TEXTBOOK OF

FORENSIC MEDICINE
AND
TOXICOLOGY
FOR MBBS
SOME OTHER BOOKS
BY SAME AUTHOR
 Forensic Medicine
AND
Toxicology
FOR MBBS

Anil Aggrawal
Director Professor
Deptt. of Forensic Medicine and Toxicology
Maulana Azad Medical College
New Delhi

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COMPANY
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AVICHAL PUBLISHING COMPANY
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Kala Amb 173 030, Distt. Sirmour (HP)
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Delhi Office:
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ISBN–978-81–7739–491–7

© Author

First Edition: 2016

Typeset at
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Printed at
Prince Print Process, Delhi

Preface
The widespread acceptance of my “Textbook of Forensic Medicine and
Toxicology” and “Essentials of Forensic Medicine and Toxicology” has led to
requests for a shorter textbook that would give just bare essentials needed for
understanding the subject and passing in exams.
In preparing the Forensic Medicine and Toxicology for MBBS, I have
rewritten content, eliminated nonessential information, and modified illustrations
in an effort to produce a comprehensive text that is shorter but equally accurate,
up-to-date, and appealing to the student. A number of new diagrams, figures and
illustrations have been included. Many more memory aids have been added, as
they were found very helpful by the students.
I am grateful to Dr. Mohit Chauhan, Senior Resident, Department of Forensic
Medicine, MAMC, who spared his valuable time to go through the entire
manuscript word by word and suggest changes. Dr. Jatin Bodwal, Specialist,
DDU hospital suggested necessary changes based on his vast experience with
UG teaching. The contributions by Dr. Bodwal on firearm injuries and asphyxia,
and by Dr. Chauhan on Identification chapters are highly appreciated.
I am thankful to the entire team of ‘Laser Tech Prints’ led by Shri Rajiv
Manchanda, who provided me with a family like atmosphere during my month
long visit to them. Special mention must be made of Shri V.K. Manchanda,
whose magnificent presence and inspiring talks always filled me up with
enthusiasm. Also worthy of praise are Ms Sangeeta Verma and Nilesh, who truly
produced what I call “Medical Art”, where a picture speaks a thousand words.
I am grateful to my publisher Dr. Vipin Gupta for reposing faith in me and going
ahead with my idea. Without his encouragement and support such a project
would never have seen the light of the day. I will always remain short of words
to pay my sincere gratitude to him.
— Author

Picture Credits

The author is thankful to the following colleagues who contributed many pictures from their vast collection.
Each picture within the text also carries the name of the contributor on the left side.
1. A. Arthy, JR, MAMC, New Delhi.
2. Abhishek Das, Upgraded Department of Forensic & State Medicine, Medical College & Hospital,
Kolkata, West Bengal.
3. Akash Meshram, Assistant Professor, Nevjabai Hitkarini College, Bramhapuri.
4. Alok Kumar, HOD Forensic Medicine and Toxicology, UP RIMS & R, Saifai 206130, Etawah, UP.
5. Anil Kumar Malik, Resident, Forensic Medicine, Pandit B.D. Sharma University of Health Sciences,
Rohtak.
6. Arun Kumar Siddamsetty, SR, MAMC, New Delhi.
7. Ashesh Gunwantrao Wankhede, Professor and Head, Forensic Medicine and Toxicology, Late Shri
Baliram Kashyap Memorial Government Medical College, Jagdalpur, Chhattisgarh-494001.
8. Ashish Bhute, Senior Resident, Maulana Azad Medical College, New Delhi-110002.
9. Avneesh Gupta, Clinical Assistant Professor, University of Michigan, Ann Arbor, MI USA.
10. Bansi Dhar Gupta, Prof. & Head, Forensic Medicine Dept., M.P. Shah Medical College, Jamnagar -
361 008.
11. Basant Lal Sirohiwal
12. Bhim Singh, Assistant Professor, Department of Forensic Medicine and Toxicology, Subharti Medical
College, Meerut, UP.
13. BN Yadav, Professor and Head, Dept. of Forensic Medicine & Toxicology, B P Koirala Institute of
Health Sciences, Dharan, Nepal.
14. Daniel E. Rusyniak, Department of Emergency Medicine, Division of Medical Toxicology, Indiana
University School of Medicine, 1050 Wishard Boulevard, Room 2200, Indianapolis, IN 46202, USA.
15. Derek Ramsay
16. Gurcan Altun, Trakya University Faculty of Medicine, Department of Forensic Medicine , TR-22030
Edirne – Turkey.
17. Henrik Elvang Jensen, Professor, Ph.D., Section of Pathology, University of Copenhagen.
18. Himmatrao S Bawaskar, Bawaskar Hospital and clinical research center, Mahad, Raigad,
Maharashtra, India 402301.
19. Hitesh Chawla, Assistant Professor, Department of Forensic Medicine, SHKM Govt. Medical College,
Nalhar, Mewat, Haryana.
20. Jagadish Rao Padubidri, District Medicolegal Consultant (Govt. Wenlock District Hospital), &
Associate Professor, Forensic Medicine and Toxicology, Kasturba Medical College, Mangalore-575001
Karnataka, India [Affiliated to Manipal University]
21. Jason Payne-James, Consultant Forensic Physician & Specialist in Forensic & Legal Medicine,
Southminster, Essex CMO 7DT, UK.
22. Jatin Bodwal, Specialist, Department of Forensic Medicine, Deen Dayal Upadhayay Hospital, Hari
Nagar, New Delhi..
23. Jean-Louis Frossard, Professor of Medicine, Head, Service of Gastroenterology and Hepatology,
Geneva University Hospital, Genève.
24. Jitendra Kumar, JR, Forensic Medicine, MAMC, New Delhi.
25. J.M. Garg
26. Jo Duflou, Clinical Director and Clinical Professor, University of Sydney, Conjoint Associate
Professor, University of NSW, Department of Forensic Medicine, Sydney, PO Box 90, Glebe NSW
2037.
27. Katsuji Nishi, Professor, Shiga University, Japan.
28. Kuldeep Panchal, Resident, Forensic Medicine, Pandit B.D. Sharma University of Health Sciences,
 Rohtak.
29. Lavlesh Kumar, Professor & Head, Department of Forensic Medicine & Toxicology, SBKS Medical
Institute and Research Centre, Piparia, Waghodia, Vadodara, Gujarat.
30. Madhumita Nandi, Associate Professor, Pediatrics, NRS Medical College, Kolkata.
31. Manivasagam M., Assistant Professor, Govt. Medical College, Omandurar Govt. Estate, Chennai.
32. Mayank Bhatnagar
33. Michael Kenneth Keng, Cleveland Clinic, 9500 Euclid Avenue, R35, Cleveland, Ohio 44195.
34. Mohit Chauhan, Senior Resident, Maulana Azad Medical College, New Delhi-110002.
35. Mukesh Sharma, In-Charge, Mobile Forensic Science Unit, Udaipur, Senior Scientific Officer (Phys.
Division), State Forensic Science Laboratory Jaipur, Rajasthan - 302 016.
36. Narendra Baluram Kumar, Assistant Professor, Department of Forensic Medicine & Toxicology,
Lokmanya Tilak municipal medical College and General Hospital, Sion, Mumbai, Maharashtra
400022.
37. Necas Pavel, Department of Linguistics, Faculty of Medicine in Hradec Králové, Charles University in
Prague, Czech Republic.
38. Nilesh K Tumram, Associate Professor, Department of Forensic Medicine, Indira Gandhi Government
Medical College, Nagpur, Maharashtra 440018.
39. N. Srinivasaragavan, Prof and Head, Dept. of Forensic Medicine, Saveetha Medical College,
Thandalam, Chennai - 602 105.
40. O. Gambhir Singh, Associate Professor, Forensic Medicine, M.A.P.I.M.S., Melmaruvathur, Tamil
Nadu.
41. Pawan Mittal, Demonstrator, Forensic Medicine, #302-D1, Medical Campus Shaheed Hasan Khan
Mewati Govt. Medical College, Nalhar (Mewat).
42. Petr Hejna, Department of Forensic Medicine, Faculty of Medicine and University Hospital in Hradec
Králové, Charles University in Prague, Czech Republic.
43. Pradeep Kumar M.V., Professor, Dept. of Forensic Medicine and Toxicology, Rajarajeswari Medical
College and Hospital, Bangalore.
44. Prateek Rastogi, Associate Professor, Dept. of Forensic Medicine & Toxicology, Kasturba Medical
College, Mangalore.
45. P. Sampath Kumar, Professor & Head, Department of Forensic Medicine, Sri Ramachandra Medical
College & Research Institute, Deemed University, Porur, Chennai - 600 116.
46. Puneet Setia, Assistant Professor, Department of Forensic Medicine, All India Institute of Medical
Sciences, Jodhpur, Rajasthan.
47. Raj Kumar, JR, MAMC, New Delhi.
48. Rattan Singh, Assistant Professor, Department of Forensic Medicine and Toxicology, Himalayan
Institute of Medical Sciences, Swami Rama Himalayan University, Ram Nagar, Jolly Grant, Dehradun
- 248016.
49. Ricardo Palao, Burn Centre, Department of Plastic Surgery and Burns, University Hospital Vall d’
Hebron, Universitat Autònoma de Barcelona, Passeig de la Vall d’hebron 119-129, 08035 Barcelona,
Spain.
50. Rishi Solanki, Senior resident, MAMC, New Delhi.
51. Ritesh G. Menezes, Professor & Head, Department of Forensic Medicine, ESIC Medical College &
PGIMSR (Ministry of Labour & Employment, Govt. of India), Bangalore.
52. Roger Byard, AO PSM, School of Medical Sciences, The University of Adelaide, Adelaide, 5005, SA,
Australia.
53. Rohit Bharti, JR, MAMC, New Delhi.
54. Rohit Goel, JR, MAMC, New Delhi.
55. Ronald Wright, 1000 Ducks Nest Road, Turtletown, TN 37391, 954-581-7952.
56. Sachin Chourasia, PG, AFMC, Pune.
57. Sanjoy Das, Professor & Head, Forensic Medicine & Toxicology & Dy. Dean (UG Studies), HIHT
University, Jolly Grant, Dehradun, Uttarakhand.
58. Shiv Ratan Kochar, Professor and HOD, Dept. of Forensic Medicine, Medical College, Udaipur.
59. Suresh, Assistant Professor, Rama Medical College, Hapur.
60. Suresh Kumar Dhattarwal, HOD, Forensic Medicine, Pandit B.D. Sharma University of Health
Sciences, Rohtak.
61. Suresh Selvi Savior, Professor, Forensic Medicine Dept. Velammal Medical College, Madurai.
62. Swapnil S Agarwal, Professor and Head, Department of Forensic Medicine and Toxicology,
Pramukhswami Medical College and Shree Krishna Hospital, Anand, Gujarat.
63. Tanuj Kanchan, Associate Professor, Department of Forensic Medicine, Kasturba Medical College,
Mangalore.
64. Tarun Dagar, Resident, PGIMS, Rohtak.
65. T.K. Bose, Head, Forensic Medicine, Calcutta National Medical College, Gorachand Road, Kolkata-
700014.
66. Verica Poposka, Institute for Forensic Medicine, Criminalistics and medical deontology, Medical
faculty, Ss. Cyril and Methodius University, Skopje, R. Macedonia.
67. Viswakanth Bhagavathula, Assistant Professor, Department of Forensic Medicine & Toxicology, P.K
DAS Institute of Medical Sciences [PKDIMS], Vaniamkulam, Ottapalam.
68. Yogesh Kumar Vashist, Demonstrator, Deptt. of Forensic Medicine, SHKM Govt. Medical College,
Nalhar, Mewat.

Abbreviations used in this Book

1. Ac – Acute
2. BAC – Blood alcohol concentration
3. BV – Blood Vessels
4. cf – confer, compare
5. Ch – Chronic
6. COD – Cause of Death
7. D/b – Differentiate between
8. d/t – due to
9. E/m – Electron microscopy
10. Ex – Example
11. FD – Fatal Dose
12. FP – Fatal Period
13. H/P – Histopathology
14. HR – Heart rate
15. ICP – Intracranial Pressure
16. k/a – Known as
17. Lit – Literally
18. MAC – Maximum allowable concentration
19. MC – Most Common
20. MLI – Medicolegal Importance
21. MOA – Mechanism of Action
22. PChE – Plasma cholinesterase
23. PMI – Postmortem Interval
24. ppb – Parts per billion
25. ppm – Parts per million
26. PO – Per Orally
27. Pt – Patient
28. SI – Simple Imprisonment
[no work allotted to prisoner]
29. RI – Rigorous Imprisonment
[work allotted to prisoner]
30. RR – Respiratory rate
31. S & S – Signs and symptoms
32. Symb – Symbol [of chemical]
33. Syn – Synonym
34. TLV – Threshold Limit Value
35. TSD – Time since Death
36. w.e.f. – With effect from
37. w.r.t. – With respect to
 Memory Aids and Mnemonics Index

S.N. Chp. Memory Aid for Page

1. 1 MA 1: Public prosecutor 5
2. 1 MA 2: Police Inquest 6
3. 1 MA 3: Summons Cases 16
4. 2 MA 1: Declaration of Sydney 21
5. 2 MA 2: Declaration of Oslo 21
6. 2 MA 3: Declaration of Tokyo 21
7. 2 MA 4: Defenses against negligence 33
8. 2 MA 5: Consent of spouse 35
9. 2 MA 6: What makes a consent valueless 36
10. 2 MA 7: Declaration of Helsinki 37
11. 3 MA 1: Cusp of Carabelli 42
12. 3 MA 2: Sex related indices 43
13. 3 MA 3: How to remember indices 44
14. 3 MA 4: Racial differences in cephalic index 44
15. 3 MA 5: Feulgen reaction 47
16. 3 MA 6: Feulgen reaction 47
17. 3 MA 7: Quinacrine staining 47
18. 3 MA 8: Medicolegal and anatomical angles
of mandible 49
19. 3 MA 9: Indices relating to sacrum 52
20. 3 MA 10: Angulation of shaft with condyles
(femur) 53
21. 3 MA 11: Eruption of temporary teeth 54
22. 3 MA 12: Eruption of permanent teeth 54
23. 3 MA 13: Calcification of permanent teeth 55
24. 3 MA 14: Ossification centers of lower end of
humerus 56
25. 3 MA 15: Ossification centers of radius and
ulna 58
26. 3 MA 16: Ossification centers of tibia and
fibula 58
27. 3 MA 17: Ages of fusion in some major bones 58
28. 3 MA 18: Ossification centers of sternum 59
29. 3 MA 19: Carpal bones 60
30. 3 MA 20: Appearance of body hair 61
31. 3 MA 21: Causes of Gynecomastia 62
32. 3 MA 22: Age of fetus 63
33. 3 MA 23: Rule of Haase 64
34. 3 MA 24: - in infant length 64
35. 3 MA 25: Infant measurements 64
36. 3 MA 26: - in infant weight 64
37. 3 MA 27: Gustafson’s Method 65
38. 3 MA 28: Major ossification centers
appearing during IU life 67
39. 3 MA 29: Closure of fontanelles 67
40. 3 MA 30: Skull suture closure 68
41. 3 MA 31: Circle of 2 68
42. 3 MA 32: MLI of age 71
43. 3 MA 33: Section of Railways Act 1989,
denoting age of criminal
responsibility 71
44. 3 MA 34: Growth phases of hair 74
45. 3 MA 35: Age of scars 79
46. 3 MA 36: Fingerprint patterns 84
47. 3 MA 37: Natural causes of alteration of
fingerprints 85
48. 3 MA 38: Modified FDI notation 91
49. 6 MA 1: Remembering multiplication
formulae 112
50. 8 MA 1: Causes of suspended animation 118
51. 9 MA 1: IOP after death 127
52. 9 MA 2: Order of putrefaction 137
53. 9 MA 3: Poisons which are destroyed by
putrefaction 139
54. 9 MA 4: Poisons which appear due to
putrefaction 139
55. 9 MA 5: Casper’s Dictum 139
56. 9 MA 6: Composition of a typical
embalming fluid 140
57. 9 MA 7: S.107, IEA 143
58. 11 MA 1: Definition of Injury 146
59. 11 MA 2: Definition of hurt 148
60. 11 MA 3: Definition of Grievous hurt 148
61. 11 MA 4: Histochemistry of wounds 155
62. 12 MA 1: Pressure abrasions 158
63. 12 MA 2: Age of bruise 163
64. 12 MA 3: Substances used for producing
artificial bruise 165
65. 13 MA 1: Composition of primer 185
66. 13 MA 2: Burning, blackening and tattooing
in various firearms 190
67. 13 MA 3: Relative distances of various
effects of firearms 190
68. 13 MA 4: Zones of rifle firearm entry wound 196
69. 14 MA 1: Coagulation temperature of
proteins 213
70. 15 MA 1: Marshall triad 223
71. 16 MA 1: Cause of death in electrocution 225
72. 17 MA 1: Age determination of antemortem
tooth loss 234
73. 17 MA 2: Thickness of skull bones 234
74. 17 MA 3: Gutter fracture 237
75. 17 MA 4: Theories of countercoup injuries 240
76. 19 MA 1: Classical signs of asphyxia 265
77. 19 MA 2: Manner of death: hanging and
strangulation 280
78. 21 MA 1: Fatal blood concentrations of
anesthetics 309
79. 23 MA 1: Organic causes of impotence 318
80. 23 MA 2: Quantity of semen 319
81. 24 MA 1: Female genital anatomy 330
82. 24 MA 2: Indications of PNDT 339
83. 24 MA 3: Preconditions for PNDT 339
84. 25 MA 1: 4 acts required for rape 346
85. 25 MA 2: Explanations and Exceptions to
S.375 IPC 347
86. 25 MA 3-15: Current definition of rape
and its punishment 349-350
87. 25 MA 16: Important sections of IEA 351
88. 25 MA 17: 4 most important sections for rape 352
89. 25 MA 18: Important components of medical
examination of rape victim 353
90. 25 MA 19: 6 components of report of rape
victim 354
91. 25 MA 20: Ano-genital injuries in rape 357
92. 25 MA 21: Tests for Semen 378
93. 26 MA 1: Stages in fetal life 380
94. 26 MA 2: Indications of MTP 382
95. 26 MA 3: Methods of Criminal Abortion 383
96. 27 MA 1: Lecithin levels and lung maturity 393
97. 27 MA 2: Position of diaphragm before and
after respiration 394
98. 27 MA 3: Foderê and Ploucquet’s tests 395
99. 27 MA 4: Changes in umbilical cord 399
100. 27 MA 5: Order of closure of fetal structures 399
101. 27 MA 6: Umbilical vein 399
102. 27 MA 7: Umbilical artery 399
103. 28 MA 1: Fregoli Syndrome 411
104. 28 MA 2: Clérambault-Kandinsky Syndrome 411
105. 28 MA 3: Cotard Syndrome 411
106. 28 MA 4: Modern and older classification of
subnormal IQs 413
107. 28 MA 5: Imbecile 413
108. 29 MA 1: O-toluidine test 427
109. 29 MA 2: Presumptive tests for blood 427
110. 29 MA 3: Hemochromogen crystal test 428
111. 30 MA 1: Forensic applications of UV light 440
112. 30 MA 2: Forensic applications of IR light 440
113. 31 MA 1: 6 important Schedules under The
Drugs and Cosmetic Rules, 1945 444
114. 31 MA 2: Hepatotoxic drugs 448
115. 31 MA 3: Hepatotoxic drugs 448
116. 31 MA 4: Poisons causing PCT necrosis 448
117. 31 MA 5: Poisons causing DCT necrosis 448
118. 31 MA 6: General Nephrotoxic agents 448
119. 31 MA 7: Major questions to ask in
poisoning cases 449
120. 32 MA 1: ABCDE of resuscitation 460
121. 32 MA 2: Best motor response in Glasgow
coma scale-1 460
122. 32 MA 3: Best motor response in Glasgow
coma scale-2 460
123. 32 MA 4: Criteria used in Glasgow coma
scale 460
124. 32 MA 5: Other resuscitative measures in
poisoning 461
125. 32 MA 6: Urine alkalinization is useful in 466
126. 32 MA 7: Urine acidification is useful in 467
127. 32 MA 8: Hemodialysis is useful in 467
128. 32 MA 9: Hemodialysis is not useful in 467
129. 32 MA 10: Drugs and Poisons NOT adsorbed
by activated charcoal 468
130. 32 MA 11: Poisoning in which activated charcoal
is not helpful/contraindicated 469
131. 32 MA 12: Indications of BAL 470
132. 32 MA 13: Indications of D-Penicillamine 471
133. 32 MA 14: Composition of coma cocktail 472
134. 33 MA 1: Liquefaction necrosis 476
135. 33 MA 2: Coagulative necrosis 476
136. 33 MA 3: Ochronosis 483
137. 34 MA 1: Allotropes of Phosphorus 490
138. 35 MA 1: Anionic site 494
139. 35 MA 2: Esteratic site 494
140. 35 MA 3: Symptoms of OP Poisoning 495
141. 35 MA 4: Signs and symptoms of OPIDP 499
142. 36 MA 1: Arsenic poisoning [main points] 509
143. 36 MA 2: Lab findings in Pb Poisoning 518
144. 36 MA 3: Main features of chronic lead
poisoning 520
145. 36 MA 4: Symptoms of ch Hg poisoning 526
146. 38 MA 1: Signs and symptoms of cobra bite 543
147. 38 MA 2: Fatal doses of venoms from lowest
to highest 548
148. 38 MA 3: MOA of scorpion venom-I 549
149. 38 MA 4: MOA of scorpion venom-II 549
150. 38 MA 5: Signs and symptoms of scorpion
stings 549
151. 38 MA 6: Main drugs in scorpion stings 550
152. 39 MA 1: Meixner test 555
153. 40 MA 1: Concentrations of various forms of
alcohol 560
154. 40 MA 2: Pupils in alcohol poisoning at the
 stage of excitement 564
155. 40 MA 3: McEwen sign 564
156. 40 MA 4: Alcohol intoxication in relation of
blood concentration 565
157. 40 MA 5: Confirmation of ethyl alcohol
poisoning 565
158. 40 MA 6: Alpha alcoholism 566
159. 40 MA 7: Gamma alcoholism 566
160. 40 MA 8: Epsilon alcoholism 567
161. 40 MA 9: Korsakoff’s psychosis 569
162. 40 MA 10: Wernicke’s encephalopathy 569
163. 40 MA 11: Toxicity of methanol metabolites 576
164. 40 MA 12: How to differentiate opioids
from opiates 580
165. 40 MA 13: Major symptoms of barbiturate
poisoning 591
166. 41 MA 1: Datura’s signs and symptoms 597
167. 41 MA 2: Reuptake of biogenic amines
blocked by cocaine 604
168. 41 MA 3: Main side-effect of cocaine 604
169. 44 MA 1: Classification of war gases and
riot control agents 637
170. 44 MA 2: Major nerve gases (paralysants) 639
171. 46 MA 1: Signs and symptoms of PCP
poisoning 656
172. 47 MA 1: Understanding oxidation at atomic
level 663
173. 47 MA 2: Methylene Blue 663
174. App1 MA 1: S.363, 366 and 369: Most imp
sections related to kidnapping 666
175. App1 MA 2: S.497, IPC 666
176. App1 MA 3: S.164A, CrPC 667
177. App1 MA 4: Two important sections are
consecutive numbers 667

Index of Tables
S. No. Chapter Page No.
Chp 1: Introduction and Legal Procedure
1. Table 1: Various types of inquests 6
2. Table 4: Powers of criminal courts 8
Chp 2: Medical Law and Ethics
3. Table 1: Functions of the Indian Medical Council 17
4. Table 2: Functions of State Medical Councils 18
5. Table 4: Types of negligence 27
Chp 3: Identification
6. Table 1: Important Identification data 41
 7. Table 3: Various important indices and their application in forensic medicine 44
8. Table 5: Long bone Indices in different races 44
9. Table 7: Classification of intersex 45
10. Table 8: Various cellular level tests for male and female features 48
11. Table 20: Accuracy in sexing adult skeletal remains 53
12. Table 21: Ages of calcification and eruption of deciduous teeth 55
13. Table 22: Ages of calcification and eruption of permanent teeth 55
14. Table 23: Number of teeth in relation to age 55
15. Table 24: Ossification of lower end of humerus 56
16. Table 25: Age of fetus 63
17. Table 26: Major ossification centers appearing during IU life 67
18. Table 27: Ages of skull suture closure 68
19. Table 30: Human hair characteristics from various body parts 76
Chp 5: Medicolegal Autopsy
20. Table 2: Viscera to be preserved according to poisoning 107
Chp 8: Thanatology, Death and Its Causes
21. Table 1: Harvard Criteria of the moment of death 120
22. Table 3: Bichat’s modes of death, based on his concept of tripod of life 123
Chp 9: Signs of Death and Changes Following Death
23. Table 1: Various colors of PM Staining and associated cause of death 129
24. Table 6: Life cycle of Musca domestica (housefly) 142
Chp 10: Artifacts
25. Table 1: Classification of artifacts 144
Chp 11: Injuries: Classification and Medicolegal Aspects
26. Table 1: Classification of Homicide 147
27. Table 2: Types of homicide according to decreasing culpability 147
28. Table 3: Age estimation of wound by histochemistry 154
29. Table 4: Immunohistochemical determination of age of wound 155
Chp 12: Mechanical Injuries
30. Table 2: Age of bruise 163
S. Page
Chapter
No. No.
Chp 13: Firearm Injuries
31. Table 1: Classification of firearms 181
32. Table 2: Some important figures regarding firearms 184
Table 3: Table showing how burning, blackening and tattooing are produced and how best they can be
33. 190
detected
Table 4: A simple mnemonic to remember commonly accepted ranges of burning, blackening and
34. 190
tattooing in various firearms
35. Table 5: Various conventional ranges and associated effects 190
36. Table 6: Odd and even rule 200
Chp 16: Electrical Injuries, Atmospheric Lightning, Radiation Injury
37. Table 1: Effects of various amounts of AC and DC on human body 224
38. Table 2: Electrical resistance of skin 225
39. Table 4: The Distance An Electric Arc Can Jump 227
Chp 17: Regional Injuries
40. Table 1: Coup and Countercoup Contusions 241
41. Table 2: Theories of Countercoup Injuries 241
Chp 19: Asphyxia
42. Table 2: Types of strangulation 276
Chp 20: Starvation
43. Table 1: Factors influencing fatal period in starvation 307
Chp 21: Deaths Associated with Anaesthesia and Surgery
44. Table 1: Causes of General Anesthetic and operative deaths 309
Chp 22: Deaths Due to Cold and Heat
45. Table 1: Stages of hypothermia and associated major effects on human body 312
46. Table 2: Characteristics of cold injury 313
Chp 23: Impotence and Sterility
47. Table 1: Nomenclature related to pathological semen quality according to WHO 319
48. Table 2: Five conditions of a valid Hindu marriage under the HMA, 1955 320
49. Table 3: Salient Differences between AIH and AID 326
Chp 24: Virginity, Pregnancy and Delivery
50. Table 2: Relationship between hymen and sexual intercourse 332
51. Table 4: Important Medicolegal dates (from LMP) 335
52. Table 5: Timings of immunological tests 336
53. Table 8: Uterus and placental site dimensions after delivery 342
Chp 25: Sexual Offences
54. Table 1: 4 possible acts and 4 possible penetrations in cases of rape 346
55. Table 2: Situations where sexual intercourse with consent is an offence 350
56. Table 3: Situations where sexual intercourse without consent is not an offence 350
57. Table 4: Situations where sexual intercourse with wife is an offence (marital rape) 350
Chp 26: Abortion
58. Table 1: Table illustrating various IPC sections related to criminal abortion 381
Chp 27: Infant Deaths Including Battered Baby Syndrome
59. Table 5: Circulation changes in a newborn 399
Chp 28: Forensic Psychiatry
60. Table 2: Modern classification of subnormal IQs compared with older system 413
61. Table 3: Classification of various supernormal IQs 413
62. Table 5: New terms used by the Mental Health Act, 1987 414
S. Page
Chapter
No. No.
63. Table 6: S.4.01 of MPC [ALI test] 421
Chp 29: Blood and Biological Stains
64. Table 1: Characteristic blood proteins with functions and genes coding for them 429
65. Table 2: Possible and impossible blood phenotypes of children if phenotypes of parents are known 429
Table 3: Expected chance of excluding a man wrongly accused of paternity by means of blood groups
66. 430
and HLA
Chp 31: Introduction, Classification of Poisons, Law Relating to Poisons and General
onsiderations
67. Table 2: Diagnosis of poisoning in the living 449
68. Table 3: Causes of Acute Abdomen Due to Poisoning 450
69. Table 4: Poisons causing vomiting and diarrhea 450
70. Table 5: Drugs and Poisons causing constipation 450
71. Table 6: Poisons Causing tremors 450
72. Table 7: Agents that cause convulsions and seizures 450
73. Table 8: Poisons and diseases/ailments mimicked by them 450
74. Table 9: Poisons causing hypotension 451
75. Table 10: Poisons causing hypertension 451
76. Table 11: Poisons causing bradycardia 451
77. Table 12: Poisons causing tachycardia 451
78. Table 13: Poisons causing Cardiac Arrhythmias 451
79. Table 14: Poisons causing Miosis 452
80. Table 15: Poisons causing Mydriasis 452
81. Table 16: Poisons causing Nystagmus 452
82. Table 17: Poisons causing bradypnea 452
83. Table 18: Poisons causing tachypnea 452
84. Table 19: Poisons causing hypothermia 453
85. Table 20: Poisons causing hyperthermia 453
86. Table 21: Some possible causes of colored urine 453
87. Table 22: A select list of radiopaque drugs and poisons 455
88. Table 23: Diagnosis of poisoning in the dead 455
89. Table 24: Poisons that can be detected by smell 456
90. Table 25: Color changes in the mucus membrane of the stomach in various poisonings 457
Chp 32: General Principles of Management
91. Table 1: Broad guidelines to follow in treatment of poisoning 460
92. Table 2: Glasgow coma scale 460
93. Table 3: Matthew-Lawson Scale of determining severity of Coma 461
94. Table 4: Solutions used for gastric lavage against different poisons 464
95. Table 5: Classification of antidotes based on the site of action 468
96. Table 6: Drugs and Poisons NOT adsorbed by activated charcoal 468
97. Table 7: Contraindications of activated charcoal 469
98. Table 8: Some common antidotes and poisons against which they are used 473
Chp 35: Agricultural Poisons
99. Table 1: Normal RBC and Plasma Cholinesterase activity in men and women 496
100. Table 2: Cholinesterase levels co-related with severity of poisoning 496
101. Table 3: Some carbamates according to their toxicity 499
Chp 36: Metallic Irritants
102. Table 2: A simple mnemonic to remember main features of chronic lead poisoning 520
S. No. Chapter Page No.
Chp 38: Animal Poisons
103. Table 4: Efficacy of PAV 547
104. Table 5: Fatal dose and total yield of venom in various snakes 548
Chp 40: CNS Depressants
105. Table 1: Some common alcoholic beverages and their alcoholic content 561
106. Table 2: Various conditions when absorption of alcohol is increased or decreased 561
107. Table 3: Ratio of Blood alcohol concentration and various body organs/fluids at equilibrium 562
108. Table 4: Alcohol intoxication in relation of blood concentration 565
109. Table 5: Fatal doses of some common opioids 582
110. Table 6: Classification of Barbiturates 590
Chp 41: Deliriant Poisons
111. Table 1: Botanical and common names of some common deliriant plants 596
Chp 44: Asphyxiants and Toxic Gases
112. Table 1: Symptoms of CO poisoning 625
113. Table 2: Classification of war gases and riot control agents 637

“Differentiate between” Index

S. No. Chapter Page No.
Chp 1: Introduction and Legal Procedure
1. Table 2: Differences between police, executive magistrate and Judicial magistrate’s inquests 7
2. Table 3: Differences in Coroner’s and Magistrate’s court 7
3. Table 5: Differences between a cognizable and non-cognizable offence 9
4. Table 6: Differences between dying declaration and dying deposition 12
5. Table 7: Differences between a common witness and expert witness 13
Chp 2: Medical Law and Ethics
6. Table 3: Differences between Professional Negligence and Professional Misconduct 27
7. Table 5: Differences between Active and passive euthanasia 34
Chp 3: Identification
8. Table 2: Racial differences in skeleton in various races 43
9. Table 4: Racial differences in cephalic index 44
10. Table 6: Sex differences in male and female sex 45
11. Table 9: General sex differences in human skeleton 48
12. Table 10: Sex differences in human skull 48
13. Table 11: Sex differences in human mandible 49
14. Table 12: Sex differences in human pelvis 50
15. Table 13: Sex differences in the human sacrum 52
 16. Table 14: Sex differences in the human sternum 52
17. Table 15: Sex differences in human ribs 53
18. Table 16: Sex differences in human thoracic bones 53
19. Table 17: Sex differences in human vertebral column 53
20. Table 18: Sex differences in human femur 53
21. Table 19: Sex differences in human scapula 53
22. Table 28: Differences in mandible in infancy, adult life and old age 69
23. Table 29: Differences between human and animal hair 76
24. Table 31: Sex differences in Teeth 89
Chp 5: Medicolegal Autopsy
25. Table 1: Differences between antemortem and postmortem clots 101
Chp 8: Thanatology, Death and Its Causes
26. Table 2: Differences between 3 major criteria of death 121
Chp 9: Signs of Death and Changes Following Death
27. Table 2: Differences between PM Staining and true congestion 129
28. Table 3: Differences between rigor mortis and cadaveric spasm 133
29. Table 4: Differences between Primary and secondary relaxation 134
30. Table 5: Differences between Putrefaction and gangrene 135
Chp 11: Injuries: Classification and Medicolegal Aspects
31. Table 5: Differences between antemortem and postmortem wounds 156
S. Page
Chapter
No. No.
Chp 12: Mechanical Injuries
32. Table 1: Differences between antemortem and postmortem abrasions 160
33. Table 3: Differences between an antemortem and postmortem bruise 164
34. Table 4: Differences between true and artificial bruise 165
35. Table 5: Differences between PM Staining and bruise 166
36. Table 6: Differences between an incised and incised looking lacerated wound 168
37. Table 7: Differences between a true incised and true lacerated wound 168
38. Table 8: Different types of lacerations and how they are typically caused 169
39. Table 9: Differences between suicidal and homicidal cut throat 173
40. Table 10: Differences between suicidal, homicidal and accidental stab wounds 176
41. Table 11: Differences between incised, lacerated and stab wounds 177
42. Table 12: Differences between suicidal, homicidal and accidental wounds 179
Chp 13: Firearm Injuries
43. Table 7: Difference between entry and exit wounds of a rifled firearm 200
44. Table 8: Differences between suicidal, accidental and homicidal firearm wounds 207
Chp 14: Thermal Injuries
45. Table 1: Differences in surface areas of adult and children 211
46. Table 2: Differences between pugilistic attitude and rigor mortis 214
47. Table 3: Differences between heat rupture and lacerated wound 215
 48. Table 4: Differences between heat hematoma and extradural hematoma 216
49. Table 5: Difference between Antemortem and postmortem burns 219
50. Table 6: Differences between burns due to dry heat, moist heat and chemicals 221
Chp 16: Electrical Injuries, Atmospheric Lightning, Radiation Injury
51. Table 3: Differences between antemortem and postmortem electrocution 227
Chp 17: Regional Injuries
52. Table 3: Differences between Drunkenness and concussion 244
53. Table 4: Differences between infarction due to SDH and stroke 250
54. Table 5: Differences between extradural, subdural and subarachnoid hemorrhage 253
Table 6: Differences between Post-traumatic intracerebral hemorrhage and spontaneous cerebral
55. 254
hemorrhage
56. Table 7: Differences between AM and PM fractures 256
Chp 19: Asphyxia
57. Table 1: Differences between antemortem hanging and postmortem suspension 275
58. Table 3: Differences between Hanging and strangulation 278
Table 4: Differences between homicidal strangulation and accidental strangulation by umbilical cord in
59. 280
infants
60. Table 5: Differences between suicidal and homicidal strangulation 281
61. Table 6: Differences between choking and café coronary 291
62. Table 7: Differences between fresh water and sea water drowning 294
63. Table 8: Differences between Emphysema aquosum and Edema aquosum 298
Table 9: Differences between accidental drowning, suicidal drowning, homicidal drowning and
64. 304
postmortem submersion
Chp 22: Deaths Due to Cold and Heat
65. Table 3: Differences between rigor mortis and cold stiffening 313
Chp 24: Virginity, Pregnancy and Delivery
66. Table 1: Differences between fimbriated and ruptured hymen 331
67. Table 3: Differences between True and a False virgin 333
S. No. Chapter Page No.
68. Table 6: Differences between superfecundation, superfetation and twins 340
69. Table 7: Differences between an affiliation case and a case involving suppositious child 341
70. Table 9: Differences in the uterus of nulliparous and Parous women 343
Chp 25: Sexual Offences
71. Table 5: Differences between cervical abrasions and cervical erosions 359
Chp 26: Abortion
72. Table 2: Differences between natural and criminal abortion 390
Chp 27: Infant Deaths Including Battered Baby Syndrome
73. Table 1: Differences between medical and legal definition of infanticide 391
74. Table 2: Differences between a stillborn and a dead born fetus 392
75. Table 3: Differences in lungs before and after respiration 394
76. Table 4: Differences between caput succedaneum and cephalhematoma 398
77. Table 6: Differences between head injury due to precipitate labor and blunt force 400
 Chp 28: Forensic Psychiatry
78. Table 1: Differences between lucid interval of head injury and insanity 413
79. Table 4: Difference between true insanity and feigned insanity 414
Chp 29: Blood and Biological Stains
80. Table 4: Different types of satellite DNA 432
81. Table 5: Differences between RFLP and STR analysis which uses PCR 436
Chp 31: Introduction, Classification of Poisons, Law Relating to Poisons and General Considerations
82. Table 1: Differences between an ideal homicidal and ideal suicidal poison 446
83. Table 26: Differences in ulcerations due to corrosives and those due to disease 457
84. Table 27: Differences in perforation due to corrosives and due to pm autolysis 457
Chp 33: Corrosives
85. Table 1: Differences between oxalic acid, MgSO4 and ZnSO4 484
Chp 34: Non-Metallic Irritants and Mechanical Irritants
86. Table 1: Differences between two most common allotropes of phosphorus 490
Chp 36: Metallic Irritants
87. Table 1: Differences between Arsenic poisoning and Cholera 508
Chp 37: Vegetable Poisons
88. Table 1: Differences between castor and croton seeds 533
Chp 38: Animal Poisons
89. Table 1: Difference between venomous and non-venomous snakes 539
90. Table 2: Difference between Cobra and Viper 541
91. Table 3: Differences between a elapid and a viperine bite 544
Chp 41: Deliriant Poisons
92. Table 2: Differences between Datura and Chili seeds 596
Chp 42: Spinal and Peripheral Nerve Poisons
93. Table 1: Differences between Strychnine poisoning and Tetanus 609
Chp 43: Cardiac Poisons
94. Table 1: Differences between root of aconite and root of horseradish 614
Chp 46: Drug Dependence and Abuse
95. Table 1: Difference between drug habituation and drug addiction 645

1. Introduction and Legal Procedure

I. INTRODUCTION
A. Forensic Medicine
Forensic medicine, Legal medicine or State medicine is the application of
medical knowledge for the purposes of law and administration of justice.
Briefly: Medicine (as applied to) Law.

B. Medical Jurisprudence
Medical jurisprudence [Latin juris, law; prudentia knowledge] is the study of
legal principles that guide medical personnel. Briefly:
Law (as applied to) Medical personnel

C. Medical Ethics
Medical ethics is the study of moral principles guiding medical men in their
dealings with their patients.
Salient features:
Graphically: Doctor Patient

D. Medical Etiquette
Medical etiquette deals with the conventional laws of courtesy observed
between members of medical profession. Or graphically:
Doctor Doctor
Violation of medical etiquette is NOT punishable under law.

II. LEGAL PROCEDURE

A. Civil Law
Deals with disputes between two private individuals or parties. Ex. Doctor D
negligently places tight plaster over patient P’s leg. Patient’s leg is paralyzed. He
brings a suit against the doctor for compensation of `10 lakhs. Patient is plaintiff;
doctor is defendant. Case is cited as P vs. D [please compare with example given
under criminal law].

B. Criminal Law
Deals with offences, which are against public interest (e.g. offences against the
person, property, public safety, security of state etc).

(1) Fundamental purpose of criminal law – is to punish those individuals who

commit crimes [as contrasted to the fundamental purpose of civil law, which is
to grant compensation to the affected individual].
(2) Civil case vs. criminal case – Civil case is a private fight between two
individuals [e.g. patient and doctor]; criminal case is a fight between the State
and the individual [e.g. State trying to prosecute a doctor].

C. Public Prosecutor
Public prosecutor [PP] is the lawyer of the state, and is the person in-charge of
prosecutions [S.2(u), CrPC].
Memory Aid 1: Public prosecutor
S.2(u)-public prosecutor

(1) Duties - He represents the State in all prosecutions.

D. Statutory Law
Law duly passed by legislature. Ex. According to S.375 IPC, sexual intercourse
with a girl under 18 years of age – even with her consent - is rape. This is called
statutory rape.

III. INQUEST

An inquest is an enquiry or investigation into the cause of death.

A. Types
There are six types of inquests (Table 1).
1. Police inquest
Police inquest refers to inquest held by a police officer.
Salient features:
(1) held u/s174, CrPC.
(2) IO- Generally the officer-in-charge of a Police Station (SHO or Station
House Officer) or Police Post conducts inquest. He is usually of the rank of
sub-inspector (SI), but no such rank has been specified in S.174, CrPC. Police
officer conducting the inquest is known as the Investigating Officer (IO).
(3) Most common type of inquest in India.
(4) Inferior to Magistrate’s inquest, because police officer is less qualified than
magistrate.
Memory Aid 2: Police Inquest
Police inquest is Poor
a. Procedure
(1) Whenever officer in-charge of a police station receives information that a
suspicious death has occurred somewhere, he immediately informs to the
nearest Executive Magistrate.
(2) Then he (IO) proceeds to the place where the body of dead person is lying.
(3) In the presence of two or more respectable persons (panchas, panch
witnesses or panchayatdars; so called because originally there used to be 5
people) makes an investigation and draws up a report of the apparent cause of
death. He describes such wounds, fractures, bruises and other marks of injury
as may be found on the body. He states how and with what weapon such
marks could have been produced.
(4) Power to summon people - Police officer may summon any person to
answer questions related to crime u/s 175, CrPC. Refusal to answer punishable
u/s 179, IPC. (6 months and/or `1000).
(5) Inquest report – The report thus prepared is called the inquest report
(panchanama), and is signed by IO and panchas.
(6) Disposal - If no foul play is suspected, body is handed over to the relatives
for disposal; if foul play is suspected, body is sent for postmortem.
(7) In both cases, the inquest report is forwarded to the District Magistrate (DM)
or Sub divisional Magistrate (SDM).

2. Magistrate’s inquest
a. Executive Magistrate’s inquest
Executive Magistrate’s [EM] inquest refers to inquest held by an executive
magistrate.
Salient features:
(1) Executive Magistrates empowered to hold inquests are: (i) District
Magistrate [DM] (ii) Additional District Magistrate [ADM] (iii) Sub-
divisional Magistrate [SDM] (iv) Special Executive Magistrate (v) Collector
(vi) Sub Collector (vii) Deputy Collector (viii) Deputy Commissioner (ix)
Revenue Divisional Officer [RDO] (x) Tahsildar and (xi) any other executive
magistrate empowered by the State Govt or DM [S.20, CrPC to S.23, CrPC;
S.174(4), CrPC].
(2) It is held u/s176(1), CrPC.
(3) Held in cases of (i) suicide of a woman within 7 years of marriage (ii) death
of a woman within 7 years of marriage in any circumstances raising a
suspicion that some other person has committed an offence in relation to such
woman [homicide etc] (iii) Exhumation.
(4) Presence of relatives - Wherever practicable, the magistrate shall inform the
relatives of the deceased whose names and addresses are known, and shall
allow them to remain present at the inquiry [S.176(4), CrPC].
(5) Imp points – It is erroneous to say that magistrate’s inquest is held in dowry
deaths [S.304B, IPC] cases. If a woman commits suicide within 7 y of
marriage, and there is no allegation of dowry, legally it is not dowry death [ch
11], yet inquest would be done by an executive magistrate.
b. Judicial Magistrate’s inquest
Judicial Magistrate’s [JM] inquest refers to inquest held by a judicial
magistrate.
Salient features:
(1) Judicial magistrate’s inquest is held u/s176(1A) of the CrPC in cases of (i)
death or disappearance of any person (a) in police custody or (b) in any other
custody authorized by magistrate or court [S.176(1A), (a)] [jail, children’s
remand home, psychiatric hospital, psychiatric nursing home etc]. Officers
empowered to hold inquests under this section are judicial magistrates and
metropolitan magistrates [both are judicial officers and trained in law]. (ii)
rape is alleged to have been committed on any woman, while in police custody
or any other custody [as above]. Death may occur even outside custody
[S.176(1A), (b)].

3. Coroner’s inquest
Currently held in - Coroner’s inquest is currently held in Australia, Canada,
UK, some states in USA and in some other countries, but not in India. During
British rule, coroner’s inquest was held in India under the Coroner’s Act, 1871.
After gaining independence, India gradually did away with the British system.
By 1977, only the cities of Kolkata and Mumbai were having Coroner’s inquest.
Since April 1978, coroner’s system has been abolished in Kolkata and since 29
July 1999 in Mumbai.

4. Procurator fiscal system

Same as the Coroner system. The coroner is called Procurator Fiscal in Scotland.

5. Medical examiner system

In medical examiner system, an official who is both legally and medically
qualified (known as the medical examiner) conducts an inquest as well as the
postmortem examination.
Salient features:
(1) Best system - Considered the best system, as the same person visits scene of
death [to conduct inquest] and conducts autopsy. Thus there is no loss of
 information.
(2) Followed in - USA (first introduced in 1877, in Massachusetts).

IV. INVESTIGATION OF THE SCENE OF DEATH

Duties of Forensic Pathologist at the Scene of Death

Record -
(1) Date, time [of arrival and departure from scene], address, location
(2) Sketching - (a) Useful, especially when pathologist wants to record own
notes, e.g. Distance of weapon from body, depth of water level at the site of
drowning etc [Fig 1.1] (b) Make to uniform scale. Be careful to accurately
note relative distances and measurements. (c) At a corner of sketch record
directions [N-S].
V. JURY
A jury is a sworn group of responsible, educated people of good social position,
who assist the judge in deciding a case.

VI. COURTS OF LAW

Courts of law are of two types:
(1) Civil and
(2) Criminal. There are 4 tiers of courts – Supreme court, high court, sessions
court and judicial magistrates court.

A. Supreme Court
It can try all kinds of criminal offences, and it can pass any sentence authorized
by law, including the death sentence [Article 134 Constitution of India].

B. High Court
Same as that of SC. [S.28(1) of the CrPC].

C. Sessions Court
6 levels of officers sit here [3 kinds of Judges and magistrates each). Powers –
Table 4.

D. Judicial Magistrates Court

Pl. see Table 4.
VII. OFFENCE
The word offence is defined slightly differently in IPC and CrPC. (A) The word
“Offence” denotes a thing made punishable by the Indian Penal Code [S.40,
IPC].(B) ”Offence” means any act or omission made punishable by any law for
the time being in force [S.2(n), CrPC].

Classification
Offence may be classified as following.

1. Cognizable or non-cognizable
This classification takes into account whether police can arrest without warrant
or not.
a. Cognizable offence
Cognizable offence means an offence for which, a police officer may arrest
without warrant. [S.2(c), CrPC]. Examples (IPC sections are mentioned within
brackets): (i) Murder [S.302] (ii) Causing death by rash or negligent act
[S.304A] (iii) Dowry death [S.304B] (iv) Abetment of suicide [S.306].

b. Non-cognizable offence
Non-cognizable offence means an offence for which, a police officer has no
authority to arrest without warrant.[S.2(l), CrPC]. Examples– (i) Causing
miscarriage with woman’s consent [S.312, IPC], (ii) Voluntarily causing hurt
[S.323, IPC], (iii) Assault or use of criminal force on grave and sudden
provocation [S.358, IPC]. Differences between the two are given in Table 5.

VIII. PUNISHMENTS
(1) Sentences authorized by law [S.53, IPC] are:
(i) Death
(ii) Imprisonment for life
(iii) Imprisonment (a) Rigorous, i.e. with hard labor, including solitary
confinement [S.73, S.74, IPC] (b) Simple
(iv) Forfeiture of property
(v) Fine
(2) Double jeopardy - No person can be prosecuted and punished for the same
offence more than once [Article 20(2), Constitution of India].

IX. SUBPOENA [SUMMONS]

Subpoena [L. sub, under; poena, penalty] is a document compelling the
attendance of a witness in a court of law under penalty on a particular day, time
and place, for the purpose of giving evidence.
Salient features:
(1) Types – Subpoena can be classified according to (i) the nature of court which
issues it [civil court or criminal court] (ii) whether a document is required to
be produced or not [Subpoena ad testificandum and Subpoena duces tecum].
(2) Failure to produce document – Imprisonment of 6 months or `1000 fine, or
both [S.175, IPC].
(3) Failure to produce thing – Simple imprisonment of 7 days [S.349, CrPC].
(4) Procedure of issue – Subpoena is issued by the court in writing, in duplicate.
It is signed by the presiding officer of the court, and bears the seal of the court
[S.61, CrPC].
(5) Things mentioned in summons: (i) Name of accused (ii) Case details, crime
number (iii) Date and time to arrive to court.
(6) Served by: (i) Court official or (ii) Police officer or (iii) some other public
servant [S.62(1), CrPC].
(7) Procedure of delivery: (i) Summon is delivered personally if practicable
[S.62(2), CrPC] (ii) Person receives one copy of summons and signs at the
back of the duplicate [S.62(3), CrPC] and returns it to the delivering official.
(8) Procedure of delivery to a Govt servant: (i) Summon delivered to head of
office in which govt servant works (ii) Head of office signs on the back of
duplicate and delivers the original copy to the concerned Govt servant [S.66,
CrPC].
(9) If person summoned resides in a different city – Court will send summon
in duplicate to the area magistrate and he will deliver the summon to the
person concerned [S.67, CrPC].

X. CONDUCT MONEY
Conduct money is money paid to a witness to meet his expenses for attending
the court.
Salient features:
(1) Civil case: (i) Conduct money is usually paid at the time of service of
summons. (ii) If money is not paid, the doctor must still attend the court and
demand his expenses at the end of his evidence. (iii) The party which calls the
doctor pays. (iv) If doctor feels that the amount is less, he must bring it to the
notice of the Judge. The judge will decide the amount to be paid.
(2) Criminal case: (i) No money is paid at the time of service of summons (ii) If
he is a doctor in private practice, he may request the court for conduct money
at the end of his evidence. Generally conduct money is paid by the court. (iii)
If he is a Govt doctor, paid by his office.

XI. EVIDENCE
“Evidence” according to S.3, IEA means and includes.
(1) all statements which the Court permits or requires to be made before it by
witnesses, in relation to matters of fact under inquiry [oral evidence];
(2) all documents including electronic records produced for the inspection of the
Court [documentary evidence]. An evidence tendered by a medical personnel
is known as medical evidence.

Types of Evidence
Evidence may be classified in two ways–
(1) How the evidence was acquired by witness.
(2) How the evidence was delivered in court [Fig 1.2].

1. According to acquisition of evidence

a. Direct evidence
Witness directly saw the crime or felt it by any of his senses. Ex (1) Doctor
conducted surgery or postmortem. Saw injuries himself (2) A passerby saw a
murder on the street.
b. Indirect evidence
Witness did not directly see the crime. It can be of 2 types.

i. Circumstantial
Witness did not see actual crime, but several related things exist, which point
strongly towards the commission of crime.
Salient features:
Admissibility - Circumstantial evidence is generally admissible in court unless
the connection between the fact and the inference is too weak to be of help in
deciding the case. Many convictions for various crimes have rested largely on
circumstantial evidence.

ii. Hearsay
Witness only heard about the crime from someone.
Salient features:
Admissibility - Generally hearsay evidence is not admitted. Two notable
exceptions (i) Dying declarations [S.32(1), IEA] and (ii) Res gestae [S.6, IEA].
Res gestae are involuntary exclamations or acts made at the time the offense was
committed. These utterances or acts are not planned, but are forced from the
individual by the excitement of the moment.

2. According to presentation in court

a. Documentary evidence

It may be of following types.

i. Medical certificates
Medical certificates are documents prepared by the doctor at the request of the
patient, and handed over to him. Ex – certificate of age, death, disability,
pregnancy, sickness, unsoundness of mind, vaccination etc.
Salient features:
(1) Accepted by a court of law only when issued by a qualified registered
medical practitioner.
(2) Certificate of ill health: (i) To be given on a recommended format -
According to S.1.3.3 of The Indian Medical Council (Professional Conduct,
Etiquette and Ethics) Regulations, 2002 [IMC Regulations 2002], should be
given in recommended format given in appendix 2. It should contain the
following (a) identification marks of the patient (b) exact nature of illness (c)
period of expected absence (ii) Confidentiality - Patient’s medical records
should be kept confidential [S.2.2, IMC Regulations 2002] (iii) Maintenance
of register – Doctor should keep one copy of certificate with him. Patient’s
signature/thumb impression, and his full address should be recorded on both
copies.
(3) Death Certificate: (i) Doctor is legally bound - If doctor has attended a
patient during his last illness, and if he has expired, the doctor must issue the
certificate without charging any fee [S10(3) Registration of Births and Deaths
Act, 1969] (ii) If doctor refuses to issue a death certificate under above
condition, fine is `50 [S.23(3) of same Act]. (iii) Death certificate must never
be issued without inspecting the dead body, and satisfying himself that the
patient is really dead [criteria to apply are Minnesota criteria – please see ch
8]. (iv) If doctor is suspicious about the cause of death, the matter must be
informed to the police.
(4) Issuing false certificates – Issuing false, fictitious or backdate certificates is
an offence u/s197, IPC. Punishment 7 y + fine. Patient using such a certificate
is punishable u/s198, IPC. Punishment same.
(5) Issuing backdate certificates – Must never be done. There are instances of
 criminals getting certificates in back date and then producing them as alibi in a
court of law. This can land doctor in serious trouble. Punishment same as for
issuing false certificate.

ii. Medicolegal reports

Medicolegal reports are documents prepared by the doctor at the request of
some investigating authority, e.g. police, magistrate etc, and handed over to him.
They may be in relation to living [e.g. injury reports], dead [Postmortem reports]
or inanimate objects [e.g. vaginal swab reports].
Salient features:
Structure of the report – It consists of 3 parts - (i) Preliminaries – (a) Serial
number [e.g. 273/2012 means that it is the 273rd MLC recorded in the year 2012]
(b) name (c) father’s/guardian’s name; husband’s name in cases of married
women (d) age, (e) sex, (f) address, (g) occupation (h) name and address of
accompanying/identifying person if any (i) two identification marks, (j) date,
time and place of examination, (k) consent (l) name and number of the police
official to whom information was sent and MLC was handed over. In case the
patient first reported to the police, and police brought the patient to doctor for
examination, the name, number and police station (PS) of accompanying police
officer. The preliminaries are to be filled up in all MLCs whether related to
physical injury, age estimation, examination for mental soundness, poisoning
[e.g. alcohol] etc. (ii) Body – Main part. Consists of (a) history as alleged by the
patient/accompanying person, (b) observations, (c) findings of physical
examination [type of each injury, its size, shape and direction, on what part of
the body inflicted, its age and remarks if any], (d) special investigations
requested etc (iii) Opinion and subsidiaries – Conclusions derived from the
observations (a) nature of injury [e.g. simple or grievous] (b) likely weapon with
which caused, and whether it was dangerous or not (c) if police wants to take the
statement of the patient, the doctor must certify if patient is fit for statement or
not.

iii. Dying declarations

Dying declarations are documents prepared on the statements of a person dying
as a result of some unlawful act.
Salient features:
(1) It is an example of hearsay evidence. It is admitted on the principle of
necessity [for a similar situation, please see ch 28 " Wills in extremis].
(2) Manner of death – May be made in all manners of death – suicide,
homicide, accident.
(3) Preliminaries - Before recording the statement, the doctor should certify that
the declarant is fit to make a statement [compos mentis] [ch 28].
(4) Who can record – Anyone. (i) Executive magistrate [EM]– Ideally he
should be called if there is time. If not possible, other persons who can record
are (ii) Doctor (iii) Police (iv) village headman (v) Any other person
[Recording by anyone other than the EM, should preferably in the presence of
2 independent witnesses, who should sign the dying declaration] (vi) The
statement can be oral, tape-recorded, or may even be made on phone, by SMS
or e-mail to someone. Evidentiary value is maximum when recorded by
magistrate, by SMS or e-mail followed by doctor.
(5) Attestation - Dying declaration recorded by the police in the presence of
medical officer. Medical officer need not attest the statement.
(6) Recording: (i) Oath – Not administered. The general belief is that a dying
person will not speak a lie (ii) Language - Dying declaration narrated in one
language (e.g. Punjabi), but recorded in another (Urdu) " Admissible. (iii)
Format – (a) If possible, it should be written by the person himself, and then
signed by him. If person is not in a condition to write, but can speak, it should
preferably be (b) video recorded. If that is not possible, then person recording
the d/dec should write the statement (c) in person’s own words. Precautions -
(I) No alteration of terms and phrases. (II) No prompting or assistance (III)
Statement must be on facts, not on opinions and judgments [my sister-in-law
might have helped my husband in burning me]. If declaration is made on
judgments, questions should be asked by the recorder to clarify facts [did you
see your sister-in-law helping your husband?]. Alternatively, it can be (d) in
the form of questions and answers; but leading questions should not be asked
[It is not proper to ask “Did your mother-in-law put fire on your body?”;
instead it must be asked “who burnt you?”] (e) if unable to speak - questions
put and signs/gestures made in reply are recorded (iv) Reading out – After
recording the statement, it should be read out to the declarant, and asked if he
agrees. If yes, his signatures or thumb impressions are taken. If signatures or
thumb impressions cannot be taken for some reason, this fact should be
 recorded. The value of d/dec would be same.
(7) Onward transmission to Magistrate – In case d/dec is taken by any person
other than magistrate, it should be forwarded to him in a sealed cover.

b. Oral Evidence
Oral evidence includes all verbal statements under oath made before the court
which it permits.

i. Dying deposition
Dying deposition is a statement of a dying person on oath, recorded by the
magistrate in the presence of the accused or his lawyer, who is allowed to cross
examine the witness.
Salient features:
(1) This is court at the bedside. Its evidentiary value is more [Table 6].
(2) Dictum - It works on the dictum “if the person cannot go to the court, the
court must go to the person”.
(3) Held in many countries like UK, Australia and many states of USA, but not
in India.

ii. Exceptions to oral Evidence

Documentary evidence is accepted by the court only on oral testimony [oral
evidence]. Imp exceptions are
(1) S.32, IEA - Statements, written or verbal, of relevant facts made by a person:
(i) who is dead [dying declaration], or (ii) who cannot be found, or (iii) who
 has become incapable of giving evidence, or (iv) whose attendance cannot be
procured without an amount of delay or expense which, under the
circumstances of the case, appears to the Court unreasonable
(2) S.33, IEA -Evidence given by a witness in a previous judicial proceeding is
admissible in a subsequent judicial proceeding, or in a later stage of the same
judicial proceeding when (i) the witness is dead or (ii) cannot be found, or (iii)
is incapable of giving evidence, or (iv) is kept out of the way by the adverse
party, or (v) if his presence cannot be obtained without an amount of delay or
expense which, under the circumstances of the case, the Court considers
unreasonable. Following additional provisos apply (vi) the proceeding must be
between the same parties (vii) the adverse party in the first proceeding had the
right and opportunity to cross-examine (viii) questions in issue are
substantially the same in the first as in the second proceeding.
(3) S.60, IEA - Opinions of experts expressed in any treatise commonly offered
for sale, and the grounds on which such opinions are held, may be proved by
the production of such treatises if (i) the author is dead or (ii) cannot be found,
or (iii) has become incapable giving evidence, or (iv) cannot be called as a
witness without an amount of delay or expense which the Court regards as
unreasonable.
(4) S.291, CrPC - Evidence of a doctor recorded in court, if taken and attested
by a Magistrate in the presence of the accused, may be given in evidence as
such in any inquiry, trial or other proceeding. But he is liable to be called if
court thinks fit [e.g. additional cross examination required, evidence is
deficient etc].
(5) S.292, CrPC - Written reports of mint officers, Security Printing Press,
Controller of Stamps and Stationery, any Central Government or State
Examiner of Questioned Documents are accepted normally without calling
them to court. However, the Court may, if it thinks fit, summon and examine
any such officer.
(6) S.293, CrPC - Reports of certain Government scientific experts: (a)
Chemical Examiner or Assistant Chemical Examiner to Government; (b)
Chief Controller of Explosives; (c) Director of the Finger Print Bureau; (d)
Director, Haffkine Institute, Mumbai (e) Director, Deputy Director or
Assistant Director of a Central Forensic Science Laboratory [CSFL] or a State
Forensic Science Laboratory [SFSL] (f) Serologist to the Government; (g) any
 other Government Scientific Expert specified, by notification, by the Central
Government for this purpose [S.293(4), CrPC]. The Court may however
summon and examine any such expert if it thinks fit [S.293(2), CrPC].
(7) Hospital Records – Routine entries made during ordinary course of work,
e.g. Dates of admission and discharge, Experts called, Pulse, BP, Signs noted,
Special investigations ordered, Temperature, Treatment given. But their
interpretations e.g. cause of disease, basis of diagnosis etc are not accepted
without oral testimony.
(8) Public records – Kept in public office, e.g. birth, marriage, death etc [S35,
74, 76, 78 IEA].

XII. WITNESS

A witness is one who has firsthand knowledge about a crime or significant event
through his senses [e.g. seeing, hearing, smelling, touching] and can help clarify
important points about the crime or event.
Salient features:
(1) Sections 118-134 [ch IX] of IEA deal with witnesses.
(2) Persons competent to be witnesses [S.118, IEA]– All persons are
competent to testify, unless they cannot understand questions put to them
because of (i) Disease of body or mind (ii) Extreme young age (iii) Extreme
old age. No age is specified. Even a mentally ill person can be a witness if he
can understand questions and give rational answers.
(3) Dumb witness [S.119, IEA]– can testify by writing or by making signs.
Such writing or signs must be made in open court. It is deemed as oral
evidence.

Types of Witnesses
Witnesses are of two types:
(1) Common (ordinary) witness
(2) Expert witness
Any of these may become a hostile witness.

1. Common witness
Common witness [lay witness, occurrence witness, witness of fact] is a person,
who tenders evidence about the facts observed or perceived by him. No
specialized knowledge is required in tendering evidence.
Salient features:
First hand knowledge principle or rule - The common witness must
demonstrate that
(i) he was capable of perceiving the fact by one of his senses [e.g. he was not
drunk at the time] and (ii) he actually observed this fact [i.e. he was present at
the site at the material time].

2. Expert witness
Expert witness is a person who is skilled or trained in some scientific or
technical subject and is capable of drawing conclusions and opinions from the
facts observed by himself, or noticed by others. E.g. Forensic pathologist, an
expert in DNA analysis, fingerprinting, firearms, handwriting or voice analysis
etc [S.45, IEA]. The value of expert medical testimony was first recognized in
the Bamberger Code (1507) and Caroline Code (1553) [please see above].
Salient features:
(1) Areas in which expert witness gives evidence: (i) upon facts which are
admitted or proved by (a) himself (b) other witnesses at the trial (ii) on
hypothetical questions. Doctor may or may not have first-hand knowledge of
the actual case. These are questions based on stated assumptions (iii) on
matters of common knowledge.
(2) Rules to follow: please see “conduct and duties of doctor in the witness box”
below.
3. Hostile witness
A hostile witness (adverse witness, unfavorable witness, unwilling witness) is
one who conceals whole or part of the truth and offers adverse testimony against
his own party.
Salient features:
(1) Reasons for turning hostile – bribed, threatened or won over by opposite
party.
(2) Who can declare a witness hostile – The party who has called the witness
will request the court to declare him hostile, whereupon court would do so.
(3) Earlier testimony - of hostile witness is rejected.
(4) Leading questions - can be asked during examination in chief from hostile
witness [S.154, IEA].
(5) Both common and expert witness may become hostile.
(6) Punishment - Hostile witness may be prosecuted for perjury u/s.193, IPC
[7 y+fine]. The Indian Evidence Act, 1872 does not expressly mention the
term “hostile witness” anywhere. It is just a convenient term to address a
witness who is concealing the truth.

XIII. PERJURY

Perjury means giving willful false evidence. The word “perjury” as such appears
nowhere in Indian law. Indian law only mentions “false evidence”, which is
synonymous with perjury.
Salient features:
(1) Definition — Perjury has 5 major components. Whoever, (i) being legally
bound by an oath or (ii) by an express provision of law to state the truth, or
(iii) being bound by law to make a declaration upon any subject, (iv) makes
any statement which is false, and (v) which he either knows or believes to be
false or does not believe to be true, is said to give false evidence
[S.191, IPC].
(2) Punishment for perjury: (i) Normal trial - 7y+fine [S.193, IPC] (ii)
Summary trial - 3 months, or ` 500 fine, or both [S.344, CrPC].

XIV. RECORDING OF EVIDENCE

(1) Sequence - The recording of evidence always in this order (i) Oath " (ii)
Examination in chief is " (iii) Cross examination " (iv) Re-examination. Judge
can ask questions at any stage. This order is defined in S.138, IEA. S.137 IEA
defines examination-in-chief, cross-examination and re-examination.
(2) Presence of accused – Recording of evidence must be in the presence of
accused, or his pleader [S.273, CrPC].
(3) Evidence may be recorded by audio-video electronic means [S.275, CrPC].
(4) Recording in summons-cases - the Magistrate makes a memorandum of the
substance of witness’ evidence or may dictate it in open Court. The
memorandum is then signed by the Magistrate and forms part of the record
[S.274, CrPC].
(5) Recording in warrant-cases — All procedures as above, but here it can be
in the form of question and answer [S.275, CrPC].
(6) Recording in Sessions court trials – procedure same as in warrant cases
[S.276, CrPC].

A. Oath
An oath is a promise made in the name of God, that the witness will speak truth
and nothing but the truth. In India, it is governed by The Oaths Act, 1969.
Salient features:
(1) To whom administered: All witnesses, jurors and interpreters [S.4(1), The
Oaths Act, 1969]. Exceptions – (a) Child <12 y, [S.4(1), The Oaths Act,
1969]. (b) Atheist - If any person does not want to swear in the name of God
[e.g. an atheist], he may solemnly affirm [S.5, The Oaths Act, 1969][solemn
 affirmation]. It will have the same value as an oath [S.51, IPC, S.3(37) The
General Clauses Act, 1897]. (c) When accused is examined as a prosecution
witness in a criminal trial [S.313(2), CrPC; S.4(2), The Oaths Act, 1969
[please see below " “trial procedure in Warrant and Summons cases].
(2) Form - Witness - I do swear in the name of God/solemnly affirm that what I
shall state shall be truth, the whole truth and nothing but the truth.
(3) Duty to speak the truth – After taking oath, all persons are bound to state
the truth [S.8, The Oaths Act, 1969].
(4) Refusal to take oath - 6 months simple imprisonment or ` 1000 fine or both
[S.178, IPC].

B. Examination-in-Chief
Examination-in-chief [syn, direct examination, EIC] is the first examination of
witness.
Salient features:
(1) Done by - Lawyer of the party which calls him (i) In a criminal case [e.g.
grievous hurt, rape, murder trial]- since State is the prosecution party, the
burden of proof lies on it. Since medical witness often proves guilt, he is
usually summoned by the State. Public prosecutor [PP; S.24, 25, CrPC;
lawyer representing the State] first examines the witness (ii) In a civil case –
Party who calls the witness first examines.
(2) Purpose: (i) to elicit all relevant facts before the court, and the conclusions
which the doctor has drawn from the facts. (ii) interpretation by the doctor of
the findings of ancillary investigations, provided by scientific labs, analysts,
serologists, toxicologists etc.
(3) Before giving evidence: (i) it is advisable that the doctor meets the PP and
discuss the report, MLC, death certificate, photographs, preserved articles etc
with him. Usually in important cases, as the witness reports in the court, PP
would himself come to the witness, show him the case file, marked with
several flags and discuss important points with him. There is nothing illegal in
doing so. (ii) If witness wants to modify any of this conclusions, it is better to
point it out to PP at this stage. (iii) Doctor may help the PP in framing proper
questions in proper sequence, so that all essential facts may be elicited. (iv)
Conversely PP is often able to tell the expected questions in cross-
examination, which doctor may prepare beforehand.
(4) Leading questions: (i) A leading question [LQ] is any question which
suggests its own answer, or which can be conclusively answered as “yes” or
“no” [S.141, IEA]. (ii) Normally leading questions are not allowed during EIC
and re-examination [S.142, IEA] (iii) Situations when LQ are allowed in EIC
- (a) If the questions are introductory in nature or undisputed (b) If not
objected to by the other party. (c) If objected to by the other party but allowed
by the judge [S.154, IEA] (d) When the witness has turned hostile.
(5) EIC is exempted - In certain cases of offences of rape, sexual harassment
(S.354 and 354A, IPC), attempt to disrobe(S.354B, IPC), voyeurism(s354C
IPC), stalking(S.354D, IPC) and insulting modesty of woman (S.509, IPC)]
[S.164 (5-A) CrPC (ch 25)].

C. Cross Examination
Cross examination of a witness is done by the lawyer of the opposite party
opposite to the one which summoned him [S.137, IEA].
Salient features:
(1) Objectives: (i) To elicit facts favorable to the cross-examining party (ii) To
test the accuracy of statements made by the witness [S.146, IEA] (iii) to
discover who he is and what is his position in life [S.146, IEA] (iv) to
discredit him, by injuring his character, including questions the answer to
which might criminate him or expose him to a penalty [S.146, IEA] (v) to
develop new or old facts (vi) To modify or explain what has been said (vii) To
remove any undue or excessive emphasis which may have been given to a
particular statement (viii) To try to weaken the evidence by showing that the
evidence was biased, contradictory, ill-founded, inaccurate, inconsistent,
influenced, untrustworthy and not impartial.
(2) In a criminal case - defense witness is cross-examined by the PP.
(3) Leading questions - may be asked in cross-examination [S.143, IEA].
(4) Other questions – Need not be confined to the facts elicited in EIC
[S.138, IEA].
(5) Competence and credibility of witness – is often tested by questioning his
qualifications, experience and number of autopsies, MLCs etc he has made. If
the witness finds the questions objectionable, he must point it out to judge
[please see “conduct and duties of doctors in the witness box” below].
(6) Person called to produce a document —cannot be cross-examined unless
 and until he is called as a witness [S.139, IEA].
(7) Questions may be asked regarding the witness’s previous convictions or
questions tending to impeach his impartiality in order to shake his credit by
injuring his character [S.153, IEA].
(8) Impeaching credit of witness — The credit of a witness may be impeached
in cross examination [and with the consent of the Court during examination-
in-chief and re-examination] (i) by the evidence of persons who testify that
they, from their knowledge of the witness, believe him to be unworthy of
credit (ii) by proof that the witness has been bribed (iii) by getting him to
deliver contradictory statements [S.155, IEA].
(9) Indecent and scandalous questions — The Court may forbid any questions
or inquiries which it regards as indecent or scandalous, unless they relate to
facts in issue, or to matters necessary to be known [S.151, IEA].
(10) Questions intended to insult or annoy - The Court shall forbid any
question which appears to it to be intended to insult or annoy, or which,
though proper in itself, appears to the Court needlessly offensive in form
[S.152, IEA].
(11) Protection from self-incrimination - If a witness is forced to give an
answer admitting any guilt or crime on his part, such answer can not be used
against him in any criminal proceeding [S.132, IEA].
(12) Medical witness – is neither a witness for prosecution, nor for defense.
Thus even if an answer is favorable to defense, witness should immediately
and unhesitatingly answer it.
(13) Cross-examination as to previous statements in writing – Sometimes
witness’s current statements may be contradictory to his own previously given
statements in writing. His earlier statements may be used to contradict him
[S.145, IEA]. If such contradictions are because of intervening medical
advances, the witness must say so.
(14) Hypothetical questions – Witness may raise objection, but if court insists,
he must answer.
(15) Time limit – There is no time limit for cross-examination and the witness
may be cross-examined for days together.
(16) Cross examination is a double edge sword – i.e. it may injure the very
case of the party cross-examining him. It happens if defense lawyer asks
questions the answer to which he himself does not know. In such cases, the
 answer may harm his own interest.

D. Re-examination
(1) Conducted by - the lawyer of the party who summoned witness.
(2) Objectives:
(i) To add details to statements, the witness made during CE
(ii) To clarify ambiguities
(iii) To correct any mistake.
(3) Objections to testimony:
(i) When an improper question is asked from witness during any stage, the
opposing lawyer may immediately object by saying “I object”, and must
give reasons for his objections.
(ii) Witness must wait till the Court gives its ruling on objection. If Judge says
“objection sustained” it means the object is right, and witness must not
answer; if he says “objection overruled” it means the objection is wrong
and the witness must answer.

E. Questions by Judge
(1) Judge may ask any question in any form, at any time [i.e. during EIC, CE,
RE], about any fact relevant or irrelevant to clear up doubts [S.165, IEA].
(2) Can recall and re-examine any person at any stage [even if already
examined] if his evidence is essential to the decision of the case
[S.311, CrPC].

XV. TRIAL PROCEDURE IN WARRANT AND SUMMONS

CASES

All offences punishable with death, imprisonment for life, or for a term
exceeding 2 y are tried as warrant cases. All other cases are tried as summons
cases.
Memory Aid 3: Summons Cases
Summons cases may be viewed as simple cases

A. Warrant Case
Warrant-case refers to a case relating to an offence punishable with more than 2
years of imprisonment, or with death [S.2(x), CrPC]. Ex - Murder is a warrant
case, because maximum punishment for this offence is death.

B. Summons Case
Summons-case refers to a case relating to an offence punishable with less than 2
years of imprisonment [S.2(w), CrPC]. Ex: Voluntarily causing hurt is a
summons case, because maximum punishment for this offence is 1 year.

2. Medical Law and Ethics

I. INTRODUCTION

(1) The medical profession is guided by various legal statutes [medical law, eg
MTP Act].
(2) Additionally, the Medical Council of India (MCI) has formulated The Indian
Medical Council (Professional Conduct, Etiquette and Ethics Regulations) in
2002, which prescribes ethical guidelines to the doctors.
(3) World Medical Association also prescribes Codes of conduct from time to
time.

II. ACTS

A. The Indian Medical Council Act, 1956

In 1933, the Indian Legislative Assembly passed the Indian Medical Councils
Act, 1933. Dr. B.C. Roy was the first Indian President of Medical Council of
India [MCI] in 1939. In 1956, it was repealed, and a new Act known as The
Indian Medical Councils Act, 1956 [IMC Act, 1956] was passed. In 1964, the
Act was amended. This Act regulates medical practitioners trained in western
system of medicine.
B. The Medical Council of India Regulations, 2000
MCI Regulations, 2000 have been made by the MCI [with previous sanction of
the Central Govt] in exercise of the powers conferred upon it by S.33 of IMC
Act, 1956. These are made to carry out the purposes of this Act, and provide for
(a) the management of the property of the Council and the maintenance and
audit of its accounts; (b) the summoning and holding of meetings of the Council,
the times and places where such meetings are to be held, the conduct of business
thereat and the number of members necessary to constitute a quorum; (c) the
resignation of members of the Council etc.

1. Indian Medical Council

Indian Medical Council or the Medical Council of India (MCI) is constituted
under The Indian Medical Council Act, 1956.
a. Constitution
(1) Constitution - According to S.3 of the IMC Act, 1956, MCI consists of
(i) One member from each State other than a union territory to be nominated
by the Central Government in consultation with the concerned State
Government
(ii) One member from each University to be elected from amongst the
members of the medical faculty of that University
(iii) One member from each State in which a State Medical Register is
maintained, to be elected from amongst themselves by persons enrolled on
such register
(iv) Seven members to be elected from amongst themselves by persons
enrolled on any of the State Medical Registers, and
(v) Eight members to be nominated by the Central Government.
(2) A president and a vice-president - are elected from among these members.
(3) Registrar - The Council appoints a Registrar, who acts as secretary and may
also act as treasurer, who looks after the day-to-day work.
(4) Tenure - The Council holds office for a term of five years.
(5) Executive Committee - The Indian Medical Council carries out its main
purposes through an Executive Committee, which consists of president, vice-
president and 7-10 other members. In 2010, following some controversies,
the President of India temporarily dissolved the Medical Council, and replaced
 it with a seven-member Governing Council.

b. Functions
Functions of the Indian Medical Council are summarized in Table 1.

i. Medical register
The MCI maintains a register of medical practitioners, known as the Indian
Medical Register [S.2(d) IMC Act, 1956].
Salient features:
(1) It contains the names of all doctors who are enrolled directly with MCI or
with any State Medical Council.
(2) It is maintained by the registrar of MCI [S.21, IMC Act 1956; S.61(1), MCI
Regulations 2000]. It is kept up-to-date by adding or erasing the names of
medical practitioners, as the case may be.
(3) Registered Medical Practitioner:
(i) IMC Act 1956 - does not define this term anywhere, but some other Acts eg
The Drugs and Magic Remedies Act 1954 and PCPNDT Act 1994 define it
as a person who holds a degree specified in S.2(h), IMC Act 1956.

ii. Maintenance of the standards of medical education

(1) The Council maintains standards of both the Undergraduate [S.19A of IMC
Act, 1956] as well as the Postgraduate [S.20 of IMC Act, 1956] medical
education.
(2) Any medical college or institution, imparting undergraduate medical
education, should have a proper space, a properly trained staff, laboratories,
equipment, library and other facilities.
(3) MCI inspects these facilities from time to time. If any college or institution
does not have these facilities, the MCI makes a representation to the Central
Government to withdraw recognition of medical degree awarded by that
college.
(4) Every five years inspection is held by the MCI to see whether the standards
are being maintained or not.
(5) Schedules: There are three important appendices to The Indian Medical
Councils Act, 1956, known as Schedules. According to S.2(h), IMC Act 1956,
a “recognized medical qualification” include only the medical qualifications
mentioned in the three schedules.
(i) The First Schedule contains recognized medical qualifications granted by
universities in India.
(ii) The Second Schedule contains medical qualifications granted outside India
(recognized by the MCI)
(iii) Third Schedule has two parts - Part I - additional recognized qualifications
granted by Indian medical institutions. Part II - additional recognized
qualifications granted by foreign medical institutions.

iii. Recognition of foreign medical qualifications

If an Indian national has acquired a degree from a foreign medical college whose
qualification is neither included in schedule 2 nor in part II of Schedule 3, he
makes a representation to the Government of India, along with the relevant
information (Course of study, syllabus, duration of the course etc). This
representation is then forwarded to the MCI, which has an authority to enter into
negotiations with any of the Medical Councils of the foreign countries, and can
recognize such foreign qualifications on reciprocal basis. The Central
Government may, by notification in the Official Gazette, amend part II of the
Third Schedule so as to include such qualification therein.

iv. Appeal against disciplinary action

If name of any doctor is removed from the State Medical Register, he may
appeal to the Central Government after exhausting all remedies under the State
Medical Council Act (within 30 days). The application should state the grounds
of the appeal and be accompanied by all relevant documents. The Central
Government confers with the MCI, and gives its decision which is binding on
the State Government and the State Medical Council.

v. Warning notice
The Council prescribes standards of professional conduct. From time to time the
MCI issues warning notices, describing acts amounting to serious professional
misconduct.

2. State Medical Councils

a. Constitution
The State Medical Council consists of (i) members elected by the registered
medical practitioners and those (ii) nominated by the State government. The
members of the Council then elect the president and the vice-president amongst
themselves.

b. Functions
The functions and working of the State Medical Council is similar to those of the
MCI. The main functions are enumerated in Table 2.

i. Maintenance of the medical register

The Council appoints a Registrar who keeps a register of medical practitioners.
This register contains the name, address, qualification and other particulars of all
medical practitioners registered with that Council. Any new or an existing
medical graduate can have his name entered on payment of prescribed fee. The
Registrar of the State Medical Council informs the Indian Medical Council of all
the additions and other amendments in the State Medical Register made from
time to time.

ii. Disciplinary control

If a doctor is found guilty of professional misconduct (see below), then the
Council may exert a disciplinary action on that doctor.

iii. Erasure of name

The causes of erasure of the name of a registered medical practitioner are:
(1) Death of doctor (2) Doctor not traceable (3) Name entered by fault or fraud
(4) Penal erasure
Penal erasure
(1) Penal erasure refers to removal of a medical practitioner’s name from the
Medical Register temporarily or permanently, as a penalty.
(2) Done when doctor is guilty of serious professional misconduct (infamous
conduct).
(3) Doctor can not practice medicine till his name remains removed from
register.
(4) If name removed permanently, doctor can not practice for life. This is
known as the Professional Death Sentence.
(5) Case studies: Temporary erasure - British doctor John Bodkin Adams
[1899 –1983] was found guilty of 13 offences of prescription fraud, lying on
cremation forms, obstructing a police search and failing to keep a dangerous
drugs register. His name was removed from the Medical Register in 1957. He
was reinstated in 1961 after two failed applications.

III. PROFESSIONAL MISCONDUCT (INFAMOUS CONDUCT)

Professional misconduct (syn. Infamous conduct, ethical misconduct, ethical

negligence, ethical malpraxis) is that act of a medical man which would be
reasonably regarded as disgraceful or dishonorable by his professional brethren
of good repute and competence.
Salient features:
Strictly speaking, professional misconduct should include only those actions for
which there are no punishments in IPC or in any other existing civil or criminal
law, yet MCI or SMC can take action by removing the name of the doctor, eg
dichotomy, putting up an extra large signboard, employment of touts etc.
However the list of professional misconducts issued by The Indian Medical
Council (Professional Conduct, Etiquette and Ethics) Regulations, 2002 [please
see below] includes many acts for which there are punishments both in IPC
[criminal misconduct] and MCI [ethical misconduct].

A. List of Professional Misconducts

The Indian Medical Council (Professional Conduct, Etiquette and Ethics)
Regulations, 2002 enumerates some instances of professional misconduct in
chapters 6 and 7. It is important to remember that a list of this nature can
never be complete and exhaustive. Depending on circumstances, even acts not
mentioned in this list may be taken as examples of infamous conduct.
(1) Adultery or improper conduct or association with a patient.
(2) Conviction by court of law of offences involving moral turpitude.
(3) Issuance of false certificates, reports and other documents.
(4) Association with unqualified persons.
(5) Contraventions of drug acts and regulations.
(6) Selling a scheduled poison to the public.
(7) Performing an illegal abortion or enabling an unqualified person to perform
an abortion.
(8) Issuance of certificate of efficiency in modern medicine to unqualified or
non-medical persons.
(9) Contributing articles to the lay press and giving interviews regarding diseases
and treatments which may have the effect of advertising himself or
soliciting practice. But it is open to him to contribute articles which educate
the public about hygienic and healthy living and also to give public lectures on
health.
(10) Using an unusually large signboard. It is also improper to affix a signboard
on a chemist’s shop or in places where he does not reside or work.
(11) Disclosing the secrets of his patients (obtained in the exercise of his
profession) to others, except when bound by law (this subject is dealt with
 later under the headings “Professional secrecy” and “Privileged
communication”).
(12) Refusing treatment on religious grounds.
(13) Publishing photographs of his patient in any medical or other journal (by
which his identity could be made out) without first obtaining the consent of
that patient. However if the identity of such a patient is concealed, the consent
of that patient is not required (to be sure, no patient under these conditions
could sue the doctor either, because he wouldn’t have a way of knowing it was
his photograph).
(14) Publicly displaying his fees, except in his consulting room.
(15) Using touts or agents to procure patients.
(16) Receiving or giving commission or other benefits from fellow doctors,
traders, chemists, manufacturers etc. Giving of commission by one doctor to
another for favor of recommending or referring the patient to him is known as
dichotomy or fee-sharing or fee-splitting.
(17) Talking disparagingly about other colleagues or doing anything that means
unfair competition.
(18) Lack of eagerness to respond in .
(19) Not attending a patient when he is already under his treatment.
(20) Addiction to narcotic drugs.
(21) Alcoholism.
(22) Using unsterile instruments, or not furnishing his patients with proper
information about drugs or diet.
(23) Covering i.e. assisting someone who has no medical qualification to attend,
treat or perform an operation on some person in cases requiring profession
skill.
(24) Running an open shop for the sale of medicines.
(25) Writing prescriptions in a secret formula known to some particular
pharmacy only.
(26) Commercialization of a secret remedy.
(27) Accepting any gift or travel facilities etc from pharmaceutical
companies.

B. The 6 A’s of Serious Professional Misconduct

The above list is quite big. Of these, the six most important offences may be
described as the 6 A’s. These are:
(1) Association with unqualified persons – e.g. employment of touts to procure
patients.
(2) Advertising – It is improper to use an unusually large sign board to advertise
oneself.
(3) Adultery–arising out of professional relationship.
(4) Abortion (unlawful) – Unlawful abortion includes prenatal determination of
sex and then inducing abortion.
(5) Addiction – Addiction to drugs or doctor supplying drugs of addiction (e.g.
pethidine) to addicts. Case study - In 2011, Britain’s General Medical Council
cancelled the license of Peter Brackenridge for 6 months, as he prescribed
Ibogaine [a hallucinogen] to a patient. Although it is used as a drug for drug
addiction [ch 46] in some countries, it is unlicensed in the UK.
(6) Alcohol – Seeing patients under the influence of alcohol.

C. Punishment and Disciplinary Action

S.82 of Professional Conduct, Etiquette and Ethics) Regulations, 2002 " If a
medical practitioner is found guilty of any of the above offences, his name may
be erased from the medical register either temporarily or permanently
(professional death sentence).

D. Oaths, Codes and Declarations Relating to Professional

Misconduct
Historically, the doctors have been voluntarily taking oaths against committing
an act of professional misconduct. Most important are:

Declarations of the World Medical Association (WMA)

World Medical Association is an association of the National Medical
Associations of all countries. It held its 1st assembly in 1947 at Paris, France.
Since then it has been holding annual assemblies at different cities. In several of
these assemblies, important ethical declarations have been adopted, which are
important for medical practitioners. Most important of these declarations are:

i. The Declaration of Geneva (1948)

The Declaration of Geneva (Physician’s Oath; modernized version of
Hippocratic Oath) was adopted by the General Assembly of the World
Medical Association (an association of national medical associations) at
Geneva in 1948. It is a declaration of physicians’ dedication to the humanitarian
goals of medicine. This declaration became important in view of the medical
crimes which had just been committed in Nazi Germany.

ii. International Code of Medical Ethics (1949)

Adopted by the General Assembly of the World Medical Association at
London in October 1949. Prescribes (i) Duties of Doctors in General (ii) Duties
of Doctors to the Sick and (iii) Duties of Doctors to Each Other. Like the
Declaration of Geneva, it also is a modern version of the Hippocratic Oath.

iii. Declaration of Helsinki (1964)

Please see “Human Experimentation” below.

iv. Declaration of Sydney (1968)

Adopted by the 22th World Medical Assembly at Sydney, Australia in August
1968. It is a statement on when to pronounce death
Memory Aid 1: Declaration of Sydney
Sydney"Death

v. Declaration of Oslo (1970)

Adopted by the 24th World Medical Assembly held at Oslo, Norway in 1970. It
is a statement on therapeutic abortion - Abortion should be performed only as
a therapeutic measure.
Memory Aid 2: Declaration of Oslo
Oslo"Abortion.

vi. Declaration of Tokyo (1975)

Adopted by the 29th World Medical Assembly at Tokyo, Japan in October 1975.
Doctors will not take part in infliction of torture.
Memory Aid 3: Declaration of Tokyo
Tokyo"Torture.

IV. RIGHTS AND PRIVILEGES OF A REGISTERED

MEDICAL PRACTITIONER

A. Rights of a Registered Medical Practitioner

The rights are
(1) Right to choose his patient (EXCEPT IN EMERGENCY).
(i) Doctor need not accept all patients who come to him for treatment.
(ii) He may arbitrarily refuse to see a patient, even if there is no other physician
around.
(iii) If patient is unable to pay doctor’s fees, he may refuse to see patient. (a) in
cases of military necessity.
(2) to add titles, qualifications etc after his name.
(3) Right to practice and dispense medicines.
(4) Right to possess and supply dangerous drugs to his patients.
(5) Right to recovery of fees.
(6) Right to give evidence as an expert.
(7) Right to issue medical certificates.
(8) Right for appointment to public and local hospitals.

B. Red Cross and Allied Emblems

Red cross is one of the three “Emblems of the International Red Cross and Red
Crescent Movement”. These are - the Red Cross, the Red Crescent, and the
Red Crystal [Fig 2.1]. The Red cross emblem was first used in 1864. [I] Who
can put up: (1) Under S.12 of the Geneva Conventions Act 1960 (to which
India is a signatory), no person can, without the approval of the Central
Government, use the Red Cross or other allied emblems [Red Crescent, Red
Crystal] for any purpose. (2) They can only be used by the armed forces medical
services, their personnel, units, installations and means of transport. [II]
Punishment for unauthorized use – `500 + forfeiture of property upon which
the emblem was used [S.13].
C. Duties of a Medical Practitioner
Medical practitioners have rights and privileges, but at the same time they have
certain duties towards their patients and society in general. These have been
outlined in various chapters of The Indian Medical Council (Professional
Conduct, Etiquette and Ethics Regulations), 2002.

1. General duties and responsibilities

These are mentioned in chapter 1 of The Indian Medical Council (Professional
Conduct, Etiquette and Ethics Regulations), 2002.
(1) Dignity - Doctor should uphold the dignity and honor of his profession.
(2) Modesty - Should be modest, sober, pleasing in personality, should have
patience. Should be eager to help patients.
(3) Knowledge - Should keep abreast of advances of medical science, and
improve his knowledge and skills by referring to latest books, journals,
attending conferences. Case studies - (i) Vigneault v. Dr. Hewson Dental
Co. – Defendant dentist in preparation for the extraction of teeth used multiple
injections of a local anesthetic " osteomyelitis of jaw developed " At that time,
block method of injection was commonly being used " possibility of
osteomyelitis was much less by this “advanced method” " defendant was held
to be negligent in not keeping abreast of the developments in his profession.
[Vigneault v. Dr. Hewson Dental Co., 15 N.E. (2d) 185] (ii) Ferrell v. Ellis -
Defendant physician attempted to disclaim liability for negligence on the
 ground that all country physicians know no better. The court held that the
standard of care is based on present conditions of medical knowledge and not
on past conditions acquiesced in by country folk [Ferrell v. Ellis, 129 Iowa
614].

2. Duties of medical practitioners to their patients in particular

These are mentioned in chapter 2 of The Indian Medical Council (Professional
Conduct, Etiquette and Ethics Regulations), 2002.

a. Duty to exercise a reasonable degree of skill and knowledge

As soon as a doctor agrees to treat a patient, a doctor-patient relationship is
established, and he owes a duty to the patient to exercise a reasonable degree of
skill and knowledge in treating his patient.

b. Legal duty to render service

(1) When a doctor agrees to attend a patient, the physician-patient relation is said
to have been established.
(2) After this, the doctor is under obligation to attend to the case as long as it
requires attention. He cannot leave the patient at his own will.
(3) Doctor can withdraw treatment under following conditions:
(i) treatment is no longer required;
(ii) patient asks him to withdraw treatment;
(iii) mutual assent of both parties;
(iv) after giving notice with a reasonable time for patient to find another doctor;
(v) physician himself becomes sick;
(vi) patient is found to be malingering;
(vii) patient is using remedies other than those prescribed by him;
(viii) patient ignoring his instructions;
(ix) patient seeing another doctor without informing him;
(x) patient is using contraband drugs, intoxicants or poisons;
(xi) patient not fulfilling his earlier financial obligations [not paying fees].
(4) Case studies: (i) Tadlock v. Lloyd - Plaintiff employed physician to attend
his sick child " physician diagnosed illness scarlet fever " The following day
he was requested to come again " He did not come " said that disease must run
its course " Several other requests were made " Finally, in response to an
 urgent appeal, he did visit the patient " Child died shortly after his arrival "
Doctor had legal duty to render service, but did not do so " found negligent
[Tadlock v. Lloyd, 65 Colo. 40].

c. Prognosis
Doctor should neither exaggerate, nor minimize the gravity of his patient’s
condition.

d. Patient must not be neglected

e. Engagement for an obstetric case

(1) If a doctor A who was engaged to attend to an obstetric case is absent, and
another doctor B is sent to conduct delivery, B is entitled for his professional
fees.
(2) When A returns, B should leave the patient only after securing the patient’s
consent.

f. Duty in emergency
No doctor can refuse a patient in emergency.

g. Duty to give instructions

Doctor must give proper instructions to the patient or his relatives regarding
administration of medicine and diet.

h. Duty to inform and warn

The doctor has the duty to inform and warn the patient regarding the possible
side effects and harmful effects of any drug or device that he is prescribing.

i. Fees and other charges

Doctor should clearly display his fees and other charges on the board of his
chamber and the hospitals he is visiting.

j. Professional secrecy (confidentiality)

Professional secrecy refers to the doctor’s obligation to keep secret all
information regarding patient that he comes to know in the course of his
professional work.
Salient features:
(1) Contract - It is an implied term of contract between doctor and patient.
(2) Information can be divulged - with patient’s consent.
(3) Situations when doctor should not reveal condition of patient: (i) Press
conferences - If patient happens to be a celebrity, do not hold press
conferences regarding his medical condition (ii) Information to parents - If
patient is major, doctor should not inform about his illness to his parents, even
if they are paying his professional fees. Doctor can communicate illness of a
minor or mentally ill person to the legal guardians. (iii) Information to third
parties – no information should be revealed, even if the third party happens to
be near relative. There are some important exceptions to this rule [please see
privileged communication below] (iv) Husband and wife – Condition of one
can not be told to the other. (v) When free treatment is provided – Doctor
still has to maintain professional secrecy (vi) Information regarding dead
person – consent must be taken from nearest relative for imparting
information to anyone (vii) Reporting in a medical journal – condition may
be revealed to readers, but identity of patient must be hidden (viii)
Postmortem findings – should be revealed only to the police. Not even to the
closest relatives. However if a patient files an application under RTI Act, 2005
(Right to Information Act, 2005), the condition may have to be revealed and
even entire PM report may have to be given to the relatives according to CIC
(Central Information Commission) judgments.
(4) Situations when doctor may reveal condition of patient (please also see
privileged communication below) (i) When one party sends another to doctor
for examination with specific intent to discover illness – When one party A
sends another party B to a doctor to discover illness, B knows that his illness
may be reported to A, and with this knowledge he submits for examination; in
such cases doctor can reveal illness to A (a) Master sends servant - to doctor
to discover if he is having an illness (eg typhoid carrier status, so he may not
be employed as a cook). Doctor can inform master (b) Govt sends an
employee or would be employee - to doctor to discover any disability or
illness to know if he is fit for govt service. Doctor can inform govt. (c)
Insurance company sends a prospective client to know if he is having a life
threatening disease. Doctor can inform insurance company. (ii) When person
in police custody, undertrial prisoner, convicted prisoner is examined.
(5) Punishment for not maintaining professional secrecy - The patient can
bring both a (i) criminal action (u/s 499, IPC – defamation) and (ii) civil
action for damages (until and unless the case is one of privileged
communication – please see below). Punishment for defamation is 2 years
and/or fine [u/s 500, IPC] (iii) He can complain to MCI or State medical
council, which can take disciplinary action.

k. Privileged communication
There occur some situations where the doctor has to divulge the patient’s details
to certain authorities. This divulgence of the details is known as privileged
communication and is an exception to professional secrecy. The situations
where privileged communication holds true are as follows.
(1) In Society’s interest: (a) Patient suffering from venereal disease " tries to
enter a swimming pool " doctor advises him against doing so, as it can cause
infection to others " patient does not agree " doctor can communicate about his
illness to swimming pool manager (b) Patient suffering from color blindness "
doctor sees him driving a truck " advises him against this, as it can cause
accidents (inability to see red lights etc) " patient does not agree " doctor can
approach road transport authority and communicate about his illness.
(2) In patient’s interest: Patient has suicidal tendencies " Doctor informs the
parents to keep watch over him, as he has tried to commit suicide " This is
privileged communication (patient can not sue doctor).
(3) In a third party’s interest: Doctor treating HIV patient “H” " He gets
information that “H” is marrying a girl “G” " Doctor warns G that H is
suffering from HIV " G refuses to marry H " H brings action against doctor for
breach of confidentiality " Can not succeed, as the information was given in a
third party’s (G’s) interest. This third party can be a legally married spouse
too.
(4) In doctor’s own interest: Patient brings negligence suit against the doctor "
Court asks what illness did he treat " Doctor informs court " privileged
communication.
(5) Court of law: A doctor has to divulge all the details about the patient if they
are asked in the court of law. If he feels that he should disclose them openly,
he should write the same and then hand the envelope over to the judge, but he
can’t refuse to divulge the facts.
(6) Notifiable diseases: if, during his practice, a doctor comes across a patient
who is suffering from a Notifiable disease, it his duty to inform the same to
the concerned authorities.
(7) Suspected crime: if the doctor comes across a patient who has committed or
has intention to commit a crime which falls under any of the sections of IPC,
he has to inform the same to the nearest police station or the magistrate [please
see ch 31 for detailed reasoning]. This is a medicolegal case [for definition of
a medicolegal case, please see ch 11].
(8) Employers: if the person being examined is found to be suffering from a
disease which can put the life of the people he is serving in danger, the doctor
must try to persuade the person to not join his duty. If he does not agree, then
the employer has to be informed. (a) waiter or cook is found to be suffering
from an infectious disease " Condition must be reported to employer. (b)
driver is found to be suffering from a disease like epilepsy, alcoholism, drug
addiction, high blood pressure, color blindness " his condition must be
reported to state transport authorities (c) Teacher suffering from infectious
diseases (eg tuberculosis) " Condition must be reported to employers.
(9) Medical for insurance: if a doctor examines a person for his insurance
policy, the person knows fully well that any adverse medical findings would
be communicated to the insurance company. He has thus given his tacit
consent for communication of medical findings to the insurance company. In
such a situation, the doctor can give all the findings to the insurance company.
(10) Waiver of professional secrecy – When a patient gives his express
permission to the doctor to disclose professional secrets.

3. Duties of medical practitioners in consultation

These are mentioned in chapter 3 of The Indian Medical Council (Professional
Conduct, Etiquette and Ethics Regulations), 2002. They concern both the doctor
who sends his patient to the consultant, as well as the consultant.
Unnecessary consultations should be avoided - The doctor should ask for
consultation from another doctor only when it is required. Patient’s consent -
Whenever doctor asks for consultation he should talk about the same with the
patient or his relatives and inform them about the reasons for the same. If they
object, he should mention the same in the case records.
4. Duties of medical practitioners to one another
These are mentioned in chapter 4 of The Indian Medical Council (Professional
Conduct, Etiquette and Ethics Regulations), 2002.
Dependence of physicians on each other - A doctor should consider it a
pleasure and privilege to render gratuitous service to all fellow doctors and their
family dependents.

5. Duties of medical practitioners to the public in general and to the

paramedical profession
These are mentioned in chapter 5 of The Indian Medical Council (Professional
Conduct, Etiquette and Ethics Regulations), 2002.
Physicians as citizens -
(i) Should disseminate advice on public health issues.
(ii) Should co-operate with the authorities in the administration of sanitary and
public health laws and regulations.

6. Duties of medical practitioner in criminal matters

These are described by s201, IPC which states - Whoever, knowing or having
reason to believe that an offence has been committed, causes any evidence of the
commission of that offence to disappear, with the intention of screening the
offender from legal punishment, or with that intention gives false information
shall be punished [the quantum of imprisonment differs according to the
seriousness of crime whose evidence was made to disappear]. The doctor must
report all cases of homicide, suicide and accident to the police, because all
these constitute offences, and fall within the meaning of S.201, IPC. Failure to
do so would make him liable to prosecution u/s 176, IPC [Omission to give
notice or information to public servant by person legally bound to give it].
Punishment is imprisonment of 6 months, or `1000 fine or both.

V. RIGHTS AND DUTIES OF PATIENTS

A. Rights of Patients
Right to treatment – All patients have a right to treatment regardless of their
age, sex, religion, economic and social status. Instances when doctor can
refuse treatment - Communication made in good faith — No communication
made in good faith is an offence by reason of any harm to the person to whom it
is made, if it is made for the benefit of that person [S.93, IPC].

B. Duties of Patients
Patient should co-operate with the doctor by giving information about the
disease process, family and personal history.

1. Infringement by doctors of patient’s rights

a. Paternalism
Paternalism [Gk. pater, father] is acting upon one’s own idea of what is best for
another person without consulting that other person.
Salient features:
(1) Paternalism and patient autonomy are two extremes of a continuum. At
one end, the doctor’s judgment and decision are supreme, and on the other, the
patient’s [Therapeutic privilege (please see below) lies somewhere in
between]. Up to 19th century, paternalism was prevalent and legal. It is no
more legal.
(2) MLI - Paternalism (in a conscious, mentally sound, adult patient), although
done in the patient’s best interests, is illegal. The doctor may be sued u/s
350, IPC [using criminal force].

b. Therapeutic privilege
Therapeutic privilege [TP] is the doctor’s privilege not to reveal to the patient
that part of the information about his illness, which he genuinely thinks would
lower patient’s morale and his will to live.
Salient features:
(1) Precautions – In order to save himself from later litigation doctor should (i)
obtain expert consultation that patient is really emotionally disturbed and
divulging information may cause more harm. Report of that consultation must
be attached to the case sheet (ii) record in patient’s case sheet (a) what he not
disclosing and (b) why (iii) As far as possible, information should be told to
patient’s spouse or next of kin.
(2) The prudent patient rule or test – Used in two ways (i) Imparting
information - This implies that the patient must be given such information
about the procedure, side effects, and complications as might be required by a
 prudent [reasonable] patient. TP extends only as far as prudent patient rule
allows. (ii) Giving treatment – If doctor exercises TP, he must ensure that he
imparts so much treatment as would be accepted by a prudent patient, if he
genuinely had all information about the disease.
(3) Examples of TP – not telling about malignancy, unavoidable fatal lesion.
HIV does not come under TP. Patient must know about it, so he can take
precautions about not spreading disease.

2. Abuse by patients of their rights

Malingering
Malingering or shamming is conscious planning, feigning and pretending a
disease for the sake of some advantage.
Salient features:
(1) Advantages - Malingering is done by people to have following advantages:
(i) by workmen to claim compensation (ii) by policemen or military people
to prevent hard postings (iii) by prisoners to avoid hard labor, or capital
punishment (iv) by govt. servants to prevent transfers (v) by businessmen to
avoid contracts (vi) by beggars to attract public sympathy.
(2) Diseases feigned - Virtually any disease may be feigned, but those most easy
to feign are amnesia, aphasia, bleeding (may injure anus or vagina to produce
anal and vaginal bleeding respectively. May take coumarin to induce bleeding
diathesis), bruises (made by juices of irritant plants, eg Dhobi’s marking nut),
burns, chest pain (may ingest digitalis to alter his ECG pattern), diabetes,
diarrhea, dyspepsia, epilepsy, hematemesis (may injure his nasopharynx with a
sharp instrument, swallow the blood and regurgitate it in front of doctor),
hemoptysis, intestinal colic, jaundice (eating large amounts of carrot produces
carotinemia, which simulates jaundice), lumbago, mental illness, neurasthenia,
ophthalmia (pour juices of irritant plants in eyes, eg ratti), paralysis,
rheumatism, sciatica, ulcers and vertigo. Sometimes patients may exaggerate a
disease they are already suffering from.
(3) M/L Importance: (i) If the patient gets a medical certificate by narrating
false symptoms, and uses it for any purpose, he may be sued u/s 198, IPC
[punishment 7 y+fine] (ii) Cheating – May be sued u/s 415, IPC [cheating].
Punishment 1 y or fine or both [S.417, IPC] (iii) Must be differentiated from
perjury [please see ch 1]. Malingering is not perjury, as patient does not
 speak a lie under oath.

VI. TORT

A tort [Latin tortus, twisted] is a civil wrong that results when a defendant
engages in conduct that harms another person. Ex of tort -
(1) A drives car recklessly and hits another vehicle " A has committed the tort of
negligence.
(2) A negligently ligates ureter of B during an abdominal operation " A has
committed the tort of medical negligence. B claims compensation " A is
tortfeasor; B is plaintiff.
(3) A writes false things on the internet that harm another person’s reputation " A
has committed the tort of defamation.

VII. PROFESSIONAL NEGLIGENCE

A. Definition
Professional negligence, medical negligence or malpraxis is absence of
reasonable care and skill, or willful negligence of a medical practitioner in the
treatment of a patient, which causes injury or death of the patient.
Salient features:
(1) Alternative definition - doing something that one is not supposed to do [act
of commission] and failing to do something that one is supposed to do [act of
omission].
(2) Reasonable care: (i) Elements - Sometimes also called “due care”. (a)
includes such reasonable care and attention that the patient may require. (b)
Must anticipate and appropriately manage known, expected or foreseeable
events and complications of patient’s disease and treatment (c) It should be
proportionate with (i) qualification of doctor - [eg an MCh is expected of a
higher level of skill than an MS, who in turn has a higher level of skill than
MBBS]. For the same level of negligence, an MCh may be held responsible,
but not MBBS (II) known inability of the patient to take care of himself – eg
unconscious patient requires higher level of care and attention than a
 conscious patient. (ii) When breached - Reasonable care is breached in 2
situations (a) when doctor unjustifiably deviates from accepted methods,
practices, procedures and treatments. (b) when he used accepted methods but
does so unskillfully.
(3) Free service - Doctor provided free medical service " injury or death of
patient occurred " doctor still liable to be prosecuted under criminal law, but
cannot be made to pay compensation under COPRA (please see below)].
(4) Components of medical negligence - For a case of medical negligence to be
established, the following components must be present (4Ds).

1. Duty
The doctor begins to owe a duty towards a patient
(1) as soon as he agrees to treat him.
(2) when he is in emergency. A doctor-patient relationship between the doctor
and the patient is established at that point in time. Doctor-patient relationship
is not formed when patient is not in emergency and the doctor did not agree
to treat the patient.

2. Dereliction of duty
Once the presence of duty has been established, there has to be a dereliction of
duty on the part of the doctor, i.e. the doctor should have been negligent in
performing his duties towards the patient.

3. Damage
(1) The damage must occur as a result of dereliction, and it must be foreseeable.
(2) Even if doctor is negligent, patient cannot sue him for compensation, if no
damage has occurred. He can however be sued criminally u/s 336, IPC
[please see below].
(3) Some examples of possible damages are:
(i) Aggravation - of a preexisting condition
(ii) Diminishing patient’s chances of recovery
(iii) Expenses incurred – eg hospital and medicine expenses, special diet etc.
(iv) Pain and suffering – causing either physical or mental [embarrassment,
fright, humiliation] pain or increasing it
(v) Loss of earning – due to absence from work
(vi) Loss of potency
(vii) Prolonging his illness
(viii) Reduced enjoyment of life – eg loss of a limb or sense
(ix) Reduction in expectation of life
(x) Death.

4. Direct causation
Damage must result directly from dereliction [proximate cause], and not from
any other cause. Proximate cause refers to a cause, which in natural and
continuous sequence, unbroken by any efficient intervening cause, produces the
injury, and without which the injury would not have occurred. It may also be
conceived of as a series of “falling dominoes”. If the final domino [damage]
can logically fall by “pushing” the first domino [dereliction], the “push” is the
proximate cause [direct causation] of fall of final domino [Fig 2.2]. Table 3
lists some differences between professional negligence and professional
misconduct.
B. Types of Negligence
Table 4 enumerates various types of negligence.
1. Medical negligence (MALPRAXIS)

a. Civil negligence (Civil Malpraxis)

Civil negligence is said to occur when patient demands monetary compensation
for the damage that he has suffered due to the doctor’s negligence. Civil
negligence comes under tort law [please see above].
Salient features:
(1) Question of civil negligence also arises - When patient refuses to pay
doctor’s fees alleging negligence, and doctor brings a civil suit against patient
to recover his fees.
(2) Court - The case goes either to civil court or to consumer forum.
(3) Punishment - The doctor only has to pay whatever compensation the court
decides. There is no criminal liability for him and he cannot be sent to jail for
his action.
(4) Additional punishments - However if the patient complains to medical
council also, it can take action against the doctor and can punish him
accordingly (e.g. removal of name from medical register temporarily or even
permanently).
(5) Standard of proof – Rests on preponderance of evidence [syn “balance of
probabilities”] i.e. there should be >50% probability of the doctor being
negligent in his conduct [please correlate with “Standard of proof” in ch 1]. It
is the duty of the patient to prove negligence.
(6) Defenses
(i) Informed consent
(ii) Contributory negligence [please see below].

b. Criminal negligence (Criminal Malpraxis)

Criminal negligence is that when patient complains to the police regarding the
misconduct of the doctor, and the police registers a case against the doctor.
Salient features:
(1) Who fights the case - State i.e. the government [not the suffering patient]
fights the case against the erring doctor.
(2) Punishment - The doctor is prosecuted under the various sections of the
Indian Penal Code (IPC) and if found guilty the doctor is liable to pay
damages as well as can be sentenced to a term in the prison.
(3) Standard of proof - In criminal negligence - in contrast to civil negligence -
the burden of proof that is required to prove the guilt is “beyond reasonable
doubt”. There should be >99% probability of the doctor being guilty. The test
is therefore more severe than the one applied for criminal negligence.

Classification
Cases of criminal negligence can be classified as follows:
(1) When no injury to the patient occurs (S.336, IPC) – Negligent action but
no injury " Patient cannot claim compensation, but he can still lodge a
criminal complaint against him under S.336, IPC if the doctor’s conduct was
so rash or negligent as to endanger patient’s life or his personal safety.
Punishment is imprisonment of 3 months, or `250 fine, or both.
(2) When injury occurs to the patient –Further subdivided into following: (i)
When hurt is caused to the patient (S.337, IPC) – Negligent action " Patient
suffers hurt [for definition of hurt, please see chapter 11] " S.337, IPC.
Punishment is imprisonment of 6 months, or `500 fine, or both. (ii) When
grievous hurt is caused to the patient (S.338, IPC) - Negligent action "
Patient suffers grievous hurt " 338, IPC. Punishment is imprisonment of 2
years, or `1000 fine, or both. When death is caused (S.304A, IPC) –
Negligent action " Death of patient " S.304A, IPC. The punishment is
imprisonment of 2 years, or fine (any amount) or both.

2. Patient negligence
Patient negligence is outright negligence by patient only. Doctor is not
negligent.
Salient features:
(1) Doctor is not liable in such cases.
(2) Examples: (i) Patient does not give correct history (ii) starts an alternative
form of treatment without informing doctor (iii) does not follow doctor’s
instructions. (iv) discontinues treatment (v) refuses to take treatment (vi)
LAMA – leaving [hospital] against Medical advice.

3. Contributory negligence
Contributory negligence is the name given to a situation, where both doctor and
the patient are negligent.
Salient features:
(1) Examples: (i) Doctor applies tight plaster cast on patient’s leg [doctor
negligent], but instructs him to report numbness " Patient develops numbness
in his toes " does not inform doctor [patient negligent] " suffers permanent
injury " Doctor entitled to the defense of contributory negligence. (ii) Doctor
prescribes drug " fails to inform the patient of its side effects [doctor
negligent] " patient starts getting side effects " fails to inform the doctor
[patient negligent] " suffers injury " contributory negligence.
(2) Burden of proof – lies with the doctor.
(3) Doctrine of comparative [or proportionate] negligence - Quantum of
injury caused by patient’s and doctor’s negligence is decided by the court and
the compensation awarded accordingly. If, say, patient’s negligence is
responsible for 80% of his injury, and doctor’s negligence for 20%, patient
would be entitled only to 20% of the compensation.
(4) Contributory negligence is a good defense in civil cases, but cannot be taken
as a defense in criminal cases.
(5) The doctrine of contributory negligence is subject to following exceptions (i)
Last clear chance doctrine - Both doctor and patient are negligent. But if it is
shown that the defendant (doctor) had a “Last Clear Chance” to avert the
damage caused to the patient, and he did not avail of this chance, he loses his
defense of contributory negligence. Example: Doctor prescribes drug to
patient " fails to inform of side-effects [doctor negligent] " Patient develops
rashes, but fails to inform doctor [patient also negligent, so concept of
contributory negligence comes into play] " Patient visits doctor on the next
 date " doctor sees rashes " fails to take remedial action " Patient suffers injury
" sues doctor " Doctor takes plea of contributory negligence. Analysis -
Patient can allege that the doctor had the “last clear chance” to avoid injury,
because on the patient’s next visit, the doctor did see his rashes and yet did not
do anything. (ii) The Avoidable Consequences Rule - Both parties are
negligent, but patient could have avoided his own injuries by being more
careful [It is in fact a variation of the Last clear chance doctrine” in as much as
he himself had the “last chance” to avoid injuries]. He could have avoided the
consequences of doctor’s negligence, but he did not carefully act upon it. So
he himself is responsible for his injuries and doctor need not pay. Example:
Doctor does not apply bandage and antibiotics to a gaping lacerated wound
(doctor negligent) " He however advises the patient not to allow the wound to
get contaminated, and visit him next week to get his wound examined again "
patient comes home and thinks that applying cow dung would heal his wound
faster " applies cow dung on his wounds " develops pus, but he does not
contact the doctor. Nor does he visit the doctor next week, as was advised by
the doctor (patient negligent) " Patient suffers injury. Analysis - Here both
doctor and patient are negligent and normally the compensation should have
been shared between the doctor and the patient. But since the patient
aggravated his own injury by doing something which was avoidable, the
doctor would be covered under the “avoidable consequences rule” and he does
not have to pay anything. (iii) Good Samaritan doctrine - One who assists
another who is in serious danger cannot be charged with contributory
negligence, unless the assistance is rash or reckless.

4. Composite negligence
Composite negligence is said to occur, when a patient suffers injury as a result
of the combined negligence of two or more doctors.

5. Corporate negligence
Corporate negligence is the negligence of a corporation [hospital]. The
individual doctor may or may not necessarily be liable in this case.

C. Important Concepts Related to Medical Negligence

1. Vicarious liability
Vicarious liability [syn vicarious responsibility, VL] means that a person is
liable for the wrongful acts or omissions of another.
Salient features:
(1) Respondeat superior [RS]- [lit, let the superior reply] Vicarious liability
arises under the principle of respondeat superior. The principle of RS holds
that the employer is responsible not only for his own negligence but also for
the negligence of his employees, if such acts occur in the course of the
employment and within its scope. (i) Also known as “captain of the ship”
doctrine. (ii) RS becomes applicable when the superior had the “right, ability
or duty to control” the activities of a violator. (iii) Difference between the two
terms - RS is the principle, while VL is the liability it puts on a superior. (iv)
RS principle ensures (a) that employers engage the best possible talent in their
hospital (b) that patient gets enough compensation due to him. Individual
negligent doctor may not have enough funds to pay the patient, but hospital
has. Also known as “doctrine of deep pockets”. Hospital has more money or
“deep pockets” so to say to compensate the patient.
(2) Preconditions: (i) There must be an employer – employee relationship (ii)
Employee’s conduct must occur within the scope of his employment [i.e.
employee did what he was legally supposed to do] and (iii) It should occur
while on the job.
(3) Compensation: (i) Both the negligent doctor as well as his employer may be
asked to compensate patient by the court. (ii) Employer may engage in a
separate “third party proceeding” to recover money from the negligent doctor.
(4) Relationships when one is vicariously responsible for the negligence of
other: (i) Senior doctor - responsible for negligence of junior doctor, resident,
intern or an assistant working under his supervision (ii) Hospital - responsible
for negligence of its doctor (iii) Two or more doctors working in partnership –
each is responsible for negligence of other (iv) Two or more doctors attending
on a patient independently – each may be help liable for the negligence of
other, if negligence produced symptoms and signs which an ordinary doctor
should have noticed and objected to. (v) Doctor referring his patient to an
incompetent doctor knowingly – Referring doctor is vicariously responsible
for negligence of incompetent doctor. (vi) Doctor writing illegible prescription
and pharmacist dispensing wrong drug – doctor is vicariously liable. (vii)
 Doctor instructing prescription over telephone and pharmacist dispensing
wrong drug – doctor vicariously responsible (viii) When an employee has
been temporarily borrowed from another – please see “Borrowed servant
doctrine” below.
(5) Relationships when one is not vicariously responsible for the negligence
of other: (i) Surgeon and anesthetist (ii) Qualified nurse acting independently,
not under the direct supervision and control of doctor – doctor not vicariously
responsible (iii) Doctor referring his patient to a competent doctor – referring
doctor not responsible [cf referral to an incompetent doctor]. (iv) Doctor
referring an already injured patient due to his negligence to a new doctor or
hospital – the latter is not vicariously responsible (v) Doctor writing clear,
legible prescription and pharmacist dispensing wrong drug – doctor not liable.

2. Borrowed servant doctrine

Borrowed servant doctrine states that if an employee is temporarily borrowed
by an employer from the principal employer, then the temporary new employer
becomes vicariously liable for any negligent act done by the employee.
Salient features:
(1) Principle – is that the lending employer temporarily surrenders control over
the employee. The new master (i) gains control over the employee (ii) directly
supervises the employee (iii) can give orders to him.
(2) The new master is responsible for the actions of hired employee [borrowed
servant] only as long as he is under his direct supervision.
(3) After the employee is returned, the original employer becomes responsible
for his negligent actions again.
(4) Ex – Resident [R] works on a regular basis in a big private hospital [H]. An
independent private specialist [S] hires an OT in H and also services of R " R
commits an act of negligence when he had been hired by S " Although R is a
regular employee of H, the latter is not vicariously responsible; S is
vicariously responsible, because negligence occurred when R was in direct
supervision of S.

3. Res ipsa loquitur

Ordinarily the professional negligence of a doctor must be proved by the patient.
Res ipsa loquitur [the thing or fact speaks for itself] is an important exception to
this rule, because here the professional negligence is so glaring and obvious that
it speaks for itself.
Salient features:
(1) Conditions to be satisfied before this rule can be legally applied: (i)
Injury to the patient would not have occurred in the absence of negligence (ii)
Doctor had exclusive control over the injury producing instrument or
treatment (iii) the patient was not guilty of contributory negligence.
(2) How proved - Generally without expert medical evidence. Common
knowledge or experience of a layman should be enough to understand and
appreciate that the negligence must have caused the injury [“Doctrine of
common knowledge” or “Common knowledge doctrine” – please see below].
(3) Applicable - to both civil and criminal negligence.
(4) Generally used - when there is no direct evidence of the doctor’s negligence.
(5) Examples: (i) Antiseptic – Failure to apply to an open cut (ii) Anti tetanus
serum – failure to give in cases of gross injuries. Patient developing tetanus.
(iii) Artery forceps, swabs etc - left in the abdomen. (iv) Blood transfusions –
mismatched (v) Breaking of needles (vi) Burns – (a) from cauterizing tool at
unintended places (b) from application of hot water bottles for excessively
long time (c) from negligent application of X-ray therapy (vii) Fluids – failure
to give in obvious dehydration (viii) Giving poisonous medicines recklessly
(ix) Prescribing overdose of medicines (x) Prolonged splinting; too tight a
bandage or plaster – loss of use of a limb (xi) Wrong amputation – eg right leg
[eye, kidney etc] has been amputated instead of the left (xii) Wrong teeth
removed (xiii) Wrong person -operated upon.

Doctrine of common knowledge

Doctrine of common knowledge” states that when negligence is of such obvious
nature that even a layman with ordinary common knowledge having no technical
expertise can appreciate it, then evidence of a medical expert to prove
negligence is not required.

D. Defenses Against Negligence

1. Actual denial
The doctor denies his responsibility straightaway and that he discharged his
duties according to the prevailing standards. His records should be proper and
complete to prove this assertion.

2. Calculated risk doctrine

Calculated risk doctrine [syn, doctrine of professional medical judgment]
asserts that doctor is not liable if he took a reasonable and calculated risk to save
life of patient and in the process patient suffered injury.
Salient features:
(1) Principle (i) Medical profession is a highly risk prone area and treatment
often involves a calculated risk and possible disagreement among experts as to
whether the risk was warranted or not. (ii) If a physician chooses for a patient
a course of treatment within a range of medically accepted choices, after a
proper examination and evaluation, the calculated risk doctrine will insulate
him from liability. (iii) To impose liability, a plaintiff must show that the
doctor’s decision was something that fell below the certified medical
determination.
(2) It is an important exception to the principle of res ipsa loquitur, since it
covers inherent risks of a medical procedure or operation.
(3) What doctor must prove – He must produce expert evidence or statistics
that the line of treatment he chose was a medically acceptable procedure under
the conditions, and that it had unavoidable risks.
(4) Examples - adverse reactions to penicillin, streptomycin, IV antibiotics,
immunizations of all sorts, blood transfusions, novocaine, X-ray dye studies,
injections into the spinal canal, injections of gold for rheumatoid arthritis, and
injections of cortisone directly into the joint.
(5) Case study: Siverson v. Weber (1962) - Dr. Charles Weber, a gynecologist,
performed hysterectomy on Lillian Siverson. 10 days later a vesicovaginal
fistula developed. Siverson brought a case of negligence against Weber. Citing
the doctrine of res ipsa loquitur, she asserted that she did not have to prove
anything. Merely the fact that hysterectomy was performed and that a fistula
developed after that meant that “the facts themselves spoke of negligence”.
The court however said that fistulas could occur even though the surgeon had
exercised the care and skill generally possessed and exercised by reputable
gynecologists and the development of a fistula, although rare, is considered an
inherent risk of the operation. It was a calculated risk taken by Dr. Weber
 [Siverson v. Weber 57 Adv. Cal. 881, 372 P.2d 97 (1962)].

3. Contributory negligence
Please see above.

4. Emergency
In emergency doctor may take some drastic measures to save life, which may
cause injury eg fracture of ribs during cardiac massage. Falls under calculated
risk doctrine also.

5. Law of limitation
Law of limitation specifies that a claim for compensation can be brought against
a doctor within a specified period. If the claim is brought after that period, the
doctor can take the defense of limitation. For cases related to consumer
protection act, the aggrieved patient must file a complaint within a period of 2
years of discovery of alleged negligence.

6. Medical misadventure
Medical misadventure [syn, Medical maloccurrence] is defined as a bad or
undesirable outcome that is unrelated to the quality of care provided.
Salient features:
It is an unintentional and unforeseen accident, disaster or mischief, which occurs
due to individual biological variations.
Types: (i) Therapeutic misadventure [TM]– when treatment is being given [eg
serious drug reaction to a common drug like aspirin; breaking of a needle during
IM inj due to sudden muscular contraction; patient dying of shock during pleural
or peritoneal tap]. (a) History of sensitivity - (i) should be obtained before
injecting any drug, especially antibiotics, biological products and sera. (ii)
Negative history and even negative tests do not however rule out possibility of
anaphylactoid reactions and death. Patient should be specifically informed of
this orally and in writing (b) In the event of a reaction - (i) an alternate drug
should be advised. (ii) If doctor fails to stop offending drug, he cannot take this
defense. (c) If a drug causes drowsiness or other accident prone side-effects,
doctor should clearly inform the patient, and advise to avoid driving, working
near dangerous machines etc. For legal immunity, it is advisable to even write
this information on the prescription sheet. (ii) Diagnostic misadventure - When
diagnostic procedures are being carried out [eg fatal allergic reaction to an ionic
contrast media before taking CT]. (iii) Experimental misadventure – Where a
patient was a participant in an experimental study.

7. No duty owed towards the patient

If the doctor had not agreed to treat patient, no duty exists.

8. Novus actus interveniens

Novus actus interveniens [Syn - Nova Causa Interveniens, an unrelated act
intervening] refers to a situation, where the doctor has been negligent, but a
completely unexpected and unforeseen act happened which further worsened the
patient’s condition.
Salient features:
(1) The new act intervening should be completely unexpected and unforeseen.
Sometimes referred to as an “Act of God”.
(2) Breaks the chain of causation between the act of negligence and the
resulting damage [Fig 2.3]. Thus injury no more remains a proximate cause of
doctor’s negligence.
(3) Analogy – Student does not prepare for exams thinking that he can cram up
on the last night"On the last night there is suddenly a failure of electricity [an
act of God]"Student cannot cram up"fails. Analysis – Student has to face
consequences at 2 places – in the examination results [a stricter option, just
like “criminal negligence”] and before his parents [a softer option, just like
“civil negligence”] His plea of NII [electricity failure on last night] will not
help him pass the examination [loss of case in a stricter option], but he may
perhaps convince his parents about his stand [a softer option].
9. Patient negligence
Please see above.

10. Res judicata

(1) Res judicata is a Latin term meaning “the thing has already been decided”
[S.300, CrPC]. Also known as the “doctrine of double jeopardy”.
(2) If a question of negligence against a doctor has been decided in one court [eg
a consumer court], the patient cannot start another proceeding in a different
court. Appeal to the higher court however is allowed. Ex - A patient who has
paid for his treatment would prefer to lodge a complaint with District forum,
since decisions are quicker. On loosing the case, he can appeal to higher
courts, i.e. State Commission, National Commission and Supreme Court. But
after getting decision from the highest court, he cannot now lodge a fresh
complaint with normal civil court. If he does, the doctor can take plea of res
 judicata.

11. Volenti non fit injuria

Volenti non fit injuria [Latin, to a willing person, injury is not done] is a legal
doctrine which means that if someone willingly places himself in a position
where harm might result, he will not be able to bring a claim against the other
party.
Salient features:
For this claim to succeed the doctor must show that an informed consent had
been taken and all side-effects had been explained, eg if patient sustains
radiation burns during therapy, and he had earlier been explained about the risks,
he cannot claim damages.

12. Countersuits by doctors

Doctor files a countersuit against the patient. Should only be resorted to when
the doctor is absolutely sure there was no fault and the litigation is frivolous and
vexatious. It is not exactly a defense, but may deter patients to go in litigation in
future, and more importantly, settle a compromise deal with the patient and
withdraw the case.
Memory Aid 4: Defenses against negligence
C3D2E – LMN2 – P R i V ate
C-Calculated risk, Contributory negligence, Countersuits
D-Denial, Delegation
E-Emergency
L-Limitation
M-Misadventure
N-No Duty, Novus
P-Patient negligence
R-Res judicata
V-Volenti non fit injuria

VIII. MEDICAL RECORDS

Medical record [MR] [syn, health record, medical chart] is a document which
records, documents and chronicles patient’s history, medical examination,
laboratory and ancillary investigations, treatment advised, operation notes,
discharge summary, details of subsequent visits and any other data regarding
patient treatment.

IX. PRODUCTS LIABILITY

Products liability occurs, when a manufacturer supplies a defective medical

instrument or gadget (product) to the doctor or hospital; doctor inadvertently
uses the defective product causing injury to the patient.
Salient features:
(1) Instances when product liability occurs: (i) Instruments - (a) Faulty,
defective or negligently designed medical or surgical instruments [eg a
defective defibrillator] (b) wrong or inadequate operating instructions (ii)
Medicines - (a) Components incorrect (b) potency too low or too high (c)
instructions of taking wrong, eg oral medicine instructed to be instilled in eye
(iii) Defective prosthetic devices - (a) artificial heart valves, limbs etc (b)
pacemakers.
(2) Legal duties of manufacturer: (i) To use due care and research in
development of all medical products, including medicines, medical and
surgical instruments etc (ii) To perform studies of its product, when adverse
reactions are reported in articles in scientific journals, and to report the results
of these studies to physicians.
(3) When is manufacturer liable: (i) Almost always, unless doctor used the
instrument incorrectly (ii) With respect to medicines if harm was caused due
to adulteration, contamination, incorrect dosage or wrong labeling of drug.
(4) When is doctor liable: (i) if the instrument functioned satisfactorily during
previous operations (ii) Incorrect use – by doctor (iii) Wear and tear - occurred
in the instrument either due to normal wear and tear, or due to mishandling by
doctor or paramedical personnel (iv) If the instrument was out of warranty,
and required periodic inspection, testing and repairing and no request was sent
to manufacturer for this (v) If instrument required periodic servicing and it
was not sent for servicing (vi) If doctor knew [or should have known] the
dangerous side effects, and could have used a substitute drug, yet decided to
use the dangerous drug for no plausible reason (vii) If manufacturer has
provided information in “package insert”, but doctor failed to convey it to
patient. Once the manufacturer has made a warning in this manner, it is the
 duty of doctor to convey this warning to the patient. Manufacturer has no duty
to ensure that such warnings in the “package insert” reach the patient.

X. MEDICAL INDEMNITY INSURANCE

Medical Indemnity Insurance [MII] [syn, Medical Malpractice Insurance

(MMI] is a contract between the doctor and an insurance company, under which
the latter agrees, in exchange for the payment of premiums, to indemnify
[reimburse or compensate] the insured doctor against claims resulting from his
professional negligence.

XI. EUTHANASIA [MERCY KILLING]

Euthanasia [Gk eu, good; thanatos, death] or mercy killing means voluntary
putting to death of a patient who is suffering from an incurable, terminal and
extremely painful condition. Euthanasia was common in ancient Greece and
Rome. This practice was challenged by Hippocrates, who spoke against it,
writing, “I will not prescribe a deadly drug to please someone, nor give advice
that may cause his death”. Among most famous recent cases of euthanasia, King
George V [1865 – 1936] was euthanized by his physician Lord Dawson by
administering a lethal injection of cocaine and morphine. John Bodkin Adams,
British general practitioner [ch 40], is thought to have euthanized several of his
patients with morphine.

A. Classification

1. According to Physician’s act

a. Active euthanasia
(1) Physician does an act of commission to bring an end to life, eg giving an
injection of lethal drugs.
(2) Case studies: (i) Howard Martin (1935-), a British doctor euthanized 18
patients by giving them morphine injections. In 2005, he was tried for the
murder of 3 patients, but was acquitted by the court, because he had no motive
to kill other than euthanizing patients who were in great pain. Nevertheless the
General Medical Council [GMC] struck his name for life.
b. Passive euthanasia
(1) Physician does an act of omission to bring an end to life, eg
(i) not using measures that would prolong life,
(ii) discontinuing or withholding extraordinary life sustaining measures [O2, IV
fluids etc] to prolong life,
(iii) failure to resuscitate a terminally ill or hopelessly incapacitated patient, or a
severely defective newborn [Table 5].
(2) Broadly active euthanasia is killing while passive euthanasia is letting die.
(3) Passive euthanasia is legal in India.

2. According to the will of the patient

a. Voluntary euthanasia
(1) Patient wants to die and makes a request to this effect [ie patient consent is
there].
(2) He must be competent to make this choice [i.e. must be mentally sound].
(3) Voluntary euthanasia is legal in: (i) Belgium (ii) Luxembourg (iii)
Netherlands (iv) Switzerland (v) U.S. - (a) Oregon (b) Washington.
(4) Classification - Divided into two further types according to involvement of
patient himself in the dying process.
b. Involuntary euthanasia
(1) Patient does not want to die, yet he is compulsorily killed.
(2) Examples:
Soldier has received vital injuries on abdomen "his intestines are hanging out "
He is in great pain " requests a doctor to save his life " doctor knows he can not
be saved " wants to end his suffering " shoots him.
c. Non-voluntary euthanasia
(1) Ending life of a person who is in coma and cannot make a decision on his
behalf [eg persons in irreversible coma, severely defective infants].
(2) Case studies: (i) Karen Ann Quinlan’s case [ch 8] (ii) Terri Schiavo’s case
[ch 8].
B. Dysthanasia
Dysthanasia [Gk dys, bad; thanatos, death] is the converse of euthanasia, and is
generally considered undesirable. This term is generally used when a person is
kept alive artificially in a condition where, otherwise, he could not have
survived, especially done for some sort of ulterior motive.

C. ML Aspects
Indian law – does not allow euthanasia [S.89, S.92, IPC]. Doctor may be
charged u/s 304, IPC.

XII. CONSENT IN MEDICAL PRACTICE

Consent means voluntary agreement, compliance, or permission.

Salient features:
(1) Indian Contract Act, 1872: (i) S.13 - Two or more persons are said to
consent when they agree upon the same thing in the same sense. Patient must
understand, what it is given for and what are the risks involved (ii) S.14 -
Consent is said to be free when it is not caused by coercion, undue influence,
fraud, misrepresentation or mistake.
(2) Components of a legally valid consent: (i) Patient >12 y [for general
physical examination]; >18 y [for surgery; please see S.88, IPC below]. In
 case of child, consent from guardian who should be >18 y (ii) Patient
understands that he can either agree or refuse to submit to examination,
diagnosis and treatment (iii) Has been provided full information on his disease
and treatment options [informed consent]. (iv) Consent should be clear, direct,
free, informed, intelligent, personal and voluntary (a) Clear " in unambiguous
words (b) Direct " directly conveyed to the doctor by patient, with no
intermediaries (c) free " without undue force (d) informed " please see below
(e) intelligent " patient should have clearly understood the implications of
treatment. No ambiguity. No communication barriers (f) personal " Doctor
should not communicate to anyone, what the patient has consented for (g)
Voluntary " of his own accord.
(3) Consent of an arrested person at police request – not necessary u/s
53, CrPC [ch 11].
(4) Consent of an arrested person at his own request: (i) Before 2008, it could
be done any time during his custody u/s 54, CrPC, if he made a request to the
magistrate. (ii) This section has been amended since 2008; the amended S.54
mandates compulsory medical inspection in all cases of arrest by the police.
(iii) A copy of the medical report is to be provided to the arrested person or his
nominee. (iv) If the arrested person is a female, her examination can be done
only by or under the supervision of a female doctor [S.54(1), CrPC]. Please
compare with corresponding S.53(2), CrPC [ch 11].
(5) Consent of victim in criminal cases – In victims of assault, rape and in
cases involving pregnancy, abortion and delivery, examination of victim is
necessary to gather evidence of crime. However if victim does not consent to
examination it cannot be done.
(6) Conflict of consent – When two persons legally competent to give consent
differ. Case must be referred to court, through IO.
(7) Consent of victim of statutory rape – ch 25.
(8) Consent of an alcoholic – ch 40.
(9) Consent of spouse: (i) Legally required - (a) for receiving artificial
insemination (b) For donation of ovum or sperm.
Memory Aid 5: Consent of spouse
Consent of spouse legally required: Giving and taking of gametes, because gametes may be construed as belonging to
spouse also

(ii) Legally not required but desirable to avoid marital conflict later - (a) MTP
(b) Sterilization (c) Any operation that can affect sexual life [eg breast
 reduction, penectomy, penis transplantation]
(10) S.87, IPC - It is not meant for doctors, because the act done by perpetrator
is not done for the benefit of the opposite party. (i) It is applicable to people
who undertake risky activities. (ii) To participate in a risky activity, the
consenting person must be >18 y. (iii) The act by the perpetrator must neither
be intended, nor known to be likely to cause death or grievous hurt.
(11) S.88, IPC - It is meant for doctors, because the act done by perpetrator is
done in good faith for the benefit of the opposite party. (i) It is applicable to
doctors (ii) The consenting person must be >12 y [S.90, IPC]. (iii) definition
of good faith given in S.52, IPC – please see below.
(12) S.89, IPC - Act done in good faith for benefit of child <12 y or a person of
unsound mind, by consent of guardian – is not punishable. Following provisos
apply (i) this exception does not extend to the intentional causing of death
[euthanasia], or to the attempting to cause death; (ii) this exception does not
extend to the doing of anything which the doer knows to be likely to cause
death, for any purpose other than the preventing of death or grievous hurt, or
the curing of any grievous disease or infirmity; (iii) this exception does not
extend to the voluntary causing of grievous hurt, or to the attempting to cause
grievous hurt, unless it be for the purpose of preventing death or grievous hurt,
or the curing of any grievous disease or infirmity; (iv) this exception does not
extend to the abetment of any offence.
(13) What makes consent valueless – Consent given (i) under fear of injury (ii)
under a misconception of fact (iii) Consent of mentally unsound person [ch
28] (iv) consent under intoxication (v) Consent of child <12 y [S.90, IPC;
please also see ch 25].
Memory Aid 6: What makes a consent valueless
Forensic Medicine Master Is Coming - Fear, Misconception, Mentally unsound, Intoxication, Child

(14) S.52, IPC - Definition of “Good faith” — Nothing is said to be done or

believed in “good faith” which is done or believed without due care and
attention.
(15) in loco parentis [in place of parent] – In emergency if parents are not
available, person in charge of child [eg a school teacher, a hostel warden] can
give consent.
(16) If inmate of jail, hostel etc refuses treatment, and he is likely to spread
disease - he can be forcibly administered treatment. Inmate of a hostel may be
 asked to leave hostel.
(17) In state mandated national programmes – eg pulse polio, vaccinations, no
consent is needed.
(18) Consent for illegal acts [eg criminal abortion] – is invalid.
(19) Consent is not a defense – in cases of professional negligence.
(20) Discharge against medical advice – If a patient wants to leave against
medical advice [LAMA], the dangers should be explained clearly in writing;
then his wish should be recorded in the case sheet and his signatures obtained.
Patient can then be discharged. In the discharge certificate, the doctor should
specifically write the dangers of leaving hospital against medical advice.

A. Kinds of Consent
Consent may be classified (a) According to information provided to patient:
(1) Uninformed consent [information completely or partly held back from
patient]. Illegal unless it falls within the concept of “therapeutic privilege”
[please see above]. (2) Informed consent [please see below] (b) According to
the way patient communicates it to the doctor. It may be (1) Implied – when
patient’s actions imply consent [eg, telephoning, SMSing or emailing a doctor
and asking for advice; (2) Express – (i) Def - When patient specifically consents
to examination either (a) verbally [oral or verbal consent] or (b) in writing
[written consent]. (ii) When required – in all procedures beyond routine physical
examination [biopsies, Blood transfusions, LP, operations, Pleural and peritoneal
tap etc] (iii) When taken – Before the act; not after it (c) Miscellaneous kinds of
consent - (1) Blanket consent – is one where the doctor takes consent from the
patient for any and every possible diagnostic or treatment procedure that might
have to be undertaken any time in the future. (i) Since doctor himself is not sure
of the kind of treatment that might be undertaken, patient cannot be explained of
its risks etc. (ii) Many nursing homes and private hospitals, take blanket consent
in the following manner “I hereby authorise staff of this hospital to perform any
surgical or anaesthetic procedure on me.” (iii) Blanket consent is invalid in the
eyes of law. (2) Proxy consent [syn, substitute consent, surrogate consent] –
Consent given by a relative, next of kin or friend in case the patient himself
cannot give consent [child <12 y, mentally unsound person, intoxication,
unconsciousness etc].
B. Informed Consent
Informed consent means that consent of patient for any procedure or treatment
can only be taken after fully informing him about the nature of his condition.
Salient features:
Consent should always be informed.

1. Components of an informed consent

(1) Informed consent has five essential components, (i) disclosure, i.e.
transmission of the information which is material to a decision; (ii)
comprehension, or substantial understanding of this information; (iii)
absence of any outside control over the decision; (iv) competence; and (v)
actual consent.
(2) Disclosure [component 1] - Patient must be told (i) nature - of his disease (ii)
Options available – All treatments, costs, risks, benefits, success and failure
rates, after-effects and prognosis of each (iii) In case of surgery – (a) Whether
it would be done under local or general anesthesia (b) Possible harmful effects
of anesthesia (c) Details of all possible operative procedures, their relative
benefits and risks (d) costs of each (iv) Risks - of not receiving any treatment
[informed refusal].
(3) Comprehension [component 2] - Language - Explanation must be done in
patient’s own language. If need be, an interpreter may be employed.
(4) Absence of any outside control over the decision [component 3] – doctor,
nurse, paramedical staff or any relative must not influence the decision. If
patient voluntarily asks for advice, it may be given.
(5) Competence [component 4]: (i) patient should be above age of consent [>12
y for GPE; >18 y for surgery; ch 3] (ii) should be mentally sound (iii) should
not be under influence of alcohol or drugs.
(6) Actual consent [component 5]: Written and witnessed - To make it legally
acceptable, (a) everything explained must be reduced to writing and (b)
signatures of patient obtained (c) in presence of two independent witnesses to
prevent any allegation that the consent was forged or obtained under
compulsion or pressure.

2. Advantages of taking informed consent [or reasons for obtaining consent]

(1) Patient cannot sue doctor (i) u/s 350, IPC (ii) u/s 351, IPC [ch 11] (iii) for
 obtaining consent by misrepresentation of facts [S.90, IPC].
(2) Legally to examine, treat and operate upon a patient without consent, even if
done in good faith is punishable under above sections.

3. Principles which form the basis of informed consent

(1) Principle of full disclosure or patient’s right to truth.
(2) Principle of patient autonomy.

Principle of full disclosure

Principle of full disclosure states that a doctor should reveal all information to
the patient, regarding his disease, treatment options etc.
Salient features:
(1) Withholding information from a competent patient is a violation of the
doctor’s role as a fiduciary [please see above] and is not justified.
(2) Exceptions to principle of full disclosure (i) Doctor need not disclose risks
of which he is himself unaware (ii) If the risk is so obvious that a person with
normal intelligence can easily understand. (iii) Therapeutic privilege [please
see above]

4. Exceptions to informed consent

(1) Emergency [S.92, IPC]. Exactly same provisos apply for mentally unsound,
intoxicated, persons <12 y and persons otherwise incapable of giving consent.
Ex. Patient consents to laparotomy " during operation doctor discovers an
unanticipated condition which endangers the life of patient " patient is under
anesthesia " consent for the new operation cannot be taken " doctor undertakes
procedure " protected u/s.92, IPC. This exception however does not extend to
causing death. Ex - Doctor finds a lesion which would cause excruciating pain
to patient, and he is sure, the patient cannot live for more than 6 months with
the lesion. He decides to commit euthanasia to save unnecessary suffering. It
is illegal.
(2) Therapeutic privilege.
(3) Waiving of rights by patient – Patient expressly waives his right to informed
consent to doctor.
(4) Case studies – Please see Jackovach v. Yocum below.
C. Informed Refusal
The concept of informed refusal states that the doctor must inform the patient
about the risks of refusing a particular operation, test, medication, or other
medical intervention.
Salient features:
Concept of informed refusal is inherent in informed consent [please see above].
It assumes importance only when the patient does not consent to treatment
despite being informed of risks of refusal. To be legally valid, such informed
refusal must be reduced to writing with signatures of patient, doctor and witness.

D. Additional Rules of Consent

(1) Necessity – Consent is required for all medical examinations. Ordinarily
express consent is not required, because implied consent is inherent in
patient’s behavior.
(2) Verbal consent – Must be obtained in the presence of a disinterested third
party, eg a nurse.

XIII. HUMAN EXPERIMENTATION

Human experimentation is conduction of medical experiments on humans.

Declaration of Helsinki (1964)

Adopted by the 18th WMA General Assembly held at Helsinki, Finland in June
1964 and amended in 1975, 1983, 1989, 1996, 2000, 2002 and 2004. Prescribes
ethical Principles for Human Experimentation.
Memory Aid 7: Declaration of Helsinki
Helsinki"Human experimentation.

XIV. THE WORKMEN’S COMPENSATION ACT, 1923

The Workmen’s Compensation Act, 1923 [WCA, 1923] is one of the earliest
labor welfare and social security legislation enacted in India.
Salient features:
Aims and objectives: (i) Provides compensation to workmen and their
dependents - in case of accidents arising out of and in the course of employment
causing death or disablement of workmen. Compensation is payable by
employer (ii) lays down various amounts payable in case of an accident,
depending upon the type and extent of injury.

XV. CONSUMER PROTECTION ACT, 1986

Consumer Protection Act 1986, [Syn, CPA, COPRA] is a legal statute whose
purpose is to provide for better protection of the interests of consumers.
Salient features:
Aims and objectives: to protect the interest of consumers - of different
commodities [eg TV, car] and services [eg banking, airline travel].

A. Consumer Disputes Redressal Agencies

There are three agencies:
(1) District Forum
(2) State Commission
(3) National Commission

1. Manner of making complaints

(1) A complaint in relation to any goods sold or delivered or any service
provided may be filed with a District Forum by (a) the consumer. If consumer
dies, his legal hair or representative (b) any recognized consumer association
(c) one or more consumers, where there are numerous consumers having the
same interest, with the permission of the District Forum (d) Central or the
State Government. Every complaint must be accompanied by a fees prescribed
by the State Govt [S.12].
(2) On receipt of a complaint - The District Forum may allow the complaint to
be proceeded with or rejected [after giving an opportunity to the complainant
of being heard]. Admissibility of the complaint shall ordinarily be decided
within 21 days from the date on which the complaint was received [S.12(3)].
(3) Frivolous or vexatious complaints – are dismissed after recording the
reasons in writing. The complainant may be asked to pay a cost of up to
 `10,000 to the opposite party [S.26].

2. Procedure
(1) Speedy trials:
(i) Every complaint is heard as early as possible and must preferably be decided
within 3 months.
(ii) No adjournment are ordinarily granted by DF unless sufficient cause is
shown and the reasons for grant of adjournment have been recorded in
writing by the Forum [S.13(3A)].
(2) If complaint refers to any service, the Forum shall refer a copy of such
complaint to the opposite party directing him to give his version of the case
within a period of 30 days. An extension of 15 days may be granted
[S.13(2), (a) ]. Notices may be served even by FAX [S.28(2)].
(3) It is not necessary for parties to be represented by lawyers.
(4) Every proceeding before the DF shall be deemed to be a judicial proceeding
within the meaning of S.193 and 228 of IPC, and DF shall be deemed to be a
civil court.
(5) Appeals against orders of District Forum:
(i) Must be made to the State Commission within 30 days from the date of order.
(ii) If there was sufficient cause for appeal later than 30 days, State Commission
can entertain it.
(iii) Fees - appellant must deposit 50% of amount ordered by DF or `25,000
whichever is less [S.15].
(6) Appeals against orders of State Commission:
(i) Must be made to the National Commission within 30 days from the date of
order.
(ii) If there was sufficient cause for appeal later than 30 days, National
Commission can entertain it.
(iii) Fees - appellant must deposit 50% of amount ordered by SC or `35,000
whichever is less [S.19].
(7) Appeals against orders of National Commission:
(i) National Commission is empowered to review its orders to avoid rush to the
Supreme Court
(ii) However even if review does not give relief to a party, the appeal must be
made to the Supreme Court within 30 days from the date of order.
(iii) If there was sufficient cause for appeal later than 30 days, Supreme Court
can entertain it
(iv) Fees - appellant must deposit 50% of amount ordered by SC or $ 50,000
whichever is less [S.23].
(8) Ensuring payment of compensation – To ensure payment of compensation,
the Consumer Courts [DF, SC, NC] can attach the property of the opposite
party and dispose it to recover amount due to the complainant. District
Collector would help the courts to recover this amount.
(9) Finality of orders – If no appeal has been preferred against order of a DF,
SC or NC, such order shall be final [S.24].

3. Limitation period
The District Forum, the State Commission or the National Commission normally
will not admit a complaint unless it is filed within 2 years from the date on
which negligence was committed. But under special circumstances complaints
after 2 years may be entertained if the Forum or Commission is satisfied that
there is sufficient reason for doing so, and it must record in writing, the reasons
for entertaining such late complaints [S.24A].

4. Who is covered under COPRA

(1) All doctors and hospitals who have charged for their service.
(2) All doctors and hospitals [including Govt hospitals, health centers,
dispensaries etc] who perform partial charitable services, i.e. who charge from
few patients only [rich] and other [poor] are not charged. All [both rich and
poor] can get benefit under COPRA.

5. Who is immune from COPRA

(1) Doctors and hospitals [including Govt hospitals] which are doing a
completely charitable service not charging anyone [i.e. neither rich nor poor
are charged].
(2) Hospitals charging a token amount for registration purpose only – It is not
payment for the purposes of COPRA.

XVI. ORGAN DONATION AND TRANSPLANTATION –

LEGAL ASPECTS
A. The Transplantation of Human Organs and Tissues Act, 1994
(No. 42 of 1994)
The Transplantation Of Human Organs and Tissues Act, 1994 [TOHOTA]
provides for (i) regulation of removal, storage and transplantation of human
organs for therapeutic purposes and (ii) prevention of commercial dealings in
human organs. The Transplantation of Human Organ rules were framed in 1995.
The Act was amended in 2011 [27th Sep].

XVII. THE PROTECTION OF HUMAN RIGHTS ACT, 1993

(1) The Act was passed in 1993 and amended in 2006. It provides for the
constitution of a National Human Rights Commission [NHRC (S.3)] at the
Center, State Human Rights Commissions [SHRC (S.21)] in States and
Human Rights Courts [S.30].
(2) Purpose - Better protection of human rights.

XVIII. MEDICOLEGAL ASPECTS OF HIV AND AIDS

A. Civil
1. Discrimination
HIV+ve person can not be isolated, quarantined or discriminated against.
2. Divorce
U/s S.13(1) of Hindu Marriage Act, 1955, a person can get divorce, if spouse has
been suffering from venereal disease in a communicable form [ch 23].
3. Employment
According to India’s National Policy on HIV/AIDS [please see above], a person
can neither be denied employment because of his HIV+ve status, nor can he be
discriminated during service, nor can he be terminated from job solely due to
HIV+ve status.

B. Criminal
Marriage or intercourse:
(1) HIV +ve person A knowingly marries B [or performs intercourse] without
 informing B of his status " B catches infection " A can be sued u/s 269, IPC.
S.269 may apply when the accused (a) did not know he was HIV+ve and (b)
did not understand how HIV is transmitted
(2) If accused disclosed his HIV+ve status to the person at risk [or honestly
believed the other person was aware of his status], there may be no case.

C. Rights of HIV+ve Patients

(1) An AIDS patient has the right to life and personal liberty [Art 21,
Constitution of India]. It means that he has the right to treatment of his
disease like any another person.
(2) They have the right to privacy. It means that they have the same right as
other patients with regard to the disclosure of their disease status to other
people and general public as a whole. In other words, one (doctor or hospital)
can’t do things like putting labels on their beds indicating their HIV
status.
(3) They cannot be isolated or quarantined on the basis of their disease.
(4) They cannot be discriminated in any sphere of life, including their job, due to
their HIV status.

D. Duty of Doctors
(1) Confidentiality:
(i) Normally a doctor must maintain professional secrecy, but in case of HIV+ve
patients, he can reveal the HIV+ve status to the prospective bride.
(ii) In case of married couple, the status of married partner can be told to the
spouse. The latter can then apply for divorce under provisions of the Hindu
Marriage Act, 1955.
(2) Careful screening of blood:
(i) for HIV status - before blood donation, transfusion, surgical operation or
organ transplantation.
(ii) Precautions - (a) screen living donors for HIV as close to the time of organ
recovery and transplantation as possible, using sensitive tests for both
chronic and acute infections, namely, serology and nucleic acid testing
[NAT] (b) inform transplant candidates of the potential risks for disease
transmission (c) advise donors that they have an obligation to avoid
behaviors that would put them at risk for acquiring HIV before organ
 donation.
(iii) Arguments in favor of routine screening (a) Charges of negligence – may be
brought by the patient, if patient discovers after the operation that he is HIV
+ve. He may allege that the infection was transmitted through these
procedures. Preoperative or pretransfusion screening will protect the doctor
from such charges
(iv) Arguments against routine screening (a) The accepted ethical standards of
autonomy, confidentiality, and informed consent are broken.

E. Miscellaneous
Multiple tattooing with same needle may cause HIV transmission.

3. Identification

I. INTRODUCTION

Identification is the determination of the individuality of a person – living or

dead.
A. Case Study
1. Bhowal Sanyasi case [1921]
A rich person Kumar Ramendra Narayan Roy [Fig 3.1] allegedly died of
biliary colic in 1909 in Darjeeling. In 1921, a Sadhu (Bhowal Sanyasi) arrived in
Dacca, and claimed that he was Kumar Ramendra, and asked for his share in
property. When denied, he filed a suit in a Dacca court in 1930, for restoration
of his legal rights. Most of his identification data was exactly the same as that
of Ramendra including pink and white complexion, brown wavy hair, light
moustache, twisted lip, sharp angle at the rim of ear, ear lobes pierced and not
adherent to cheeks, broken left upper first molar, a fleshy point in the right lower
eyelid, size 6 for shoes, irregular scar on left ankle, syphilitic ulcers, boil mark
on the head and back, operation mark near the groin, tiger claw mark on the right
arm and even a minute mole on the dorsum of the penis. He was declared by the
court to be Kumar Ramendra Narayan Roy and entitled to the property.
However the Bhowal Sanyasi died shortly after the decision of the court in July
1946.

II. CORPUS DELICTI

Corpus delicti [from Latin corpus, body; delictum, crime] is the legal principle
requiring positive proof of crime before someone can be convicted of
committing that crime. Also known as the body of crime, foundation of crime or
essence of crime.
Salient features:
(1) Corpus delicti includes anything which positively prove a crime.
(2) In case of homicide, it would include the dead body, photograph of dead
body, blood stained clothes showing weapon marks, blood stained
weapon, bullet, severed body parts (eg head) etc.
III. IDENTIFICATION DATA

Table 1 enumerates important identification data. Please also see Fig 3.2.
A. Race
Three races are recognized: (i) Caucasoids (ii) Mongoloids, and (iii) Negroids.
Race – as mentioned above - can be determined by:

1. Skin
(1) Caucasoids are white skinned,
(2) Mongoloids yellow skinned, and
(3) Negroids black skinned
(4) Indians - brown
(5) Skin color changes in advanced decomposition and burns -> determination
of race may become difficult.

2. Eyes
(1) Caucasoids have blue eyes.
(2) Black in other races.
(3) People of mixed races (e.g. Indians) may have brown eyes.
3. Hair
(1) Caucasoids have light colored, reddish or golden hair. They are curly or
wavy and cross section is oval.
(2) Mongoloids have dark colored hair. They are straight, and cross section is
round.
(3) Negroids have dark colored hair. They are wooly and arranged in tight
spirals, and cross section is kidney shaped (Fig 3.3).

4. Skeleton
Racial differences in the skeleton are enumerated in Table 2. (1) Prognathism –
A quick test is to occlude the lower jaw in its proper dental occlusion, and with a
pencil attempt to touch the base of the nasal aperture and chin at the same time.
This can be done in Caucasoid skulls, but not in Negroid and Mongoloid skulls.
Memory Aid 1: Cusp of Carabelli
Cusp of Carabelli is present in Caucasoids.
a. Skull
Cephalic index
Cephalic index (CI) [syn index of breadth] is the ratio of the maximum width
(B) of the head divided by its maximum length (L), multiplied by 100. CI as a
criterion of race was introduced in 1842 by Anders Retzius (1796 – 1860). It is
now known that besides race, local environmental conditions also influence the
CI. Its validity in race determination has been challenged.
C.I. = # 100
Memory Aid 2: Sex related indices
All sex related indices [Table 3] are higher in females except chilotic line index and corporobasal index,
which are more in males. Both start with C.
Salient features:
(1) Measurements: (i) Maximum length of skull = Summit of glabella to
furthest occipital point.
(ii) Maximum breadth of skull = greatest breadth, at right angles to sagittal
plane. (iii) measured by sliding calipers. If not available, use osteometric
board.
(2) As seen from the top, a longer skull is dolichocephalic and a more rounded
skull is brachycephalic. Brachycephaly can occur in any other race also if the
coronal suture fuses prematurely [flat head syndrome].
(3) Races can be determined to some extent by CI [Table 3]. An average Indian
has a mesaticephalic skull.

Memory Aid 3: How to remember indices

There are about 15 important indices [Table 3], all of which can be remembered using the following 3
simple rules:
1. Think up 2 most natural dimensions of the related bone
2. Keep smaller dimension in numerator; larger in denominator
 Only one index – medullary index – is not so multiplied. Strictly
3. multiply with 100.
speaking it is a co-efficient. Conventionally co-efficient is measured between 0
and 1. When it is expressed as a percentage, it is called an index.
Example 1 – Remembering cephalic index
1. Cephalic is skull. 2 most natural dimensions are length and breadth.
2. Breadth is smaller so we get B/L.
3. Multiply above by 100.
Example 2 – Remembering sternal index
1. Sternal refers to sternum. 2 most natural dimensions are height of manubrium [M] and height of body
[B]
2. M is smaller so we get M/B.
3. Multiply above by 100.
With some practice, all indices can be similarly derived. In fact the definition of index is that it is “the
percentage expression of the ratio of a smaller dimension over a larger one”.
(4) Use of indices – In forensic medicine, indices are used for solving 3 major
questions – race, sex and species origin [human or animal] [Table 3].

b. Long bones
(1) Brachial index [Latin Brachium, arm]
[syn, radio-humeral index] = # 100

(2) Crural index [Latin crus, leg] [syn, tibio-femoral index] = # 100

(3) Intermembral index = # 100

(4) Humerofemoral index = # 100

B. Religion
(1) Hindu males are not circumcised and wear a sacred thread.
(2) Muslim males are circumcised, have corns and callosities on lateral aspects
of knees and feet and have a black spot on their forehead [From making
sujood, (placing of the forehead on the ground in prayer)].
(3) Hindu females wear sindoor on head, nose rings and ear rings.
Memory Aid 4: Racial differences in cephalic index. Pl. correlate with Table 4.
Du MB Horse
C. Sex
Normally sex determination is easy from external examination (Table 6), but it
may be difficult in cases if (i) Advanced decomposition (ii) Concealed sex (iii)
Hermaphroditism (iv) Skeleton.

1. Intersex
An intersex is an intermingling in one individual of characters of both sexes in
varying degrees, including physical form, reproductive organs, hormonal profile
and sexual behavior.
Salient features:
(1) Incidence is 0.018% without the inclusion of Klinefelter’s syndrome and
Turner’s syndrome, and 1.7% with their inclusion.
(2) Intersex may be classified in a number of ways. The simplest classification is
according to presence of gonads and accompanying external sexual
characteristics [Table 7].
a. Gonadal agenesis
In gonadal agenesis, the testes and ovaries are entirely absent.
Salient features:
Sex chromatin is absent (46, XY).
b. Gonadal dysgenesis
In gonadal dysgenesis, the testes and ovaries are present, but they fail to develop
normally.
Salient features:
(1) Gonads are mainly composed of fibrous tissue (streak gonads).
(2) Gonadal dysgenesis are divided into two types: (i) Klinefelter’s syndrome
(ii) Turner’s syndrome.

i. Klinefelter’s syndrome
Klinefelter’s syndrome, “47, XXY”, or “XXY syndrome” is a condition in which
the affected individual has two X chromosomes and one Y chromosome.
Salient features:
A. Anatomical structure - male; nuclear sexing – female; sex chromosomes
[gonosomes]– 47, XXY [XXY Males] Most common; 48,XXXY, 48,XXYY, and
49,XXXXY have also been described. B. Incidence - Occurs in 1:600 males.
Most common sex chromosome disorder. C. Named after American
endocrinologist Harry Klinefelter (1912 -1990), who described the condition in
1942 D. Signs and symptoms: (1) Diagnosis - Usually diagnosed when there is
(i) a delay in onset of puberty, (ii) behavioral disorders and (iii) mental
retardation [in contrast to Turner’s syndrome, where intellectual function is
intact]. (2) Body dimension related - (i) Height -ed [due to extra copy of SHOX
gene. Please see below] (ii) narrow shoulders, (iii) broad hips. (3) Sex related
features - (i) Testicles are small [microorchidism] (ii) .testosterone (iii) Leydig
cell function"normal to moderately reduced (iv) Azoospermia [absent
spermatogenesis] (v) Sterility [most common genetic cause for male sterility]
(vi) Gynecomastia. (4) Hair - (i) Axillary and pubic hair absent. (ii) Hair on
chest and chin are reduced. (5) Serum and urinary gonadotrophins- -
Pathophysiology
s
Primary hypogonadism"serum testosterone."FSH and LH-. (6) Miscellaneous -
(i) Diabetes mellitus (ii) Osteoporosis (iii) thromboembolic disease (iv) varicose
veins E. Histology – Testicular atrophy with hyalinization of seminiferous
tubules.

ii. Turner’s syndrome

Turner’s syndrome (also known as Ullrich-Turner syndrome) is a condition in
which the affected individual has only one X chromosome and no Y
chromosome [monosomy X].
Salient features:
[A] Anatomical structure - female; nuclear sexing – male; sex chromosomes –
45, XO. [B] Incidence - Occurs in 1:2500 girls [C] Signs and symptoms –
Turner syndrome manifests itself differently in each female; no two individuals
display the same symptoms. (1) Diagnosis - Can be recognized at birth by (i)
low birth weight, (ii) edema of dorsum of hands and feet and (iii) loose skin
folds in the nape of the neck (Webbed neck or pterygium colli). Other signs and
symptoms are (2) Stature related - (i) Short stature [most common feature;
becomes evident by about age 5]. (ii) slow growth (iii) Micrognathia [small
lower jaw] (iv) shortened 4th metacarpal (3) Sex related - (i) Premature
ovarian failure [very common]. (ii) Rudimentary ovaries gonadal streak
[underdeveloped gonadal structures] (iii) Amenorrhoea [primary] (iv) Sterility
(v) Lack of development of primary and secondary sexual characteristics (vi)
Serum and Urinary gonadotrophins- [pathophysiology same as in KS] (4) Face
related - (i) Ptosis (ii) Visual impairments [glaucoma, etc] (iii) Ear infections
and hearing loss (iv) high-arch palate [narrow maxilla] (v) Low-set ears (vi) Low
hairline (5) Chest related - (i) Broad chest [shield chest] (ii) Poor breast
development (iii) widely spaced nipples (6) Upper limb related - (i) Cubitus
valgus [-ed carrying angle (>15°) of the elbow] (ii) palmar crease (iii) Small soft
upturned fingernails (7) Body related - (i) High waist-to-hip ratio [hips are not
much bigger than the waist] (ii) -ed wt, obesity (iii) pigmented moles (8)
Anomalies of heart – (i) Bicuspid aortic valve, (ii) Coarctation of aorta (iii)
septal defects (9) Other anomalies - (i) Horseshoe kidney [other renal defects
also] (ii) spina bifida. (10) Endocrine - (i) Hypothyroidism (ii) Diabetes mellitus
(iii) Cushing’s syndrome (11) Intelligence - Most patients have normal
intelligence [E] Histology – Ovaries do not contain primordial follicles.

c. True hermaphroditism
True hermaphroditism refers to a condition in which the affected individual has
both ovarian and testicular tissue.
Salient features:
(1) Very rare condition
(2) Gonads - There may be an ovary on one side and a testis on the other, but
more commonly the gonads are fused in the form of ovotestis.
(3) Position of gonads – Abdominal, inguinal or labio-scrotal
(4) Function - Neither gonad is completely functional.
(5) External genitalia – ambiguous.
(6) Internal sex organs – Uterus may be present in some cases
(7) Karyotypes - are mosaics [46XX/46XY, or 46XX/ 47XXY].

d. Pseudohermaphroditism
Pseudohermaphroditism, is the condition in which the affected individual has
gonads of one sex, but external genitalia of opposite sex.
Salient features:
(1) Two types are seen – Male pseudohermaphroditism and female
hermaphroditism
(2) Male pseudohermaphroditism: (i) Genetics and external sex - Nuclear
 sex is XY, but external sexual characteristics and internal sex organs (some or
all) are female. (ii) Causes - (a) Androgen insensitivity syndrome (AIS)
[earlier name “testicular feminization syndrome”]- The gonads are testes [due
to the influence of the Y-chromosome]. No ovaries or uterus. The absence of
uterus in fact is regarded as a condition for the diagnosis of testicular
feminization. (b) 5-a-reductase deficiency [5-ARD] –
(3) Female pseudohermaphroditism: (i) Genetics and external sex - Nuclear
sex is XX, but external sexual characteristics and internal sex organs are male
(ii) Causes- (a) Congenial Adrenal hyperplasia [CAH].
In 2014, the Supreme Court directed the Center and State govts that they must
recognize transgenders as 3rd gender. All documents including
voter/Aadhar card and passports etc will have a third category called
“transgenders”. They will be considered as OBCs and shall be provided
reservation in educational institutions and jobs. Govt must provide separate
toilets in public places for them and separate facilities for them for HIV/Sero-
surveillance measures. The court clarified that their verdict pertained only to
eunuchs and not to other sections of society like gay, lesbian and bisexuals.

2. Concealed sex
Concealed sex is hiding one’s sex by wearing dress of the opposite sex.
Salient features:
(1) Criminals often do it to avoid being caught by the police. This can be
detected by physical examination.
(2) Concealed sex is different from transvestism (eonism), in which also the
person wears clothes of the opposite sex. But in the latter, there is a
psychological compulsion instead of a motivation to avoid detection (see also
chapter 25).
(3) Colonel Sir Victor Barker‘s case is one of the most amazing cases of
concealed sex. Barker (1895 – 1960) was born a female (Valerie Lilias
Barker), who acted like a man between 1923 and 1929. She married twice to
males and once to a female (posing as a male)! During the period she posed as
male, she played for a cricket club, moved about in the streets in Khaki shorts
with a shirt open at the neck and dropped in at pubs for drinks. She was
sentenced to nine months imprisonment for making a false statement in the
marriage register.
3. Determination of sex
Determination of sex [in living and dead in medico legal practice] can be done
by
(1) Examination of external genitalia
(2) Sex chromatin
(3) DNA based methods
(4) Skeleton
a. Examination of external genitalia
Useful in cases of concealed sex. In other cases, may be unreliable and
confusing. Please see intersex above.

b. Sex chromatin
A normal person has 46 chromosomes (males 46, XY; females 46, XX). Sex
chromatin is the condensed chromatin of the inactivated X chromosome in
females (Barr body). While sex chromosomes refer to both X and Y
chromosomes, sex chromatin refers only to inactivated X chromosome. [A] Sex
chromatin is: (i) characteristic of females [found in about 30% to 40% of
female cells] (ii) shape - planoconvex in shape (iii) size - about 1µ, in diameter
(iv) location - Lies against the inner surface of the nuclear membrane (v) Stage
seen in - present only during interphase; disappears during mitosis (vi) Tissues
seen in – Visible in all nucleated cells (not seen in RBC), but easily seen in (a)
buccal smears (b) saliva, (c) skin (d) hair follicles (e) dental pulp and (f) bone
marrow. Karyotyping (study of chromosomal constitution of cell nuclei for sex
determination) of fetus is done from (g) amniocytes (h) lymphocytes and (i)
fibroblasts (vii) Stain – (a) X chromosome – demonstrated by Feulgen reaction
using acriflavine Schiff reagent [X chromosome seen as bright yellow spot].
Memory Aid 5: Feulgen reaction
XY FAST -
X chromosome looks bright Yellow in Fluorescent Feulgen reaction using Acriflavine Schiff reagenT
Memory Aid 6: Feulgen reaction
Feulgen reaction is +ve in Females
(b) Y chromosome – demonstrated by quinacrine dihydrochloride [Y
chromosome seen as bright fluorescent body – commonly referred to as an f-
body] (viii) discovered in - 1948 by Barr and Bertram [hence the name Barr
body] (ix) Putrefied bodies – Sex chromatin may be demonstrated in putrefied
bodies, but not if putrefaction has reached up to cellular level. Uterus and
prostate resist putrefaction for a long time; in advanced putrefaction, sex can be
determined by identifying uterus and prostate.
Memory Aid 7: Quinacrine staining
MCQ - Male Chromosome colors with Quinacrine
[B] Davidson’s bodies: (i) Location - Barr bodies seen on the nucleus of
neutrophils. Appears like a drumstick (Fig 3.5). (ii) seen in 3% female
neutrophils. (iii) Diameter - of the round head at the end of the drumstick is
1.5µ. (iv) Stain – Demonstrated by Jenner-Giemsa method or Feulgen method
(v) Named after William M. Davidson of King’s college hospital medical
school, London, who first described these bodies in 1954.
c. Sexing of the skeleton
(1) Human bones display sexual dimorphism [different shapes in sexes].
Recognizable sex differences do not appear until after puberty except in
pelvis, in which sexual dimorphism is present since fetal life.
(2) There are two methods for sex determination from skeleton (i) morphologic
[roughness, shapes etc, more subjective] and (ii) metric [measurements; more
objective]. Sex differences in skull are typically morphologic, while sex
differences in femur are typically metric. An admixture of both is mostly used.
Normal “carrying angle” of the elbow varies between 5 to 15 degrees. This angle
permits the forearms to clear the hips in swinging movements during walking,
and is important when carrying objects. This is more in girls.
(3) Sex differences in minor bones: (i) Metacarpals - Metacarpal 2 is best for
sex determination; metacarpal 3 is worst. (ii) Patella - (a) Vol – Male > 15 cc;
Female < 11 cc. Measured by putting patella in a container of water.
(4) Accuracy of sexing adult skeletal remains – According to American
anthropologist Wilton Krogman (1903–1987) the percentage accuracy of
determining sex when one or more bones are given is as follows [Table 20].
(5) Medullary index of bones – Medullary index of long bones [tibia, humerus,
radius, ulna etc] is
Diameter of medulla
Diameter of shaft
# 100. Attempts have been made to determine age and sex from this, but have
been largely unsuccessful.
(6) From bone marrow – DNA based methods of determination of sex [please
see above].
Memory Aid 8: Medicolegal and anatomical angles of mandible. Pl co-relate with (Fig 3.6)
1. Remember MAndible
Medicolegal angle is upper angle
Anatomical angle is lower angle
2. Remember MAAS
Medicolegal angle deals with
A
ge
Anatomical angle deals with Sex. Further, it behaves
the same way as subpubic angle, i.e. it is - in females
3. Remember 75 " 100 " 125 " 140
75º " Subpubic angle in males
100º " Subpubic angle in females
<125º " Anatomical angle in males
>125º " Anatomical angle in females
>140º " medicolegal angle in infants and old age.
[90º in adults]
Memory Aid 9: Indices relating to sacrum
1. State Bank Corporation - Sacral, Base-Wing, Corporobasal.
2. For males, figures are in a neat sequence - 105"65"45. Female indices are greater for first 2 and lesser
for 3rd. The differences are 10, 15 and 5 - another easily remembered sequence.
M Diff F
Sacral 105 10 115

Base-Wing 65 15 80

Corporobasal 45 -5 40
3. For base-wing index, remember WBC, i.e. W comes at top and B at bottom. Another way to remember
is reading the index backwards i.e. Base - Wing"W/B
4. Pl also note that numerator of 1st index and denominator of 2nd index interchange their position in the
3rd index.
D. Age
1. Age estimation in the living
a. Methods of determination
Age of an individual can be determined from (i) teeth (ii) bones (iii) secondary
sexual characters and (iv) general development (v) Miscellaneous features.
i. Teeth
For deduction of other parameters from teeth please see below under the heading
“Teeth and bitemarks [forensic odontology]”. Criteria from which age can be
determined are (a) Eruption and calcification of teeth and root resorption (b)
Aspartic acid racemization (c) Tooth Development stages [TDS].
(a) Eruption and Calcification
1st Deciduous teeth
(1) Deciduous [Latin – de, down; cadere, to fall] teeth are also known as baby
teeth, milk teeth or temporary teeth.
(2) Total number of deciduous teeth are 20.
(3) The dental formula of children is
2102
2102
.
(4) Ages of eruption of deciduous teeth - can be remembered by two different
mnemonics:
Memory Aid 11: Eruption of temporary teeth
Mnemonic (1) South Indian Idlis, mothers can make.
1. South"Indicates lower teeth appear first (especially incisors)
2. Indian"(i) Incisors [1st], central (lower)"6 months (ii) Incisors [1st], central (upper)"8 months
3. Idlis"(i) Incisors [2nd], lateral (upper)"10 months [Lateral incisors are an exception; upper appear first]
(ii) Incisors [2nd], lateral (lower)"12 months
4. Mothers"Molars [1st]"14 months
5. Can"Canine"18 months
6. Make"Molars [2nd]"24-30 months.
The ages start at 6 months. After this go on adding 2 months to go to next step.
Nothing appears at 16, 20 and 22 months. Counting of teeth is always done from
medial to lateral, i.e. 1st incisor is medial, 2nd lateral and so on.

Mnemonic (2) It is a visual mnemonic. Draw 10 temporary teeth of one half of mandible in the form of a
graph [Fig 3.8] other half need not be drawn, as it is identical. (i) Incisors would appear in a clockwise
fashion starting from lower central incisor [6 m]. (ii) Teeth erupt from medial to lateral with a gap of 6
[except 1st molar which erupts at 14 m]. Best depicted in lower jaw with the sequence 6, 12, 18, 24 (iii)
Double headed arrows indicate that upper and lower teeth erupt at same age.
Ages of eruption and calcification of deciduous teeth are summarized in Table
21.
2nd Permanent teeth
(1) Total number of permanent teeth are 32.
(2) The dental formula of adults is
2123
2123

(3) Ages of eruption of permanent teeth -Table 22.

Memory Aid 12: Eruption of permanent teeth
Mnemonic
1. Order of eruption of permanent teeth is in the following sequence
Mama Is In Pain; Papa Can Make Medicine
Mama Molar, 1st Papa Premolar, 2nd

Is Incisor, 1st Can Canine

In Incisor, 2nd Make Molar, 2nd

Pain Premolar, 1st Medicine Molar, 3rd

Mnemonic
2. Mother is in bed; baby comes Monday morning. Same as above, except that B"Bicuspid

Mnemonic
3. It is a visual mnemonic. (i) Draw all 8 permanent teeth of one quadrant in the form of a graph [Fig
3.9]. (ii) First fill up ages of eruption of molars which are a table of 6 [6,12,18 y]. (iii) Now fill up ages for
rest of teeth. Teeth appear from medial to lateral with a gap of 1 y except canine which appears at 11 y.
Memory Aid 13: Calcification of permanent teeth
Remember following steps:
1. For beginning of calcification of permanent teeth – remember 0,6,12,18,24,30,36.
2. Sequence of teeth remain as earlier [as in Memory aid 12].
3. Now allot numbers to teeth, keeping first molar at birth [0m]
4. M1=0m
I1=6m
I2=12m
P1=18m
P2=24m
C=6m [because canine and central incisors begin with same letter]
M2=30-36m; M3=8-10 y [Mnemonic - 8th tooth calcifies at 8 y].
5. For greater accuracy, change 6 m to 4 m for both I1 and C.
6. For completion of calcification, just add 3 y to the ages of eruption for all teeth.

(4) Dentition [permanent] is delayed in: (i) Local conditions – Same as in

deciduous teeth. Additionally (a) Ankylosis of deciduous teeth (b) Apical
periodontitis of deciduous teeth (c) Impacted primary tooth (d) Injuries to
primary teeth (e) Lack of resorption of deciduous tooth (f) Premature loss of
primary tooth (ii) Systemic conditions – Same as in deciduous teeth
(5) Mixed dentition – Between 6-11 y, the child has both temporary and
permanent teeth. This is the period of mixed dentition. In mixed dentition, the
total number of teeth are always 24 [Table 23]. During this period following
formula gives age:
Number of permanent teeth = (Age in years – 5) x 4.
(6) Successional and superadded teeth [Fig 3.10] – Successional teeth are
those permanent teeth which replace some other teeth. Thus their eruption does
not change the total number of teeth of the individual. In contrast superadded
teeth are those which are added to the existing set of teeth; they do not replace
any teeth. Thus their eruption always -es the number of teeth. Incisors, canines
and premolars are successional teeth while all molars are superadded teeth.
ii. Bones [determination of age in the living]
[A] General: (1) Formation of bones - In a fetus bones form in two ways: (i)
Intramembranous ossification (ii) endochondral ossification [formation in
hyaline cartilage]. (2) Primary and secondary centers: (i) Initial site of
ossification is referred to as the primary center [eg shaft of humerus, femur,
tibia]. This center lays down most of the bone. Typically, a long bone [eg femur]
is already ossified throughout its shaft [diaphysis] at birth. (ii) The one which
appears afterwards is the secondary center (eg head of humerus, head of femur
etc). Generally they appear towards the bone ends [eg each side of the long
bone]. Both primary and secondary centers appear in X-rays initially as white
spots. As bone lays around them, the whitish area -s in area, till only a black
plate remains between primary and secondary centers. This is the growth plate
[please see below] (iii) Secondary center may be single [eg head of humerus,
femur] or multiple [eg lower end of humerus, which shows 4 secondary centers –
medical epicondyle, trochlea, capitulum and lateral epicondyle]. (iv)
Metacarpals, metatarsals, phalanges, clavicles and ribs possess an epiphysis at
one end only. (v) Not all bones have secondary centers; some bones ossify from
a single primary center only [eg all carpals and most tarsals]. (vi) The earliest
bone to begin ossification is clavicle (45 days, or 1½ months). (vii) Most
primary centers appear during fetal development [with some exceptions eg. most
carpals and tarsals]. (viii) Number of ossification centers – (a) End of 11th IU
wk – 806 centers. Many of these unite with one another (b) At birth - Approx
450 ossification centers remain. (c) These gradually enlarge throughout
childhood and united together to form 206 bones of the adult. (3) Ossification
of a typical bone: Growth plate [growth cartilage, metaphysis] – is a layer of
hyaline cartilage that persists between the diaphysis and epiphysis. In an X-ray it
appears as a black line, which may be confused by an inexperienced person with
a fracture line. In the dead, it appears as a circular groove, and cuts with the
consistency of tough wax. In very old skeletal materials, growth plates putrefy
completely causing separation of epiphysis and diaphysis. This may be confused
with fractures by inexperienced persons. To demonstrate them adequately in a
living person, X-rays of all joints should be taken both in AP as well as lateral
views.

(a) Long bones

1st—Ages of appearance
[I] Upper end of humerus [Fig 3.12]"Remember the arithmetic series 1, 3, 5 :
Head of humerus appears at 1; Greater tuberosity at 3; Lesser tuberosity at 5.
Remember that in English alphabet g comes before l, and in arithmetic 3 comes
earlier than 5: G"L 3"5 All three centers unite by 6 y, i.e. 1 y after the last centre
comes. [II] Lower end of humerus [Fig 3.12]"There are four major centers to
remember: Medical epicondyle, trochlea, capitulum and lateral epicondyle.
Memory Aid 14: Ossification centers of lower end of humerus
1. Capitulum - appears at one [remember “c” for child. Children are younger so it comes very early, i.e. at
1]
2. Trochlea - appears at Ten (remember “T”)
3. Lateral Epicondyle - appears at 11 (Remember “lateral”. Both beginning and ending letters are “l”. If
we keep them together, they look like 11)
4. Medial Epicondyle - appears at 5-7 [Five-Seven].
[My Excellent Forensic Science]
5. LTC (Lateral epicondyle, Trochlea and Capitulum) join together to form a conjoint epiphysis, which
then joins with the shaft.
6. Medial epicondyle joins the shaft of humerus separately [Table 24].
[III] Radius and ulna: Make a representation of the two bones [Fig 3.13]. Make
a capital “N” beginning from the lower end of radius as shown, and write
numerals 2"5"6"9 (1) Lower end of radius appears at 2 years (2) Upper end of
radius appears at 5 years (3) Lower end of ulna appears at 6 years (4) Upper end
of ulna appears at 9 years [IV] Femur: Remember 1 -> 4 -> 14 [formed by the
first two digits]. Head of femur appears by 1 year, greater trochanter by 4 years
and lesser trochanter by 14 years [Fig 3.14].
Angle of neck with shaft 150° in newborn. Angle in adults is different depending
on sex [Table 18]. [V] Tibia and fibula: Make the bones (as in case of radius
and ulna) and write a capital “U”. Now write the numerals 0"1"1"4 [Fig 3.15]
(1) Upper end of tibia appears at 0 years, i.e. just at birth [in 80% cases; in rest it
appears soon after birth] (2) Lower end of tibia appears at 1 year (3) Lower end
of fibula appears at 1 year (4) Upper end of fibula appears at 4 years.
2nd—Ages of fusion
Age of fusion may be remembered by an easy mnemonic. Imagine a person
reclining on a sandy beach [Fig 3.16]. His elbows are sinking in the sand
somewhat. Draw four lines parallel to the horizontal plane. The lowest one
passes through the elbow, the next through the hip and ankle joints, the next
through the shoulder and knee joint, and the uppermost through the wrist joint.
Epiphyses falling on a particular line fuse at a particular age. All epiphyses
around the elbow joint complete fusion by 16 years, all epiphyses around hip and
ankle joints by 17 years, all epiphyses around shoulder and knee by 18 years,
and all epiphyses around the wrist by 19 years.
Following three centres fall upon the lowest line – ossification centres around
elbow joint.
(1) Medial epicondyle unites with the shaft at 16 y
(2) Upper end of radius unites with the shaft at 16 y
(3) Upper end of ulna unites with the shaft at 16 y. Following three centers fall
on the second line from below.
(4) Head of femur unites with the shaft at 17 y.
(5) Lower end of tibia unites with the shaft at 17 y.
(6) Lower end of fibula unites with the shaft at 17 y. Following four centers fall
on the third line from below.
(7) Head of humerus unites with the shaft at 18 y.
(8) Lower end of femur unites with the shaft at 18 y.
(9) Upper end of tibia unites with the shaft at 18 y.
(10) Upper end of fibula unites with the shaft at 18 y. Following two centers fall
on the fourth line from below.
(11) Lower end of radius unites with the shaft at 19 y.
(12) Lower end of ulna unites with the shaft at 19 y.
3rd—Epiphyseal scar
Epiphyseal scar is a radiodense band seen in X-rays at the junction of the
epiphysis and metaphysis, which represents closure. It signifies recent union,
and disappears a few years after. Rarely multiple transverse lines are seen at
diaphyseal ends. They often indicate growth disturbances due to scurvy, rickets
etc [scars of arrested growth].
(b) Skull
(1) Determined by X-rays. Changes given in detail in a subsequent section.
(2) For suture closure, x-ray requested should be
(i) Anteroposterior (Towne’s) X-ray of skull
(ii) Posteroanterior X-ray of skull
(iii) Submentovertical X-ray of skull.
(c) Hyoid
(1) Hyoid ossifies from 6 centers - 2 for the body and one for each cornu.
(2) Ossification begins in
(i) Greater cornu"10 m [IU life].
(ii) Body"just after birth.
(iii) Lesser cornu"16 y.
(3) Completion of ossification -
(i) Apices of greater cornu"20-30 y
(ii) Greater cornu of hyoid unites with the body at 40-60 y.
(d) Sternum
(1) Anatomy - Sternum consists of three parts – the manubrium sterni, the body
of the sternum and the xiphoid process. The body of the sternum has four
sternebrae. Thus the whole bone may be visualized as being composed of 6
parts [manubrium sterni + 4 sternebrae + xiphoid process].
(2) Centers appear from above downwards, and unite from below upwards. The
union occurs in two different “waves” so to say – hence the two upward
arrows.
(3) The centers for the manubrium sterni and the sternebrae appear during the IU
life. Remember the figures 5m"5m"7m"7m"10m"3y. All months refer to
intrauterine period. The center for xiphisternum appears at 3 years of age.
(4) In the first “wave” of union, the four sternebrae unite from below upwards.
The figures are:
(i) Union of 3rd and 4th sternebrae at 15 years
(ii) Union of 2nd and 3rd sternebrae at 20 years
(iii) Union of 1st and 2nd sternebrae at 25 years.
(5) In the second “wave” of union:
(i) xiphisternum unites with the body at 40 years.
(ii) Manubrium sterni unites with the body at 60-70 years, and quite often
remains ununited.
(e) Clavicle
(1) Clavicle is the first bone to begin ossification.
(2) Primary centers -Two centers appear in the shaft between the 5th-6th weeks
of IU life, and fuse at 45th day.
(3) Secondary centers:
(i) Medial end appears between 11-19 y [average – 15 y] and unites with the
shaft between 18-25 y [average - 22].
(ii) There is no lateral end of ossification in clavicle.
Memory Aid 18: Ossification centers of sternum
Sternum – 1st piece, i.e. Manubrium sterni appears at 5 [S looks like 5]. Last piece. i.e. 4th sternebra
appears at ten – second letter of sternum is t]. All other pieces appear in “pairs”, i.e. MS and 1st sternebra
at 5; 2nd and 3rd sternebrae at 7.

(f) Scapula
(1) Coracoid - 1 y [A]; 15 y [F]
(2) Subcoracoid - 16 y [A]; 17 y [F]
(3) Acromion - 16 y [A]; 20 y [F]
(4) All epiphyses of the scapula join the bone - 20 y.
(5) 30-35 y " Lipping starts on the ventral margin of glenoid cavity
(6) 35-40 y " Irregular lipping around clavicular facet and inf surface of
acromion process
(7) 45 y " Localized bony atrophy
(8) 50 y " Cristae scapulae.
(g) Carpals
Write down the first letters of all carpal bones as shown.
Memory Aid 19: Carpal bones
Mnemonic 1 - She Looks Too Pretty; Try To Catch Her. [lateral to medial; proximal to distal]
Mnemonic 2 - Teacher teaches Cunningham; Students like to play [lateral to medial; distal to
proximal]
Now encircle the pisiform bone. Start from capitate bone and make a full circle
as shown. The ages (all extra uterine) are:
(1) Capitate"2 months
(2) Hamate"3 months
(3) Pisiform"We pass this bone, as this is encircled
(4) Triquetral"since this starts with “tri” we cannot assign the next number. It
has to be “tri” or 3. So Triquetral appears at 3 years
(5) Lunate"4 years
(6) Scaphoid"4-5 years
(7) Trapezium and trapezoid"4-5 years (Trapezium comes slightly earlier than
Trapezoid)
(8) Pisiform: We finally land on this bone. It appears between 9-12 years. It is
the last carpal bone to appear.
(h) Vertebrae
(1) At birth - Vertebral body shows a series of deep radial furrows both on the
 upper and lower surfaces
(2) birth-10 y – Furrows -in prominence with age
(3) 10-25 y – Furrows start . ing in prominence
(4) >45 y – Osteoarthritic changes, lipping, osteophytes.
(i) Symphysis pubis
(1) For changes in symphysis pubis [SP], please see below In the living, CT can
demonstrate these changes.
(j) Hipbone
(1) Ischiopubic ramus unites by 7-8 years.
(2) For iliac crest and pubis, remember 14"20; i.e. both iliac crest and pubis
appear at 14 years of age and unite by 20 years.
(3) Iliac crest - union occurs from before backwards, i.e. the crest begins uniting
at anterior superior iliac spine and the union gradually proceeds backwards.
(4) For ischium, remember 16"20; i.e. ischium appears at 16 and unites at 20.
(5) For acetabulum, remember 13"15; i.e. the acetabular cup assumes the shape
of a triradiate cartilage, which becomes noticeable in radiographs by 13 years.
This is generally taken as the “age of appearance” of triradiate cartilage.
(6) The triradiate cartilage disappears by 15 years.
(k) Sacrum
(1) 20 y - Bodies of sacral vertebrae begin to unite with one another. They unite
at margins but not in the central area.
(2) 25 y -Sacrum is one bone, even though central area may remain unossified up
to 50 y; sometimes even later.
(3) The union occurs from below upwards. Sometimes a gap may remain
between S1-S2 due to lapsed union [please see above].
(l) Patella
(1) Centers in males – Appear between 1½ -4 y.
(2) In females - between 2½ -6 y [Significantly the centers appear later in
females].
(3) Patella assumes adult contours by 14 years in females and 16 years in males.
(4) Sometimes additional ossification centers appear which remain ununited,
producing bipartite or multipartite patella. This is more common in sporting
persons.
(m) Tarsals
(1) For secondary centers of calcaneum remember 7 Appearance ->16 (F)usion.
(2) Navicular appears at 3 years (just like xiphisternum in the upper half of the
body).
(3) Cuneiforms - Lay down:
(i) cuboid
(ii) lateral cuneiform
(iii) intermediate cuneiform and
(iv) medial cuneiform in their anatomical fashion. Ossification centers in these
bones appear from lateral to medial side [skip IC]. The years are 0, 1, 2, 3.

iii. Secondary sexual characters

Not very helpful. Give a very vague idea about the age. Best known staging of
secondary sexual characters is by James Tanner (1920-2010). He was a British
Pediatrician, who worked at the Institute of Child Health at the University of
London. Developed formal stages of sexual development in puberty [Sexual
Maturity Ratings or SMR].

(a) Tanner’s stages of breast development [girls]

(1) Tanner stage 1 [B1, prepubertal, before 9-10 y]:
No discernible breast tissue in prepubertal girls.
(2) Tanner stage 2 [B2, Breast bud stage, thelarche, 10-11 y]:
(i) Breast development begins with an -in the pigmentation and diameter of the
areola and the development of a small amount of breast tissue.
(ii) Breast development not seen beyond areola.
(3) Tanner stage 3 [B3, 12 y]:
(i) Breast development occurs beyond areola;
(ii) areola experiences early changes [pigmentation, Montgomery glands].
(iii) One mound stage - Further breast enlargement, but there is no separation of
the contours of the areola from the breast. This is all one mound.
(4) Tanner stage 4 [B4, 13 y]:
Two mound stage - Formation of a double mound; secondary mounding of the
areola above the plane of the breast, and of papilla [nipple] above areola.
(5) Tanner stage 5 [B5, final or mature stage]:
(i) One mound stage again - Recession of the areola into the general contour of
the breast. Projection of nipple only. Loss of double mound
(ii) further growth of the breast.
(b) Tanner’s stages of genital development [boys]
(1) Tanner stage 1 [G1, prepubertal, 9-10 y]:
(i) Testes, scrotum, penis are small sized.
(ii) No rugosities in scrotum.
(iii) Testicular volume 4-5 cc each. Testicular volumes can be measured by
orchidometers, ultrasonography or simply by measuring length [L] and
width [W] of testes" π/6 x L x W2, testis being regarded as an ellipsoid.
(2) Tanner stage 2 [G2, prepubertal, 10-11 y]:
(i) Skin of scrotum reddens
(ii) Scrotum shows changes in texture (slight rugation).
(iii) Enlargement of penis, scrotum and testes
(iv) Testicular volume 6-7 cc each
(3) Tanner stage 3 [G3, prepubertal, 12 y]:
(i) Further growth of scrotum, testes and penis. The latter -es at first mainly in
length; very slight -in breadth
(ii) Testicular volume 15 cc each.
(4) Tanner stage 4 [G4, prepubertal, 13-14 y]:
(i) Scrotal skin darkens.
(ii) Glans develops.
(iii) Further enlargement of penis, scrotum and testes
(iv) Testicular volume 20 cc each.
(5) Tanner stage 5 [G5, prepubertal, 15-16 y]:
(i) Genitalia adult in size and shape.
(ii) Testicular volume 25-30 cc each.
(c) Tanner’s stages of pubic hair development [both sexes]
(1) Tanner stage 1 [PH1, prepubertal, <12 y]:
(i) No pubic hair [< 12 y]
(2) Tanner stage 2 [PH2, prepubertal, 12-13 y]:
(i) Sparse growth of long, slightly pigmented downy hair, straight or very
slightly curled, chiefly at base of penis or along labia. [12-13 y]
(3) Tanner stage 3 [PH3, prepubertal, 13-14 y]:
(i) Darker, coarse extending on to mons pubis, pigmented, start curling and
spread around
(4) Tanner stage 4 [PH4, prepubertal, 14-15 y]:
(i) Cover most parts but do not go up to thighs
(5) Tanner stage 5 [PH5, pubertal, >15 y]:
(i) Mature pubic dense hair extend to the inner thighs (>15 years).
(d) Secondary sexual features in males according to age
(1) 14 y:
(i) fine downy hair begin to appear around the pubes.
(ii) Testes become larger and firmer.
(iii) Penis begins to enlarge
(2) 15 y:
(i) Hair moderately grown on pubes.
(ii) Begin to appear in axilla
(3) 16 -18 y:
(i) Hair on pubes well grown.
(ii) Begin to appear on face [moustache, beard]
(iii) Adam’s apple becomes more prominent
(iv) Voice – becomes hoarse
(v) External genitalia have an adult appearance.
(4) 20 y:
(i) Color of hair becomes darker
(ii) Hair become thicker
(iii) Hair begin to appear on the inner sides of the thigh, scrotum and anus.
Memory Aid 20: Appearance of body hair
Hair on the body appear from below upwards

(e) Secondary sexual features in females according to age

(1) 13 y"
(i) Breasts - begin to develop
(ii) fine, pale downy hair appear on mons veneris [about 2 m after breast change]
(iii) Labia – develop
(iv) Menstruation – starts
(2) 14-15 y"
(i) Pubic hair is well-grown
(ii) Hair appears in axilla.
(f) Fallacies of secondary sexual characteristics
(1) Sexual precocity-(i) McCune–Albright syndrome [syn, Albright
syndrome] – Secondary characteristics appear earlier than average age.
(2) Breast in males [Gynecomastia]– (i) Causes – Pl see memory aid.
Memory Aid 21: Causes of Gynecomastia
CT SCAN – Cimetidine, Testosterone, Spironolactone (antiandrogen), Cannabis, Alcohol, Nifedipine

b. Procedure for determination of age

(1) Request - Age is determined by a doctor on
(i) private request, [eg when a couple want to marry in court and require an age
certificate]
(ii) police request [eg age determination in a girl to determine if it was a case of
statutory rape]
(iii) court order [eg to know if a child is juvenile]
(2) Preliminaries – please see ch 1"Medicolegal reports" Preliminaries.
Important additions are (i) Age – record both as alleged by subject as well as
that alleged by police or contesting party
(3) Body of report – please see ch 1. Note especially
(i) ht and wt
(ii) Secondary sexual characters – eg distribution of hair on body, development
of genitals, breasts etc, voice
(4) Opinion and subsidiaries – please see ch 1. Opinion should be based on
physical, dental and radiological examination. If there is a conflict between
them generally the levels of preference should be as follows; greatest regard to
radiological data followed by "dental followed by"physical findings.

c. Age of the fetus

i. Stages of development of fetus

Pl. see ch. 26.

ii. Month wise development of fetus

Following dates are from LMP. The months are lunar (28 days each).
(1) End of 1st month:
(i) Length – 1cm
(ii) Wt - 2.5g
(iii) Eyes – seen as 2 dark spots
(iv) Mouth – seen as cleft
(v) Nucleated red cells - begin to form in placenta
(2) End of 2nd month:
(i) Length – 4 cm
(ii) Wt - 10g
(iii) Hands and feet – Webbed
(iv) Anus – seen as a dark spot
(v) ossification centers – in clavicle and maxilla
(vi) Placenta begins to form
(3) End of 3rd month:
(i) Length – 9 cm
(ii) Weight – 30 g
(iii) Eyes – (a) closed (b) pupillary membrane appears
(iv) neck is formed
(v) Early fingernail development.
(vi) Intestines in abdomen.
(4) End of 4th month:
(i) Sex: distinguishable externally.
(ii) Neck: Well defined.
(iii) Head: erect.
(iv) Brain: convolutions begin to form
(v) Lower limbs: well developed.
(vi) Placenta and fetus are equal in weight [17 wks].
(vii) Meconium: begins to form [13th week] In the first trimester, placental
growth is more rapid than that of the fetus. It is at beginning of small
intestine [duodenum].
(5) End of 5th month:
(i) Ears stand out from head.
(ii) Vernix caseosa appears.
(iii) Early toenail development.
(iv) Meconium: at beginning of large intestine
(6) End of 6th month:
(i) Head and body (lanugo) hair visible.
(ii) Skin wrinkled and red.
(iii) Eyebrows and eyelashes – appear
(iv) Skin – red, wrinkled. S/c fat begins to be deposited
(v) Meconium – at transverse colon
(vi) Testes – close to kidneys
(7) End of 7th month (age of viability):
(i) wt 1100 g.
(ii) Fingernails – present and thick.
(iii) Lean body.
(iv) Eyes - (a) partially open (b) pupillary membrane - disappears.
(v) Meconium – in entire large intestine
(vi) Testes – at external inguinal ring
(vii) Ossification center – appears in talus. This is the most imp center
medicolegally since it appears at age of viability. For all IU ossification
centers, please see above.
(viii) Neonate born at this age has a 90% chance of survival without physical or
neurological impairment.
(8) End of 8th month:
(i) Eyes open.
(ii) Scalp hair – thicker, length -1.5 cm
(iii) Skin slightly wrinkled.
(iv) Nails – (a) Fingernails reach tip of fingers (b) Toenails present.
(v) Body filling out.
(vi) Left testis – in scrotum.
(9) End of 9th month:
(i) Fingernails reach fingertips.
(ii) Skin pink and smooth.
(iii) Scrotum – wrinkled, contains both testes
(10) End of 10th month:
(i) Length – (a) Crown-Heel – 50 cm [48-52 cm] (b) Crown-Rump – 30 cm [28-
 32 cm] (c) Umbilicus – placed midway between pubis and xiphoid cartilage
(ii) Weight – (a) 3.4 kg [2.5-5 kg]. (b) male infant weighs about 100 g more than
female (c) Weight is more variable than length
(iii) Circumference of head – 33-38 cm [Head circumference at any given time is
roughly equal to 2/3rd of CH length – same is true of CR length also please
see below]
(iv) Head =1/4 x body length
(v) Scalp hair – dark, 3-5 cm long
(vi) size of anterior fontanelle – 4 x 2.5cm
(vii) face – not wrinkled
(viii) Lanugo hairs – absent, except on shoulders
(ix) skin – covered with vernix caseosa
(x) Nails - (a) Fingernails - extend beyond fingertips. (b) Toenails – just reach
toe tips. (c) Nose and ears – cartilages have formed
(xi) Umbilical cord – Length 50-55 cm. Thickness 1 cm.

Memory Aid 22: Age of fetus [Pl co-relate with Table 25 below.]
Write figures 1-10 in a vertical row as in Table 25. These represent lunar months (end of). Now write
features appearing at each month as below:
(1) At 1m 2 dark spots; at 2m 1 dark spot
(2) 1 imp thing happens at 1m - nucleated RBC in placenta
(3) 2 things are webbed at 2m - hand and feet [mentioned later also in a different mnemonic]
(4) By now we have 2 features each for 1 and 2 months; total 4 features. Use following mnemonic now:
Post Mortem So Tough – Arrange them in front of figures 3, 4, 5 and 6 from above downwards, so
that P comes in front of 3; M in front of 4; S in front of 5 and T in front of 6. Now proceed as below.
(5) Pupillary membrane - 3 , 7 [appearance, disappearance]
(6) Meconium - 4, 5, 6, 7: 4-duodenum, 5-beginning of LI [cecum], 6-Beginning of TC, 7-
entire LI.
(7) S kin related - 5, 6: 5-vernix caseosa appears; 6-head and body hair visible, eyebrows, eyelashes
appear.
(8) Testes - 6, 7, 8, 9 [start 2 m after meconium]: 6-Close to kidneys, 7-external inguinal ring, 8-left
testis descends [Mnemonic to remember that left descends first - Lecture Theatre; or co-relate with left
umbilical vein - Left is left], 9-both testes in scrotum.
(9) Fingernails - [start 2 m after testes]- 8,10 : 8-Fingernails reach tips of fingers, 10-Fingernails
beyond tips; Toe nails just at tips. Remember: Toe nails are at Tips at Ten.
(10) Now weights – In front of numerals 1, 2, 3, write 2.5 g; 10 g; 30 g respectively [Note that for
3 months, just 0 has to be added]. At 7 months [viabIl Ity]– 1100 g. [Take 2 vertical “I”s from
viability and add 2 “0”s 1100]
(11) Now first formations [Mostly mentioned in earlier mnemonic also]: 1- Nucleated RBC
in placenta; 2 - Webbing of hand and feet; 3 - Neck; 4 - Brain convolutions; 5 -
Vernix caseosa; 6 - Hair [eyebrows, eyelashes]. Nothing much forms after 6m. In fact
disappearance starts at 7m pupillary membrane disappears.
(12) 4 Imp things happen at 4 m:
(i) sex – distinguishable [most imp]
(ii) neck – well defined [begins to form at 3 m]
(iii) brain convolutions - begin to form
(iv) Placenta and fetus – equal in wt [17 wks]
(13) Talk of 10 months now –
(i) length -50 cm
(ii) umbilical cord - 50 cm
(iii) umbilicus - midway between xiphoid and pubis

iii. Rule of Haase

[A] Rule of Haase states that during the first 5 months of development of fetus,
the crown-heel (CH) length in cm is equal to the square of its age in lunar
months; afterwards it is equal to 5 multiplied by its age in lunar months. Thus
CH length of a fetus from 1-5 lunar months is: 1 m"12= 1 cm; 2 m"22= 4 cm; 3
m"32= 9 cm; 4 m"42= 16 cm and 5 m"52= 25 cm. From 6-10 lunar months it is:
6 m"6x5= 30 cm; 7 m"7x5= 35 cm; 8 m"8x5= 40 cm; 9 m"9x5= 45 cm; 10 m
(full term)"10x5= 50 cm; (1 lunar month = 28 days). [B] CR length is
medicolegally more important than CH length because of (1) The variability in
the length of the legs (2) Difficulty of maintaining them in extension. Despite
this, Rule of Haase deals with CH length [Memory Aid 23: H for
H
aase"thus C
H
], because that is easier to remember. Karl Friedrich Haase (1788-1865), a
German gynaecologist reported the birthlength statistics for the Berlin Charité
for 1875. In a footnote he added this famous mnemonic. CR length at any given
time is roughly equal to 2/3rd of CH length.

iv. Development after birth

(a) Length
Length (i) at birth = 50 cm;
(ii) at end of 6 months = 60 cm;
Memory Aid 24: - in infant length
At 6 m, add a “0” after 6 to get length " 60 cm

(iii) at end of 1st year = 68 cm; (iv) at end of 4th y =100 cm [double the length at
birth].
Memory Aid 25: Infant measurements
1. HS - Height is slow to increase.
2. Double the double, i.e. 4
3. Now write 4 5
4. Now write bigger unit first (y) and smaller later (m) in front of 4 and 5. Joining them together gives
circumference of head at 1 y [45 cm]
5. 4 y height doubles; 5 m weight doubles.
6. Head circumference till 1 y is 2/3 of CH length.
7. At 1 y, when height is 68 cm and circumference is 45 cm.

(b) Weight
Birth weight (i) at birth = 2500 gm (average); (ii) at 5 months = doubles.
Memory Aid 26: - in infant weight
At 5 months, wt is 5 kg.

(iii) at 1 year = triples [7.5 kg].

(c) Head circumference

Head circumference (i) at birth = 33 cm (average); (ii) 1 year = 45 cm.

2. Age Estimation in the Dead

a. Methods of determination
Virtually all criteria used in the living can be used in the dead also. But certain
additional criteria become available in the dead.
i. Teeth
(a) Gustafson’s Method
In 1950, Swedish forensic odontologist Gösta Gustafson (1906 - 2001)
developed an objective method for determining age from teeth in the dead.
[A] Criteria – Six criteria are used [Fig 3.18]:
Memory Aid 27: Gustafson’s Method
[Mnemonic 1]
SCRIPT
Secondary dentin, Cementum apposition
Root resorption, AttrItion
Periodontosis, Transparency of root
OR
[Mnemonic 2]
Always Purchase Second Class Railway Ticket
Attrition, Periodontosis
Secondary dentine, Cementum apposition
Root resorption, Root Transparency
(1) Secondary dentin:
(i) With advancing age, dentin develops within the pulp cavity decreasing its size
[Fig 3.18]
(ii) Initially it is deposited in the upper part of the pulp cavity. Gradually it
extends lower down till the apex of the root, filling up the entire pulp cavity
(iii) Dentine forms at an average rate of 4 µ/day for man.
(iv) Scoring : S0 – No deposition; S1 –Deposition in the upper part; S2 – Pulp
 cavity half filled; S3 – More than half to whole pulp cavity filled.

(2) Cementum apposition:

(i) Cementum is a specialized calcified substance covering the root of a tooth.
(ii) It is light yellow and slightly lighter in color than dentin.
(iii) Cementum is formed continuously throughout life; a new layer of cementum
is deposited to keep the attachment intact as the older layer of cementum
ages. It can thus be used to calculate age. (iv) Scoring: C0 –Normal layer of
cementum; C1 – Deposition slightly greater than normal; C2 – Great layer
of cementum; C3 – Heavy layer of cementum
(3) Root resorption:
(i) Resorption of root starts at the apex, and extends upwards
(ii) Shows characteristically as sharp grooves
(iii) Scoring: R0 – No root resorption; R1 – Root resorption only on small
isolated spots; R2 – Seen over a large area; R3 – Great areas of both
cementum and dentin affected.
(iv) It is the least reliable of all criteria.
(4) Attr Ition:
(i) Wearing down of incisal or occlusal surface due to mastication
(ii) Scoring: A0 – No attrition; A1 – Attrition within enamel; A2 –Attrition
reaching dentin; A3 – Attrition reaching pulp
(5) Periodontosis:
(i) Regression of gums and periodontal tissues surrounding the teeth occurs as
age advances
(ii) Gradually necks and roots are exposed
(iii) Finally teeth may become lose and fall off
(iv) Scoring: P0 – No periodontosis; P1 – periodontosis just begun. Less than
1/3rd of root exposed; P2 – 1/3rd to 2/3rd of root exposed; P3 – More than
2/3rd of root exposed.
(6) Transparency of root:
(i) Cause of transparency - (a) C anals in the root are at first wide and filled with
air. Light cannot pass through them as it is diffracted (b) As age advances,
they are filled by mineral, making the entire area uniform. No diffraction of
light occurs and root becomes visible (c) Transparency first appears in the
apical region and then ascends upwards
(ii) Scoring: T0 – No Transparency; T1 – Transparency over apical region; T2 –
Transparency over apical 1/3rd of root; T3 – Transparency over apical 2/3rd
of root.
(iii) Most objective criteria, because area of root transparency can directly be
measured by microscope
(iv) It is the single most reliable criteria followed by secondary dentin formation.
[B] Technique:
(1) Most suitable teeth – are anterior teeth (incisors). Merit .s as one goes back
from incisors to molars. Molars are quite unsuitable
(2) Observation of paradentosis – Before extraction of incisors, paradentosis is
measured, and score noted
(3) Tooth extracted, cleaned under running water, disinfected in 3% H2O2 and
dried at room temperature.
(4) Embedded in resin, and ground down perpendicular to the axis
(5) When the thickness of tooth is reduced to 1mm, transparency is estimated
(6) Tooth is now further ground down to 100μm and other changes noted.
Scoring of all 6 criteria done as mentioned earlier. All scores are added.
Minimum score can be 0 [No change (0) in any criteria. On an average this
 happens up to 15 years] and maximum 18 [maximum change (3) in all
criteria] (7) Age can directly be read from an already plotted regression line
[made from known cases] on a graph. (8) Rate of error is ±4 to 7 years. It -s
after 50 years of age.
(b) Boyde’s method
(1) Ameloblasts produce enamel at the rate of 4 µ/day.
(2) Therefore the enamel of the crowns of teeth shows incremental striae in
histologic sections [striae of Retzius].
(3) When viewed microscopically in cross-section, they appear as concentric
rings [similar to the annual rings on a tree]. In a longitudinal section, they
appear as a series of dark bands.
(4) The neonatal line is the darkest band, which represents the disrupted
enamel formation due to the stress of being born.
(5) Occasionally systemic disturbances in the human body [eg fever] can cause
some lines to appear darker than those surrounding them.
(6) Boyde in 1963 suggested that counting the enamel rings outside of neonatal
line can reveal age of a child.
(c) Age from size and weight of teeth
Stack’s method - Size and weight of anterior deciduous teeth (incisors and
canines) are known to -with age. Thus age of a child can be calculated by
measuring exact height and weight of anterior teeth.,

ii. Bones [determination of age in the dead]

Please also see above [Bones "determination of age in the living]. In the dead,
following additional parameters become available.

(a) Ossification centers during IU life

Demonstration of ossification centers:
(1) Naked eye - All ossification centers on naked eye examination would appear
as brownish red spots surrounded by bluish white cartilage. Significantly the
same centers appear as whitish spots in radiographs. (a) Sternum - (I)
Sectioning - Place sternum flat on a wooden board and cut with a cartilage
 knife in its long axis in midline. 1-5 ossification centers are seen depending
upon the age of fetus. (II) Visualizing against bright light – Alternatively
hold sternum against bright light. Centers of ossification will appear as dark
spots within the bone [Fig 3.20]. [Table 26]. (b) Lower end of femur and
upper end of tibia – (I) Leg is flexed against the thigh (II) A transverse
incision is made in the knee joint (III) Patella removed (IV) End of femur
pushed forward through the wound (V) Make a number of parallel cross-
sectional incisions through the epiphysis starting from the articular surface and
continuing till diaphysis is reached. Look for brownish red centers (VI)
Diameters of ossification center - (1) At 36 wks, when the center appears, it is
pinpoint in size (2) At 37-38 wks - diameter is 4-5 mm (3) At full term –
diameter is 6-8 mm (VII) Examine upper end of tibia in same way (c) Tarsals
– (I) Grasp foot behind the heel in left hand, with toes pointing towards the
dissector (II) Make incision between the interspace of 3rd and 4th toes
backwards through the sole of the foot and heel (III) Centers for talus and
calcaneum should be seen as brownish red spots; if not seen, make thin
incisions on either side till they are visible. The upper one is talus; lower is
calcaneum. If not visible, it is interpreted as not appeared.
(2) By staining - Alizarin Red is used as a marker to stain centers of
ossification.
(b) Skull
(1) Number of bones:
(i) Calvaria [8]– 1 frontal, 2 Parietal, 2 temporal, 1 occipital, 1 ethmoid and 1
sphenoid.
(ii) Face and jaw [14] – 2 inferior nasal concha, 2 lacrimal, 2 maxillae, 2 nasal, 2
palatine, 2 zygomatic, 1 mandible and 1 vomer.
(2) Fontanelles:
(i) Posterior fontanelle closes by 2 months
(ii) anterior by 2 years.
(iii) Two postero-lateral fontanelles [mastoid fontanelles] close shortly after birth
(iv) Two antero-lateral fontanelles [sphenoidal fontanelles] at 6 months.
Memory Aid 29: Closure of fontanelles.
Fontanelles close from back to front.

(3) Ossification:
(i) Basiocciput unites with basisphenoid – 18-21 y
(ii) Condylar portions of occipital bone unite - (a)with squama – 3 y (b)with
basiocciput – 5 y.
(iii) Inferior nasal concha - ossifies from a single center, which appears at 5th
month of IUL in the lateral wall of the cartilaginous nasal capsule.
(4) Suture closure: [Fig 3.22]
(i) Skull sutures obliterate earlier in males than in females.
(ii) Suture closure begins at the inner table [5 y earlier] and progresses outwards.
(iii) Metopic suture – closes at 3 y. Persists in 5-10% cases
(iv) Other sutures - Table 27.
Memory Aid 30: Skull suture closure. Please correlate with Table 27.
1. Spheno-occipital is the earliest to fuse (20 years)
2. Coronal, sagittal and lambdoid start fusing together at 25 years. The frontal ones (coronal and sagittal)
finish at 40 years while posterior one (Lambdoid) finishes a little later – at 45 years (remember “back
benchers”)
3. Two minor sutures are Pterion (at front) and Masto-occipital (at back)
4. Front one (pterion) starts when front sutures close (40 years)
5. Back one (Masto-occipital) starts when back sutures close (45 years)
6. Pterion takes 25 years to close (65 years)
7. Masto-occipital takes 35 years to close (80 years) [remember “back benchers” again]
8. Asterion closes by 50 years.

(5) Other age criteria in skull:

(i) 7 y - Vault almost reaches adult dimensions.
(ii) <10 y - skull is smooth and ivory like on both outer and inner surfaces
(iii) 25 y – Muscular markings become more prominent especially (a) Masseteric
attachments (b)Nuchal lines and (c) Temporal line
(iv) 40 y - the surface begins to assume a “matted” granular rough appearance.
(v) 45-50 y - (a) On the inside of skull, pacchionian depressions for arachnoid
granulation bulges - in number as well as depth, even to the point of
penetrating the outer table of the vault. (b)Groove for middle meningeal
artery becomes deeper
(vi) >50 y – (a) Diploe becomes less vascular (b) Thins out, as it is gradually
replaced by bone (c) There is no consistent change in the thickness of skull.
(c) Mandible
(1) Mandible ossifies in dense fibromembranous tissue
(2) Each half ossifies from one center which appears near mental foramen at 6th
week of life (just after the appearance of primary center for the clavicle)
(3) Two halves of mandible – Start uniting from below upwards in the 1st year.
Completely unite by 2 y.
(4) Head of mandible completely ossifies by 30 y.

Memory Aid 31: Circle of 2.

Nature has made an interesting circle around the skull, which we call the “circle of 2” [Fig. 3.23]. As many
as 5 structures unite at 2 (or a related figure) along this circle.
A. Symphysis menti unites at 2 years.
B. Metopic suture unites at 2 years (more correctly 2-8 years).
C. Anterior fontanelle unites at 2 years.
D. Posterior fontanelle unites at 2 months (more correctly 2-6 months).
E. Basisphenoid unites at 20 years.
(d) Ribs
(1) It was reported in 1984 that sternal ends of ribs, particularly 4th rib show age
related changes similar to pubic symphysis [please see below].
(2) surface is billowy in adolescence, while margins are sharp and cup shaped in
middle aged adults, and irregular in old age
(3) For age determination right 4th rib is chosen.
(e) Symphysis pubis [SP]
(1) SP is the single best criterion for determining age after 25 y. Method is
similar to that of rib end
(2) It requires bones free of cartilage
(3) While pubic symphyses of humans shows age changes, those of other
primates metamorphose more quickly and usually synostose with advancing
age.
(4) The young adult human SP has a rugged surface traversed by horizontal
ridges and intervening grooves. This surface loses relief with age and is
 bounded by a rim by age 35 Subsequent erosion and general deterioration of
the surface are progressive changes after this age [Fig 3.25].
(5) SP changes were first observed by Todd in 1920, based on a series of 306
males of known age. He noted evidence of billowing, ridging, ossific nodules,
and texture on the symphyseal surface. Using these observations on his sample
of known ages, Todd recognized ten phases of SP age, ranging from 18 y to
50+ y.
(6) In 1955, Brooks modified Todd’s system.
(7) In 1957, McKern and Stewart modified Todd’s system in their own way,
using skeletal remains of 349 males who had died in the Korean War. Their
ages were documented from military records. They divided the symphyseal
surface longitudinally into two halves, or “components”:
(i) the “dorsal demiface” [Fig 3.25].
(ii) the “ventral demiface” and added a 3rd component
(iii) the “symphyseal rim.”
Six developmental stages [from 0-5] were recognized for each of the 3
components [Fig 3.25]. Developmental stage for each component is calculated
and added. The resultant score gives the age of the specimen. This system, like
that of Todd, was derived from an all-male sample.
(8) Drawbacks of McKern and Stewart’s 3-component system:
(i) The components do not vary independently
(ii) The system is unduly complex.
(9) Because of these drawbacks, in 1986, Darryl Katz and Judy Suchey
modified the Brooks’ 1955 system. This is now widely known as Suchey–
Brooks (SB) system, and is currently the most widely accepted system,
although even this system continues to evolve and is yet to reach its final
form. Like McKern and Stewart, they also suggested 6 phases, but with some
differences. Significantly they made casts of SP [of all phases] which could be
compared with the unknown sample. This method was obviously better than
comparison with photographs. The casts made by Diane France, consist of a
set of 12 models – 2 from each of the 6 phases; one illustrating an early
pattern and one showing a later pattern.
(10) Changes [McKern and Stewart’s method] – Changes are complex and must
be attempted by an expert only. Broadly they are:
(i) 20 y – Symphyseal surface is markedly irregular and uneven. Ridges run
 transversely across the articular surface
(ii) 20-40 y – (a) Ridges gradually disappear (b) Surface has a granular
appearance (c) Ventral and dorsal margins form
(iii) 40-45 y – symphyseal surface has an oval smooth surface, with raised upper
and lower ends
(iv) 45-50 y – A narrow beaded rim develops on the margins
(v) 51-60 y – (a) Symphyseal surface erodes (b) breakdown of ventral margin
begins
(vi) 61-70 y – Surface is irregularly eroded.

3. ML importance of age
Memory Aid 32: MLI of age
CIRCLE MIKE JIM [MERE MCI KI JAI - is another useful mnemonic, where ‘A’
becomes ‘Abortion’]
C-CRIMINAL RESPONSIBILITY, CONSENT
I-INFANTICIDE
R-RAPE
C-CRIMINAL ABORTION
L – [dummy letter]
E-EMPLOYMENT
M-MAJORITY
I-IMPOTENCE AND STERILITY
K-KIDNAPPING
E-EVIDENCE
J-JUDICIAL PUNISHMENT
I-IDENTIFICATION
M-MARRIAGE CONTRACT

(1) Criminal Responsibility:

(i) 7 y - Any act which is done by a child under 7 years of age is not an offence
[S.82, IPC]. This is because such a child does not have mens rea [ch 28].
Corollary - A male child <7 y cannot be accused of rape [ch 25].
(ii) 7-12 y - A child >7 y of age is presumed to have “attained sufficient maturity
of understanding to judge the nature and consequences of his conduct”.
However if a child between 7 and 12 years can show that he did not attain
such understanding, his action would not be considered an offence
[S.83, IPC].
(iii) 12-18 y – A child between 12 and 18 years would be tried only by a Juvenile
Justice Board [JJB] [Children’s court in layman’s terms]
(iv) Railways Act [RA] 1989 - (a) u/s 168(1), a child of any age below 12 years
can be convicted. But no punishment will be given to such a child. Instead
the father or guardian will have to execute a bond for such amount and for
such period as the court may direct for the good conduct of such person.
Memory Aid 33: Section of Railways Act 1989, denoting age of criminal responsibility
S.168 – Remember 16. Half of it is 8. Put that in front. A child of any age can be convicted according
to this section.

(b) If child repeats offence, the bond amount shall be forfeited [168(2)]. (c) If a
father or guardian fails to execute a bond he shall be punishable with
`50 fine [168(3)]. (d) The offences for which child may be convicted are (I)
maliciously wrecking a train [S.150], (II) causing damage or destruction of
railway property [S.151], (III) maliciously hurting persons travelling by
railway [S.152], or (IV) endangering safety of persons traveling by railway
willfully [S.153] or (V) negligently [S.154]. (e) It is wrongly taught
 sometimes that under the Indian Railways Act, the age of criminal
responsibility is 5 years. This is not true. A child of any age can be convicted.
The important diff is that in conviction of children <12 y, the father or
guardian will execute a bond of good conduct of the child; no punishment will
be awarded to the child.
(2) Consent:
(i) 12 years – A child >12 y can give consent for general physical examination
[Act not intended to cause death, done by consent in good faith for person’s
benefit – S.88, IPC, S.90, IPC]
(ii) 18 years – A person >18 y can give consent for undergoing surgery. (iii)
S.87, IPC - ch 2.
(3) Infanticide – For a charge of Infanticide, infant must be proved to be <1 y.
In India there is no specific law on infanticide [ch 27].
(4) Rape:
(i) sex with consent with wife of <15 y"Marital rape
(ii) sex with consent with any other girl <18 y"Statutory rape [ch 25].
(5) Criminal Abortion – Woman who has passed the child bearing age [usually
45y] cannot be charged of procuring criminal abortion.
(6) Employment -
(i) child <14 y cannot be allowed to work in any factory [please see below under
MLI of 14 y].
(ii) Young person 14-18 y – (a) can work in a factory only when a certificate of
fitness has been given to him by a certifying surgeon (b) The certificate
must be in custody of manager. (c) Such young person must carry a token
giving a reference to such certificate [S.68 The Factories Act, 1948]
(7) Majority – A person attains majority when he/she attains the age of 18 years
[S.3, Indian Majority Act, 1875]. If person is under guardianship, the age of
majority is 21 y [please see below under MLI of 21 y].
(8) Impotence And Sterility:
(i) Males - Before puberty, a boy is sterile, but not impotent.
(ii) Females - become sterile after menopause [approx 45 y]
(9) Kidnapping:
(i) Kidnapping from lawful guardianship — Taking away a boy <16y or a girl
<18y or person of unsound mind away from a guardian without his consent
[S.361, IPC]
(ii) Abduction — Taking away a person by force or deceitful means
[S.362, IPC].
(iii) Punishment for kidnapping — 7 y + fine consent [S.363, IPC].
(10) Evidence - Persons of all ages are competent to testify as witnesses
[S.118, IEA][ch 1].
(11) Judicial Punishment:
(i) “Juvenile” or “child” - means a person who has not completed 18th year of
age [S.2(k) The Juvenile Justice (Care and Protection of Children) Act
2000, or JJA 2000]
(ii) Juvenile in conflict with law - means a juvenile who is alleged to have
committed an offence and was <18 y as on the date of commission of such
offence [S.2(l), JJA 2000]
(iii) Punishments that cannot be given to a juvenile who has committed an
offence - (a) death (b) life imprisonment (c) imprisonment in default of
payment of fine or in default of furnishing security [S.16, JJA 2000]
(iv) If juvenile is between 16-18 y - and JJB thinks that offence committed by
him is so serious or his conduct and behaviour is such that it would not be
in his interest or in the interest of other juveniles in a special home to send
him to such special home, it may order the State Govt to keep such juvenile
in a safe place [S.16, JJA 2000]
(v) Punishments that can be given to a juvenile who has committed an
offence - (a) allow the juvenile to go home after advice, admonition and
counselling. Parent or guardian is also counselled. (b) direct the juvenile to
participate in group counselling and similar activities; (c) order the juvenile
to perform community service; (d) order the parent of the juvenile or the
juvenile himself to pay a fine, if he is over fourteen years of age and earns
money; (e) direct the juvenile to be released on probation of good conduct.
(f) Release the juvenile on probation of good conduct and place him under
the care of any fit institution for up to 3 y. (g) send him to special home for
up to 3 y [S.15, JJA 2000]
(vi) Borstal school - Please see below.
(12) Identification – Approximate age is important in all identifications, eg
when a newborn is lost, it cannot be replaced by an older child, say of 2-3
months.
(13) Marriage Contract – age of marriage of female is 18 y and of males 21 y
 [ch 23].
(14) Miscellaneous – use of children in pornographic materials is punishable.

4. Various ages of medicolegal importance

a. 12 y
(1) Crime committed by a child between 7-12 years of age - is not an offence,
if he hasn’t attained sufficient maturity of understanding [S.83, IPC]. Judge
decides the issue.
(2) General physical examination – Age of consent is 12 y [S.89, IPC].
(3) Consent – intended by any section of IPC is not a valid consent, if age of
child is <12 y [S.90, IPC]
(4) Indian Oaths Amendment Act 1939 - Unsworn evidence of a child <12 y is
admissible if the court thinks he does not understand the nature of an oath.
(5) Bombay Shops and Establishments Act 1948 - Child <12 y cannot be
employed.
(6) Exposure or abandonment of a child < 12 y by parents or person having care
of it - 7 years and/or fine [S.317, IPC]
(7) Man rapes his own wife of <12 y - Punishment as if he raped any other girl
of <12 y. [10 y-life]. If age of wife is 12-15 y - punishment of 2 y [maximum]
or fine or both [S.376(1), IPC]. This clause may appear paradoxical as the
minimum legal age for marriage in India is 18 years for girls. But despite this
law, many marriages of young girls are going on in India [for details, please
see ch 23].

b. 16 y
(1) Child passports - In many countries, different rules apply for a child <16 y
for getting passport.
(2) Age of voting - in Austria [Since 1st July 2007. It became the first member
of the European Union, and the first of the world’s leading democracies, to
adopt a voting age of 16 for all purposes], Brazil, Cuba, Ecuador, Nicaragua.
(3) Juvenile is between 16-18 y of age"has committed an offence so serious in
nature or his conduct and behaviour have been such that it is neither in his
interest nor in interest of other juveniles to keep him in a special home"the
Board may order the juvenile to be kept in such safe place that it thinks fit and
 report the case to the State Government [S.16 Juvenile Justice Act 2000].
(4) Kidnapping of boy– Taking away boy <16 y [and girl <18 y, or any person
of unsound mind] from lawful guardianship without the consent of such
guardian [S.361, IPC]
(5) Selling intoxicating drugs - A licensed vendor is not permitted to sell any
spirit or intoxicating drug to persons <16 y [S.22, United Provinces Excise
Act, 1910].
(6) Childhood, Minority: (i) Child - (a) means a boy or girl <16 y. If child
commits an offence, he is called a youthful offender, and cannot be sentenced
to death [The Bombay Children Act 1948]. (b) means a person <16y [S.2(aa)
The Immoral Traffic (Prevention) Act, 1956]. (ii) Minor - (a) means any
person <16 y [Bombay Prevention of Hindu Bigamous Marriage Act 1946].
(b) means a person 16-18 y [S2(cb) The Immoral Traffic (Prevention) Act,
1956].
(7) Kidnapping or maiming a minor boy for the purpose of begging - If
merely kidnapped [10 y+fine]. If also maimed [life+ fine]. For the purposes of
this section a minor is a male <16 y (or a female <18y). Imp because ages for
minors are different for males and females [S.363A, IPC].

c. 18 y
(1) Age of marriage - for girls [(i) S.5(iii), Hindu Marriage Act 1955; (ii) S.4(c),
Special Marriage Act, 1954 (ch 23)].
(2) Kidnapping of girl- Whoever takes or entices any girl <18 y [or boy <16 y,
or any person of unsound mind] out of the keeping of the lawful guardian
without his consent fine [S.361, IPC]
(3) Adulthood, Majority etc:
(i) Adult - Person >18 y is an adult [S.2(a) The Factories Act, 1948; S.2(1) (b)
The Mines Act, 1952]
(ii) Child – A female <18 y, and a male <21 y [S.2(a) The Prohibition of Child
Marriage Act, 2006]
(iii) Juvenile - (a) Person <18 y is a “juvenile” or “child” [S.2(k) JJA 2000]. (b)
If juvenile is accused of committing an offence and an enquiry is going on
he must be kept in “Observation homes” [S.8 JJA] (c) If after enquiry,
juvenile is proved to have committed an offence, he is called a “juvenile in
conflict with law”. Irrespective of what his current age is, if at the time of
 commission of offence, he was <18 y he is “juvenile in conflict with law”
[S.2(l), JJA]. He must be kept in “special homes” instead of jails [S.9, JJA].
He may be kept in special home for maximum of 3 y [S.15(1) (g), JJA] (d)
Juvenile cannot be sentenced to death or life imprisonment, or committed to
prison in default of payment of fine or in default of furnishing security
[S.16(1), JJA].
(iv) Major - (a) A person attains majority when he/she attains the age of 18 years
[S.3, Indian Majority Act, 1875]. If person is under guardianship, the age of
majority is 21 y [please see below]. (b) Major means a person >18 y
[S.2(ca) The Immoral Traffic (Prevention) Act, 1956]. Person between 16-
18 y is a minor [S.2(cb) of same Act].
(v) Minor – is a person <18 y [(I)S.4(a) The Hindu Minority and Guardianship
Act 1956 (II)S.2(hb) The Transplantation of Human Organs and Tissues
Act, 1994].
(vi) Young person - person <18 y [S.2(d) The Factories Act, 1948].
(4) S.87, IPC -A person <18 y cannot give valid consent to suffer any harm
which may result from an act not intended or not known to cause death or
grievous hurt [example: boxing, cricket, fencing]. 17 y old boy [i.e.<18y] asks
an older boy to do boxing with him "Older boy explains it could injure
him"younger boy says, it doesn’t matter"They start boxing"Younger boy
receives fatal injury"dies"Older boy is responsible. He cannot take plea that
younger boy had consented. If however the younger boy was >18 y, the older
boy could take the plea of consent.
(5) Age of consent for undergoing surgery [please see MLI of age above].
(6) Procurement of girl <18 y for illicit intercourse – Whoever procures such
girl is punishable [10 y+fine; S.366A, IPC]
(7) Selling person <18 y for prostitution - Whoever sells, lets to hire, or
otherwise disposes of any person <18 y for the purposes of prostitution or
illicit intercourse with any person or for any unlawful or immoral purpose is
punishable [10 y+fine; S.372, IPC]
(8) Buying or hiring person <18 y for prostitution - Whoever buys, hires, or
otherwise obtains possession of any person <18 y for the purposes of
prostitution or illicit intercourse with any person or for any unlawful or
immoral purpose is punishable [10 y+fine; S.373, IPC]
(9) Abetment of suicide of child <18 y - Death + fine [S.305, IPC]
(10) Culpable homicide -is not murder if the person who died was >18 y and he
risked death with his own consent [S.300, IPC, exception 5]
(11) Children’s home - A child [Under Children’s Act 1960] is sent to children’s
home on commission of an offence, but is not retained there beyond the age of
18 years.
(12) Children and Young Person’s Act 1933 of England - A person <18 y
can’t be sentenced to death.
(13) Kidnapping or maiming of a minor girl for the purpose of begging - If
merely kidnapped [10 y+fine]. If also maimed [life+ fine]. For the purposes of
this section a minor is a female <18 y (or a male <16 y). [S.363A, IPC]
(14) Age for voting - in India and most other countries [Australia, UK, USA]
(15) Statutory rape - Sexual intercourse with a woman <18 y even with consent
is rape [S.375, IPC].
(16) Age of consent for MTP [S.34. (a) MTP Act 1971].
(17) Divorce by a girl between 15-18 y - A wife may divorce her husband
without any ground if her marriage (whether consummated or not) was
solemnized when she was <15 y, and she repudiated the marriage after
attaining that age but before the age of 18 y [S.13(2)(iv) The Hindu Marriage
Act 1955].
(18) Donation of organs - (a) Age of giving consent for organ donation (b) A
“donor” is a person>18 y who voluntarily authorizes removal of any of his
human organ or tissue or both for therapeutic purposes. [S.2(f) The
Transplantation of Human Organs and Tissues Act, 1994].

E. Hair [Forensic Trichology]

Study of hair is known as trichology, and its application for administration of
law and justice, forensic trichology.
Salient features:
(1) Composition - Human hair is composed of proteins [<65-90%], water [<15-
35%], and lipids [<1-9%].
(2) Growth: (i) Rate - Hair grows at the rate of 0.4mm/day [1cm/month]. Nails
at the rate of 0.1mm/day.
Memory Aid 34: Growth phases of hair
ACT
1. Anagen phase: 2–3 years (occasionally much longer)
2. Catagen phase: 2–3 weeks
3. Telogen phase: 2–3 months

1. Structure of hair
a. Longitudinal section
The structure of hair is quite like that of a pencil.
(1) It consists of a shaft
(2) and root
(3) ending in a bulb.

b. Transverse (cross) section

(1) Cuticle:
(i) This is the outermost layer [Fig 3.26].
(ii) consists of - (a) thin, non pigmented scales [flat overlapping cells arranged in
a root-to-tip direction]. (b) Each cuticle cell [scale] is 5–10 µm long and
0.3–0.5 µm thick. (c) The cuticle layer in human hair is approximately 5–10
scales thick.
(iii) Function – to protect the cortex
(iv) Scales [cuticular cells] - are broadly divided into two types - (a) Coronal –
when each scale encircles the shaft completely and (b) Imbricate, when the
scales do not encircle the entire shaft. Each type is further divided into
several subtypes.
(v) Examination of cuticular scales – An impression from the surface of hair is
made in a thin film of cellulose acetate or finger nail varnish. A drop of soln
is spread thinly on a glass slide. Hair is cleansed in alcohol and is laid over
the wet film. After the film has dried [in about 10 m], the hair is stripped off
the slide quickly and the scale impressions are examined microscopically.
(2) Cortex:
(i) Middle layer.
(ii) Consists of longitudinally arranged elongated cells without nuclei.
(iii) Within these cells, fibrils are present
(iv) granules of pigment lie over the fibrils
(3) Medulla:
(i) innermost layer
(ii) Consists of keratinized remains of cells and air sacs.

2. Information from hair

Hair may be examined to reveal following information:
a. Hair or some fibre
Structure - Look under the microscope for structure. (I) Hair - Hair structure
would be unique as illustrated above. (II) Textile fibers - are divided into two
categories: natural or synthetic. Natural fibres are cotton, jute, linen, silk and
wool. Synthetic fibres include acetate, acrylic, aramid, nylon, polyester, and
rayon. Each fibre will show its own unique structure [Fig 3.27]. Characteristics
such as relative thickness of cell walls and lumen, cell length, and the presence,
type, and distribution of dislocations are important in identification of all natural
fibres.
(1) Coir: (i) Comes from the husk of coconut. (ii) Very dense and stiff fibre. (iii)
Dark brown or opaque (iv) chemical tests for lignin - Can be used for all plant
derived fibres.
(2) Cotton: (i) These are fibers from the cotton plant’s seed pod (ii) Solubility –
Insoluble in alkali. Soluble in 75% Sulphuric acid. (iii) Most commonly
encountered natural fiber (iv) The cross section of the fiber is bean-shaped,
swelling almost round when moisture absorption takes place. (v) Each cotton
fiber is composed of concentric layers (vi) Fibres show double refraction when
observed in polarized light.
(3) Jute: (i) Comes from flax just like linen but the plants are processed slightly
differently (ii) Jute fibres are smooth without transverse lines (iii) The cell cavity
is not uniform (iv) The ends are blunt.
(4) Linen: (i) Comes from flax, a bast fiber taken from the stalk of the plant (ii)
Has a narrow lumen (iii) Fibres show cross lines or folds about which the fibre is
often swollen.
(5) Silk: (i) These are fibers from the cocoon of the silkworm (ii) Shows
crossover marks and a triangular cross section with rounded corners. (iii)
Consists of long clear threads without any cells (iv) Smooth and finely striated.
(6) Wool: (i) These are fibers from animal coats: Sheep, goats, rabbits etc (ii)
Show an outer layer of flattened cells with overlapping margins (iii) Interior is
composed of fibrous tissue.
(7) Synthetic fibres – Differentiated by noting (i) their solubility in solvents like
HCl, HNO3, acetone, and dimethyl sulfoxide. (ii) Physical characteristics like
density, refractive index, melting/softening point (iii) infrared spectroscopy. For
more on fibres, please see ch 30 – Forensic Science Laboratory.
b. Human or animal
(1) Issue of human or animal hair arises in
(i) Killing of an animal protected under the Wildlife Protection Act, 1972
(ii) Bestiality. It can be differentiated from human hair [Table 29. Fig 3.28].
(2) Medullary index:
(i) Medullary index =
Diameter of medulla
Diameter of whole hair shaft

(ii) Value – Humans<0.3; Animals>0.5 [Table 29]. Value differs in hair from
different parts of the body; thus sometimes useful to know the part of the
body, hair is derived from.

c. From what part of body derived?

(1) Medullary index – please see above
(2) Morphology [Table 30]:
(i) Head – long, soft, taper gradually from root to tip. Often traces of oil found
smeared on them
(ii) Beard and moustache – thicker than the hair from any other part of body.
Traces of shaving cream, or aftershave may be found on surface
(iii) Eyebrows, eyelashes – stiff, thick and taper to a point. In females, traces of
 eye cosmetics may be found smeared on them.
(iv) Nostrils – stiff, thick. May show nasal mucus smeared on them.
(v) Beard, axilla, chest, arms, legs and pubis - Table 30.
d. How much violence was used?
(1) Force used - Considerable force is required to pluck out a thick bunch of
healthy growing hair from the scalp
(2) Tearing of scalp – An adult may even be lifted or dragged by the hair and
yet they may not come off. So strongly are they attached that sometimes even
scalp would be torn from the skull, but not the hair.

e. Sex
(1) Male hair –Coarser, Darker, Thicker
(2) If hair follicles present:
(i) Barr bodies [in females]
(ii) From DNA profile [Amelogenin]
(3) Hair diameter - Significant differences between sexes. Please also see Table
6 above.

f. Age
(1) Scalp hair – With -ing age, there is (i) graying and thinning; (ii) growth is
slower. (iii) -ed loss.
(2) Facial hair – -in women at about menopause
(3) Body hair:
(i) Human fetus and newly born child - show lanugo hair [fine, non medullated,
non pigmented (colorless), soft, scale pattern simple]
(ii) Adults – coarse, medullated, pigmented, tougher, more complex scale pattern
(4) Axillary and pubic hair:
(i) Initially soft and fine.
(ii) Later become coarse, pigmented and curly.
(iii) In women, there is loss of axillary hair at menopause. Please also see
“secondary sexual characters” above for ages of appearance.
(5) Pigmentation – Initially -es with age; afterwards hair start losing
pigmentation.
(6) Number of hair follicles - .with age. There is an associated -in the
proportion of telogen hair follicles.
(7) Hair diameter – has been measured with Atomic Force Microscopy [AFM]
and has been found to -for the first 40 y of life, after which it begins to ..
Thickness of scalp hair varies with age.
(8) Scalp hair density –-es up to 40 y. Then .es with age.
(9) Cuticles - of older people
(i) Show more damage. Damage is similar to that of chemo-mechanically
damaged hair fibers.
(ii) Show many cracks and miscellaneous cuticular debris. Because of this, hair
become brittle with age.
(iii) Scale edges - show uneven saw-tooth appearances.
(iv) Scale edge ghosts and endocuticles - more frequently seen
(v) Surface roughness -significantly -ed.
(vi) Stiffness - between the hair and the tip altered.
10. Hair roots – from children dissolve rapidly in KOH soln, but not in older
people.

g. Has the hair been altered by bleaching, dyeing or disease?

(1) Bleached hair: (i) brittle (ii) dry and (iii) straw yellow
(2) Dyed hair: (i) Color is not uniform (ii) roots are of different color (iii) hair is
brittle, lusterless and rough (iv) scalp skin is also colored (v) Color of head
hair different from hair on other parts.
h. Blood groups from hair
Please see ch 29.

i. Is the hair identical with the hair of suspect or victim?

Comparison of (1) color (2) length (3) scale pattern (4) DNA analysis [ch 29] if
root is available.

j. Dit it fall naturally or was it forcibly removed?

Examine base – see if root is visible
(1) If forcibly pulled out – hair bulb is larger and irregular. Sheath is ruptured
[Fig 3.29].
(2) If fallen naturally – hair bulb is smaller, atrophied and distorted. Root sheath
is absent.

k. Trace elements in hair

Trace elements in hair [eg P,S] are in different conc in different individuals,
depending on their race, age, sex, environment, diet etc. These can be estimated
by Neutron Activation Analysis [NAA] to establish identity [please see Gaetane
Bouchard murder case below under “case studies”].

l. Hair and DNA

(1) Both nDNA and mtDNA analyses [ch 29] can be applied to hair samples.
(2) Plucked hairs - usually have live follicle cells that can be used for nDNA
sequence analysis. Cut hair or hair lost naturally during the telogen [quiescent]
phase do not have live cells associated with the sample.
(3) Cut or shed hair - mtDNA sequencing methods can be used to associate or
distinguish hair samples from different individuals.

m. What is the cause of injury?

(1) Injury can be:
(i) Mechanical - (a) Broken (b) Crushed (c) Frayed (d) Glass cut (e) Tangled (f)
Twisted
(ii) Burnt
(iii) Chemicals [corrosives etc]
(2) Examine tip:
(i) Tip pointed and non-medullated"normal uncut hair
(ii) Shows sharp ends"(a) indicates cut by a sharp weapon [Fig 3.29] (b) Time of
inj - (I) Recently cut – sharply cut edge with a projecting cuticle (II) After a
week – End becomes square, smooth (III) After 1-2 months – Round, blunt
(IV) After 3-4 months – end becomes elongated, but medulla is absent.
(iii) Crushed ends"Heavy blunt weapon. Unprotected cortex splits and frays
(iv) Ragged ends"indicate frequently brushed hair (v) singed"Death by fire.

3. Medicolegal importance of hair

Each of the above questions answered has an MLI. In addition following is the
MLI of hair
(1) Age – of a person can be determined by distribution of hair on his body.
(2) Sex – can be determined by
(i) Barr bodies
(ii) Body distribution
(iii) Texture
(3) Identification – especially when some known hair peculiarity is known, eg
wavy hair, bleached, colored and dyed hair etc, very long hair.
(4) Injuries on hair, hair tip and hair bulb – can help in determination of
nature of weapon.
(i) Blunt and sharp weapons produce different kinds of injuries.
(ii) Fire and firearms can produce singeing of hair tips.
(iii) Scalds – hair are not singed in scalds; thus burning and scalding can be
differentiated.
(5) Trace evidence [ch 30] – Remains identifiable on body, clothes, weapons etc
for a long time; thus identifiable even in crimes committed long before. It may
be the only link between the accused and his crime and weapon.
(i) Sexual offences – bestiality, rape, sodomy [hair of either partner found on the
other]
(ii) Vehicular accidents – vehicles causing injuries on victims may be
identifiable long time after by hair adhering to them [ch 18].
(6) Time of death – length of hair on face.
(7) Toxicology from hair - Please see ch 31"Diagnosis of poisoning"Hair
analysis for poisons. Also ch 36"s Arsenic.

F. Deformities, Diseases, Moles, Birthmarks

[A] Deformities and diseases - eg amputations, arthritic changes, asbestosis,
bilobed ear, bowed legs, cleft palate, calcified leiomyomata, club foot (talipes),
dental implants, dentures, hare lip, horseshoe kidneys, nail deformities, old
fractures, poliomyelitic leg, polydactyly, prosthesis (implanted valves,
orthopedic nails, pins and screws, pacemaker, plates in skull), silicosis, skull
deformities [please see above under “skull”], souvenir bullets, stones in gall
bladder and kidneys, spine curvature, surgically removed organs (appendix,
gallbladder, kidneys, ovaries, prostate, tonsils and uterus), surgical scars,
undescended testicles and web fingers or toes etc can help identification in
highly putrefied bodies. [B] Mole, also known as a nevus, is a pigmented pin-
point spot over the skin. (i) Color - varies from gray to brown or jet black. (ii)
Frequency - Very common. An average person has over 20 pigmented moles
(iii) Situation - usually situated on the face, neck or back, but they may occur
anywhere (iv) Hairs - may be hairy or non-hairy (v) congenital condition, but
many pigmented moles do not appear until adult life. [C] Birthmarks are
blemishes on the skin present in a baby since birth or formed soon after.
Birthmarks may be (i) vascular (eg Port-wine stains) or (ii) pigmented (eg
Café-au-lait spots). Port-wine stains are flat, pink, red or purple marks that
appear at birth, often on the face, arms, and legs, and continue to grow as the
child grows. Café-au-lait spots are flat spots having the color of coffee with
milk. Many birthmarks disappear as baby grows, and are thus not useful as
identification features [eg macular stains, strawberry marks (capillary
hemangioma) and Mongolian spots].

G. Scars
A scar is a fibrous tissue covered by epithelium devoid of hair follicles, elastic
tissue, sebaceous and sweat glands and pigment; they are usually produced after
the healing of a wound involving the dermis.
Salient features:
(1) If the wound involves only the epidermis [as in abrasions], it will regenerate
without the formation of a scar.
(2) Permanency - Scars once formed are permanent. That is why they serve as
good identification features.

1. Characteristics
(1) All scars are usually depressed, but may be raised above the surface if keloid
formation has occurred (occurs especially in Negroes)
(2) An incised wound - leaves a linear scar
(3) A lacerated wound and a suppurating wound leave a prominent, irregular,
firm scar.
(4) A bullet wound causes a circular depressed scar.
(5) Burns leave an irregular scar.
(6) Scars from scalds are spotted in appearance. They show splashing marks as
well as signs of dribbling (flowing down).
(7) Stab wounds may leave different shaped scars, depending upon the shape of
the cross-section of the knife. May be oval, elliptical, triangular or sometimes
irregular.
(8) Corrosive acids leave an irregular scar. There may be signs of splashing and
dribbling.
(9) Vaccination scars are circular or oval, flat or slightly depressed. They are
not good identification features because they are likely to be present on
several people in almost the same location.
(10) Diseases like smallpox and syphilis may leave characteristic irregular scar
marks over the body.

2. Classification
(1) Accidental scars – eg from burns, cuts, injury to eyes, loss of limbs, scalds
etc
(2) due to disease – eg smallpox
(3) surgical scars – eg incisional scars [Fig 3.31].
3. Growth
Scars produced in childhood grow in size as child grows, especially if situated
on chest or limbs.

4. Age of scars
Scar forms on by secondary intention in about 2 weeks. After this period, the age
of scar is calculated as follows
(1) Up to 2 months – Vascular; angry red
(2) 2-6 months – Soft, sensitive and tender
(3) After 6 months – White, firm, tough, hard, glistening, corrugated.
Memory Aid 35: Age of scars
VAST
VAscular : up to 2 m
Soft, Sensitive, tender : 2-6 m
Tough : >6m

5. Examination
(1) Good lighting and magnifying glass – Essential (because old scars may
often be very faint and unrecognizable).
(2) Description - should include, their number, size, shape, location, nature of
surface (whether smooth or irregular), whether fixed or free, its level in
relation to the body surface (whether raised above the surface or depressed),
 whether glistening or not, and its tenderness.
(3) Ends - rounded or tapering (can often help determine the nature of the
weapon used to inflict the wounds)
(4) Probable direction – of the original wound (note tailing).
(5) If the scar is faint - can be made more visible by the application of heat, UV
light or surface friction.
(6) Demonstration of scar in a dead body – can be done by microscopy (scars
lack elastic tissue). Elastic tissue is however present in striae gravidarum.

6. Erasure
Scars can be erased by
(1) Skin grafting and
(2) Excision with suturing of edges of excised area. This results in another scar,
but which is less prominent than the earlier one.

7. MLI
(1) Identification
(2) Shape of scar – Can reveal nature of offending weapon
(3) Age of scar – if it corresponds to the date of attack, it is a good corroboratory
evidence
(4) Linea albicantes – indicate previous pregnancy.

H. Tattoos
Tattoos (Tahitian tatau, a mark) are special marks, designs, pictorial diagrams
(e.g. of Gods and Goddesses), or alphabetical messages (e.g. name of self,
husband, or a friend etc) made or written permanently on the skin of the body.
Tattooing has been practiced since ancient times. The body of “Ötzi the Iceman”,
dated 3300 BC, bears 57 tattoos. Several Egyptian mummies have been found to
have tattoos.
Salient features:
(1) Site - Tattoos can be found on just about any part of the body, though the
commonest site is front of forearm. Other common sites are upper and lower
limb, back of neck, abdomen, breasts and vulva (prostitutes), penis
(homosexuals), buttocks. Even facial tattoos are known.
(2) Method of examination – Record exact size, shape, design, color, site.
 Photography is better.

1. Technique
Coloring matter (dye) is injected deep in the dermis with sharp needles, or an
electric vibrator, so that the mark becomes indelible. An inaccurate technique
would deposit the pigment in superficial layers of dermis only, which would
cause obliteration of the tattoo mark eventually.

2. Dyes
(1) Henna and Mehndi in India.
(2) Salts of heavy metals - Aluminum (green, violet); barium (white); cadmium
(red, orange, yellow); chromium (green); cobalt (blue); copper (blue, green);
iron (brown, red, black); lead (yellow, green, white); mercury (red); nickel
(black); titanium (white), ultramarine [double silicate of aluminum and
sodium; blue] and zinc (yellow, white). Metal oxides used are ferrocyanide
and ferricyanide (yellow, red, green, blue).
(3) Organic chemicals - Azo-chemicals (orange, brown, yellow, green, violet)
and naphtha-derived chemicals (red).
(4) Homemade or traditional tattoo inks - Made from pen ink, soot, dirt or
blood.
(5) UV (Blacklight) Reactive Tattoo Ink - Blacklight tattoos will not glow in
the dark but glow under UV light. These work on the principle of
fluorescence; the inks are made of florescent material.
3. Permanency
(1) Once imprinted, tattoos remain on the body almost indefinitely, until and
unless they are removed by specialized procedures.
(2) Rate at which the tattoos fade depends upon (a)composition of dye (b)
depth up to which the dye is inserted - Dye should be injected to the right
depth. Dye injected superficially gradually fades in some years. Dye injected
too deep is removed by phagocytes (c) Site:
(i) Parts protected by clothing retain tattoos much longer than those which are
exposed to sunlight
(ii) Tattoos on hand disappear early due to constant friction

4. Faded tattoos
Faded tattoos may be made visible by
(1) UV lamp
(2) Infrared photography (Can also reveal old tattoos superimposed by new
tattoos) [please see ch 30, under the heading photography]
(3) Removal of epidermis:
(i) makes the tattoo very clearly visible on dermis.
(ii) In decomposed or burnt bodies – can be done easily.
(iii) In fresh bodies – Apply heat on suspected tattooed area (a) By placing a
spirit soaked burning cotton over the area. (i) Examination of lymph nodes
nearest to faded tattoo [eg in case of forearm tattoos, axillary LN] – Incise
LN and note color"If an abnormal color [eg black, red] is noted, tattoo
presence confirmed. Helpful also if the person had intentionally removed
tattoos during life. The color should be mentioned in the pm report [please
correlate with ch 5"description of an organ].
5. Complications
Abscess, AIDS, allergic reactions to tattoo inks, bruise (if bv is punctured),
erysipelas, fungal infections, hepatitis, gangrene, leprosy, septic inflammation,
syphilis, tetanus, tuberculosis may occur. A few cases of burns on black tattoos
caused by MRI scans have been documented. Black ink commonly contains iron
oxide; the MRI scanner causes the iron to heat up causing burns.

6. Removal
(1) A criminal often removes tattoos, lest he may be identified.
(2) Examination by UV, Infrared [or other methods described above] is helpful.
(3) Following methods are used.

a. Surgical removal
(1) Excision and skin grafting
(2) Scarification - scars are formed by cutting, branding or burning the skin.
(3) Dermabrasion - Surgical procedure involving controlled abrasion of the
upper layers of the skin with mechanical means (eg sandpaper) or LASER
(CO2 or Erbium:YAG).

b. LASER
LASER treatment causes tattoo pigment particles to heat up and fragment into
smaller pieces. These smaller pieces are then removed by phagocytosis
[normally tattoo dye particles are too big to be removed by phagocytosis. That is
the reason of their permanency].
c. Corrosives
Corrosives produce a scar causing disappearance of tattoo. Substances used are
Formic acid, papain in glycerine, tannic acid and zinc chloride.

d. Cover-up
This is not true removal, but covering of an old tattoo with a new tattoo.
Necessitates darker inks to effectively hide the older tattoo.

e. Miscellaneous
(1) Carbon dioxide snow
(2) Diseases (natural removal). Confluent Smallpox (in the smallpox era),
chronic eczema
(3) Electrolysis.

7. ML importance [of tattoos]

a. Drug addicts, HIV transmission

(1) Drug addicts get the front of their arms tattooed to hide the needle puncture
marks to mask their addiction habit from policemen [ch 40].
(2) If drug addict is HIV+ve, there is risk of HIV transmission if same needle is
used.

b. Identification
Tattoos are an important aid to identification. If the number of tattoos are large,
or if the shape of tattoo is very peculiar, identity can be made from tattoo alone.
Other information that can be derived from tattoos is identity numerals [as in
prisoners], initials and dates, name (own, spouse, friend) and regimental or
nautical details.
Case studies:
Shark Arm Case – James Smith (resident of Sydney, Australia), former boxer
and a small time criminal went missing on April 7, 1935. On 25 April, a human
arm was regurgitated by a captive tiger shark kept in an aquarium; it had been
captured shortly after April 7, the arm bore a tattoo mark showing “two men
boxing”. His wife and brother identified it as the arm of James Smith as it had
exactly the same tattoo. Investigations led to the arrest of Patrick Brady, who had
killed Smith and thrown the body in sea.

c. Medical Tattoos
A medical tattoo is one used for medical reasons. It may be made
(1) to show illnesses or allergic reactions
(2) As a warning that a patient suffers from a chronic disease that can exacerbate
suddenly and that will require immediate specialist treatment (eg congenital
adrenal hyperplasia; patient may need steroid replacement therapy during
ordinary illness).
(3) As an aid in radiotherapy. In order to minimize damage to surrounding
tissues, the radiotherapist seeks to keep the irradiated field as small as
possible. Marking a number of points on the body with tattoos can aid
radiotherapists in adjusting the beam properly.
(4) During breast reconstruction after mastectomy or breast reduction surgery.
Tattooing is sometimes used to replace the areola which has been removed
during mastectomy.
d. Mental state
The presence of tattoos of various types tell about the mental state of the person,
as well as his likes and dislikes. They can also tell about the past experiences of
the person.

e. Occupation
Prostitutes, homosexuals, sailors, boxers etc may have peculiar tattoos at
peculiar sites.

f. Protective tattoos
In many cultures tattoos are regarded as the protective amulets. Can reveal
country of origin.
(1) Burma:
(i) Soldiers believe that tattoos on their thighs make them invincible in war.
(ii) The snake tribes of Pakokku believe these tattoos protect them from the
vipers and cobras. Each member of this community goes under weekly
tattooing. Black Ink mixed with snake venom is used for tattooing The
entire body - arms, legs, chest, back, face and even the scalp - is tattooed
[venom tattoos]. May be scientifically sound
(2) India – There is a popular belief among Hindus that a tattoo of a God like
Lord Hanuman can protect them from all kinds of evils and pains.
(3) Japan - Women of Ainu group believe that if they get tattooed like a
goddess, the evil spirits of diseases would run way from them.

g. Religion
The presence of tattoos of a particular God or Goddess tells about the religion of
the person.

h. Miscellaneous
(1) May be an indicator of social status. Generally persons of high social status
avoid tattoos.
(2) Country of origin
(3) Perversions – drawing of indecent figures
(4) May reflect travel history, involvement in wars, sex interests etc.
(5) May cause hypersensitivity reactions.

I. Occupation Marks
Occupational marks or stigmata are special marks on the body of a person,
produced as a result of his profession or habits. These may sometimes be helpful
in identifying a person. Sherlock Holmes often impressed his colleague Watson
by telling the occupation of his clients simply by observing occupational marks.
Occupational marks may be temporary or permanent.

J. Anthropometry (Bertillon system, Bertillonage)

Anthropometry (Gk anthropos, man; metron, measure" literally “measurement of
man”) refers to the measurement of eleven key dimensions of the individual for
the purposes of identification.
Salient features:
(1) Earliest system of criminal identification.
(2) Started by Alphonse Bertillon (1853 –1914) in the year 1883.
(3) Principle - Based on the two facts (i) Dimensions of the skeleton do not
change after the age of 21 years. (ii) Quetelet’s law [please see above under
“Stature”]. According to Quetelet’s law, there is one in four chance of two
persons having exactly same height. Bertillon reasoned that if one more
measurement was added - for example the length of the trunk - the chance of
finding the both measurements exactly the same decreased to one in sixteen.
By extending the number of measurements to eleven, the cumulative
probability of two criminals having exactly the same measurements would be
411 or over 4 million to one.
(4) The system included (i) Descriptive data – e.g. (a) color - of hair, eye and
skin [complexion], (b) shape - of ears, nose and chin (ii) Body marks – e.g.
tattoos, scars, moles (iii) Body measurements - 11 parameters were used by
Bertillon. No individual has all 11 parameters exactly the same. The
parameters used were: (1) Height: Standing (2) Height: Sitting (3) Reach:
Arms outstretched (middle finger-tip of one hand to middle finger tip of other)
(4) Length of head (5) Width of head (6) Length of right ear (7) Width of right
ear (8) Length of left foot (9) Length of left forearm (10) Length of left middle
finger (11) Length of left little finger (iv) Front and side photographs. Also
called portrait parlé (Fr. The Speaking Portrait), because it was like making a
 speaking portrait of a person.
(5) Disadvantages - (a) Measurement requires use of instruments and trained
operators. Otherwise two operators may give different values for same person
(b) applicable only to adults (c) Calculation errors are there (d) photographs
are not reliable (e) Like fingerprinting, anthropometric data is not left at the
scene of crime. Presence of criminal at the scene cannot be established by
anthropometry
(6) Current status - This system has now been replaced by dactylography.

K. Dactylography
Dactylography (Gk daktylos, finger; graphein, to write) [syn. Fingerprinting,
dermatoglyphics, Galton system] is a method of identification, based on unique
epidermal ridge pattern on the tips of fingers.
Salient features:
(1) It is the most important, accurate and unfailing method of positive
identification.
(2) It is a better method of identification than even DNA profiling. DNA
profiling would be same in identical twins, but fingerprints are different even
in identical twins.
(3) Paternity by fingerprints – Patterns are not inherited and paternity cannot
be proved through fingerprint patterns.
(4) Epidermal ridges (also called friction ridges) are raised portions of the
epidermis on the fingers (also seen on toes, palms, soles). Their function is to
amplify vibrations and to assist in gripping rough surfaces and wet surfaces.
Sweat gland pores open on their top"Responsible for fingerprints. A subsidiary
ridge [syn incipient, nascent or rudimentary ridge] is an incompletely
developed ridge [thinner]. Sweat pores do not open over them; they do not
produce fingerprints.
(5) Embryology: (i) 6-8 weeks after conception - Volar pads form. These are
ball like structures that make up the contour of the fetal hand. (ii) 10-12 wks -
volar pads begin to recede (iii) 13th wk - Skin ridges appear (iv) Between 10-
16 wks - local factors like amniotic fluid pressure influence fingerprint
pattern. That is why fingerprints are different even in identical twins. (v) 21st
wk – fingerprint pattern is complete.
(6) Permanence: (i) Fingerprints remain permanent throughout life and even
 after death. (ii) Even in advanced decomposition, fingerprints can be
identified.
(7) Transmission of fingerprints – Patterns can be easily emailed and printed,
enabling intercontinental criminals to be caught easily.

1. Types of Fingerprints
a. According to fingerprint pattern
Four types are known [Fig 3.35]. Depend on presence of core and delta. A ridge
recurving on itself is called the core. Convergence of ridges from three
directions is called a delta (or triradius). Rule: If a pattern contains neither core
nor delta, it is an arch; if it contains 1 core and 1 delta, it is a loop; if it contains
no core and 2 delta, it is a whorl. Composites will have mixed patterns. Types:
(1) Loops [most common, about 67%]. Ridges enter from one side, recurve and
exit from the same side they entered [Show one core and one delta]. These are
further divided into (a) radial – ridges enter and exit from radial side (b)
ulnar – from ulnar side.
(2) Whorls [next most common, about 25%]. Ridges make a complete 360°
circuit around the center of the print [show 2 deltas].
(3) Arches [7%] – Show neither core, nor deltas. Further divided into two types.
(i) plain arch - Ridges enter from one side, rise to a slight bump and exit out
from the opposite side. (ii) tented arch. Similar to arch, but ridges stand at an
angle of 45° or more.
(4) Composite [1%] - A mixture of above types in a single print.

Memory Aid 36: Fingerprint patterns

[Most common patterns to least common patterns]
Mnemonic (1) Lily Works At Cafe
Loops [67%], Whorls [25%], Arches [7%], Composite [1%]
Mnemonic (2) Love Wife And Children
2. Comparison of fingerprints
(1) Identification - is done by comparing many details of characteristics
[minutiae] which occur throughout the ridge areas, eg ridge termination,
bifurcation etc [Fig 3.36].
(2) ACE-V:
An acronym for 4 stages of the examination process: Analysis, Comparison,
Evaluation, and Verification.
(3) Points to be compared:
(i) There is no fixed rule.
(ii) Different countries adopt different number of points to be compared.
(iii) Generally 16-20 points of comparison are accepted as proof of identity.
3. Fingerprints on human skin
(1) Can be done to detect fingerprints of murderer, rapist etc. Especially useful
 where hands have been used, eg throttling.
(2) Body at crime scene - should be processed immediately, and before its
touching by anyone else.
(3) Recommended technique - Superglue fuming of deceased’s body, followed
by the application of magnetic powders
(4) Fingerprints from refrigerated bodies - cannot be recovered because
condensation washes away prints, and interferes with fingerprinting
techniques. Yet an attempt may be made after taking out the body and
allowing the moisture to evaporate.

4. Alteration of fingerprints
Alteration of fingerprints may be (a) Natural (b) Occupational (c) Intentional
[mutilation].

a. Natural
Fingerprints are better protected than other parts of the body, and are thus not
easy to change [eg in burns, the fingers reflexly bend inwards against the palm
protecting fingerprint patterns]. Following changes are most important
(1) Overall pattern retained, but there is change of distance between ridges – in
(i) Acromegaly
(ii) Infantile paralysis
(iii) Rickets.
Memory Aid 37: Natural causes of alteration of fingerprints
AIR – Gives 3 most common natural causes when overall fingerprint pattern is retained, but there is change
of distance between ridges

(2) Complete loss of pattern – in (i) Burns (ii) Coeliac disease

(3) Epidermal ridge atrophy - in (i) Coeliac disease
(4) Incomplete atrophy of ridges - in (i) Dermatitis
(5) Permanent impairment of fingerprint pattern - in (i) Electrical injury (ii)
Leprosy (iii) Radiation exposure
(6) Ridge alteration - in (i) Acanthosis nigricans (ii) Eczema (iii) Scleroderma
(iv) Skin atrophy.

b. Occupational
In manual laborers working with cement, gravel, lime, sand etc, fingerprint
ridges may get damaged.

c. Intentional
(1) Used by: (i) Criminals to avoid detection by police (ii) Illegal immigrants
(iii) Refugees
(2) Methods used are
(i) Abrading with a rasping device [a tool similar to a file, used for shaping wood
or other material]
(ii) Burns
(iii) Cauterization
(iv) Corrosives
(v) Rubbing against a hard surface
(vi) Self inflicted wounds [by knifes, needles, biting or chewing skin off]
(vii) Skin grafting [plastic surgery] from other portions of body, eg chest.
(viii) Transmogrification - changing into a different pattern, by removing two or
more portions of fingerprints and exchanging their places. By doing so,
finger ridge patterns become so unusual that they at once arouse suspicion
(3) Except in skin grafting, some part of the skin is generally left undamaged,
which can lead to identification.
(4) Attempted mutilation also produces additional characteristics, making
identification easier.
(5) In most cases [eg burns], fingers on healing begin showing original pattern.

5. Poroscopy
Poroscopy is the examination of impressions left by the sweat openings on
fingerprint ridges [Fig 3.36].
Salient features:
(1) First described by Edmond Locard
(2) Each mm of fingerprint ridge contains 9-18 pores
(3) Uniqueness - They are unique in size, shape, extent, position and number in
a given individual
(4) Permanence - Pores are permanent and do not change during life
(5) Medicolegal Importance – Useful when only fragments of fingerprints are
available.
6. MLI [of fingerprints]
(1) Identification of (i) criminal (ii) deserters (iii) persons suffering from
amnesia (iv) Unknown persons found dead (v) unconscious persons involved
in accidents etc (vi) decomposed bodies (vii) accidental or intentional
exchange of babies.
(2) Fingerprinting in burnt bodies [ch 14].
(3) To maintain identity records [eg in army, police].
(4) Authentication of sensitive documents [eg driver’s license, migration records,
passport].
(5) Prevention of impersonation.
(6) Documents are often signed by thumb impressions by illiterate persons.
(7) Cheques, bank notes and other legal documents sometimes may be found to
bear a latent fingerprint
(8) Reveal drug use - Secretions, skin oils and dead cells in a human fingerprint
contain residues of chemicals and their metabolites present in the body. Drugs
eg cannabis, cocaine, marijuana, methadone and nicotine can be identified
from fingerprints.
(9) Time of fingerprints – Can be calculated roughly. Salts in fingerprint
residues are stable relative to the esters and proteins. Thus fresh fingerprints
will reveal all; older fingerprints would reveal salts, but not the other
components.
(10) Sex from fingerprints:
(i) From DNA profile [Amelogenin]
(ii) Females deposit more sebaceous residue than males.
(11) DNA profile from fingerprints – An average fingerprint leaves between
0.04 to 0.2 ng of DNA from which a DNA profile can be prepared.
(12) Association with blood groups:
(i) Blood group A+ and O+ have highest incidence of loops [52% & 54.3%
respectively] followed by whorls (33.4% & 30.6% respectively)
(ii) Incidence of whorls is highest in blood groups A- and O- [53.3% & 50%
respectively] followed by loops [46.7% & 30% respectively).
(iii) Blood group AB shows highest loops [55% in Rh+ve & 52.5% in Rh-ve],
followed by whorls [32.5% in Rh+ve & 27.5% in Rh-ve] and arches [12.5%
in Rh+ and 20% in Rh-].
(iv) Frequency of whorls is highest in blood group B in both Rh+ and Rh-
 subjects, followed by loops and arches.

L. Footprints
Footprints are prints left in the soil or any other surface by either a bare foot
(bare footprint) or shoe (shoeprint). These can be used for identification.

M. Other Prints (Palatoprints, Lip Prints)

1. Ear prints
[A] When a human ear is pressed against a surface, materials present on the ear’s
surface (waxes, skin oils, etc.) are left behind, forming a two-dimensional “ear
print” [Fig 3.37].
2. Lip prints (Cheiloscopy)
The study lip prints is called cheiloscopy. Forensic cheiloscopy is the study of
lip prints for the purposes of law and administration of justice.
Salient features:
(1) Like fingerprints, lip prints have various patterns which are different in any
two individuals. These patterns are identified and then matched to obtain at a
positive identification.
(2) There may be differences in patterns of upper and lower lips and right and
left halves.

3. Nose prints
Used to identify pet animals [eg dogs], but not yet used in humans.

4. Palate prints
Palatoscopy, palatoprints or rugoscopy, is the study of palatal rugae to establish
identity.
Salient features:
(1) The anterior part of the palate has rough raised ridges (palatal rugae), which
are different in every individual, much like fingerprints.
(2) Prints of palatal rugae [Fig 3.38] are known as palatoprints. They can be
used and matched for positive identification.
5. Tongue prints
Tongue prints include its shape and the unique surface textural features found
on its surface.

N. Superimposition
Superimposition is the technique applied to identify a dead person when both his
skull and antemortem photograph are available [Fig 3.39]. Two techniques are
used (1) Photographic superimposition (2) Video superimposition.

1. Photographic superimposition
Technique –
(1) Processing of Photograph - (a) Position - The photograph need not be the
frontal view of the person. It can be a lateral, semi-lateral view or any other
view. Essentially all major bony prominences namely cheek bones, chin, nasal
prominence, outline of top of skull etc must be clearly visible, because these
would ultimately be matched with the photograph. (b) Recent - In case of a
growing child, most recent photograph is better. More recent grown skull may
not match with the protuberances of an old photograph.
(c) Size - If the photograph is small, it must be enlarged to exact life size. [i]
From an object in picture - This can be done by noting any physical object
in the picture (ear ring, nose ring, hair pin, picture in background, a design on
worn cloth, tie etc) and obtaining it from the family of deceased. Photograph
is enlarged till the picture of object (in picture) attains a size exactly equal to
the size of object obtained from family. [ii] From interpupillary distance – If
no object is present in the picture, or if the object present in picture is not
available, enlargement to life size can be done from interpupillary distance.
This is constant in a given person irrespective of where his gaze is.
Considering the orbits to be two rectangles, diagonals are made; the pupil lies
at the point where the diagonals meet. Interpupillary distance is thus
calculated. The picture is enlarged till the interpupillary distance of the picture
becomes exactly equal to that calculated from skull. The picture is then
exactly life size. (d) A transparency of this picture is then prepared.
(2) Preparation of skull – (a) Ideally entire skull should be available, but if
 mandible is not there, one can still perform the technique (b) If skull had
attached soft parts, they must be removed (c) Mounting – Skull is mounted on
a moveable skull rest which can be rotated on all three axes. Position of the
skull can be suitably adjusted (d) Skull is so adjusted that its outline
corresponds that of the photograph on transparency (e) A photograph of skull
is taken and a transparency prepared (f) The transparency of the life size
photograph is now superimposed on the transparency of the skull [Fig 3.39].
(3) Comparison – Several points are then compared.
(4) Photograph – The superimposed transparencies are then photographed for
court display. Lay judges can be shown this photograph and points of
comparison explained.
(5) Presumptive test only – Superimposition is a presumptive test.

O. Reconstruction of Features from Skull

Facial reconstruction [syn, facial approximation] is based on the fact that face
is influenced by the underlying bone tissue.
(1) Traditional Method:
(i) Average thickness of soft parts of the face is measured at several
predetermined points.
(ii) Using this data, small wooden or plastic sticks of appropriate thickness are
 pasted on the skull
[Fig 3.40].
(iii) Clay is then applied over the skull in such a way, that it just comes up to the
level of sticks.
(iv) Soft features of mouth, nose, ears etc are applied using the racial data
extrapolated from skull [eg negroid etc].
(v) Color of eyes is similarly applied.
(2) Computer method – skull is scanned and data fed in computer. From the
tissue thickness data, the computer “clothes” the skull with soft tissues.
Advantage is that the tissue thickness or other facial features can be altered
easily on the computer screen if a new fact comes to light later.
(3) Advantages – reconstructed features when published in a newspaper etc is
likely to draw much greater public response.

P. Teeth, Bitemarks, Oral Structures [Forensic Odontology]

Forensic odontology or forensic dentistry is the application of the knowledge of
dentistry for the purposes of law and administration of justice. Forensic
odontostomatology is a wider discipline, which uses knowledge of all oral
structures [lips, palate] and secretions [saliva] for the purposes of law and
administration of justice.

1. Identification from teeth

[A] No two persons have identical dentition in all respects. Dental identification
can thus be done by comparison of records between missing person and dead
body. Comparison is done by gross examination and radiography. [B] Why teeth
are especially suited for identification - because they are protected from fire and
trauma etc by external oral structures. Highly resistant to putrefaction also.
Disaster dentistry is use of teeth in identifications in mass disasters [ch 4].

a. Gross examination
Following things are compared
(1) Restorative work – Note especially (i) Bridge work (ii) Conservative dental
work (iii) Crowns (iv) Dental fillings (v) Dentures - (a) Full or Partial (b) If
partial, upper or lower (c) Type (d) Shape (e) Look for patient’s name or code
number included in them (f) Restorative materials used (vi) inlays (vii)
Prosthesis if any.
(2) Special and unusual features:
(i) Present teeth - Number, spacing and situation. Note especially (a) whether
deciduous or permanent (b) caries (c) decayed teeth (d) undersized or
oversized teeth (e) loosened teeth (f) chipped teeth (g) broken teeth (h)
Fractures (i) Surface (j) configuration (k) Incisal edges
(l) ridges (m) Accessory cusps.
(ii) Absent teeth – Number and situation. Note especially if they are (a)
unerupted (b) erupted and extracted by medical intervention. Time period of
extraction [there may be evidence of old or recent healing] (c) erupted and
fallen (d) If fallen whether due to natural causes or trauma (e) Any evidence
of fresh loss.
(iii) General condition of teeth - (a) Age related changes [eg Attrition,
periodontosis etc] (b) Cavities (c) Cleanliness (d) Color and Staining
[please see below under MLI].
(iv) Peculiarities of arrangement - (a) Crowded teeth (b) Deformities (c) Ectopic
teeth (d) Malposition (e) Overlapping (f) Rotation.
(v) Supernumerary teeth.
(vi) Mesiodistal width of teeth.
(vii) Peculiarity of jaws, eg prognathism [prominence of the lower jaw,
overbite].
(viii) Oral pathology [eg disease, gingival hyperplasia, old injury].
(ix) Unusual findings – eg Diastema [space between two teeth], Palatal tori
[Bony protrusions on the palate].
(3) Diseases – Syphilis [Hutchison’s teeth].

b. Radiography
(1) Useful in – Identification, especially in badly burnt, putrefied or mutilated
bodies; in mass disasters etc [please also see “X-rays in identification” below].
(2) Antemortem X-rays - In all cases, antemortem X-rays are necessary for
comparison. More recent the antemortem X-rays, the more reliable the
comparison

2. Age from teeth

Please see above under the heading “Age”.

3. Sexing from the teeth

Please see Table 31.
4. Stature from teeth
Take combined mesiodistal width [CMDW] of 6 maxillary anterior teeth [i.e. all
4 upper incisors + both upper canines]. The formula is as below.
Stature in mm = CMDW [in mm] x 13.65 + 982.421

5. Race from teeth

(1) Size:
(i) Large – in Amerinds, Eskimos, Melanesians
(ii) Small – in Lapps and Bushmen
(2) Mutilation of teeth by filing and inlaying with precious metals and stones –
indicates tribals [tribal custom, cultural peculiarity]
(3) Cusp of Carabelli - [syn Carabelli’s tubercle, tuberculus anomalus of Georg
Carabelli] is a small additional cusp at the mesiopalatal angle of maxillary
first molars [Table 2]. It is most common among Caucasoids (75-85%) and
rarest in Pacific Islanders (35-45%).
(4) Shovel shaped teeth [Fig 3.4]– in Mongoloids
(5) Taurodontism – “Bull like” teeth [L, taurus, bull; Gk, odous, tooth]. Found
 in molars only. Seen in Eskimos.
(6) Eruption cyst - Benign cyst in the gums associated with a deciduous or
permanent tooth after it has erupted through the bone. Most prevalent in the
Caucasian race.
(7) Hypodontia and double teeth – More common in Taiwanese children.
Hypodontia - Patient is missing 6 teeth or less, excluding the 3rd molars.

6. Personal habits
(1) Smoking:
(i) Cigarette smokers - smoke marks mainly the lingual (inner) surface of upper
anterior teeth
(ii) Pipe smokers – develop oval-shaped notches on the occlusal (biting) surfaces
from clenching the pipe stem. Similar pattern also in people who chew
cigarette holders
(2) Loss of tooth substance:
(i) Serrated occlusal surfaces - carpenters, cobblers, seamstresses and women
who open bobby pins with their teeth [because they use their teeth to hold
nails and pins]
(ii) Anterior tooth loss – trauma caused by wrestling or fighting or using the
teeth in certain professions and sports [eg power grasping in holding sled
reins or fish lines]
(3) Abrasions on labial and occlusal surfaces of teeth – sandblasters and
stonemasons
(4) Dissolved enamel structure – persons who consume excessive amounts of
citrus fruit juices and carbonated drinks
(5) Alteration of positions of teeth – Musicians who play mouth instruments

7. Pink teeth
[A] Pink teeth can occur during life or postmortem. During life they occur
mainly in CO poisonings. After death they develop in about 1-2 weeks
especially near the gumline. [B] Mechanism of development - Seepage of
hemoglobin or it’s derivates into the dentinal tubules. Prerequisites are (i)
hyperemia and congestion (ii) extravasation of erythrocytes into pulp capillaries
(iii) autolysis (iv) damp and humid environment. Therefore, most often seen in
drowning. In victims of drowning the head usually lies in a head-down position.
From this it can be assumed that pink teeth could be because of PM lividity.
Although seen in drowning most often, they are not pathognomonic of any
condition. They have been described in victims of drowning, hanging, knifing,
barbiturate poisoning, carbon monoxide and CO2 poisoning. In addition, pink
teeth have also been observed in many cases where the cause of death was not
known.
8. Bitemarks
An odontoglyphic or a bitemark is a patterned injury produced by the voluntary
action of teeth being forced into a softer object.
Salient features:
Bitemarks can be left by humans, animals [both land and sea] and insects.
Human bites
Human bitemarks can be offensive, defensive, self-inflicted, or consensual.

9. Dental charting
Dental charting is a means to provide a quick graphic description of a person’s
teeth.
Salient features:
(1) There are >150 different methods of dental charting in use around the
world. The most common ones are described below.
(2) Advantages:
(i) Provide a quick overview of patient’s teeth
(ii) Records can be stored easily
(iii) Since only mathematical symbols are used, can be understood by
professionals knowing different languages
(iv) can be transmitted easily over internet, phone and telegrams.

a. Zsigmondy system (1861)

Earliest system was proposed by Austrian dentist Adolph Zsigmondy. The
entire mouth was divided in 4 quadrants, and teeth in each quadrant were
represented by Roman numerals in children, and Arabic numerals in adults.
Deciduous
Right V IV III II I I II III IV V Left
V IV III II I I II III IV V
 Permanent
Right 8 7 6 5 4 3 2 1 1 2 3 4 5 6 7 8 Left
87654321 12345678

b. Palmer system (1870) [Fig 3.41]

Zsigmondy system modified by Ohio dentist Corydon Palmer, because Arabic
numbering system (1,2,3 etc) could be confused with Roman numbering system
(I, II, III etc). Used very widely in UK and several other countries.
Deciduous
Right E D C B A A B C D E Left
EDCBA ABCDE

Permanent
Right 8 7 6 5 4 3 2 1 1 2 3 4 5 6 7 8 Left
87654321 12345678
In both Zsigmondy and Palmer notations, if a tooth has to be represented, use is
made of a symbol
(

) which designates the quadrant in which the tooth is located. A number indicates
the position from the midline. Thus
3
represents upper right permanent canine. Similarly
A
represents lower left first deciduous incisor.
Disadvantages – Since letters of English alphabet are used, only English
speaking nationals can understand it.
c. FDI (Theilman) notation (1971)
Two digit notation. Quadrants are 1,2,3 and 4 in adults and 5,6,7 and 8 in
children.

1 2
Right Left
4 3
5 6
Right Left
8 7
Charting - Quadrant number comes first. Teeth number comes after this.
Permanent
Right 18 17 16 15 14 13 12 11 21 22 23 24 25 26 27 28 Left
46 77 46 45 44 43 42 41 31 32 33 34 35 36 37 38
 Deciduous
Right 55 54 53 52 51 61 62 63 64 65 Left
85 84 83 82 81 71 72 73 74 75

Both universal system and FDI system use several two digit numbers which refer
to different teeth. This is resolved by insertion of a hyphen between the two
digits of the FDI notation [Thus 18 is more appropriately written as 1-8]. They
are spoken also differently. Example: 16 in universal notation is “upper left third
molar” – pronounced as “sixteen” 16 in FDI notation is “upper right first molar”
– pronounced as “one six”

d. Modified FDI notation

Same as FDI, except that numbers of the lower quadrant start on a new line.

1 2
Right Left
3 4
5 6
Right Left
7 8

Memory Aid 38: Modified FDI notation

M"N
In Modified, numbers start on a New line

10. MLI [of teeth, bitemarks, oral structures]

(1) Teeth:
(i) Identification, age, sex, race. [please see above]. Especially useful in mass
disasters
(ii) Blood group from dental tissues [ch 29]
(iii) Loss of tooth – is grievous hurt [S.320, IPC; ch 11]
(iv) Poisons – As, Hg etc may be detected
(2) Dentures – useful in identification [please see “Dental prostheses” above]
(3) Information from color changes in teeth:
(i) Intrinsic – Coloration is due to changes in the composition or thickness of the
dental tissues (a) Alkaptonuria – brown (b) Congenital erythropoietic
porphyria – Color Red-brown. Red fluorescence under UV light. (c)
Congenital hyperbilirubinemia - yellow-green (d) Amelogenesis imperfecta
 - Varies from ‘snow-capped’ enamel to a yellow to yellow-brown (e)
Dentinogenesis imperfecta - bluish or brown. Demonstrate opalescence on
transillumination. (f) Tetracycline staining - yellowish or brown-grey (g)
Fluorosis – chalky white to a dark brown/black appearance (h) Enamel
hypoplasia - pitting and grooving which predisposes to extrinsic staining of
the enamel. Later it becomes internalized (i) Pulpal hemorrhagic products –
Black (j) Root resorption – pink appearance at the amelo-cemental junction
(k) Ageing – gradual darkening of teeth occurs with age.
(ii) Extrinsic - Discoloration is outside the tooth substance; lies on the tooth
surface. It can be metallic and non-metallic
(4) Bite marks:
(i) Identification [bitemarks left in human tissues or on foodstuffs]
(ii) In children may indicate child abuse [ch 27]
(iii) On cheeks, breasts etc of female may suggest sexual assault
(5) Oral structures – lead line in plumbism and some other metallic poisons [ch
36].
(6) Age determination - of antemortem tooth loss or extraction [ch 17].

4. Mass Disaster

INTRODUCTION

A. Definition
Mass disaster (also known as mass fatality incident) is any event that produces
more fatalities than can be handled using local resources.

B. Classification
Mass disasters can be (1) Natural and (2) Man made (due to acts of omission or
commission).
(1) Natural: (a) Biological - Disease epidemic [eg cholera, plague] (b) Chemical
- Mass poisoning [consumption from naturally contaminated wells, eg arsenic
 contaminated wells in some parts of the country, Mass CO2 poisoning] (c)
Other - (i) avalanches (ii) blizzards (iii) cold wave (iv) cyclone (v) drought
(vi) earthquakes (vii) famines (viii) floods (ix) heat wave (x) hurricanes (xi)
landslide (xii) limnic eruptions [please see ch 44 for details] (xiii) shipwrecks
(xiv) storms (xv) tornados (xvi) tsunami (xvii) volcanic eruption (xviii)
wildfires and bushfires
(2) Man made: (a) Accidental - (i) Airplane crashes (ii) Building collapse (iii)
Dam bursts (iv) Fires [Uphaar film hall tragedy](v) Adulterated food [causing
food poisoning] (vi) Adulterated liquor [eg hooch tragedy (methyl alcohol
poisoning)] (vii) Mining accidents (viii) stampedes in unruly crowds [during
sporting events, football tragedies eg Ibrox park, Heysel, Hillsborough, places
of worship eg Mecca, temples etc] (ix) Transportation [air, rail, river, road,
sea, waterways] (b) Civil disturbances - riots and demonstrations (c) Industrial
– (i) Explosions (ii) Fires (iii) Leakage of toxic substances [Bhopal MIC
disaster of 1984] (d) Terroristic - (i) bombings (ii) special terroristic incidents
like 9/11 WTC incident, 26/11 Mumbai incident (e) Warfare – CBRN -
chemical, biological, radiological, and nuclear warfare.
 5. Medicolegal Autopsy

I. INTRODUCTION

Autopsy, [syn; necropsy, post mortem examination, sectio cadaveris, thanatopsy]

is the examination of a person’s body after his death. It is an essential part of
death investigation. An autopsy is of the two types – medicolegal autopsy and
hospital autopsy.

A. Medicolegal Autopsy
Done when some legal issue is involved (homicide, accident, suicide, any other
suspicious death). In India, any registered medical practitioner can conduct an
medicolegal autopsy on the request of the investigating officer. Permission of
relatives not required.

B. Hospital Autopsy
Done for academic purposes, research etc. No legal issue is involved (also
called clinical autopsy or pathological autopsy). Permission of relatives
required.

II. OBJECTIVES OF A MEDICOLEGAL AUTOPSY

Among the objectives are 6Ws and 1H [often jokingly referred to as 6 wives and
1 husband]:
(1) What injuries are present? [description of injuries]
(2) When did the injuries occur? When did the victim die? [time of injuries and
of death]
(3) Where did the death occur?
(4) Which injury caused death? [cause of death]
(5) Who is the victim? [identification in unknown bodies]
(6) Why were the injuries produced [Manner of death - suicide, homicide or
accident]
(7) How were the injuries produced [self-inflicted, by others, which kind of
weapon was involved]
(8) Collection of evidence (a) External - To collect incriminating evidence
from the dead body (e.g. semen in case of rape, grease and dirt in case of
automobile accidents, rope fibers in case of strangulation) (b) Internal - To
retain relevant organs and tissues as evidence
(9) Fetus - In case of fetus, to find its age and thus its viability
(10) In newborn infants to determine live birth or dead birth
(11) Co-relation - To correlate with ante mortem diagnosis.

III. POSTMORTEM INSTRUMENTS

Common postmortem instruments and their common usages are given in [Fig
5.1].
(1) Forceps – Various forceps used in PM facilitate manipulation of anatomical
 structures. They are also used to stabilize tissues and assist in dissection. All
forceps perform essentially the same function but differ in the design of their
tips and their intrinsic delicacy of form.
(i) Toothed forceps are useful for stabilizing and moving tissues, but they are
traumatic and may lacerate structures.
(ii) Smooth atraumatic forceps are more appropriate when trauma must be
avoided, as in exploring traumatized structures, or for delicate vascular
manipulation.
(iii) DeBakey forceps are good general-use instruments with atraumatic flat tips
and tiny fine serrations.
(iv) Fine-toothed Adson forceps and
(v) stout-toothed Bonney forceps are more commonly used in surgery but may
be used for PM also. Adson is ideal for skin closure, while Bonney is
excellent for facial closure [after facial dissection].
(2) Knife blades – In India, Bard-Parker knife blades are commonly used.
These are made functional by attachment to a standard no. 3 Bard-Parker
knife handle. Choose the size and shape of the blade based on the intended
indication. In surgical practice, abdominal or thoracic skin incisions are
typically made with no. 10, 20, or 22 blades, whereas more delicate incisions
require the smaller no. 15 blade. However such distinction in PM is more or
less of an academic nature. In surgery, the sharp-tipped no. 11 blade is ideal
for entering and draining an abscess or for making an arteriotomy by incising
a blood vessel in preparation for vascular procedures.
(3) Needles - come either straight or curved.
(i) Straight needles are rarely used in PM, but may be used if curved are not
available
(ii) Curved needles -are usually half circle or three-eighths circle. Sewing in a
deep hole may require a five-eighths circle needle, whereas sewing up of
smaller structures often requires quarter circle needles. Needles can have
an eye for threading the suture (French eye) or an already attached suture
(swaged). Surgeons mostly use swaged needles [needle-suture
combination], but they are rarely used in PM. Etymologically, a swage is a
blacksmithing tool used to shape metal. Thus a swaged needle is
manufactured by placing the suture into the hollow shank of a needle and
then compressing the needle around the suture, holding it firm. Some
 sutures are swaged to needles in such a manner that they pop off if excess
tension is applied between suture and needle.
(iii) Large needle [with twine]– This is a general purpose needle most
commonly used for sewing up bodies after PM.
(iv) Needle tips - are either tapered or cutting. Tapered needles are
circumferentially smooth and slide between the elements of tissues,
whereas cutting needles are triangular in cross section and cut through
tissues like a tiny knife. More tougher tissues, eg mummified bodies may
require cutting needles.
(4) Dissecting scissors – cutting of tissues, general purpose cutting
(i) Iris scissors - are fine and are used for delicate dissection and cutting.
(ii) Mayo scissors -are sturdier and are used for cutting thick or dense tissues,
such as fascia, scar, or tendons.
(iii) Metzenbaum scissors - are versatile, general-use instruments.
(iv) Richter Dissecting scissors - comes with angular blades, one sharp and one
blunt point. Useful for reaching inaccessible areas eg below pubis to cut out
prostrate.
(v) Scissors with one pointed and one blunt end – used for cutting tough
tissues, fibrotic scars etc.
IV. EXAMINATION OF CLOTHINGS AND ORNAMENTS

A. Clothings
(1) List - all clothings
(2) Describe -
(i) Burns [if present]
(ii) Buttons [loss of]
(iii) Color
(iv) Creases [lack of]
(v) Design
(vi) Disarrangement [indicates struggle]
(vii) Staining [blood, feces, grease, mud, poison, saliva, semen, urine,
vitriolage], and their relative distribution. Are the stains in several layers, eg
a layer of semen over blood or vice-versa. Can help reconstruct events
(viii) Tears [indicates struggle]
(ix) Type of garment
(x) wetness [as in drowning]
(xi) wrinkles [presence of].

V. EXTERNAL EXAMINATION OF THE BODY

External examination is very important, especially in cases of trauma, where a

number of injuries are visible externally. Following points must be noted
(1) Record height, weight, age, sex
(2) General features
(3) Hands - (a) Trace evidence
(4) Skin
(5) Eyes
(6) Palpate (a) Abdomen (b) breasts [In females] (c) testes [In males].

VI. INTERNAL EXAMINATION

(1) First cavity to be opened –

(i) General rule - As a rule of the thumb, skull should be opened first. Reasons
(a) smell of poisons is best appreciated before odorous gases from abdomen
are released. Brain can give out smell of poisons like alcohol, phenol,
organophosphorus etc. (b) Blood drained out – through vessels going to
the brain. Creates a bloodless field in the neck, which is ideal for
appreciating antemortem neck injuries [ch 10, 19].
(ii) If a cavity shows obvious signs of injury – It may be profitable to start
examination with the affected cavity [eg abdomen in case of stab abdomen].
Reasons – (a) Pathologist is less exhausted initially and his best energies are
spent on the main cause of death (b) Findings in other cavities may be co-
related appropriately with those in the chiefly affected first [eg bleeding in
abdomen will help understand better a pale brain]
(iii) In infanticide - after skull, abdomen should be opened next [ch 27].
(iv) For other precautions, please see ch 10"Artifacts introduced during
autopsy"extravasation of blood.
(2) Incisions – Following incisions are standard, but they may have to be
adapted to special situations [eg in stab wounds in the midline of chest and
abdomen, the midline incision may have to be diverted sideways].

A. Skin Incisions
1. I-shaped incision
(1) Most common
(2) Starts from just under the chin in midline and goes up to the pubic
symphysis, sparing the umbilicus (Fig 5.2). The umbilicus is spared as it
consists of dense fibrous tissue which is difficult to stitch.

2. Y-shaped incision
(1) Incision -
(i) Starts from the two mastoid processes, which form the two limbs of the Y
[Fig 5.2].
(ii) The two limbs move medially to meet at the level of xiphisternum, from
where it goes downwards exactly as I-shaped incision
(2) Used -
in cases of neck trauma, where layer dissection of muscles is needed
(3) Precautions -
Air embolism - Neck dissection should be performed particularly carefully,
being alert not to injure the large neck veins.

3. Modified Y-shaped incision

(1) Starts from below both anterior axillary folds, goes below the breasts, meets
at xiphoid process and proceeds down to symphysis pubis [Fig 5.2].
(2) Used - in females to preserve appearance [incision line is not visible on
exposed face and neck].

4. T-shaped (subclavicular) incision

(1) Straight incision from suprasternal notch till the pubic symphysis
(2) From the suprasternal notch, the incision is extended horizontally on both
sides to the acromion processes [Fig 5.2]. Gives a wide exposure of base of
neck
(3) Used – when exploration of base of neck is necessary as in dissection of
 vertebral arteries.

B. Method of Removal of Organs

1. Virchow’s method
(1) Advocated by Rudolph Virchow (1821–1902), German pathologist.
(2) Organs are removed separately one by one and then studied individually.
(3) Adv - Quick
(4) Disadv - causes loss of continuity; difficult to evaluate interrelationships.

2. Rokitansky’s method
(1) Advocated by Carl Rokitansky (1804–78), German pathologist.
(2) in situ dissection
(3) Adv – good in children; infected bodies
(4) Disadv – Difficult in adults.

3. Letulle’s method
(1) Advocated by Maurice Letulle (1853-1929), French pathologist.
(2) All organs from tongue till prostate [oral, cervical, thoracic, abdominal,
pelvic] are remove en masse in a single block
(3) Adv -
(i) excellent preservation of organ inter-relationships, their regional lymphatic
drainage, and their vasculature
(ii) body can be handed over to relatives quickly
(4) Disadv – Organs difficult to handle.

4. Ghon’s method
(1) Advocated by Anton Ghon (1866-1936), Austrian pathologist.
(2) Compromise between Virchow’s and Letulle’s. Cervico-thoracic, abdominal
and pelvic organs are removed as 3 separate blocks [en bloc method]
(3) Adv -
(i) excellent preservation [as in Letulle’s]
(ii) Handling of organs easier than in Letulle’s
(4) Disadv – If disease process extends across the three blocks, interrelationships
may be difficult to study.

C. Examination of Organs

1. Head
a. Skull
(1) A wooden block is placed under the shoulders. It extends the neck.
(2) Head is stabilized by a head rest which has a semicircular groove to hold the
back of neck.
(3) The hair is parted with a comb in a line joining the mastoid processes,
passing over the vertex, and the scalp incised down to the bone along it. The
incision should be deep enough to penetrate the periosteum.
(4) The two scalp flaps are then reflected down to the supraciliary ridges in front
and to the external occipital protuberance behind [Fig 5.3]. If the reflection is
difficult, a scalpel blade can be used to cut the loose connective tissue as the
other hand continues to peel the scalp. The knife edge should be directed
toward the skull and not toward the scalp [otherwise it would create
“buttonholes” in the scalp]. The anterior flap is reflected to a level approx 2
fingerbreadths above the supraorbital ridge [Fig 5.3]. The posterior flap is
reflected down to a level approx 2 fingerbreadths above the occipital
protuberance.
i. Dissection of Head in infants
(1) Child’s brain attains mature size and weight at about 5 y
(2) In newborns and infants, different approaches for removal of brain are
adopted for two reasons
(i) firm adherence of dura to the skull [ch 17]. It tends to dip into sutures
(ii) Importance of keeping the falx and tentorium intact [their injuries are
common in difficult births].
(3) Two approaches are used -
(i) Beneke’s technique - Opens skull in 2 flaps. (a) The scalp is reflected as in
adults. (b) Points to be noted at this stage - (I) Any caput formation or
hemorrhage (II) width of the sutures, size of fontanelles, degree of
calcification [to assess hydrocephalus] (III) Any separation of the occipital
plates caused by birth trauma (IV) Incision of the atlanto-occipital
membrane will reveal tonsillar herniation and posterior fossa hemorrhage.
(V) A sample of CSF from the cisterna magna can be removed if necessary,
using a sterile needle. (c) Removal of skull - (I) cutting along the suture
lines will destroy the falx and the superior sagittal venous sinus. Therefore
cut is made about 0.5 cm on either side of the sagittal suture (II) A scalpel is
used to make an incision starting from anterior fontanelle at its posterior
margin, about 0.5 cm [5mm] on the right side of midline [point A in Fig
5.4]. The incision will cut both skull and dura together. After an incision of
about 2 cm or so, introduce one end of a heavy duty scissors inside skull,
and cut posteriorly up to point B and anteriorly up to point C. This will
 allow the right side of skull to come out like a flap [B-A-C]. (III) Similarly
dissect the left side of skull making similar incisions and reflect the flap E-
D-F [Fig 5.4]. This leaves an intact area in the temporal squama on either
side [BC on right side and EF on left], which serves as a hinge as the bone
flaps are reflected. (IV) A midline strip approx 1 cm wide [5mm either side
of midline], is now left at the top, containing the superior sagittal sinus and
the falx. The older the infant, the narrower the sagittal strip will be because
ossification advances toward the midline, as age advances. (d) Now vertex
of the brain can be seen [barring for a 1 cm wide strip at the top]. Make sure
that gloves are wet before touching the brain. Now Examine (I) the
terminations of pial veins entering into superior sagittal sinus (II) Any
hemorrhages around (III) Gently push each cerebral hemisphere to the side
turn by turn and examine falx cerebri for any tears (IV) medial parts of each
cerebral hemisphere (V) space between two dural layers of the falx (e) Now
open superior sagittal sinus and look for any thrombi (f) Separate falx at its
antero-inferior insertion (g) From the sides examine tentorium for tears and
for hematoma between its layers (h) Remove brain as in adult (i) Open
dural sinuses at base of skull and examine.
(ii) Baar’s technique – Opens skull in 4 flaps [“butterfly” manner of removal] –
Procedure is same except that in this case, 4 flaps [Fig 5.4, B-A-C, E-D-F,
H-G-I and K-J-L] are removed like the 4 wings of a butterfly. This
technique is preferred by most pathologists.
b. Brain

Examination of brain
(1) Surface and base of brain - examine for any obvious signs of disease, eg
encephalitis.
(2) Cerebral vessels – note atherosclerosis, aneurysms, or evidence of other
disease, especially in those forming the circle of Willis.
(3) Cortical contusions and hemorrhages – are detected best in fixed brains;
conversely small hemangiomas and ruptured Berry aneurysms are best
detected in unfixed brains.
(4) Ruptured berry aneurysms – put the brain under a gentle flow of running
 water. Ruptured walls of berry aneurysms “fan out” under the stream, much
like those of a ruptured balloon. Size of Berry aneurysms vary from few mm –
few cm, and are usually present at the junction of vessels.
(5) Note presence of cerebral infarctions – These can be due to atheroma,
thrombus for due to -ed ICP causing obstruction to venous outflow.

2. Chest

a. Heart
i. External examination
(1) Hold in anatomical position - Assess its size and shape.
(2) Examine epicardial surface - for evidence of
(i) adhesions
(ii) aneurysms
(iii) flaccidity [may indicate underlying infarction]
(iv) focal hyperemia
(v) pericarditis
(vi) rupture
(vii) Small white “soldier’s” patches are often seen, particularly anteriorly over
the right ventricle. They represent either previous trauma or episodes of
subclinical pericarditis.
(3) Weight - Heart should not be weighed at this point, as it will inevitably
contain blood clot which would falsely elevate the weight obtained, leading to
mistaken impressions of hypertrophy.

ii. Examination of the coronary arteries

Dissection of the Coronary Arteries – Two methods are mainly used –
transverse sectioning [more common] and longitudinal opening. In both the
origin of the arteries must be identified and their course within the epicardium
followed. This is variable, and in difficult cases it may be necessary to first
identify the ostia by inspecting the aortic sinuses from above. Look for any
evidence of thrombus or loose atheroma; its extent and severity should be
assessed, and the affected areas noted. If the arteries are sectioned transversely,
an estimation of the percentage of luminal stenosis should be made, and must be
represented by diagrammatic charts
(1) Transverse Sectioning Technique - (a) A sharp scalpel blade is used to slice
completely through the arteries at intervals of about 2-3mm. (b) Proximally,
where atheroma and thrombus are more likely, the transections should be even
closer together. (c) Note – Calcification, Plaque hemorrhage, Plaque rupture,
Stenosis, Thrombi etc (d) If vessels heavily calcified, it will be necessary to
cut the vessel with a sharp pair of artery scissors; it will give a gritty feel as if
one is cutting through chalk. (e) Advantages – (I) Percentage block can easily
be estimated (II) Antemortem thrombi can be demonstrated without risk of
dislodging them. In longitudinal opening method neither is possible. Thrombi
can easily be dislodged and pushed further along.
(2) Longitudinal Opening Technique - (a) A sharp pair of very fine artery
scissors is used to open the arteries from the ostia, extending as far down their
course as possible. (b) Advantages - (I) Gives a good idea of the length of the
plaque. Helps to assess the length of the vessel occupied by a thrombus or by
complicated atheroma or both (II) allows to track any sizeable small branches,
and to look at narrowing of their openings (III) gives a view of the intimal
tears (IV) If the vessel wall is markedly calcified, less damage and distortion
occurs than by transverse sectioning.
(3) Clinical Correlation - Significant or severe disease is indicated by a stenosis
of 75% or more. In the absence of occlusive thrombus, death should be
ascribed to atherosclerosis only if the stenosis is severe.

iii. Dissection of the heart

(a) Along the path of blood flow
(1) Several methods have been described, but the best is opening along the path
of blood flow [Fig 5.5]. An enterotome is used for dissection.
iv. Internal examination of the heart
(1) Weight - Whichever method of examination has been used, all post mortem
blood clots should now be removed and the heart weighed.
(2) Morphology of the chambers - examined closely and any septal defects
noted.
(3) Endocardium - examined for evidence of fibrosis, attached antemortem
thrombi, and subendocardial hemorrhages.
(4) Subendocardial hemorrhages [syn, Sheehan’s hemorrhages]–First
described in the 1930s by the English pathologist Harold Sheehan (1900-
1988) in cases of abortion and acute hemorrhage associated with pregnancy.
(i) Mostly seen in (a) left ventricle (b) left side of IV septum, opposing papillary
muscles and adjacent columnae carnae.
(ii) Shape - flame shaped, confluent, tend to occur in one continuous sheet rather
than patches.
(iii) When bleeding is severe, endocardium may be raised like a flat blister
(iv) Seen in the following conditions - (a) Acute heavy metal poisoning,
especially arsenic (b) Deaths due to obstetric complications (ante-partum or
post-partum hemorrhage, ruptured tubal pregnancy, ruptured uterus,
abortions) (c) Deaths due to shock especially hemorrhagic shock (d)
 Intracranial damage [cerebral edema, head injuries, surgical craniotomy,
tmours]
(v) Mechanism of production - obscure but may be due to sudden and profound
hypotension within the ventricles"BP within the coronary system for some
moments remain normal"causes a pressure gradient across the endocardium
(at least of 80 mm Hg, if we assume the pressure within the ventricle at 0
mm Hg and in the coronary system at a diastolic level of 80 mm
Hg)"superficial vessels rupture"subendocardial hemorrhages. The theory
however fails to explain these hemorrhages in cases of head injury. If the
vagus nerves of goats are severed and then they are killed by head injury,
Sheehan’s hemorrhages fail to appear. This suggests that these hemorrhages
may be mediated by autonomic nervous system.
(5) Valves - Examine number of cusps and leaflets, fusion between them and
evidence of vegetations, fibrosis, or calcification. The valve circumference is
then be measured with a ruler or a length of string. Average measurements are
given in appendix at the end of book.
b. Lungs
Removal - by cutting through each of the main bronchial stems distal to the
carina with a large pair of scissors or PM40. A large bronchial stump should
remain attached to the lung by making the cut as away from lung as possible.

3. Gastrointestinal system

a. Stomach
(1) Removal - Stomach is removed after applying ligatures at each end"Placed
on a clean dish"Open along greater curvature [reasons ch 31].
(2) Contents -
(i) Examine for nature of food, its state of digestion, smell, color, character,
presence of foreign and suspicious matter.
(ii) Clear contents in a clean jar.

b. Liver
Removal and examination of accessory structures
(1) Removed by itself or when still attached to stomach and duodenum.
(2) The latter is done when patency of bile ducts are to be examined. Duodenum
is exposed where ampulla of Vater opens and gall bladder pressed. Greenish
bile is seen to ooze from the ampulla if bile ducts are patent.
(3) Open the bile duct with a fine pair of scissors and look for calculi, strictures
and tumors
(4) Open hepatic artery and portal vein
(5) Examine lymph nodes in the neighborhood.

4. Genitourinary system

Kidneys

(1) Renal ostia - As the abdominal aorta is opened along its anterior midline, the
renal artery ostia are examined for thrombi, emboli and atherosclerosis.
(2) Renal vessels – examine for thrombi
(3) Kidneys – note
(i) Congenital malformations – agenesis, aplasia, hypoplasia, horseshoe kidney,
pancake kidney [both kidneys are fused into a single mass in the pelvis]
(ii) size and shape - (a) Normal size 11 x 6 x 3cm, in adults. (b) Normal Wt –150
g [males, each kidney], somewhat less in females. (c) Causes of atrophic
kidneys - (I) arteriosclerosis of renal arteries, (II) chronic obstruction, (III)
glomerulonephritis
(iii) Note smoothness or granularity of surface.

5. Spinal cord
(1) Methods of removal -
(i) anterior approach
(ii) posterior approach
(2) Anterior approach –
(i) Advantages – body need not to be turned over (a messy procedure if
evisceration has already taken place) allowing the nerve roots and dorsal
ganglia to be dissected.
(ii) Disadvantages - more difficult
(3) Posterior approach -
(i) Advantages – (a) quicker and easier, but should be performed before the rest
of the PM, to avoid mess. (b) Allows for removal with less tension on the
cord (c) allows the SC and brain to be removed in continuity
(ii) Disadvantages- (a) does not allow easy examination of the nerve roots or
dorsal ganglia (b) When body is returned to relatives, the sheet may become
blood soaked through oozing of blood from posterior incision. To reduce
this oozing, it is advisable to put a plastic sheet inside before sewing up the
incision.
6. Blood
(1) Postmortem clotting -
(i) Initiates within 1 hour of death.
(ii) Simultaneously, clot lysis also initiates.
(iii) Since the two processes occur simultaneously, the presence of absence of
clots in a dead body depends on which process prevails. It may be
completely clotted, completely fluid or partly clotted and partly fluid.
(iv) Generally in small capillaries, blood is completely clotted by 8 h [time of
fixation of pm staining - ch 9]. But at the same time blood may be partly
fluid in large vessels.
(v) Amount of blood clots vary from body to body, and from site to site within
the same body.
(2) Clotted blood for toxicologic analysis:
(i) When fibrin clot is present it always entraps large numbers of RBCs, so that
the clot is relatively RBC-rich.
(ii) For drugs with an unequal distribution between RBCs and serum [eg (a)
alcohol - distributed only in the water portion of blood (b) chloroquine -has
an RBC: serum ratio of 32:1], examination of clots may give spurious
results
(3) Clotted blood for DNA analysis - ch 29.
(4) Hb levels and poison concentrations - no proven correlation exists.

a. Agonal thrombi
Agonal [Gk agon, struggle] thrombi are firm, stringy, tough, pale yellow
thrombi which form during terminal phase of life in the cavities, usually on the
right side of heart, especially in persons dying slowly with circulatory failure,
and diseases such as lobar pneumonia, in which the coagulability of the blood is
increased.
Salient features:
(1) Beginning of process – occurs in (i) atrial appendage (ii) apex of ventricles
or (iii) in the angles of the ventricular surfaces of tricuspid valve
(2) Right heart – Extends and fills both right auricle and ventricle, pulmonary
artery and even its finest branches to give an appearance of tree like cast
(3) Left heart: (i) usually less extensive (ii) When it passes through aorta it
bears projections, corresponding in shape, though not in size, to the sinuses of
Valsalva.

b. Postmortem clots
(1) Postmortem clots form after death. They should be differentiated from
antemortem clots [Table 1].
(2) Types – Two types
(i) Black currant jelly type – forms when blood clots rapidly. Heavier RBCs do
 not have time to settle down; they are found distributed throughout the clot.
The clot is lumpy, moist, slippery, soft and uniformly dark red.
(ii) Chicken fat type – forms when blood clots slowly. Heavier RBCs have time
enough to settle down. Two layers are seen in the clot; a lower redder layer,
which is quite similar to black currant jelly type clot, and an upper pale or
bright yellow layer of serum and fibrin
(3) Cardiac polyps - These are pm fibrinous, pedunculated clots in the heart.

c. Unclotted blood
Blood remains fluid after death in certain conditions [ch 9"pm lividity]. PM clots
are greatly reduced in number in these conditions.

D. Procedure after Completion of Autopsy

(1) Clean body cavities – of blood, fluids
(2) Sew all cuts, clean body, hand over to police.

VII. EXAMINATION OF WEAPON

If weapon is submitted along with body, it must be examined after the autopsy is
over. Co-relations of injuries must be made. The weapon may be blunt, sharp or
firearm.

VIII. THE AUTOPSY REPORT

(1) Autopsy report [syn, postmortem report] is a medicolegal report. Like all
MLRs it consists of preliminaries, body and opinion. For details, please see ch
1.
(2) Headings – An ideal autopsy report should have following headings
(i) Preliminaries – name, age, sex etc
(ii) History
(iii) Date, Time, Place, Assistants, Attendees
(iv) Presentation, Clothing, Personal Effects, Associated Items
(v) Evidence of Medical Intervention
(vi) Postmortem Changes
(vii) Postmortem Imaging Studies
(viii) Identification
(ix) Evidence of Injury
(x) External Examination
(xi) Internal Examination
(xii) Histology samples Listing
(xiii) Microscopic Descriptions
(xiv) Toxicology Results, Laboratory Results, Ancillary Procedure Results
(xv) Pathologic Diagnoses
(xvi) Summary and Comments
(xvii) Cause of Death Statement.

IX. AUTOPSY ROOM HAZARDS

A. Commonly Acquired Infections

Micro-organisms have been classified into 4 hazard groups by the ACDP
(Advisory Committee on Dangerous Pathogens) on the basis of pathogenicity to
humans, risk to laboratory and autopsy workers, transmissibility to the
community, and whether effective prophylaxis is available.
(1) Group 1 [category 1]- An organism that is (i) most unlikely to cause human
 disease
(2) Group 2 [category 2]:
(i) may cause human disease
(ii) may be a hazard to laboratory workers, but lab exposure rarely produces
infection
(iii) effective prophylaxis or treatment is usually available
(iv) unlikely to spread to the community.
(v) Ex – (a) adenoviruses, (b) herpesviruses (c) ortho and paramyxoviruses (d)
picornaviruses (e) unconventional slow viruses.
(3) Group 3 [category 3]:
(i) may cause severe human disease
(ii) serious hazard to laboratory workers
(iii) usually effective prophylaxis or treatment available
(iv) presents a risk of spread to the community.
(v) Ex – (a) Hantaviruses (b) HBV (c) HIV (d) Japanese B encephalitis (e)
rabies (f) Rift Valley fever (g) Tuberculosis - Anatomists and autopsy
pathologists usually got skin TB through cuts when doing autopsies on
infected corpses [anatomist’s wart, prosector’s wart] (h) Yellow Fever.
(4) Group 4 [category 4]:
(i) causes severe human disease
(ii) serious hazard to laboratory workers
(iii) usually no effective prophylaxis or treatment
(iv) high risk of spread to the community.
(v) Ex – (a) Viral hemorrhagic fevers - Hantavirus, Ebola virus (b) Russian
spring-summer encephalitis (c) smallpox [if released for biowarfare]

B. High Risk Autopsy

The high risk autopsy [syn, hazardous autopsy] is defined as postmortem
examination of a deceased person who has had, or is likely to have had, a serious
infectious disease that can be transmitted to those present at the autopsy, thereby
causing them serious illness and/or premature death.
Salient features:
(1) Bodies infected with group 3 and 4 organisms are high risk autopsies [eg
HBV, HIV etc].
(2) Pathogens may be acquired by inhalation (of aerosols), ingestion, direct
inoculation, entry though pre-existing breaks in the skin, and through the
mucous membranes of the eyes, nose, and mouth. Any procedure that may
result in infection through one of these routes constitutes a hazard.
(3) HIV:
(i) HIV remains viable in high concentrations in blood up to 2 months.
(ii) may be transmitted through cuts while doing autopsy, needle pricks during
collection of blood and other body fluids, mucosal splashes, skin contact
with superficial injuries.
(iii) HIV is present mostly in brain, colon, lungs and lymphoid tissue.
(4) Airborne transmission - does not occur with HIV and HBV.

1. Universal Work Precautions

(1) Tagging - All infected bodies should be wrapped and tied in double layer
tough plastic bags. Both body and bag should have a red color tag mentioning
“Biologically Hazardous”
(2) Handling of bodies - Workers who have external injuries, exudative lesions
or weeping dermatitis should not handle bodies with infectious diseases [eg
AIDS]
(3) Handling sharp instruments:
(i) Use either chain mail or Kevlar gloves.
(ii) If not available, wear double gloves and over the gloves, wrap leucoplast
over fingers of the left hand [for a right handed person].
(iii) Most common digits pricked during autopsy in a right handed person are left
index finger, left middle finger and left thumb in that order. These three
digits should certainly be protected. (iv) If despite all precautions, there is a
cut, the finger should immediately be dipped in bleach solution [sodium
hypochlorite] and then washed with soap and water. No effort should be
made to “milk” blood towards the cut.
(4) Protective clothing - should be worn. Consists of face mask, full sleeve
overall [instead of simple surgical gowns], goggles, head cap, plastic visor,
protective gloves [double gloves or chain mail], waterproof plastic apron and
rubber gum boots of knee length with shoe covers
(5) Handling specimens for lab examination - Should be handled with gloved
hands only
(6) Treatment of used instruments - Should be washed in glutaraldehyde
solution
(i) Cidex Plus - is a high-level disinfectant [3.4% glutaraldehyde]. Instruments
dipped for 20 min.
(ii) Cidex OPA [ortho-Phthalaldehyde] - 15 min. After treatment with
glutaraldehyde, the instruments should be washed with soap, detergent and
water, dried and then rinsed in methylated spirit and then air dried.
(7) Soiled cotton and gauze - collect in a double plastic bag"Send for
incineration
(8) Laundry material - eg towels etc should be soaked in 1% bleach for 30
min"washed with detergent and hot water"autoclaved
(9) Completion of autopsy - take a complete bath with soap and water.
X. COLLECTION OF SPECIMENS

A. Fresh Bodies [Undecomposed]

1. Anal swabs
For spermatozoa if anal intercourse is suspected
2. Bile
(1) When - For determining presence of poisons, particularly those excreted
through the biliary system.
(2) How -
(i) Method 1 - Passing a needle, attached to a syringe, into the lumen through
gall bladder wall. Bile aspirated and collected into a container
(ii) Method 2 - The gallbladder is dissected from the adjacent liver and bile is
squeezed into a sterile container.
(iii) Method 3 - Expression through cystic duct after evisceration.

3. Bite marks
Bite marks should be swabbed with a saline moistened cotton swab. Dry and
place in a test tube and plug with cotton. Saliva of the assailant can reveal his
blood group [in secretors]. DNA analysis can be done from mucosal cells in
saliva.

4. Blood
Collection for toxicology is described here. Blood for microbiology"please see
below. Collection of blood for toxicology in the living"ch 31.

a. General Guidelines
(1) Site -
(i) Best site to collect blood for toxicological analysis is a peripheral vessel like
iliac, femoral or subclavian [being at periphery least affected by
postmortem diffusion]
(2) Quantity taken"10-20 ml.
(3) Preservatives – please see below under the section “preservation of viscera
in suspected poisoning”.
(4) For grouping - a piece of filter paper or clean cotton gauze is used to soak
up some blood, dried and sent to lab.

b. Before autopsy
(1) From femoral v – withdraw 10-20 ml by a syringe.
(2) From jugular or subclavian v – use similar procedures.
(3) From heart – preferable not to take for toxicology because of postmortem
diffusion [please see below], but is highly desirable for microbiological
studies. For procedure, please see below.

c. During autopsy
Blood can be collected after removal of viscera. Sites to sample in .ing order of
preference are
(1) Femoral v
(2) Iliac v – elevate leg to ease flow
(3) Subclavian v – Hold a small container under the cut end of subclavian v. and
elevate arm.

i. Precautions
(1) Scooping up:
(i) Never take directly from heart or scoop out of thoracic or abdominal cavities
[please also see ch 31].
(ii) Reasons -(a) Contamination - with gastric or intestinal contents, lymph,
mucus, pus, serous fluid and urine [ch 10"Toxicological artifacts]. (b) PM
glycogenolysis in the liver "-ed glucose in right atrial blood (c) Postmortem
diffusion – please see below.
(2) If blood is being collected for volatile substances [chloroform, ether], use
small glass bottles lined with aluminum foil. Fill up to top to avoid loss of
volatile substances into headspace. Store at 4°C.
(3) Erroneous results can be obtained if
(i) clotted or
(ii) hemolyzed blood is taken.
(4) Massaging or milking limbs to - flow – Should not ideally be done as blood
is being taken for toxicology. It can produce significant alterations in drug
concentrations in the expressed blood [drug moving from muscles to blood
 stream].
(5) Samples taken for alcohol estimations – Must contain and anticoagulant and
preservative [prevents alcohol formation by microorganisms]- please see
below, and also ch 40.

ii. Postmortem diffusion

Postmortem diffusion [syn PMD, postmortem redistribution, PMR] is the passive
diffusion of poisons from stomach and intestines to adjacent organs after death
giving spuriously high levels.
Salient features:
(1) Diffusion mainly occurs from stomach to the liver (especially the left lobe).
For this reason, whenever a liver sample is taken, it must be taken from the
middle of the right lobe, which is a relatively sequestered region of the liver.
Also occurs in base of left lung, spleen, heart, pericardial fluid, aorta and IVC.
(2) Causes – (i) Barriers formed by living cell membranes breakdown after
death, enabling molecules to move freely through tissues (ii) Severe
trauma"gastric rupture"gastric contents may spill over in thoracic
cavity"chances of PM diffusion are still more
(3) MLI – It is an important medicolegal considerations in all poison deaths [eg
alcohol (ch 40)].

d. Blood stains
Very rarely only blood stains may be available as body has been disposed of.
Toxicology is possible from stains [Please see ch 29 for collection of blood
stains].

5. Bone marrow
For diatoms [please see ch 19].

6. CSF
(1) by lumbar puncture on intact body before autopsy
(2) withdrawing fluid using a needle and syringe from cisterna magna. Pass
needle through the atlanto-occipital membrane, just below the occiput, into the
cistern.
(3) From lateral ventricles directly [after removal of skull].
7. Cyst fluid
Collect from hydatid cysts. Examine for echinococcus hooklets.

8. Feces
Collect 5-10 g from sigmoid colon or rectum. Examine for protozoa and
helminths.

9. Lungs
(1) Mobilize lung
(2) Tie off main bronchus with a strong ligature
(3) Divide hilum
(4) Immediate put in a nylon bag, which should be heat sealed. Plastic
(polythene) not suitable as it is permeable to volatile poisons.

10. Saliva
For spermatozoa if oral intercourse is suspected

11. Tissue
Small pieces of tissues collected into a thermos flask containing liquid nitrogen
[for enzymes]

12. Urethral discharge

For microscopy and culture in case of STD

13. Urine
Urine can be obtained at two stages
(1) before the dissection - (a) catheterizing the urethra [usually for
microbiological analysis] (b) syringing through the anterior abdominal wall
directly above the pubic symphysis
(2) after the abdomen is opened -(a) incising bladder and collecting urine
directly with a ladle. Such specimens can be useful for toxicology, but not for
microbiology. [Ch 31"method of collection in the living].

14. Vaginal swabs

For spermatozoa

15. Vitreous humor

(1) Take 10 cc syringe and 20 gauge needle
(2) Insert in eye ball
(3) apply gentle suction. Aggressive removal or employment of vacuum tubes
results in retinal tissue getting dislodged, causing contamination.
(4) All vitreous [About 1-5 mL] from each eye is removed, as conc near the
retina are different as compared from centre of the globe. Volume is somewhat
. in infants.
(5) If samples are too viscous"Centrifuge"use supernatant.

XI. PRESERVATION OF VISCERA IN CASES OF SUSPECTED

POISONING

A. When Viscera should be Preserved?

Viscera should be preserved in following cases:
(1) Advanced decomposition
(2) Cause of death not found - after complete autopsy
(3) Criminal abortions
(4) Death due to burns [CN can be found in such cases. Please see chapter on
burns]
(5) Death of a machine operator in a factory [may be under the influence of
alcohol or drug]
(6) Drug induced deaths [penicillin etc]
(7) History of addiction, alcoholism etc
(8) History of intoxication
(9) Road side vehicular accidents [often alcohol or addiction drugs are found in
the driver and occasionally in the victim]
(10) Surgical and anesthetic deaths [to rule out deaths due to anesthetic gases]
(11) Suspicion of poisoning - Death is suspected to be due to poisoning either
by (i) police [eg when open drug sachets etc are found at scene of death.
Request comes from IO] or (ii) doctor [peculiar smell from viscera]. For
technique of collection, please see above.
B. What Viscera should be Preserved?
Following viscera must be preserved (Fig. 5.9)
(1) Stomach and contents – because most poisons are taken orally [of primary
value for estimating the quantity ingested in acute poisonings]
(2) Small intestine and contents – same reason as above.
(3) Liver (200-300 g) – Because
(i) it is the major detoxifying poisons
(4) Kidney – One half of each as one kidney may be dysfunctional. Because it is
the major excretory organ [Poison detected in liver and kidney is proof of
absorption. Therefore it is important to keep the contents of stomach and
intestines in separate bottles].
(5) Blood – 30 ml. Poison in blood is proof of absorption.
(6) Urine – 30 mL. Poison in urine is proof of absorption and excretion.
[Poison found in urine – unless added with an evil intention - is proof of
absorption and excretion]
(7) Food or medicine – Found at the scene of crime. Presence of poison in food
or medicine is a very strong evidence of poisoning. Table 2 gives a list of
body fluids/viscera to be preserved in special cases.
C. Preservatives
(1) Saturated solution of common salt – Most common preservative used in
India. Not to be used in corrosive acids (use rectified spirit instead)
(2) Rectified spirit – except in cases of (i) acetic acid (ii) alcohol (iii) chloral
hydrate (iv) chloroform (v) ether (vi) formaldehyde (vii) formic acid (viii)
kerosene (ix) paraldehyde (x) phenol and (xi) phosphorus. These are soluble in
rectified spirit and may be leeched away from tissues.
(3) Preservatives for blood – (a) For 10 mL of blood, use 100 mg sodium
fluoride (enzyme inhibitor) + 30 mg potassium oxalate
(anticoagulant)"shake thoroughly (e) Alternative preservatives for alcohol –
For 10 mL of blood [or urine], 50 mg of phenyl mercuric nitrate or sodium
azide.
(4) Preservatives for Urine – Urine should be taken in addition to blood.
Preservatives used (a) an equal quantity of saturated solution of common salt
(b) equal quantity of rectified spirit (c) some fine grains of thymol (d) one gm
of sodium benzoate (e) 5 mL concentrated HCl (the last two for about 200-500
 ml of urine). Some important pointers: (1) Formalin should never be used
as a preservative" Makes the extraction of poisons difficult, especially non-
volatile organic compounds (2) Samples of preservative - should be sent
separately to rule out contamination [ch 10" Toxicological artifacts] (3)
Preservatives for virological analysis - (a) Frozen at -90°C in liquid
nitrogen flasks (b) If this facility not available - 50% glycerol saline [glycerol
in buffered saline] (4) Heparin and EDTA should never be used as
anticoagulants. They interfere with the detection of some poisons (eg
methanol).

Conditions when preservative is not necessary

(1) When viscera can be analyzed within 24 hours
(2) If sample can be kept in a refrigerator or ice box
(3) For hair, nails, bones
(4) lungs for detecting inhaled poisons.

6. Examination of Decomposed
Bodies, Mutilated Bodies,
Fragmentary Remains and Bones

I. AUTOPSY ON DECOMPOSED BODIES

All human remains must be examined, because even the most highly
decomposed bodies provide some information.

II. AUTOPSY OF MUTILATED BODIES AND

FRAGMENTARY REMAINS

Forensic anthropology is the application of physical anthropology for the

purposes of law and administration of justice.

A. Questions to be Answered
Following questions are asked by police in relation to mutilated bodies or
fragmentary remains.

1. Human or animal
(1) If head, trunk, limbs available – very easy
(2) If only muscles etc are available – perform precipitin test with antihuman
globulin.

2. One or more bodies

(i) Anatomically fit together all parts and count bodies (ii) If only parts are
available, apply logical count eg (a) two limbs of the same side"two persons (b)
two opposite limbs of different lengths"2 persons (c) two opposite limbs of
grossly different weights"2 persons (d) two limbs of different colors"2 persons
(e) two limbs of different DNA profiles"2 persons (f) Three ears"definitely more
than one person, but may be 2 or even 3. Confirm sides. Perform DNA (g)
multiple fingers"sort according to side and count. If unsure, perform DNA.

3. Sex
(1) If head, trunk, limbs available – very easy. Look for distribution of hair,
development of breasts, striae gravidarum
(2) If not available, look for non gravid uterus and prostate – they resist
putrefaction for long.
(3) DNA based methods – ch 3.

4. Age
Can be determined from (1) General development (2) eruption of teeth (3)
ossification centers (4) obliterations of the sutures of skull [ch 3].

5. Stature
In mutilated bodies, following pointers may be helpful
(1) If only torso available - (a) Arms outstretched"Distance between tips of
middle fingers of both hands is equal to height (b) Length from vertex to
 symphysis pubis is roughly half of total height [if the age is >14 years. If age
<14 y, trunk is longer than the lower limbs] (c) Length from sternal notch to
symphysis pubis # 3.3 = Height
(2) If only lower half of body available – As above. Measure height from
symphysis pubis to heel and multiply by 2
(3) If only vertebral column available – Length of vertebral column # 100/35 =
Height
(4) If only one arm available – Multiply length of arm by 2. Add 30 cm for two
clavicles. Add 4 cm for sternum. Gives height
(5) If only part of one arm available – Length of forearm from tip of olecranon
process to tip of middle finger # 19/5 = Height
(6) If only head available – Height of head from vertex till tip of chin # 7 =
Height
(7) If only palm available – 34.5 + (5.77 # Palm Length in cm) + (2.7 x Palm
Breadth in cm) = Height in cm
(8) If only middle finger (of hand) available – Length of middle finger # 21.5 =
Height
(9) If only index and ring fingers are available
(10) If only foot available – Foot length # 100/15 = Height
(11) Can be measured from long bones too (please see below)

6. Identity
Identity can be determined from (1) clothing (2) deformities (3) fingerprints (4)
hair (5) moles (6) scars (7) superimposition (8) tattoos (9) teeth etc. Please refer
to ch 3 for details.

7. Manner of separation of parts

Margins of the separated parts must be examined to determine if they are (1)
cleanly cut (2) disarticulated at the joints (3) gnawed by animals (4) hacked (5)
lacerated or (6) sawn.

8. Time since death

From condition of parts. For details, please see ch 9

9. Cause of death
Look for signs incompatible with life, eg
(1) cut or rupture of a large blood vessel, [eg jugular vein]
(2) evidence of fatal injury such as cuts and stabs to a vital organ [eg heart or
brain]
(3) fractures [esp of skull, ribs, cervical vertebrae, hyoid etc)
(4) marks of burning
(5) If body recovered from a body of water, look for diatoms
(6) Perform toxicology from available tissues. Metallic poisons can be detected
for years in hair, nails and bones
(7) Signs of natural disease [eg blocked coronaries]
(8) Emaciated body might point to death by starvation. For details, please see ch.
20.

10. Injuries antemortem or postmortem

Examine margins of parts for evidence of vital reaction. Gross examination,
histopathological, enzyme histochemistry and immunohistochemistry is useful.
[For details please. see ch 11 on injuries].

11. Miscellaneous info

Handedness of the individual – can be determined by measuring muscle mass
in both upper and lower limbs on each side. Muscle mass is -er on the dominant
side. Right dominance in upper limb may not necessarily correspond with right
dominance in left limb and vice-versa.

III. EXAMINATION OF BONES

Forensic osteology is the application of knowledge of bones for the purposes of

law and administration of justice.

A. Questions to be answered
Following questions are usually asked by police in relation to bones

1. Whether these are bones or only rubble

(1) Naked eye inspection - shows peculiarities of bones, eg trochanters,
 tuberosities, condyles etc, which would not be visible in rubble
(2) Density of bone - is different from that of rubble [sp gr of bone = 2; rubble
lesser or greater, but rarely 2]
(3) Microscopy
(4) Precipitin test - possible when bones are within 15 y; plasma proteins are
extractable up to this period [details in ch 29]. Not possible with burnt or
cremated bones.

2. Human or animal
(1) Comparative anatomy:
(i) differentiation is done by studying details which are different in man and
animals.
(ii) Easy when entire bones are available, but difficult when bones are burnt,
fragmented or otherwise mutilated.
(iii) Also difficult with very small bones eg metacarpals, metatarsals, ossicles,
phalanges etc.
(iv) Hand and foot bones of bear resemble human bones greatly.
(v) Virtually impossible with sesamoid bones.
(2) Precipitin test
(3) Microscopy – but bones of great apes cannot be distinguished
(4) Chemical analysis - of bone ash.

3. One or more individuals

Look for incompatibilities, which will indicate more than one individual (i) Age
– bones belonging to persons of different ages, indicate more than one person.
(ii) Sex– eg if only two bones are available, say skull and pelvis, they are
compatible with one person. But one bone of male and another of female
indicate two persons. (iii) Race – bones of two different races, indicate at least 2
different persons (iv) Stature - determined from two bones (v) Side – eg two
femurs are normally compatible with one person. But if they are of same
side"indicate 2 persons. (vi) Number – 2 skulls indicate two persons. 3 femurs
indicate at least two persons, but if all are of same side"3 persons and so on. (vii)
Articulation – normally one femur and tibia of same side indicate one person,
but if they cannot be articulated together, they indicate different persons. (viii)
State of putrefaction – some fresh and some very old indicate different
individuals (ix) Other studies - (a) bone weight (b) density studies (c) neutron
activation (d) radiography (e) serological testing (f) trace element analysis.

4. Stature
a. If complete skeleton is found
(1) By articulation - Articulate (skeleton. Add 2.5 cm for soft tissues of scalp,
vertebral bodies and heels.
(2) By Weight – Matiegka has given a formula [Matiegka’s formula] for
calculation of skeletal weight from stature and vice-versa. Skeletal weight (g)
= 1.2 # D2 # H. Here “H” is standing height in centimeters [this can be
calculated by articulating skeleton], and “D2” is the average of the squares of
four measurements–transverse dimension of the lower end of the (i) humerus
(ii) forearm (iii) Femur, and (iv) ankle.

b. If incomplete skeleton is found, but individual bones not fragmented

(1) Individual bones are measured by osteometric board [Fig 6.2] and
multiplication factors applied.
(2) Osteometric Board:
(i) Hepburn board modified by Trevor is most commonly used
(ii) Has a rectangular base [1]
(iii) A ruler [2] is fixed along one of its long sides
(iv) Upright boards - One is fixed at one side [3]; second slides along the board
[4]
(v) Procedure – one end of the bone is placed against the fixed board; the
moveable board is brought up to the other end; Ruler then shows the length
of the bone.
(3) Long bones - Multiplication factors for all six long bones [femur, tibia,
 fibula, humerus, ulna and radius]
(i) provided by different workers (a) Breitinger [1937] (b) Dupertuis and
Hadden’s [1951] (c) Muñoz [2001] (d) Pearson - Oldest. Developed in 1899
by the British anthropologist Karl Pearson [1857 – 1936] (e) Telkkä
[1950] (f) Trotter and Glesser [1952].
(ii) A simple rule of thumb is that humerus is 20%, tibia 22%, femur 27% and
the spine 35% of individual’s height in life.
(iii) If long bones are not available - Articular length of metacarpals may be
used.

c. If fragmented bones are found

Steele and McKern’s formula is used.

d. If only skull available

Height of skull # 8.

e. Stature from teeth

Please see ch 3 [forensic odontology].

5. Time since death

(1) Skeletal changes depend upon
(i) Accessibility to scavengers [carnivorous animals and insects]
(ii) Burial or non burial
(iii) Climatic conditions [temp, humidity]
(iv) Soil type.
(2) Determination of Time since death:
(i) up to 6 months - (a) Heavy [because of the preservation of the organic
stroma] (b) Greasy to touch. Greasiness persists for several years (c) bad
odor (d) color – pale ivory, if directly placed under sunlight [bleaching by
sun] (e) Sawing – (I) Bone would be hard to saw (especially the shafts of
limb bones such as the femur) (II) uniform through the whole thickness.
(III) Smell of burning organic tissue if vigorous sawing produces heat. In an
older bone (>5 y), the loss of the collagenous stroma will lighten the bone
and make it easier to cut. (f) Nitrogen content - 4.5%. It progressively .es
with time
(ii) 6 m – 1 y - (a) Soft tissue remnants [tendon, ligament tags] adherent,
especially around the joint ends. (b) Periosteum visible as fibrous material
closely adherent to the shaft surface. (c) Cartilage present on articular
surfaces.
(iii) 1y - 5y - Microradiography and electron microscopy reveal vacuoles in
compact bone left in soil for 5 y.
(iv) 50-100 y - (a) Nitrogen content – between 4-4.5%
(v) 200 y – UV fluorescence of cut surface is useful up to 200 y [Fig 6.3].
(vi) >350 y - (a) Nitrogen content ≤2.5%.

6. Signs of pathology
a. Gross examination
(1) Anemia - Cribra orbitalia, a fine porosity visible on the ceiling of the orbits
 is a sign of severe anemia.
(2) Syphilis:
(i) Characteristic tibial lesions (“sabre shins”) are indicative of treponemal
infection.
(ii) purify IgG from powdered bone"use ELISA" reactivity with T. pallidum
antigen.
(3) Stones – in kidneys, gall bladder
(4) Tuberculosis – signs of Pott’s disease, Other bone anomalies.

b. Biochemical analysis
Heavy metal poisoning, eg lead

7. Signs of Trauma
Examine ends of long bones - Note if bones are (i) Cut by sharp instruments (ii)
Gnawed by animals – (a) Crabs, fish, turtle – leave shallow marks (b) Deer and
sheep – hold bones with back teeth"fork shaped or double pronged fragments (c)
Dogs, fox and wolves - cause splintering of bone (d) Rodents – produce parallel
“chisel marks” due to gnawing (iii) Hacked (iv) Sawn.
8. Cause of death
Can be ascertained in some selected cases only
(1) Bullets - found lodged in crucial bones, eg skull, vertebrae. Even in bullets
are found in non-vital bones eg femur, one can be fairly certain that the victim
was exposed to a volley of bullets.
(2) Burns - If bones are burnt, possibly the victim was burnt to death. Very
difficult to know if body was burnt after killing.
(3) Deep cuts - on crucial bones eg ribs on left side overlying heart indicating
the victim was stabbed. Cuts on lumbar vertebrae indicate abdominal stabbing.
Type of weapon can often be made out by studying cuts.
(4) Diatoms - can indicate drowning
(5) Diseases of bones - eg malignancies
(6) Fractures - of bones containing vital structures eg skull, vertebrae, multiple
ribs, hyoid bone
(7) Poisons - Metallic poisons can be detected in bones, even after burning.

9. Miscellaneous info
(1) Bones discarded after anatomical dissection – Some stains are seen in the
nutrient canals.
(2) Harris lines - [syn, growth arrest lines, HLs Lines of Arrested Growth
(LAGs)] – First described by Harris in 1933 are transverse radiopaque lines
of -ed bone density that are only visible by radiographs or in cross-sections.
(i) Seen in most bones, but most frequently in distal half of tibia.
(ii) Cause - Episodes of temporary arrest of longitudinal growth caused by stress
[eg disease, illness, malnutrition, psychogenic stress, trauma]. Can be used
to predict these stresses in the individual.
(3) Natural disintegration of body – articular surfaces are smooth.
(4) Stride length - Femur length has a positive relationship with stride length.
Opinion can be formulated regarding person’s gait, biomechanics, movement,
and posture. If video or closed-circuit television footages from video
surveillance systems are available, these can be linked to the deceased whose
femur is being examined.

B. MLI (of mutilated bodies and bones)

(1) Cremation litigation – Mishandling of cremated remains may result in
doubts and litigation. There are reports of families receiving two sets of
cremains each purported to be of their relative.
(2) Human rights investigations
(3) Mass disasters
(4) separation of recent from ancient remains
(5) All other questions answered above may be raised in one or other civil or
criminal case.

7. Exhumation

Exhumation (Latin ex, out of; humus, ground) [syn disinterment] is authorized
digging out of the coffin of a dead person from his grave, in order to establish his
cause of death, or to decide upon some other relevant fact, such as the person’s
identity.
Salient features:
(1) Incidence - Exhumation is rarely done in India, because the bodies are
mainly disposed off by cremation. Only certain communities bury their dead.
(2) Time limit – No time limit in India. Can be done any number of years after
burial.

I. REASONS FOR EXHUMATION

A. Criminal

1. Determination of cause of death

(i) Homicide (ii) suspected homicide (iii) homicide disguised as natural,
accidental or suicidal death (iv) suspicious poisoning (v) death as a result of
criminal abortion (vi) criminal negligence.

2. Retrieving evidence
(i) some vital object which may throw more light on the case, such as bullet from
the dead body (ii) poison from body.
B. Civil

1. Identification
Identification of the deceased for
(1) burial of the wrong body inadvertently or by fraud,
(2) settling of inheritance
(3) survivorship claims [disputed identity].

2. Others
(1) Accident death claim
(2) Civil negligence
(3) Insurance
(4) Workmen’s compensation claim [ch 2].
(5) When the site of a graveyard is moved e.g. for redevelopment.
(6) When the relatives wish to relocate the grave for some reason.

II. AUTHORIZATION

(1) Magistrate – In India, the body can be exhumed only upon the written order
from an executive or judicial magistrate [S.176(3), CrPC]. Police CAN NOT
order exhumation.
(2) Coroner - In countries with coroner system [eg UK].
(3) Medical examiner – in USA.

III. PROCEDURE

(1) Information to relatives – Wherever practicable, the magistrate should

inform the relatives of the deceased whose names and addresses are known,
and shall allow them to remain present at the inquiry [S.176(4), CrPC] [ch 1].
(2) Officials present at the time of exhumation: (i) magistrate (ii) medical
officer (iii) police officer
(3) Identification of grave: (i) Done in association with local priest. Identifying
features are (a) Burial plot location (b) Grave marker (c) Headstone (ii) Note
distance of grave from some permanent objects eg a prominent grave, fence,
 gate, road, rocks or trees.
(4) Time – Early in the morning. Advantages (i) Exhumation, postmortem and
reburial can be conducted on the same day (ii) Less curious onlookers, and
less police presence is necessary. However if still onlookers are there, areas
should be screened off (iii) Presence of natural light
(5) Removal of earth: (i) Earth should be removed in layers [10-15 cm at a
time]. Note should be made about the condition of soil, water content and
vegetable growth. (ii) Burial pit should be opened up to 30 cm on all sides of
the body. This enables the investigator to stand at side of grave and clear the
body [please see below].
(6) Measurements – Measure the depth of grave from the surface to the skull as
well as surface to feet [gives inclination of body]
(7) Before recovery of body: (i) Photography - With the body in situ
photograph it"Clear the body surfaces with the use of a soft brush or whisk
broom"Photograph the body in situ again (ii) Drawing – of the grave as well
as body or skeleton should be made now. This enables various measurements
to be recorded on the drawing, eg height of body, extent of flexion or
extension of limbs etc, grave’s distance from notable landmarks etc.
(8) Recovery of body: (i) If body is with a coffin – Note condition of coffin;
whether eaten up by worms, sodden, soggy, damaged, worn out, peeling on
the outside etc. Whether dry or filled up with water. If filled up with water,
remove as much as possible, preserve, label and send for toxicology. Now
lower a plank or strong PVC sheet to the level of earth on which coffin
rests"Gently lift coffin on to the plank or PVC sheet"Remove from
grave"Transport entire coffin to mortuary (ii) If body is without a coffin - (a)
If decomposition is not advanced – Use same procedure to remove body as
above. Body is gently lifted and placed on to the plank or PVC sheet (b) If
decomposition is advanced – There is possibility of body disintegrating and
breaking away as soon as it is attempted to be lifted. So an alternative
procedure is followed. Dig down beside and beneath the body"Insert a
wooden plank under the body"Lift up the wooden plank. (c) If body is
skeletonized – Use same procedure as above [advanced decomposition]. In
addition, after removal of skeleton, remove earth from below and sides of the
body and sift it in a finely-meshed screen. This can often recover smaller
bones [carpals and tarsals , epicondyles, epiphyses, phalanges, sesamoid
 bones, teeth, tuberosities] as well as objects [bullets, gall stones, kidney
stones, medical prosthesis eg nails, plates, tips of knives and arrows etc].
(9) Identification – Body should now be identified by close relatives and friends
either from features [if intact] or from clothes, objects kept within the grave,
appearance of coffin etc.
(10) Note – condition of body, burial clothes
(11) In suspected poisoning: (i) Collect all personal effects, clothings, nails,
hair, bones etc and send for toxicological analysis (ii) Collect samples of earth
[about 1kg] that are in actual contact with body and also from above, below
and each side of the body. Also from a site well away from the grave [Fig
7.1]. (iii) Also preserve samples of burial clothes and coffin to preclude the
possibility of contamination from these sources.
(12) First autopsy or second autopsy – please see ch 5.

8. Thanatology, Death and its Causes

I. INTRODUCTION

A. Thanatology
Thanatology (Gk Thanatos, the God of Death) is that branch of science that
studies death in all its aspects.

II. STAGES OF DEATH

A. Somatic Death
Somatic death is the permanent, irreversible death of an organism as a whole.
Historically the concept of when somatic death occurs has kept changing.
Traditionally the concept was that it occurs when there is irreversible cessation
of heart, lungs and brain [Bichat’s criteria - please see below]. The concept was
gradually changed to brain death and eventually to brain stem death. With
modern technology, bizarre situations can arise. Circulation and respiration of a
brain stem dead individual can be maintained artificially. By classical criteria,
such an individual would be somatically alive, which is an absurd situation.
Salient features:
(1) According to modern concept, somatic death coincides with the death of
brain stem. It involves complete and irreversible stoppage of vital brain
stem functions.
(2) Legally a person is dead after somatic death.
(3) It is death as a common man understands it.

B. Molecular Death
Molecular death is the death of all individual cells within the body. All
biochemical (molecular) activity within the cells comes to a stop. It comes 2-3
hours after somatic death.
1. Demonstration of supravital period in the dead
Electrical excitability of muscles - The Orbicularis oculi muscle is tested by
inserting needle electrodes into the upper eyelid at a distance of 1.5–2 cm, and at
a depth of 0.5–0.1 cm. The Orbicularis oris muscle is tested by inserting similar
electrodes at 1 cm distance from the mouth angles, at same depth as above [0.5–
1 cm]. Muscles are then stimulated using constant current rectangular impulses
of 10 mA at 50 cycles/s. The muscular reaction is graded according to the
intensity and spread of contraction. Different intensities can be related to
different periods of death.

C. Antemortem, Postmortem and Perimortem Injuries

(1) Antemortem injuries - Injuries that occur during life.
(2) Postmortem injuries - Injuries that occur after molecular death.
(3) Perimortem (around death) injuries - injuries caused between somatic and
molecular death [supravital period].
(4) Agonal period – is the period just before death.

III. SUSPENDED ANIMATION

Suspended animation [syn apparent death] is a state where the heartbeat and
the respiration of a person become so weak, that they cannot be detected by
routine clinical methods. The person thus appears clinically dead but he is not
since the brain stem is functioning.
Salient features:
(1) The metabolic rate of life is so reduced that the oxygen requirement of
individual cells is satisfied through oxygen dissolved in body fluids.
(2) Testing for brain stem reflexes [please see below] would establish that the
victim is not dead.

A. Causes

1. Voluntarily induced
By yogis during samadhi.
2. Accidental
Pl see memory aid 1.
Memory Aid 1: Causes of suspended animation
(1) Anesthesia, (2) Barbiturates, (3) Coma (4) Cholera (5) Concussion, (6) Deep shock (7) Drowning,
(8) Electrocution, (9) Frozen state (Hypothermia)
(10) yoG is [voluntarily induced, but may be remembered by the student here as a memory aid], (11)
Hanging
(12) Heat stroke, (13) Hypothermia, (14) Hysteria
(15) Illnesses [prolonged], (16) Infections [Cholera, Typhoid], JKL, (17) Mesmeric trance, (18) Newborn,
(19) Opiates.

B. ML Importance
(1) Premature burial or cremation - Before 19th c, when modern methods of
diagnosis of death were not available, some people were undoubtedly buried
as dead, when they were actually in a state of suspended animation. In many
cases, the “dead” person awoke just before he was about to be buried, but in
many others they were actually buried. (i) Sommer’s movements - Several
coffins dug up years later due to some reason, showed that the limbs of dead
person were in different position, than when he was buried [In 1833, this was
attributed by Sommer to contraction of muscles after death due to rigor
mortis. These were the so-called Sommer’s movements].
(2) Postmortem – Persons in suspended animation have been brought for PM
examination. This reflects the need for more careful diagnosis of death in
emergency wards.

IV. THE MOMENT OF DEATH

The moment of death refers to the exact moment, when the person dies. The
concept of the moment of death has radically changed over the years.

A. Classical Criteria of Death

Criteria of death refer to criteria and tests which confirm death.
Salient features:
(1) Bichat’s criteria - Before the era of heart transplantation, the criteria of
death were the so-called tripod of life, advanced by French physician Marie
Bichat (1771 –1802). Also known as Bichat’s tripod of life. Bichat believed
that life could be compared to a tripod (Fig 8.1), with the three legs
representing brain, heart and lungs. If any leg perished, very soon (i.e. within
minutes) all legs would perish, and the tripod of life would fall (death).
(2) Atria mortis [Latin, Gateways of death, death’s portals of entry]- Since death
could “enter” only by stoppage of these organs, each was called an “atrium
mortis” [please, atria mortis].
(3) The rule of the thumb at that time was: breathing stops within 20 seconds of
cardiac arrest, and heart stops within 20 minutes of stoppage of breathing.
Brain would die within 3 minutes of the stoppage of any of the other two.
Tests were developed to determine the death of each organ.
1. Tests for circulation
Stethoscope was invented in 1819. But it was Bochet in 1846 who suggested
cardiac auscultation for 2–3 min to diagnose death. Because in suspended
animation the stethoscope could not detect heart sounds, it could not gain wide
acceptance.
a. Magnus test [Syn, ligature test] [Fig 8.2]
Suggested by an Italian Hugo Magnus in 1872. The test consisted of tying a
string around one of the fingers of the supposedly dead man. The pressure
applied had to be just above that in veins, but just below that in arteries. This
would occlude the veins but not the arteries. If the circulation was still
maintained the finger distal to the ligature would swell. Although stethoscope
had been discovered by Laënnec in 1816, it was still very basic in design, and it
could not be used reliably to listen to heart sounds, especially if it was beating
very feebly. Magnus test was in vogue for some time, but is now completely
outdated.
b. Icard’s test
Suggested by Séverin Icard of France in 1895. It consisted of subcutaneous
injection of a compound [Fluorescin with sodium bicarbonate; pl co-relate
with Fluorescein test (ch 29). Fluorescin is a colorless amorphous substance;
oxidation by heme produces fluorescein which is fluorescent. fluorescein also
causes urine to fluoresce in ethylene glycol poisoning (ch 40)]. If the circulation
was still going on, the whole skin would turn a vivid yellow. If the person was
already dead, no such change would be seen. This test is now completely
outdated.
c. Diaphanous test (transillumination test)
Hand with closed fingers was held against a strong source of light. During life, it
appears red and translucent. After death, it is yellow and opaque.
d. Finger nail test
Pressure applied on nail bed. During life normally nail bed is red; on pressure it
turns pale, and on release of pressure becomes red again. After death remains
pale throughout.
e. Other tests
(1) Cutting of small artery"Jerky flow during life. Continuous or no flow after
death.
(2) Heat test - Application of heat [heated matchstick; hot melted wax]"Blisters
appear during life, not after death.

2. Tests for respiration

a. Winslow’s test
Winslow’s test was suggested by the Danish physician Jacques-Bénigne
Winslow (1669-1760). A small pot containing water, milk or mercury was kept
just below xiphisternum. Slightest motion of the chest-walls, such as occurs even
with the faintest respirations, is indicated by the rippling on the surface of the
water, or by the movements of a reflected image (such as a candle-flame) from
the surface of the mercury. The absence of such movements indicates the
absence of any motion of the chest-walls, and the probable stoppage, therefore,
of respiration.
b. Mirror test
Mirror held in front of mouth and nostrils. Becomes dim due to water vapor in
breath
c. Feather test
Feather placed in front of nostrils or mouth. Movement during life. No
movement after death. Sometimes soap bubbles or a candle was held to the nose
to detect respiration.
d. Others
Submerging the body in water to detect bubbles produced by respiration.

3. Tests for brain function

Tests for “sensibility”

(1) Blowing a strong stimulant such as hellebore or mustard into the nose
(2) inserting a sharp instrument under the nail
(3) cauterization or incisions
(4) scalding with hot water or oil
(5) trumpeting or loud noises.

4. Miscellaneous tests
(1) Ripault sign - External pressure to the eye causes permanent (vs. temporary)
distortion of the roundness of the pupillary aperture.
(2) X-ray fluoroscopy -to search for organ movement was suggested in 1910.
All above tests are now completely outdated.

B. Brain Death
With the advent of heart transplant in 1967, the definition of death needed
to be revised and made more logical (Table 1). Transplant surgeons needed a
“live” and “beating” heart from a “dead” donor (beating heart donor). This was
not possible with the old illogical definition, where all three vital organs needed
to perish before death could be pronounced. Advent of modern resuscitative
measures could also keep heart and lungs “alive” for long intervals even after the
brain of the individual was dead.

Harvard criteria of Brain Death (1968)

In 1968 the Harvard Criteria of the moment of death [Table 1] were
developed. Laid stress on determining the activity of only the brain to determine
death [Fig 8.4]. The criteria suggested that the activity of the heart and lung are
important not by themselves, but as a sign of brain activity.

a. Unreceptivity and unresponsivity

The patient is totally unaware of the externally applied stimuli (unreceptivity).
Even the most intensely painful stimuli evoke no vocal or other response, not
even a groan, withdrawal of a limb, or quickening of respiration
(unresponsivity).
b. No movements or breathing
There should be no spontaneous muscular movements, nor any breathing
movements for at least one continuous hour. The breathing movements are to be
observed by turning off the respirator for 3 minutes and observing closely
whether there is any effort on the part of subject to breathe spontaneously.
c. No reflexes
(1) The pupil should be fixed and dilated, and unresponsive to bright light.
(2) Ocular movement [to head turning and to irrigation of the ears with ice
water] should be absent.
(3) Corneal and pharyngeal reflexes are absent.
(4) Spinal reflexes [eg knee jerk] are also absent.
d. Flat electro-encephalogram
Flat or iso-electric EEG [at 5µV/mm] is of great confirmatory value.
e. Repetition of tests
(1) All tests should be repeated again after 24 hours with no change.
(2) Respirator must be put back on during the intervening period. It can only be
taken off after the patient has been declared dead. This was done to offer legal
protection to physicians, otherwise, it could be argued that they turned off
respirator on a living patient.

C. Brain Stem Death (Modern Criteria of the Moment of Death)

Even the brain consists of many parts, the cerebral cortex, brain stem,
cerebellum etc. If some cells of the brain were dead, and others alive, how was
one going to say that the person was dead? In 1971, Mohandas and Chou (two
neurosurgeons from Minnesota) suggested that even within the brain, the most
important part was the brain stem (Fig 8.4). Thus one must look only for the
brain stem death. The reasons for this assertion were
(1) Resistance to anoxia - Among all brain cells, medullary neurons are most
resistant to anoxia. Thus if they are dead, all brains cells can reasonably be
assumed to be dead
(2) Vital centers - Brain stem is responsible for all vital functions of the body
(3) Gateway - All cortical pathways pass through the brain stem. Thus if
brain stem was dead, all pathways would be dead. The criteria for brain stem
death (now popularly known as the Minnesota Criteria) suggested by them
were as follows.

1. Minnesota criteria of Brain stem death (1971)

(1) No spontaneous movement
(2) No spontaneous respiration when tested for a period of 4 minutes at a time
(3) Absence of 5 major brain stem reflexes [Fig 8.3]
(4) EEG not mandatory. All the above findings must remain unchanged for at
least 12 hours [Table 2].

2. Indian law on brain stem death

[A] S.2(d) of The Transplantation of Human Organs and Tissues Act, 1994 -
please see ch 2. [B] S.3(5) of the same Act - “where any human organ is to be
removed from the body of a deceased person, the doctor must confirm that (i)
life is extinct in such body or (ii) where it appears to be a case of brain-stem
death, such death has been certified under section 3(6). [C] S.3(6) of the same
Act - Where any human organ is to be removed from the body of a person in the
event of his brain-stem death, no such removal shall be undertaken unless such
death is certified by a Board of medical experts consisting of (i) the registered
medical practitioner, in charge of the hospital in which brain-stem death has
occurred (ii) an independent specialist nominated by the doctor specified in
clause [i] (iii) a neurologist or a neurosurgeon to be nominated by the registered
medical practitioner specified in clause [i] and (iv) the registered medical
practitioner treating the person whose brain-stem death has occurred.
V. MODES OF DEATH

Mode of death in an old concept of death based on Bichat’s concept of the

tripod of life.
VI. GORDON’S CLASSIFICATION OF DEATH

Gordon’s classification of death is an old way of classifying medico-legal

deaths taking tissue anoxia as the fundamental cause of all deaths. Gordon came
to the conclusion, that in all cases of deaths of medico-legal importance, tissue
anoxia must supervene in one or the other way, before death occurred. There are
four major ways in which tissue anoxia can occur, and thus death was classified
into four types.
A. Anoxic Anoxia
[syn, asphyxia, hypoxemic hypoxia, hypoxic hypoxia] O2 content of blood is .ed.
It occurs in following ways:

1. .ed Oxygen in the Ambient Air

(1) Getting trapped in a closed almirah, closet, old unused refrigerators etc
(2) Exposure to noxious gases such as sulphur dioxide, chlorine, sewer gas, etc.
(3) Hypothetical situation of trying to inhale in a vacuum.
(4) Anesthetic agents [ch 21]
(5) High-altitude.

2. .ed supply of oxygen

(1) Mechanical Interference with the Passage of Air - Hanging, strangulation,
choking, drowning.
(2) Ventilation disorder.

3. .ed pulmonary blood supply

Perfusion disorders.

4. .ed pulmonary gas exchange

Diffusion disorders.
Last two are unimportant medicolegally.

B. Anaemic Anoxia
Oxygen carrying capacity of the blood is reduced. Eg
(1) acute massive hemorrhage
(2) poisoning by CO.

C. Stagnant Anoxia
Blood is incapable of movement. E.g.
(1) heart failure (heart unable to pump the blood),
(2) embolism [heart pumping the blood, but there is obstruction to the flow of
blood] and shock.
D. Histotoxic Anoxia
Tissue loses the capacity to utilize oxygen. Histotoxic anoxia is of 4 types.

1. Cellular histotoxic anoxia

Oxygen cannot be taken up due to failure of tissue enzyme system by poisoning,
eg CN [Ch 44], PH3, H2S, overdose of hypnotics and anesthetics.

2. Pericellular histotoxic anoxia

Oxygen cannot be taken up due to .ed permeability of cell membrane, eg in
nitrous oxide or lipid soluble anesthetic agents like halogenated hydrocarbons
[chloroform, cyclopropane, ether, halothane, trilene].

3. Substrate histotoxic anoxia

Oxygen cannot be taken up due to failure of efficient cell metabolism, eg
hypoglycemia.

4. Metabolite histotoxic anoxia

Oxygen cannot be taken up due to due to accumulation of end products of cell
respiration, eg CO2 poisoning, uremia.

VII. NEGATIVE OR OBSCURE AUTOPSY

Negative autopsy is one, when gross and histopathological examination,

toxicological, microbiological, serological and other laboratory examinations fail
to reveal a cause of death. The term “negative autopsy” is used in a wrong sense by several books,
which tend to include so called “defective autopsies” within this term. Whenever a well-established PM
procedure, technique or ancillary investigation is not done, be it due to ignorance, lack of training or due to
non-availability of resources etc, it is a defective autopsy. There are thus four kinds of autopsies (i)
Normal autopsy - cause is apparent from gross examination (ii) Defective autopsy – cause was
ascertainable, but was not ascertained due to some constraint on the part of doctor, hospital, facilities etc
(iii) Obscure autopsy - Gross findings are minimal, indecisive, or obscure as in adrenal insufficiency,
anesthetic overdose, myxedema, rare plant poisons, thyrotoxicosis etc. Subsequent examinations such as
histology, microbiology, serology or toxicology reports establish the diagnosis. (iv) Negative autopsy -
Cause is not clear from gross as well as subsequent examinations. Some pathologists merge obscure
autopsies with normal autopsies to avoid confusion.
Salient features:
(1) Rate of negative autopsies"5-10% of all autopsies.
(2) Mostly seen in – children and young adults.

A. Causes of Defective Autopsy

Lack of competence or inadequate training of doctor - (a) Inadequate crime
scene examination – (i) presence of legal drugs [eg cardiac medications, asthma
inhalers, rare drug prescriptions] (ii) presence of illegal drugs [eg open drug
ampoules, drug paraphernalia, open drug sachets, illicit drugs] (iii) Position of
the body when first found – Positional asphyxia (eg hyperflexion of the neck
from collapse in the corner of a room) may leave no anatomic findings. (iv)
Suffocation by the placing of a plastic bag over the head can cause asphyxia in
the absence of anatomic findings. The bag may be removed by a careless or
ignorant policeman, or by a relative before the body is sent for pm (b)
Inadequate examination of clothings - (i) may contain drugs (ii) may show burn
marks in low voltage electrocutions (c) Inadequate history. (i) Personal h/o
allergies, chest pain, diabetes mellitus, dizziness, epilepsy, prior
electrocardiograms [whether positive or negative], syncopal episodes (ii) family
h/o sudden death/lethal heart disease (iii) activities of the deceased just before
the time of collapse - Exercise, emotional stress, altercation in which the victim
received a blow to the chest [Commotio cordis] may suggest sudden cardiac
death (d) Inadequate or improper external examination – (i) Electrocution with
hidden and/or insignificant entry mark [as in low-voltage electrocutions](ii)
Insect bite (iii) Snake bite (iv) Needle marks in drug addicts [fresh and old].
Sometimes these may be hidden by an overlying tattoo (v) therapeutic
transdermal patches [eg for nitroglycerin and fentanyl] (e) Inadequate or
improper internal examination - (i) Air embolism (ii) anomalous coronary
arteries [eg origin of the left coronary artery from the right sinus of Valsalva, the
right coronary artery from the left sinus of Valsalva, origin of the coronary artery
from a pulmonary artery, ostial stenosis from aortitis, congenitally narrowed
coronary ostium, coronary artery bridging] (iii) blunt injuries to heart (iv)
concussion (v) Pituitary tumors (vi) Pneumothorax (vii) whiplash injury [self
reducing neck injuries] (f) Insufficient laboratory examinations – as in (i)
Allergy and hypersensitivity and drug idiosyncrasy [IgE determination would
reveal cause] (ii) Biochemical disturbances [eg porphyrias, potassium deficiency,
uremia etc] (g) Insufficient toxicological analysis – rare poisons eg tetrodotoxin.
B. Causes of Obscure or Negative Autopsy
Obscure or negative autopsy may be due to: Unsuspected or obscure
conditions, which leave minimal, indefinite or obscure signs – (a) Concealed
trauma - [please see below] (b) Endocrine dysfunction [eg uncontrolled diabetes
causing diabetic ketoacidosis, hyperinsulinemia causing profound
hypoglycemia] (c) Cardiac conditions - (i) Brugada syndrome (ii) Coronary
artery spasm (iii) long QT syndrome (iv) Wolff–Parkinson–White (WPW)
syndrome (v) Early MI – No changes may be detectable up to 3 hours [please
see below under the heading “sudden and unexpected death] (vi) Flutter and
fibrillation [histological examination of SA node, AV node or Bundle of His may
reveal diagnosis] (d) Natural conditions and diseases - (i) Epilepsy (ii) Fear,
anger, extreme happiness or other emotional outburst (iii) Work stress (e)
Poisoning (f) Miscellaneous - (i) Hypersensitivity reactions (ii) Laryngeal spasm
[choking, dry drowning] (iii) Status epilepticus (iv) Vagal inhibition. Many of
these autopsies would not be negative, if conducted by a thoroughly trained
pathologist in well-equipped lab, with all tests conducted properly.

Concealed Trauma
a. Cerebral concussion
May cause death without any marks of injury – external or internal [ch 17].
b. Commotio cordis
Please see ch 17
c. Hidden neck injuries
Railway spine"ch 17
d. Reflex Vagal inhibition [RVI]
Vasovagal shock [syn, instantaneous physiological death, nervous apoplexy,
reflex cardiac arrest, vagal inhibition, vagal shock, vasovagal inhibition of the
heart, vasovagal syncope] is sudden death, occurring within seconds or minutes
due to minor trauma or relatively simple and harmless peripheral stimulation [eg
touching of neck].
Salient features:
Mechanism: (i) Pathophysiology - minor trauma to neck"- pressure on
baroreceptors situated in carotid sinus, carotid sheath and carotid body [situated
about the level of angle of mandible]"transient -in BP locally in the
sinus"Afferent impulses are transmitted through small Hering’s nerves to the
glossopharyngeal nerves"further transmitted to tractus solitarius in the
medulla"Vagus stimulated" reflex slowing of HR, dilatation of BV, fall in BP
[Fig 8.5]. The term “vagal inhibition” or “vasovagal inhibition” is a
misnomer, because it gives the impression that vagus is inhibited. The correct
term should be “vagal inhibition of the heart”; the vagus is actually stimulated
which in turn causes inhibition of heart. (ii) In normal persons – this process
causes minimal effects [. in HR of <6/min; . in BP of <10 mm Hg]. But in
sensitive persons it may cause sudden death.
VIII. SUDDEN AND UNEXPECTED DEATH

Sudden and unexpected death is death occurring within 24 hours of the onset of
symptoms in an individual who was not known to be suffering from any disease,
injury or poisoning.

A. Sudden Unexplained Death Syndrome [SUDS]

Sudden unexpected death syndrome [SUDS], or Sudden unexpected nocturnal
death syndrome (SUNDS) is a specific name given only to sudden unexpected
death of adolescents and adults during sleep.

1. Cardiovascular system
Diseases of the CVA are the leading cause of death in men between 20 and 65
years of age.
a. Coronary artery disease
About 80% of CVS deaths are due to coronary artery disease.
b. Other CVS causes
(1) Aortic Dissection (2) Cardiomyopathies (3) Coronary Artery Anomalies (4)
Coronary Artery Spasm (5) conducting system disorders (6) Dissecting
Coronary Aneurysm (7) endocarditis (acute) (8) Takotsubo Cardiomyopathy
(TTC)

2. Respiratory system
(1) Acute edema of glottis (2) Acute edema of lungs (3) Air embolism

3. CNS
Most common CNS causes of sudden death are (1) epilepsy (2) nontraumatic
subarachnoid hemorrhage (3) intracerebral hemorrhage (4) meningitis, and (5)
tumors. Occasional rare lesions such as (6) cysticercosis may also be
responsible.

4. GIT
Main causes are: (1) Acute hemorrhagic pancreatitis (2) Appendicitis (3) Cancer
of esophagus (4) Enlarged spleen [rupture].
 9. Signs of Death and Changes
Following Death

I. SIGNS OF DEATH AND CHANGES FOLLOWING DEATH

Signs of death appear in the following order:

(I) Immediate:
(1) Insensibility and loss of voluntary power
(2) Cessation of respiration
(3) Cessation of circulation
(II) Early:
(1) Changes in the skin
(2) Changes in the eye
(3) Supravital reaction of the skeletal muscles
(4) Cooling of the body (Algor mortis)
(5) Postmortem lividity (Livor mortis)
(6) Changes in the muscles (Rigor mortis, RM)
(III) Late:
(1) Decomposition (combination of autolysis and putrefaction)
(2) Modifications of putrefaction (adipocere, mummification).

II. IMMEDIATE CHANGES

Bichat’s concept of tripod of life was based on first three changes.

A. Insensibility and Loss of Movement [Cessation of CNS

Function]
This sign is due to loss of brain activity. Earliest sign of death, but not an
infallible sign. May be seen during life also under following conditions: (1)
Catalepsy (2) electrocution (3) Epilepsy (4) Fainting attack (5) Narcosis (6)
Trance (7) Vagal inhibition. Loss of brain activity is better determined by brain
stem reflexes and EEG.

B. Cessation of Respiration
Respiration ceases immediately after death. Can be checked by stethoscope
(unreliable). Respiration stops for very short periods without death in following
conditions: (1) Drowning (2) Drug-induced (e.g. opiate toxicity) (3) Obstructive
sleep apnea [OSA] (4) Preterm infants [immaturity of CNS] (5) Voluntary act.

C. Cessation of Circulation
Circulation ceases immediately after death. Can be checked by stethoscope
(unreliable) or ECG [please. see ch 8 for earlier tests for circulation].

III. EARLY CHANGES

A. Changes in the Skin

Skin becomes ashy-white, pale and loses elasticity, within a few minutes of
death. Lips are dry, brownish and hard due to drying.

B. Changes in the Eye

1. Loss of corneal reflex

Loss of corneal reflex is one of the 5 Minnesota criteria of brain stem death
(please see previous chapter for details).

2. Opacity of the cornea

(1) Cornea becomes opaque about 6 hours after death (this is the time period up
to which cornea can be harvested for corneal transplantation).
(2) If the eyelids remain open after death, desiccation of sclera occurs giving rise
to somewhat triangular shaped discolored areas [Taché noire de la sclérotique
(French for “black spots of the sclera”) or simply Tache noire (black spots)].
 These are yellowish in color in the beginning, but as dust settles in, they
become dark red (Fig 9.1) or later even black. Sometimes they may be bright
red, giving rise to an artifactual appearance of subconjunctival hemorrhages.
The eyes look sunken and are softer after death due to fall of Intraocular
Pressure (IOP). Normal IOP during life is between 10 to 20 mm Hg [Average –
15 mm]. One hour after death, it is 12 mm Hg; after 2 h, 10 mm Hg; after 3 h,
8.5 mm Hg; after 4 h, 7.5 mm Hg and after 8 hours, 5 mm Hg.1 Measurement
of IOP can thus give a rough estimate of the pm interval [PMI].
Memory Aid 1: IOP after death [in mm Hg]
IOP figures after death are same as figures for circumferences of heart valves. Pl see mnemonic for heart
valves in Appendix [weights and measurements of organs]

Value IOP [in mm Hg] Circumference of heart valve [in cm]

15 At death -

12 After 1 hour Tricuspid

10 After 2 hours Mitral

8.5 After 3 hours Pulmonary

7.5 After 4 hours Aortic

5 After 8 hours -
3. Pupils
Normal pupil size during life is between 1-8 mm. No appreciable change in
pupil size occurs after death. Pupils react to atropine and pilocarpine, for about 2
hours after death (till molecular death occurs). If pressure is applied by fingers
on two or more sides of the eyeball, the pupil may become oval, triangular or
polygonal.

4. Retinal vessels
(1) Segmentation of the retinal blood columns – Occurs immediately after
death. On ophthalmoscopic examination:
(i) the continuous blood column in the retinal blood vessels breaks up into small
segments, which then collide with each other (Kevorkian sign, railroading,
trucking or cattle trucking).
(2) Color of retina – Retina becomes pale after death, and becomes more and
more pale as time of death -es. Disk outline becomes hazy after a few hours.
5. Biochemical changes
During life, K+ concentration is low in the vitreous humor but much higher in
peripheral tissues such as retina. After death K+ from peripheral tissues starts
diffusing in the vitreous raising its concentration.

C. Cooling of the Body (Algor mortis)

Cooling of the body [Algor mortis (L. Algor, cold; mortis, death), chill of death]
occurs after death since all metabolism comes to a stop.
Salient features:
(1) Transfer - During life heat is constantly transferred from one body part to
 other by conduction as well as convection [through flow of blood]. After death
this occurs only through conduction, as blood flow stops.
(2) Heat production - There is some production of heat during initial period
after somatic death due to two mechanisms: (i) ATP molecules breaking down
[up to 2 h only] (ii) Anaerobic glycolysis [much longer]. Because of this,
rectal temp falls little or not at all during first 2 hours.
(3) Cooling – occurs from the surface of the body to the surroundings. It occurs
due to temp difference between the body and surroundings [air, water etc]. If
the temperature of surroundings is higher, the body temp may actually rise.
(4) Core temp: (i) Core temperature is the temp of the viscera. It is slightly -er
as compared to surface temp of the body. (ii) Core temp is a better guide to
TSD than surface temp.
(5) Ambient temperature – Human body rarely reaches the ambient
atmospheric temperature unless the latter is at or near freezing point. This is
because of the heat released due to enzymatic and bacterial actions on the
body.
(6) Site to take temp from: (i) Rectal - Best method.
(7) Method of recording temp: (i) By touching – Quick, but not accurate. Can
only tell if death occurred recently [body warm] or not [body cold] (ii) Lab
thermometer – 25 cm long, with a range from 0-50°C, inserted 10 cm above
the anus. Left there for 2 min. (iii) Thermocouple – A small electronic
thermocouple with a digital readout
(8) Things to be recorded: (i) temp of body (ii) temp of environment (iii) Time
of recording
(9) Number of recordings - at least 5 at half hour intervals, so rate of fall may be
obtained.
(10) Calculation of TSD:

(i) TSD [in hours] =

Rectal Temp at the time of death–Rectal Temp at the time body was found
Rate of Temp Fall

When death is not due to hypothermia, hyperthermia etc, rectal temp at the time
of death may be taken as 98.4°F. The formula thus becomes
98.4°F Rectal Temp at the time body was found
Rate of Temp Fall
(ii) Average rate of fall - (a) during summers - 0.75°F/h (b) during winters -
1.5°F/h.

1. Factors affecting rate of cooling

(1) Environmental temp – When the environmental temp is low (winters) heat
loss is faster and vice-versa.
(2) Build:
(i) Rate of heat loss is directly proportional to the surface area/body wt
[SA/BW] ratio.
(ii) Children who have -SA/BW ratio, lose heat faster.
(iii) Lean and thin adults lost heat faster than fat adults
(3) Physique – Fat bodies cool slowly; lean bodies faster. Because fat is a bad
conductor of heat.
(4) Environment:
(i) Air - (a) Well ventilated room – cooling faster than in a closed room (b)
Humid atmosphere – cooling faster than in dry atmosphere
(ii) Water - (a) Body immersed in cold water - cools faster (b) Running water -
Cooling faster than in stagnant water (c) Water containing sewage effluent
or other putrefying organic matter - Cooling slower than in fresh water
(5) Position of body – Cooling faster in bodies lying spread-eagled, than in
crouched positions. In the former more surface area is exposed to environment
(6) Covering – if body clothed, cooling is slower. Heavier the clothing, slower
the cooling.

2. MLI of algor mortis

Helps to estimate TSD.

3. PM caloricity
PM caloricity is a condition when the temperature of body -es after death instead
of .ing.
Salient features:
Conditions when it occurs: (i) Dead body is lying in the open in hot
summers – Most common (ii) Infections - like cholera, malaria, septicemia,
tetanus, typhoid etc.

D. Postmortem Lividity (Livor mortis)

Postmortem lividity (syn: cadaveric lividity, darkening of death, hypostasis,
livor mortis (L. Livor, blueness; mortis, death), livores, postmortem hypostasis,
postmortem lividity, Postmortem staining, subcutaneous hypostasis, suggillation)
is the (i) bluish-purple or purplish-red discoloration (ii) which appears after
death, (iii) on the most dependent parts of the skin (iv) due to collection of blood
in the capillaries and small veins (rete mucosum) of the most superficial layers
of the dermis (v) due to gravity [Fig 9.5].
Salient features:
(1) Cause: (i) Stoppage of circulation (ii) tendency of blood to sink by gravity to
the most dependent parts; its collection in toneless BV and capillaries (iii)
Backward flow – of venous blood to the capillaries from the venular end [adds
to the blueness of pm staining]
(2) Color: (i) Hue – Bluish purple, but may vary in different parts of the body
 (ii) Intensity – depends upon the amount of reduced Hb in the blood. Large
amounts of reduced Hb produce deep purplish coloration (iii) Portions drained
of blood – become correspondingly pale (iv) may depend on cause of death
[Table 1].
(3) Place: (i) In general – well marked in lobes of ears and in tissues underneath
fingernails (ii) back of chest and abdomen in supine position. Most common
(iii) front of chest and abdomen in prone position; (iv) lower legs and hands in
hanging (v) Face in drowning [in drowning, face is the most dependent part].
On the contrary, antigravity regions of the body are drained of blood and
become pale.
(4) Visibility: (i) More clearly seen in (a) fair skinned people (b) young having
good nutrition and normal hemogram (ii) Less clearly appreciated in (a) dark
colored people (b) old, anemic persons
(5) PM staining and congestion: (i) True congestion - Table 2. (ii) Hypostatic
congestion – may occur even a few hours before death in persons dying
slowly with circulatory failure, eg asphyxia, CCF, cholera, coma [deep],
poisonings.
1. Development

a. Time period
i. 0.5-2 hours
Appears as mottled patches.
(1) These are discolored patches of about 1-2 cm diameter, which can be
mistaken for bruises [please see ch 12 for differences].
(2) These patches are initially seen on the upper surfaces of the body, especially
the legs due to uneven dilatation of vascular bed. The areas then combine,
enlarge and slide down to produce extensive discoloration on dependent parts.
(3) Plasma also accumulates. Good culture media for bacteria; contributes to the
cutaneous blisters of early putrefaction.
(4) The time period may be more than normal in anemia and cachexia [1-4 h]
and less than normal [few minutes] in persons dying of circulatory failure
[because of an already developed hypostatic congestion].
ii. 4 h
Well developed like a sheet but not fixed.
iii. 8 h
Fixation occurs in 8 h [range 6-12 h].
(1) Fixation means that if the body is turned over to a different position, the pm
staining would not disappear.
(2) Causes:
(i) Clotting of blood within capillaries [ch 5]
(ii) By 8 h, capillaries become permeable"blood leaks through them "stains
tissues
(iii) Plain fluid also leaks causing hemoconcentration "tends to keep blood in
same location
(iv) rigor mortis of muscles occurs around capillaries "doesn’t allow the blood to
move away.
iv. >8 h
Persists till putrefaction sets in.

b. Influencing factors

(1) Vol of blood – in circulation at the time of death

(2) Length of time blood remains fluid after death
(3) More marked in conditions where blood does not readily coagulate, causing
more accumulation to occur. The conditions are:
(i) Amniotic fluid embolism [hypofibrinogenemia]
(ii) Anticoagulants
(iii) Asphyxia
(iv) CO poisoning
(v) Puerperal sepsis
(vi) Retained abortion
(vii) Septicemia.
2. Distribution
Depends upon following factors:

a. Pressure
Any kind of pressure prevents capillaries from filling up. This can be: Pressure
by body parts – Pressure of one body area pressing another, eg upper arm
pinned beneath the back of the body. Areas of body mutually pressing each other
would be pale [mirror image blanching].

b. Position of body
i. Body lying on back [supine]
(1) first appears on neck, then spreads over the entire back extending up to the
flanks and sides of the neck. Blotchy areas may appear on the upper surface of
limbs
(2) Not seen in pressure areas [contact pallor]:
(i) occipital region
(ii) shoulder blades [typically “butterfly-like”; Fig 9.5]
(iii) buttocks
(iv) posterior aspects of thighs
(v) calves and
(vi) heels.
ii. Body lying on face [prone]
(1) Looseness of connective tissue - Because the connective tissues in front are
relatively loose [as compared to those at back] following special appearances
are seen
(i) Color of lividity - intense
(ii) Ecchymosis, petechiae, Tardieu’s spots - common, especially in areas of
shoulders and chest. May be mistaken for asphyxial death
(iii) Cutaneous blisters - may develop on chest and abdomen containing blood
(2) Nose - Minute bv in nose may rupture "bleeding.
iii. Body lying on one side
Pm staining will be seen on one side, with opposite side completely pale.
iv. Suspended
Body suspended as in hanging "PM staining develops on dependent parts of
hands and legs, undersurface of chin, breasts, genitals and soles. If suspension
continues for several hours, petechial hemorrhages develop in these areas.

3. PM staining in poisoning
Give in Table 1. Additional points
(1) Bright pink – in hypothermia etc [at . temperatures Hb as a -er affinity for
O2] and bodies taken out from cold water [wet skin allows oxygen to pass
through]. The color is most marked over large joints.
(2) Chocolate color – is due to formation of methemoglobin, which is a form of
Hb where one or more Fe atoms are in a ferric state [Fe3+]. Caused by
oxidizing agents [Table 1].

4. Internal hypostasis
(1) In supine position – in
(i) cerebrum and cerebellum - posterior portions
(ii) Heart – dorsal portions. Simulates myocardial infarction
(iii) Intestines – lowermost coils. Simulates strangulation
(iv) Kidneys, larynx, liver, spleen – dorsal portions. Simulates congestion
(v) Lungs – dorsal portion. Simulates pneumonia
(vi) Stomach – posterior wall. Simulates congestion. Can be differentiated as
absent from anterior wall
(2) In prone position or other abnormal positions – depending upon the
position, the part which is most dependent develops hypostasis.

5. Changes
(1) With onset of putrefaction - capillary endothelium shows lytic
changes"blood diffuses into surrounding tissues"it undergoes secondary
changes [eg sulfhemoglobin formation]"area acquires greenish color"Thus
PM staining acquires a green color or mergers with the color of putrefaction.
(2) Microscopic – At this stage neither the cellular outlines nor the capillaries
are identifiable. Thus it is impossible to determine if the blood present locally
was intravascular [pm staining] or extravascular [contusion]. Both give the
same appearance.
(3) Advanced putrefaction - There is destruction of blood. Entire body acquires
a very dark black color. It is impossible to see any separate color due to PM
 staining"PM staining disappears.

6. ML importance [of PM lividity]

(1) It is a sign of death
(2) It must not be confused with bruise [for differences, please see ch 12 –
Mechanical injuries]
(3) Estimation of time since death
(4) Indicates the position of body after death
(5) Indicates movement of the body to another position, if it is done after pm
lividity has fixed in the earlier position
(6) Color may indicate cause of death.

E. Changes in the Muscles

After death, all muscles of the body (voluntary, involuntary and cardiac) pass
through 3 states (i) Primary relaxation [primary flaccidity] (ii) Rigor mortis
[RM] and (iii) Secondary relaxation [Secondary flaccidity].

1. Primary relaxation
Primary relaxation [or flaccidity] is complete relaxation of muscles in the
period immediately after somatic death [Table 4].
Salient features:
(1) Relaxation of skeletal muscle causes following changes (i) contact
flattening [flattening of muscles in contact with the surface, eg gluteal and
scapular muscles, when body is supine] (ii) Eyelids - lose tension (iii) Lower
jaw - falls (iv) joints become flexible
(2) Relaxation of involuntary muscle causes following changes (i) pyloric
sphincter – duodenal contents move up"bile staining of stomach walls (ii) anal
sphincter – emptying of rectum. (iii) bladder sphincter – emptying of bladder
(3) Persists - throughout supravital period [i.e. about 3 h]. All cellular functions
continue as in supravital period [ch 8].
(4) Muscle protoplasm – slightly alkaline.
2. Rigor mortis
Rigor mortis [L. rigor, stiffness; mortis, death] (syn cadaveric rigidity, death
stiffening, RM) is a state of stiffening of muscles, with very little shortening of
fibers, that occurs soon after death.
a. Mechanism
ATP molecules continue to deplete from the surface of myosin. When they are
completely consumed, “permanent”, irreversible cross-linkages form between
actin and myosin filaments (actinomyosin complex). There is no appreciable
shortening of sarcomere [Fig 9.7(3)]. During life muscle is alkaline [pH 7.3].
Since the pH of muscle reaches 5.8 (acidic), the rigor (produced under initial
conditions of abundant glycogen and ATP) is known as acid rigor.
b. Order of appearance of rigor
It appears in all muscles in this order: Cardiac muscle [1 h]"Involuntary
muscles"Voluntary muscles
c. Duration of RM
(1) Rigor mortis appears - in the entire body in 12 hours
(2) Persists – for another 12 hours
(3) Then disappears – in next 12 hours in the same proximodistal fashion in
which it appeared. The body is again relaxed in 36 h [secondary relaxation].

d. Conditions altering onset and duration of RM

All the following conditions can be easily explained on the basis of formation of
actinomyosin complex. If muscular ATP reserve was more at the time of death,
and its consumption slower after death, it would take longer to deplete and RM
would develop late, and vice-versa.
i. Age
(1) Rigor mortis appears in all ages, even in fetuses. It is wrongly taught
sometimes that RM does not appear in fetuses <7 m. It is not true. Author has
seen hundreds of fetuses below this age with well-developed RM. As long as
there is muscle, the actinomyosin complex would form, and RM would set in.
Muscles in a fetus begin to form at 8 weeks. A fetus <8 weeks may not show
RM simply because he does not have muscle. The rigor mortis is decidedly
weak in young fetuses, and probably some authors confused a weak RM with
no RM.
(2) Stillborn fetuses at full term – would develop RM
(3) In children and old people – feeble; develops rapidly; passes away early
(4) Healthy adults – strong and well marked; develops slows; lasts longer; passes
away late.
ii. Nature of death
(1) RM sometimes absent in - septicemia
(2) RM appears early and passes away early [duration short] in
(i) Conditions causing great exhaustion and wasting -(a) bacterial infections [esp
gas gangrene, where putrefaction begins early] (b) cancer (c) cholera (d)
starvation (e) tuberculosis (f) typhoid
(ii) Death preceded by convulsions - (a) DDT (b) OP (c) Strychnine (d) Tetanus
(iii) Violent deaths - (a) Cut throat (b) Electrocution (c) Firearms (d) Lightning
(3) RM appears late and passes away late in: (i) Apoplexy (ii) Asphyxia (iii)
CO (iv) Hemorrhage [severe] (v) Neuromuscular disorders (vi) Perfusion with
normal saline (vii) Pneumonia.
iii. Muscular state
(1) Onset slow, duration long, strength substantial - Muscles healthy and were
at rest before death
(2) Onset slow, duration short, strength weak – emaciated, weak persons
(3) Onset rapid, duration short: (i) Convulsions (ii) Exercise [heavy and
violent] (iii) Exhaustion (iv) Fatigue (v) Running [excessive as to save from
assailant. Rigor appears (vi) quicker in legs than other body parts] (vii)
Strenuous work (viii) Struggle.
iv. Atmospheric conditions
(1) Onset slow, duration long – Cold dry weather
(2) Onset rapid, duration short – Hot weather.

e. MLI of RM
(1) It is a sign of death
(2) Helps in estimation of TSD to some extent
(3) It indicates position of body at the time of death. If for examples arms are in
rigidity extending up in air, it may indicate that they were initially resting on a
chair, which was subsequently moved away.

f. Conditions simulating RM
i. Heat stiffening
ii. Cold stiffening
iii. Chemical stiffening
iv. Gas stiffening
(1) In about 2-3 days after death, putrefactive gases collect in s/c tissues,
muscles and around joints to stiffen the joints [putrefactive rigor mortis].
(2) Both upper and lower limbs are abducted, flexed and rigid; hands are open
 and fingers wide apart.
(3) The rigidity persists till gases escape during advanced putrefaction.
(4) This condition is especially seen in bodies recovered from water.
v. Cadaveric spasm
Cadaveric spasm [syn cataleptic rigidity, instantaneous rigidity, instantaneous
rigor, postmortem spasm] is a rare condition, in which the muscles that were in
contraction at the moment of death, remain in contraction after death without
passing through the stage of primary relaxation.
Salient features:
(1) Predisposing conditions: (i) Cerebral hemorrhage (ii) CNS injuries [eg
Firearm wounds to the head] (iii) Convulsant poisons [eg strychnine] (iv)
Excitement (v) Exhaustion (vi) Fatigue (vii) Fear (viii) Pain [severe] (ix)
Sudden death
(2) Last action - of the person is preserved or “frozen” for several hours after
death
(3) Mechanism – Unclear. Some theories are (i) ATP depletion at time of death
– appears most attractive. Muscular contraction starts during last moments of
life, i.e. neuromuscular stimulation, but contraction is retained because of low
levels of ATP
(4) Muscles involved – usually a single group of voluntary muscles. Rarely
entire body as seen in soldiers shot in battle [battle-field rigidity].
(5) Cannot be simulated – eg by keeping the weapon in victim’s hands.
(6) Disappearance – occurs along with rigor mortis in other muscles
(7) MLI: (i) Differentiation between AM and PM drowning – by grass, weeds
[Fig 9.9], leaves etc found firmly grasped in hands (ii) Weapon [eg blade,
knife, pistol etc] gripped tightly in hand – strongly favors suicide. Attempts to
put weapon in victim’s hands after murdering him does not produce the same
tight grip (iii) Objects grasped in fist – of victim may give information about
the assailant, eg hair, pieces of cloth [eg piece of shirt pocket], buttons etc.

3. Secondary relaxation
Secondary relaxation [or flaccidity] is complete relaxation of muscles after rigor
mortis has passed away [Table 4].
Salient features:
(1) Mechanism - 3 theories (i) Action on muscles of alkaline liquids produced
 by putrefaction (ii) Excessive acid produced during RM"Dissolution of
myosin (iii) Autodigestion
(2) Secondary relaxation in heart – may mimic pathologic dilatation, or
myocardial degeneration. Because of RM and secondary relaxation appearing
in heart, it is not possible to opine if heart stopped in systole or diastole.
IV. LATE CHANGES

A. Decomposition
Decomposition involves two processes: (i) Autolysis and (ii) Putrefaction.
1. Autolysis
Autolysis is the breakdown of cells and organs through an aseptic chemical
process caused by intracellular enzymes.
(1) Cause - Soon after death cell membranes break down with release of
cytoplasm containing enzymes (glycolytic, proteolytic, lipolytic) . The
enzymes autodigest the tissues even in the absence of bacteria
(2) Modification - Since it is a chemical process, it is accelerated by heat and
slowed by cold.
(3) Sequence - Organs rich in enzymes (glandular tissue) will undergo autolysis
faster than organs with lesser amounts of enzyme (eg, pancreas autolyses
earlier than heart and spleen)
(4) Dead fetus in utero – there is aseptic environment. Autolysis results in
maceration of fetus
(5) Gastric mucosa – Autolysis causes softening and rupture of stomach and
lower esophagus. In intracranial lesions, when the person lies comatosed for
long periods, this process may start even before death.

2. Putrefaction
Putrefaction is due to fermentation by bacteria. After death, the bacterial flora of
the GIT spread throughout the body, producing putrefaction.
Salient features:
(1) Commencement: (i) At Cellular level – Putrefaction begins immediately
after death at cellular level, but these changes are not visible grossly (ii)
Visible changes - (a) Putrefaction usually is visible externally after rigor
mortis (RM) has passed off. (b) In summers however, visible changes may
commence before RM has passed off completely.
(2) Cause: Bacterial enzymes derived mostly from anaerobic organisms from
the intestines (main is Cl. Welchii. Others are B. aerogenes, B.capsulatus, B.
coli, B. proteus, Staphylococci and Streptococci).

a. External phenomena
Chief external phenomena of putrefaction are (i) Color changes and (ii)
Development of foul smelling gases.
i. Color changes
Greenish discoloration of right iliac fossa (RIF) – This is the earliest sign of
putrefaction
(1) It is more clearly appreciated in fair skinned people than in the dark skinned
(2) Time - Occurs in 18 h in summer and 36 h in winter.
(3) Mechanism - Just below RIF lies cecum. It lies very superficially, its
contents are in a fluid state and full of bacteria. They migrate out and (a) break
up sulfur containing amino acids [cysteine, cystine and methionine] to form
H2S, which combines with Hb to form sulfhemoglobin (SulfHb), which is
greenish in color. (b) cause deamination of L-phenylalanine. Produce NH3 and
phenylpyruvic acid which combine with Fe3+ to form a green complex.
ii. Development of foul smelling compounds
(a) Chemical processes in putrefaction are those of reduction. Proteins and
carbohydrates are reduced to simpler compounds (amino acids, CH4, CO, CO2,
H2, H2S, mercaptans, NH3 and PH3). Many of these gases are inflammable, and
they can be ignited [these gases may give rise to preternatural combustion (Ch
14)].
(b) Foul smell – Foul smell from the cadaver is mainly due to the production of
ptomaines [syn, cadaveric alkaloids]. Most ptomaines are biologic amines
[low molecular wt compounds produced by bacteria through decarboxylation of
free amino acids, releasing CO2 in the process]. Two most common ptomaines
are cadaverine [NH2(CH2)5 NH2 produced by decarboxylation of lysine], and
putrescine [NH2(CH2)4 NH2; produced by decarboxylation of ornithine].
(c) Effects of gases: (1) Blisters – (i) Form because of collection of gases
between epidermis and dermis [postmortem blisters]. Fluids and liquid fat may
also be pushed in the blisters (ii) Must be differentiated from antemortem blisters
[ch 14]. (iii) Blisters form first on areas where tissues contain more plasma due
to hypostatic edema [back, lower surfaces of trunk, thighs] (iv) Time of
development: Summers-36 h, Winters-48 h. (2) Bloating of features [2-3 d] –
May be more marked when the head of the cadaver is in most dependent position
[accumulation of fluids]. Appearance quite similar to that of strangulation: (i)
Eyes – softened. May bulge from sockets (ii) Lips – swollen and discolored (iii)
Tongue – blackened and thrust between the teeth (iv) Face – swollen and
discolored. Identification becomes difficult or even impossible. In late stages,
face is transformed into a bulbous green mass. (3) Emptying of heart – Blood is
pushed out; blood for analysis not available in heart. (4) Expulsion of fetus
from uterus [postmortem delivery]– may be seen in pregnant women in 2-3 d.
Rigor mortis of uterus may be an additional reason. (5) Expulsion of urine and
feces – in 2-3 d. Due to formation of gas and relaxation of sphincters. (6)
Floatation of body in water – In drowned bodies, formation of gases cause the
body to come up and float [please also see ch 19 - Asphyxia]. (7) Postmortem
aspiration – Gases in the stomach force the food up in the throat, from where it
may fall into larynx. Differentiation from true antemortem aspiration – Food not
found beyond the bronchi in PM asp, while in AM asp, it will be found up to
terminal bronchioles. (8) Shifting of the position of PM staining [36-48 h] –
PM Staining displaced in any direction. Position of body immediately after death
can not be ascertained, if body seen at this stage. (9) Skin slippage: (i)
Epidermis becomes loosened, and separated (Fig 9.11). (ii) Skin of hands and
feet may come off in a “glove and stocking” fashion. (iii) Exposed subdermal
tissue dries giving a yellow parchment like appearance. Fingerprints can be
taken from skin deprived of epidermis [please see ch on identification]. (10)
Skull – Sutures of skull [especially of children] separated, with flowing out of
liquified brain [3-5 d] (11) Soft tissues become crepitant – Entire body swells
due to collection of gases in the tissues. If a suitable area, say, chest is pressed,
the crepitant collection of gases can be felt. Feels like a sponge. (12) Swelling of
entire body – May make even a thin body appear obese. (13) Microscopically –
Breakdown of vessel walls and cell membranes leads to water logging of tissues
with protein rich fluid. This helps in the growth of bacteria.
iii. Other changes
(1) Cornea – becomes white, flattened or compressed [12-18 h in summers; 1-2
d in winters]
(2) Fingertips –become leathery and wrinkled. Nails become prominent [36-48
hours]
(3) Fat – Body fat, especially omental and mesenteric liquefies into a translucent
yellow fluid.
(4) Loosening of appendages - Loosened and can be easily pulled out (i) Hair
[3d] (ii) Nails [4d] (iii) Teeth [5d]
(5) Postmortem luminescence - Body may start emanating light in the dark.
The light comes not from the body, but from luminescent bacteria
[Photobacterium fisherii] and fungi [Armillaria mellea].
(6) Fissures or splits – may form in skin. May simulate antemortem incised
wounds or lacerations.

iv. Appearance of maggots

(1) Maggots appear in 1-2 days. They have proteolytic enzymes and penetrate
the skin rapidly.
(2) This allows air to enter underneath the skin"More maggots enter body
 cavity"Activity of maggots may -body temperature to above that of normal
body temp.
(3) Decomposition and maggot activity -temp of body.
(4) May produce small round holes which may be confused with firearm
wounds.

b. Internal phenomena
Internally decomposition proceeds more slowly than at the surface.
(1) 36 h - Inner surfaces of vessels are discolored reddish brown, especially the
aorta. Due to Hb released from RBC, which stains the walls. This is the
earliest internal putrefactive change
(2) 36-48 hours:
(i) Clotted blood becomes fluid.
(ii) Fluid blood starts collecting in serous cavities. Such effusions are usually
less than 100 ml.
(3) 48-72 hours - Viscera are discolored dark red to greenish yellow, greenish
blue, greenish black and finally black. They are softer and greasier to touch
(4) 5-10 days:
(i) Colliquative putrefaction begins.
(ii) Abdomen – Bursts. Stomach and intestines protrude Thorax – bursts
especially in children.
(iii) Tissues – become loose and soft. Converted into a thick, semifluid, black
mass. Separated from bones and fall of
(iv) Body fat – especially mesenteric, omental and perirenal liquefies into a
translucent yellow fluid, which fills the abdominal cavity between organs.
Marked in obese people.
(v) Cartilages and ligaments – softened towards the final stages
(vi) Miscellaneous – in ruptured ectopic pregnancy, small fetuses may
completely disappear.

i. Order of putrefaction
(1) General rule - The softer the organ, the more blood it contains and the
nearer to sources of bacteria it is, the faster it putrefies
(2) In general, organs show putrefactive changes in the following order - (a)
Larynx and trachea (b) Brain of infants (c) Stomach, intestines (d) Spleen (e)
 Omentum and Mesentery (f) Liver (g) Adult Brain (h) Heart (i) Lungs (j)
Kidneys (k) Adrenals (l) bladder (m) Esophagus (n) Pancreas (o) Diaphragm
(p) Blood vessels (q) Gall bladder (r) Skin, muscle, tendons (s) Prostate, virgin
uterus (t) bones.
Memory Aid 2: Order of putrefaction
Large tree bird sits on liver. Adult bird has long kidneys, a bad Ependix and
big muscles.
Large tree - Larynx and trachea
b i rd - Brain [infants]
s i t s - Stomach, intestines Spleen
On - Omentum and Mesentery
Liver - Liver
Adult bird - Brain [adults]
Has - Heart
Long - Lungs
Kidneys - Kidneys
a - Adrenals
bad - Bladder
E pen di x - Esophagus Pancreas Diaphragm and
b i g - BV Gall bladder
muscles - Muscles.
NB - The last soft organs to putrefy are prostate in males and virgin uterus in
females. Bones are the last organs [including both soft and hard] to putrefy.
These facts are easily remembered on their own.
Liver
Timings are for summer. In winter same changes take twice the time
(1) Soft and flabby – 12-24 h
(2) Multiple blisters – 24-36 h
(3) Honeycomb liver [Fig 9.12]:
(i) Cl.welchii collect in tissue spaces in characteristic small clumps
(ii) Produce gas which soon -in size
(iii) Resulting lesions first appear as small, opaque, yellowish grey, dendritic
figures in parenchyma.
(iv) Later form bubbles making liver look like a honeycomb [foamy liver,
honeycomb liver, vesicular liver; Fig 9.12].
(4) Color:
(i) Initially greenish; later coal black
(ii) In early stages, discoloration is seen around the branches of portal vein
(5) Newborns - Liver putrefies earlier in newborn children than in adults
(6) Gall-bladder - putrefies much later than liver.

c. Skeletonization (last stage)

Skeletonization is the last stage of putrefaction, when the body is reduced to a
bare skeleton.
Salient features:
(1) Time required – varies considerably
(2) Body lying exposed in air – Carnivores [Dogs, Jackals, vultures], Flies and
their larvae [Maggots], Insects [Ants, Cockroaches] and Rodents [rats] reduce
the body to a skeleton within a few days
(3) Body in water – body attacked by aquatic animals [crabs, crustaceans, fishes
etc]. Clothing protects body from animals for long periods. In warm weather
 algae may deposit on exposed parts of body offering some protection against
aquatic animals.
(4) Buried bodies:
(i) Factors modifying rate of skeletonization (a) Access to air (b) Acidity of soil
and soil water (c) Amount of soil water (d) Climatic and seasonal variation
(ii) Bodies buried without coffins - (a) in shallow grave – Putrefaction delayed to
a moderate extent (b) in deep grave – Decomposition is markedly delayed
[due to .temp, exclusion of air, absence of animal life]. (c) Mass burials in a
common grave - Bodies lying in the center of grave are better preserved
than those at the periphery (d) Average time period for complete
skeletonization in a buried body in India – 1 y
(iii) Bodies buried with coffins - (a) If coffin is of good quality and airtight –
disintegration does not complete till several decades (b) Poor quality coffin
which admits air and water – bodies may decompose within months
(5) Bones lying on surface – As proteinaceous portion decomposes, the bones
are reduced to just calcium, which then crumble. Bones which decompose
faster – flat bones, bones of infants and old.
(6) Buried bones – decay according to acidity of soil. Neutral soil does not
destroy bones. Acidic soil causes decay in 25-100 y depending upon acidity.

B. Conditions Affecting the Rate of Putrefaction

1. External

a. Air
(1) In normal conditions – unbroken skin acts as an impermeable barrier to
bacteria
(2) Free access to air"hastens putrefaction [air conveys organisms to the body].
(3) Moist air"hastens putrefaction.
b. Clothing
(1) Loose clothing:
(i) Initially - -putrefaction [because body temperature is maintained and is not
allowed to fall]
(ii) Later - .putrefaction [because access of airborne organisms, flies, insects etc
is prevented]
(2) Tight clothing – includes belts, boots, socks, suspenders and undergarments
[tight fitting]
(i) Initial and late stages both - .putrefaction [tissues compressed"blood driven
out"organisms do not find medium to grow]. Also access to organisms is
prevented as above.
c. Manner of burial
Putrefaction is less: (i) Body buried soon after death (ii) Buried in dry soil (iii)
buried in sandy soil (iv) Buried in lime.
d. Moisture
(1) Moisture is necessary for putrefaction
(2) Conditions associated with -ed moisture -the rate of putrefaction: (i)
anasarca (ii) bodies recovered from water (iii) Organs which contain more
water putrefy faster.
e. Temperature
(1) Putrefaction begins at"10°C.
(2) Temp increase of 10°C"doubles the rate of all chemical reactions, including
putrefaction
(3) Season – rate of putrefaction is twice in summer as in winter.
(4) Putrefaction is optimum between"21°C-38°C.
(5) Putrefaction is arrested"<0°C and at >48°C.
(6) Dead bodies are best preserved at"4°C.

2. Internal

a. Age
(1) Newborns:
(i) If unfed – slow, because body is sterile
(ii) If fed – fast
(iii) If IV drips etc were given – fast, because bacteria can enter quickly through
punctures
(2) Bodies of children putrefy faster than those of older people [less water
content].
b. Sex
No effect on putrefaction.
c. Condition of the body
Fat and flabby bodies putrefy faster [-fat and fluid, -er retention of heat].
d. Cause of death
(1) Putrefaction is rapid in deaths due to: (i) Anasarca [generalized] (ii)
Asphyxia (iii) Inflammatory conditions (iv) Peritonitis and (v) epticemia
(2) Putrefaction is delayed in deaths due to: (i) Anemia (ii) Debility and (iii)
Wasting diseases. (iv) Poisons which either have preservative action on tissues
or a destructive [or inhibitory] action on bacteria or both.

i. Poisons which delay putrefaction

(1) Carbolic acid
(2) Heavy metal poisoning [chronic], especially arsenic
(3) Strychnine [if death occurred following a few seizures]
(4) Zinc chloride. These should not be confused with poisons which resist
putrefaction [i.e. which are not destroyed by putrefaction; can be detected
even in putrefied bodies].
ii. Poisons which resist putrefaction
(1) Barbiturates [ch 40] (2) Corrosives (3) Cyanide (4) Datura (5) KCN (6)
Metals (7) Nicotine (8) Pancuronium [Pavulon] (9) organophospnates (10)
Phosphorus (11) strychnine. Heavy metals and strychnine both delay and resist
putrefaction. Cyanide both appears after and resists putrefaction.
iii. Poisons which are destroyed by putrefaction
(1) Aconitine (2) morphine (3) succinylcholine.
Memory Aid 3: Poisons which are destroyed by putrefaction
Destroy is same as SMASH
S - Succinylcholine
M - Morphine
A - Aconitine
iv. Poisons which hasten putrefaction
(1) Chronic alcoholism
(2) H2S
(3) Strychnine [if death occurred after prolonged and repeated seizures"-heat
production].
v. Poisons which appear due to putrefaction
(1) Alcohol - Bacterial and fungal fermentation yields ethyl alcohol, which may
vitiate the interpretation of postmortem alcohol concentration. Levels of alcohol
produced by putrefaction are almost always <200 mg%. (2) CO [ch 44] (3)
cyanide (4) Ptomaines (5) Substituted phenols, especially p-hydroxy phenyl
derivatives.
Memory Aid 4: Poisons which appear due to putrefaction
APPEAR
A – Alcohol
P – Ptomaines
P – Phenols [substituted]
3C – Carbolic, CO, CN

e. Mutilation
(1) Mutilated bodies, or bodies with excessive wounds "Rapid putrefaction [(i)
organisms gain easy access]
(2) Dismemberment"Putrefaction of limbs is slower than that of trunk [(i)
Blood drains out of limbs (ii) intestinal organisms cannot gain access].

C. Casper’s Dictum
Casper’s dictum [syn Casper’s law, Casper Regel, Casper’s Rule] states that the
time taken for same amount of putrefaction to occur when the body is in air,
water and buried in earth is in the ratio of 1:2:8. Putrefaction occurs fastest in air
and slowest in earth.
Memory Aid 5: Casper’s Dictum
AWE (Air, Water, Earth)

D. ML Aspects of Putrefaction
(1) Time of death - can be ascertained
(2) Cause of death – becomes difficult to ascertain, except in cases of Firearm
injuries, fractures, drowning and Poisoning. Hair, teeth and bones resist
putrefaction and several poisons [esp metals] can be detected in hair and
bones. Several poisons resist putrefaction [please see list above]. Diatoms
may be demonstrated in bones.
(3) Infanticide - level of diaphragm may spuriously be altered by gases of
decomposition [ch 27].
(4) Poisons:
(i) can hasten or delay putrefaction,
(ii) can resist putrefaction and
(iii) may destroy during putrefaction
(iv) may appear after putrefaction [defense lawyer may argue that the poisons
appeared due to putrefaction]. These lists are given above.
(5) Raygat’s test - May be vitiated by putrefaction [ch 27].

E. Modifications of Putrefaction

1. Adipocere
Adipocere (Latin adipo fat, cera wax) is a modification of putrefaction in which
a friable, crumbly, water insoluble grayish-white to brown wax-like material is
produced in the dead body by the breakdown and conversion of body fats to fatty
acids (FA), mainly oleic, palmitic, and stearic acids.
Salient features:
(1) Nomenclature - Adipocere is also known as corpse wax, grave wax or
mortuary wax.
(2) Areas where formed [Distribution]:
(i) It is most prominently formed in areas where fat is excessive [face, cheeks,
breasts, abdomen, buttocks].
(ii) Limbs, chest wall and other parts of the body are less commonly affected.
(iii) Can occur wherever fat is present.
(iv) Rarely entire body be converted into adipocere.
(v) Internal adipocere – Starts earlier, because body’s own water is used. Fatty
tissue present between individual fibres of (a) Skeletal muscle - Small
muscles are dehydrated, very thin and acquire a uniformly grayish color.
Large muscles show a pinkish or reddish color in depths. (b) nerves and (c)
Myocardium. Fat in the substance of (d) liver [especially if fatty liver] –
Retains its shape (e) kidneys (f) other internal organs. Adipocere then forms
a matrix for remnants of tissue fibres, nerves and muscles. Grossly the
organs retain their shape; histologically only cell outlines can be made out.
(g) Lungs and intestines – thin, parchment like (h) May rarely form in the
fat of bone marrow in fractured bones
(vi) Skin – As adipocere forms, (a) epidermis disappears due to decomposition
and shedding (b) Dermis becomes darkened (c) Multiple whitish-grey,
rounded outgrowths [1-10 mm in diameter], resembling moulds, are seen on
 the surface. (d) These are protruding clusters of crystals from underlying
adipocere
(3) Conditions required: (i) Hot and humid environment.

2. Mummification
Mummification is a modification of putrefaction in which the skin becomes
brittle, contracted, dried, firm, leathery tough, parchment like, shrunken and
wrinkled, turning yellow-brown to black in color. [from Latin mumia, bitumen;
because of the blackened skin, bitumen was once thought to be used by
Egyptians to produce mummies].
Salient features:
(1) Conditions required: (i) Hot and dry environments, eg air heated buildings,
deserts. Hot environment helps evaporate water away from the corpse, making
it desiccated and dry (ii) enclosure in warm and dry environments – unwanted
newborn children have been killed and hidden in trunks and kitchen
cupboards, where their mummified bodies are recovered a few years later.
(2) Internal organs: (i) Consistency - Hard and shrunken. May adhere together
to form a single mass. Individual organs may lose their identity and disappear
(ii) Color"Dark brown and black
(3) Entire body: (i) loses wt, becomes brittle, stiff and thin (ii) emits no foul
smell (iii) if unprotected – gradually breaks into fragments, becomes powdery
and disintegrates. May also be attacked by flies, insects, larvae and moths (iv)
if protected [as by wrapping in bandages (done by Egyptians)] – preserved for
centuries
(4) Histologically demonstrable tissue are (i) Cartilage and bone (ii) Collagen
(iii) Elastic tissue and (iv) Muscle [cardiac and skeletal]
(5) Partial mummification: (i) occurs in some cases, with only some parts [eg
head, limbs, trunk] mummified and others not. (ii) Occasionally some parts
show mummification [arms and legs], while others adipocere [cheeks,
abdomen, buttocks]
(6) Medicolegal Importance: (i) Identification - Features are relatively well
preserved (ii) Determination of cause of death is possible – Because injuries
are preserved. (iii) Time and place of death - can be ascertained. Time
required is same as that of adipocere formation.
V. EMBALMING

Memory Aid 6: Composition of a typical embalming fluid

PG Bounced a WAD in VP’s Mouth
1. Preservatives – FM [Formaldehyde, Methanol]
2. Germicides – BGP (similar sounding to BJP) [Benzalkonium chloride, Glutaraldehyde, Phenol]
3. Buffers
4. Wetting agents – WiGS [Glycerine, glycols; sodium lauryl sulphate, sorbitol]
5. Anticoagulants
6. Dyes – T A PE R - Toluidine red, Acid fuchsin, amaranth, erythrosine, rhodamine, rose Bengal
7. Vehicle
8. Perfuming agents – LOCUM – Lavender, Oil of cloves, Cinnamon oil, Menthol, Methyl salicylate
9. Muscle relaxants – MgCl2

VI. ESTIMATION OF PM INTERVAL (PMI)

[A] Postmortem interval (PMI) or time since death (TSD) is the time period
between death and examination of the body. It is important because of following
reasons: (i) credibility of suspect - one can check the credibility of a suspect’s
statement (ii) Moment of crime - It informs when the crime was committed (iii)
Vital leads to the police - It gives police a vital lead and a starting point for their
enquiries (iv) Exclude suspects – if a suspect was not in the city during the time
of death, he can be excluded (v) checks alibi – It can confirm or disprove an
alibi. [B] Importance of PMI - Determination of PMI is important both in
criminal and civil cases. In criminal cases it is important to catch the killer; in
civil cases, it may become important in deciding (i) who inherits the property
(please see the example under the heading “commorientes” below) and (ii)
whether at the time of death the insurance policy was in force. [C]
Determination of PMI: (i) Exact time of death can not be determined, except
in very rare cases, where the wrist watch of the victim stopped due to drowning,
the blow of a weapon or fall from height. In most cases, the enormous biological
and environmental variations make it very difficult (ii) The pathologist should
give a range of PMI rather than a fixed PMI. To estimate PMI one must make
use of immediate, early and late changes (as the case may be) as mentioned
above. In addition, one can make use of following parameters.

A. Electrical Contractility of Muscles

Can be used to calculate TSD up to first 2-3 h [supravital period. Please see ch
8].

B. Nasal Ciliary Motility

Nasal cilia maintain motility up to 18 h after death.

C. Food in the Stomach

(1) Average emptying time of stomach -approx 3 h [one feels hungry 3 h after
last meal]. Thus if the time of last meal is known, tsd can be calculated.
(2) State of digestion – of food inside stomach also indicates time of death.
(i) Digestion is an active antemortem process, which does not continue after
death. Although acids and enzymes are present, the peristaltic movements
necessary to churn food with them are absent.
(ii) Recognition of meal - If complete digestion has taken place [>4 h], nature of
food cannot be recognized. This generally happens when food has passed in
the intestine. As long as food is in stomach, it can generally be identified.
Identification of meals generally corroborates or negates the story of
witnesses, especially if the death was sudden.

D. Postmortem Chemistry [Thanatochemistry]

1. Blood
Carbohydrates:
(1) Glycogenolysis in liver"Glucose diffuses in nearby vascular channels "-ed
glucose [in vena cava and R side of ht]"Spurious pm diagnosis of diabetes
mellitus may be made.
(2) Right atrial blood is sampled, which contains glucose diffusing from
glycogenolysis in the liver
(3) Glycolysis in the PM period occurs at a rate of 12.8 mg/100 ml/h.
(4) However blood glucose levels are not useful as PMI indicator because of
several variables – Diabetes, cause of death [-glucose levels occur in asphyxia,
 CO poisoning, -ed Intracranial pressure].

2. CSF
About 15mL is removed through LP. Specimen of choice in child abuse cases
when eyes are to be examined histologically.
Carbohydrates:
(i) Glucose - .es very rapidly after death
(ii) Lactic acid - -es sharply and regularly up to 10 h. Thereafter continues to -,
but at a lower rate
(iii) Inositol – Normal level during life : 1.7±0.45 mg%. -es regularly after death,
with levels reaching up to 72 mg%.

3. Vitreous
Interpretation
Variation between two eyes may be up to 10%.
(1) Carbohydrates:
(i) Glucose – Normal vitreous glucose levels are approximately half the serum
levels. With -ing PMI, there is a consistent .in levels. Within 4-5 h, levels
are zero in non-diabetics.
(ii) Lactic acid – normal values are 80-160 mg%. After 20 h, they - to 210-260
mg%.
(2) Electrolytes:
(i) Potassium – Found to be most useful so far. During life, K+ concentration is
low in the vitreous humor [5.8 mmol/L] but much higher in peripheral
tissues such as retina. After death K+ from peripheral tissues [retinal cells
and vascular choroid] starts diffusing in the vitreous -ing its concentration.
This occurs in a linear fashion. Formulae most popular in this regard are:
(a) Time since death [in hours] = 7.14 # [K+]in mmol/l – 39.1 (Sturner’s
formula) (b) Time since death [in hours]= 5.26 # [K+]in mmol/l – 30.9
(Madea’s formula) (c) Time since death [in hours]= 4.32 # [K+]in mmol/l –
18.35 (James’ formula) (ii) Sodium – Normal levels are 2480-3500 mg/L
[or 118–154 mmol/L] Postmortem change is too insignificant to be of any
help.

4. Pericardial fluid
(1) More quantities [10-15 mL] can be obtained as opposed to 5mL of CSF and
1-2 mL of vitreous.
(2) Potassium - -es at an average rate of 0.30 mmol/h.
(3) Sodium -.es at a rate of 0.37 mmol/h in the first 85 h after death.
(4) Calcium – Doesn’t change appreciably after death.

5. Synovial fluid
Levels of sodium, potassium, calcium, chloride, urea, creatinine, and glucose in
synovial fluid show that they behave in the same way as in vitreous.

E. Hair
(1) Hair does not grow after death; yet it appears to have grown in dead
individuals. It is due to shrinkage of skin, which make the hair look taller.
(2) Time since death:
Fungal Growth - (a) Over 30 genera of fungi have been detected on hair after
death. (b) Order of succession - (I) Initial stage colonization - Hair is first
occupied by fungi with high competitive saprophytic ability able to rapidly
utilize the less complex nutrients [for hair composition, please see ch 3] (II)
Mid stage colonization - occupied by fungi with less competitive saprophytic
ability. Both initial and mid stage colonization is by non-keratinophilic fungi
(III) Last stage colonization - Keratinophilic fungi. Utilize keratin, the most
resistant part of hair.

F. Muscle Proteins and Enzymes

(1) Calcineurin A (CnA) - .es in skeletal muscle after death.
(2) Creatine phosphokinase (CPK) -.es after death
(3) Myofibrillar protease - -es after death
(4) Protein phosphatase 2A (PP2A) - -es after death in first 24 h.

G. Entomology of the Cadaver

Entomology is the scientific study of insects. Forensic entomology is the
application of insect biology for the purposes of law and administration of
justice. An important area of forensic entomology is estimation of time of death,
where the order of appearance of flies on dead body often indicates the probable
time of death.

H. The Scene of Death

(1) Cell phone records – Death must have occurred between last call attended
and first call unattended. Not foolproof, since unattended call may be
intentional and attended call may be by someone else.
(2) Milk bottles - Number of uncollected milk bottles at door step indicate
number of days person is dead. Useful if there was a lonely occupant living
in a house.
(3) Newspapers - Earliest newspaper uncollected at door step gives the possible
date of death. Death must have occurred one day previously. Disposal of body
parts wrapped in newspapers may indicate the day of death. Please see
 Ruxton case [ch 6].
(4) Stopped wrist watch – in cases of drowning, fall from height, blunt trauma
etc where weapon struck watch and stopped it, may rarely give exact time of
death. Firearm wounds of chest may stop a pocket watch exactly at the time of
death. Case study - The author was once involved in a case, where a person
was shot in the chest. He used to keep a pocket watch in the upper left hand
pocket of his vest. The bullet had scraped the watch before entering the chest.
The watch had stopped showing 8:47pm.
(5) Dates on uncollected mail
(6) Sales receipts and dated slips of paper in deceased’s pockets
(7) Statements from neighbors – when they last saw the deceased
(8) State of food on the table – fully completed, half eaten etc.
(9) State of dress – whether the person was in normal dress or night dress
(10) Corpse lying on grass – Look at grass underneath the corpse. The state of
drying, yellowness etc can indicate time of death.

VII. PRESUMPTION OF SURVIVORSHIP AND DEATH

[B] S.107 Indian Evidence Act – Presumption of survivorship - When the

question is whether a man is alive or dead, and it is shown that he was alive
within 30 years, the burden of proving that he is dead is on the person who
affirms it.
Memory Aid 7: S.107, IEA
Section hundred and seven [S.107, IEA] deals with survivorship

[C] S.108 Indian Evidence Act – Presumption of death - When the question is
whether a man is alive or dead, and it is proved that he has not been heard of for
7 years by those who would naturally have heard of him if he had been alive, the
burden of proving that he is alive is shifted to the person who affirms it.
1 Balci Y, Basmak H, Kocaturk BK, Sahin A, Ozdamar K. The importance of measuring intraocular
pressure using a tonometer in order to estimate the postmortem interval. Am J Forensic Med Pathol. 2010
Jun;31(2):151-5.

10. Artifacts

I. GENERAL

[A] An artifact [L. arte, by skill; factum, thing made] is (i) any change caused to
a body after death unintentionally and which is (ii) physiopathologically
unrelated to the natural state of the body tissues or to the disease process to
which the body was subjected to before death.

II. CLASSIFICATION
A. Artifacts Introduced Between Death and Autopsy
1. Agonal artifacts (produced just after death)
Regurgitation of gastric contents - in respiratory tract after death may be
confused with genuine antemortem aspiration.
2. Resuscitation artifacts
Injection marks
3. Artifacts due to handling of the body
Abrasions – Due to inept dragging of the body by the police from the scene of
crime to their vehicle for transportation.
4. Artifacts related to postmortem lividity
Prinsloo and Gordon artifact - Generally thought to be due to pm lividity, but
is actually due to “leakage” of blood outside the vessels. Described under the
heading “Postmortem hemorrhage”.

B. Artifacts Introduced During Autopsy

1. Air in blood vessels
Can be introduced by: pulling the dura in the sagittal line [air enters in bv at the
top of brain].
2. Skull fractures
Using chisel and hammer to open skull – May produce artificial fractures
[usually in the middle fossae], or may cause fractures already present to enlarge.
Presence of a blood streak within the fracture can sometimes help to differentiate
artifactual fractures.
3. Visceral damage
(1) Aorta – Descending aorta may show transverse intimal tears, if neck
structures are pulled too hard to eviscerate thoracic viscera. May cause tears of
neck structures also.
(2) Brain – rough handling during removal may produce tears of midbrain
(3) Liver – Rough handling during removal may produce tears of diaphragmatic
surface which resemble antemortem lacerations.
4. Extravasation of blood
Spurious air embolism – cutting of bv during autopsy" sucking of air in
circulation"may enter cerebral, coronary and other bv"appear like a genuine
antemortem air embolism.
 11. Injuries: Classification and
Medicolegal Aspects

I. INTRODUCTION

A. Injury
1. Legal definition
Any harm whatever illegally caused to any person, in body, mind, reputation or
property (section 44 IPC). In general, it is violation of another’s rights for
which the law allows an action to recover damages. Ex - (i) “Z” inflicts burns
on “P’s” body. He has caused injury [harm to body] (ii) “Z” threatens “P” on
phone. He has caused injury [harm to mind] (iii) “Z” spreads false rumors that
“P’s” character is bad. He has caused injury [harm to reputation] (iv) “Z” burns
“P’s” car. He has caused injury [harm to property].
Memory Aid 1: Definition of Injury
BMR is an important concept of Physiology - Body, Mind, Reputation, Property
2. Medical definition
Damage inflicted on the body by an external force. Only the 1st part of legal
definition constitutes medical definition. For other significant terms which have
different medical and legal definitions, pl see ch 26.

B. Wound
A break in the natural continuity of any of the tissues of the living body.

C. Trauma
[from Gk traumata, “to wound”, “I injure”] A physical or psychological injury
[physical trauma, psychological trauma].

II. CLASSIFICATION OF INJURIES

A. Medical Classification
Doctors when communicating among themselves would refer to this
classification.
(1) Mechanical injuries - (a) Due to blunt force - (i)Abrasions (ii) Contusions
(iii) Lacerations (iv) Fractures and dislocations (b) Due to sharp force - (i)
Incised wounds (ii) Chop wounds (iii) Stab wounds (c) Firearms - Firearm
wounds
(2) Thermal injuries - (a) Due to cold - (i) With tissue freezing (I) Frostbite (II)
Frostnip (ii) Without tissue freezing (I)Trench foot (II) Chilblains (b) Due to
heat - (i) Burns (ii) Scalds
(3) Chemical injuries - (a) Due to corrosive acids (b) Due to corrosive alkalis
(c) Due to corrosive salts
(4) Physical agents - (a) Electricity - (i) High tension (ii) Low tension (b)
Lightning (c) X-rays (d) Radioactive substances
(5) Explosions.

B. Legal Classification
Courts would generally follow this classification.
1. Hurt
Hurt would fall u/s 319, IPC. Law does not mention the word “simple injury“
anywhere, and thus this term should best be avoided. By common usage, “simple
injury” is used as a synonym of hurt.
2. Grievous hurt
Grievous hurt would fall u/s 320, IPC. All injuries which are not simple are
grievous and vice-versa.

C. Medicolegal Classification
Doctor when advising the court would follow this classification.
1. Suicidal injuries
Hesitation cuts etc.
2. Homicidal injuries
Fatal wounds on head, chest, abdomen. Would not include non-fatal defense
wounds [ch 12].
3. Accidental injuries
4. Self inflicted injuries
Caused by self to mislead police (Fabricated injuries)
5. Defense wounds
Received by victim, mostly on his hands, during defense. Generally non fatal [ch
12].
6. Iatrogenic injuries
Surgical incisions, thoracotomy wounds etc.

III. HOMICIDE

Homicide is killing of a human being by another human being. It can be

classified according to the following scheme (Table 1).

A. Lawful
1. Justifiable homicide
Justifiable homicide is one in which the person committing it is at no fault in a
legal sense. It is commanded or authorized by law. Usually a legal officer is
involved who commits the homicide in order to carry out a perfectly legal
[justified] task.
2. Excusable homicide
Excusable homicide differs from justifiable homicide in that one who commits
an excusable homicide is at fault to some degree, but the degree of fault is not
enough to constitute a culpable homicide.
B. Unlawful
In unlawful homicide, the degrees of culpability (degrees of fault) would differ
in different cases.
1. Culpable homicide (S.299, IPC)
Culpable homicide is causing death by (1) doing an act with the intention of
causing death, or (2) with the intention of causing such bodily injury as is likely
to cause death, or (3) with the knowledge that he is likely by such act to cause
death, commits the offence of culpable homicide.
2. Murder (S.300, IPC)
Culpable homicide is murder (1) if the act by which the death is caused is done
with the intention of causing death, or (2) if it is done with the intention of
causing such bodily injury as the offender knows to be likely to cause the
death of the person to whom the harm is caused, or (3) if it is done with the
intention of causing bodily injury to any person and the bodily injury intended
to be inflicted is sufficient in the ordinary course of nature to cause death, or
(4) If the person committing the act knows that it is so imminently dangerous
that it must, in all probability, cause death or such bodily injury as is likely to
cause death, and commits such act without any excuse.

IV. LEGAL PROVISIONS REGARDING HOMICIDE, SUICIDE

AND RELATED ACTS

*"imp; **"v.imp

A. IPC
(1) S.299 IPC*"Definition of culpable homicide
(2) S.300, IPC*"Definition of murder
(3) S.301, IPC"Culpable homicide by causing death of person other than person
whose death was intended
(4) S.302, IPC*"Punishment for murder. Death or life imprisonment and fine.
Honor killing - An honor killing is the murder of a person by one or more
fellow family members when they believe the victim brought dishonor upon
the family. Victims are usually unmarried females who engage in lover affairs,
or marry someone from a different caste. These cases are tried u/s 302, IPC.
 Honor killings had been reported in Egypt, India, Iran, Jordan, Lebanon,
Morocco, Pakistan, Syrian Arab Republic, Turkey, Yemen, and other
Mediterranean and Gulf countries.
(5) S.303, IPC"Punishment for murder by life-convict. This is the only section in
the entire IPC, where only death has to be given. No fine.
(6) S.304, IPC*"Punishment for culpable homicide not amounting to murder
(imprisonment for life or fine or both)
(7) S.304A, IPC**"Causing death by negligence. 2 y, or fine, or both
(8) S.304B, IPC**"Dowry death. Punishment minimum 7 y. No fine.
(9) S.305, IPC"Abetment of suicide of child or insane person. Punishment death
or imprisonment for life and fine.
(10) S.306, IPC"Abetment of suicide. Punishment"10 y+fine
(11) S.307, IPC"Attempt to murder. Punishment"10 y+fine
(12) S.308, IPC"Attempt to commit culpable homicide. Punishment"3 y, or fine
or both (if hurt is not caused to the victim); 7 y, or fine or both (if hurt is not
caused to the victim)
(13) S.309, IPC*"Attempt to commit suicide. Punishment"1 y, or fine or both.
Salient features:
(i) This is the only section in the entire IPC, where a person cannot be
prosecuted if he is successful in his crime. (ii) Dyadic death (“pairs of death”)
is homicide followed by suicide or a double suicide pact (e.g. a pair of lovers
committing suicide together, because they were not allowed to marry. Other
reasons may be infidelity, jealousy, poverty, property disputes or
unemployment). (iii) Multiple methods of suicide – If a person is unable to
commit suicide by one method, he may resort to another method. At autopsy
evidences will be found of all attempts [e.g. a person consuming rat poison first.
When he finds he is still alive, he may slash his wrists, and finally jump out of
the window] (iv) Suicide attack – Human bomb in order to kill a large number
of persons. (v) Most common method of suicide – Varies from place to place,
and from culture to culture. In one South Indian study organophosphorous
poisoning was found to be the most commonly used method for suicide (25.4%).
(vi) Decriminalization of suicide – S.124 of the proposed Mental Health Care
Bill 2013 attempts to decriminalize suicide. It says “Notwithstanding anything
contained in section 309 of IPC, any person who attempts to commit suicide
shall be presumed, unless proved otherwise, to be suffering from mental illness
at the time of attempting suicide and shall not be liable to punishment under the
said section” [S.124(1)]. Furthermore it says, “The appropriate Government shall
have a duty to provide care, treatment and rehabilitation to a person, having
mental illness and who attempted to commit suicide, to reduce the risk of
recurrence of attempt to commit suicide.” [S.124(2)] However, pending the
passage of the Mental Health Care Bill 2013, S.309, IPC is yet to be limited or
repealed.

B. Other Acts
S.25, Hindu Succession Act, 1956 - A person who commits murder or abets the
commission of murder shall be disqualified from inheriting the property of the
person murdered, or any other property in furtherance of the succession to which
he or she committed or abetted the commission of the murder.

V. HURT (S.319, IPC)* *

Hurt means bodily pain, disease or infirmity caused to any person.

Memory Aid 2: Def inition of hurt
BiDI " Bodily pain, Disease, Infirmity

VI. GRIEVOUS HURT (S.320, IPC)* *

[A] Grievous hurt is hurt of a more serious nature. There are 8 clauses in the
definition of grievous hurt(GH). Clause 8 has further 3 sub clauses. (1)
Emasculation (2) Permanent privation of the sight of either eye (3) Permanent
privation of the hearing of either ear (4) Privation of any member or joint (5)
Destruction or permanent impairing of the powers of any member or joint (6)
Permanent disfiguration of the head or face (7) Fracture or dislocation of a bone
or tooth (8) Any hurt (i) which endangers life or (ii) which causes the sufferer to
be during the space of twenty days in severe bodily pain, or (iii) unable to follow
his ordinary pursuits.
Memory Aid 3: Def inition of Grievous hurt
E1very S2tudent H3 as re member4 ed I5njury’s D6efinition, but F7orgot it within 20days8 of
P8assing E8xaminations.

[B] Illustrations (1) Emasculation – Refers to taking away the masculine

power (i.e. penetrating power during intercourse) of male. This is the only clause
that applies only to males. (i) Cutting of penis - X cuts penis of Y"X has
emasculated Y"caused GH. (2) privation of the sight of either eye – Privation
means even partial loss of sight. Operative interference is not to be taken into
account. Ex. (i) Retinal detachment (ii) Gouging out eyes. (3) Permanent
privation of the hearing of either ear – Same examples and reasoning as
above, but w.r.t. ear. (i) Tympanic membrane - Teacher X slaps student Y"Y’s
tympanic membrane is ruptured and he cannot hear"X has caused GH (4)
Privation of any member or joint – A member is any part of the body, which is
capable of performing a distinct function, and/or is not able to regrow. Hands,
feet are members, but not nails and hairs. Blood is not a member, because it can
regenerate. For the same reason skin and body fluids (milk, saliva, tears, urine,
CSF, semen etc) are not members. (i) Nails - If nail is trimmed, it is not GH
(because it can regrow), but if avulsed from base, it is GH (because it cannot
regrow). (5) Destruction or permanent impairing of the powers of any
member or joint – This clause is attracted if privation is not caused to member
or joint (i.e. not amputated), but has been destroyed or permanently impaired (i)
X strikes a hammer on Y fingers, so that his fingers are reduced to pulp"GH (6)
Permanent disfiguration of the head or face – Ex (i) Abrasions v lacerations
– Abrasions of face are simple (as they heal without scarring); lacerations of face
are grievous (as they heal with scarring) (7) Fracture or dislocation of a bone
or tooth – Ex. (i) Cut on a bone is a fracture and thus GH. (viii) Dislocation of
shoulder – Grievous hurt, because dislocation of a bone occurs. It is also a rare
example of grievous hurt which can be corrected within minutes. (8) Any hurt
(i) which endangers life or (ii) which causes the sufferer to be during the
space of twenty days in severe bodily pain, or (iii) unable to follow his
ordinary pursuits.Exp – Any hurt which endangers life – Pointers [A] It is
an injury which has a 50% chance to end in fatality.

VII. DOWRY DEATHS

A. Legal Provisions Relating to Dowry Deaths

(1) S. 304B, IPC"Where the death of a woman is caused by any burns or bodily
injury or occurs otherwise than under normal circumstances (i) within seven
years of her marriage and (ii) it is shown that she was subjected to cruelty
or harassment by her husband or his relative for dowry, such death shall be
called “dowry death”, and such husband or relative shall be deemed to have
caused her death. Punishment is imprisonment minimum 7 years; maximum
life. There is no fine.
(2) S.498A, IPC"Treating a married woman with cruelty – If the woman’s
husband or any of his relatives treats her with cruelty, he/she will be
imprisoned for up to 3 years and will also be fined. Cruelty has been defined
as any willful conduct which is of such a nature as is likely to drive the
woman to commit suicide or to cause grave injury or danger to her life. It also
includes her harassment with a view to coerce her for dowry. Habitual
drunkenness by husband has been regarded as cruelty to woman (please see ch
40).

VIII. TORTURE

A. Definitions
[A] General Definition - Torture (Latin tortus, to twist) is infliction of intense
pain (e.g. from burning, crushing, wounding etc) to punish, coerce, or afford
sadistic pleasure. [B] Declaration of Tokyo (1975) - Torture is deliberate,
systematic or wanton infliction of physical or mental suffering by one or more
persons acting alone or on the orders of any authority, to force another person to
yield information, to make a confession, or for any other reason.
B. Methods

1. Physical torture
(1) Beating:
(i) Commonest form of torture
(ii) Instrument used – blunt instruments like belt, bicycle chains, lathi, metal or
wooden bar, whip etc.
(iii) Target and injuries produced - (a) Back [Most common] - abrasions,
contusions, lacerations are produced (b) Abdomen – rupture of viscera may
occur (c) Head – head injury, skull fractures, intracranial hemorrhages.
(iv) Detection (a) In the living - via ultrasound (b) In the dead- Bruising in the
back is not seen superficially because of thick fascial planes [same is true of
soles also – please see falanga below]. Deep dissection is necessary to
reveal bruising. Aseptic necrosis may be seen.
(2) Chepuwa - A Bhutanese torture technique. Both thighs or legs are tightly
clamped with bamboo for a number of days. The 2 sides of the clamps are
pressed with torturer’s legs or he may stand on the 2 sides of the clamps.
(3) Electric torture - Also called cattle prod. Types
(i) Picana: (a) victim is strapped to a wooden table and wetted to aid the flow of
current. (b) Current [DC, usually powered by an automobile battery] is
applied to sensitive parts of the body eg head, temples, eyes, mouth, teeth,
tongue, breasts, nipples and genitalia (c) a doctor is present to make sure
that the victim has no heart problems and can survive the interrogation (d)
Effects - May result in the loss or fracture of teeth.
(ii) La parrilla (metal grill): Electric shocks given while the victim is tied to a
metal bed frame.
(4) Falanga - [also known as bastinado, falaka, falaqa, foot whipping and
phalanga]
(i) Beating of the soles of the feet with canes or rods.
(ii) Favored by perpetrators, because (a) Extremely painful and debilitating
[there is clustering of nerve endings in the feet] (b) Foot being weight
bearing organ, injuries take long time to heal (c) leaves few physical marks
(iii) Detection – As in beating above. Dissection of soles may be necessary
(5) Force Feeding – of boiling water, mustard oil, pepper, saturated salt water,
 vinegar, urine and feces
(6) Forced standing:
(i) Types (a) standing on both feet (b) On one foot [could be in hot sun to
increase pain]
(ii) Called Planton in Latin America and stoika in the Soviet Union. An
attractive option for torturers because like water torture, it leaves no marks
(iii) Effects (a) Swelling of the ankles and feet to twice their size within 24 hours
(b) moving becomes agonizing (c) Development of large blisters (d)
Increasing of the heart rate and fainting.
(7) Knee capping - Victim is shot through the knee joint. Common in Northern
Ireland.
(8) Submarino:
(i) Dry submarino (submarino seco)-Near suffocation by pulling a plastic bag
[usually a shopping bag sometimes containing chillies and/or petrol] over
the head and face
(ii) Wet submarino (submarino mojado)-Face of the victim is forced under water
usually contaminated with excrement, urine, vomit or blood. Victim may
die of drowning. Feces [or other extraneous material] in lungs at autopsy.

2. Mental torture
(1) Blindfolding
(2) Deprivation techniques – Deprivation of sleep by use of continuous high
pitched sound. Deprivation of the use of toilet, clean habitable place, isolated
captivity [social deprivation]
(3) Mock execution - Victim is deliberately but falsely made to feel that his
execution or that of another person is imminent.
(4) Providing false information to victim – e.g. tragedy involving wife and
children
(5) confinement - in a dark place
(6) Threat of permanent, severe disfigurement to victim or his loved ones [e.g.
wife, children]
(7) Witness torture – Victim is forced to witness the torture of another person.

C. Medicolegal Aspects
Torture is punishable in Indian law under following sections (a) S.330, IPC -
Voluntarily causing hurt to extort confession, or to compel restoration of
property is punishable with imprisonment up to seven years, and also fine. (b)
S.331, IPC - Voluntarily causing grievous hurt to extort confession, or to compel
restoration of property is punishable with imprisonment up to ten years, and also
fine.

IX. CAUSES OF DEATHS FROM WOUNDS

A. Immediate Causes
1. Shock
Shock is a circulatory disturbance characterized by hypoperfusion of cells and
tissues, which in turn may be due to . in the vol of blood or cardiac output. In
wounds it is mainly due to hemorrhage, but also because of other causes.
a. Causes
i. Cardiogenic shock
(1) Due to myocardial failure".cardiac output.
(2) Myocardial failure in turn may be due to
(i) extrinsic compression [cardiac tamponade]
(ii) intrinsic myocardial damage [MI]
(iii) outflow obstruction [eg pulmonary embolism]
(iv) Pulmonary embolism
(v) ventricular arrhythmias
(vi) Ventricular rupture.
ii. Hypovolemic shock
Hypovolemic shock is due to loss of blood [eg massive hemorrhage] or plasma
volume [eg vomiting, diarrhea, severe burns (burn shock)].
Salient features:
(1) When it is due to excessive bleeding, it is known as hemorrhagic, traumatic
or wound shock. It is the most common cause of hypovolemic shock in
forensic practice.
(2) Bleeding diathesis – Victims with hemophilia or other bleeding diathesis may
succumb to relatively minor injuries
(3) Quantity of blood loss – may be approximately judged by observing (a)
scene of death – amount of blood lying around the victim
(4) Classification - It could be classified according to (a) etiology (b) source of
 bleeding (c) destination of bleeding (d) Time period of bleeding (e) Quantity
of blood loss.
Important points of each are as below:
(1) Etiology – (a) Traumatic – Due to wounds involving blood vessels, or
severe laceration of viscera (b) Spontaneous – Bleeding diathesis etc.
(2) Source of bleeding - (a) Cardiac (b) Arterial (c) venous (d) capillary
(3) Destination of bleeding - (a) External [outside the body] (b) Internal [within
the body].
(4) Time period of bleeding - (a) Primary hemorrhage - Occurs immediately
after injury (b) Secondary hemorrhage - Delayed for several hours (up to 24
hrs) after injury. Due to (i) -in BP, which accompanies recovery from shock
(ii) muscular movements, which loosen blood clots, and (iii) erosion and
sloughing of vessel walls due to infection [cf; ch 17"Primary and secondary
head inj and intracranial hemorrhages].
(5) Quantity of blood loss: (i) Sudden loss of blood is more dangerous that the
same quantity of loss occurring slowly. (ii) Measuring blood loss - (a) Clot of
a fist size – contains 400-500 ml.
iii. Septic shock
(1) Causes: (i) Overwhelming microbial infections [bacterial and fungal] (ii)
Superantigens [eg toxic shock syndrome]
(2) Vasodilation and peripheral pooling of blood occurs as part of a systemic
immune reaction to infection.
(3) Mechanism of death - is unclear; aside from -ed lymphocyte and enterocyte
apoptosis there is only minimal cell death, and patients rarely have refractory
hypotension.
(4) Septic shock due to Gram –ve infections are sometimes called endotoxic
shock.
iv. Less common causes
(1) Anaphylactic shock - denotes systemic vasodilation and -ed vascular
permeability caused by an IgE–mediated hypersensitivity reaction. Acute
widespread vasodilation results in tissue hypoperfusion and hypoxia.
(2) Neurogenic shock - anesthetic accident, spinal cord injury. Loss of vascular
tone occurs"peripheral pooling of blood.
(3) Surgical shock – Occurs during or immediately after surgical procedures.
Occurs due to combination of:
(i) anesthesia
(ii) loss of blood and plasma
(iii) infections
(iv) emotional factors
(v) liberation of substances from severely traumatized tissues.

b. Stages of shock
(1) If the injury is massive (eg a massive hemorrhage from a ruptured aortic
aneurysm), death is immediate.
(2) In all other cases, shock evolves through three general stages:
(i) Initial nonprogressive stage- Reflex compensatory mechanisms are
activated and perfusion of vital organs is maintained
(ii) Progressive stage - characterized by tissue hypoperfusion and onset of
worsening circulatory and metabolic imbalances, including acidosis
(iii) Irreversible stage - sets in after the body has incurred cellular and tissue
injury so severe that even if the hemodynamic defects are corrected,
survival is not possible.

c. PM appearances
i. General
(1) Circulatory changes:
(i) Congestion of all internal organs
(ii) Edema of viscera
(iii) Petechial hemorrhages in serous membranes
(2) Degeneration and necrosis - of various organs.
ii. Brain
(1) Changes occur if victim survives for 12-24 h.
(2) Findings:
Ischemic encephalopathy: Sequence – shrinkage or swelling of neurons"nucleus
becomes pyknotic"death of neurons"replaced by fibrillary gliosis.
iii. Heart
(1) Fatty changes: (i) After 18 h of survival - seen in about 20% cases. (ii) 3-4
days – become well marked in all cases
(2) subendocardial hemorrhages.
iv. Lungs
Findings are same as in ARDS [please see below].
v. GIT
(1) Contents – blood stained fluid. Blood is dark red and fluid.
(2) Mucosa – congested and edematous, shows hemorrhagic erosions,
ulcerations and necroses [Hemorrhagic enteropathy].
vi. Liver
(1) Gross – no appreciable change
(2) microscopic – Due to perfusion deficit. Fatty changes after 18 h. Gradually
extend from central areas to lobules.
vii. Spleen
Enlargement and softening [in septic shock].
viii. Kidneys
(1) Pathology - Changes are due to .in renal blood flow (RBF)"ischemic renal
injury. Changes begin within 24 h. Become marked in 7-10 days.
(2) Shock kidney:
(i) Gross – Normal in size. May be slightly enlarged in some cases
(ii) Microscopic - Acute tubular necrosis.
ix. Adrenals
Focal lipid depletion in cortical cells – begins after 24 h. Well marked in 3-4
days.
x. Other organs
Necrotic foci – in lymph nodes, pancreas, spleen

2. Reflex vagal inhibition

Please see ch 8.

3. Air embolism
Air embolism [syn, gas embolism] is entry of air bubbles in vascular system. It is
an immediate cause of death in certain wounds e.g. wounds of neck.
Types:
(1) Venous – more common. So common that when only the phrase “air
embolism” is mentioned, it is presumed to be venous air embolism [please
also see ch 11].
(2) Arterial – caused when air in sufficient quantities enters (i) a vein of the
pulmonary system"reaches left side of the heart"blocks arterioles and
 capillaries in different parts of the body [brain, heart] or (ii) directly into the
arteries of the systemic circulation.

a. Causes of air embolism

i. Venous embolism
(1) Artificial respiration – forced respiration by mechanical respiratory
aids"rupture of overinflated alveoli"interstitial pulmonary emphysema"air
penetrates pulmonary lymphatics"enters venous system via thoracic duct.
(2) Criminal abortions – when air or soap solutions are injected in the uterine
cavity [ch 26]
(3) Crush injuries of chest
(4) Decompression sickness or Caisson’s disease [may cause both arterial and
venous embolism]
(5) Oral genital sex, especially in a pregnant woman [ch 25]
(6) Surgical and other iatrogenic procedures:
(i) Central venous catheterization (CVC), including central lines, pulmonary
catheters, subclavian artery catheterization, hemodialysis catheters and
Hickman (long-term) catheters
(ii) cesarean delivery, manual extraction of placenta
(iii) hemodialysis
(iv) Injection of air under pressure in fallopian tubes (to test patency)
(v) IV injections given with a faulty technique
(vi) Neurosurgical procedures, especially those performed in the Fowler’s
(sitting) position (e.g., air encephalography, posterior fossa surgeries)
(vii) Otolaryngological surgeries
(viii) positive pressure ventilation in newborn infants [over distension of
airspaces"alveoli rupture+ pulmonary vascular damage"entry of air into
pulmonary vasculature]
(ix) thoracocentesis
(x) During transfusion, when positive pressure is being used.
(7) Wounds of
(i) neck involving jugular or subclavian veins
(ii) craniofacial region (especially wounds of sagittal sinus)
(iii) chest and abdomen.
ii. Arterial embolism
(1) Crushing and penetrating wounds the chest [may penetrate a lung vein and a
bronchiole and allow air to enter vein]
(2) Surgical procedures on the thorax [any cardiac surgical operation that uses
extracorporeal bypass, thoracentesis, thoracic surgery]. Because the
pulmonary vein pressure is low [10 cm H2O], any factor producing an -ed
pressure gradient between airway and pulmonary vein allow entrance of air
into the vein.
(3) Paradoxical embolism
(4) overexpansion of the lung by decompression barotrauma.

b. Pathophysiology
If volume of air is large - Air enters venous system" carried to right heart and
pulmonary arteries" mechanical obstruction and churning [turbulent flow] of
blood"Production of erythrocyte and platelet aggregates, fat globules, fibrin and
froth [complexes of air bubbles, microbubbles]"further occlusion of
vasculature"death.

c. Paradoxical air embolism

(1) Occurs when air passes into the arterial system via anomalous structures
(i) atrial or ventricular septal defect
(ii) patent foramen ovale [incidence in general population "ch 27]
(iii) pulmonary AV malformations [AVM].
(iv) In the absence of AVM, gas bubbles may pass when (a) there are large
volumes of venous air (b) administration of vasodilators and (c) volatile
anesthetic agents [have a pulmonary vasodilating effect].
(2) Arterial tree is embolized paradoxically. The paradox is how the air entering
the veins can embolize arteries. Mechanism is same as that of fat embolism
[please see below].

d. Minimum amount of air that causes fatal air embolism

(1) Venous embolism - 100 ml in adults. If injected in a limb vessel,
comparatively larger volumes are required, as air is absorbed rapidly.
(2) Arterial embolism – 2-3 ml, because air travels directly from lungs to the
left side of the heart, from where it is forced into the coronary or cerebral
arteries [ch 5].
e. Fatal period
Death from air embolism [venous or arterial] occurs within a few minutes, and is
rarely delayed beyond an hour.

f. Diagnosis at PM
Please see ch 5.

4. Mechanical injury to a vital organ

(1) Most vital organs - brain, heart and lungs [ch 8]. Severe injury to any of
these would result in rapid death.
(2) Other vital organs – if severely injured may also result in death, eg liver,
spleen etc
(3) Slight injury:
(i) May result in death, if the organ was previously diseased.
(ii) Some examples where minor trauma may cause death (a) Opening up of
recently stitched wounds [eg vital abdominal wounds] (b) Perforation of ch
intestinal ulcer (c) Rupture of an aneurysm, enlarged liver or spleen.
(iii) In such cases, if the offender (a) did not have intention to kill (b) did not
know the condition of victim and (c) amount of injury caused would not be
fatal to a normal person, then he cannot be charged for murder or even
culpable homicide. He would be charged with causing hurt or grievous hurt
[please also see “culpable homicide and murder compared” above].

5. Natural diseases
A natural disease may be aggravated by trauma. Please see below "Trauma and
disease.

B. Remote Causes
(1) These are cases when victim dies from the effects of trauma, long after it was
inflicted.
(2) Liability:
(i) If cause of death can be traced to the original trauma, assailant is responsible.
(ii) If medical attention was provided and was allegedly negligent in nature,
liability may lie on the doctor also [please see “surgical operation” below].
1. Crush syndrome
Crush syndrome (traumatic rhabdomyolysis, Bywaters’ syndrome) is a life
threatening medical condition characterized by shock and renal failure following
a crushing injury to skeletal muscle.

2. Disseminated intravascular coagulation (DIC)

DIC is a state of hypercoagulation that occurs in a variety of disease states,
including severe trauma, particularly to the brain.

3. Embolism
An embolus is defined as a detached intravascular physical mass that is carried
by the blood to a site distant from its point of origin. 95% of all emboli consist of
thrombi dislodged from an intravascular thrombus.

4. Gangrene or Necrosis
Gangrene is death of an area of the body accompanied by putrefaction.
Salient features:
Types: (i) Dry gangrene – (a) Mechanism – Injury" thrombosis"loss of blood
supply (ii) Wet [moist] gangrene - (a) Mechanism - untreated infected
wound"bacterial infection"Swelling"stoppage of blood flow"invasion of muscles
by bacteria. Gas gangrene is a special type of wet gangrene caused by Clostridia.

5. Infection
Caused by:
(1) Organisms normally present on body surfaces - (i) B. pyocyaneus (ii)
Friedlander’s bacilli
(2) Organisms invading tissues from environment - (i) C. diphtheriae (ii) Cl.
tetani
(3) Organisms from both body and environment - (i) Cl. welchii (ii) Coliform
bacilli (iii) Staphylococci (iv) Streptococci.

6. Neglect
(1) Negligence:
(i) of doctor, eg not paying attention to complications
(ii) of patient himself. Willful disobedience, eg not taking medicines
(2) Improper treatment

7. Surgical operation
Surgical operation, anesthesia or other medical intervention–for treating
injury may cause death.

8. Supervention of disease from a traumatic lesion

(1) Damage of artery by bullet"false aneurysm" rupture"death
(2) Fibrous scar tissue formation - Traumatic lesion" healing"scar tissue
formation"scar tissue contracts"complications
(i) fibrous scar in hollow muscular organ–obstruction, stricture
(ii) fibrous scar in arteries"under constant
tension"traumatic aneurysm"rupture" death
(iii) Abdominal wound"heals"fibrous scar" strangulated hernia"death
(3) Injury to spinal column"paraplegia"bed sores, septic cystitis, general
exhaustion"death
(4) Thoracic trauma"injury to coronary artery"coronary thrombosis"death.

X. AGE OF WOUNDS

Age of wounds can be determined by observing the amount and extent of

healing. Age of wounds can be determined by (i) Gross changes (ii)
Histopathology (iii) Enzyme histochemistry (iv) Immunohistochemistry. For
ageing by gross changes, please refer to individual types of injuries (abrasion,
contusions etc).

A. Enzyme Histochemistry
[A] Enzyme histochemistry is a technique to demonstrate enzymes in tissues.
[B] Sequence - Immediately after a wound is produced, two zones can be
demonstrated around it 1.a central zone 0.2-0.5mm wide and (1) a peripheral
zone 0.1-0.3mm wide. The enzymatic activity .s in central zone and -s in the
peripheral. The technique can be combined with biochemical examination to
detect vasoactive amines (serotonin and histamine), which are the earliest to
appear (Table 3).
Memory Aid 4: Histochemistry of wounds
Remember like this.
• First to appear corresponds with Free histamine; and
SeCond to appear corresponds with Serotonin, Calpains and Cathepsins. But this is not so.
So transpose them. Thus we get following:
✦ First to appear [10 min] " Serotonin, Calpains, Cathepsins
✦ Se Cond to appear [30 min] " Free histamine
• Last two are acids and alkalis respectively. Thus we have:
✦ 4 h " Acid phosphatase
✦ 8 h " Alkaline phosphatase

B. Immunohistochemistry

XI. VOLITIONAL ACTS AFTER INFLICTION OF FATAL

WOUNDS

In severe and fatal injuries, the question often arises, if the victim could have
performed some volitional acts involving physical and mental exertion eg
speaking, walking, throwing, killing someone back in revenge etc. after
receiving the injuries.
(1) Length of time victim can live depends on
(i) nature of injury
(ii) Rate of bleeding
(iii) Degree of associated shock
(iv) Different individuals may react differently to same injury
(2) Trauma to brain -
(i) Frontal lobe damage "does not incapacitate immediately.
(ii) If brain stem is destroyed [as in judicial hanging]" immediate incapacity
(iii) Severe injuries to brain "(a) victim may survive rarely although the extent of
damage is expected to have caused instant death. (b) May remain
unconscious for several minutes before finally succumbing to injuries (c)
Death may occur with no obvious naked eye changes to the brain
(iv) Single stab wound of skull and brain"May not be immediately fatal, and
victim may walk, run or do some other voluntary activity before death.

XII. ANTEMORTEM VS. POSTMORTEM WOUNDS

(1) AM v PM wounds – [L. ante, before; post, after; mortis, death]. PM wounds
may be caused by animals [dogs, cats, rodents etc], deliberate attempts to
confuse police, mutilomaniacs, lust murderers [ch 25] etc.
(2) Differences - In many situations, it becomes vital to know if injuries are
antemortem [AM] or postmortem [PM].
(3) Diff - Table 5.
(4) Perimortem wounds [L. peri, around; mortis, death] – Wounds caused
during supravital period [ch 8]. Since molecular death has not occurred,
cellular reaction and enzyme histochemistry may be +ve. However since heart
has stopped, spurting etc may not be present.
XIII. MEDICOLEGAL QUESTIONS ON TRAUMA

Following questions on trauma are frequently asked by lawyers in courts.

A. Can There be No Signs of Trauma Externally, Yet Internal

Injury May Be so Great as to Cause Death?
Yes, this is possible. In blunt injuries to abdomen (pliable body surfaces), there
may be no external signs of trauma, yet liver and spleen may be damaged, and
cause enough bleeding to cause death.

B. How Would You Quantify Degree of Trauma?

This is mostly subjective. Trauma is roughly estimated as mild, moderate, severe
and extreme.

C. What are the Situations in Which Acceleration-Deceleration

Forces Play a Vital Part?
(1) Vehicular accidents [ch 18]
(2) Shaken baby syndrome [ch 27].

D. Can the Wounds be Altered from their Original Appearance?

Yes, it is possible both in the living and in the dead (i) In the living: (a) by
medical treatment- Kennedy phenomenon (please see chapter on firearms) (b)
by healing (ii) In the dead: (a) by resuscitative measures (b) by postmortem
predators (insects, animals) (c) by decomposition.

E. Is it Possible for a Person to Die During Altercation?

Yes, if the deceased already suffered from heart disease. Sudden altercation may
-BP and heart rate. If the coronaries are already thrombosed, it may precipitate a
subintimal hemorrhage leading to death.

F. Were More than One Weapon Employed in this Case?

(i) Gang wars and group fights - Generally several people attack with different
weapons. Different weapons would produce different injuries, which would
enable the pathologist to opine that more than one weapon were used (e.g. if an
incised wound and a bruise are present on the body, it can be opined that both a
sharp and a blunt weapon were used) (ii) Suicide – If a suicide fails by one
method (e.g. cutting wrists), he may employ a firearm to end his life. Presence of
incised and firearm wounds would indicate, two different weapons.

12. Mechanical Injuries

Mechanical injuries are injuries produced by mechanical force – blunt, sharp or

firearms.

I. ABRASIONS

An abrasion is an injury involving destruction of epidermal layers of the skin

and dermal papillae.
Salient features:
(1) Force - producing abrasions can be of two types (a) tangential (b)
perpendicular.
(2) Effects - Tangential force generally produces scratch and graze abrasions,
while perpendicular force produces pressure and imprint abrasions (Fig 12.1).
Most commonly the force involves a mixture of the two.
(3) Healing - Abrasions always heal without scarring. If the injury extends to
subepidermal areas [below the level of dermal papillae], it would result in
superficial scarring. They are termed as superficial lacerations (Fig 12.2).
(4) Weapons - with rougher surfaces and with more movement produce more
severe abrasions.
(5) On a wet skin – difficult to see. Become more prominent after the skin dries.
Body recovered from drowning must be allowed to dry before inspection
begins.
(6) On drying – abrasions become dark brown or black
(7) Description – Each abrasion must be described separately.

A. Types of Abrasions
1. Scratch abrasions
Scratch abrasions [syn, linear abrasions, scrapes, scratches] are abrasions with
appreciable length, but no significant width (Fig 12.3).
Salient features:
(1) How produced - They are typically produced by sharp, pointed objects such
as fingernails, pins or thorns. (a) When produced by tip of knife or razor, they
are called point scratches. (b) Nails produce typically curved scratch
abrasions, known as semilunar abrasions. Abrasions produced by fingernails
may barely be recognizable when very fresh and moist. Upon drying they
become dark brown or black and prominent.
(2) Direction - Surface layers of the skin are “heaped up” in the direction of the
movement. This leaves a clean area at the start of abrasion and epithelial tags
at the end.

2. Graze abrasions
Graze abrasion [syn, glancing, grinding, scraping or sliding abrasions] is
essentially a collection of innumerable scratch abrasions.
Salient features:
(1) Most common abrasions.
(2) Comprise of uneven, longitudinal parallel lines (grooves or furrows) with the
epithelium heaped up at the ends of these lines. This heaping up indicates the
direction in which force was applied.
(3) Abrasions may extend partially into the dermis because of corrugations of
the dermal papillae. Bleeding occurs in such abrasions.

a. Typical examples

(1) Dragging at rough road side, as occurs in road side vehicular accidents
[brush burn, friction burn, gravel rash, road rash, scuff abrasion]. Dirt,
grit or gravel may be found sticking to abrasions, which would indicate the
surface, where the person was dragged.
(2) Glancing kick with a boot [application of tangential pressure]
(3) Pedestrian walks into the side of a moving vehicle [ch 18"injuries to
pedestrians"primary impact inj].

3. Pressure abrasions
Pressure abrasions [syn, crushing or friction abrasions] are abrasions produced
by crushing of epithelium, when a relatively small force is applied
perpendicularly to the skin for large time periods.
Salient features:
Impact abrasions also occur by perpendicular forces to the skin. The difference is
that in pressure abrasions, the pressure may not be much, but the time period
during which pressure is applied is considerable. Because of this, tissue fluid is
gradually extruded out and the skin becomes dry and parchment like.
Memory Aid 1: Pressure abrasions
Parchmentization is the hallmark of pressure abrasions.
In impact abrasions, the time period is negligible, but the pressure applied is
tremendous. Substantial extrusion of fluid is not there and skin is not dry and
parchment like. (1) Typical examples: (i) Corneal abrasion - Use of contact
lens for more hours than indicated leads to abrasion of the outer layer of the
cornea. (ii) Nappy abrasions (nappy rashes) - in babies due to pressure of
nappies on soft baby skin (iii) Ligature marks - of hanging and strangulation (iv)
Shoe bite (v) Teeth bite marks.

4. Impact abrasions
Impact abrasions [syn, contact or imprint abrasions] are abrasions produced by
crushing of epithelium, when a relatively large force is applied perpendicularly
to the skin for minuscule time periods.
Salient features:
(1) Impact abrasions are slightly depressed below the surface, unless an
underlying bruise or local edema bulges the tissues.
(2) in forcible impacts – (i) dermis is damaged (ii) there is an underlying bruise
(3) by a solid object – often produces abrasions only at the periphery, where the
skin is forced downwards with more force.
(4) Impact by a smooth surface – abrasion without any pattern. Object cannot
be identified [cf patterned abrasions]
(5) Typical examples: (i) Headlamp rim marks, or radiator grille marks - in
head-on vehicular collisions. (ii) Recoil/muzzle impression - in tight contact
wounds [ch 13]. (iii) Shoe sole marks – in kicking (iv) Tire marks of a car, bus
or truck on pedestrian - in run over accidents. Marks may be soiled with
grease, paint flakes and road dirt.

Patterned abrasions
Patterned abrasions are a special subset of pressure and impact abrasions,
whereby the pattern of the object causing them is faithfully reproduced on the
skin, enabling its identification.
Examples – (i) bicycle chain (ii) Cat-o-nine tails – It is a special whip having 9
thongs, each containing a number of knots. It produces a very typical patterned
abrasion consisting of a series of linear abrasions showing knot marks at specific
distances. Sometimes superficial lacerations are also produced. (iii) falling down
on a metal grid, (iv) serrated knife, (v) shoe (vi) spiral weaves of electric wires
or ropes, (vii) striking by a weapon having a highly patterned surface (viii)
weave of coarse fabric.
5. Miscellaneous
(1) Tattooing and pseudo-tattooing - ch 13
(2) Dicing injuries – ch 18.

B. Age of Abrasions
Abrasions heal from periphery to the centre, by new growth of epithelial cells.
Age of abrasions can be determined by (i) gross examination and (ii)
microscopic examination [histologically].
1. Gross examination
(1) Fresh – Bright red
(2) 1 day – Blood and lymph dries up. Bright red scab forms
(3) 2-3 days – Reddish brown scab
(4) 4-7 days – (i) Scab becomes dark brown (ii) Epithelium grows under the
 scab and covers defect. Scab becomes ready to fall
(5) >7days – Scab dries, shrinks and falls off, leaving depigmented area.
Gradually the area would get pigmented.

2. Microscopic (histological) examination

(1) 4-6 hours – Cellular infiltration in abraded area
(2) 12 h – Three layers are seen
(i) Surface layer – fibrin and RBCs
(ii) Middle layer – infiltrating polymorphs
(iii) Deep layer – abnormally staining collage
(3) 48 h –
(i) Scab well formed
(ii) Epithelial regeneration is seen at the margins of scab
(4) 4-5 days – If abrasion is small, it is completely covered by epithelium
(5) 5-7 d – subepithelial formation of granulation tissue
(6) 8 d – Reticulum fibres appear
(7) 9-12 d – Collagen fibres appear
(8) >12 d – Regression starts. Remodelling of epithelium occurs. Becomes
thinner.

C. Postmortem Abrasions
(1) Cause –
(i) when dead body is dragged to conceal it,
(ii) rolled down a hill
(iii) thrown in water and it buffets against reefs, stones and other objects within
water
(iv) animals gnaw or scratch the dead body
(2) Differentiation between AM and PM is difficult or even impossible when -
(i) produced just before or after death [impossible even by microscopic
examination]
(ii) superficial in nature
(iii) advanced decomposition
(iv) burns occur as added injury. Table 1 gives some imp differences between
the two.
D. Medico Legal Importance of Abrasions
(1) Direction of force – can be estimated from tissue tags
(2) Force of impact – can be judged
(3) Foreign matter sticking over abrasions – may give an idea of scene of
crime [eg grass, gravel, sand etc]
(4) Imp and only sign – of internal injury sometimes
(5) Manner of production –
(i) Generally accidental or homicidal in nature
(ii) May be self-inflicted for leveling false charges against enemies
(6) Nature –
(i) Usually simple, because they heal without scarring (ii) Do not pose danger to
life, until and unless multiple and massive, or involve underlying vital
organs
(7) Time of assault – can be calculated
(8) Type of offence – is indicated by site of abrasions
(i) around anus - homosexuality
(ii) around breast, cheeks, neck, inner side of thighs – indicate sexual assault
(iii) over face – indicate struggle
(iv) over mouth and nose – in smothering
(v) over neck – indicate throttling, especially crescentic abrasions
(9) Weapon – can be identified from patterned abrasions. Sometimes peculiarity
of the offender’s nails can be estimated [eg long, crooked, broken, irregular
etc).

E. Differential Diagnosis
1. Burns
After death abraded epidermis becomes brown, leathery, parchment like,
prominent and stiff and may begin to resemble burns.
2. Erosions produced by ants
(1) Ants gnaw the body after death and produce whitish or brownish erosions.
(2) Differentiating features:
(i) Margins - abrasions have irregular margins
(ii) Site –Since ants attack moist areas, the abrasions are found at
 mucocutaneous junctions, around eyelids, nostrils, mouth, ears, axillae,
knuckles, groins, genitalia and any moist folds of the skin.
(iii) Examination by hand lens – may reveal crescent shaped ant bite marks
(iv) Vital reaction - Absent.

3. Excoriations of skin by excreta

Seen in infants – persistence of excreta around napkin area"slight
excoriation"these areas dry up and become depressed and parchment like. Color
varies from pale-yellow to deep copper.
4. Drying of the skin
Scrotal area may dry up and produce reddish brown or yellowish discoloration
resembling abrasions.
5. Pressure sores
Seen only in pressure areas. History of long immobilization may be there.

II. BRUISES (CONTUSIONS)

A bruise [Fig 12.8] is an effusion of blood into the tissues underneath the skin
due to rupture of blood vessels (arterioles, venules and veins). When the effusion
of blood is in other tissues and organs (muscles, lung, heart, brain, spleen,
mesentery etc), it is called a contusion.
Salient features:
(1) Situation – Bruise is usually situated in the dermis and subcutaneous
tissues – some-times in the fat layer
(2) Color – Lighter in the center, than at the periphery, because extravasated
blood is pushed outward
(3) Cause – Bruises (and contusions) are caused by blunt force, eg iron rod,
lathi, fist, stone, cricket bat, hockey stick, whip, boot etc.
(4) Associated findings - (a) painful, tender (b) crushing and tearing of s/c
tissues; (c) usually no destruction of skin (d) may occur in association with
abrasions or lacerations. If abrasions and contusions occur together, it is
customary to call them “abraded contusion” if contusion is more prominent
and “contused abrasion” if abrasion is more prominent.
(5) Size - (a) Petechial hemorrhages – 0.1-2 mm (b) Ecchymosis – 2-5 mm (c)
Bruise – more than 5 mm. Size of a bruise may be larger than the surface of
the weapon which caused it, because blood continues to ooze (d) Hematoma
– (i) Usually associated with substantial trauma, when a large BV is injured.
(ii) More than 5 mm with appreciable swelling. (iii) Lesion rises above surface
of skin. (iv) Forms a fluctuant mass (v) Unlike a standard bruise, a hematoma
can be aspirated in the same way a collection of pus is aspirated.
(6) Shape –(a) Does not correspond with offending weapon, because of (i)
constant oozing of blood (ii) tissue swelling. However if death occurs
immediately after infliction, the oozing stops and shape may be similar to that
of weapon (b) Often a bruise has a doughnut like configuration, with the
center a lighter shade. This results from outward pressure of extravasated
blood by the impact.
(7) Margins – blurred
(8) Extent – -force"bigger bruise
(9) Compare with corresponding opposite part – may display minor swelling.
(10) D/d – Mongolian spot (hyperpigmented skin in the lumbosacral region).
Mongolian blue spots in a child. They may look like bruises and raise
suspicion of child abuse.
(11) Differentiating features-
(i) Present since birth.
(ii) Location is always lumbosacral.
(iii) Color changes will not occur in Mongolian spot.

A. Classification
Bruises are classified in 3 types depending on their location [Fig 12.9]
(1) Intradermal bruise - (a) Location - Bleeding occurs in dermis (Fig 12.9).
(b) Amount - of extravasated blood is small, but because of its superficial
position, and relative translucency of epidermis above it, the pattern is distinct
(c) This type of bruising occurs especially when the impacting object has
alternating ridges and grooves, as the skin will be forced into the grooves
and be sharply distorted [ex: vehicle tire running over body, kick by ribbed
rubber soles of “trainer” shoes. Stomping (kicking and jumping on a person
together) may also produce intradermal bruises].
(2) Subcutaneous bruise - Bleeding occurs in subcutaneous tissue. Most
common type of bruising. Appears soon after injury
(3) Deep bruise - (a) Bleeding occurs in deep subcutaneous tissue just above
muscle, or between muscular bundles. (b) Not apparent immediately after
injury, but 1-2 days after (delayed bruising). (c) In suspected cases, infrared
photography [ch 30] is essential (d) If this facility not available, examine
again after 48 hours.
B. Factors Modifying Size and Shape
1. Age
(i) Children and old people bruise easily [soft and delicate subcutaneous tissues
in children. Loss of flesh and atherosclerotic changes in old] (ii) Adults
(especially muscular) bruise less easily.
2. Sex
(i) Women bruise more easily than men [more s/c fat. More delicate tissue].
Even a firm grip on the arms of a delicate woman may produce bruising (ii) Men
bruise less easily
3. Obesity
Fat people bruise more easily [greater amount of s/c fat]
4. Color of skin
(i) Fair skinned people – bruising is better appreciated visually (ii) Dark
skinned people – Bruising is not easily appreciable. May be better appreciated
on touching (raised area due to tissue swelling can be felt). Always compare
with the identical area on the opposite side.
5. Effect of embalming
Bruises are more prominent in embalmed bodies because (i) embalming fluids
form a dark pigment complex with blood (ii) Since pressure is used to force
embalming fluid into BVs, it also forces blood through the damaged areas (iii)
Transparency of blood is increased.
6. Condition and type of tissue
(i) Vascular and loose tissue (eg face, vulva, scrotum)" More bruising, because
there is sufficient space for blood to collect (ii) Firm, fibrous, strongly
supported tissue (scalp, back, palms, soles)"Less bruising (iii) Good muscle
tone (boxers, athletes)"Less bruising because of good muscle tone, which
prevents blood from extravasating (iv) Resilient areas (abdomen, buttocks)
bruise less.
7. Weapon used
(i) If weapon is a yielding weapon (eg sandbag), bruising may not be seen. (ii) If
it is a cane or whip, railroad bruise may be seen (please see under patterned
bruising).
8. Associated diseases
(i) Arteriosclerosis – bruising occurs easily (even on coughing and slight
exertion), because diseased vessels rupture easily (ii) Blood dyscrasias – may
cause prominent bruising even on minor trauma because of defective clotting
mechanism (eg hemophilia, leukemia, prothrombin deficiency, purpura
hemorrhagica, scurvy, vitamin k deficiency). Purpuric spots can be
differentiated from true bruises by following points (a) Purpuric areas are
clearly demarcated from surrounding skin (b) They never show tissue swelling
(iii) Poisonings – Hepatotoxic poisons may cause major bruise to appear from
minor trauma because of prothrombin deficiency (eg alcohol, phosphorus).
Chronic alcoholics bruise more easily.
9. Gravity shifting of blood
The site of bruise does not necessarily indicate the site of violence. Sometimes
the two may be entirely different. When extravasated blood at the site of injury
tracks along fascial planes or between muscular layers under the influence of
gravity to reappear at a site below the injured site, it is known as ectopic,
migratory or percolated bruise. Ex: (i) Spectacle hematoma - [Fig 12.10] (a)
Blunt injury to the forehead"blood extra-vasates in forehead region"gravitates
down and collects around the eye (b) Blunt injury to skull"fracture of anterior
cranial fossa (ACF)"blood extravasates below ACF"gravitates down and collects
around the eye (black eye). Because of its peculiar position, known as spectacle
hematoma, panda eyes or raccoon eyes. Contusion of eye may also be as a
result of direct trauma (punch in the eye). (ii) Bruise behind the ear [mastoid
ecchymosis, Fig 12.11] may indicate fracture of posterior cranial fossa rather
than a direct blow behind the ear. (iii) Injury to the scalp"bruising of the face (iv)
fracture of jaw"Bruise appears in neck (v) fracture of pelvis"Bruise appears in
thigh (vi) fracture of femur"Bruise appears on lower outer aspect of thigh (vii)
Blunt injury to upper part of thigh"Bruise appears above knee (viii) Kick on the
calf"Bruise appears around ankle.
10. Miscellaneous factors
(i) If injured part is thickly clothed, bruising may not be seen (ii) Persons on
anticoagulants, antiplatelet drugs, SSRI"More extensive bruising. SSRIs
inhibit platelet activity.
C. Patterned Bruising
A patterned bruise is that which reflects the pattern of the striking surface. Such
bruises are very medicolegally very important, because they can tell about the
striking object. Ex.: Railway track bruise - Also known as railway line or
tram line bruise. Caused when the skin surface is struck by a pliable instrument
such as a broom handle, cane (as that used by police), narrow planks, wood and
metal rods or whip. The bruise appears as two parallel lines of bruising with an
undamaged zone in the centre (like a railway track).

D. Age of Bruise
(1) Mechanism - Bruise heals by destruction and removal of the extravasated
blood. RBCs disintegrate by hemolysis"Hb liberated"broken down into
hemosiderin, hematoidin and bilirubin by the action of enzymes. Because of
formation of different pigments, color of the bruise changes with its age.
(2) Rate of healing – Healing faster if
(i) area is more vascular
(ii) Contusion is smaller
(iii) Individual is young, well-nourished and healthy.
(3) Color changes:
(i) Start - at the periphery and extend inwards towards the center.
(ii) Color changes [Table 2]
(iii) Rate of color change [healing]– Highly variable, and one should be very
cautious in interpreting age from colors [please see above for factors
affecting rate of healing]. In extensive and deeply situated bruises, color
takes a longer time to appear externally.

Memory Aid 2: Age of bruise

(4) Special cases -
(i) Subconjunctival bruising – color changes do not occur. They change straight
from red to yellow
(ii) CO poisoning – bruise have a cherry red color.

E. Deep Tissue and Organ Contusions

(1) All organs may be contused
(2) Contusion of brain:
(i) may cause impairment of function, confusion
(ii) Contusion of vital centers [eg those controlling BP and respiration]- Even
small contusions may cause coma and death.
(iii) Pathogenesis – (a) causes swelling (b) Metabolic by products accumulate
which are toxic to the brain
(3) Contusions of the heart –
(i) Prevent adequate cardiac emptying"Ht failure
(ii) If involve SA or AV node or Bundle of His"may cause serious disturbance of
normal rhythm or stoppage of cardiac function"Death
(4) Contusion of visceral organs – may cause rupture" bleeding into body
cavity"Death.

F. Postmortem Bruises
Postmortem bruise is one that appears after death.
Salient features:
(1) Causes - It may be due to (i) an antemortem injury or (ii) postmortem injury.
 (i) Antemortem injury - Sometimes if death occurs soon after blunt impact,
bruise may appear after death. This is due to (a) passive oozing of blood from
damaged BV under the influence of gravity (b) hemolysis of stagnant
blood"pigment diffusing out locally and producing a stain on the surface
[come-out bruise] (c) Pressure of putrefactive gases may further push blood
out of damaged BV. (d) Blood gravitates down to the most dependent areas,
rendering non dependent areas much more paler. Paler areas in non dependent
parts may reveal bruises [because of greater contrast], which were not visible
earlier. Therefore even if no bruise was detected during life, it may be
worthwhile to search for it at autopsy.
(2) Differences between AM and PM bruise are given in Table 3.

G. Artificial Bruises
Artificial or false bruises are fake bruises produced by rubbing some irritant
substances on the skin.
Salient features:
(1) They produce discolorations which look like bruises, but can be
differentiated (Table 4).
(2) Reasons - They are produced (i) to bring a false charge of assault against an
enemy (ii) by prisoners to bring a false charge of torture against policemen
(iii) by malingers to go on leave
(3) Substances used for producing artificial bruises are (i) Calotropis gigantea
(ii) Plumbago rosea (iii) Semecarpus anacardium [marking nut] of these at
least Calotropis gigantea [madar] has a wrong reputation of producing
artificial bruise. Author has rubbed the juice of madar several times on his
own arms, with absolutely nothing happening. He has in his possession
several videos of this too. (iv) Unusual Agents like Dithranol have also been
used.
Memory Aid 3: Substances used for producing artificial bruise
Can M D Pass – Calotropis [wrongly attributed], Marking nut, Dithranol, Plumbago
H. Demonstration of Bruises at Autopsy
(i) Examination of whole body under UV light [please see ch 30 for all things
visible in UV light] (ii) Contusions of scalp – Demonstrated by reflecting the
scalp (iii) Contusions of neck – layer dissection of neck (iv) Contusions due to
torture and beating – Long parallel incisions through the skin (v) Microscopy
in cases of doubt.

I. Complications
(1) Death from shock - An average bruise contains about 20-30 ml of blood.
Multiple bruises can cause death from shock.
(2) Infection - stagnant blood serves as a good culture medium for bacterial
growth, especially of clostridial group
(3) Fat embolism - Rarely a large bruise may cause sudden compression of the
subcutaneous tissue"release of s/c fat"Pulmonary fat embolism
(4) Necrosis and Gangrene - may sometimes result from extensive bruising.

J. ML Importance
(1) Age of bruise – Determined by color changes. Can confirm or refute the
story of victim
(2) Alcoholics – are more prone to bruising because
(i) keep falling due to unstable gait
(ii) cirrhotic disease causes bleeding diathesis. With the passage of time they
accumulate bruises all over their body. This may give an appearance as if
they have been involved in a fight. All bruises will however be of different
ages.
(3) Decomposition – can cause merger of contusions with blurring of their
patterns.
(4) Differentiation from PM staining - They must be differentiated from pm
staining (hypostasis) [Table 5].
(5) Distribution of bruises – Can indicate the character and manner of injury
(i) Child abuse – Bruises of different ages all over the body indicate that the
child was beaten regularly. Indicates child abuse
(ii) Manual strangulation – Position of finger tip and thumb bruises over the
neck (as in the above case) can indicate method of asphyxia, as well as
position of assailant
(iii) Pinning on the ground – deduced by bruising of shoulder blades
(iv) Restraint signs - 3-4 coin sized bruises on one side of arm (produced by
finger tips) and one larger bruise on the opposite side (produced by thumb)
would indicate that arms were held together by the assailant. From the
relative positions of smaller bruises with the larger one, the position of the
assailant can be deduced. This can be sign of forcible restraint.
(v) Sexual assault – Can be deduced by bruising of inner aspect of thighs
(6) Extraneous material – Same ML value as in lacerations
(7) Manner of production:
(i) Self inflicted – Very rare because painful. May be seen in hysteria and
mentally ill persons.
(ii) Accidental – (a) Very common (b) Seen on prominences [forehead, nose,
elbows, knees] (c) Manner of causation – can be deduced from presence of
dirt, Grease, Mud, Oil and Sand
(iii) Homicidal - (a) On any part of the body (b) Associated injuries eg
lacerations, stabs etc can reveal their manner of production
(8) Medicolegal value - Bruises are medicolegally less valuable than abrasions
because:
(i) Ectopic bruises - appear away from the site of injury. Thus exact site of injury
is not denoted by location of bruise
(ii) Direction of force – not indicated
(iii) Shape and size - does not correspond to the offending weapon [due to
constant oozing of blood]. Thus bruises caused by different weapons, fist,
fall etc cannot be differentiated very well
(iv) Time of appearance – of deep bruises may be too long after infliction of
injury
(v) Visibility - not very well visible in dark skinned persons
(9) Micro-contusions - are seen in firearm entry wounds surrounding each
individual tattoo point [ch 13].
(10) Patterned bruises – May indicate the surface features of offending
weapon. May connect the victim with the weapon. May help recover it [eg
cane, chain, ligature, shoe, tire, whip]
(11) Six penny bruises:
(i) These are discoid shaped bruises of about 1-2 cm in diameter, usually in a
group of three to five.
(ii) They resemble English six penny coin, and are caused from fingertip
pressure.
(iii) Causes - (a) Child abuse [ch 27] (b) criminal abortion, rape and attempted
rape - present over thighs, lower abdomen, perineum (c) throttling - over
neck: [ch 19]
(12) Size – can indicate the degree of violence.

III. LACERATIONS

Lacerations are tears or splits of skin, mucus membrane, muscle or internal

organs, produced by application of blunt force to the body, which stretches
tissues beyond their limits of elasticity.
Salient features:
(1) Also called ruptures
(2) Displacement of tissues is most common – when soft tissues are crushed
against bone, e.g. scalp, facial bones, shoulders and shin.

A. General Characteristics
(1) Margins – irregular, ragged, uneven
(2) Edges:
(i) Angular impact - (a) skin on the side of wound opposite to the direction of
motion is usually torn free and undermined. (b) Skin on the other side, i.e.
 the side from which blow was delivered is abraded and bevelled
(ii) Perpendicular impact - Equal undermining on all sides.
(3) Depth – depends on
(i) degree of force
(ii) depth of soft parts at the site of injury
(4) Shape and size:
(i) May not correspond - with the weapon which produced it
(ii) Linear – produced by long, thin objects eg crowbars, pipes.
(iii) Irregular, ragged or Y-shaped – produced by objects with flat surfaces
(iv) if curved - convexity of curvature points towards the direction of application
of force
(v) Stellate [star shaped] – produced by blunt round object
(vi) Crescentic– Produced by a blunt object with an edge, eg hammer head
(vii) Semicircular – striking head against wall or other hard surface. Due to
convexity of head
(viii) Patterned lacerations
(ix) Swallow tails at one end – seen sometimes due to tearing at angles of
lacerations [Fig 12.13].
(5) Gaping – present due to pull of elastic and muscular tissues.
(6) Bruising:
(i) in skin or s/c around the wound
(ii) If the force is exerted by the object moving in a downward direction, the
lower margin of the wound shows more bruising, and undermining.
(7) Tissue bridges [Fig 12.14]:
(i) Tissue bridges or bridging fibres are seen at the base of wound. This is
because deeper tissues [BV, connective tissue, elastic fibres, nerves etc] are
unevenly divided.
(ii) Tissue bridges become apparent, when the edges of the wound are gently
separated manually
(iii) MLI - their presence immediately indicates blunt force
(iv) Internal organs - Bridging is also seen in internal organs eg liver, kidneys,
pancreas and spleen.
(8) Hair bulbs – crushed
(9) Hair and epidermal tags – Deeply driven in the wound
(10) Hemorrhage:
(i) less in laceration. Because vessels are crushed and torn across irregularly. (a)
They can retract (b) Blood clots readily
(ii) Exceptions – scalp lacerations, where hemorrhage is more. Temporal artery
is firmly bound"unable to retract.
(11) Foreign matter – usually present in the wound.
B. Types
(1) Tear, the most general type of laceration, and encountered most commonly,
occurs when blunt force is applied to skin having sufficient amount of
underlying fat and muscle (eg thigh).
(i) caused by a heavy blunt weapon (cricket bat, hockey stick, lathi)
(ii) has ragged and bruised margins.
(2) Split laceration occurs when blunt force is applied to skin direcly overlying a
bone, with miminal amount of underlying fat and muscle. (scalp, zygomatic
process, chin, tip of shoulder, back of elbow, anterior superior iliac spine,
shin).
(i) Mechanism - Skin is split between the weapon and the underlying bone.
(ii) Appearance – mimics an incised wound [called incised looking lacerated
wound. Examination with hand lens is helpful (Table 6).
(iii) Table 7 lists differences between a true incised and true lacerated wound.
(3) Stretch laceration is caused if the force is applied in such a manner that skin
is overstretched, resulting in a large flap. Ex. a glancing kick by foot.
(4) Cut laceration is produced by heavy cutting weapons [axe, boat propeller,
bush knife, chopper, hatchet, industrial and farm machinery, lawn mower
blade, machete (a large heavy knife used for cutting sugarcane), meat cleaver]
wielded with a tremendous amount of force.
(i) It may best be conceived as a “cross” between a true laceration and a true
incised wound. The edges of the weapon do cut the skin, but since the edges
are heavy, they crush and bruise the margins of the wounds too.
(ii) The wounds show an ugly, wide gape
(iii) The underlying bones are frequently fractured, or show deep grooves or
cuts.
(iv) Also called chop wounds.
(5) Avulsion is produced if grinding compression [eg fast moving tire of a heavy
motor vehicle (eg run over inj; ch 18), or a rotating heavy industrial machine],
is applied, causing avulsion (separation) of large areas of skin from its
underlying attachments and is lost (Fig 12.16).
(i) Wound is devoid of any overlying skin.
(ii) also known as flaying.
(iii) Underlying muscles are heavily bruised. Table 8 summarizes various types
of laceration and how they are typically caused.
C. Age of Lacerations
Age determination is difficult unless clear signs of healing are present [eg
Fibroblasts, Granulation tissue, Organizing infiltrate].

D. AM and PM Lacerations
Antemortem lacerations would show (1) Bleeding (2) Blood-staining of margins
(3) Bruising (4) Eversion (5) Gaping (6) Vital reactions. PM lacerations would
show none of these.
E. MLI
(1) Age of lacerations –
(i) Fight - indicates time of struggle
(ii) Disputed pregnancy - age of perineal lacerations indicates the possible date
of delivery [please see ch 24 for more details]
(2) Combinations of lacerations with abrasions and bruises – Abrasions,
bruises and lacerations may be seen together. Each injury may be produced by
different blows by the same weapon, or they may be produced at the same
time (as in explosions). Punching (with a fist), kicking and stomping (with a
shoe wearing foot) can produce all three injuries with different blows.
(3) Extraneous material – may be present in lacerations (eg dirt, dust, grass,
grease, sand, stone particles). This may connect the injuries with the place of
occurrence
(4) Firearms [Lacerations produced by]– By pistol whipping [buffaloing].
(i) It is the act of holding a handgun by its barrel, and clubbing the victim with
the butt, in effect using it as a blunt weapon.
(ii) location - Predominantly on forehead.
(5) Manner of production -
(i) Accidental - falls etc
(ii) Suicidal lacerations – are very rare, because a person virtually never uses a
blunt object for suicide (very painful and rarely effective). May be seen in
suicidal jumping from high buildings.
(iii) Homicidal - (a) Lacerations on the vertex generally indicate homicide. (b)
Bagh Nakh [tiger claws] is a claw-like weapon inspired by the armature of
big cats. It fits over the knuckles or is concealed under and against the
palm. It consists of four or five curved blades affixed to a crossbar or glove,
and is designed to lacerate skin and muscle. Some incorporate a spike or
blade on one end of the crossbar. This form is known as a bichawa bagh
nakh because the blade is based on that of the bichawa (scorpion knife).
(6) Shape of lacerations –
(i) can very rarely indicate the nature of offending weapon. (patterned
lacerations).
(ii) Causes – (a) chains (b) Pistol whipping [please see below]. Please also see
above under the heading “shape and size”.
(7) Tendons and muscle lacerations without corresponding lacerations on
 skin – Can indicate violent muscular contractions and spasm (convulsant
poisons like strychnine, convulsive natural disorders like epilepsy, tetanus). In
such cases, lacerations in hollow viscera may also be seen.

IV. INCISED WOUNDS

An incised wound (cut, slash, slice) is a clean cut wound through the tissues,
caused by a sharp-edged instrument. In an incised wound, length is its maximum
dimension [cf. stab wound].
Salient features:
(1) Force – delivered over a very narrow area, corresponding with the cutting
edge of the instrument
(2) Skips in pattern - A series of incised wounds, separated from one another by
bridges of normal skin are produced - (i) when there are bony ridges (ii)
tendons or (iii) if a dull weapon was used over areas of loose, thin, atrophic,
folded and wrinkled skin, eg back of hand in an elderly victim..

A. Causes
(1) Typical instruments which cause incised wounds – Blade, knife, razor,
scalpel, sword
(2) Single or multiple strikes – Usually caused by a single strike. A “sawing
motion” may produce a more complex wound.
(3) A curved sharp weapon (eg a sickle) produces a stab from the pointed end,
and an incised wound from the blade with an intervening intact skin.
(4) Glass – Wounds by glass (eg broken bottles, broken glass pieces) are
typically incised. If the bottle is very thick [eg a cola bottle], the broken pieces
would be equally thick, and may produce bruising around margins, giving the
appearance of a cut laceration.

B. Characteristics
1. Length
(1) Greatest dimension - Length is the greatest dimension in incised wounds [cf
stab wounds].
(2) Length has no relation to the cutting edge of the weapon, because a cutting
 weapon may be drawn to any distance creating an incised wound of any
length.
2. Width
Width may be greater than the edge of weapon - due to
(i) retraction of divided tissues
(ii) shaking of blade.
3. Margins
(1) Clean-cut, well-defined
(2) if knife is serrated – may produce a saw-toothed cut
(3) Edges -
(i) usually everted
(ii) Inverted – if a thin layer of muscle fibre is adherent to the skin, pulling it
inwards [eg in scrotum]
(4) Abrasions and contusions -
(i) Not seen on margins if weapon was perfectly sharp
(ii) may be seen if the cutting edge was blunted; because then the incision is
produced more by pressure than by the sharpness of the cutting edge.
4. Shape
(1) usually spindle shaped – due to greater retraction of edges in the center
(2) Crescentic – if blade is curved or struck surface is convex
(3) Zigzag – if skin folds are loose, as in axillary folds, scrotum etc
(4) Gaping – is greater if underlying muscle fibres are cut transversely or
obliquely [due to retraction]. Lesser when cut longitudinally.
5. Direction
(1) Incised wound is deeper at the beginning [Fig 12.17 (A) ], because more
pressure is applied on the knife at this point. This is known as the head of the
wound.
(2) As the assailant draws the knife away from head, it is gradually withdrawn.
This causes the wound to become increasingly shallow towards the tail [Fig
12.17 (A) and (B) ]. Finally as the knife leaves the tissue, the depth is so less
that only the skin is cut alone. The portion where the epithelium alone is cut is
known as tailing of the wound. It indicates the direction of the incised
wound. Because only epithelium is injured, the tail of the incised wound
typically shows no bleeding.
6. Beveling cut
[A] A beveled cut refers to a cut which is not perpendicular to the skin surface,
but at an angle [Fig 12.18]. [B] Direction of weapon: (1) Vertical – If weapon
enters vertically the edges of wound would make a nearly 90° angle with the
skin surface [Fig 12.18(1)] (2) Oblique – If weapon enters obliquely [Fig
12.18(2)], one edge would make an angle >90° with the skin surface (beveled
edge). The other edge (under mined edge) makes an angle <90° with the skin
surface. It mostly lies submerged under the surface. (3) Nearly horizontal – If
weapon enters nearly horizontally [Fig 12.18(3)], a wound with a flap is
produced. [C] Manner – Beveling usually indicates homicide, and may indicate
relative position of the assailant and victim.

7. Hemorrhage
(1) Hemorrhage is more as the vessels are cut cleanly.
(2) Spurting will occur if an artery has been cut.

C. Cut Throat Wounds

1. Suicidal and homicidal
Please see Table 9.
D. Age of Incised Wounds
1. Gross
(1) Fresh – Hematoma formation
(2) 12 h –
(i) Edges red, swollen, adherent with blood and lymph
(ii) Leukocytic infiltration
(3) 24 h – Dried clot in the form of crust or scab.

2. Histopathology
(1) Few min –
(i) Reactive changes in tissue histiocytes
(ii) Dilatation of capillaries
(iii) Swelling of vascular endothelium
(iv) Margination and emigration of neutrophils
(2) 12 h –
(i) Reactive changes in fibroblasts
(ii) Monocytes appear in exudate
(3) 16 h – Mitotic divisions begin in monocytes
(4) 24 h –
(i) Epithelium begins to grow at the edges
(ii) A continuous layer of endothelial cells cover the surface
(iii) Vascular buds begin to form
(5) 72 h – Formation of vascularized granulation tissue
(6) 4-5 d – New fibrils are formed
(7) 1 wk – scar formation if wound is small.

E. MLI of Incised Wounds

(1) Reconstruction of crime – Incised wounds help to reconstruct the crime and
to corroborate or refute the story of the victim by enabling to determine (a) the
nature of the weapon – sharp edged (b) Age of injury and (c) Direction of
force
(2) Decomposed body - Differentiation between incised and lacerated body is
difficult
(3) Body with incised wounds immersed in water soon after death - Blood in
wounds is lysed by water. It is difficult to make out if the wounds were AM or
PM. Same is true of lacerations and stab wounds also.
(4) Manner of injury –may be accidental, suicidal or homicidal.

V. CHOP WOUNDS

Chop wounds (or slash wounds) are same as cut lacerations. Please see under
the heading “Type of lacerations”.

VI. STAB WOUNDS

A stab wound is one which has depth as its maximum dimension [cf. incised
wound]. It is produced when force is delivered along the long axis of a narrow or
pointed object, such as an arrow, dagger, knife, nail, needle, screw driver, spear
etc. into the depths of the body.
Salient features:
(1) How caused - either when the instrument is driven in body, or the body is
 pressed against or falls against the instrument.
(2) - (a) Punctured wound (Fig 12.20) is a stab wound caused by a circular “ice
pick” shaped object. Wound caused by other instruments (eg daggers etc)
would be called stab wounds. A punctured wound typically terminates in flesh.
It may be due to (i) Insertion of pins, needles or threpeutic injections in flesh
(ii) Snake bite (iii) Drug addiction [there will be older scars around from
earlier injections]. In case of deaths due to therapeutic injections, drug
addiction or snake bite, excised tisse around the punctured wound must be
sent frozen for chemical analysis. Homicidal needle punctures may often be
missed, especially when inflicted at base of skull near nape of the neck
(injurying the medulla), axilla (injurying a major b.v.), or through natural
orifices (fornix of upper eyelids, inner canthus of the eye, ears, nostrils,
vagina, rectum). The locations of such punctured wounds are intentionally
chosen to hide their location. These are known as concealed puncture
wounds [concealed trauma – ch 8; concealed firearm wounds – ch 13].
Needle punctures are a common method of infanticide (through anterior or
posterior fontanelles). (b) Penetrating wound (Fig 12.20) enters into a body
cavity (chest, abdomen, skull, knee joint, orbit, scrotum, etc) without coming
out. Should be described in a sequential order, i.e. entrance wound, depth and
direction of track, specific location of termination Ex - (i) Stab wound to the
chest or abdomen [having no exit] (ii) Gunshot wound to the head [having no
exit] (iii) Needle injury to the eye (iv) Tracheostomy wound (v) Intracardiac
injection [as in resuscitation attempts] (vi) Drainage tubes in chest and
abdomen (c) Perforating wound (Fig 12.20) has both an entry and exit
wound [same terminology is used in relation to fracture of skull [ch 17] and
firearm wounds; penetrating wounds occur when a bullet enters the body and
does not exit – has only an entry wound; perforating wounds occur when the
bullet passes completely - has both an entry and exit wounds]. Should be
described in a sequential order as above, i.e. entrance wound, path of wound,
exit wound.
(3) Entry and exit Ex - (i) Stab wound to the chest or abdomen [with exit] (ii)
Gunshot wound to the head [with exit] (Fig 12.21)- In perforating wounds,
wound of entry is (a) larger (b) has inverted edges. Exit is (a) smaller [due to
tapering of blade] (b) has everted edges. In firearm wounds entry is smaller;
exit is larger [ch 13].
A. Characteristics
1. Length
Length of stab wound ‘l’ is normally less than width ‘w’ of weapon. To
predict the correct width ‘w’ of the weapon, the edges of the wound must be
brought together [by fingers, or by an adhesive tape. This releases tension in the
elastic fibres, so the wound displays its original length ‘l’, which should then be
measured [Fig 12.22].
2. Width
Width of stab may not indicate the true thickness of blade, because of retraction
of wound edges, after knife is withdrawn.
3. Margins
(1) If weapon has sharp edges [eg knife, dagger]– Margins are clean cut
[incised stab wound]
(2) If weapon has rounded edges [eg cricket stump, ice-pick, pencil, screw
driver etc]– Margins are contused and lacerated [lacerated stab wound].
4. Depth
(1) Greatest dimension - Depth is the greatest dimension in stab wounds.
(2) Assessing depth – In the living, a stab wound must never be probed in order
to assess depth, as it may disturb a loose clot and may lead to fatal
hemorrhage, and produce false tracks. It should always be done in the OT,
when the wound is being repaired. In the dead - Radiopaque dye must be
injected in the track and X-ray taken Alternatively incision is made at the side
 of stab wound, and tissues dissected parallelly. Reveals depth, without
disturbing the actual wound A pliable rubber tubing may be introduced gently,
then taken out and measured. Once inside, the tube may be made more rigid
by inserting a probe.
5. Shape
(1) Cleavage lines of Langer:
(i) These are the lines within the skin along which the dense feltwork of
intimately intermingled dermal collagen and elastic fibres is arranged [Fig
12.23]. Named after Austrian anatomist Karl Langer (1819-1887),
professor of anatomy at Budapest and Vienna, who first described them in
1861.
(ii) They are arranged in parallel rows, which are same in all persons
(iii) In the extremities – they run longitudinally; In the neck and trunk -
circumferentially
(iv) Stab wound which runs across the wound causes gaping; a parallel cut does
not and an oblique cut produces an oval or sometimes a crescentic or
semicircular wound.
(2) Shape of stab wound – Normally it is slit shaped with two acute angles. But
it would depend upon -
(i) Cleavage lines of Langer. Same weapon may produce different sized wounds
on different parts of body, depending upon the course of these lines
(ii) Depth of penetration
(iii) Direction of thrust
(iv) Movement of blade within wound
(v) Movement of victim
(vi) Shape of weapon
(vii) Tenseness or wrinkling of skin.
(3) Shapes of weapon influencing shapes of stab wounds:
(i) Single edged weapon -produces tear drop [or rain drop], triangular or wedge
shaped [Fig 12.24]. The angle caused by sharp edge is sharp and the one
caused by blunt edge is rounded, blunt or squared off. Sometimes the blunt
edge causes a split, such that the wound appears like the tail of a fish
[fishtailing, fishtail wound].
(ii) Double edged weapon – produces elliptical, slit like or spindle shaped
wound. Both ends are sharp.
(iii) Single edged weapon producing spindle shaped wounds – (a) If some length
of knife near the tip was double edged, and the skin was too elastic. The
angle corresponding to blunt edge would reflect the shape of initial few cm.
As weapon is thrust deeper, excessive elasticity would “let in” the weapon
without corresponding change in shape (b) If weapon penetrated at an
oblique angle. As the knife perforates at an angle, the blunt edge does not
impart its shape as it does not contact it.
(iv) Single or double edged weapons producing a wound with both ends blunt –
if weapon was thrust up to the level of ricasso [short, unsharpened section
of blade between the cutting edge and guard]. In both the above cases a
correct shape of weapon can be given by examining the serosal planes
[pleural, pericardial, peritoneal surfaces, liver capsule] and muscle fasciae,
which clearly show the wedge shape. Thus in multiple wounds examination
of all wounds is necessary before opining upon the nature of weapon.
Possibility of multiple weapons [both single and double edged] must also
be kept in mind.
(v) A round object with a pointed end like an ice pick or a spear – produces a
circular wound. May resemble a small caliber bullet wound. Leon Trotsky
[1879 – 1940], the famous Russian revolutionary was assassinated by a
mountaineering ice axe much like an ice pick.
(vi) A round object with a blunt end [eg pointed stick, ball point pen, metal rod]
– (a) produces a circular wound with bruised, inverted and ragged ends. (b)
Blunter the tip, the coarser or more stellate would be the whole it makes (c)
as such weapons are likely to be rusted and dirty, foreign material eg dirt,
splinters, rust etc would be found within the wound
(vii) Pointed square weapon eg a screw driver – produces a cross-shaped injury,
each of 4 edges producing its own “cut”.
(viii) Fall on a pointed article – would produce circular wound
(ix) Stabbing with a fork – produces a cluster of punctured wounds depending
upon the number of prongs. A two edged fork would produce two separate
wounds, their distance depending upon the angle at which it is struck. An
open scissors would produce a similar wound.
(x) Thick relatively blunt-edged weapons eg bayonets – produce penetrating
wounds with excessive laceration around
(xi) Stabbing followed by rocking, twisting or victim moving around – L or V
 shaped wounds, with one limb corresponding to main or primary wound
and the other an extension of it as it exits
(xii) Knife with a serrated edge – produced a ragged wound.
6. Direction
(1) Penetration at an angle – bevelled margin on one side and undermining
[undercut] on the other [Fig 12.18],
(2) Weapon withdrawn partially and thrust again – externally only one entry
wound would be visible. But two or more punctures seen in soft parts.
7. Opinion
Proper examination of stab wound would enable the pathologist to opine upon
(1) Amount of force used
(2) Dimensions of the weapon
(3) Direction in which weapon hit the victim
(4) Movement of knife within the wound
(5) Taper of blade
(6) Type of weapon.
B. Complications
(1) Air embolism – especially in stabs of neck vessels
(2) Choking due to inhalation of blood
(3) Hemorrhage
(4) Infection
(5) Pneumothorax.

C. MLI of Stab Wounds

(1) Concealed puncture wounds – used homicidally. Please see above.
(2) Depth of wound – indicates force used
(3) Direction and dimension of wounds – Indicate relative positions of
assailant and victim
(4) Manner of production – Suicide, accident or homicide may be determined
[Table 10]. (i) Hara-kiri [syn Seppuku, “cutting the belly”] – (a) Unusual
form of suicidal stab wound on the abdomen. (b) At one time used as a capital
punishment. (c) Procedure - The victim inflicts a single large wound on the
abdomen with a tanto or wakizashi [ceremonial Japanese swords], while in a
 sitting position; or falls forwards upon it, and pulls out intestines (d) Cause of
death - (I) Excessive bleeding (II) Sudden . in intra-abdominal pressure ".ed
cardiac return" Sudden cardiac collapse.
(5) Multiplicity of wounds – Indicates overkill [more wounds inflicted than
were necessary to kill]. This happens in sexual and revenge murders
(6) Shape of wound – Indicates class and type of weapon [eg single edge,
double edged]
(7) Time of attack – Can be determined by assessing the age of stab wound
(8) Must be differentiated from incised and lacerated wounds [Table 11].
VII. DEFENSE WOUNDS

Defense wounds are caused by immediate and instinctive reaction of the victim
to save himself, either by raising the arm to prevent the attack, or by grasping the
weapon [Fig 12.26].
Salient features:
(1) Incidence – Seen in about 40% of all homicides.
(2) Nature of Defense wounds – (a) When attacking weapon is sharp - (i)
Incised wounds (ii) perforations of forearms or hands [rarely] (b) When
attacking weapon is blunt - (i) abrasions and bruises (ii) rarely fractures of
carpals, metacarpals and phalanges (c) Defense wounds “due to attack” –
When the victim “attacks” but the basic purpose is to defend himself. This
may cause wounds (i) on the victim [eg on knuckles of hand or fingers, when
the attacker was struck in the mouth] (ii) on the attacker [teeth bite marks on
the hands and forearms of the attacker]. This is a rare case where Defense
wounds are on the attacker and not on the victim.
(3) Location – (a) Palm, when the victim tries to seize the weapon [“active”
 defense wounds] (i) If single edged weapon is used - incised wound is either
on the palm or on the bends of fingers or thumb [Fig 12.27] (ii) If double
edged weapon is used – incised wounds are found both on the palm and
fingers (b) Back and ulnar aspects of forearm, when the victim raises the
hands or arms for protection [“passive” defense wounds] (c) interdigital
spaces Knuckles rarely thighs and feet, if the victim is thrown on ground, and
she curls up and kicks the assailant.
(4) Defense wounds are absent - (a) when it is a case of suicide or accident (b)
in cases of homicide when (i) victim is unconscious (ii) taken by surprise (iii)
attacked from back (iv) weak, debilitated, old, very small infant (v) drunk or
under influence of drugs
(5) Injuries simulating Defense injuries - Offensive injuries may sometimes
simulate Defense injuries Victim punches assailant on his anterior teeth with
his fist"may sustain knuckle lacerations which may look like Defense injuries
Victim punches assailant on his head or chin"may sustain fractures of
metacarpals
(6) Medico legal importance - Homicide - Defense wounds indicate homicide
Sexual assault - If they are present in females, especially on thighs.
VIII. OFFENSE WOUNDS

Offense wounds [syn, protective wounds] are reverse of defense wounds and are
caused by offense rather than defense.
Salient features:
(1) Injuries - (i) Abrasions, (ii) contusions, (iii) lacerations over knuckles, (iv)
boxer’s fractures [ch 17]
(2) Lacerations - may be caused if a fist was planted on the victim’s open mouth
with exposed teeth. The injury should be matched with dislocated or fractured
teeth. Saliva of victim would be detected in such lacerations. Teeth of victim
would reveal blood of assailant [Locard’s exchange principle].

IX. SELF-INFLICTED WOUNDS

Self inflicted [syn, fabricated, fictitious, forged or invented wounds] are those
inflicted by a person on his own body or by another with his consent.
Salient features:
(1) They may be created ab initio or an existing injury may be deepened or
enhanced
(2) Reasons - (i) By an assailant - To change appearance of wound so he may
not be connected with the crime or so that he may pretend self defense (ii) By
a victim - (a) To blackmail an enemy (b) To charge an enemy with assault or
attempted murder (c) To make a simple injury appear more serious (iii) By
military men - To escape service or to get leave (iv) By policemen, servants,
watchmen acting in collusion with thieves and robbers - To show they were
defending property (v) By prisoners - To bring a false charge of attack against
police officers (vi) By women - To bring a false charge of rape against an
enemy. (vii) by mentally ill – eg paranoid schizophrenics may inflict hundreds
of small wounds upon themselves (viii) Religious mendicants – may cut away
their penis, scrotum and testes in order to achieve celibacy.
(3) Nature - (i) Incised – mostly (ii) burns, Contusions, Stabs – next most
common (iii) lacerated, firearm wounds – rarely. Author has dealt with a case
of self inflicted firearm wound in the right thigh. The allegation was that his
enemy had shot him. However it was a near discharge phenomenon. The track
of wound was virtually vertical, entering just below the inguinal ligament and
exiting from just above the knee.
(4) Characteristics - (i) General – (a) Multiple, (b) parallel, (c) superficial (d)
generally on accessible areas, but rarely may be found on back. Author has
dealt with several cases, where the perpetrator fixes a razor blade at the end of
a cleft-stick and makes cuts on back with the help of a mirror. (e) An injury
covered by clothing and unaccompanied by any damage to it is self inflicted,
as the perpetrator lifts cloth to inflict injury. It cuts are seen on cloth, they are
inconsistent with the injury (f) Old linear scars in nearby areas or other parts
of body suggest similar occurrences earlier. However they are often seen in
mental patients too. (g) Rarely a person may inject local anesthetic before
inflicted such wounds. Needle puncture mark must be looked for around the
wounds. (h) history is inconsistent with injuries, eg an injury may be old, and
history given may be of recent assault and vice versa; history may be of attack
with lathis, but examination may reveal incised wounds etc. Additional
characteristics of specific wounds are (ii) Incised wounds are (a) They are of
 equal depth at origin and termination. (b) avoid sensitive and vital areas eg
face [eyes, ears, nose, lips] (c) direction – on top of head, behind forwards
[tailing in front]; from above downwards on outer side of upper arms;
horizontal or from below upwards on forearms and abdomen; variable on
chest, and from below upwards on abdomen and legs. (iii) Stab wounds (a)
Site – fleshy areas eg upper arms; virtually never on chest. (iv) Burns –
superficial; mostly on left upper arm. Usually produced by lighted cigarette
tips, but unusual objects may be used.

X. THERAPEUTIC WOUNDS

Therapeutic or iatrogenic wounds are wounds produced by doctors during

treatment (eg. surgical wounds of chest and abdomen for drainage tubes,
tracheostomy, thoracotomy, laparotomy, cut-open wounds for IV catheters etc).
Salient features:
(1) Sometimes these wounds may be mistaken for traumatic wounds (Fig 12.28).
It is thus best to study original MLC and operation notes before starting pm.
(2) Sometimes an original traumatic wound may be enlarged and used for
therapeutic purposes (i) drainage tube may be inserted in a homicidal stab
wound (ii) gunshot wound of the abdomen may be used for colostomy.

XI. MEDICOLEGAL IMPORTANCE OF WOUNDS

It must be determined if the wound was suicidal, homicidal or accidental in
nature (Table 12).

13. Firearm Injuries

I. INTRODUCTION
A. Firearm
A firearm is a thermodynamic machine in which the potential energy of the
gun-powder is transformed into the kinetic energy of the projectile.

B. Ballistics
Ballistics is the science which deals with the motion of projectiles.
1. Internal ballistics
Internal ballistics deals with what happens to a cartridge and its bullet from the
time the trigger of the gun is pulled until the bullet exits from the gun barrel.
Also known as initial, interior or proximal ballistics.
a. Muzzle velocity
Muzzle velocity is the speed at which a projectile leaves the muzzle of the gun
(cf striking velocity). Muzzle velocities range from subsonic (i.e. less than the
speed of sound 340 m/s or 1200 ft/s) for some air guns to supersonic [about
1,800 m/s (5900 ft/s)] for tank guns.
2. External ballistics
External ballistics - deals with what happens to a bullet or projectile from the
moment it leaves the gun barrel to the moment of impact on a target or object.
Also known as exterior ballistics or intermediate ballistics.
3. Terminal ballistics
Terminal ballistics – deals with study of behavior of missiles after they penetrate
their target.
a. Wound ballistics
Wound ballistics is a subset of terminal ballistics when the target is living tissue
(human or animal).
b. Striking velocity
It is the velocity of the projectile at the point of impact (cf muzzle velocity).
4. Forensic ballistics
Forensic ballistics is scientific investigation of firearms in a criminal or civil
matter.

II. CLASSIFICATION OF FIREARMS

Table 1 gives classification of firearms based on five criteria, of which first is
most popular.
A. According to Condition of Barrel
1. Rifled firearms
A rifled firearm is one which has spiral grooves (riflings) inside its barrel, which
impart spin to bullets. Just as the grooves inside a bolt make the nut turn around,
grooves inside rifled weapons make the bullet revolve (Fig 13.1).
When bullet exits the rifled firearm, it is revolving around its own axis at 3000
rev/sec (Fig 13.2). This stabilizes the bullet, and gives it better penetrating
power. If no rifling were present inside the firearm, the bullet would topple over
very soon. Rifled firearm is more lethal. It is used to shoot large animals. It fires
bullets (cf smooth bore firearms which fire pellets). Ex. Pistol, Revolver, Rifle,
Carbine, Air rifle.

a. Lands and Grooves

A rifled firearm has spiral grooves inside its barrel. They range from 2 to more
than 20 [6 grooves are commonest. They may be clockwise or anticlockwise
(depending on manufacturing company). The raised portions inside the barrel are
known as lands, and the grooved portions, the grooves (Fig 13.3). The land
width is generally in the range of .069-.090”; groove depth is usually between
0.002” and 0.005” (lead bullets require deeper grooves than copper jacketed
bullets).

Primary and secondary markings

In all rifled firearms, the bullet is slightly larger than the barrel [so that it can
provide perfect obturation]. Thus as it passes through the barrel, not only do the
lands and grooves leave their mirror image on it (primary markings, Fig 13.4),
but also the unique linear markings which are specific to each gun (secondary
markings) [ch 30"class evidence and individualizing evidence]. The sides of the
barrel in fact act as a “machine die” to reproduce all markings on the bullet,
which comes out carrying a faithful reproduction of all markings inside the
barrel. [A] Primary markings can reveal the manufacturer of the gun (since
each company has different number of riflings, their widths and depths, the
direction of their rotation and twist etc). They are part of class characteristics of
a fired bullet [please see below] [B] Secondary markings [Fig 13.4] can
pinpoint the individual gun, and are due to individual variations in each gun.
These can in turn be due to (i) unavoidable individual variations in minor details
of rifling at the time of manufacturing itself (ii) repeated wear and tear of each
gun (iii) gun cleaning activities by the user (iv) metallic fouling – each time a
shot is fired, the bullet leaves some metal inside the barrel, which hardens.
Because of the infinite possible variations, each gun leaves its own characteristic
secondary markings on the bullet, which are often called the “fingerprint of the
gun”. The phrase is however not entirely correct; while fingerprints do not
change during the life an individual, markings made by guns change gradually
over the life of a gun – as it wears out more and more. They can also altered by
the gun owner very easily by cleaning it repeatedly. They are synonymous with
individual or accidental characteristics of a fired bullet [please see below]. [C]
Primary, secondary and other markings described below are not seen if bullet
was discharged without the agency of a firearm [eg heat-induced firing; please
see above].

b. Caliber or Gauge
Caliber (Gauge) is the internal diameter of a rifled firearm.
Salient features:
(1) Traditionally it is measured between two opposite lands (Fig 13.5) [Groove
or rifling diameter is the distance between two opposite grooves].
(2) Units - (i) measured either in caliber units [one caliber equals 1/100 inch] or
mm.
c. Examples of rifled firearms
i. Revolver
A revolver is a rifled firearm that has a cylinder containing multiple chambers
(usually 6) where cartridges are placed for firing.
ii. Pistol
Pistol is a hand arm which uses cartridges contained in a vertical magazine [syn,
clip], placed within the butt.
iii. Rifle
A rifle is a firearm with a long barrel, the bore of which is rifled.
(1) Muzzle velocity – 450-1500 m/s [average – 800 m/s]
(2) Pressure in firing chamber – 20 ton/sq inch
(3) Range – 1000-3000 meters [Table 2].
iv. Carbine
A carbine [German: Karabiner] is a shortened version of rifle (having a shorter
barrel) firing the same ammunition at a lower velocity, used especially by
mounted troops.
Salient features:
(1) Barrel – is <55 cm in length
(2) Muzzle velocity – varies according to the make. A typical carbine [The M1
carbine] has a muzzle velocity of 600 m/s. There are carbines with lesser and
higher muzzle velocities, eg Standard .30 carbine"(580 m/s) and M4
carbine"880 m/s.
(3) Range – 300 meters.
v. Other firearms
Gyrojet – A family of unique firearms developed in the 1960s. Named for the
method of gyroscopically stabilizing its projectiles. Firing small rockets rather
than inert bullets, they had little recoil and didn’t require a heavy barrel to resist
the pressure of the combustion gases. Velocity on leaving the tube was very low,
but increased to around 1,250 feet per second at 30 feet. The result was a very
lightweight weapon with excellent ballistics. Now they are out of production.
Fuel is kept at the base of projectile, which keeps burning during its flight.
Because of this, the entrance wound shows a singeing effect even at very large
distances.
2. Smooth bore firearms
A smooth bore firearm is one whose barrel is smooth from inside. It fires
multiple pellets instead of single bullets. The pellets do not rotate on their axis
as does the bullet. A smooth bore firearm [Ex. Shotgun, Musket (smooth)] is
less lethal, less accurate and has a lesser range than a rifled firearm. It is used to
shoot small, moving targets (birds, hare etc), which change their direction
unpredictably. Multiple pellets ensure that at least one pellet hits the “moving”
target.
a. Bore
Bore is the internal diameter of a smooth bore firearm. What is caliber (please
see above) to a rifled firearm is bore to a smooth bore firearm. Traditionally (and
for historical reasons), it is not expressed in inches or mm, but in a very
different way – the bore. The bore is defined as the number of equal sized
spherical balls made from 1 pound (454 g) of lead, each of which exactly fits
the inside of the barrel. Thus the 12 bore gun is one whose diameter is that of a
ball of lead of such a size that 12 such balls could be made from 454 g of lead.
The smaller the bore, the larger the diameter of firearm. A 20 bore gun has a
smaller diameter than that of a 12 bore gun (Fig 13.10).
b. Examples of smooth bore firearms
i. Shot gun
A shotgun (also known as a scattergun or peppergun) is a firearm that fires
several spherical pellets (shots) simultaneously. Sometimes a single projectile
(slug) is also fired.
Salient features:
(1) Shoulder arm
(2) Barrels: (i) Like rifles, they may be single barreled or double barreled. (ii)
The barrels may lie side by side or one above the other [Over-and-under
shotgun]. Single barrels and side-by-side are more common. (iii) Length -
 varies from 18–36” (45–90 cm), with 26 and 28” the most common. [U.S.
federal law requires a minimal barrel length of 18” for a gun to be classified
as shotgun]. The length of the barrel makes handling and hiding difficult;
barrels are thus often shortened [sawn off] for criminal activities.
(3) Range - Effective, 30–40 m; terminal, 50 m.
(4) Muzzle velocity – 300 m/s.
(5) Bore – (for definition, please see above) May vary from 4 to 40. (i) .410 -
This is the only bore, which is referred to by the size in inches [spoken as
“four-ten”]. If converted to bores, it would be 68 bore. So called because it
was originally made from worn out .303 rifles. It fires a single lead shot of 6.2
g with a muzzle velocity of 1700±100 ft/sec. In India, it was originally used
by Railway Protection Force, but its use is now obsolete.
(6) Insertion of cartridges - Shotgun is made to “break” or open on a hinge for
insertion and extraction of cartridge cases
(7) Loading – can be done in two ways just as in rifles. Muzzle loading shotguns
are commoner than muzzle loading rifles
(8) Choke – If the entire barrel from breech to muzzle end is of same diameter, it
is called a cylinder bore, true cylinder or unchoked gun. If a shot gun has a
cylinder barrel, the individual pellets tend to scatter, decreasing the probability
that the target will be hit. To keep the pellets together, the terminal 7-10 cm of
the barrel is constricted. This constriction is referred to as choke.
ii. Musket
A musket is a muzzle loading, smooth bore firearm designed for use by infantry.
A soldier armed with a musket is called a musketeer.
Salient features:
(1) It is a shoulder arm
(2) muzzle velocity – 350-600 m/s.

3. Air guns
An air gun can be rifled (air rifle, air pistol), or smooth bore. It fires projectiles
by means of compressed air or other gas (CO2 ), in contrast to a firearm which
burns a propellant.
Salient features:
(1) Most air guns use metallic projectiles as ammunition. Air guns that only use
plastic projectiles are classified as airsoft guns. It is not really a separate
class of firearms.
(2) Muzzle velocity – 80-105 m/s [average – 100 m/s]
(3) Range – Effective, 30 m; Terminal, 40 m
(4) Injuries – Usually minor. Death can occur from injury to head, heart and
abdomen.
(5) Exit wounds – usually not seen, because of low kinetic energy.

III. CARTRIDGE
A cartridge, (called a “round”, when it is loaded within the gun), is a single unit,
comprising of four components (i) the case (shell) (ii) the projectile (bullet in
case of rifled firearm, and pellets in case of smoothbore firearms), (iii) propellant
(gunpowder) and (iv) primer. The latter three are enclosed within the case, which
is made to fit the firing chamber of a firearm precisely. Fig 13.8 depicts a rifled
firearm cartridge; Fig 13.9, a smooth bore firearm cartridge. Cartridges are
always used in breech loaders. In muzzle loading guns each component of the
cartridge, eg gunpowder, wads, ammunition etc is introduced separately from the
muzzle end [please see “loading mechanisms” above].

A. The Rifled Firearm Cartridge

The rifled firearm cartridge (Fig 13.8) - It consists of a metal case (1) in
which is filled the propellant [gunpowder] (2). The metal provides strength and
hardness to the case; it must withstand pressures up to 40,000 pounds per square
inch, generated by the gases produced. The base is rimless in case of pistol, but
has a rim (3) in revolver and rifles both (in the figure it shows a rim). The
primer (4) is filled in the rim (in rim fire ammunition, as in the picture). The
bullet (5) fits into the upper end of the case, the case mouth (6) the edges of
which are “pressed” into the body of the bullet, leaving an impression on the
bullet - the cannelure (7). It serves to hold the bullet in place. The bullet may
have knurls (8), which hold lubricant. Lubricant serves two purposes (i) it
lubricates the interior of the barrel as the bullet grazes past it. This makes it
easier to clean it later. (ii) provides for a better seal for gases coming from
behind. Knurls may be visible on the outside (as in the diagram), or beneath the
neck of the cartridge case and not visible.
B. The Smoothbore Firearm Cartridge
The smoothbore firearm cartridge [Fig 13.9] – It consists of a paper or plastic
case (1), which keeps all components in place, and provides a waterproof
container for the propellant (2) (gunpowder). The base is covered in a thin brass
covering, (12) to provide it with strength; it must be hard enough to withstand
ramming (pushing in) and extraction (pulling out). In “high brass” cartridges
(more powerful) the brass extends further up along the sides of the shell, while
in “low brass” cartridges (less powerful) the brass does not extend so far up. The
brass not only provides strength to the base of cartridge, but the difference in
appearance also provides shooters with a way to quickly differentiate between
high and low powered ammunition. Sometimes entire cartridge may be made up
of solid brass. At the bottom is the propellant (2) and the primer (4). There is a
rim (3) at the base to hold the cartridge securely in chamber; it also makes
extraction easy. The powder is covered by an overpowder card disc (5). It acts
as the gas seal (known as obturation), and is placed firmly over the powder; it
may be made of paper or plastic. Without the overpowder card disc (5) [and two
components above it (6) and (7)] the gas would just blow through the shot rather
than propelling it. Over it is the wad (6) [also known as card wad or cushion].
It is designed to compress under pressure, to act as a shock absorber and
minimize the deformation of the shot, to take up as much space as is needed
between the powder and the shot and to act as a piston for the shot above (for
this purpose the diameter of wad is kept greater than that of the bore of the gun).
Wad also contains grease, which lubricates the bore, each time a shot is fired.
Functions of card wad thus are (I) Obturation (II) shock absorber (III) to act as
piston for shot (IV) lubrication (V) They also act as spacers, setting the correct
volume for the propellant and shot charges. One of the functions of overpowder
card disc (5) is to protect the powder from the “grease soaked wad”. Wads are
made of cork, felt, glazed board, plastic or straw board. Above this is undershot
card disc (7). It prevents the shots from getting lodged in the felt wad. Also
serves to hold the shot together as it moves down the barrel. Both wad and
undershot card disc play a part in obturation too. Above this are the pellets (8),
and over it is the overshot card disc (9). Overshot cards give a stable platform
for the crimp (10) - one of the most critical factors of a proper shotgun cartridge.
At the moment of fire the firing pin strikes the base of the primer cup (11)
igniting the primer, which in turn sets fire to the gunpowder. Cartridges are
numbered according to the shot they contain. The total length of smoothbore
cartridge varies from 5-7 cm.
C. Components of a Cartridge
1. Primer
Primer is shock-sensitive explosive mixture that ignites when struck
mechanically. It is a primary explosive [ch 15][hence the name primer]. Primer
is kept in a small metal cup that is inserted into a recess in the center of the base
of the cartridge. When the trigger is pressed, the firing pin strikes the cup and
crushes the primer between the cup and an anvil to produce a shower of sparks
[incandescent particles] and hot gas that pass through a flash hole to ignite the
powder charge.
a. Composition of Primer
Memory Aid 1: Composition of primer
B L2 A S T –
1. Barium nitrate
2. Lead peroxide
3. Lead styphnate
4. Antimony Sulfide
5. Tetracene
Others:
(1) Diazodinitrophenol [DDNP]
(2) Mercury fulminate
(3) Pentaerythritol tetranitrate [PETN]
(4) Potassium perchlorate. Mercury fulminate is not used now in most countries
because mercury tends to corrode brass walls of cartridge on long storage. It is
being used in India though.

2. Propellant
A propellant is a material that is burnt to propel ammunition. It may be black
powder, smokeless powder or a combination of the two.
Salient features:
(1) Propellants are secondary explosives [ch 15]
(2) Primer merely provides a spark to set the propellant on fire. To put it
figuratively, while primer is the spark plug, propellant is the petrol.

a. Black powder
Black powder (also called gunpowder) is a mixture of potassium nitrate (75%),
charcoal (15%) and sulfur (10%) by weight. Black powder was first produced by
Roger Bacon in 1250.
Salient features:
(1) Functions of each component: (i) Charcoal - fuel (ii) Sulfur - (a) binding
agent (b) fuel (c) .es the temp of ignition (d) -es the speed of combustion (e)
 improves shelf life by reducing water absorption (iii) KNO3 - Oxidizer.
(2) Size of grains - Black powder is essentially a surface burning powder, larger
the surface area, the quicker it will burn. Larger surface area is achieved by
grinding the black powder very fine. The four most commonly used
granulations are graded as FFFFg, FFFg, FFg, and Fg (also known as 4Fg,
3Fg, 3Fg and Fg respectively). More the F’s, finer the grain, with FFFFg
being the finest and Fg the coarsest. Thus 4Fg would burn fastest and Fg,
slowest.
(3) Production of gas - One gram of black powder on burning produces 280 cc
of gas. The chemical formula involved is: 10KNO3 + 3S + 8C"2K2CO3 +
3K2SO4 + 6CO2 + 5N2. A typical cartridge may contain between 1-20 grams
of black powder, depending on the size of projectile, it is expected to propel.
P53 Enfield rifle introduced by the British in 1853 contained 4.4 g [68 grains]
of black powder.
(4) Gunpowder is a low explosive having a low brisance [please see chapter 15
– Explosion injuries].
(5) Obsolete now - Today black powder is used only in muzzle-loading firearms,
blank cartridges, refilled shotgun cartridges and country made cartridges. It is
rarely if ever used in standard, factory-made cartridges.

b. Smokeless powder
Smokeless powder is a misnomer – it is not entirely smokeless; it only produces
less smoke than the black powder. Thus blackening is produced even with
smokeless powders. Smoke is however somewhat grayish white, and it produces
blackening of a much lighter color.
Salient features:
(1) Composition - Nitrocellulose alone (single-base powder); nitrocellulose+
nitroglycerin (double-base powder); nitrocellulose+ nitroglycerin +
nitroguanidine (triple-base powder). Triple base powders are usually restricted
to large caliber ammunition.
(2) Burning - Produces much less flame and smoke. They are more completely
burnt than black powder
(3) Color – Varies from bright orange to bluish black
(4) Shape – minute globules, flakes, square, rectangles, irregular discs, cylinders
and long threads.
(5) One gram of nitrocellulose on burning produces 950 cc of gas.
(6) Smokeless powder is not used in muzzleloading firearms; it can damage the
firearm and might injure shooters and bystanders.

c. Semismokeless powder
Combinations of black powder [80%] and smokeless powder [20%]. Though
some advantages have been claimed for the powder, the mixing procedure is
very dangerous. This has prevented its extensive production and use.

3. Projectile [bullets and pellets]

a. Bullets (used in rifled firearms)

i. Nomenclature of bullet
Traditionally the bullet is made of soft metal (eg lead) with varying amounts of
antimony and/or tin added to it to provide hardness. Its various parts are (i)
Bourrelet - Finely machined ring of metal just behind the ogive (ii) Caliber –
its cross sectional diameter (iii) Heel – base (iv) Meplat - The flat area at the tip
of bullet [in flat nosed bullets only] (v) Nose - Tip of bullet (vi) Ogive - The
curved area extending backwards from the nose to the main cylindrical portion.
ii. Types of bullets
Bullets may be classified according to (a) shape of nose (b) shape of heel (c)
their material (d) their covering (e) special purpose they serve (f) Forensic
scientist’s point of view.
(a) According to shape of nose
(1) Hollow point [Fig 13.10(1)]- is an expanding bullet that has a pit (hollow) in
its tip so that it expands upon entering a target. It serves two purposes
(i) maximizing tissue damage and blood loss
(ii) decrease penetration (controlled penetration is necessary where over-
penetration could cause collateral damage, as on an airplane).
(2) Round nose [Fig 13.10(2)]- has a semiblunt, conical shape
(3) Spire point [Fig 13.10(3)]- Made with two straight lines, joined to the shank
at a specified angle [typically 9-12 degrees]. The spire shape is like a pencil
tip or “church spire” in shape.
(4) wadcutter [Fig 13.10(4)]- Bullet specially designed for shooting paper
targets, usually at close range and at subsonic velocities typically under 800
 ft/s. Used in handgun and airgun competitions. Has a flat front (with a
relatively sharp edge along the perimeter) that cuts a very clean hole through
the paper target, making it easier to score. Because the flat nosed bullet is not
well suited for feeding out of a magazine (used in pistols), wadcutters are
normally used only in revolvers. To address this problem, semiwadcutter is
used
(5) semiwadcutter [Fig 13.10(5)]- is designed to be fired from pistols. It
consists of a conical section (a) that ends in a smaller flat surface (b), and a
thin sharp shoulder (c) at the base of the cone. The flat point punches a clean
hole, and the shoulder opens the hole up cleanly.

(b) According to their covering

(1) Non-jacketed [syn, unjacketed]– Made up of lead. As they travel down the
barrel, lead is scratched off, and sticks to the inside of barrel (lead fouling of
the barrel). To prevent lead fouling, these bullets are lubricated with grease or
some other lubricating compound. This is contained in knurls (Fig 13.8).
Copper gilding is used extensively in .22 high-velocity rimfire ammunition.
(2) Jacketed:
(i) Two types (a) Full Metal Jacket (FMJ); Total Metal Jacket (TMJ) bullets -
Bullet nose is fully encased by a jacket; base is base (b) Full Metal Case -
Both the base and the nose of a bullet are fully encased by the jacket;
typical of military bullet where expansion is not desired
(ii) used in semi-automatic pistols.
(iii) Have a lead or steel core covered by an outside jacket. It is made up of
gilding metal, gilding metal-clad steel, cupro-nickel (copper and nickel), or
 aluminum.
(iv) Jackets generally range from 0.0165 to 0.030 in. in thickness.
(v) Advantages – (1) Imparts additional strength to the bullet. Help to prevent
the bullet from breaking apart (2) higher muzzle velocities are achieved (3)
Prevent lead fouling as well as jamming of the gun that occurs if a large
number of lead bullets are fired [due to lead deposition on barrel and other
areas of the gun] (4) prevents damage to bores from steel or armor-piercing
core materials.
(vi) Deformation – Full metal jacketed bullets exit undeformed; unjacketed
bullets show deformations
(vii) Armor-piercing bullet [APB] - (a) APB is a special jacketed bullet fired
from small arms [Armor-piercing rifle and pistol]. They are meant to
penetrate bullet-resistant vests [commonly known as bulletproof jackets]
and other tough targets like automobile doors.
(3) Partially jacketed [syn - Semi-Jacketed, SJ bullet, soft-nosed bullet, Soft-
point bullet – Jacket is left open at the tip, exposing some of the lead inside.
Exposed lead expands upon impact.
(c) According to special purpose they serve
(1) Dum-dum bullet (Fig 13.11):
(i) A special type of expanding bullet [please see below]
(ii) A British military bullet developed for use in India during the late 1890s.
(iii) Jacketed .303 bullet with the jacket nose open to expose its lead core.
(iv) Immediately balloons out on impact with the target thus increasing the
damage.
(v) The phrase ‘Dum-Dum’ is now taken to include any soft-nosed or hollow
pointed bullet.
(2) Expanding bullet:
(i) Expands on impact, increasing in diameter to produce a more serious wound.
(ii) Also known as mushroom bullet, because of the mushrooming that occurs
on impact.
(iii) The two typical designs are the (a) hollow point bullet [please see above]
and the (b) soft point bullet. (c) Dum-dum bullet is a special type of
expanding bullet
(3) Frangible bullet:
(i) Made of bonded powdered iron [or lead], which fragments on impact.
(ii) Caliber – mostly .22
(iii) Normal use – target practice by police, shooting galleries, to stun cattle
(iv) Recovery and matching - of fragments is difficult because of fragmentation
(v) They do not ricochet [please see below]
(vi) If bone is penetrated, they are usually recovered in an eroded state.
(vii) D/d - An x-ray would reveal several fragments which look like small
pellets. One may wrongly conclude that the victim was hit by a shot gun
(4) Tracer bullet - Special kind of bullets that contain a powder in their base
that burns very brightly during their flight. This enables the shooter to follow
the bullets’ trajectories, so he can adjust his aim accordingly. It is used both in
ground as well as aircraft guns.
(d) According to Forensic scientist’s point of view
(1) Crime bullet - Bullet with which crime is committed. This bullet is
recovered from the body of the victim, and is produced in court as evidence;
hence also known as evidence bullet. Crime bullet is fired by the criminal
(2) Test bullet - Bullet that is fired from a suspect weapon by the forensic
scientist, so he can compare the markings on the bullet with that of the crime
bullet. If the markings match perfectly, the suspect weapon is the actual
weapon used for crime. Both crime and test bullet when presented in the court
as evidence are known as exhibit bullet.

b. Pellets and slugs (used in smooth bore firearms)

i. Types
Pellets are of four types
(1) Soft or drop shot [made of soft lead] and
(2) Hard or chilled shot [made of lead; hardened by antimony]
(3) Steel shot [made of steel. Individual steel pellets weigh less than
comparatively sized lead pellets, and thus travel less] and
(4) Plated shot [lead shot plated with copper or nickel or both.
ii. Shot size and form
In any one given cartridge, the number of pellets may vary from 1 to several
thousand.
(1) Dust shot is the smallest size of shot. Up to 2600 tiny particle like shots in a
12 bore cartridge. Used to shoot house sparrows
(2) Bird shot - 200-400 shots (.05-.18” in diameter) in a 12 bore cartridge.
Mainly used to hunt birds in flight (hence the name). Birdshot sizes are
numbered similar to the shotgun gauges; the smaller the number, the larger the
shot. Generally birdshot is just called “shot”, such as “number 9 shot” or “BB
shot”.

IV. FIREARM WOUNDS

A firearm wound is an injury produced by a firearm.

Salient features:
(1) Types:
(i) Entrance [syn, entry, in-shot] wounds
(ii) Exit [syn, out-shot] wounds
(2) Confusing appearances - Firearm wounds are normally recognized easily.
However they may sometimes simulate other injuries
(i) Bullet strikes glass before striking body – simulate lacerated wounds
(ii) Glancing wounds – simulate incised or lacerated wounds
(iii) Wounds by rifled weapons – simulate wounds inflicted by burning pointed
stick or red-hot poker
(3) Differentiation:
(i) Firearm wound causes crushing of tissues [produce an actual hole]
(ii) Stab wounds tend to seal after the knife is withdrawn.

A. Wounding from Firearms

1. Effects of distance on Firearm wounds
[Fig 13.13] shows the ejection of flame, smoke and unburnt powder particles
from the gun just as it is fired. Flame travels the shortest distance; smoke goes
farther; and unburnt powder particles go farthest.
a. Flame
(1) Flames causes burning, searing, scorching and singeing.
(2) Burning is used in relation to skin and singeing in relation to hair.
(3) In the hair – Keratin melts due to excessive heat and then resolidifies on
cooling, producing a clubbed, rounded appearance at the tips
(4) Searing and scorching are areas of intense burning; typically seen in near
contact wounds.
(5) Darkening and parchmentization of burnt area – occurs after death due to
drying.
b. Smoke
(1) Produced by complete combustion of gun powder.
(2) Responsible for blackening [syn, fouling, smudging]. Primer residues also
do not enter the skin, and produce blackening
(3) Smoke simply deposits on the skin, without actually entering inside the
dermis [Fig 13.14].
(4) Appearance – Normally black, but if powder is smokeless, grayish or white
deposit.
(5) How to detect:
(i) Take a wet cotton gauge, sponge or towel and try cleaning the wound; the
 blackening would vanish. Cotton would be blackened.
(ii) IR photography – detects blackening on both skin and clothing.
(iii) In bone - Lead may be rubbed off from bullet, which may look like soot.
Test for metals would be negative in true blackening.

c. Unburnt powder
(1) Produced by incomplete combustion of gun powder, which has the
consistency of very fine sand.
(2) Appearance:
(i) Multiple punctate abrasions - seen as small dark brown dots [individual tattoo
point] surrounding the wound.
(ii) Individual tattoo points - are surrounded by a small magenta colored zone of
micro-contusion. Caused by the trauma of high speed impaction of powder
grains with rupture of small bv.
(3) How to detect:
(i) Take a wet cotton gauge, sponge or towel and try cleaning the wound;
tattooing would not vanish. Cotton would not be blackened.
(ii) Can be identified under a hand lens or dissecting microscope, picked up for
analysis [by a little probing] and even ignited with a red hot wire for
confirmation.
(iii) IR photography – detects tattooing on both skin and clothing.
(4) Measurement - Tattooing must be measured in all directions around the
wound. Tangential wounds produce unequal tattooing [also burning, singeing
and blackening] around the wound [Fig 13.15].
(5) Range - If tattooing is visible, the wound is termed an intermediate-range
gunshot wound [please see below].
(6) Miscellaneous points:
(i) Palms and soles are very resistant to powder tattooing [thick skin resists entry
of powder].
(7) Table 4 gives important ranges.
2. Ranges

Please see Table 5.

Memory Aid 3: Relative distances of various effects of firearms
1. Burn Black Train - Burning, blackening, tattooing [from inside to outside]. Simple, but with
lesser detail.
2. TuB2erculoSiS – Tattooing, Blackening, Burning, Singeing and scorching [from outside to inside]. This
memory aid adds details to burning effects too.
a. Contact
(1) Characteristics:
(i) Range - The term is applied when the muzzle of the weapon is held against
the surface of the body at the time of discharge.
(ii) In all contact wounds, soot, powder, carbon monoxide [carboxyhemoglobin,
COHb], and vaporized metals from the bullet, primer, and cartridge case are
deposited in and along the wound tract. Their concentration .es with -ing
depth.
(2) Classification - Contact wounds may be
(i) hard
(ii) loose
(iii) angled or
(iv) incomplete [a variation of angled].

i. Hard contact
Characteristics:
(1) Muzzle of the weapon is jammed “hard” against the skin, indenting it, so that
the skin envelops the muzzle; contact is so hard that gases cannot escape out
(2) immediate edges of the entrance are seared by the hot gases of combustion
and blackened by the soot
(3) This soot [along with unburnt powder] is embedded in the seared skin and
cannot be completely removed either by washing or by vigorous scrubbing of
the wound [Fig 13.16]. This is thus a special case, where burnt powder
[smoke] also produces tattooing.

ii. Loose contact

Characteristics:
(1) The muzzle, while in complete contact with the skin, is held lightly against it.
(2) Gas preceding the bullet, as well as the bullet itself, indents the skin, creating
a temporary gap between the skin and the muzzle through which gas can
escape. This temporary gap cannot be produced in hard contact wounds.
(3) Soot carried by the gas is deposited in a zone around the entrance
(4) This soot can be easily wiped away.
(5) A few unburnt grains of powder may also escape out this gap and be
deposited on the skin around the zone of soot [Fig 13.17].
iii. Angled contact
Characteristics:
(1) The barrel is held at an acute angle to the skin so that the complete
circumference of the muzzle is not in contact with it.
(2) Gas and soot escaping from the gap, where contact is not complete, radiate
outward from the muzzle, producing an eccentrically arranged pattern of soot.
(3) The soot is arranged in two different zones. (a) More noticeable zone – [often
the only one seen] is a smaller blackened seared area of skin or cloth having a
pear, circular, or oval configuration [Fig 13.18] (b) Less noticeable zone - is a
larger fan-shaped zone of light-gray soot that radiates outward from the gap.
On the skin (the less noticeable zone with respect to soot) this light zone is
usually washed away, or obscured by bleeding or removed in cleaning the
wound for examination.
(4) A few unburnt grains of powder may also be deposited in these zones.
(5) The entrance wound is normally present at the base of the seared blackened
zone. All or at least the majority of the seared blackened zone will be on the
opposite site of where the muzzle was in contact with skin, and thus “points”
the way the gun was directed.
(6) As the angle between the barrel and the skin -es, i.e., the barrel moves toward
a perpendicular position to the skin, the entrance hole will be found more
toward the center of the zone.
(7) If the angle between the barrel and the skin .es, the gap between the muzzle
 and skin becomes larger, and more material can escape through the gap.
(8) At some point, the gap becomes sufficiently large that unburnt grains of
powder escaping through the gap will skim over the zone of seared skin,
fanning out from the entrance, impacting distal to the entrance wound in a fan
shaped pattern of powder tattooing.

iv. Incomplete contact

Characteristics:
(1) This is a variation of angled-contact wound.
(2) Muzzle of the weapon is held against the skin, but because the body surface
is not completely flat, there is a gap between the muzzle and the skin [Fig
13.19].
(3) Difference with angled contact – In angled contact, the barrel is held
intentionally at an angle. In incomplete contact there is no intention to hold it
 an angle; angle is produced because of curvature of surface.
(4) A jet of soot-laden gas escapes from this gap producing an area of seared,
blackened skin. Powder grains may also be deposited on the skin.
(5) Location of this seared, blackened zone can be anywhere in relationship to
the muzzle circumference, depending on where the gap is.
(6) Incomplete contact wounds are most often seen in self-inflicted contact
wounds of the head due to long arms, i.e., rifles and shotguns.
b. Near contact
(1) Characteristics:
(i) Range - The term is applied when the victim is within the range of flame
(ii) Muzzle of the weapon is not in contact with the skin, being held a short
distance away.
(iii) The distance, however, is so small that the powder grains emerging from the
muzzle do not have a chance to disperse
(iv) Flame effects - Present. There is an entrance wound, surrounded by seared,
blackened skin. The zone of searing is wider than that seen in a loose
contact wound.
(v) Overlying it is a wide zone of soot
(vi) The soot in the seared zone is baked into the skin and cannot be completely
wiped away.
(vii) Small clumps of unburned powder may be present in the seared zones.
(viii) Up to this distance the shot is also called “point blank“.
(2) Classification - Contact wounds may be
(i) straight near contact
(ii) angled near contact.
c. Intermediate
Characteristics:
(1) Range - The term is applied when the victim is within the range of tattooing.
(2) Tattooing - Present. Powder grains expelled from the muzzle produce
tattooing. These markings are the sine qua non [essential requisite, hallmark]
of intermediate-range gunshot wounds.
(3) Blackening – May or may not be present.
d. Distant
Characteristics:
(1) Range - The victim is outside the range of flame, blackening and tattooing
(2) No burning, singeing, blackening or tattooing are seen. The only marks on
the body are those produced by the mechanical action of the bullet [entry
wound].

B. Wounds from Shotguns

1. Ranges
(1) Table 4 gives general ranges.
(2) Some provisos are:
(i) Larger the caliber, the greater the distance to which the powder is discharged.
(ii) The cards travel for 2 m
(iii) Wads travel for 2-5 m
(iv) Wads produce minor injury up to a distance of 3 m.
2. Entry wounds
Entry wounds from shotguns depend upon
(1) Distance from which weapon is discharged
(2) Size of the shot
(3) Nature of the explosive
(4) The firearm.

a. Distance
At close range, the shotgun is the most formidable and destructive of all small
arms. Discharge from a shotgun produces a long shallow cone of shots. Its apex
is at the muzzle of the gun. Farther along the victim is, larger the wound is [Fig
13.20].

i. Hard Contact
Characteristics
(1) Cruciate laceration [syn, cruciate wounds, stellate laceration]:
(i) Laceration in the shape of a cross [+ or x].
(ii) Seen especially if there is bone immediately underneath [eg skull].
(iii) Caused by gases entering beneath the skin, and coming out through the same
wound [blowback phenomenon].
(iv) Sometimes there may be subsidiary linear tears extending from the cruciate
wound.
(2) Bone underneath – shows
(i) a large irregular hole with fissured fractures running from the margins
(ii) Crazy-paving fracture - is sometimes seen in skull. Involves base of skull,
roof of orbits and middle ears [bursting fractures, burst head].
(iii) Burning, blackening and tattooing of bone – In skull wounds frequently soot
may enter the inner surface of skull and may blacken it from inside. Dura
may also be blackened.
(3) Soiling and burning – of the wound minimal or absent, because all material
discharged from gun is driven within the wound.
(4) Track of wound:
(i) Seared and charred by flame
(ii) Blackened by powder and smoke
(5) Blast effects - shattering and destruction of tissue are maximal. Effect .es and
range -es.
(6) Backspatter [syn, German - Rückschleuderspuren]– It is the ejection of
blood, cloth fibres, hair and tissue fragments from the entry wound towards
the firearm.
Salient features: (i) Occurrence and degree - depends on (a) anatomical
location of wound (b) range and (c) caliber of weapon. (ii) Etiology [of
backspatter]- (a) Relevant for contact wounds - (i) negative pressure in the
barrel created immediately after firing (ii) Expansion of gas trapped s/c. (b)
Relevant for all ranges -(i) intra-cranial pressure generated by the temporary
cavity and (ii) tail splashing - backward streaming of blood and tissue along
the lateral surfaces of the bullet. This may represent an early stage of the
temporary cavity effect. (iii) Seen in all firearms, but more common with
shotguns. (iv) Seen at all ranges, but blood and tissues etc are found within the
muzzle of gun only in contact and close ranges. (v) MLI - Crime scene
reconstruction. It can be found inside the barrel, outside the weapon, on the
 person shooting and on persons or objects nearby. Assists in differentiation
between suicide and homicide.
(7) If entry is through a cloth:
(i) Ammunition hole in the cloth touching the muzzle - may be surrounded by a
flat ring corresponding to the outline of the muzzle
(ii) Loose fibres of the cloth - in the center of hole may be turned in and stuck in
the wound. Sometimes they may be turned outwards due to pressure of
gases returning from the entry wound
(iii) Smoke - (a) may enter within clothing, and may blacken each layer of
clothing within, and even skin. (b) If cloth is bloodstained, soot may not be
recognizable. IR and UV photography may be helpful. Also examine the
cloth from inside, where soot may be recognizable
(iv) Entry hole in cloth - shows singeing. Synthetic clothes may show melting of
fibre tips
(v) A ring of burning - may be seen around the wound also.
(8) Other features - same as those of loose contact and near contact.

ii. Loose Contact and near contact

(1) Blast effects:
(i) Lesser than those seen in hard contact;
(ii) Cruciate wounds are less commonly seen.
(iii) Shotgun wounds up to this range cause much more destruction than rifled
weapon due to larger amount of gunpowder producing greater amount of
gas.
(2) Dimensions:
(i) Single
(ii) Usually round, but may be oval in angled shots
(iii) Equal to the bore in size
(3) Margins:
(i) Often ragged [because of individual shots at the periphery] and torn [because
of gases]
(ii) Usually inverted, but may be everted due to rebounding gases
(iii) Charring, blackening and tattooing - (a) around the wound and also within
the wound. (b) Corona– is seen sometimes. (I) It is a circular zone of soot
deposited around the hole with a clean area between it and the hole. (II)
 Cause - Due to faster-moving gases near the hole not allowing soot to
deposit there. As the effect of gases lessens at greater distances, it is seen
only up to near contact range. (III) Seen in all firearms up to near contact
range
(iv) Contused [caused by impact of heavier particles of unburnt gun powder]
(v) Color – (a) of entry wound as well as track is pinkish due to CO within the
gases combining with Hb to form COHb. (b) Intensity - gradually .es along
the track, till it almost disappears near exit. But very rarely it may be
present in exit wounds also. (c) COHb may be demonstrable in blood also.
(vi) Muzzle impression [muzzle imprint] – seen around the wound. (a) Causes -
It is an impact or imprint abrasion caused by (I) firm mechanical pressure
of impact of metal rim against the skin (II) s/c expansion of gases lifting the
skin forcibly up against the muzzle from within.[copy abrasion, imprint
abrasion, recoil abrasion]. (b) Appearance - Rarely it presents a perfect
imprint of the muzzle end, but mostly it is an incomplete, indistinct bruise.
(c) Double barreled shotgun – Leaves a tell-tale impression, which may
help in identifying the firearm. The impression caused by the unused barrel
is often more distinct [Fig. 13.21]. (d) If muzzle impression is present, other
collars may be absent as all material is driven inside the wound. (e) May be
absent due to - (I) explosive damage associated with discharge [because
gases have restricted space for expansion; blast effect]. In head wounds, the
entire contour of head and face may be destroyed, location of actual entry
being virtually impossible. (II) Recoil"Immediate removal of weapon away
from wound
(4) Track of wound – as in hard contact
(5) Underlying tissues – Entry of gases has following effects
(i) s/c tissues - show severe disruption. A pocket may sometimes form
containing blood mixed with soot and gunpowder
(ii) Chest wounds – Skin and s/c tissues may be peeled away from the rib cage to
form a pocket, which collapses after sometime.
(iii) Abdominal wounds – Coils of intestine may lie outside
(iv) extrusion of soft tissues [eg fat] through the wound [due to a “tail vacuum”
produced by rapid entry of gases in the wound].
(6) Depth of the wound – Contains
(i) pellets
(ii) Brightly colored plastic granules – if they were present as a filler between
the shots [please see above]
(iii) felt, wads or plastic cups.
(7) Bone underneath – may show fractures as in hard contact, but since gases
do not enter wound, blackening and tattooing of bone absent.
(8) Entry within mouth:
(i) abrasion or bruising of both lips
(ii) splitting of angle of mouth [due to blast effect]
(9) If entry is through a cloth – Same as in hard contact above.

iii. Up to 1 meter
(1) Wound – Appearance same as in loose contact and near contact wounds
(2) Burning, singeing, blackening and tattooing – around the wound present.
(i) Burning – (a) Wide flare of narrow rim of hyperemia or even blistering
caused by flame (b) Unequal burning in angled wounds [Fig 13.15]
(ii) Blackening and tattooing – More extensive than in near contact wounds.
Intensity .es as distance -es.
(3) Color – pinkish, as above. Seen up to a distance of 60 cm.
(4) If power piston is used:
(i) It opens up between 30-60 cm. If victim is standing beyond this range, there
would be a circular entrance wound, with a typical “flower petal” or
“Maltese cross” pattern abrasion around it.
(ii) These petal marks can occur even if the entrance site is covered with
clothing.
(iii) By 90 cm, the petals fold back; beyond this range this characteristic abrasion
would be absent.
(5) Depth of the wound – Same as above. Plastic granules [if present within the
shot] may produce very fine punctate abrasions around the pellet holes
[Pseudo-tattooing].
iv. 1-2 meters
(1) Central aperture – up to 2 m, all shots travel together [en masse] and enter
through a single hole. There is a single central aperture of diameter 3-4 cm. As
distance -es, the size of hole also -es.
(2) Distance at which outer shots just begin to separate:
(i) variable (a) 1 m – with sawed-off gun (b) 2 m – with unchoked guns (c) 4 m –
with full choke guns.
(ii) Appearance - Central aperture has jagged margins [scalloping]. The wound
appears as if a rat has gnawed at the margins [rat hole].
(3) Up to 2 m – Cards and wads are found deep within the wound. If found
within the wound, bore of gun may be estimated.
v. 2-4 meters
(1) Just after 2 m:
(i) Central aperture - irregular
(ii) Individual pellet holes - are seen at the periphery of central aperture. Their
entry wound is round and shows a rim of abrasion around their margins
(iii) Cards and wads – strike the body below the shotgun wound and fall off,
producing bruises
(2) 3 m – Central aperture is surrounded by separate openings, in an area of
about 8-10 cm in diameter
(3) As distance -es:
(i) Diameter of central aperture progressively .es
(ii) Individual pellet wounds -in number
(iii) Occasionally few individual pellet holes may coalesce producing larger
entrances than those produced by individual pellets
(4) Examination of individual pellets – recovered from wound would reveal
deformation. Cause - lead is softer"rubs against the inside of
barrel"deformation. Intense heat inside barrel may cause melting and fusion of
several pellets.
vi. >4 meters
(1) Shots spread widely - All pellets enter the body separately, producing its
own track
(2) In head shots:
(i) pellets may not have sufficient energy to enter skull. If at all they enter, they
do not enter the entire thickness of the brain
(ii) Cavitation – minimal or does not occur
(iii) Infarcts – may be produced by lacerations of blood vessels by pellets or
bone fragments.

b. Size of the shot

(1) At close range wounds produced by shots of different sizes are similar
(2) Penetrating power of large shot > small shot
(3) Smaller the shot, more minutely irregular are the edges.

c. Nature of the explosive

Smokeless powder causes less blackening and tattooing than black powder, and
it is somewhat grayish white rather than black.

d. The firearm
Appearance of wound depends upon
(1) Bore
(2) Length of barrel – shorter barrels usually produce deposits over larger areas
(3) Presence or absence of choke, and in case of presence, its degree.

3. Exit wounds
(1) Syn – In all firearms, they are also known as outshoot wounds.
(2) Generally not present – due to low kinetic energy [because of .mass and
.velocity of pellets]. They exit in following conditions:
(i) Nature of projectile – balling or welding of shot [please see below], large
caliber buckshot, rifled slug
(ii) Part of body struck - Thin [neck, extremities]. Occasionally head. However
entrance wounds in mouth or nose are not accompanied by exit wounds
because of resistance offered by hard palate. In such cases, shots may be
seen to lie between the skull and scalp at the back or side of head.
(iii) Manner in which struck - (a) Contact wounds (b) Tangential wounds [where
some pellets have a very short track through the body]
(3) Appearance of exit wounds [when present]:
(i) Disruption - Greater than in entrance wounds
(ii) Margins – everted [because the unsupported skin is struck from within]
(iii) No burning, singeing, blackening and tattooing
(iv) If the skin is well supported – may show “shored” exit wounds. Please see
below.
(4) In contact wounds of head – following features are seen:
(i) Krönlein shot [syn, Krönleinschuss]- (a) In contact wounds, occasionally a
large exit wound is produced, and the gases entering through the wound
cause the expulsion of entire brain out of the skull, which may be found
relatively intact at some distance from the body [evisceratio cerebri
sclopetaria totalis]. (b) This phenomenon is only seen in contact wounds,
where gases enter inside the wound, and is much more common in high
velocity missiles [muzzle velocity [600–800 m/s]. (c) In high velocity
missiles, temporary cavitation produces an enormous force within the brain,
which may also cause expulsion of brain [please see “cavitation of brain”
above]. (d) May be seen in exit wounds of other firearms also eg pistols,
revolvers and rifles. (e) Named after German surgeon Rudolf Ulrich
Krönlein (1847-1910) who first described it in 1899.
(ii) Eyeball – may be blown out of socket.
4. Special effects

a. Billiard ball ricochet effect

Billiard ball ricochet effect is excessive spreading of shot pellets due to passage
through an intermediate target such as a glass window.
b. Balling or welding of shot
Balling [syn, welding] of the shot is exactly the reverse of billiard ball ricochet
effect.
Salient features:
(1) Here the shots stick together and travel for large distances as a single mass. Spread is thus less than
what it should be and causes the forensic pathologist to estimate less distance than actual.
C. Wounds from Automatic Pistols and Revolvers

1. Entrance wounds
a. General
(1) Components of an entrance wound - from center to the periphery are as
follows [Fig 13.23].
Memory Aid 4: Zones of rifle firearm entry wound
Mnemonic 1: Wild Goat Ate Chara - Wound defect, Grease collar, Abrasion collar, Contusion collar
[from within outwards]
represents Entry wound. Either may be
Mnemonic 2: CAGE [from without inwards]. E
remembered according to comfort level.
(2) Revolvers and automatic pistols - cause similar wounds [both entry and
exit]. However penetrating power of pistol bullets is much greater because of
greater velocity. Pistol bullets are also more often coated with hard metal.
i. Wound defect
This is the actual entrance wound of the bullet
ii. Grease collar
Grease collar [syn – bullet wipe, bullet wipe soiling, burnishing, dirt collar,
grease ring, lead ring, leaded edge, metal fouling, metal ring] is a ring of grease
seen around the entry wound in the form of a gray coloration. It is present at all
distances.
Salient features:
(1) Cause – As bullet moves down the barrel, it collects debris and metal from
barrel, dirt, gun oil, powder and primer residue, soot etc over it. This is
deposited on to the skin, as the bullet penetrates the body. [Fig 13.8].
(2) Less common – in jacketed bullets
(3) If wounded area is covered by clothing, seen on clothing only [importance of
examining clothings]
(4) Detection:
(i) Naked eye
(ii) IR photography
(5) Wiping – collar produced by grease can be wiped, but not that produced by
metal, which enters inside the skin. The term “fouling” is used in two
contexts:
(i) fouling of the barrel [please see above], and
(ii) fouling of the entrance wound [as mentioned here].
(6) MLI - may link the entrance wound to a weapon because metallic elements
from the grease collar may be linked to those from the weapon.
iii. Abrasion collar
Abrasion collar [syn - Abrasion ring, marginal abrasion] is a ring of abrasion
around the entry wound which is present at all distances.
Salient features:
(1) Cause: (i) friction - between the bullet and the epithelium, which occurs as
the bullet indents and perforates the skin. (ii) massive temporary
overstretching - of the skin adjacent to the bullet perforation (iii) rotational
movement of bullet [opinion differs on this cause].
(2) Width of abrasion ring - varies with the caliber and type of the firearm
(3) Appearance: (i) Color - Reddish at first; becomes reddish brown or dark
brown as it dries (ii) concentric or eccentric – depends on the angle of bullet
entry [Fig 13.24]. (iii) Patterned abrasion collar – Sometimes pattern of fabric
may be imprinted on skin if fabric is interposed in between.
(4) Peeled keratin – is often seen outer to the abrasion collar. The stratum
corneum of skin is raised to form a slightly frayed edge.
(5) Absent – when tissues are soft and yielding, eg abdomen, buttocks.
iv. Contusion collar
Contusion collar [syn, Contusion ring] is a ring of contusion around the entry
wound which is present at all distances.
Salient features:
(1) Cause - damaged blood vessels in the dermis.
(2) Abrasion and contusion collar may often overlap.

b. Hard contact
(1) Muzzle impression [syn, recoil impression] is seen only in hard contact
wounds.
(2) All features same as those seen in shotgun hard contact, eg backspatter, blast
effects, fractures etc [please see above].
(3) If entry is through a cloth – same features as in shot gun above at this
range.

c. Contact shot
The description is true for all 4 variants of contact wounds [please see above]
(1) Discharge from muzzle eg flame, gases, metallic particles, powder and
smoke are blown inside the track. Because of this blackening and tattooing are
absent or minimal. These features begin when muzzle to target distance >1
cm. Corona may be present in loose contact wounds.
(2) Burning and singeing - due to flame and hot gases. Can be seen both
macroscopically and microscopically.
(3) Size - Wound is large; tissues within lacerated; shows cavitation due to gases
 entering within
(4) Shape – Cruciate, elliptical, stellate or triangular,
(5) Edges – Normally inverted, but may be everted if there is bone underneath.
Due to gases coming out after entering the wound.
(6) Abrasion and contusion collar - present
(7) Bone underneath, entry through cloth, track of wound, underlying
tissues – same as in shotgun wounds at this range.

d. Near contact
(1) All features present in shotguns at this range are also present here, eg
backspatter, corona etc
(2) Entrance wound:
(i) Shape - circular.
(ii) Edges - inverted. However gases rebounding from within the wound may
level them up or even evert the margins.
(iii) Burning and singeing - present
(iv) Surrounding skin - hyperemic. Shows bruising, burning, blackening,
tattooing. Abrasion collar, dirt collar and grease collar present.
(v) Surrounding hair - Burnt and singed. Ends clubbed due to intense heat.
(3) Bone underneath, margins, track of wound, underlying tissues – same as
in shotgun wounds at this range.

e. Intermediate
(1) Intermediate range in case of pistols and revolvers is up to 45 cm [Table 4,
Table 5].
(2) up to 15 cm:
(i) Burning and lacerating effects of gases present. Lost beyond this range due to
dispersion
(ii) Small fragments of metal derived from the interior of barrel or bullet itself
are embedded in the skin surrounding the entry wound.
(3) Entry wound:
(i) Shape - rounded; slightly smaller than the diameter of the bullet [retraction
due to elasticity of skin]. Due to this, caliber of bullet cannot be determined.
(ii) Margins - bruises, inverted, zone of abrasion and grease collar, blackening
and tattooing.
f. Distant
(1) Entry wound:
(i) Shape - same as in intermediate range.
(ii) Margins - inverted. No burning, blackening or tattooing.
(2) Special appearances:
(i) Distant entry wounds of palms and soles - irregular, often having a stellate
appearance. There is usually no abrasion ring. Thus they may look like exit
wounds.
(ii) Deformity and fragmentation - (a) Presence of a full or partial metal jacket
has a major effect on deformity. (b) Bullets with full metal jackets - often
remain in one piece and usually do not deform much. (c) Trail - These
projectiles typically do not leave a trail of lead fragments along their path.
(d) Semi jacketed, hollow-point, nonjacketed, and soft-point bullets - tend
to deform on impact or break apart, leaving a telltale trail of metal
fragments through the soft tissues. (e) Mushrooming - Hollow-point
handgun bullets usually deform by simple mushrooming with minimal
fragmentation, whereas high-velocity soft-point rifle bullets usually
undergo marked fragmentation. (f) ”Lead snowstorm” appearance - This
fragmentation of high-velocity bullets creates a “lead snowstorm”
appearance on radiographs. The area over which the lead snowstorm
fragments are deposited in the soft tissues widens as the distance from the
entry site -es. Thus, a conical distribution of lead fragments is seen on
radiographs, with the apex of the cone pointing toward the entry site. (g)
Deformation, fragmentation, cavitation, dissipation of KE and stretching
are the major causes of lethal effects of bullets (h) Such deformities and
fragmentation may be seen in closer shots also. However as closer shots are
more likely to exit, these are described here in distant shots.

g. Skull
i. Beveling
Beveling is the scraping away of bone chips from the unsupported table of skull
caused due to intense vibration set up by the bullet.
Salient features:
(1) Mechanism: (i) Outer table - As bullet strikes the skull, it sets up intense
 vibrations in the skull. Outer table is supported by the inner table, and thus
shows a clean punched-in hole. However the inner table is unsupported and
bone chips scrape away from it, causing bone chips to come away from it in
the shape of a cone. It produces a sloping surface on the inner table [beveling]
(ii) Inner table – Situation gets reversed; now outer table is unsupported and
shows beveling.
(2) Bone chips – from the inner table at the entry may produce lacerations in the
dura, and get driven inside the brain forming their own accessory tracks.
(3) Asymmetry of beveling – helpful in determining angle of fire. Also
corroborated by different levels of entry and exit wounds.
(4) Exit wound – is larger due to (i) deformity and (ii) tumbling of bullet
(5) Radiography - can reveal beveling of the bone, and thus direction of bullet
travel may be determined even in the living by X-raying the skull.
ii. Puppe’s rule
Puppe’s rule is used to determine sequence of shots when more than one shot
have been fired at the cranium. First enunciated by Georg Puppe (1867-1925)
of Germany.
Salient features:
(1) Principle - First bullet will cause certain fracture lines to radiate from the
hole it causes [Fig 13.25]. The fracture lines emanating from the second bullet
hole (b) will stop at the lines caused by the first hole. The fracture lines
emanating from the third bullet (c) would stop at the lines caused by first as
well as second and so on.
(2) Rule is applicable to multiple instances of blunt force caused by any object,
or even multiple objects, eg a bullet first and then an iron rod etc. Also
applicable to other flat bones eg sternum, hip bone
(3) Also determines the sequence of shots in a glass window or some other
similar object.
h. Shot through clothing
(1) If entry occurs through clothing, an examination of clothing can reveal range
of fire.
(2) Contact shot:
(i) clothing shows cross-shaped perforation
(ii) Deeper layers of cloth and skin around bullet hole are blackened
(iii) Pieces of cloth may be carried inside the wound along with the bullet
(3) Close shot - Clothing may absorb or filter out all discharge products except
the bullet.
(4) At all distances - if a lead of full metal jacketed bullet is used, a gray to
black rim is produced on the clothing [bullet wipe]. It is the equivalent of
grease collar seen in unclothed entry wounds [please see above], and caused
due to same reasons.

i. MLI [of entrance wounds from pistols and revolvers]

(1) Caliber Determination from Entrance Wounds:
(i) in skin – Not possible due to elasticity [small wound than bullet], tumbling
and explosive effects [larger wound than bullet].
(ii) in bone – possible to some extent. A small bullet may produce a larger
wound [explosive effect, tumbling], but not vice-versa. Bone does have
some elasticity though; thus a 9-mm bullet may produce a 8.5-mm defect,
but not much smaller.

2. Exit wounds
(1) Shape – Extremely variable. They may be crescentic, cruciate, elliptical,
round, slit like or stellate [star shaped].
(i) Slit like wounds - are produced by (a) Body factors - (I) folding skin [axilla,
umbilical area, groin, buttock crease] (b) Bullet factors - (I) a bullet exiting
sideways or a (II) tumbling bullet. May resemble a stab, incised or lacerated
wound
(ii) Stellate wounds – seen in exit wounds of head. May resemble contact
entrance wounds.
(2) Size:
(i) Usually bigger - than entry
(ii) Both entry and exit may be of same size - with high velocity bullets
(iii) Exit is smaller than entry in some exception cases - (a) breaking of bullet -
within the wound, with only a portion exiting (b) bullet entering through
folded or creased skin (c) contact wounds [due to tearing of soft tissues by
inrushing gases] (d) Tangential entry - with focal avulsion of tissues (e)
Tumbling or yawing of bullet
(3) Large variation in shape and size is due to:
(i) Deformation of bullet
(ii) Tumbling of bullet
(iii) Breaking up of bullet in the tissues and exiting as several pieces. If jacketed,
 the jacket may separate completely or in part.
(iv) The bullet may contact bone and/or cartilage, and their fragments may be
blown out of the body with the bullet.
(v) unsupported skin at exit tends to shatter and tear. The resulting defect may
bear little relationship in shape to the missile that caused that defect.
(4) Edges:
(i) Everted, puckered, torn. Eversion of wound often differentiates exit from
entry wound. However both entry and exit wounds may be everted in (a)
Fatty persons [due to protrusion of fat] (b) Putrefaction [due to protrusion
of gases].
(ii) No burning, singeing, blackening, tattooing; no abrasion or contusion collar
[exception - shored exit]
(iii) Pieces of contused hemorrhagic s/c fat may protrude through the defect.
(5) Thermal artifacts – A bullet is hot when it enters the body and still so at the
time of exit. Rarely burning as a thermal artifact may be seen at the site of
bullet exit as at the site of entrance. However blast effect of muzzle gas would
be absent.
(6) Exit wounds may not be seen:
(i) in distant shots
(ii) If bullet fragments within body [Frangible bullets; please see above].
(7) Differentiation from entrance wounds:
(i) May not be easy always, and may look alike.
(ii) Reliance must not be made on information from police, victims, or onsite
witnesses as it may be false or inaccurate.
(iii) Helps in determining (a) direction of fire (b) posture of victim at the time of
fire (c) number of bullets in the body – Can be determined by the “Odd
and even rule“. The rule states that if the total number of bullet holes (both
entrance and exit) is odd (or even), then the number of bullets remaining in
the patient is odd (or even) as well [Table 6].
(iv) Table 7 lists some imp differences.
(8) Shored [syn, supported] exit wounds: Exit wounds shored or supported by
a firm material or object pressed against the skin.

D. Wounds from Rifles

(1) Appearance - Wounds are similar to those produced by revolvers and
 pistols, but produce more damage
(2) Burning, blackening, tattooing - Table 4.

1. Contact wounds
a. Contact wounds of head
Extent of damage - These are most devastating wounds, producing a bursting
rupture of the head.
b. Rifle discharge in mouth
1. Massive wounds from the gas and the temporary cavity occur.
2. Lacerations of the corners of mouth, nasolabial folds, medial to the eyes, at
the bridge of the nose and along the nasal ridge.
c. Contact wounds of the chest and abdomen
External appearances
The wound of entrance is typically circular in shape and usually larger in
diameter than those due to pistol bullets. The wounds do not have the peculiar
explosive appearance of similar wounds in the head. There is almost never
tearing of the skin due to gas.
2. Intermediate-range wounds
Severity of injuries: Both intermediate range and distant head wounds, show a
wide range in the degree of severity, depending on the type of bullet and the
entrance site in the head.
3. Distant wounds
Entry wound is usually smaller than the diameter of bullet; appears as if it was
made by forcing a lead pencil into skin.
4. Exit wounds
(1) At all ranges, exit wounds of the chest and abdomen have the same
appearance. They are larger and more irregular than the entrance wounds, with
the majority of exit wounds ≤25 mm in diameter.
(2) If the bullet strikes a bone, extensive shattering and communion takes place.
In such cases, exit may be as large as the palm of the hand.
(3) Sometimes several small holes are found around the large exit. These are
caused by fragments of bone being driven out.

E. X-ray Examination of Gunshot Wound Victims

X-ray helps to
(1) determine defects, fractures etc
(2) determine the break-up pattern of the bullet
(3) locate air embolism accompanying large vessel damage by the missile
(4) locate the bullet, bullet fragments, jackets, pellets etc
(5) show the track of bullet, demonstration of ricochet etc [a radiopaque dye may
be instilled in the track before taking X-ray]
(6) type of ammunition used [caliber etc].

F. Peculiar Effects of Firearms

1. Artifacts
(1) Kennedy phenomenon - Name given to problems in interpretation of
wounds caused by surgical alteration or suturing of gunshot wounds.
(2) Rayalaseema phenomenon – Victim first stabbed " Then to mislead the
police, a bullet is stuffed into the stab wound. Once common in Rayalaseema
district of AP.
2. Atypical entrance wounds
a. Ricochet bullet
A ricochet bullet is one which before striking an object strikes some intervening
object first, and then after ricocheting and rebounding from the intervening
object, hits the object.
Salient features:
(1) Types of ricochet – (a) External ricochet – Bullet rebounds off some
external object (eg roof) (b) Internal ricochet – Bullet rebounds off some
internal body surface (eg inside of skull, chest)
(2) Occurs rarely – Most of the times the bullet either breaks up on striking
intervening object, or penetrate it.
(3) Occurs with inferior firearms and low velocity bullets
(4) Critical angle – 10°-30°.
b. Bullet graze or slap
Bullet strikes at such an acute angle, that instead of entering the body, it simply
causes an abrasion. It may appear as an elongated, elliptical or triangular reddish
brown abrasion. Underlying dermis may or may not be involved. Adjacent skin
should be examined; it may show ecchymosis.
c. Peculiar flight characteristics of bullet
i. Yaw, pitch, tumble, precession, and nutation
ii. Tail wobble or tail wag
(1) The tail of the bullet wobbles for a few microseconds after it leaves the
muzzle [50 meters for pistol; 150 meters for rifle]
(2) Produces atypical entrance wounds and causes greater tissue damage at these
ranges.
3. Bullet embolism
If bullets or pellets enter a large vessel, they move along the blood flow and
become embolized at a distant part.
4. Concealed firearm wounds
Entrance wounds may be hard to locate if present inside the ear, mouth, nostrils,
axilla, anus or vagina. If bullet is found inside the body and no entry wound may
be located, search should be made of such areas.
5. Entrance-exit anomalies
a. Single entrance and multiple exits
Occurs in following circumstances:
(1) Bone acting as secondary missile – bullet strikes bone" chips off a piece or
more of bone"Bone pieces act as secondary missiles and exit through separate
tracks. Such a bullet may also split producing further exits.
(2) Jacket acting as missile – Jacketed bullet strikes victim"jacket separates
within body and exits separately from bullet. Part of the jacket may sometime
remain within the body. In such cases despite multiple exits, radiologically
jacket would be visible inside, albeit part of it only.
(3) Splitting - Bullets splits up within the body in 3-4 pieces and each piece
comes out through a separate track. Happens especially when it strikes bone.
b. Multiple entrances and exits from a single shot
(1) Situations when this occurs:
(i) the victim was running or sitting in an unusual position
(ii) Bullet hit irregular surface of the body eg breast, buttocks
(iii) bullet struck victim in such an orientation that several parts of the body
came in its line successively.
(2) Investigation: Examination of clothing [or skin, if an unclothed portion was
hit] for burning, blackening and tattooing. These phenomena, if present, would
be seen only in the 1st entrance wound, only wound 1 would show these
phenomena. Other entry wounds, eg 3 and 5 would resemble wounds caused
by distant fire].
(3) Number of bullets present in the body - Please see “odd and even rule”
above.
c. Entrance wound is present; no exit wound but bullet not in the body
(1) This occurs when bullets exit through natural orifices. Ex (i) Bullet enters
mouth [eg through a cheek wound]"spit out (ii) Bullet enters nose [eg through
a face wound]"sneezed out (iii) Bullet enters stomach"vomited (iv) Bullet
enters trachea"coughed out (v) Bullet enters intestine or colon"defecated (vi)
Bullet enters uterus"passed out through vagina (vii) Bullet strikes a bone at
right angle"ricochets back and comes out through the same wound through
which it entered.
(2) Sometimes such bullets are found unaccountably on the stretcher. This
should warn the surgeon [or pathologist] of the possibility of bullet’s exit
through one of the natural orifices.
(3) This is an exception to “Odd and even rule” [please see above].
d. One entrance, one exit; bullet within the body
May occur occasionally when the area around exit was heavily clothed, or
victim’s body was juxtaposed against a hard object [eg cement floor]. Bullet
enters "attempts to exit"makes an exit wound, but returns to the body, as it
encounters the hard object. Causes a shored exit wound. The hard object at the
exit site must be examined for damage.

6. Fetal firearm wounds

Gunshot wounds of the pregnant uterus are relatively uncommon. Maternal
death in such cases is rare. The gunshot injury to the fetus or placenta usually
results in IUD or premature delivery with or without evidence of injury to the
child. If fetus was “quick” and death occurs, assailant would be tried u/s316,
IPC [ch 26].

7. Firearm going off by itself

If there is some defect in the mechanism, the firearm may discharge by any
mechanical pressure applied anywhere on the gun. Country made firearms and
old worn out guns may discharge on being pushed, or thrown or by being
dropped on the ground.

8. Souvenir bullets
A souvenir bullet is one which has been lodged in the body for a long time
without causing ill effects.
Salient features:
(1) Location - Lies usually in an inaccessible place, eg, near or inside a vertebra
and the surgeon considers it best to leave the bullet alone
(2) Souvenir pellets – from shotgun. Individual pellets may be tedious to
extract, so the surgeon may decide against removing them
(3) Scar – indicates the original entrance wound
(4) Dense fibrous tissue – forms around the bullet [encapsulation]
(5) Chronic lead poisoning – may occur over the years, as lead gradually
absorbs from the bullet or pellets [ch 36]
(6) Synovial fluid – in the joints around bullet location may display -Pb.
(7) Souvenir bullet as an artifact - It is not the cause of death. An
inexperienced pathologist may however label it so [ch 10].

9. Unexplained bullets in the body

Major rules explaining number of bullets inside body:
(1) Rule 1 - Odd and even rule [please see above]
(2) Rule 2 - No. of bullets in body = no. of entry wounds – no. of exit wounds. If
the number of bullets in the body are different [either more or less] than the
number of “entrance-exit” wounds, the absence or presence of some bullets
has to be explained. This happens mostly in case of tandem bullet or
piggyback bullet.
Tandem bullet
Tandem bullet is a pair of bullets going off by a single fire due to a defective
firearm.
Salient features:
(1) Mechanism: (i) When Old, rusty, unused for several years and worn out
weapon is used – (a) It may not provide perfect obturation to the bullet. Bullet
travels a little distance within the barrel and sticks somewhere within the
barrel [lodged bullet] (b) When a second bullet is fired [striking bullet], the
first bullet [lodged bullet], being firmly stuck within the barrel provides
perfect obturation and both bullets move out together. The two bullets together
are called the tandem bullet. (ii) When a mismatched cartridge is used –
Generally happens when a smaller cartridge is loaded in a larger gun.
(2) Trajectory: (i) Tandem bullets tend to follow the same trajectory, but only
for a short distance because the two together form an unstable projectile. (ii)
The bullets are thereafter separated and follow different trajectories. (iii) If the
tandem bullets hit the target before separation, a single hole of entry may be
observed. (iv) If the bullets separate before they hit the target two entry holes
on the same or on different targets may be observed. (v) The phenomenon of
two separate regular entry holes by a single effective firing can be established
if the recovered bullets are identified as tandem bullets.
(3) Peculiarities: (i) 1 entrance; 2 exit – If the target is near, tandem bullets
would enter through a single entry wound; then separate inside the body and
come out of different exit wounds. (ii) 1 entrance, 1 exit, 1 bullet inside the
body – Rule 2 above is flouted. Situation explained like this"Tandem bullets
entered through single entrance wound"Separated inside body"one exited and
one remained inside body.
(4) Imp – Tandem bullet is different than tandem or duplex cartridges; in the
latter, the cartridge itself contains 2 bullets – one behind the other. They come
out in separate lines and enter through two different entry wounds.
V. MEDICOLEGAL QUESTIONS

A. Is the Injury Caused by Discharged of a Firearm?

(1) Around wound look for: (i) muzzle impression (ii) abrasion (iii) contusion
and (iv) grease collars (v) blackening and (vi) tattooing.
(2) Presence of bullets and pellets in body.
(3) Corresponding cuts in clothes
(4) entrances and exits
(5) track
(6) presence of (i) cards (ii) wads (iii) shotgun fillers (iv) metal jackets and (v)
other residual matter associated with firearms.

B. Can Firearms Produce Lacerated Wounds?

Yes, by pistol whipping [buffaloing]. Please see ch 12 for details.

C. What Kind of Weapon Fired the Shot?

1. Examination of cartridge, wads, ammunition etc

Cartridges are retrieved from crime scene. Wads and ammunition may be
retrieved either from crime scene or from the wound. They can reveal the type of
gun.
(1) Characteristic cartridges and ammunition - reveal the type of gun they
were fired from
(2) If wad is found to be a plug of paper, cotton or cloth - gun should be a
muzzle loader
(3) If wad is more formally shaped and circular discs of felt or cardboard
are also found - it should be a breech loader. From the diameter of discs and
wads, bore of the gun can also be determined.
(4) Characteristic stains around clothes or skin – can reveal whether black or
smokeless powder was used.
(5) Chemical and microscopic examination of stain – reveals the particular
brand of gunpowder used.

2. Examination of bullet
(1) Class and individual characteristics of the crime bullet are compared with
those of a test bullet [please see above].
(2) Class characteristics are same in all guns of a certain make and model. Thus
if class characteristics of crime and test bullet are matched, one can tell the
make and model of the gun.
(3) Class characteristics are:
(i) Caliber
(ii) Primary markings - (a) Number of lands and grooves (b) direction of twist of
rifling [left or right] (c) rate of twist (d) width of lands and grooves
(4) Individual characteristics are characteristic of a particular gun. They are
most important in pinpointing the exact weapon from which the bullet was
fired. That is why they are also known as fingerprints of a firearm.
(5) Comparison microscope:
(i) A comparison microscope [Fig 13.27] is essentially two microscopes joined
together with a single eyepiece. This permits simultaneous observation of
half the view of each microscope, side by side in the eyepiece.
(ii) A line in the center of the field of view separates the views of the two
microscopes.
(iii) If two bullets [or cartridge cases] can be brought into position under the
respective objectives so that their individual markings appear to flow from
one to the other at the dividing line, an identification is established.
(6) Procedure of comparison:
(i) When a suspect gun is presented to the ballistic expert along with the crime
bullet, he test fires a bullet from the suspect gun into a bag of rags, a box
filled with cotton waste [bullet traps], oiled sawdust, water tanks [bullet
recovery tanks] or some other similar non abrasive material, which does not
leave its own markings.
(ii) Test bullet is then compared with the crime bullet under a comparison
microscope. If each striation matches faithfully, the suspect gun is the actual
crime gun [bullet fingerprinting].
(7) Extraction of bullet at autopsy – Since comparison of each and every
single striation is important, the surgeon or the autopsy pathologist must
extract the bullet from body by cotton or rubber tipped forceps, or preferably
with bare hands, but never with needle, toothed forceps or scissors, which can
leave their own markings on the bullet, rendering the comparison useless.
(8) Other marks on bullets – A lead bullet may often carry weave pattern of the
cloth on it. Such a bullet found at the scene of crime can give away the type of
cloth victim was wearing, even if his body has been disposed of.

3. Examination of cartridges
(1) These may be found at the crime scene in cases of pistols and rifles.
(2) Identification criteria:
(i) Shape and size of case; manufacturer’s stampings on the case head – reveal
caliber, type and manufacturer of cartridge
(ii) Markings on cartridges – [please see above under the heading “other
markings”] can reveal the make and model of gun.
(iii) Comparison of markings – between crime cartridge and test cartridge [as in
the case of bullets] can identify the exact gun from which a particular
cartridge was fired.
D. From what Distance and Direction was the Shot Fired?
(1) Range of fire at short ranges - determined by presence of burning, singeing,
blackening, tattooing etc.
(2) At greater ranges, when these signs are absent:
(i) look for spread of pellets and
(ii) test fire in case of shotgun [quite accurate] and
(iii) nature of wounds and penetration in rifled firearms [only an inspired guess]
(3) Direction – Look for entry and exit wounds [Table 7] and the intervening
track. Possibility of bullet deflection and movements of body parts must be
kept in account.

E. Which Person Did the Bullet Hit?

A bullet found at a scene may be linked to the specific individual through which
the bullet had passed by examining tissue deposited on the bullet. This is
possible even if no tissue is visible with naked eye. The tissue can be removed
by swabbing the bullet and a DNA profile prepared [ch 29]. This procedure is
useful if the criminal has removed the body, but forgot to remove the bullet
which was hidden in grass etc.

F. Did the Suspect Fire the Gun?

This is determined by detecting gunshot residue (GSR) [also known as firearm
discharge residue (FDR) or cartridge discharge residue (CDR)] over the hands of
the suspect. GSR
Salient features:
(1) Distance traveled by GSR - Can travel out from the gun to distances of 3–5
feet or even farther. At the farthest distance, only a few trace particles may be
present. Thus even if a person was standing in the vicinity of firearm
discharge, GSR can be detected on his clothes, in his nose, hair etc.
(2) Composition - Gunshot residues are composed of (a) unburned and partially
burnt propellant, (b) particles from primer, (c) smoke, (d) grease, (e) lubricants
and (f) metal particles from the cartridge as well as the weapon.
(3) Organic and inorganic GSR – [A] Organic GSR [OGSR] consists of
nitrocellulose, nitroglycerine, nitroguanidine, hydrocarbons, methyl and ethyl
 centralite and many other diverse compounds and originates from (a)
propellant (b) firearm lubricants and (c) products of their combustion.
[B]Inorganic GSR [IGSR] consists of nitrates, nitrites, and metallic particles
and originates from (a) the primer, (b) propellant, (c) cartridge case, (d)
projectile jacket, (e) its core and (f) weapon barrel.
(4) Size – Diameter of GSR particles ranges from 0.5µ to 10µ.
(5) Mechanism of formation - GSR escapes from weapon openings in
vaporized form and solidifies into particulate matter on coming in contact with
environment (suspect’s hands, face, hair, clothes, around wound of entrance
etc).
(6) The detection is done by following techniques:
(i) Color Tests – (a) Paraffin test - Also known as the dermal nitrate test, the
diphenylamine test, or the Gonzales test [developed in 1931 by Teodoro
Gonzales]. [A] Technique: (1) Molten paraffin wax is applied to the back
of suspect’s hands with a brush (2) Wax solidifies on cooling. It is then
peeled off the hands (3) The surface of this wax cast is treated with
diphenylamine/sulfuric acid reagent by spraying. (4) Blue color is
produced if nitrites and nitrates are present (important constituents of GSR).
[B] Fallacies – False +ve results are obtained with several common
substances eg certain paints, pharmaceuticals, fertilizers, fingernail polish,
leguminous plants, tobacco, tobacco ash and urine. The test is obsolete now.
(b) Harrison and Gilroy test - Detects metal-containing components of
GSR, eg lead, antimony, and barium, originating from the primer and the
bullet. [A] Technique: (1) Suspect’s hands are swabbed with cotton cloth
dampened with 0.1 M HCl. (2) The swab is allowed to dry and is then
tested with 1-2 drops of a 10% alcohol solution of
triphenylmethylarsonium iodide. (3) The appearance of an orange ring
indicates the presence of antimony. (c) Griess Test [pronounced grease]–
Detects nitrites in GSR. (ii) Anodic Stripping Voltammetry (ASV) (iii)
Atomic Absorption Spectroscopy (AAS) and Flameless Atomic
Absorption Spectroscopy (FAAS) (iv) Scanning Electron Microscope-
Energy Dispersive X-ray (SEM-EDX) (v) Laser-induced breakdown
spectroscopy (LIBS).

G. Is a Given Hole in a Cloth Produced by the Passage of a Bullet

Through it?
In criminal investigations it is often necessary to determine whether or not a
given hole or mark [in car, cloth, door, skin, wall etc] has been produced by a
bullet. If a bullet passes through an object some of its material [cobalt, copper,
lead, nickel] is rubbed off at the periphery of the hole [bullet hole peripheries
(BHP)]. This material can be detected by AAS, NAA, and SEM-EDX [already
described above]. Additionally following color tests may be used [collection
techniques same as for GSR].
(1) Sodium Rhodizonate test – in presence of lead"reddish violet color
develops.
(2) Dithiooxamide Test [DTO, also known as rubeanic acid]- in presence of
(i) copper"green-black color develops.
(ii) Cobalt"brown
(iii) nickel"blue. The copper test is more sensitive than the test for cobalt and
nickel.

H. How Long Did the Victim Survive?

Depends upon the extent of injuries
(1) Vital organs involved - If multiple wounds are there in vital organs"Death
could be immediate
(2) Vital organs not involved - If vital organs [i.e. brain, heart and lungs] were
not involved and death occurred due to hemorrhage and shock"Death may
take place after few hours.
(3) Infection - If infection is present"Death must have occurred more than 36 h
after infliction of injury.

I. Suicide, Accident or Homicide?

Table 8 gives major differences between suicidal, accidental and homicidal
wounds. Other important points are:
a. Nature of the entrance wound
1. Victim characteristics
(1) Contact wound: likely to be suicidal, unless found on inaccessible parts eg
back of neck, chest or abdomen
(2) Distant shot – homicidal or accidental, but almost never suicidal.
(3) No corresponding hole in overlying clothing – likely to be suicidal, as
suicides normally pull clothes away to expose skin.
b. The position and direction of the wound
[A] Position - Table 8 [B] Direction - (1) vertically downwards – as over the
top of skull would indicate homicide (2) Obliquely downwards and
backwards – over the chest may indicate suicide, because it is difficult for a
suicide to maintain a completely horizontal line over the chest.
c. The number of wounds
(1) Single wound – eg on temple may indicate suicide. Other factors need to be
taken into account also. For instance if the weapon is missing from the crime
scene, even a single wound may indicate homicide. Cases have been described
when a suicide shot himself and then threw the weapon outside the window to
make it appear like a homicide.
(2) Multiple wounds – Especially over vital regions such as brain and heart
would strongly favor homicide. A projectile passing through the heart or brain
would immediately incapacitate the victim, and if it was a suicidal wound, he
would not be in a position to shoot again. A phenomenon hesitation shots
(flinch shots) has been described, very similar to hesitation cuts. Hesitation
shots are shots fired either away from the body or on non fatal parts of the
body, just before the final fatal shot. The victim, when he points the gun at his
head, subconsciously pulls away from it at the moment of discharge, with the
result that the bullet misses him completely. This may be repeated 2-3 times
before he finally gathers courage to kill himself. Very rarely he may point the
gun at some non fatal parts of his body, eg foot and fire. On examining the
room in such cases, an investigator may see a number of bullet holes on the
walls, and may wrongly draw conclusion that there had been gunfight.

d. Other characteristics
Victims hands would show (a) gunshot residue [GSR] (b) Blood splashes
[backspatter].

2. Disposal of the body

If attempts have been made to remove the body from the scene (presence of drag
marks etc), it is a case of homicide.

3. Miscellaneous
Multiple methods of suicide (combined suicides), eg by poisoning, hanging and
finally shooting indicate suicide.
14. Thermal Injuries
I. BURNS

Burn is an injury which is caused by the application of heat, chemical

substances to the external or internal surfaces of the body causing tissue
destruction.
Salient features:
(1) Exclusions - The definition excludes heat applied by hot liquids, which is
known as scalds.
(2) Application of heat - may be (i) direct or external e.g. flame, heated body or
(ii) indirect e.g. corrosives, X-rays etc which produce heat within the body.
(3) Temp for producing burn: (i) <44°C – Burn cannot be produced as heat is
conducted away via the capillaries of the skin. (ii) 44°C – minimum temp
required to cause burn. At this temp, heat must be applied for minimum 6 h to
produce a 2nd -3rd degree burn. MLI – forgotten hot water bottle applied
against an unconscious or geriatric patient may cause burns inviting
negligence charges. (iii) Between 44°C–51°C - - in temp by 1°C halves the
duration of exposure necessary to cause same amount of burns (iv) At 65°C –
only 2 s required for burns (v) >70°C – instantaneous.

II. CLASSIFICATION OF BURNS

Burns may be divided pathologically or clinically.

A. Pathological Classification
In 1832, Guillaume Dupuytren (1777–1835), a French military surgeon divided
burns into 6 degrees. Later Wilson [as well as Austrian dermatologist Hebra
(1816-1880)] merged them into 3 degrees (Fig 14.1). To some extent the degree
of burns can be estimated by clinical assessment [i.e. naked eye examination].
More precise degree [depth] of burn can be measured by a high frequency
ultrasound device.
1. 1st degree dupuytren
Erythema or reddening of skin. Ex. One touches a hot object and immediately
retreats. His fingers are reddened and inflamed.
2. 2nd degree dupuytren
(1) Blisters - A blister (bulla) forms, which is covered by white avascular
epidermis, bordered by red hyperemic skin
(2) Contents of blister – exudate containing protein and chloride [please see
Table 5 for the contents of pm blister]
(3) Base of blister - red
(4) There is capillary dilatation and transudation of fluid into the tissues causing
swelling.
(5) Singeing of hair - present
(6) Burn is confined to epidermis.
(7) Repair – is complete without scar formation. Wilson and Hebra
 Classification combines 1st and 2nd degree to just one - 1st degree burns
(epidermal burns).
3. 3rd degree dupuytren
(1) Epithelium completely destroyed.
(2) Burn reaches upper layers of dermis.
(3) Destruction of the papillary layer of the dermis
(4) Pain fibers exposed. Most painful burns.
(5) Shock produced is much more than in 1st and 2nd degree burns.
4. 4th degree dupuytren
(1) Whole dermis is destroyed with all dermal appendages and fatty tissue
(2) The burns are painless because pain fibers are destroyed
(3) Appearance – (a) Brownish black due to charring and eschar formation (b)
Shriveled, depressed areas of coagulated tissue (c) bordered by reddish skin
(4) Repair – occurs with scar formation. Contraction of scar tissue may produce
disfigurement or impaired function. Wilson and Hebra Classification
combines 3rd and 4th degree to just one – 2nd degree burns (dermo-epidermal
burns).
5. 5th degree dupuytren
(1) Muscles are destroyed [Fig 14.2]
(2) Burns are painless due to destruction of nerve fibers.
6. 6th degree dupuytren
(1) Burns reach up to bone level
(2) Burns painless
(3) There is complete charring Wilson and Hebra Classification combines 5th
and 6th degree to just one – 3rd degree burns (deep burns).

III. EFFECTS OF BURNS

Effects of burns depend on following factors:

A. Surface Area
Total surface area of body in an adult is 1.8 sq m. Surface area of burns is
measured by following methods.
1. Rule of nine
According to this rule all areas of the body have areas in multiples of nines as
follows (Fig 14.3): head and neck 9%, front of chest 9%, back of chest 9%, front
of abdomen 9%, back of abdomen 9%, right upper limb 9%, left upper limb 9%,
front of right lower limb 9%, back of right lower limb 9%, front of left lower
limb 9% and back of left lower limb 9%. This makes 99%. The remaining 1% is
allotted to genitals. The rule was first pronounced in 1951 by Dr. A.B. Wallace,
a Scottish surgeon who practiced at Bangour General Hospital, near Edinburgh.
It is thus sometimes also known as “Wallace’s rule of nine”. Children have
larger head and neck compared to adults, and smaller lower limbs. The ratio of
their surface area is thus somewhat different (Table 1).
2. Rule of palms
Palmar surface of patient [including digital surface area] is roughly equal to 1%
of his own body surface area. Useful in case of isolated and scattered burns.
3. Lund and browder chart
The Lund and Browder chart [LB chart], first proposed in 1944 by Charles
Lund and Newton Browder is regarded as the most accurate in measuring % of
burns and is widely used in everyday clinical practice. It takes into account the
fact that 3 areas of body – head, thigh and leg - have variable % areas during
different ages. These are designated as A, B and C respectively, and their body
percentage is read directly from table. 13 areas have fixed %. These are - (1)
front of neck [1%] (2) back of neck [1%] (3) Right UL [9½ %] (4) Left UL
[9½ %] (5) Anterior chest and abdomen [13%] (6) Posterior chest and
abdomen [13%] (7) Genital area [1%] (8) Right gluteal region [2½ %] (9)
Left gluteal region [2½ %] (10) Dorsum of right foot [1¾ %] (11) Sole of
right foot [1¾ %] (12) Dorsum of left foot [1¾ %] (13) Sole of left foot [1¾
%]. Fixed area thus adds up to 60%. Rest 40% is divided among A [½ of head],
B [½ of one thigh] and C [½ of one leg], which represent variable areas. The
variable areas at all ages would always add up to 40%. The formula is: 2xA +
4xB + 4xC = 40%. Pl note that in this chart, %age of some areas does not
coincide with that suggested by rule of nine, eg upper limbs have 9.5% instead
of 9%; anterior chest and abdomen have 13% instead of 18% and so on. It is
because rule of nine is only an approximation.

B. The Degree of Heat

(1) Higher the heat more severe the damage
(2) Temp and time required for cremation – please see ch 6"Cremains.

C. The Duration of Exposure

Higher the duration, more severe the damage.

D. Age
Children are more susceptible.

E. Sex
Women are more susceptible.

F. Site of Burns
Burns on head and neck, face, trunk and anterior abdominal wall are more
dangerous.
IV. CAUSES OF DEATH IN BURNS

A. Immediate
Immediate causes (death within 24 hours) are
(1) Accidents – occurring in an attempt to escape from a burning building or by
injuries due to falling masonry, timber or other structures on the body
(2) Primary (neurogenic) shock due to pain
(3) Carbon monoxide intoxication – If burns occurred in a confined area
4.Acute respiratory insufficiency, lack of oxygen.

B. Late
Late causes [death from 24 h-few months] are
(1) Biochemical disturbances – due to fluid loss and destruction of tissue, eg
hypokalemia
(2) GIT disturbances:
(i) Curling’s ulcers [please see below]
(ii) Dilatation of stomach
(iii) hemorrhage into intestines
(3) Complications of burns: (i) Gangrene (ii) Pyemia (iii) Tetanus
(4) Embolism:
(i) Fat embolism – rare
(ii) Pulmonary embolism – from thrombosis of leg veins due to tissue damage
and immobility
(5) Inhalation of toxic substances -
(i) CO inhalation
(ii) Cyanide inhalation - cyanides are produced during the combustion of nylon
clothes [please also see ch 44"cyanide"building fires]
(iii) Smoke inhalation
(iv) Inhalation of other burn products [Non specific toxic substances]
(6) Respiratory tract injury: (i) edema of glottis (ii) Pulmonary edema
(7) Secondary shock – due to fluid loss from burnt surface
(8) Septicemia – Most important cause in late deaths.
(9) Toxemia - due to absorption of various metabolites from the burnt tissue
(10) Miscellaneous causes: (i) Free radicals (ii) Oxygen deprivation.

C. Very Late
Very late causes [death after several years] are: Marjolin’s ulcer - Malignant
transformation of a burn scar.

V. PM APPEARANCES
A. External
1. Clothes
(1) Cotton fabrics burn faster than wool; victim may get more severe burns if
wearing cotton fabrics. Nylon and polyester melt and stick to skin, and may
produce far more serious burns.
(2) Long loose garments catch fire easily and are thus more dangerous than
close fitting garments.
(3) Examination of clothes - Clothes should be removed, preserved in plastic
bags or air tight bottles and sent for examination for the presence of kerosene,
petrol etc. Smell the clothes is indicative.
2. Stature and weight of the body
Markedly reduced due to
(1) organic matter of the body consumed as fuel and
(2) loss of tissue fluid
(3) skeletal fractures 4.pulverization of intervertebral discs. Thus they cannot be
used to establish the identity of the body. The stature may be less by several
cms and wt loss may be up to 60%.
3. Facial features
(1) Face:
(i) Swollen and distorted.
(ii) In severe burns, soft tissues of the face may be completely burnt, exposing
the skull.
(iii) Features are changed due to contractions.
(2) Eyes - In most cases
(i) the eyes are closed, and the shrunken lids can be opened incompletely and
that too with difficulty.
(ii) Cataract – may be seen as a result of coagulation of proteins in the lens of the
eye. This may occur at temperatures of 150°C and above.
(iii) Jaundice may be seen [liver failure]
(3) Nose and mouth – may show froth due to pulmonary edema [due to heat
irritation of air passages and lungs]. Mouth is usually open with shrunken lips
(4) Tongue – Burnt. Protruding (due to contraction of the tissues of face and
neck).
(5) Crow’s feet – These are areas without burns or soot deposits on the forehead,
in the angles of the eyes, and in naso-oral folds. Mechanism - This is due to
 non-penetration of smoke into the base of wrinkles, which may form due to
pain. Thus crow’s feet may indicate antemortem burns.
(6) Neck - Unsooted creases [mechanism similar to that of crow’s feet] may be
found all over the body, eg in the neck and groins. In the neck such unsooted
creases may mimic a ligature mark [pseudoligature mark].

4. Pugilistic attitude
Pugilistic attitude [L. pugil, boxer][Syn. Boxing attitude (or posture), defense
attitude (or posture), fencing attitude (or posture), heat rigor, heat stiffening] is
the characteristic attitude adopted by the body after severe burns. It is similar to
the one commonly adopted by boxers during fight, and hence the name.
a. Causes
Burns, falling in hot liquids, high voltage electric shocks.
b. Mechanism
(1) Pugilistic attitude is due to
(i) coagulation of muscle proteins
(ii) dehydration and
(iii) contracture of muscles due to heat. Flexors being bulkier than extensors are
contract more.
(2) Temp required – > 50°C; well-established at 75°C. Myosin coagulates (in
mammals) at 50°C, and albumin coagulates at 73° C. If, therefore the body is
subjected to a temperature exceeding 73°C, all these proteins are coagulated.
This rigidity is stronger than that produced by rigor mortis.
(3) Normal rigor mortis does not appear in such muscles.
Memory Aid 1: Coagulation temperature of proteins
MAL
Myosin – coagulates first (50°C)
ALbumin - coagulates later (73°C)
Temperatures are rough multiples of 25 (50, 75)
c. Main features [Fig 14.6]
Due to contracture of muscles
(1) Head slightly extended
(2) Arms
(i) held out in front of the body and
(ii) flexed at elbows and wrists
(3) Fingers hooked like claws
(4) Legs flexed at hips and knees.
(5) Body – showing opisthotonus [arching of body backwards] due to
contraction of paraspinal muscles
(6) Delayed decomposition – due to intense heat producing “heat fixation” of
tissues and inactivating autolytic enzymes.
d. Appearance of muscles
(1) Contracted, desiccated, even carbonized on the surface. A zone of brownish
pink “cooked meat” lies beneath this. Further below, normal red muscle may
be seen.
(2) Degree and severity of contractures – depend on intensity of heat and
duration for which heat was applied.
(3) Stiffening remains until muscles and ligaments soften from decomposition.
e. Interpretation
(1) It occurs irrespective of whether the victim was alive or dead at the time of
burning. Thus pugilistic attitude is not a sign of antemortem burns.
(2) Pugilistic attitude is never seen in the living victim. Case study – A case of
burns was brought to the author for PM. Pugilistic attitude was present. The
story was that the victim survived for 4 hours and even gave her dying
declaration in which she admitted it was accidental burns. Author opined that
this was not possible.

5. Algor mortis, livor mortis, rigor mortis

Difficult to judge in a case of burn. Thus time of death is difficult to determine.

6. Burnt areas
(1) Burnt areas
(i) have a patchy distribution and vary in size and shape. Shape may often take
 shape of ornaments worn [patterned burns].
(ii) They show reddening, blistering or charring depending upon the depth of
burns.
(iii) Depth of burn in different areas may be different, and must be assessed
separately.
(iv) There may be blackening over some areas due to deposition of soot.
(v) In severe burns, skin may be leathery, stiffened and yellow-brown. As the
skin dries after death, it may leave a stiff, parchment-like surface.
(vi) RBCs may hemolyze in vessels and stain vessels presenting a branching
pattern.
(2) Extent of burns – should be assessed [i.e. percentage area of body involved]
(3) Blisters – may be seen as small islands away from the periphery; or whole
burnt area may form one large blister, or there may be a confluence of several
blisters. Blisters are also seen in
(i) CO poisoning
(ii) Deep coma
(iii) Gasoline exposure [AM or PM] and
(iv) putrefaction. Differentiation – When blisters due to other causes rupture,
they leave a moist, pale, raw, yellowish surface, which tans and becomes
dark brown and leathery as it dries. Blisters due to burns reveal an angry
red base.
(4) Hands and feet – if burnt, the skin, including fingernails and toenails
detaches as a glove [due to appearance of fluid between the layers of the skin;
degloving].
(5) Burns absent – Burns may be absent sometimes
(i) in gums
(ii) in armpits
(iii) Hands and feet – Rarely if burning is sudden and intense, they may drop off
and may be preserved with very little damage [because they fall away from
the source of fire]
(iv) Unburnt areas on wrists and ankles – may indicate victim was bound before
the fire started
(v) On abdomen – if person was sitting and face falls forwards between knees
(vi) on buttocks – if person was in a sitting posture
(vii) in portions of body where clothing is tight eg under the (a) belt (b) brassiere
 (c) shoes or (d) tight buttoned collar. The unburnt areas may reveal true
color of skin and may establish racial identification in some cases. Unburnt
area around tight buttoned collar may look like a strangulation mark [please
also see unsooted creases of neck above].
(6) Flash burns – Seen in burns due to
(i) Explosions
(ii) Ignition of highly inflammable liquids or gases
(iii) Sudden ignition of fine particulate matter. Their characteristics are (a) seen
only on exposed areas of skin (b) Depth is usually 1st or 2nd degree
[Dupuytren] (c) uniformity [in depth]
(7) Microscopic appearance:
(i) Cutaneous erythema, characterized by dilated capillaries
(ii) Leukocytic infiltration [within 6 hours]
(iii) epidermal cells show (a) necrosis (b) swelling of nuclei, and (c)
condensation of nuclear chromatin
(iv) edema of subepidermal connective tissue.
7. Heat ruptures
(1) Heat ruptures [or tears] are produced by splitting of the soft parts. If skin is
completely burnt, underlying muscles may show rupture. They may be partly
cooked and brownish. Sometimes the muscles may be converted into black,
brittle masses.
(2) They may be antemortem or postmortem.
(3) Mechanism:
(i) Excessive heat – Due to excessive heat, skin contracts [antemortem heat
ruptures]
(ii) Disturbance of body - Sometimes external disturbance of the body may
produce heat ruptures, eg when a severely burnt body is moved, the charred
skin cracks easily producing tears. Such tears are commonly seen around
the places where the body was held – shoulders, elbows, knees [postmortem
heat ruptures].
(4) Site – May be anywhere, but usually over extensor surfaces and joints
(5) Size – Several cm in length
(6) D/d – May resemble lacerations [rarely even incised wounds] [Table 3].
8. Hair
(1) Singed and burnt, but may be spared in armpits.
(2) In lesser degree of burns, ends may be bulbous or clubbed.
(3) Color – Color of hair may sometimes reveal the temp reached.
(i) Gray hair become brassy blonde or even golden at 250°F
(ii) Brown hair become slightly reddish when exposed to 400°F [for 10-15 min]
(iii) Black hair do not change color on exposure to heat.
9. Miscellaneous findings
(1) Identification marks – eg moles, scars and tattoos may be destroyed in 5th
and 6th degree burns.
(2) Abdominal wall – may show rupture. Caused by
(i) burning of the abdominal wall
(ii) expansion of gases within the intestines exerting pressure on weakened
abdominal wall. Intestines may be seen protruding through this gap, which
may themselves be ruptured rarely.
(3) Anus – Gaping may be seen because of shrinkage of the perianal tissue. This
may be misinterpreted for sodomy or homosexuality
(4) Pre-existing lesions – may become smaller and change in shape due to
shrinkage of the skin. For example, originally slit like stabs may assume a
circular shape. Lesions may sometimes migrate toward the center of the
thermal damage.
(5) Complete destruction - If the flame is unchecked, the body is reduced to a
shapeless, coal like mass and finally to a heap of grey and yellow ashes. These
are known as cremains.

B. Internal
1. Heat hematoma
Heat hematoma is the collection of blood in the extradural space due to
excessive heat.
Salient features:
(1) Degree of heat required – occurs mostly when the heat is enough to cause
charring of the skull.
(2) Appearance:
(i) Gross - Honeycomb appearance due to presence of air bubbles inside
(ii) Color - light chocolate color, or pink if blood contains CO.
(iii) Consistency - Soft and friable [bubbles]
(iv) Thickness – 1.5 mm to 1.5 cm. Volume up to 120 ml.
(v) Differences from antemortem EDH – please see Table 4.
(3) Adjacent area of brain – is hardened and discolored (due to heat)
(4) Distribution – of heat hematoma follows closely the distribution of the
charring of the outer table of skull. Found also along the superior sagittal
sinus. Most common site is parietotemporal region.
(5) Mechanism of development – Not clear. Could be expansion of blood in the
diploe (due to heat) and rupture of dural venous sinuses.
2. Heat fractures (Thermal fractures)
Heat fractures are postmortem fractures produced by excessive heat.
Salient features:
(1) Appearance - Bones are burnt and assume a gray-white color. Usually
shows a fine superficial network of heat fractures on its cortical surface, which
may crumble on handling
(2) Types - Three types; skull fracture, long bone fracture, other fracture.
a. Skull fractures
(1) Frequency - Occur most commonly in areas where the skull has been
severely burned
(2) Site – either side of skull above temples
(3) Types:
(i) Due to -of intracranial pressure by steam - (-a)Akin to an intracranial
explosion (-b)Separation of ununited sutures occurs (-c)displacement -
fractures show wide gaping defects and widely separated bony margins.
Elevated fracture [Fig 14.10] (-d)fractured tables – both
(ii) Due to rapid drying of bone with contraction – (a) fractured tables - Only
outer table is fractured (b) Displacement – none (c) Fracture – stellate (d)
may cross a suture line.
b. Long bone fractures
(1) Cause – excessive shrinkage of muscles, pulling tendons and bones
(2) Appearance – Bones may show curving due to drying out [curved
fracture].
c. Other fractures
Hyoid – May be so cooked and fragile that it may fracture, or sometimes even if
intact, fractures on even most gentle manipulation.

3. Air passages
(1) Mucosa:
(i) of entire air passage from nose till terminal bronchi is congested and
edematous.
(ii) Laryngeal edema .es rapidly with -ing PM interval and only wrinkling of
mucus membrane may be seen.
(iii) Microscopically – eosinophils in walls
(iv) may be thickened
(v) May show frank burns if flame or superheated air is inhaled
(2) Vocal cords – destroyed along with overlying epithelium
(3) Aspirated black carbon particles [soot]- seen embedded in mucus lying on
 the surface in nose, mouth, larynx, trachea and bronchi.
(4) Presence of carbon particles [soot] in terminal bronchioles – on
histological examination is a very strong proof of antemortem burns.
(5) Amount of soot depends upon:
(i) Duration of survival - in smoke contaminated atmosphere
(ii) Type of combustible objects -present on victim’s body and around
(iii) Type of fire – eg smoldering fire burning partially wet objects produces
more smoke
(6) Demonstration of soot – Sometimes soot may not be clearly differentiable
because of underlying dark, congested mucosa. In such cases, clean mucus
from trachea with a cotton swab and smear it on a piece of white paper. It
would blacken due to carbon particles.
(7) Smaller peripheral air passages:
(i) may be blocked - by mucus, soot and mucosal cells. The latter are shed from
larger air passages higher up due to burn injury.
(ii) may show vomitus – inhalation of smoke" vomiting"inhalation of vomit.
(8) Ulceration and secondary infection – in cases of death after a few days of
survival.

4. CVS
(1) Heart – full of clotted blood. Histology shows interstitial edema and
fragmentation of myocardial fibres.
(2) Pericardium, endocardium-show petechial hemorrhages.

5. Lungs
(1) Lungs – Markedly edematous and congested. Sometimes shrunken. Airless,
discolored, hardened, heavy. May present picture of shock lung [ch 11]. In late
deaths, show bronchopneumonia.
(2) Pleurae – inflamed, show petechial hemorrhages
(3) blood vessels of lungs – may contain fat droplets due to a physico-chemical
alteration of fat already present in blood. Must not be confused with true fat
embolism.

6. GIT
(1) Mucosa:
(i) of esophagus, stomach may be congested because of entry of hot gases up to
this region.
(ii) May show petechial hemorrhages, often with erosions and even acute ulcers
(2) Aspirated black carbon particles - seen embedded in mucus lying on the
surface in pharynx, esophagus and stomach. Can reach up to stomach due to
peristaltic movements and hot gases reaching up to this point. Generally not
seen beyond stomach, even in survivors.
(3) Inflammation and ulceration – of Peyer’s patches and solitary glands in
intestines.
(4) Curling’s ulcers:
(i) Acute peptic ulcer of the duodenum, generally seen after about 7-10 days in
extensive burns, but may be seen as early as after 1 day. Appear as sharply
punched out mucosal defects. Especially common in children. There may
be bacterial or fungal colonies in the floors of ulcers.
(ii) Incidence – 10%
(iii) Site – 1st part of duodenum [most common]. May be seen all over
duodenum, stomach and even large intestines.
(iv) Mechanism – (a) -ed ACTH and corticosteroids released as result of burn
stress. (b) -ed levels of blood histamine (c) gastrointestinal ischemia (d)
Hemoconcentration. (e) thrombosis of vessels due to burns
(v) Complications – (a) may erode large vessels "massive hemorrhage"late death
(b) may perforate"late death.

7. Viscera
(1) Well preserved - Even in badly burnt bodies viscera are usually well
preserved because body tissues are poor conductor of heat
(2) Show marked congestion. Sometimes may show a “cooked” appearance, i.e.
hardened and discolored
(3) Puppet organs – All internal organs may shrink to very small size due to
loss of water. They are firm, hardened, and cooked by the heat. Systematic
observations of cremations show that this change occurs between 30-50 min.
If the fire continues, the surface of the organs becomes increasingly
bosselated [marked or covered with many bosses (protuberances)] and is
reduced to a sponge like residual structure in the end. The tissue is completely
desiccated and disintegrates into ash at the slightest touch
 [“Zermürbungspunkt” (crumbling point)].
(4) Liver:
(i) shows cloudy swelling
(ii) Fatty changes – due to burns or even due to treatment with tannic acid
(5) Spleen – softened. There is edema and necrosis of lymphoid germinal
centers.
(6) Kidneys:
(i) show cloudy swelling, capillary thrombosis and infarction.
(ii) heme casts in renal tubules
(iii) hemoglobinuria if >30% surface area is burnt
(iv) microcirculatory insufficiency and renal ischemia due to thrombosis
(7) Adrenals – enlarged, congested.

8. CNS
(1) Brain:
Cooked appearance – (a) Color – yellow to light brown (b) Firm (c) Shrunken
(2) Dura – leathery. May be split with brain oozing out forming a mass of frothy
paste.

9. Blood
(1) Hemoconcentration
(2) Color – cherry red, due to formation of carboxyhemoglobin [COHb]"may
turn brownish due to heat
(3) COHb levels - usually >10%; in some cases may reach up to 70-80%.
Children and old persons may die at much lower levels [30-40%]. Presence of
COHb associated with external burns is the surest sign of antemortem burns.
(4) COHb levels depend upon –
(i) Victim related factors – (a) Activity of victim (b) Hb content of blood (c) Rate
and depth of respiration
(ii) Extrinsic factors - (a) Conc of CO in inhaled air (b) Duration of exposure
(5) Causes of absent COHb:
(i) Adequate supply of O2 - causing .production of CO
(ii) Convection air currents - driving away CO laden air
(iii) Flash fires - eg in conflagrations of chemical plants
(iv) Inhalation of superheated air - constriction of air passages"death occurring
 due to suffocation
(v) Instantaneous or near instantaneous [rapid] death - eg in explosions, warfare
(6) Other gases found in blood:
(i) Ammonia, H2S, oxides of sulphur – due to burning of wool or silk
(ii) HCN – due to burning of domestic furnishings made up of polyurethane [ch
44]
(iii) Oxides of nitrogen – due to burning of nitrogen containing substances, eg
Nitrocellulose films [produce nitrogen oxide, nitrogen tetroxide]
(7) Histology – macrophages may show soot particles.

10. Miscellaneous
(1) Tissue edema
(2) Serous cavities – contain excessive fluid
(3) Infection – in delayed deaths.

VI. AGE OF BURNS

A. Macroscopic and Histological

Age of burns is quite inaccurate, as it depends on a number of variables (extent
and depth of burns, age and nutrition of victim, causative agent). Broad
guidelines are as follows:
(1) Immediate – erythema
(2) 1 hour – (a) Vesication (b) BV in the floor of blister are dilated
(3) 6 hours – (a) Epidermis – Coagulated, thinned out and deeply staining. Cells
in the deeper layers become elongated, with their long axes oriented at right
angles to the skin surface (closely resembling streaming in electrical mark) (b)
Dermis - Inflammatory reaction starts with infiltration of polymorphonuclear
leucocytes
(4) 12-24 h – Exudate begins to dry
(5) 36 hours – If burn area is not kept clean, pus forms. After the formation of
pus, it becomes very difficult to tell the age of wound. If pus does not form,
the healing proceeds as follows
(6) 2-3 days – Dry brown crust forms
(7) 4-6 days – Superficial slough falls
(8) 2 weeks – Deep slough falls
(9) 2-3 weeks – Granulation tissue covers the surface
(10) Several weeks to months – Scar forms.
(11) 10-25 years later – Marjolin’s ulcer may form. It is an ulcerating squamous
cell carcinoma in an area which suffered burn injuries (after French surgeon,
Jean Marjolin, who first described the condition in 1828). It is slow growing,
painless carcinoma, which does not spread by lymph (due to local destruction
of lymphatic channels). Treatment is usually surgical. May be medicolegally
significant if original burn injury was work related, or due to negligence.

VII. ANTEMORTEM AND POSTMORTEM BURNS

Differences between AM and PM burns are given in Table 5. If destruction of

body is considerable, their differentiation may be difficult or even impossible.
Salient features:
(1) Line of redness [Fig 14.11]:
(i) Appearance
- It is a zone of hyperemia between burnt and unburnt area. A reaction to burns.
(ii) Time of production – Seen in antemortem burns. But may be seen if heat
is applied in the early supravital period (please see chapter on thanatology)
too, i.e. up to about 1 hour after death. Burns produced within this period are
difficult to differentiate from true antemortem burns. Presence of COHb is a
useful indicator. (iii) Absent – (a) when death is immediate (b) when whole
body is burnt [No unburnt area; so no zone differentiating burnt and unburnt
areas] (iv) Extent – involves whole thickness of skin (epidermis and dermis)
(v) Width – varies, but usually between 5-20 mm (vi) Pathogenesis – due to
capillary dilatation (vii) Permanency – Persists after death.
(2) Antemortem blister: (i) Appearance – Appears as a raised dome and
contains fluid [exudate]. (ii) Time of production – Seen in antemortem burns.
Very rarely blisters with a red rim may be seen in PM burns due to
contraction of dermal capillaries. This forces blood to the periphery of
blister, producing a reddish rim.
VIII. ML IMPORTANCE

(1) Branding – Application of red hot iron rods on skin is very common among
the illiterates and tribals of India to treat a vast variety of conditions from
jaundice to neurological disorders. Patient may present with multiple burn
scars in various stages of healing which may arouse suspicion of physical
abuse and torture.
(2) Manner of infliction of burns:
(i) Homicide– Very common in India, mostly in the form of dowry deaths
(ii) suicide – very common among females
(iii) accident – bursting of inferior quality stoves, gas cylinders etc
(3) Necklacing is the practice of extrajudicial execution carried out by forcing a
rubber tire, filled with petrol, around a victim’s chest and arms, and setting it
on fire. Common in South Africa.
(4) Negligent conduct with respect to fire or combustible matter - so as to
endanger human life"punishment of 6 months or `1000 fine or both [S.285,
IPC].

IX. SPONTANEOUS HUMAN COMBUSTION (SHC)

Spontaneous human combustion (or simply spontaneous combustion) is more

or less an anecdotal phenomenon, where a live person is supposed to go up in
flames on its own, without any outside source of heat. In the past centuries, the
defense sometimes used to raise the plea of SHC, and in some cases it was even
accepted by the courts. However it is highly doubtful if such a phenomenon
actually occurs.

X. PRETERNATURAL COMBUSTION

Preternatural combustion is a phenomenon, where a putrefying dead body

catches fire spontaneously due to formation of inflammable gases, such as
hydrogen, hydrogen sulphide and methane (Ch 9). A flame is necessary for
ignition. Preternatural combustion is different from SHC; former occurs in
the dead and putrefaction is a must. SHC is seen in live people, or immediately
after death [please see “wick effect” hypothesis above].

XI. SCALDS

A scald is an injury which results from the application of liquids or from steam.
Salient features:
(1) Cause: (i) Hot non sticky liquids. (a) Water at 55°C" produces full thickness
scalds in 25s (b) at 70°C"same damage in just 1s. Can occur through clothing,
with no damage to it (ii) Sticky liquids – eg oils, syrup, tar cause more severe
 scalds than hot water. (iii) Superheated steam (a) If touches skin"soddens the
skin"Becomes dirty white in color (b) If inhaled"scalds on skin are not seen,
but death can still occur. Thermal inj to resp tract"Edema of mucus
membrane"obstruction"death by asphyxia
(2) Types: (i) Immersion burns – caused by immersion in hot liquids. May be
accidental or homicidal (ii) Splash or spill burns – by splashing. Mostly
accidental (iii) Steam burns
(3) Destruction - not as deep as in burns
(4) Redness [erythema] - appears at once; due to vasoparalysis; blistering takes
place after a few minutes
(5) Blister Characteristics: (i) formed due to -ed permeability of capillaries (ii)
have a hyperemic zone around them [Table 5] (iii) Reddening and swelling of
the papillae in the floor (iv) Blister fluid contains WBC and RBC (v)
Soddening and bleaching, but no singeing, blackening, charring (vi) Blistered
skin removed"raw pink surface"If left exposed"becomes brownish, dry and
hard
(6) Cause of death: (i) shock (ii) Fluid and electrolyte disturbance (iii)
secondary infection

A. Degrees of Scalds
Divided into three (1) Erythema (2) Blister formation (3) Necrosis of dermis.

B. ML Importance
(1) Accidental - Scalds are mostly accidental
(i) Bursting of hot water bottles, pressure cookers, boilers etc
(ii) Splashing of fluids from cooking utensils
(iii) Pulling over kettles or saucepans by children. If children suck the spouts of
kettles containing hot liquids, can cause severe scalds of mouth and
respiratory tract
(2) Suicide – by scalding is rare
(3) Criminal offences by scalding:
(i) Murder – rare
(ii) Grievous hurt - Boiling water may be thrown on a victim in order to injure. If
face is disfigured, it is a grievous hurt [S.320, IPC]
(iii) Child abuse by scalding [ch 27].

15. Explosion Injuries

I. INTRODUCTION

[A] Explosions can be (1) Natural [volcanic] (2) chemical (bombs) (3) nuclear
(4) electrical (produced by a high current electrical fault) (5) magnetic (during
solar flares) and (6) mechanical (steam boiler bursts). Most commonly in
medicolegal practice are chemical (bombs) and less commonly mechanical. [B]
Explosion injuries are seen in bombings, the most common method of
destruction employed by terrorists today. [C] Molotov cocktail (also known as a
petrol bomb) has been a favorite of guerillas and terrorists. It consists of a glass
bottle partly filled with flammable liquid, usually petrol (gasoline) or alcohol
(generally methanol or ethanol). The mouth of the bottle is stoppered with a
cork, and a cloth rag is fixed securely around the mouth. The rag is soaked in a
flammable liquid immediately prior to using it. The rag is lit and the bottle
thrown at the target. The bottle shatters on impact, spilling the flammable liquid
over the target, which is then ignited by the burning rag. It is a common practice
to throw several unlit, full bottles to saturate an area, then finish with a lit one.
This avoids the risk of throwing several lit devices. If one uses lit bottles each
time, the enemy would see the flaming bottles approaching and know which
direction to start shooting. There is also the possibility of missing target or
dropping the device after being lit. Many substances such as white phosphorus,
tar, palm oil, acids etc may be added to the basic Molotov cocktail to enhance its
use as a weapon. The bomb is named after Vyacheslav Mikhailovich Molotov
(1890–1986) a Soviet politician, who first advocated it. [D] Letter bombs are
explosive devices sent by mail through parcels. They consist of the detonating
fuse, the explosive, the electronics for initiation and the energy source. The
cause injuries – sometimes fatal – to the unsuspecting person who opens such
parcels. [E] Booby Traps - A bomb designed to explode in the presence of a
person, when he is engaged in activities like opening a door, picking something
up [eg a policeman trying to pick up some incriminating object], switching
something on. Often used in guerrilla warfare, and by criminals wanting to
protect drugs or other illicit objects and property.

II. CLASSIFICATION OF BLASTS

Three types of blasts are seen (a) air blasts (b) underwater blasts (c) solid blasts

A. Air Blasts
Most frequently seen. Please see “Primary blast injuries” below.
B. Underwater Blasts
The blast in water differs from that in air, physically in that there is no after-
wave of negative pressure. The most common organ suffering damage in
underwater blast is intestines. Reasons: (a) Generally people affected are those
who are taking bath. Only their abdomen is under water (b) They are wearing
life jackets on their chests. (c) Density of both water and body is same. So
most blast energy is transferred to the body, unlike the air blasts, where most
energy is reflected. Ribs provide some kind of shield to this kind of blast energy.
There is no such shield on abdomen.

C. Solid Blasts
Solid blast is seen when the blast forces a solid material against the body e.g.
victim is standing on the relatively rigid deck of a ship when an underwater
detonation occurs. In this case, the energy of the shock wave is transferred
through the structure of the ship to the feet of the victim. The shock wave then
travels upward through the inferior extremities resulting in fractures of the
bones of feet, ankles, knees and hips. In addition, intraabdominal blunt force
injuries without accompanying surface injuries may occur. The victim may also
be propelled a considerable distance and strike intermediatry targets.

III. INJURIES DUE TO BOMBS

Injuries seen in explosions are as follows:

A. Primary Blast Injuries

Primary blast injuries occur due to the direct pressure effects of the blast wave
on the victim [Barotrauma]. These are more severe when the blast occurs in a
confined space, primarily due to repeated reflection of the blast wave. Organs
most likely to suffer damage due to these injuries are those which contain air,
e.g. auditory apparatus, respiratory system, gastrointestinal system. Blast
waves tend to get reflected at air-fluid interphase, and since these organs contain
such a boundary, they are more liable to get injured. The organ most sensitive to
blast effects is the ear. Classic injuries seen in terrorist bombings are rupture of
the tympanic membrane, damage to the Eustachian tube, the ossicular
chain and to the organ of Corti within the cochlea. While ear is the most
sensitive organ to blast effects, injuries to the lungs are the greatest cause of
mortality. Lungs would often reveal the fatal lesion in cases of deaths due to
terrorist bombings. Shock wave passes to the lungs directly through the chest
wall, as well as through the air via oronasal orifices. Main injuries seen are a
widespread alveolar damage, tears in the visceral pleura, pulmonary hemorrhage,
atelectasis, pneumothorax, hemothorax, pneumomediastinum and traumatic lung
cysts. Air emboli are common which can be due to traumatic alveolar-venous
fistulae. Subcutaneous emphysema and chest wall damage, including injuries to
the ribs are also seen.

B. Secondary Blast Injuries

Secondary blast injuries are produced by flying missiles (nuts, bolts, nails etc)
generated by the explosion. These injuries resemble classic ballistic wounds,
except that the entrance wound is very irregular. Small missiles striking the body
produce the classic triad of punctate lacerations,
A
brasions and
B
ruises (Marshall Triad). This triad is very characteristic of bombings. X-rays of
victims should be taken to reveal them [detection of small metallic particles].
Memory Aid 1: Marshall triad
LAB
Laceration
Abrasion
Bruise

C. Tertiary Blast Injuries

Tertiary blast injuries are produced either when the victim is actually lifted up
and thrown around by the blast wind, or when some heavy piece of masonry
breaks and falls upon the victim. These injuries resemble the classic blunt force
injuries.

D. Burns
These are sometimes called quaternary injuries. The characteristic burns seen
in explosions are flash burns. They are not due to flame, but due to radiant heat
of high intensity. Since the duration of exposure is infinitesimally small, these
injuries are superficial in nature. Furthermore, since the heat applied is the
same, they are of uniform depth. If an object happens to be between the seat of
explosion and the victim, it would cast its “shadow”, just as it would if there
were a flash of lightning. Areas protected by clothing (bra, waste bands, belt,
shoes) are safe.

E. Fumes
If the bomb explodes in a confined area, CO would be produced, and cause
asphyxiation.

F. Explosive Injury
Typical injury seen in this category is the “dust tattooing”, which occurs due to
small particles of dust entering and lodging in the subcutaneous tissues. They
cannot be washed off, since they penetrate inside the dermis.

G. Complete Disruption
If the victim happens to be sitting over the explosive device, or if he is in very
close proximity, his body would be completely disrupted. The individual body
parts are thrown wide apart. These bodies are most difficult to identify.

16. Electrical Injuries, Atmospheric

Lightning, Radiation Injury

I. INTRODUCTION

Electrical injuries are produced by electricity. The damage produced by

electrical injuries depends on:
A. Nature of Current (AC v DC)
(1) Alternating current (AC) is 4-5 times more dangerous than direct current
(DC).
(2) Frequency – AC between 40 and 150 cycles per second have the greatest
lethality. One reason for the greater lethality of AC is that it induces tetanic
contractions in the victim’s hands, making it impossible to let go of electric
wire. DC throws back the victim. In India, the domestic supply is 220-240
Volts A.C. at 50 Hz.

B. Amperage v Voltage
Contrary to popular belief, it is the amperage, which is the most important factor
in determining the lethality of electric currents, and not the voltage.

C. Amount of Current
The amount of current in amperes is given by the formula A = V/R, where A is
the current in amperes, V the voltage and R the resistance of intervening tissue in
ohms. Table 1 gives the effects of various amounts of currents on human body.
D. Path of Current
Electric current runs from the point of contact to the point of grounding,
following the shortest path (Fig 16.1). When current runs from arm to arm (Fig
16.1(A)) or from arm to leg (Fig 16.1(B)), the heart comes in way (may lead to
ventricular fibrillation).
When current runs from head to arm or head to leg [Fig 16.1(C, D)], respiratory
center comes in the way. This may lead to respiratory paralysis.
E. Duration of Current
Joule’s first law states (please see below) that heat produced is directly
proportional to duration (t) of current.

II. TREATMENT

(1) Scene safety – If the victim is in contact with the source of electricity, he
should not be pulled off with bare hands. The current should be switched off
first. If this is not possible, rescuer must wear rubber shoes and gloves and
then attempt to remove him
(2) Defibrillation – must be tried in low voltage currents
(3) Emergency measures - Give artificial respiration, closed chest cardiac
massage.
III. CAUSE OF DEATH

Death due to electrocution depends on

(1) amount of current
(2) area of contact
(3) duration of current
(4) pathway of current [please see above]
(5) resistance of the body
(6) type of current and
(7) voltage. Low voltage currents are <1000 v. High voltage are >1000 v.

A. Low Voltage (household) Currents

Ventricular fibrillation. Victim may sometimes do some volitional acts
(walking, talking etc) for 20-30 sec before dropping dead. Ventricular fibrillation
is occasionally self-reversible. The heart reverts to spontaneous rhythm
following a short time of fibrillation. Thus in cases of low-voltage electrocution,
resuscitation and defibrillation must be tried; this may prevent death.

B. High Voltage (industrial) Currents

Paralysis of the respiratory center (RC). RC is damaged by the hyperthermic
effects of the current.
Memory Aid 1: Cause of death in electrocution
In low voltage currents organ at lower level is involved [heart];
In high voltage currents organ at higher level is involved [RC]

IV. SCENE OF DEATH

The examination of scene may be much more important than the post mortem
(1) Photographs - Photographic documentation of the body, scene and any
nearby electrical devices or conductors.
(2) Examination of any electrical equipment (eg electric washing machine,
cooler, electric iron etc) - found near the body by an electrical engineer or
someone fully qualified in electrical assessment.
(3) Electrical circuits - Analysis of the electrical circuitry within, and
 sometimes connecting to the building where the victim was found is required.

V. PM FINDINGS

If death occurs due to electricity, it is known as electrocution. The PM findings

are as follows:
A. External
1. Electric entry mark
May or may not be present. If present, it is the most diagnostic PM finding of
electrocution. Its absence does not rule out electrocution.
(1) If absent – (a) Prerequisites: (i) Large surface area from where current enters
(ii) low skin resistance. Both these conditions are aptly met when
electrocution occurs in the bathtub, or when a live electric wire is grasped with
a wet hand (iii) Low voltage current also leaves no mark (b) Diagnosis - in
such cases is entirely dependent upon the circumstances of death.
(2) If present – Three types may be seen as below:
a. Joule burn (endogenous burn)
i. General
Joule burn is typically produced in low voltage (household) currents, where heat
is produced by conversion of electrical energy to heat energy within the tissues
(hence called endogenous burns also). The name is after British physicist James
Joule (1818 – 1889), who first worked out a relationship between current and
heat produced, now known as Joule’s first law or Joule effect. It is expressed
as: Q = I2 # R # t where Q is the heat (in Joules) generated by a current I flowing
through a conductor of electrical resistance R, for t seconds [I and R are
expressed in amperes and ohms respectively]. Most resistant tissue of the body is
(i) skin (Table 2) followed by (in order of .ing resistance) (ii) bone (iii) fat (iv)
nerve (v) muscle (vi) blood and (vii) body fluids. [cf, resistance to firearm
ammunition offered by tissues (ch 13)].
ii. Characteristics of Joule burn
(1) Appearance -(a) Crater [most common] (i) Round or oval shallow crater (ii)
1-3 cm in diameter (iii) has a ridge of skin about 1 mm high around part or
whole of circumference (iv) Occasionally the mark may take the shape of the
conductor [Fig 16.2] (v) Floor is pale (vi) Periphery may be blanched due to
arteriolar spasm caused by current. Sometimes there may be a hyperemic
border outside the blanched area. (b) Broken blister – Sometimes the skin
may break at the site of electrical contact. It then resembles a broken blister.
(c) Incised wound – In some cases, especially when a wire was involved, the
skin would be linearly divided, mimicking an incised wound. Also known as
electric splits. (d) bullet wound – Rarely, the mark may penetrate muscle and
even bone, simulating a bullet wound. (e) If skin is wet, may not be visible.
Becomes more apparent when the skin dries up. In one case, current marks
were not discernible in a body lying in the rain, but became visible the next
day after the body was moved and the skin dried out. (f) Charring – when
there is more prolonged contact (g) Metallization – Electrical metallization in
electrocution was first shown to occur by Schrader in 1932. A number of
methods were later devised to detect it (i) Color – of the electric mark depends
upon the composition of the electrode (A) Aluminum – silvery (B) Copper –
Reddish brown (C) Iron – Brownish black. The color is because of deposition
of metal. The metalized skin desquamates within a few weeks. (ii) In rare
cases, metallic coating may be seen on nails too. (iii) Metallization is a
definite evidence that the burn was produced by electricity and not by flame.
Even during touching of skin with hot metallic conductors (in the absence of
 electricity), metallization does not take place. (iv) Acroreaction test - This
test demonstrates metallization. (A) It is a much simpler microchemical test
for metals (B) applicable for entry marks; not exit marks (C) Procedure - Treat
metalized skin with acid (HCl or HNO3). A portion of the acid is then taken
with a tiny wedge of filter paper treated with a suitable reagent. Production of
color is indicative of metal [e.g. potassium ferrocyanide detects iron by the
production of Prussian blue]. (v) Other tests – (A) histochemical (B)
microprobe analyzer (C) polarographic analysis (D) scanning electron
microscope [SEM] (E) Spectroscopic (F) stereomicroscopic (G) transmission
electron microscope and (H) variable-pressure scanning electron microscope
(VP-SEM) with energy dispersive X-ray (EDX) microanalysis may determine
the nature of the metal, which may be compared with the suspect electrode.
These methods may be used even if decomposition has set in. (vi) Depth of
penetration – Spectroscopic analysis has shown that while aluminum,
magnesium, manganese, molybdenum and zinc penetrate the skin up to 3 mm,
chromium, copper and iron penetrate up to 5 mm. No suitable explanation has
been found for the difference in penetrating power.
(2) Site – (a) May be on palmar aspects of fingers and hands usually, as these
areas come in contact with electricity mostly (b) Rarely on genitals or anus –
in sexual perversions (c) May be under intact clothing or under hair – If
under hair, may remain unnoticed. Scalp must be thoroughly palpated, and if
any suspect lesion felt, hair carefully shaved from that area. (d) Inside mouth
– (i) Accidental – when children place a live plug between their lips. Joule
burn may be on tongue or buccal mucosa (ii) homicidal - in children. Done
intentionally to hide from investigators
(3) Temperature – directly underneath the Joule burn may be as high as 95°C.
(4) Smell – of recent current marks resembles that of burnt cork.
(5) Histology – (a) Microblisters – The epidermis is elevated with microblisters
developing within the squamous epithelium as well as in the external horny
layer. These blisters result from the cooking effect on the tissue. (b) Electric
channels – Cells are separated in the form of sharp slits. This pattern is known
as electric channels or vacuolation. (c) Palisading and streaming of the nuclei
– Nuclei of epidermal cells are stretched, elongated and placed at right angles
to the dermis, to produce a palisade type appearance [streaming of the nuclei]
(d) Collagen – Stains blue in ordinary H&E stain [due to its thermal
 denaturation] (e) Nuclei of vascular media – are twisted so as to resemble
spirals. This may occur at points quite distant from the site of contact with the
electrode. They are localized in the arterial walls, because of blood being a
good conductor of electricity. Indeed most current passes through the body via
blood vessels. (f) Vascular intima – tearing of elastic fibres and overlying
intima. May cause secondary thrombosis and gangrene.

iii. Postmortem electrocution

Joule burns are not characteristic of antemortem electrocution. However there is
no vital reaction in pm electrocution. Differences are given in Table 3.
b. Flash or spark burn (exogenous burn)
Flash or spark burn is typically produced in high voltage (industrial) currents,
when sparking occurs between the conductor and the victim. Also known as
exogenous burns, because the source of heat is outside.
Salient features:
(1) Crocodile skin:
(i) High voltage currents can jump several millimeters across air and cause
lesions [in dry air a current of 100 kV can jump upto 35 mm].
(ii) Such high voltage currents produce extremely high temperatures (upto
4000°C).
(iii) Causes keratin of the skin to melt over multiple small areas.
(iv) On cooling, molten keratin over these areas fuses into multiple hard
brownish nodules [as resolidified wax], as in the skin of a crocodile (Fig
16.3) [another phenomenon seen due to keratin melting and resolidifying is
clubbed appearance of hair tips in firearm wounds – ch 13].
(2) Arc eye - Electric arc produces heat and UV light. Clinically this produces a
superficial and painful keratitis [arc eye]. If the patient survives, the onset of
symptoms occurs 6-8 hrs after exposure. The characteristic features are
(i) intense bilateral lacrimation
(ii) blepharospasm
(iii) photophobia. The injury resolves spontaneously within 36 hours.
Fluorescein staining of the eye [both in the living and at pm] reveals many
punctate erosions of the cornea.
c. Electric splits
(1) In some cases the point of entry shows lacerations in the form of electric
splits
(2) They may be round, oval, linear or of irregular shape
(3) Skin is shed; some of this is found attached to the conductor
(4) Wrinkling of skin may be present

2. Electric exit mark

(1) Site - This mark appears where the body was earthed or ‘grounded’ [Fig
16.4].
(2) More damage of tissues than at entry marks
(3) Often seen as splits.

3. Other external findings

(1) Face – pale
(2) Eyes – (i) Congested (ii) Pupils – dilated
(3) Rigor mortis – appears early
(4) PM Lividity – well developed
(5) Seminal ejaculation [Fig. 16.5] – Due to contraction of seminal vesicles
caused by electrical flow through body.
(6) Secondary burning – may be present due to ignition of clothing
(7) Additional findings in high tension electrocutions –(a) Charring of the body
(b) Amputation of extremities.
B. Internal
(1) Congestion – of all internal organs.
(2) Petechial hemorrhages – along the line of passage of current. Depending on
route, may be present in brain, spinal cord, endocardium, pericardium and
pleurae.
(3) Brain – Irregular tears and fissures
(4) Muscles and tendons:
(i) Zenker’s degeneration - of skeletal muscles in the path of current [severe
glassy or waxy hyaline degeneration of skeletal muscles. Grossly the
muscles appear pale and friable; microscopically, the muscle fibres are
swollen, have a loss of cross striations, and show a hyaline appearance.
Rupture and small hemorrhage are also seen].
(ii) Release of myoglobin – Myoglobin is released into general circulation. This
 may cause renal shutdown, as occurs in extensive crush injury [please. see
ch 11 on injuries also, under the heading “Crush syndrome”].
(5) Bones and joints:
(i) Bone pearls [syn osseous pearls, wax drippings, wax pearls]– (a) Seen in high
voltage currents. (b) Mechanism - (I) Heat generated by current melts
calcium phosphate. "seen radiologically as typical round density foci
(II)Vaporization within bone"seen on the surface of bone with naked eye as
grayish white, hollow nodules of the size of a pea
(ii) Necrosis of bone
(iii) Fractures – (a) due to violent muscular contractions or falls. All
electrocution deaths should be radiographed for this reason. (b) fractures
may be hair thin [microfractures]. May be missed on X-ray. Have an
irregular zigzag course [osseus schisis] (c) Bones most commonly fractured
in upper limb [in order of frequency]- (I)coracoid process (II)head of
humerus (III)neck of humerus (IV)ulna (d) Bone most commonly fractured
in lower limb - neck of femur (e) Fracture of spinal processes. It is
postulated that these regions are susceptible to fractures due to the large
bulk of surrounding muscle [and thus stronger tetanic contractions]. A
disproportionately large number of the fractures are bilaterally symmetric,
suggesting again susceptibility of certain bones within a relatively extensive
path of electrical current. (f) Late bone injuries – are seen due to tissue
ischemia from diminished or obstructed blood supply
(iv) Electrical injury of skull – (a) Occurs due to arcing when transformer and
switch operators and persons working on utility poles inadvertently touch
the cable with vertex of the head. (b) Skull may be split open. (c) Orbital
contents extruded eye sockets. (d) Effects attributed to boiling of the brain
and formation of steam within skull. (e) Decapitation may also occur.
(v) Subluxation of joints – especially shoulder joint
(6) Current pearls - Small balls of molten metal, derived from the metal of the
contacting electrode is carried deep into the tissues.
(7) Heart:
(i) Auricles - Dilated
(ii) Petechial as well as larger hemorrhages – on endocardium, pericardium and
myocardium, particularly at the base of aortic cusps.
(iii) H/P - Fragmentation, rupture and twisting of myofibres, interstitial edema
 and foci of colliquative necrosis
(iv) Electron microscopy – detachment of the external myocardial membrane
(8) Vascular:
(i) Microscopic lesions in media
(ii) Intima is relatively protected due to cooling effect of circulating blood
(iii) massive coagulation necrosis of the entire vessel wall
(iv) Hemorrhage and thrombosis. May occur immediately or up to 1-6 weeks
after the accident. May lead to thromboembolism
(v) Tissue edema [edema electricum] due to immediate and late vascular injury
(9) Kidney and urine:
(i) Lower nephron nephrosis [due to myoglobin entering nephrons]
(ii) Urine – shows myoglobin
(10) Fetus – If pregnant female receives electric shock, abortion may occur.
Sometimes fetus may survive too.
(11) Additional findings in high tension electrocutions – (a) Viscera – may be
ruptured (b) Bone - (i) Periosteum elevated (ii) Fractures
(12) Electroporation - Injury of tissue through direct cellular Damage.

VI. ML ASPECTS OF ELECTRIC INJURIES

(1) Electric crematorium - ch 6.

(2) Electroconvulsive therapy [ECT] - fractures may be sustained during it,
bringing allegations of negligence against the doctor. Most famous example of
this is the Bolam case [ch 2].
(3) Manner of death:
(i) Accidental - Virtually all electrocutions are accidents, with suicides rare and
homicides even rarer. (a) Accidents occur mostly when live electric wires
are touched, especially when the victim is barefooted and the ground is wet.
A case is recorded where a 14 y old boy suffered a fracture of radius from
his electric guitar. He had been playing it when he reached to turn on a
floor lamp which was improperly grounded. The boy felt a sudden shock
and noted that some of his guitar strings “popped” and burned his arm.
Physical exam revealed a small linear burn on his proximal forearm, soft
tissue swelling and tenderness of his distal forearm. A plain radiograph of
his right forearm revealed a buckle-type fracture of the radius. (b)
 Accidental electrocution during autoerotic practices – Can occur. A case of
death has been described where one electrode was attached to the anus; an
attempt was being made to attach the other to the penis, when accidental
electrocution occurred. Death occurred by myocardial fibrillation.
Pornographic literature around the scene had been hidden by the parents to
avoid embarrassment. It was discovered by the investigators.
(ii) Suicidal - (a) uncommon method of suicide. (b) Used by both males and
females, but predominantly by males (c) Suicidal electrocution can be
staged to mask a homicide by other means (d) Methods - (I) Climbing a
pylon and grasping the wire carrying high voltage current (II) Victim fasten
one end of a long wire to one of the limbs (usually the wrist)"throws the
other end of the wire (weighted by a heavy object) over the transmission
line (III) Victim winds the wires around his waist or limbs, plugs wires in
domestic electrical supply and switches on the current. (IV) Miscellaneous
– placing the end of an electric line in the mouth; Using an electric saw to
simulate an industrial accident.
(iii) Homicidal - (a) Homicide by electrocution is rare (b) Methods -(I) Live wire
is placed across a road where the prospective victim is expected to walk or
drive (II) Setting up an electrical circuit within an object that victim is
expected to touch (III) Putting a live wire, or a defective electrical appliance
in the bath tub as the victim is taking a bath. (IV) By simply tricking the
victim - A woman and her young son were homicidally electrocuted in 1980
by the ex-husband of the woman. He deceived his ex-wife by telling her
that he was playing a harmless game where a bulb could be lit when placed
on her bare skin. Thus, he persuaded her to be part of the circuit. He then
wound flexible conducting wires around the limbs of the victims and
electrocuted them by switching on the current.
(4) Judicial Electrocution – is the method of imparting death penalty in some
states of the US. For all official methods of judicial execution, please see ch
40. (a) Electric chair - The condemned criminal is strapped to a wooden chair
(sometimes called “the Old Sparky”). (c) PM findings - (i) Temperature -
Beneath the electrodes, the skin and brain temperature may rise as high as
60°C. (ii) Histologically rupture of neuroaxons and blood vessels of the brain
occurs. (iii) Right leg immediately goes into cadaveric spasm. (iv) Often
ejaculation of semen occurs.
(5) Pregnancy and electric shock– If a pregnant mother receives an electric
shock, the fetus may be aborted. It may lead to claims of civil compensation,
if the shock was received during work through faulty machine. (a)
Mechanisms (i) Fetal skin offers 200 times less resistance than does skin of a
newborn(ii) Both hyperemic pregnant uterus and amniotic fluid are
excellent good conductors (iii) Uterine contractions – are induced by electric
current, which lead to premature expulsion of fetus. (b) How to say positively
that fetus died due to electric current – (i) Pregnancy was normal before
electric shock (ii) There was no history of abortion in earlier pregnancies (iii)
Electric shock proven (iv) No other factor can be explained as being
responsible for abortion (v) Stage of development of fetus corresponds to the
stage of pregnancy and degree of maceration is proportional to the time
elapsed between electric shock and death of fetus. (c) Other significant
points (i) Current enough to kill fetus – 25mA for 0.3 secs [AC] (ii) PM
findings on fetus killed by electricity – [A] Dilatation of the heart chambers
[B] hemorrhages in brain, kidneys and liver (iii) Criminal abortion – has
been tried via electricity. (iv) Electroshock therapy of pregnant mother –
can cause [A]abortion [B]temporary disturbance of fetal heart rhythm. The
doctor may face negligence suit in both. In the latter, it has been alleged that
the fetus suffered late ill effects due to disturbance.
(6) TASER - A TASER (Thomas A. Swift’s Electric Rifle) is an electroshock
weapon [an electrical gun] that uses electrical current to disrupt voluntary
control of muscles.

VII. LIGHTNING

Lightning is an atmospheric discharge of electricity accompanied by thunder,

which typically occurs during thunderstorms, and sometimes during volcanic
eruptions or dust storms. Lightning is a natural phenomenon which occurs
following a massive buildup of electrostatic charge in cloud formations
[particularly cumulonimbus clouds]. It is estimated that a lightning flash occurs
approx 8 million times/day throughout the world. As ice particles form within
the clouds, +ve and -ve charges build up in the upper and lower levels of cloud
respectively. The -ve charge at the base of cloud creates a corresponding +ve
charge on the ground underneath. When enough voltage is built up, charge
begins to flow in the air down to earth. This is seen as a visible lightning flash.
Discharges occur within the cloud too.
Salient Features:
(1) Speed - In the atmospheric electrical discharge, a leader of a bolt of lightning
can travel at speeds of 220,000 km/h
(2) Frequency - There are some 16 million lightning storms in the world every
year.
(3) Time - required for passage to earth lies between 0.001 and 0.0001 s [10-3-
10-4 s]. Flashes lasting as long as 1 second have been reported and are called
“hot lightning.” These are more dangerous than the short flashes.
(4) Electrical charge: (i) The electrical discharge is between a negatively
charged cloud and a positively charged object on earth [negative lightning].
5% of lightning flashes are from positively charged clouds [positive
lightning]. Positive lightning tends to occur during winter, during tornadoes,
during violent thunderstorms and in mountainous regions. It tends to be more
powerful than negative lighting and might have a different injury profile. (ii)
Attracted at the highest points [this is the principle of lightning conductors]
(5) Temperature – is about 50,000°C
(6) Amperage - Lightning produces very high currents [between 12,000 and
200,000 Amperes]
(7) Voltage - is equivalent to a 1 million volts DC. However up to 1000 million
volts has been described
(8) Energy dissipated in a typical lightning flash: (i) 500 million Joules. (ii)
Conversion of this energy - occurs into (a) Mechanical energy - leads to
massive movements of air [“wind” of lightning; causes mechanical trauma to
victims also]. (b) Sound Energy – energy from lightning heats the air up to
18,000°F. This causes a rapid expansion of the air causing thunder (c) light –
seen as a flash.

A. PM Appearances
1. Clothes
(1) Usually burnt, especially at the point of entrance or exit. Body may or may
not show associated burns
(2) Torn [due to “wind” of lightning,]
(3) May be stripped off the body and thrown to some distance
(4) Rarely may remain undamaged
(5) Melting belt buckles and zippers
(6) Shoes may be ripped apart
(7) Objects in the pockets:
(i) Metallic objects - [eg coins, medallions, nail cutters, pen-knife etc] may be
found molten, fused together or even magnetized [cf H2S, where they are
blackened and serve as a clue to exposure – ch 44].
(ii) Plastic objects - eg pens, credit cards, cell phones may be completely molten
and distorted.
(iii) USB drives - become completely useless.
2. External
Keraunopathology [Gk keraunos, a thunder bolt] deals with pathological
changes seen in lightning injuries.
a. Burns
Except surface burns, all are due to heat generated from within the body
[endogenous burns] rather than being applied from the outside. Burns of the
body with no accompanying heat damage to overlying clothes is common in
lightning and indicates endogenous burns. One of the earliest instances was
described in 1680. After a lightning incident in Westmoreland (present-day
Cumbria), one woman suffered burns of the feet at the heel and toe. Her
stockings and shoes were completely unharmed.
i. Endogenous burns
(1) Linear burns:
(i) Site: moist creases and folds of skin, eg such as beneath the breasts, down the
mid-chest, and in the midaxillary line.
(ii) Length: varies from 3-30 cm or more
(iii) Width: 0.3-2.5 cm
(iv) Depth: usually first and second-degree burns
(v) Time of development: may be present initially or develop as late as several
hours after the lightning strike. Late burns are most likely steam burns
secondary to the vaporization of sweat or rainwater caused by the flashover
phenomenon on the victim’s skin.
(2) Punctate burns – multiple, closely spaced, discrete circular burns
(i) diameter - ranges from a few mm to 1 cm. Usually too small to require
grafting in case of survival
(ii) Depth – may be full thickness and resemble cigarette burns.
(iii) Tip-toe sign [Fig 16.6]- Small, circular, full-thickness burns involving the
sides of the soles of the feet and the tips of the toes. This is the exit mark of
lightning.

(3) Arborescent burns [Fig 16.7] – [syn, arborization, feathering, ferning,

filigree burns, keraunographic markings, keraunographism, Lichtenberg’s
flowers lightning marks]. These are irregular, superficial, thin, tortuous
markings on this skin resembling the general pattern of a fern or tree. These
are the most characteristic findings in lightning. There are references to these
markings in the Bible, in which they were described as representing
photographic imprints of the victim’s surrounding vegetation.
(i) Site – most common over shoulders, front of chest, flanks
(ii) Usually pink to brownish in color and are sometimes lightly palpable.
(iii) Time of development – Not certain if produced instantaneously or after
some time.
(iv) Not associated with burning. There is no associated damage to the skin.
(v) Seen only in 20% - 33% cases.
(vi) Do not lie either along vascular channels or nerve pathways
(vii) Histopathology - shows no pathological changes in epidermis, dermis,
nerve, or collagen. The absence of H/P changes indicates that they are
purely a physical phenomenon, and not a class of burn.
(viii) disappear in about 1-2 days among survivors. Sometimes after death also.
(ix) Mechanism of formation – There are several theories (a) break down of
RBCs due to high current"Hb stains surrounding tissues. The lysis occurs
not within vascular channels, but along the path of electric current. This
accounts for markings not corresponding to vascular channels.
Disappearance is accounted for by pigment dissipating away with the
passage of time. Most acceptable theory. A similar branching which truly
corresponds vascular channels is seen in burns [ch 14]. (b) Minute
depositions of copper – in dermis (c) Boiling of intercellular fluid following
fascial planes (d) These are representation of static electricity discharges
along superficial vasculature and nerves (e) inflammatory response –
elicited by electron showers (f) current following the lines of moisture in
skin creases. (g) The figures are fractals [a mathematical concept]. Many
natural features exhibit fractal like shapes [eg coastlines].

ii. Exogenous burns

Surface burns – These are burns caused by external heat. May occur if the
victim’s clothing is ignited or if the victim was wearing or carrying metal.
Necklaces, belt buckles, rings, pocket change, and other such items in the grasp
or in contact with a lightning strike victim can lead to second- or third-degree
burns to the adjacent skin as the objects become heated rapidly by the electric
energy. Metallic objects may be fused due to excessive heat. Hair may be singed
b. Mechanical lesions
Blast like, disruptive lesions. Due to expanded, displaced air (i) Contusions (ii)
Fractures [Skull, facial, limb] (iii) Lacerations [external and internal organs] (iv)
Wounds [all kinds] (v) Ears - (a) hemotympanum (b) rupture of tympanic
membrane

3. Internal
(1) Brain:
(i) Shows congestion, edema
(ii) Hemorrhages - Epidural, SDH, SAH, intracerebral hemorrhage, Peri and
intraventricular hemorrhage, Basal ganglia hemorrhage [direct or thermal],
brainstem hemorrhages
(iii) Leptomeninges – congested, lacerated
(iv) Coagulation of parenchyma
(v) Postcardiac arrest hypoxic–ischemic encephalopathy and associated cerebral
infarction
(2) Lungs:
(i) Congested
(ii) Patches of hemorrhages underneath the pleura
(iii) Pulmonary contusion [blast effect]
(3) Heart - Myocardial infarct (rare); myocardial contraction bands
(4) Muscle - necrosis, myoglobinuria, renal failure (rare compared with high-
voltage AC electrocution
(5) Spinal cord – damage. Direct or secondary to fracture
(6) Eyes and ears: (i) cataracts (ii) corneal edema (iii) secondary otitis media;
(iv) Tympanic membrane perforation; (v) uveitis; (vi) vitreous hemorrhages.

B. Cause of Death
(1) Cardiopulmonary arrest- most common cause
(2) Damage to CNS
(3) Electrocution
(4) respiratory center paralysis
(5) thermal injuries
C. ML Importance
(1) Fatality-<50% people struck by lightning are killed.
(2) Manner – always accidental
(3) Keraunomedicine deals with medical aspects of lightning injuries.

17. Regional Injuries

I. INTRODUCTION

Epidemiology:
(1) Age - Most injuries are commonly seen between 20–35 y
(2) Sex – More frequent in males.

II. HEAD INJURIES

A head injury is any trauma that leads to injury of the scalp, skull, or brain. The
injuries can range from a minor swelling on the scalp to serious brain injury. No
case of head injury should be taken lightly. All cases of head injury should be
hospitalized for at least 24 hours for observation.
Memory Aid 1: Age determination of antemortem tooth loss
There are total 7 stages – 2 in days; 3 in weeks; 2 in months. Now write them down as below.
• 1st stage – only fresh blood;
• 2nd and 3rd stages – deal with organization;
• 4th stage – fibrous;
• 5-7th stages – deal with bone.
ü 7 numbers to remember are – 0, 1, 1, 2, 3, 6, 12.
ü These are easy to remember because they are in a logical sequence. Q in superscript denotes a possible
viva or MCQ question.
Only fresh blood
(1) 0 d [Fresh] – fresh blood
Main focus - organization
(2) 1 d – Early organization
(3) 1 w – complete organizationQ
Main focus - Fibrous
(4) 2 w – clot replaced by fibrous tissueQ
Main focus – bone formation
(5) 3 w – partial bone [socket partially filled with bone]Q
(6) 6m – bone cont’d [filling with bone continues]
(7) 12 m (1 y) – bone complete

A. Skull
1. Fractures
a. Factors influencing skull fractures
Skull fractures depend on thickness, density and elasticity which varies from
person to person.
Thickness
(1) Thickness of skull -
(i) Average thickness - 6 mm. Different skull bones are of different thickness
though.
(ii) Occipital bone is thickest at 15 mm
(iii) Frontal bone - 8 mm;
(iv) Parietal bone - 7 mm;
(v) Temporal bone - 4 mm.
(vi) Skull is thinner where it is protected by thick muscles.
(vii) Buttresses - Skull is thicker in the midfrontal, midoccipital, parietosphenoid
and parietopetrous buttresses.
Memory Aid 2: Thickness of skull bones (from thickest to thinnest)
After Office to party
Occipital"Frontal"Parietal"Temporal

(2) The thickness of outer table of skull is twice that of inner table.
(3) The inner table is thinner and more brittle than the outer table which is
more resilient.
(4) The skull is thicker in some races (thicker in Negro than in Caucasians). In
all races, bones of the skull are thinner in women and children than in men.

b. Signs of skull fractures

i. Halo sign, ring sign
Clear, pink, watery CSF will leak from the nose [in ACF fracture] or ears [in
PCF fracture]. Drops of CSF on the white sheet wrapped around body form a
pink ring around a slightly blood-tinged center, resembling a target [halo sign,
ring sign]. Seen in live patients also around pillowcases, handkerchiefs etc.
ii. Battle’s sign
(1) After English surgeon William Battle (1855 – 1936), who first described this
sign.
(2) Ecchymosis over the mastoid indicates fracture of posterior cranial fossa).
(3) Results from extravasation of blood along the path of the posterior
auricular artery.

c. Types of skull fractures

Skull fractures may be classified according whether they communicate with the
outside environment or according to their site and appearance.
i. According to communication with outside environment
Fractures of the skull may be (a) simple or (b) compound. In compound skull
fractures, the cranial cavity comes in contact with the outside environment
increasing the risk of contamination and infection. It happens when there is a
laceration over the fracture or when a nasal sinus is fractured along with. In
simple fractures there is no such communication.
ii. According to site and appearance
(a) Comminuted fracture
Comminuted fracture (comminuted:“to reduce to powder”, “to pulverize”; from
L. minuere, “to lessen”) is one in which there are two or more intersecting lines
of fracture which divide the bone into three or more fragments.
Salient features:
(1) Caused by - (i) Fall from height on a hard surface (ii) hoof of an animal
[animal kicks] (iii) vehicular accidents (iv) weapons with a large striking
surface [axe, cricket bat, heavy iron bar, hockey stick, poker]
(2) Often resembles a spider’s web or mosaic [Spider web fracture or mosaic
fracture].
(3) If the fragments are pushed inwards, it would be called a depressed
comminuted fracture. Sometimes small pieces may be lodged in brain
(4) lines of fissured fracture are often seen radiating outwards from comminuted
fractures.
(b) Depressed fracture
Depressed fracture is a fracture, in which the fractured bone is driven inwards
into the skull cavity.
Salient features:
(1) Produced by local deformation of skull
(2) Causes:
(i) Weapons – Typically produced by heavy weapons with a small striking
surface [eg axe, chopper, hammer, spanner, stick, rock, stone]
(ii) Other causes – (a) Fall on a sharp corner of a piece of furniture
(3) Outer table is driven into the diploë and inner table shows comminuted
fracture. Rarely only the inner table may be involved, leaving the outer table
intact
(4) Depth – of the fracture is directly proportional to the force of impact
(5) Signature fracture [syn, fractures à la signature]- is a special variant of
depressed fracture in which the shape of fracture “mirrors” the striking surface
of the weapon. Medicolegally they are very important because they can reveal
the weapon.
(6) MLI -
(i) Identification of weapon from signature fractures
(ii) Compression of brain"severe dysfunction, coma and death.
(c) Diastatic (sutural) fracture
Diastatic fracture [Gk, dia, apart; histanai, stand] is the traumatic separation of
cranial bones at a suture line.
Salient features:
(1) Age - Seen only in young persons [because of non union of sutures]
(2) Suture involved – Most commonly, sagittal suture [Fig 17.2]
(3) Cause – blunt trauma
(4) Association with other fractures - Generally occurs along with other
fractures, but may be seen alone.

(d) Elevated fracture

(1) Skull pieces are pushed outwards.
(2) Very rare.
(3) Causes:
(i) a long, sharp wounding object [eg machete] elevates the fracture fragment by
a lateral pull of the object or rotation of the head.
(ii) Through and through penetration of skull. The exit wound causes elevated
fracture [Fig 17.3]
(iii) Elevation of free fragment while retrieving the weapon
(iv) Tangential force applied to the calvarium associated with rotation of head.
(v) Burns – pressure of gases from inside cause outward displacement of skull
fragments [ch 14].

(e) Fissured fracture

Fissured fracture is a linear fracture involving the whole thickness of skull, or
only the inner or outer table.
Salient features:
(1) Frequency – Commonest type of skull fracture
(2) Mechanism:
(i) General deformation of skull - caused by forcible pressure against a broad
resisting surface, as in (a) blows with weapons with a large striking
surface and (b) falls on ground or flat surface – one or several fracture lines
are seen radiating from the point of impact; depression of bone fragments
 may not be seen
(ii) Movement of head - (a) Head is free to move - fracture starts at the point of
impact (b) Head is fixed – If head is fixed [as when the person is sleeping
on ground], the head is “sandwiched” between weapon and the hard
surface. In such cases, fracture line may start at a point opposite the point of
impact. Sometimes the skull may get “ballooned out” between the two
pressure points, and fracture line may start at the base of skull [commonly]
or at the vertex [less commonly]. The line of fracture runs parallel to the
axis of compression
(3) Association with other fractures –
(i) May be found alone or associated with other type of fractures
(ii) May be found only on the inner table. This happens because after impact, the
more resilient outer table rebounds back to its original shape, while the
more brittle inner table fractures.
(4) Site of fracture – may be indicated by an extensive hematoma of scalp.
(5) Characteristics of fracture line:
(i) Breadth - hair’s breadth.
(ii) Course - irregular. Sometimes it reaches a suture"follows its course for a
while"then starts again its own way.
(iii) Hemorrhage - almost always present. This makes the fracture line look red.
This is also a useful way to differentiate between AM and PM fractures.
Red color can also be used to detect fractures at autopsy [ch 5].
(6) Determination of cause – As a broad rule fracture caused by fall are at the
level of pinna, while those due to blows are above this level. Injuries at top of
head may indicate direct force over head, or fall.
(f) Growing fracture
Growing skull fracture (syn. GSF, craniocerebral erosion), is a rare
complication of skull fractures seen mainly during first 3 years of life, and is
characterized by progressive enlargement of the fracture line.
Salient features:
(1) Incidence – 0.05 to 1.5% of skull fractures in childhood.
(2) Age - More than 50% of the GSFs occur under the age of 12 months and
90% under the age of 3 years. Virtually never found after 8 yrs of life.
(3) Bone involved - Usually located in the parietal bone.
(4) Separation – Usually seen in fractures, where the separation at the time of
 injury is > 4 mm.
(5) Time when enlargement occurs - 4 to 8 weeks later.
(6) Why occurs during young age group – (a) Interposition of dura in fracture
- Dura adheres more tightly to the bone in this age group and therefore is more
easily torn in skull fractures. Part of it gets interposed in the fracture line
preventing osteoblasts from migrating to the fracture site, inhibiting healing
[most important cause] (b) Interposition of epidural hematoma in a similar
way (c) Lack of nutrition - Dura acts as a periosteum of the skull bones, the
latter’s blood supply coming mainly from dural vessels. Laceration of dura
with or without its interposition between the fractured pieces of skull
interrupts its blood supply causing nutritional deficiency of the skull bones.
This results in enlargement of the skull defect. The enlargement starts from the
inner table (d) Continuous pressure - from tissue herniation through the bone
gap. (e) rapid growth of skull - Skull grows very rapidly during this period,
preventing stability needed for fracture union (f) Raised intracranial pressure.
(g) Gutter fracture
Gutter fracture is a long, narrow, fracture of the skull, produced by partial
removal of the outer table.
Salient features:
(1) Causes – most commonly due to a glancing bullet [Fig 17.4, Fig 17.5].

Memory Aid 3: Gutter fracture

Gutter # is produced by G lancing bullet.
(2) Types: (i) First-degree gutter fracture - Only the outer table of the skull is
 grooved by the bullet, with resultant carrying away of small bone fragments.
(ii) Second-degree gutter fracture - In addition to above, pressure waves
generated by the bullet fracture the inner table [Irregular depressed fracture].
Dura mater and brain may be torn (iii) Third-degree gutter fracture - It is
synonymous with keyhole fracture [please see below]. (iv) Bullets at a still
lower level cause “perforating wounds” where there is production of separate
entrance and exit wounds in the bone.
(h) Keyhole fracture
The bullet perforates the skull in the center of the tangential wound [Fig 17.5].
The outer table is fragmented, and there are depressed fragments of the internal
table if not comminution and pulverization of both tables in the center of the
wound track. Fragments of bone can be driven into the brain causing death.
(i) Penetrating or perforating fracture
(1) Cause – firearms, pointed sharp weapons [axe, dagger, knife, nail]
(2) Penetrating fracture-
(i) Characteristics - There is only entry, eg nail driven in the skull.
(ii) Manner - Accidental, suicidal, homicidal or due to supernatural beliefs.
(3) Perforating fracture - Characteristics: There is both an entry and exit, eg
 firearms.
(4) Size and shape -
(i) Almost clean cut
(ii) corresponds with that of the cross section of weapon.
(j) Pond (indented) fracture
A pond fracture is a circular depressed fracture of the skull.
Salient features:
(1) Victim – Occurs only in infants
(2) Appearance – Like a simple dent of the skull, much like the indentation of a
table-tennis ball produced by finger pressure. Also known as ping-pong
fracture.
(3) Causes -
(i) Blunt object
(ii) Fall [of an infant from lap of mother]
(iii) Forcible impact against some protruding object
(iv) Obstetric forceps blade [Fig 17.6].
(4) Fracture – occurs only in the outer table [around the periphery of the dent].
Inner table is not fractured
(5) Associated injuries –
(i) Dura mater is not torn
(ii) Usually brain is not damaged.
(k) Ring (Foramen) fracture
A ring fracture (foramen fracture) is a circular fracture around the foramen
magnum.
Salient features:
(1) Appearance – Fissured fracture running 3-5 cm outside the foramen
magnum, all around [Fig 17.7]
(2) Cause:
(i) fall from height onto feet or buttocks – most common [body weight passing
up the vertebral column on to the base of skull]
(ii) heavy weight falls on the vertex.
(3) Prognosis - Usually lethal, because of associated brainstem injury.
(l) Signature fracture
Please see depressed fracture above.
(m) Base of skull fractures
(1) Causes:
(i) Application of force to skull specifically to the base (a) directly. Ex – ✦ An
oblique blow of great force applied to one side of the back of the head"may
start a fracture in the underlying posterior fossa"it may cross the middle line
to enter the middle fossa of the opposite side"may advance further and may
end in the anterior fossa. (b) indirectly through the face [above] or spinal
column [below]. When caused by transmitted force (through face or spine),
they are usually isolated. Ex – ✦ Force of a blow on the mandible [eg an
upper cut in boxing]"may be transmitted through the maxilla and its internal
angular processes to the base of the skull"may cause an isolated fracture of
the cribriform plate of the ethmoid.
(2) Blows on the chin occasionally fracture the mandibular fossa.
(ii) Application of force to skull anywhere – Due to general deformation of skull.
Ex – ✦ A fall on the back of the head or blow on top of the head usually
 produces independent fractures of the orbital roofs, especially in old people.
(iii) Sudden violent - in internal pressure - Produces fractures of the roofs of
orbits, especially in suicidal gunshot wounds of the skull. Caused by sudden
release of gases in the skull.
(iv) Extension of fracture from vault
(3) Influencing factors:
(i) Fracture patterns are strongly influenced by petrous buttresses. Fracture lines
which approach these buttresses from middle or posterior cranial fossa are
either turned towards its apex or base according to the angle at which they
strike them.
(ii) The middle of the body of petrous bone is fractured only when the force is
very great.
(4) Characteristics:
(i) Most basal fractures tend to meet at and overrun the pituitary fossa.
(ii) Fracture lines usually open into the basal foramina.
(iii) Sphenoid fissure is most commonly involved.
(iv) The foramen magnum is not spared despite its thick margins.
(v) Longitudinally or transversely directed force will generally produce fractures
in the corresponding axis.
(5) Types:
(i) Incomplete – do not traverse entire base
(ii) Complete or hinge fractures - Traverse entire base creating a “hinge”.
Divided in 3 categories [Fig 17.8]. (a) Type I -run in the coronal plane,
extending from the lateral end of one petrous ridge, through the sella
turcica, to the lateral end of the contralateral petrous ridge [Motorcyclists
fracture; details in ch 18]. Most common type of hinge fracture. Due to
impacts on the side of the head and, less commonly, to impacts on the tip of
the chin [indicated by chin laceration, and less commonly by mandibular
fracture] (b) Type II - run from front to the contralateral back, passing
through the sella turcica. (c) Type III - run from side to side in the coronal
plane but do not pass through the sella turcica.
iii. According to relationship with impact
(a) Coup fractures
Occur at the site of impact
(b) Contrecoup fractures
(1) Site - Occur opposite to the site of force.
(2) Mechanism - Usually occur when head is not supported. Sudden disturbance
of fluid brain content "transmits force received to the opposite side"cranial
vault opposite to site of trauma gets fractured.

d. Age of skull fractures

(1) Healing - occurs without formation of callus
(2) Development of external callus - delayed due to damage to periosteal bv.
(3) Age:
(i) 1 wk - Edges of fissured fractures stick together
(ii) 2 wks - (a) edges slightly eroded (b) inner table of skull shows pitting and
 deposition of lime salts.
(iii) 3-5 wks - (a) edges become slightly smooth (b) bands of osseous tissue run
across the fissure.
(iv) 3 months - Complete healing occurs. If there is much loss of bone, the defect
is filled only with fibrous tissue.

e. D/d
Mendosal suture
2. Mandibular fractures
The frequency of fractures of different parts of mandible in .ing order are (1)
Condyle [36%] (2) Body [21%] (3) Angle [20%] (4) Parasymphyseal [14%] (5)
alveolar [3%] (6) ramus [3%], (7) coronoid [2%] and (8) symphysis [1%].

B. Traumatic Injuries of the Brain

Traumatic brain injury (TBI) occurs when an external force traumatically
injures the brain.
1. The mechanism of cerebral injury
Brain injury may be caused simply by shaking, without actual blow or fall on the
head [ch 27"Shaken baby syndrome].
a. Blunt head trauma
Results in Acceleration/Deceleration injuries.
(1) Linear acceleration in frontal impact is more dangerous than that in side
impact (falx absorbs part of the impact)
(2) Internal structure of the skull:
(i) determines the most probable location of traumatic injuries of the brain in
closed head injury.
(ii) Skull surface of the anterior cranial fossa is quite rough. Furthermore the
most anterior frontal vault of the skull is limited in size. As the brain
accelerates forward or rotates into the frontal areas of the skull, the
infraorbital frontal lobes are impacted by the rough prominences above the
orbits"results in contusions or lacerations of bases of frontal lobes"Frontal
Lobe Syndromes may occur
(iii) sphenoid ridges of the skull provide a significant structural impediment to
the temporal poles"an accordion-like compression of the temporal tips
occurs"damage to a number of important structure which temporal lobes
 contain [amygdalae, hippocampi, and limbic structures]"disturbances of
memory, mood.
b. Penetrating head trauma
(1) In civilian situations - Penetrating head trauma by missiles is less frequent
than blunt force trauma to the head.
(2) In military situations - missile injury to the head is more common than
blunt trauma. Missiles are usually bullets, but they also include knives,
crossbow bolts, and shrapnel. Even nails, and screwdrivers can become
missiles.

2. Contusions of the brain

a. Mechanism of production
Contusions of the brain may be produced in six ways (Fig 17.9):
i. Coup contusions
Occur at the point of impact due to in-bending of the bone, with compression
of the brain.
ii. Countercoup contusions
(1) Countercoup [syn, contrecoup] contusions occur in the brain directly
opposite to the point of impact.
(2) Classically associated with falls.
(3) Most common in frontal and temporal lobes. Virtually never seen in
occipital lobes.
(4) Seen more frequently than coup contusions.
(5) Generally more severe than coup lesions.
(6) Both coup and countercoup contusions are present over the crests of gyri.
iii. Intermediary coup contusions
Occur in the deep structures of the brain (white matter, basal ganglia, corpus
callosum, brain stem) between the location of coup and countercoup points,
along the line of impact.
iv. Fracture contusions
(1) Associated with fractures of the skull.
(2) If fracture occurs at the point of impact, they would be same as coup
contusions. They would be called fracture contusions, if fracture occurs
away from point of impact.
Memory Aid 4: Theories of countercoup injuries
LP done by Registered Nurse every HouR
1. Lindenberg - Positive pressure
2. Russel - Negative pressure
3. Holbourn - Rotational sheer stress theory

v. Gliding contusions
(1) Caused by displacement of the gray matter of the cerebral cortex during
angular acceleration of the head.
(2) Occur at the junction between the gray matter and the white matter (cf.
coup and countercoup contusions, which occur at gyral crests).
(3) Associated with diffuse axonal injuries.
vi. Herniation contusions
(1) Due to impaction of medial portion of the temporal lobes against the edge
of the tentorium, or cerebellar tonsils against the foramen magnum
(2) Independent of site and direction of impact.
b. Morphological appearances
Morphologically, cerebral contusions are of three types:
i. Contusion hemorrhages
Contusion hemorrhages are located at the crest of a gyrus. They are multiple in
number, streak like and densely arranged (Fig 17.14). They point radially
towards the white matter.
ii. Contusion necrosis
Contusion necrosis, just as contusion hemorrhage tends to be in the cortex, at
the crest of a gyrus, sparing the sulci. It is wedge shaped, with the base of the
wedge at the cortical crest. The lesion becomes visible 10-12 hours after
injury.
iii. Contusion tears
Contusion tears are caused by stretching and shearing forces within the tissues
produced by blunt force. They are the dominant types of contusions in infants
up to the age of five months. At this age, skull is easily deformed and the brain
is quite soft. The tears usually involve the white matter of the upper frontal
convolutions, orbital lobes and temporal lobes.

3. Diffuse axonal injury (DAI)

Diffuse axonal injury (DAI) refers to extensive lesions in white matter tracts
spread over wide diffuse areas. DAI is generally produced by rotational motions
of the head. Because of this, it is also known as shearing brain injury or
axonal shear injury.
a. Mechanism of DAI
(1) Earlier mechanical theory - The hallmark of DAI is axonal damage.
Earlier it was thought that the main cause of axonal damage was tearing due to
mechanical forces during the trauma. Because of different tissue
consistencies within the brain layers and relative fixation of certain parts of
the brain to the rigid skull, the deep and superficial portions may not move
at the same rate. This results in shear strain that manifests as axonal injury
and rupture. Since different tissue consistencies and different degrees of
fixation of brain are responsible for DAI, the lesions are predominantly found
in some special locations such as the white-gray matter junction and corpus
 callosum (because it is rigidly attached to the falx) [Fig. 17.15].
(2) Modern biochemical theory: (i) Stretching of axons during injury causes
physical disruption of axolemma [membrane covering the axon]"(ii) This
opens up Na+ channels in the axolemma"(iii) Voltage changes"(iv) voltage-
gated Ca2+ channels open"(v) Ca2+ flows into the axon"(vi) intracellular
presence of Ca2+ activates phospholipases and proteolytic enzymes"(vii)
damages mitochondria and cytoskeleton; separation of axon"(viii) Axons
swell up; there is impaired transport and accumulation of axonal transport
proteins [fast transport β-amyloid precursor protein (β APP) and the slow
transport neurofilament (NF) protein] within axonal swellings"(ix) neuronal
death.

b. Clinical features
The clinical presentation of DAI depends on the severity of injury. Both severe
[Glasgow coma scale (GCS) 3 to 8] and moderate [GCS 9 to 12] head injuries
have been associated with DAI.
(1) Mild DAI - Coma lasts 6-24 hours [coma lasting <6 hours is termed as
severe concussion – please see below]. Patients with mild DAI usually present
with a history of brief loss of consciousness and good neurologic status
without subsequent deterioration. One-third to one-half of mild head injury
patients develop a postconcussion syndrome. They usually have subjective
complaints including difficulty concentrating, memory problems,
headache, or disequilibrium; and neuropsychologic testing reveals deficits
 in information processing.
(2) Moderate DAI -Coma lasts > 24 h without prominent clinical signs of
brain stem dysfunction.
(3) Severe DAI - Coma lasts > 24 h with brain stem dysfunction signs.

c. PM/Histological appearances
(1) Grossly there are no pm findings. In some cases there may be petechial
hemorrhages through white matter.
(2) Breakage of axons at the time of brain trauma (primary axotomy) rarely
occurs. More commonly breakage occurs in the course of hours to days after
injury, even several months later (secondary axotomy) due to biochemical
mechanisms described above.
(3) Most significant finding is bulb formation at the terminal end of the severed
axon (“terminal clubbing” or “retraction balls”) [Fig. 17.15].
(4) In severe DAI axonal pathology is accompanied by tears in the white
matter and intraparenchymal hemorrhage.

4. Cerebral concussion
Concussion (Latin concutere, “to shake violently”) is a clinical syndrome
characterized by the immediate and transient post-traumatic impairment of
neural function such as alteration of consciousness, disturbance of vision or
equilibrium due to mechanical forces.
Salient features:
(1) Common post concussion Signs and Symptoms [PCSS]- anxiety, bell rung
[excessive noise sensitivity], confusion, depression, dizziness
numbness/tingling, drowsiness, easy distraction, excess sleep, fatigue, feel “in
a fog”, feel “slowed down”, headache, inappropriate emotions, irritability,
light intolerance, loss of consciousness, loss of orientation, memory deficits,
nausea, nervousness, noise intolerance, personality change, poor balance, poor
concentration, poor coordination, ringing in the ear(s) , sadness and stupor.
These are used not only for the initial evaluation but for each subsequent
follow-up assessment, which is periodically repeated until all PCSS have
cleared at rest and exertion.
(2) A second head injury during the recovery phase after a concussion can lead
to death or permanent major disability [second impact syndrome].
MLI
(1) Concealed trauma – causes death without any gross signs [ch 8].
(2) Drunkenness - Head injury and concussion can often mimic alcoholic
intoxication. Table 3 gives salient differences between drunkenness and
concussion.
5. Cerebral edema
Cerebral edema is an excess accumulation of water in the intracellular or
extracellular spaces of the brain.
a. Classification of Cerebral edema
i. Vasogenic
(1) Causes –
(i) cerebral ischemia [late stages]
(ii) focal inflammation
(iii) hypertensive encephalopathy
(iv) trauma [Massive cerebral swelling can occur within 20 min following head
trauma]
(v) tumors
(2) Mechanism - Due to a breakdown of tight endothelial junctions which make
up the BBB.
(i) physical disruption by arterial hypertension or trauma
(ii) tumor-facilitated release of vasoactive and endothelial destructive
compounds [arachidonic acid, bradykinin, eicosanoids, excitatory
neurotransmitters, free radicals, histamine]
(3) Subtypes:
(i) Hydrostatic cerebral edema - seen in acute, malignant hypertension. Results
from direct transmission of pressure to cerebral capillary with transudation
of fluid into the ECF from the capillaries.
(ii) Cerebral edema from brain cancer - Cancerous glial cells (glioma) of the
brain - secretion of vascular endothelial growth factor (VEGF) " weakens
junctions of BBB
(iii) High Altitude Cerebral Edema [HACE] - due to the effects of hypoxia on
the mitochondria-rich endothelial cells of BBB.
ii. Cytotoxic
(1) Causes - (i) cardiac arrest (ii) Encephalopathy (iii) Hypothermia [severe] (iv)
intoxications [dinitrophenol, hexachlorophene, isoniazid, triethyltin] (v)
Ischemia [early] (vi) pseudotumor cerebri (vii) Reye’s syndrome (viii) stroke
or hypoxia [early]
(2) Mechanism - BBB remains intact. Edema is due to the derangement in
cellular metabolism"inadequate functioning of the Na+ and K+ pump in the
glial cell membrane"cellular retention of Na+ and H2O"swollen astrocytes in
 gray and white matter.
(3) PM appearances – in cytotoxic cerebral edema there is - in intracellular
fluid in contrast to vasogenic cerebral edema where there is - in intravascular
cerebral blood volume and - in interstitial fluid. In the former [cytotoxic],
brain is enlarged, firm and has a relatively dry cut surface; in the latter
[vasogenic] the brain is similarly enlarged but is softer and has a very watery
cut surface.
iii. Osmotic
(1) Causes - (i) excessive water intake (ii) hemodialysis (iii) hyponatremia (iv)
rapid reduction of blood glucose in hyperosmolar hyperglycemic state (HHS)
[formerly hyperosmolar non-ketotic acidosis (HONK)] (v) Syndrome of
inappropriate antidiuretic hormone secretion (SIADH)
(2) Mechanism - Normally brain osmolality is < than that of serum osmolality
brain osmolality becomes > than that of serum osmolality in above
causes"creates a reverse pressure gradient"edema.
iv. Interstitial
(1) Causes - obstructive hydrocephalus.
(2) Mechanism - rupture of the CSF-brain barrier"trans-ependymal flow of
CSF"CSF penetrates the brain and spread to the extracellular spaces and the
white matter. Differentiated from vasogenic edema in that interstitial cerebral
edema CSF contains almost no protein.

b. Extent
Cerebral edema may be
(1) Focal – adjacent to the area of injury
(2) Diffuse -
(i) Unilateral [involves one hemisphere only]. Occurs mostly in relation to
ipsilateral acute SDH
(ii) Bilateral [involves both hemispheres].
c. PM Appearances
(1) Dura - stretched and tense
(2) Brain - bulging
(3) Wt -
(4) Cerebral surface – smooth (i) Gyri – pale, flattened with thinning of gray
matter (ii) Sulci – obliterated
(5) Cut surface – pale
(6) Signs of herniations.
6. Cerebral compression
Cerebral compression results from an - in the size of brain.
Salient features:
(1) - in size of brain - may occur due to edema [please see above], space
occupying lesions or trauma.
(2) The magnitude of brain swelling - does not necessarily correspond to the
severity of the injury.
(3) Effects of cerebral compression [please see pathological effects of EDH
below].

C. Intracranial Hemorrhages
Intracranial hemorrhage [ICH] is any bleeding inside the skull.
Salient features:
(1) Hemorrhage – small and thin layered bleeding
(2) Hematoma – Large and space occupying bleeding [for definitions of
petechial hgs and ecchymosis, please see ch 19].
(3) Types -
(i) Primary – occurs immediately after trauma
(ii) Secondary [syn, Delayed traumatic intracranial hemorrhage (DTICH),
Reactionary hemorrhage]– First described in 1891 by Bollinger who called
it “traumatische Spät-Apoplexie”. (a) occurs within first 10 days of injury,
particularly in the first 3. (b) Incidence after severe head trauma - 2-10%.
(c) Mechanism. (II) Due to weakening of capillary walls and subsequent
rupture.
1. Extradural hemorrhage
Extradural hemorrhage [syn epidural hemorrhage, EDH] is bleeding into the
extradural space. As the bleeding clots and forms a large firm mass it is often
referred to as hematoma.
a. Causes
(1) Traumatic [main]
(2) Spontaneous. Very rare. Seen in (i) coagulation disorders, (ii) dural vascular
malformations (iii) frontal sinusitis and (iv) infections.
b. Epidemiology
(1) Incidence – least common type of meningeal bleeding
(i) 1-2% of all treated head injuries
(ii) 5-10% of autopsies in fatal head injuries
(2) Age -
(i) Most common – 10-30 y
(ii) rarest - <2 y and >60 y. At these ages dura is more firmly attached to the
inner table.
c. Mechanism
(1) Fracture of skull – In 90% cases, the fractures is fissured type. In rest it is
depressed fracture"Blood vessel [bv] ruptures"blood starts collecting in
space"As more and more blood collects, dura gets stripped further and
further"Stripping of dura causes further damage to communicating v between
skull and dura"More bleeding"Because stripping of dura is a slow process,
typically EDH develops over several hours. Bleeding may continue for several
hours or even a day after injury.
(2) Impact to skull without fracture - Skull and dura separate momentarily"An
empty extradural space is created at the site of trauma"If bv does not rupture,
nothing further happens and immediately dura and skull come to adhere once
again; if bv ruptures, mechanism is same as above. EDH without fracture of
skull is rare.
(3) EDH in neonates – is extremely rare because of firm adherence of dura to
the skull. If occurs, limited to single bones because of adherence of the dura to
the skull along the suture lines.
d. Vessels involved
Depend on site of trauma. EDH is mainly produced from inj to arteries. Veins
are generally unable to produce EDH, because their bleeding cannot generate
sufficient pressure to strip dura from bone. However EDH can be of venous
origin and also of mixed origin.
Blow over lateral convexity of head. Can cause 4 types of injuries (i) fracture of
pterion [weakest part of the skull; overlies anterior branch of middle meningeal
artery, Fig 17.16]"injury to anterior branch – EDH tends to run into the middle
cranial fossa (ii) fracture of squamous temporal bone.
e. Characteristics
(1) Site:
(i) Directly underneath the site of impact [in almost all cases]
(ii) Countercoup EDH – very rare. Seen only if skull is grossly deformed
(iii) At base of skull – rare
(iv) Usually unilateral. The sites are (a) Temporoparietal area [most common]
(b) Frontotemporal (c) Parieto-occipital (d) Occasionally – frontal region,
anterior or posterior fossa
(v) Rarely bilateral – occurs in bilateral trauma or when a median structure eg
 sagittal sinus has been injured.
(2) Size and shape:
(i) Clot is oval or circular and sharply defined
(ii) Dimensions - (a) Diameter 10-20 cm (b) Thickness 2-6 cm (c) Weight 30-
300 g
(iii) Adherent to dura mater
(iv) Presses dura inward
(v) Causes a localized concavity of external surface of brain
(3) Associated hemorrhages – about 50% have a concomitant hemorrhage
[SDH, SAH or intracerebral]
f. Pathological effects
These pathological effects are not unique to EDH; They would be seen in any
space occupying lesion [SOL], or generalized cerebral swelling causing cerebral
compression
(1) Herniations.
(2) Classification:
(i) Supratentorial herniation - (a) subfalcial [Cingulate] (b) Uncal
[transtentorial]. (c) downward [central, transtentorial] (d) External
[transcalvarial]
(ii) Infratentorial herniation - (e) Tonsillar [downward cerebellar] – also known
as coning [because tonsils herniate like a cone]. (f) Upward [upward
cerebellar or upward transtentorial].
(3) Kernohan’s notch – It is a unilateral grooving of a cerebral peduncle Caused
when the midbrain is pushed against the contralateral tentorial
edge"compresses the cerebral peduncle. During life, it results in a hemiparesis
that is ipsilateral to EDH. While Kernohan’s notch is on cerebral peduncles,
uncal grooving is on uncus.
(4) Cerebral edema
(5) Duret’s hemorrhages - These are secondary teardrop shape hemorrhages in
the brainstem. Range from small streaks to massive confluent hemorrhages.
g. Symptoms and signs
(1) There may be initial unconsciousness due to concussion. In about 25% of
cases, initial unconsciousness does not occur
(2) -ing weakness - on the side opposite to that of EDH. Occurs in face and arms
first, then spreads to legs. Symptoms may worsen due to cerebral edema or
 diffuse axonal injury [DAI]
(3) Pupils –
(i) dilated, unresponsive to light, usually on the side of hemorrhage [anisocoria -
unequal pupils].
(ii) Later there is bilateral dilatation and fixation of pupils
(4) Decerebrate rigidity and death - in about 20-50% cases. Cause of death is
respiratory failure due to compression of brain stem.
h. Sequelae
(1) Small hematomas – may undergo resorption by phagocytes derived from
perivascular dural cells
(2) Large hematomas occasionally may become smaller - due to escape of
blood through a fracture into s/c tissues. If escapes in scalp"may form a
hematoma underneath the scalp.
i. Chronic EDH
EDH is mostly of acute nature; however rarely a patient may report several days
after the injury. The term chronic EDH is typically used, when a patient reports
13 days after injury, because microscopic ossification of an EDH occurs at this
period. Ch EDH has however been reported up to 6 y after injury.
(1) Cause - Generally due to venous bleeding which is much slower. May
originate from sinuses or from the diploic veins.
(2) They represent 7-14% of EDH. In 25% cases the cause is not determined.
(3) Infection of the ch EDH occurs but is uncommon.
j. D/d
Dural metastases – secondary to neoplasia eg bronchogenic carcinoma. Patient
may present with hemiparesis and plain CT scan findings highly suggestive of
EDH. Such metastasis may also present as ch SDH.
k. Cause of death
Secondary pressure on brain stem"stoppage of respiration.
l. PM examination
Gentle removal of hematoma - may show
(1) a rupture in the vessels [may be visible during operation also] and
(2) a fissured fracture of the skull nearby. It is often confined to the inner table.
m. Dating of EDH
(1) Recent effusion – bright red
(2) 4th day - Bluish-black to brown
(3) 12-25 days - Pale brownish yellow
(4) Few months – coagulum becomes firmer and laminated.
n. MLI
(1) Minimum amount associated with fatality – 100 mL.
(2) Lucid interval [syn, latent interval]:
(i) Mechanism - Initial trauma [Fig 17.17, point A] causes unconsciousness. An
artery in extradural space may rupture and bleeding may begin slowly.
Initial unconsciousness resolves within a few minutes [B]. The person may
remain active for a period varying from few hours to a week [B-C]. This is
the lucid interval.
(ii) Incidence – 30-40% of head injuries only
(iii) Not seen in massive injuries to brain – because recovery from initial
consciousness is late and EDH develops much before that time; thus the
unconsciousness due to two conditions overlaps.
(iv) Also seen in (a) Subdural hematoma [please see below] (b) Fat Embolism
Syndrome [FES] (c) mental illness [ch 28].
(v) MLI - (a) During this period the person is responsible for all actions. (b)
Doctor may be charged with negligence if he discharges the patient
prematurely at point A.
(3) EDH, SDH etc can be preserved for chemical analysis in late deaths, when
drug has disappeared from peripheral blood [ch 40"MLI of ethyl alcohol].
2. Subdural hemorrhage
Subdural hemorrhage is bleeding into the subdural space. As the bleeding clots
and forms a large firm mass it is often referred to as hematoma.
a. Anatomy
(1) Subdural space is very narrow and contains a small amount of fluid
permitting the thin and tough arachnoid to move relative to dura
(2) The cerebral veins [bridging veins] cross this space to reach sinuses
(3) Arachnoid is attached to the dura by arachnoid granulations and venous
sinuses
(4) In Fig 17.18, space 1 is the extradural space [as can be seen, there is no
actual potential space here]; space 2 is subdural space, and space 3 is
subarachnoid space. Normally rupture of middle meningeal artery will cause
bleeding in extradural space, but if associated dura is torn, bleeding can occur
in subdural space. Similarly arteries of the Circle of Willis (where aneurysms
are most commonly found) normally cause bleeding in subarachnoid space,
but if associated arachnoid is torn, bleeding can occur in subdural space. Since
subdural space is the “middle space”, bleedings from adjacent spaces can
come in this space through a tear in the corresponding membrane.
(5) Hemorrhage:
(i) Origin - mostly venous or capillary. Rarely arterial [please see below].
(ii) Volume – ranges from a few drops to 150 mL [sufficient to cause death], or
sometimes even more.

b. Causes
(1) Traumatic ruptures – are the main cause. Rupture of
(i) parasagittal bridging or communicating veins near sagittal sinus [most
common]. These veins rupture when brain moves relative to dura. Seen in
shaken baby syndrome [ch 27]
(ii) aneurysms or a malformed superficial bv through the arachnoid into subdural
space [Fig 17.18]
(iii) cortical vessels
(iv) dural venous sinuses
(v) inferior cerebral veins entering sinuses at the base of skull
(vi) middle meningeal artery [with associated laceration of dura] so that it bleeds
directly into the subdural space, instead of epidural space [Fig 17.18].
(2) Anticoagulants -
(i) Dicoumarol
(ii) heparin
(iii) Warfarin. SDH may occur even in the absence of history of trauma.
(3) Contusions and lacerations - of brain and dura
(4) Metabolic disorders –
(i) Galactosemia
(ii) Glutaric aciduria type I.
(iii) Menkes disease. These diseases may indeed be mistaken for shaken baby
syndrome [ch 27].
(5) Old adhesions - between brain and dura breaking up
(6) Perinatal -
(i) Following labor – due to head moulding in newborns. Usually in the posterior
fossa and massive.
(ii) Precipitate labor – [ch 27]
(7) An already formed SAH - may bleed into subdural space, if dura tears due
to blunt force
(8) Secondary to disease -
(i) Bleeding diathesis
(ii) Cerebral aneurysm
(iii) Cerebral tumor
(9) Miscellaneous -
(i) Arachnoid cyst rupture
(ii) -CVP
(iii) Hypernatremia.

c. Epidemiology
(1) Incidence – Commoner than EDH
(2) Age -
(i) Common in childhood and old age
(3) Degree and type of trauma –
(i) May occur from relatively insignificant trauma insufficient to produce any
other visible mark. Thus it may be seen in the absence of fractures of skull,
cerebral injuries [eg contusions or lacerations] or unconsciousness
(ii) About 70% due to falls; 25% due to vehicular accidents; 5% due to other
reasons
(iii) Fatal SDH – usually associated with contusions and lacerations of brain and
fractures of skull.
(4) Site - Supratentorial – upper lateral surface of cerebral hemispheres [most
common]. Gradually the blood drains down under gravity to cover the entire
cerebral hemispheres. Large accumulations occur in cranial fossae also [all 3,
but most commonly in ACF and MCF]
(5) Accumulation – is quicker than EDH, but occasionally may be as slow as
EDH. With slower accumulation, considerably larger sizes of SDH may be
tolerated.
(6) May be associated with
(i) alcoholism [Reasons (a) liver damage" coagulation factor deficiency; (b)
more falls; (c) more involvement in fights]
(ii) countercoup injuries.

d. Types
Divided in 3 types according to time interval between trauma and onset of
symptoms [apathy, change in behavior, confusion, dizziness, drowsiness,
headache, lethargy, nausea and vomiting, seizures, weakness].
(1) Acute – immediately to 3 days
(2) Subacute – 3 days to 3 weeks
(3) Chronic – > 3 weeks.
i. Acute SDH
Cause –
(1) rupture of (a) large bridging veins (b) one of the cortical arteries (c) larger
dural sinuses – usually torn by penetrating wounds or depressed fractures.
Produce clots in unusual positions, eg posterior fossa underneath the occipital
lobes or between the hemispheres over the corpus callosum.
(2) cerebral lacerations.
ii. Subacute SDH
(1) Occurs when bleeding is from smaller bridging veins.
(2) Associated brain damage is less likely
(3) Blood film is thin and watery due either to dilution with CSF or hemolysis.
iii. Chronic SDH
(1) Location –
(i) Over frontal and temporal [extending to base],
(ii) near midline [may be bilateral] and
(iii) parietal lobe
(2) Extent –
(i) localized and deep, or
(ii) as a widespread film on surface
(3) Epidemiology - Seen in old persons. Etiology"brain atrophies in old
age"more space in SDH"vessels traversing it have less cushioning"break more
easily
(4) Time course of development – please see dating of SDH below.

e. Sequelae
(1) Cerebral shift and herniation [mostly transtentorial].
(2) Encapsulation - SDH may develop its own membrane formed by dural cells.
The capsule is firmly attached to the dura. Arachnoid does not take part in this
encapsulation.
(3) Extramedullary hematopoiesis – may occur rarely in SDH. Evidence is the
presence of nucleated RBCs in various stages of maturation in the patient’s
subdural space.
(4) Flattening of cerebral gyri:
(i) Same side – due to direct pressure
(ii) Opposite side – displacement of cerebral hemispheres to the opposite
side"gyri of opposite side are pressed against the bone.
(5) Fresh bleeding – Causes
(i) SDH may draw in water due to osmosis" expands"compresses brain
tissue"causes new bleeds by tearing other blood vessels.
(ii) Original clot gets absorbed"chemical changes occurring in it cause a further
hemorrhage to occur in it
(iii) Further trauma.
(6) Infarction – must be differentiated from infarction due to stroke [Table 4].
(7) Organization – Ossification or hyalinization may occur rarely. Symptoms -
focal epilepsy, progressive hemiplegia.,
(8) Reabsorption of clot
(i) Smaller SDH- completely reabsorbed with no trace
(ii) Larger SDH - replaced with granulation tissue.
(9) Secondary brain hemorrhage – due to compression of brain stem
(10) vasoconstrictors may be released from SDH" ischemia under
SDH"ischemic cascade"brain cell death.
f. Dating of SDH
(1) 24 h:
(i) SDH consists of - partially liquid and partially soft fragments of red-black,
gel-like, clotted blood.
(ii) Adherence to inner dural surface - (a) Most clots do not adhere (b) Some
clots that do adhere are loose and slide along the surface when pressed.
(iii) Microscopy - (a) No cellular reaction from dura (b) RBC – intact (c)
Leucocytes – trapped (d) Fibrin – in discontinuous layers between the dura
and the hemorrhage
(2) 24-48 hours:
(i) Color – Reddish brown with -ed fibrin deposition
(ii) Neutrophils invade hemorrhage
(iii) Proliferation of fibroblasts at the interface of the dura and hemorrhage
(3) 2-5 d:
(i) -ed presence of the above
(ii) soft clots – stick loosely to dura; resist pressure to move them along surface
(iii) Microscopy - (a) Endothelial proliferation (b) scattered macrophages are
present in the clot (c) Occasional spindle cells invade clot from dura (d)
RBCs – (I) Early RBC breakdown (II) hemosiderin granules are
demonstrable (III) Margins of clotted RBC - become indistinct (e)
Neomembrane – Appears on the outer [dural side] (I) 3-4 cells thick closer
to day 3 (II) up to 7 cells thick closer to day 5
(4) 1 week:
(i) Outer neomembrane is yellow; grossly visible around the edges of clot
(ii) Inner membrane [arachnoid side] has not yet appeared
(iii) Coagulated blood is orange brown. Definitely adheres to dura
(iv) Microscopy - (a) Newly formed capillaries enter the hemorrhage along with
the more abundant fibroblasts, giving the appearance of a typical
granulation tissue (b) More intracellular hemosiderin accumulates (c)
Laking [hemolysis] of RBCs
(5) 2-3 weeks:
(i) Outer [dural] neomembrane thickens and becomes more vascular. Proceeds to
partially cover inner surface of clot, which is beginning to liquefy
(ii) Clot – orange to yellow brown
(iii) Foci of red-black blood are common. Reflect the tendency of granulation
tissue to bleed
(iv) Microscopy - (a) day 10 - Neomembrane is up to 15 cells thick (b) Up to 14
days - (I) Hemosiderin-laden macrophages (II) Neomembrane – thickness
[twice that of the native dura]. Becomes more vascular. Hugely dilated
capillaries (c) Up to 21 days - (I) Hemorrhage is absorbed with rare RBCs
remaining (II) More obvious vascular proliferation (III) Inner neomembrane
– thin and incomplete (IV) Outer neomembrane - mostly loosely arranged
fibrovascular tissue
(6) 4 weeks:
(i) Outer [dural] and inner [arachnoidal] membranes are complete and grossly
visible. Outer membrane is approximately the thickness of the dura
(ii) Most blood is now semiliquid and orange brown
(iii) Collagen is deposited
(iv) Formation of arteries
(v) If there was an arachnoidal laceration, SDH adheres to it, otherwise not.
 Arachnoid does not contribute to the process of organization.
(7) 1-6 months:
(i) Rare hemosiderin-laden macrophages
(ii) Fusion of neomembrane and dura
(iii) Blood is mostly resorbed, leaving a thin gold colored membrane adherent to
dura
(iv) Rare blood vessels
(8) 6-12 months:
(i) Thin neomembrane that is difficult to distinguish from native dura
(ii) Hemosiderin-laden macrophages still present.

g. Subdural hygroma
A subdural hygroma [Gk, hygros, moist; oma, tumor] [syn, hydroma] is a
subdural collection of CSF without blood.
Salient features:
(1) Causes: (i) Arachnoid cyst rupture (ii) CSF leakage through an arachnoid
tear [valve mechanism] (iii) Entry of microorganisms into the subdural space
"inflammatory changes with a serous reaction (iv) Post-operative - (a) After
ventricular drainage [frequently bilateral] (b) Failure of the brain to re-expand
- after surgical resection of a long-standing mass lesion (c) excessive drainage
- during the implantation of a CSF shunting device.
(2) Significance – Subdural hygromas on CT scans may be misinterpreted as
chronic subdural hematomas, and vice versa.

h. Cause of death
Secondary pressure on brain stem"stoppage of respiration.

i. PM examination
Unlike EDH, the bleeding points are so small that they cannot be discovered at
operation or PM.

j. MLI
Lucid interval – Seen in subdural hematoma also. If accompanied by cerebral
contusion, a lucid interval is relatively less common because the primary
disturbance of consciousness persists far longer.
3. Subarachnoid hemorrhage
Subarachnoid hemorrhage is bleeding into the subarachnoid space. As the
bleeding clots and forms a large firm mass it is often referred to as hematoma.
The latter is more often used when it is present over the spinal cord [spinal
subarachnoid hematoma].
a. Anatomy
(1) Subarachnoid space [SAS] - Unlike extradural space, subarachnoid space –
space between arachnoid and the very thin pia – is a real space.
(2) Pia dips up and down along the surface of gyri and sulci, while arachnoid
doesn’t.
(3) Contents of SAS –
(i) Brain bv
(ii) Connective tissue network
(iii) Cranial nerves
(iv) CSF – produced by choroid plexuses of lateral and 4th ventricles.
b. Arachnoid cysts
Arachnoid cysts are CSF filled collections that occur between two arachnoid
layers.
c. Causes
(1) Trauma - Most significant cause of SAH. SAH is further classified in 3
subtypes:
(i) brain injury associated [seen in association with contusions and lacerations of
brain and pia-arachnoid]
(ii) traumatic rupture of basal cerebral vessels [ruptures normal basal vessels or a
preexisting berry aneurysm]
(iii) traumatic focal [bleeding occurs only in focal areas].
(2) Non-traumatic (Spontaneous) - please see ch 8.
(3) Hanging – ch 19.
d. Epidemiology
(1) Incidence – Most common ICH. In fact in all cases of significant head injury
some degree of SAH is seen.
(2) Associations - May be seen alone or with other craniocerebral injuries,
including fractures.
(3) Like all delayed traumatic hemorrhages, it can also be delayed after trauma.
e. Clinical aspects
(1) Symptoms -
(i) severe headache with a rapid onset [“thunderclap headache”]
(ii) vomiting,
(iii) confusion or a lowered level of consciousness,
(iv) seizures
(2) Diagnosis - confirmed by a CT scan or LP.
f. Microscopic dating of SAH
(1) <1 hour - Fresh blood in subarachnoid space
(2) 1-4 h -
(i) Occasional neutrophils seen
(ii) Some RBCs begin to break down
(iii) RBCs begin to creep down the Virchow–Robin spaces
(3) 4-12 h -
(i) -ed neutrophils
(ii) Perivascular lymphocytes
(iii) Rare macrophages
(4) 12-24 h -
(i) Hemosiderin and fibrin
(ii) -ed numbers of lymphocytes and macrophages
(5) 24-48 h -
(i) -ed neutrophils and macrophages
(ii) Definite hemosiderin deposition
(6) Up to 3 days - Peak neutrophilic infiltrate
(7) Up to 5 d -
(i) Laking of RBCs
(ii) -ed lymphocytes
(iii) Intense fibrin deposition separating islands of RBCs
(iv) Early collagen formation.

4. Intracerebral hemorrhage
Intracerebral hemorrhage [ICH] is a subtype of intracranial hemorrhage that
occurs within the brain tissue.
Salient features:
(1) Timing in relation to injury – Most ICH occur at the time of accident, but
bleeding is often slow due to oozing from venules and capillaries. As
hematoma expands, it injures more vessels and more bleeding occurs. Rarely
bleeding may occur several weeks or even months after trauma during which
brain softens ultimately rupturing the vessel.
(2) Location: (i) Relatively deep seated traumatic ICH - usually accompanied by
other types of injuries, eg cortical contusions and lacerations. (ii) Superficial
traumatic ICH - generally occur alone.
(3) Symptoms – patient becomes deeply unconscious from the moment of
injury.
a. Causes
(1) Angioma or malignant tumor of brain
(2) Capillary hemorrhages – seen in Asphyxial states, Blood dyscrasias, Fat
embolism, Softening due to Anoxia, Arterial thrombosis, Sinus thrombosis
(3) Cerebral trauma
(4) Hypertensive cerebrovascular disease – Generally due to rupture of
lenticulostriate artery. Causes spontaneous hemorrhages in the region of basal
ganglia. Common in middle aged and elderly persons. Other areas of
hemorrhage are thalamus, external capsule, pons and cerebellum.
5. Intraventricular hemorrhage
An intraventricular hemorrhage [IVH] is a bleeding into the brain’s ventricular
system.
Salient features:
(1) Types: (i) Primary - (a) bleeding is confined to the ventricular system. (b)
Uncommon [3% of all spontaneous intracerebral hemorrhages (ICH)]. (c)
median age - 55 y [range 9 to 91 years] (d) Sex - Males and females are
equally represented (e) 50% patients have a history of hypertension (f) Causes
– Mostly non-traumatic. (I) Coagulopathies, acquired or inherited (II)
Fibromuscular dysplasia (III) Intraventricular aneurysms. (IV) Intraventricular
tumors (V) Moyamoya disease (VI) Pituitary apoplexy (VII) Puerperal
toxemia (VIII) Sympathomimetic abuse [eg methamphetamine] (IX) Vascular
malformations [usually AV malformations or fistulae] (X) Vasculitis (ii)
Secondary – (a) More common. (b) An intracerebral or subarachnoid
hemorrhage occurs first which bleeds into the ventricular system. (c) IVH
 complicates 40% of ICH and 10% of SAH cases.
(2) Source of bleeding – choroid plexus, vessels of septum pellucidum.

D. Respirator Brain
Respirator brain is a characteristic brain change, which occurs when brain stem
death has occurred and cerebral circulation has ceased, but the patient has been
kept on a respirator for >12 h.

E. Sequelae of Head Injury

1. Head injury and offending
(1) Head injury is linked to -ed rate of subsequent offending.
(2) Evidence:
(i) There is -ed irritability, aggression, impulsivity and lack of foresight, which
predispose to offending.
(ii) Follow-up studies of those who have suffered head injury indicate -ed rates
of arrest, conviction and incarceration post injury.
(iii) There is an -ed rate of past head injury in samples of people who have
committed violent crimes.

2. Post traumatic automatism

Post traumatic automatism refers to a disturbance of consciousness, associated
with automatic, repetitive, and uncontrollable behavior that occurs after head
injury.
Salient features:
(1) There is subsequent amnesia for the automatic events.
(2) Most typical signs are: (i) Thrashing or flailing limbs in a non-directed
manner (ii) Refusing to be directed [eg onto a stretcher or into an ambulance]
(iii) Wildly swinging arms if directly confronted or restrained (iv) Aimless
wandering in a “robotic” fashion.
(3) Post traumatic automatism may be advanced as a defense by the offender, if
he has committed a crime (say a murder). A successful claim of automatism
results in an absolute acquittal. Before certifying, the forensic specialist should
note following points. (i) There should be a documented concussive brain
injury. (ii) The automatism must occur in the stage of post-traumatic
amnesia. (iii) The automatism behaviour must represent a reactive and
 purposeless response to stimulation or confrontation. (iv) No premeditation,
planning, or concealment should be demonstrable. (v) There should be
absence of goal directed, purposeful, or proactive behaviour.
3. Post traumatic amnesia
Post-traumatic amnesia (PTA) is characterized by a transient state of confusion
and disorientation following head injury. The hallmark of this state is
anterograde amnesia (AA), which is the impaired ability to remember events
after the trauma.
Interrogation of persons having sustained head injuries
Because of the possibility of retrograde amnesia, it may not always be fruitful
for police to interrogate a victim who has sustained head injuries. Leading
questions should not be asked from him.
4. Increased intracranial pressure
-ed intracranial pressure is seen after
(1) Abscesses and tumors of brain and its coverings
(2) Diffuse cerebral edema
(3) Dural sinus thrombosis [ch 5]
(4) Hemorrhages [Cerebral hemorrhage, Extradural and subdural hemorrhage]
(5) Infarction of brain
(6) Leptomeningitis.
5. Miscellaneous
(1) Aneurysms,
(2) Arterio-venous fistula,
(3) Dural sinus thrombosis [Central Venous sinus thrombosis] [DST, CVST ch
5].

III. INJURIES OF THE SPINAL CORD

A. Railway Spine
Railway spine (concussion of the spinal cord) is the name given to a
constellation of neurological signs and symptoms, appearing after a railway
accident.
Salient features:
(1) These were very common in early days of railway travel (19th c), because the
 railways were not specially designed for passenger safety.
(2) Since no external injuries were noted on the victims, it was thought that the
symptoms were due to concussion of the spinal cord.
1. Cause
Railway accident (generally due to heavy forces involved in railway accidents).
May also be seen in
(1) other vehicular accidents
(2) severe blows to the back
(3) compression from dislocation or fracture of vertebrae
(4) fall from height
(5) bullet injury.
2. Mechanism
Concussion of the spinal cord, caused by
(1) momentary collision of the cord against the wall of the canal, or
(2) transient deformity in the profile of the canal due to violent deceleration or
(3) rotational strains.
3. Symptoms
(1) Time of appearance - Appear immediately or after a few hours. Sometimes
after several days
(2) Symptoms - Mainly neurological: (i) headache and giddiness (ii) restlessness
(iii) weakness of limbs (iv) Paralysis (v) back pain (vi) urinary and/or fecal
incontinence (vii) loss of sexual power (viii) disorders of special senses (ix)
insomnia (x) amnesia (xi) failing memory.
(3) Duration - Usually transient. Classically they used to disappear after
compensation was granted. This gave rise to a widespread suspicion that this
condition was merely “invented” by some interested parties in order to get
money.
(4) Current concepts - It is now known that these symptoms represent
Posttraumatic Stress Disorder (PTSD) [ch 11"Trauma and neurological
disease].
4. Treatment
Conservative.
5. PM Appearances
Nothing specific. There may be petechial hemorrhages in spinal cord. Mostly
railway spine results in negative autopsy [ch 8].
B. Whiplash Injury
Whiplash injury is an injury to the neck caused by sudden hyperextension of the
neck followed by hyperflexion or vice-versa.
(1) Mechanism – Caused due to sudden and violent hyperflexion and
hyperextension of the spine. Of these two, hyperextension is more dangerous
because flexion injuries are protected by the contraction of strong posterior
neck muscles. In comparison, the anterior longitudinal ligament which
protects from injuries during hyperextension is quite weak.
(2) Injuries:
(i) Dislocation of upper cervical spine
(ii) Fatal contusion and laceration of spine without fracture of spine
(iii) Fracture dislocation in lower spine (C5-6)
(iv) Fracture dislocation in the upper dorsal spine (T5-7).
(3) Causes:
(i) Motor vehicle accidents – Most common [ch 18]. (a) Stationary vehicle
struck from rear (most common)– Sudden hyperextension of the head
followed by sudden flexion [to prevent hyperextension, modern cars now
have a head-rest at the top of the seat] (b) Moving vehicle crashing into a
stationary object – Hyperflexion of head"strikes windscreen"Rebounds and
goes into hyperextension
(ii) Rabbit punch – Rabbit punch is a sharp blow to the back of neck [spinous
process of an upper cervical vertebra] or to the base of the skull. Because of
the fear of whiplash injury, the rabbit punch is illegal in boxing and many
other combat sports. The name is derived from the use of the technique by
hunters to kill rabbits with a quick, sharp strike to the back of the head.
(4) Clinical presentation - (i) cognitive/psychological symptoms (ii) Dizziness
(iii) Headaches (iv) Neck, shoulder, or back pain (v) paresthesias (vi) vertigo.
If these symptoms persist for some months, it is known as chronic whiplash
injury.

IV. INJURIES TO BONES

A. Fractures
1. AM and PM fractures
2. Age of fractures
Age of fractures can be estimated by
(1) Naked eye and histological examination [in the dead] and by
(2) Radiological examination [in the living]. Fractures heal in 4 stages.
(i) Stage of inflammation – Lasts up to 7 days [total 1 week]
(ii) Stage of soft callus formation (or reparative or proliferative phase) – 1 week
to 4 weeks [total 3 weeks]
(iii) Stage of hard callus formation [or maturing or modeling phase] – 4 to 12
weeks [total 8 weeks]
(iv) Stage of remodeling (or remodeling phase) – [up to 2 years]
(v) Rarely formation of false joints.

V. BOXING INJURIES

1. Punch-drunk syndrome
Punch-drunk syndrome [syn - boxer’s syndrome, chronic traumatic
encephalopathy, Dementia pugilistica, pugilistic Parkinson’s syndrome] is a
neurological disorder which affects professional boxers and others who receive
multiple serious blows to the head.
Salient features:
(1) Most important chronic boxing injury
(2) Onset - The condition develops over a period of years, with the average time
of onset being about 15 years after the start of a career in boxing.
(3) Number of years the boxer has been in profession is more important in
determining its onset, than the number of serious blows the boxer received. It
is because even minor, unnoticed traumatic events are important.
(4) Symptoms - The major symptoms are (i) ataxia (ii) dementia (iii) memory
impairment (iv) slow thought process (v) slurred speech (vi) stiff limbs (vii)
tremors [much like those seen in Parkinsonism], and (viii) outbursts of
violence. The condition is called “punch-drunk” because the symptoms are
similar to those shown by a drunk person. Famous boxers who have suffered
from this syndrome include Jack Dempsey, Beau Jack, Joe Louis and
Muhammad Ali.
(5) utopsy shows (i) Cortical atrophy (ii) perforation of septum pellucidum (iii)
slight hydrocephalus (iv) thinning out of fornices and adjacent corpus
callosum (v) presence of scars and patches of gliosis throughout the brain
tissue.

2. Boxer’s hemorrhages
Pontine hemorrhages.

3. Post-traumatic hypopituitarism
Due to direct injury and vascular problems.

4. Other cerebral injuries

(1) Cavum septum pellucidum (CSP) - Septum pellucidum develops a
separation between its two leaflets (septal laminae). This cavity contains CSF. It
was once called the “fifth ventricle”, but the term is not favored now, because
CSF in CSP is noncommunicating (2) diffuse axonal injury, (3) cerebral edema
(4) ischemia and herniation (5) cerebral atrophy (6) enlargement of the ventricles
(7) cerebellar changes (8) loss of neurons in the substantia nigra (9) chronic
encephalopathy (10) dissecting aneurysms.

5. Ocular injuries
(1) choroidal tears (2) Retinal detachment (3) vitreous hemorrhages.

18. Traffic Accidents

AUTOMOBILE ACCIDENTS

A. Injuries to Pedestrians
Three types of injuries are seen:
(1) Primary impact injuries are caused by the initial strike, i.e, the first part of
the vehicle that strikes the victim (usually legs). The victim then revolves
round his center of gravity (located at symphysis pubis), and is thrown back
on the vehicle, causing further injuries.
(2) These are known as secondary impact injuries.
(3) Then the victim is thrown on the ground. This causes secondary injuries [Fig
18.1].
(4) Finally the victim may be run over by the vehicle, causing crush injuries. A
diagram indicating the three types of injuries, their extent and location can
help reconstruct the accident.
1. Primary impact injuries
Part of body struck – Depends upon
(1) Position of person - in relation to the vehicle when struck, i.e. walking with
the traffic, against the traffic or crossing the road. If walking with the traffic,
he would be struck from behind, and back of legs are struck. Following
situations are most important.

a. Pedestrian struck from behind; both feet fixed to the ground

Whether the feet are fixed or not fixed depends upon nature of the road surface;
whether it is slippery or not; whether it has rained or not. Injuries produced are
(1) Bumper injuries - Injuries at site of bumper impact, in the form of
abrasions, contusions, lacerations, internal haemorrhage in the calves etc.
Bumper fractures - part of bumper injuries. Most characteristic fracture in
vehicular accidents. Characteristics - (a) Usually tibia is fractured, although
very rarely fibula may also fracture. (b) The fractured fragment of tibia is
wedge shaped, and is displaced forwards. The base of the wedge indicates the
site of impact, and the apex points in the direction in which the vehicle was
travelling. (c) If bumper fractures are only in one leg or in both legs but at
different levels, it suggests victim was walking or running (d) In children – the
 bumper usually produces fracture of femur. Femoral head may be driven
through acetabulum (e) Identification of vehicle – Height of bumper fracture
from the ground = height of bumper of offending vehicle (f) Behavior of the
driver of the vehicle – (I) When brakes are applied - height of bumper dips
down. Thus height of bumper fracture is less than the height of the bumper of
offending vehicle. (II)when accelerator is pressed - height of bumper goes up.
Height of bumper fracture is more than the height of the bumper of offending
vehicle (g) Sometimes the fracture may be spiral.
(2) Impact against mudguard or headlamp:
(i) fracture of pelvis, Pubic ramus fracture
(ii) fracture dislocations of the sacroiliac joints.
(iii) Imprint abrasions - Due to head lamps and radiators
(3) Vehicle type:
(i) If vehicle has a straight and high front end [eg bus, trailer, truck, van], the
entire body may come in contact with front end at once.
(ii) Injuries - would depend on how victim was positioned [including positions
mentioned below]. (a) Frontal impacts- Head injuries, chest injuries,
fracture of ribs (b) Side impacts – Injuries [lacerations etc] of arms (c) Rear
impacts - (I) injuries to buttocks and sacroiliac joints (II) Fracture-
dislocation of the lumbar or thoracic spine, sacroiliac joint (III) The
fractured portion of the vertebral column may move forward causing
transection of the spinal cord and thoracic aorta. (IV) Associated
fracture of adjacent ribs. Secondary impact injuries are virtually non-
existent in such cases, as there is no way a victim can recoil back on the
vehicle. He instead is pushed to the ground and suffers secondary injuries.
(4) Protruding objects – from vehicles may cause serious, and often
characteristic injuries.

2. Secondary impact injuries

(1) If feet slide forward, the whole body falls backwards, with a secondary
impact of the head against the windshield [Fig 18.1].
(2) Injuries: If victim falls on hood – Tangential force directed by hood to the
buttock and thigh"Causes separation of the skin and s/c tissues from the
muscle"produces a pocket in the upper thigh and buttock"Collection of large
amount of blood in this pocket, which is often not visible externally
(3) If feet not firmly fixed on ground and vehicle is at high speed - The victim is
“scooped up”, i.e. thrown into the air. He may land over the roof of the
vehicle, somersaults [head may strike roof] and may even be deposited on the
road behind the vehicle, where he may be run over by other vehicles. Atlanto-
occipital dislocation and partial disruption of intervertebral discs are quite
common in this situation.

3. Secondary injuries
(1) Due to striking of victim on ground:
(i) May be caused after secondary impact injuries, or
(ii) immediately after primary impact injuries, when the victim is thrown high up
in air and strikes the ground.
(2) Injuries:
(i) All kinds – including abrasions, contusions, lacerations, fractures etc
(ii) fracture skull – due to victim falling over road
(3) Waddell and Drucker’s triad [syn, Waddell’s triad]-
(i) Primary impact, secondary impact and secondary injuries may together
constitute the Waddell and Drucker’s triad.
(ii) The injuries described in the original paper were (a) Injury around the knee
[primary impact by bumper] (b) Injuries to proximal femur or pelvis
[secondary impact inj]. (c) Contralateral craniocerebral injury -
[secondary inj].

4. Run over injuries

(1) Abrasions:
(i) Grazes
(ii) Impact or imprint abrasions – in the form of tire marks. They are spread out a
little due to yielding and flattening of body from pressure.
(2) Avulsions [ch 12]:
(i) The rotatory effect against a fixed limb may strip off almost all tissues down
to the bone.
(ii) The avulsed wound may be segmental or circumferential [completely
encircling arm or leg]
(iii) If head is involved, complete avulsion of an ear may occur
(iv) If intestines or scrotum are involved – extrusion of intestines or testes occurs
(3) Head injury with egg-shelling of skull – skull may be crushed from sided to
side or forced open with extrusion of brain.
(4) Multiple fracture of ribs – if tire passes over chest
(5) Abdominal rupture – with extrusion of contents [if tire passes over
abdomen]
(6) Crushing and hemisection of body - if vehicle is very heavy [eg truck] and
tire passes through middle of body, eg abdomen
(7) Crushing of legs – if tire passes over legs
(8) Burns – due to
(i) heat produced due to friction consequent upon dragging
(ii) Exhaust gases
(9) Special situations:
(i) If brakes are applied – wheels will lock"Shearing action of tangential
force"Long lacerations, complete amputation of a limb, decapitation
(ii) If victim is a child – fractures may not occur because of elasticity of
cartilaginous skeleton.

5. Rolling over injuries

(1) Mechanism - Produced when a vehicle with low chassis “rolls” the victim
along the roadway, instead of “running him over”.
(2) Injuries:
(i) Abrasions – (a) Graze abrasions (b) Patterned abrasions – caused by parts on
the undersurface of chassis
(ii) Burns - from exhaust system
(iii) Fractures – of bones all over body
(iv) Grease soiling
(3) Site - Present circumferentially all round the body [eg graze abrasions
circling around body].

B. Injuries to Vehicle Occupants

Injuries would depend upon type of impact. 2 broad types are recognized – Non
ejection and ejection injuries.

1. Non-ejection injuries
a. Frontal impact
(1) Most common - About 80% of vehicular accidents are frontal in nature, eg
two vehicles colliding head-on or vehicle striking a fixed object, such as a
lamp post, tree or a wall, causing violent deceleration.
(2) Sequence of events upon frontal impact – Driver and passengers receive
some common [deceleration injuries] and some different set of injuries [due to
differences in secondary collision].
i. Driver
(1) Secondary accident - The driver (if not wearing seat belt) slides forwards so
that his legs strike the fascia/parcel-shelf area [instrument panel and dashboard
area], and his chest and lower abdomen strikes the lower edge of the steering
wheel. This is known as second collision, second impact or secondary
accident.
(2) Facial impact on windscreen – windscreen injuries of face [imprint abrasions,
bruises, fracture jaws, facial bones;
(3) Flexion across steering wheel - The body flexes across the steering wheel
and begins to rise. Causes steering wheel injuries on the chest and abdomen
[chest contusions, bilateral rib fracture, lacerations of liver]. Modern cars are
fitted with energy absorbing compressible steering wheel column"results in
less serious steering wheel injuries.
(4) Rarely driver’s chin may be suspended against steering wheel causing
accidental hanging [ch 19]
(5) Flexion of spine - The head [which is heavier] goes forwards causing flexion
of the cervical and thoracic spine. If followed by hyperextension, results in
whiplash injuries [ch 17].
(6) Head strikes windscreen - The upward and forward component of the force
of impact causes the head to strike the windscreen. Thus windshield is
prevented from shattering and drivers [and other occupants] may sustain only
relatively minor incised wounds. These are typically vertically oriented and
clustered on the forehead.
(7) Windscreen broken and body ejected - The windscreen may be broken due to
impact by the head or face, and the whole body may be ejected through the
broken glass, to land on the bonnet or even on the roadway ahead.
(a) Air bag injuries
Salient features:
(1) Although airbags . the incidence of fatal injuries, ironically they themselves
may be cause of serious injuries.
(2) Epidemiology:
(i) Incidence - At least one airbag related injury occurs in 43% of airbag
deployments.
(ii) Age - Adults of short stature and children are particularly liable
(iii) Severity - (a) The majority [96%] of injuries are minor, eg lacerations,
thermal, mechanical, or corrosive burns of the skin and the eyes. (b) Only
0.2% are considered as serious lesions. The risk of serious injuries or
fatalities is particularly high in children sitting in the front passenger seat
[chest, abdomen, or cervical spine traumas].
(3) Fatal lesions – Caused by impact of chest against air bag. Multiple rib
fracture with bilateral hemothorax, SDH, laceration of pericardium and right
atrium with hemopericardium, retropharyngeal hematoma with airway
obstruction.
(4) Non fatal lesions:
(i) Ocular injuries – Most common. Caused by impact of face against air bag, or
the projection of an object [eye glasses, tobacco pipe] into the face
(ii) abrasions, contusions, lacerations of face, chest and limbs
(iii) Orthopedic injuries – (a) Mainly occur in upper and lower limbs [for lateral
airbags] (b) fracture of ribs and sternum (c) pulmonary contusions (d)
cardiac trauma (e) spinal lesions [eg cervical spine fracture] -less common.
(f) Forearms are most frequently involved, especially on the distal third. (g)
Hand lesions - usually minor and rare.
(b) Deceleration injuries
Deceleration injuries include a variety of thoracic injuries resulting when the
moving thorax decelerates rapidly as a result of impact against a stationary or
relatively stationary object.
Salient features:
(1) Injuries: (i) aortic injuries [laceration, transection]. (ii) sternal fracture (iii)
flail chest (iv) myocardial injuries – (a) Contusions and lacerations (b)
contusions of pericardium and myocardium may be seen even without fracture
of ribs. (c) Posterior surface of heart – shows injuries from impact against the
spine (d) Avulsion – May be completely avulsed from its base and may be
lying loose in the chest cavity (e) Lacerations – of auricles and ventricles.
 Either from fractured ribs and sternum, or through external objects (v)
Tracheobronchial disruption (vi) Lungs – (a) Vertical line of bruising on
posterior surface – due to blunt impact of lung against vertebral column (b)
Air bullae and blood blisters – under the pleura, overlying the bruised areas
(2) Aortic injury: (i) “classic” deceleration injury (ii) Location - aortic isthmus,
a few centimeters distal of the ostium of the left subclavian artery [Most
common] (iii) Associated with large magnitude forces (iv) Most frequently
seen in frontal and near-side crashes (v) Appearances – (a) Aortic rupture –
circular, clean cut; appears as sharp as if transected with a knife (b) Ladder
tears - multiple transverse intimal tears, adjacent to main rupture [Fig 18.2].
(vi) Mechanisms - (a) Differential deceleration - of the heart and aortic arch
relative to the anchored segments of the thoracic aorta (b) -ed intravascular
pressure and hemodynamic forces in vehicular crashes (c) severe whiplash
effect on thoracic spine (d) Osseous pinch - Aorta is crushed or “pinched”
between the vertebral column and the inner surface of the manubrium, first
rib, and clavicle during anteroposterior thoracic compressive deformation. (I)
Consistent location of aortic injury - Adequately explained, since the aortic
isthmus will be compressed between the bony anterior thoracic structures and
the fourth vertebral body. (II) Also provides an explanation for aortic injuries
occurring in low-speed crushing injuries.
(3) Two or more deceleration injuries – are mostly fatal. Thus while in clinical
cases, only one of the above types are seen, in autopsy cases, two or more than
two are seen.
(c) Seat belt injuries
Salient features:
(1) Mechanism of protection: (i) Restrains body – Keeps it away from
potentially injurious objects like steering wheel and windscreen. (ii) Spreads
deceleration force – over broad surface area of strap (iii) Reduces G-forces –
 strap stretches during deceleration"time of deceleration -es, causing reduction
of G-forces (iv) Prevents ejection
(2) Reduction in risk of death - 40%. Nancy Cruzan died because she was not
wearing seat belts [ch 8].
(3) Although seat belts .the risk of aortic injuries, the same is not true of side
impact crashes.
(4) Seat Belt Syndrome [SBS]: (i) Caused by lap-strap seat belts - Frontal
collision"driver forced forwards violently"Jack-knifes over the lap belt at the
waist"Injuries [lap belt syndrome] (a) Surface injuries to lower abdomen
[abrasions, contusions, hematomas] (b) Injury to abdominal viscera at the
midlumbar level [avulsion, contusion, perforation and tear of intestine; bowel
transection, particularly near points of fixation, eg duodenum, suspensory
muscle of duodenum [ligament of Treitz], cecum, ileocecal valve and root of
mesentery; omental and mesenteric lacerations; lacerations of spleen, liver,
pancreas, cecum and bladder; rupture of abdominal aorta, vena cava, common
iliac artery, diaphragm, especially left hemidiaphragm] (c) fracture and
dislocation of the thoracic and lumbar vertebrae [Chance fractures; ch 17]
and spinal damage causing paralysis. Most characteristic “triad of injuries”
associated with rapid deceleration against a fixed fulcrum is spinal trauma
[Chance fractures (ch 17)], seat belt aorta (ch 17), and bowel injuries. (ii)
Caused by Modern 3-point belts – These were developed to minimize the
incidence of SBS. Abdominal injuries were .ed, but the diagonal strap
introduced new injuries. It contributes to hyperflexion or hyperextension of
the neck"fracture of cervical and upper thoracic vertebrae, Carotid laceration,
Tracheal transection, Injuries to brachial plexus (iii) Accidental strangulation -
Children may slide under the lap strap, and the diagonal strap passes across
throat. May cause accidental strangulation [ch 19]. Other types of belts are
much less common.
(5) Strangulation by seat belts - please see ch 19.
(d) Under-running
(1) If a small vehicle eg a car is following a larger vehicle eg a truck at a high
speed [tail-gating], and truck suddenly stops, the smaller vehicle may continue
to run underneath the larger vehicle, causing severe crushing of the car [under-
running].
(2) Occupants – may receive severe crushing injuries. Their recovery is very
difficult.
(3) If tailgating vehicle is a motorcycle:
(i) the motorcyclist’s head and shoulders are smashed against the tailboard.
(ii) In extreme cases decapitation may occur.

ii. Front seat passengers

Same sequence as that seen in driver, except that they do not strike the steering
wheel. They instead strike the dashboard.
iii. Back seat passengers
(1) Mechanism:
(i) violent deceleration
(ii) no seat belts
(2) Injuries:
(i) Most common - to head and knees, due to striking of head to front seat
including head rests
(ii) Sometimes thrown over the front seat and strike the car’s front structures, or
even ejected through the windscreen.
b. Side impact
(1) Frequency - Second most common – after frontal collisions
(2) Circumstances:
(i) An offending vehicle strikes on the side of the victim vehicle
(ii) vehicle skids sideways into a fixed object
(3) Place - Commonly occurs at intersections; therefore frequent occurrence in
urban areas
(4) Injuries:
(i) Severe; because side of car has thin metal walls. No other components to
absorb impact
(ii) Occupant sitting on the struck side is injured most
(iii) Injuries caused by shattering of side-windows. (a) When driver [or other
vehicle occupant] impacts one of these tempered glass windows during a
crash, the glass breaks into fragmented cubes. (b) This may cause dicing
injuries [caused by “dice” shaped glass fragments] on the face, shoulders,
and arms. These are small linear, right angled, V-shaped or sometimes
irregular cuts, lacerations or abrasions [Fig 18.3]. (c) Location of victims -
A driver will have dicing injuries on the right side of the body and a
passenger will have them on the left. In left hand driven vehicles, the
 pattern would be opposite. May help locate position occupied by the
victims in the car, if they were ejected out.

C. MLI [Automobile Accidents]

1. Manner of death
Most automobile accidents are accidental; few are suicidal and still fewer are
homicidal. Pattern of injuries, and circumstances of death often indicate the
manner.
a. Accidental
(1) Driver may stop - and may try to assist victim
(2) Hit and run - Driver looses nerve"drives away in order to avoid arrest.
b. Suicidal
(1) Automobile accidents can rarely be suicidal. Sometimes these may be
masqueraded as an accident.
(2) Pointers:
(i) The typical scene is when an old depressed individual, suffering from
incurable disease and chronic pain is found to have died following an
accident.
(ii) He drives the car himself at very high speed, and strikes it against a tree.
(iii) No skid marks [indicating application of brakes] are found.
(iv) Shoe sole shows a deep impression of accelerator pedal, as if shoes were
hardly pressed on it.
(v) No alcohol and drugs are found in the body, ruling out drunken driving.
(3) Motive - for masquerading a suicide as an accident is to help relatives claim
full insurance amount; for suicide claim is not given.
c. Homicidal
Premeditated murder of a pedestrian with an automobile. Driver hopes to avoid
the blame altogether if he is able to successfully drive away, or at least get away
with a lesser charge u/s 304A.

2. Accident faked to conceal crime

(1) Person killed by other means"body placed in vehicle"vehicle pushed off a
cliff, or set on fire to make it look like an accident
(2) Investigation:
(i) Careful evaluation of all injuries
(ii) If vehicle caught fire during fall, burns should be antemortem and there
should be soot in fine branches of bronchi
(iii) If body shows signs of putrefaction, the time of which is inconsistent with
that of accident, it may indicate an already dead body being kept inside
vehicle.

3. Miscellaneous
(1) An already dead body lying on a street may be run over by a vehicle,
especially if the street was dark. All run over injuries would be PM in nature.
Some other obvious cause of death would be present eg a stab wound etc.
(2) Primary skin tuberculosis has been reported after vehicular accident. Also
seen after incised wounds [ch 12].

19. Asphyxia

I. INTRODUCTION

A. Definitions
(1) Asphyxia (Gk a, not; sphyzein, to throb) is exclusion of air from lungs.
Literal meaning is without throbbing or pulse, which occurs soon after
asphyxia. (For Gordon’s classification, please see ch 8).
(2) Hypoxia is deprivation of adequate oxygen supply at tissue level that results
from asphyxia.
(3) Anoxia is complete deprivation of adequate oxygen supply at tissue level.
Normal oxygen saturation of arterial blood is around 95 mm Hg (12.7 kPa).
Persons > 60 years of age may have a somewhat lower saturation – around 80
mm Hg. Mild hypoxia"60 mm Hg. Severe hypoxia"40 mm Hg. Fatal
hypoxia"20 mm Hg (1/5 of normal).

B. Classification of Asphyxial Deaths

1. According to mechanism of production
(1) Mechanical (a) When exclusion of air from lungs is by ligature around the
neck, and: (i) Constriction force of ligature is weight of the body " Hanging
(ii) Constriction force of ligature is anything other than the weight of the body
" Strangulation (b) When exclusion of air from lungs is by any means other
than ligature around the neck " Suffocation (i) External orifices of respiration
(mouth, nose) are blocked " Smothering (ii) Foreign object is pushed through
mouth up to posterior pharyngeal wall " Gagging (iii) Foreign object enters
trachea " Choking (iv) Mechanical obstruction by interference with
respiratory movements " Crucifixion, Hog tying, Pickwickian syndrome,
Traumatic asphyxia, Positional [syn,postural] asphyxia, wedging (c) When
exclusion of air from lungs is by mechanical entry of liquid into lungs "
 Drowning. For sub classification of each entity, pl refer to the appropriate
section. Only mechanical asphyxias are the subject matter of current chapter.
Other causes of asphyxial deaths are:
(2) Pathological -
(i) Acute poliomyelitis [paralysis of respiratory muscles]
(ii) Bronchitis
(iii) Edema of glottis [eg hypersensitivity reaction due to drugs (penicillin)]
(iv) Laryngeal spasm
(v) Tumors and abscess around neck.
(3) Toxic -
(i) Hb binding of oxygen lowered [CO]
(ii) Tissues unable to utilize oxygen [CN]
(iii) Respiratory center paralyzed [barbiturates, opium, strychnine]
(iv) Muscles of respiration paralyzed [Gelsemium]
(4) Environmental -
(i) High altitude
(ii) insufficient oxygen in environment [eg enclosed places, trapped inside a box,
trunk, refrigerator etc]
(iii) irrespirable gases in the environment [CO, CO2, Sewer gas, Chlorine etc]
(5) Traumatic -
(i) Bilateral pneumothorax
(ii) Pulmonary embolism [blood clot, amniotic fluid, fat, air etc]
(6) Iatrogenic - Anesthetic deaths
2. According to time of survival
(1) Rapid asphyxia [survival <15 min]1 – Hanging, throttling, choking
(2) Slow or protracted asphyxia [survival >30 min] – CO intoxication, opiates,
initial resuscitations followed by death.

II. CLASSICAL SIGNS OF ASPHYXIA

[A] Classical signs are asphyxia are (1) Cyanosis [Fig 19.2] (2) Congestion of
internal organs (3) Petechial hemorrhages (4) Edema (5) Engorgement of the
right side of the heart (6) -ed fluidity of the blood [see square boxes in Fig 19.1].
Memory Aid 1: Classical signs of asphyxia
CCTV FoR Everyone
Congestion
Cyanosis
Tardieu’s spots [petechial hgs]
Fluidity of blood
Rt side heart engorged
Edema
[B] Mechanism - Application of ligature, pressure of chest or restriction of
respiration by other means generally results in compromise of the movements of
the chest, which normally facilitates venous return.
This causes (1) obstruction of venous return (2) Acute -in venous pressure and
(3) back pressure in the venous system. Since lungs cannot expand fully it also
results in (4) collapse of pulmonary vasculature. Normal expansion of lungs is
also responsible for “sucking in” of blood into the lungs from the right heart.
Since this mechanism also comes to an almost halt, pooling occurs in the right
heart. These mechanisms together produce classic signs of asphyxia (Fig 19.1).
Hypoxia that results from lack of oxygenation is supposed to release
fibrinolysins which are supposed in turn to -the fluidity of blood. These “classic
signs” of asphyxia are no more considered pathognomonic of asphyxia. These
are very general signs seen in almost any autopsy. In fact they have been called
as the ‘obsolete diagnostic quintet’ [considering congestion and edema
together]. The explanations given above are however generally advanced for
these signs as seen in asphyxia.
[C] Petechial hemorrhages: (1) Size: (i) Small pin-point collections [0.1-2.0
mm] of blood lying in the skin, the sclera, conjunctivae, skin of eyelids,
forehead, upper cheeks, lining of the mouth and throat, muscles of the temples,
and under thoracic serous membranes such as the pleura or pericardium. (ii)
Bleeding spots 2.0 mm are called ecchymoses [for definitions of hemorrhage
and hematoma, which are still larger bleedings please see ch 17, under the
heading intracranial hgs]. (2) Petechiae due to asphyxia - known as Tardieu’s
spots [syn Tardieu’s ecchymoses; Tardieu Flecken]. First described by the
French pathologist Ambroise Tardieu in 1866. (3) Mech of asphyxial petechiae
- -in venous pressure above the noose"rupture of capillaries and small venules.
Typically they are pinpoint to pinhead size. Larger petechiae are infrequent and
when they occur, result from confluence. (4) Density of petechiae: (i) Serves as
an indicator for the duration of process. -duration "-petechiae (ii) Sometimes
they may be so diffuse [and minute] that the head and neck may present a dusky
appearance, which may be mistaken for congestion, especially when they are in
s/c tissues. (5) Petechiae in other deaths – seen also in (i) plethoric and obese
individuals dying of natural deaths (ii) Acute right ht failure with markedly -ed
venous pressure. (iii) Cardiopulmonary resuscitation. These petechiae are
usually larger than the asphyxial petechiae. [D] Engorgement of the right side
of the heart - has been found in many causes other than asphyxia. (1)
Mechanism - Has been claimed to be due to (i) greater distensibility of the right
heart, (ii) the influence of violent respiratory movements and muscular spasms
[not convincing because administration of curare still causes fullness of right
heart] (iii) an alleged strong contraction of the pulmonary arterioles opposing the
discharge of blood from the right ventricle, (iv) diminished suction power of the
left ventricle and (v) influence of rigor mortis on the left ventricle after death,
though no explanation has been offered as to why the right ventricle should
behave differently to the left in this respect.

III. HANGING

Hanging is that form of death which is caused (i) either by exclusion of air from
lungs or oxygenated blood from the brain (ii) by means of a ligature round the
neck, (iii) the constricting force being the weight of the body. When a person
survives hanging incident, it is called near hanging.
A. Classification
Hanging can be classified according to (1) position of knot (2) position of feet
(3) manner of hanging.
1. According to position of knot
(1) Typical hanging – if knot is at occiput
(2) Atypical hanging – if knot is at any other position.
2. According to position of feet
(1) Complete hanging – if feet do not touch ground
(2) Incomplete or partial hanging – if feet or other parts of the body touch
ground (for details please see “ML aspects of hanging”).
3. According to manner of hanging
(i) Suicidal (ii) Homicidal [eg lynching] (iii) accidental [eg autoerotic asphyxia]
(iv) Judicial.

B. Cause of Death
It is not necessary for ligature to completely encircle the neck in order to cause
death. It may be applied only to the anterior part or sides of neck. Happens
generally with “stiff” and “rigid” ligatures, eg steering wheels of cars, transverse
ladder rungs, during accidental hanging [More examples given below under the
heading “accidental hanging”].
1. Asphyxia
(1) Mechanism - Trachea is occluded"No air supply to lungs"No
oxygenation"Death.
(2) Earliest theory. This mechanism was suggested in 1870 by Tardieu [please
see above]. He thought that hanging was not associated with cerebral ischemia
because intimal tears of the carotid and pale brain were not commonly seen at
autopsy.
2. Occlusion of neck blood vessels
(1) Mechanism - Neck b.v. are occluded"Blood supply to the brain is
stopped"cerebral ischemia [or venous congestion] occurs"Death.
(i) Cerebral ischemia"occurs when both arteries and veins are occluded
(ii) Venous congestion"occurs when only veins are occluded, but arteries are
patent. Blood keeps flowing to the brain, but cannot return
(2) Evidence in favor of occlusion of neck b.v. – (a) In 1880, Hoffman tried to
infuse the neck vessels of hanging victims, including those of children [while
 they were still hanging], but could not do so. This led him to propose that
occlusion of the neck vessels occurs during the hanging process [in addition
to asphyxia] (b) In 1895, Reineboth performed tracheostomy in rabbits and
hanged them in two groups. In the first group noose was placed above the
tracheostomy opening and in the second group, below. If asphyxia was the
real mechanism of death, rabbits in the first group would not die. But they still
died although slower [15-20 minutes vs. 5-6 min]. (c) In 1897, Brouardel of
France observed the retinas of hanged animals by ophthalmoscopy, and
discovered they were devoid of blood. Indicated cerebral ischemia. (d) A
number of individuals have hanged themselves with the noose above the
larynx and a permanent tracheostomy opening below.
3. Reflex vagal inhibition of the heart
Mechanism - Pressure over carotid arteries"Carotid body stimulated"Vagal
stimulation"Cardiac inhibition"Death.
4. Fracture dislocation of cervical vertebra
Occurs mainly in hangings associated with a long drop (as in judicial hangings).
5. Current thought
Consensus of opinion is that
(1) asphyxia is the main cause of death in complete hanging, while
(2) occlusion of neck b.v. is the main cause in incomplete hanging.
(3) Very few authors believe in reflex vagal inhibition theory.
(4) Earlier belief that commonest cause is combined asphyxia and venous
congestion is no more considered correct.

C. Fatal Period
(1) Suicidal hanging – If death occurs due to asphyxia, fatal period is 5-10 min;
if death is due to occlusion of neck b.v. death takes longer - 12-20 mins.
(2) Judicial hanging [i.e. with a long drop]- instantaneous
(3) Delayed deaths – Few days. If the victim is saved initially from hanging, he
may succumb hours, days or weeks later to (a) aspiration pneumonia (b)
edematous or hemorrhagic swelling – of pharyngeal tissues or aryepiglottic
folds (c) emphysema – massive s/c and mediastinal emphysema from tracheal
and laryngeal lacerations (d) infections (e) edema of larynx and lungs (f) brain
pathology [abscess, hypoxic encephalopathy, infarction and softening].
Mechanism – In hypoxic injury, higher cortical centers suffer first [being
 most sensitive to O2]"unconsciousness"hypostatic pneumonia"further
anoxia"injury to basal ganglia, and finally of respiratory and other vital
centers"death.

D. PM Appearances

1. External
a. Description of ligature
Ligature material if present around the neck should always be described. Note
especially
(1) Nature of ligature – eg bed sheet, belt, dhotie, leather strap, metallic chain,
nada, rope, sacred thread, saree, scarf, turban and wires (plain metal wires,
electrical wires etc). When a narrow wire is used, it may “eat into” the flesh of
the neck [“cheese-cutter” method]. A cheese cutter is a kitchen utensil used to
cut a large solid block of cheese into slices, using a thin metal wire. In jails
and prisons, convicts typically tear sheets into strips, or they may use
whatever is handy eg T-shirts, undershorts, trousers, or even socks.
(2) Its color and composition [eg silk, cotton, nylon etc]. May help co-relation
if similar cloth is found in possession of someone.
(3) Pattern and texture of ligature – Does the ligature show any particular
pattern [eg weaving patterns in ropes]? Pattern and texture of ligature is often
produced upon the skin in the form of a patterned abrasion.
(4) Intact – Whether ligature is intact or has been cut off.
(5) Cut ends – if cut, whether appears torn or cut sharply by scissors.
(6) Extraneous material on ligature – blood, fragments of epidermis, hair,
fibres, saliva, vomit, any other suspicious substance.
(7) Length – Is the length of ligature sufficient to hang from the point from
where victim’s body was found hanging.
(8) Width – (a) does it correspond with the ligature mark (b) Narrow ligature
tends to produce deeper groove, because wt of body is distributed over
narrower area. Broad ligatures produce narrower grooves.
(9) Multiplicity – (a) Does the ligature show multiple turns round the neck(b) If
there are two turns, it may produce a double mark round the neck – one
circular, the other oblique(c) Skin may get caught between multiple turns, and
show multiple rings of congestion.
(10) Strength – is the ligature strong enough to support the weight and jerk of
the body.
(11) Circumference – Circumference of the ligature. Compared with the
circumference of the neck, it can be decided if the neck was horizontal or
oblique.
(12) Tightness – Note how tight the ligature is wrapped. (a) Tighter ligatures
produce deeper grooves all round the neck. Impression from knot may also be
found (b) Slip (running) knot does not produce uniform pressure all round; it
is maximum just opposite the knot and then tapers off gradually at the sides.
(c) If the point of suspension is in the occipital region, front of neck would
show the deepest groove (with neck tilted forwards); if below the chin, the
deepest groove would be at the back (with neck tilted backwards). (d) Knot
and small adjacent lengths of ligature may be stretched away from the body,
and may not even be in contact with the skin. Ligature mark will be absent in
this area and impression from knot not found.
(13) Padding – a piece of towel may sometimes be found between the skin and
ligature [placed by victim in order to reduce pain]. Found usually in accidental
hanging, especially sexual asphyxias [please see below].
(14) Spontaneous breakage - Sometimes the ligature may break spontaneously
and body may be found lying on the ground. In such cases, it becomes
imperative to determine if the death was due to hanging or strangulation. It
can be done by (a) examining the other end of ligature which must be found
tied to the suspension point (eg fan, tree etc)(b) Broken ends of ligature must
coincide.
(15) Knot – (a) Record the location and type of knot. (b) Location – whether at
occiput, below the chin, below either ear (subaural) or any other specific
location. In all cases, it is always above the rest of the ligature. This produces
an inverted ‘V’ shaped ligature mark, the apex of ‘V’ corresponding with the
site of the knot. (c) Type - It may be fixed or running (Fig 19.4). Granny
[syn, lubber’s] and reef [syn, f lat, square] knots are rather common. But
some other special types of knots are exceedingly rare and may sometimes
give away the profession of the person. Even simple knots can reveal
predilection or hobby of the person, eg a sailor or a scout may use a reef knot
rather than a granny knot. (d) Removal of ligature – Knot should never be
opened. (i) Photography – First step is to take photographs [at close range]
 before removal of ligature (ii) The ligature should now be cut opposite the
knot, and the two cut ends secured with a string (Fig 19.5) [for more on
Forensic knot analysis, please see chapter 30 – Forensic Science
Laboratory].

b. Ligature mark
Ligature mark is a type of pressure abrasion due to continued pressure by
ligature on the neck.
Salient features:
(1) It is seen both in hanging and strangulation [Table 3]. Strangulation mark is
described later.
(2) Appearance - It is usually seen as a furrow or groove in the tissue which is
soft and pale initially, but as the skin dries up, becomes hard (parchment like)
and dark brown. It runs from midpoint of the neck upwards, outwards and
backwards [from either side of the neck] to reach behind the neck where it is
deficient [Fig 19.6]

(3) It is the most important and specific sign of death from hanging.
(4) Following things must be noted (i) Its position - Usually it is at the front of
neck, but rarely at the back of neck also. If the head has been hanging on one
side, it may be one-sided [Fig 19.7].
(ii) If in front its position with respect to thyroid cartilage – Ligature mark is
situated (a) above the thyroid cartilage in 80% cases (b) at the level of thyroid in
15% cases and (c) below the level of thyroid in only 5% cases. Likelihood of
ligature being below the level of thyroid is more in partial suspension. (iii) its
direction, whether continuous or interrupted (eg if a piece of cloth such as shirt
collar is interposed between it and the skin), depth and width, areas of neck
involved and its relation to local landmarks (iv) Compare with (a) weight of
body – Heavier the body, deeper the ligature mark (b) Degree of suspension –
Complete suspension produces deeper mark; partial suspension, much shallower
(c) Time of suspension – Longer the suspension, deeper the groove. With long
suspension times, even lesser weight of body and wider ligatures can produce
deeper grooves. Sometimes a thin line of congestion or hemorrhage is seen along
the edges of the groove. If present, it is strongly suggestive of antemortem
hanging (d) ligature material – if ligature mark is showing a pattern (patterned
abrasion), does it match with that of the ligature? Ligature pattern is better
appreciated by using a magnifying lens and examining under oblique lighting.
(v) Effect of slippage of ligature - (a) As the victim ties ligature round his neck,
it may produce a very faint and superficial impression (b) when victim suspends
himself, the ligature moves upwards, and produces a second deeper impression
above the initial impression. (c) If the ligature material is rough (eg rope), the
two ligature marks may be joined by fine abrasions representing the movement
of ligature upwards (vi) Fibres – Although the ligature mark may look clean,
there always are small fibres sticking to the ligature mark. Strip them off with a
sticking tape [Fig 19.6], secure it on a glass slide and see under microscope.
Fibres must match with that of the ligature found at the scene. Case study - In
one case of homicidal strangulation, with missing ligature, the author could tell
the color of the ligature (red) by lifting the fibres from the ligature mark by a
cellotape and observing them under microscope. Nothing was visible on the
ligature mark with the naked eye, and if cellotape method had not been used, the
case may have remained unsolved. (vii) Reexamination after some hours – If
body is fresh, ligature mark may not be very evident. After drying the mark
becomes more prominent (viii) Pattern of ligature mark – If the ligature mark
is in the form of a patterned abrasion, photograph and describe the pattern. If
pattern is not clear in ordinary light, examine in oblique light or under UV light.
Compare with the pattern of the ligature recovered, and see if they match. (ix)
Absent ligature mark – If the ligature mark is absent, it does not exclude
hanging. Causes of absent [or indistinct] ligature mark - (a) Soft ligature material
eg scarf, towel etc (b) Beard, or a piece of clothing getting caught between
ligature and skin (c) Decomposition – may obliterate ligature mark (d) when
pressure is applied only on the front of the neck, eg by arm of a chair or rung of
a bladder (x) Ligature mark present in the absence of hanging – (a) If soon
after death, ligature is passed around neck and body is dragged along ground
with its help, a ligature mark very similar to that of hanging may be produced (b)
in infants and obese persons, skin folds on neck may resemble a ligature mark,
especially if s/c fat has been coagulated by refrigeration (c) Jewellery or clothing
around neck [eg shirt collar]"Neck tissues swell due to decomposition"a false
mark resembling that of hanging [or strangulation] may be produced. Please also
see pseudostrangulation below. (xi) Histological examination – of the ligature
mark is a must. Presence of vital reaction indicates antemortem hanging. (xii)
Suspension peak – The junction of the noose and the vertical part of the rope
[point A in Fig 19.8] is pulled upwards and away from the skin due to weight of
the body. Thus no ligature mark is left at the back. A triangle ABC is formed the
apex of which (A) is called the suspension peak or point. This suspension peak is
the distinguishing feature of hanging from strangulation, as weight of the body
does not act on the ligature in strangulation. Such a suspension peak is typically
absent when the knot is in front because of projecting chin, on which knot often
leaves its mark.

c. Other Signs
(1) PM Staining – on legs, feet, soles, hands, forearms [glove-stocking like
distribution], undersurface of breasts, penis [most dependent parts of the
body]. Blood may extravasate in these areas in the form of petechial hgs.
Upper part pale. If body is unsuspended before fixation, and made to lie down
in a supine position, it disappears from these areas and reappears in new
dependent parts.
(2) Head – inclined to the side opposite to that of knot
(3) Neck – elongated and stretched
(4) Face:
(i) Usually pale [occlusion of carotids and vertebral arteries]
(ii) rarely congested [occlusion of jugular veins and vertebral venous plexus but
not of vertebral arteries]
(iii) may be swollen [same reason as above causes leakage of edema fluid into
the tissues]. If body is cut down, swelling may disappear
(iv) Eyes – frequently protruded and firmer than usual due to congestion
(v) Conjunctiva - congested
(vi) Le facies sympathiques – If ligature knot presses on cervical sympathetic,
the eye on the same side is open and its pupil dilated; the other eye is closed
and its pupil constricted. It was once believed to be a hallmark of
antemortem hanging. Believed to result as a result of unequal tension on the
neck structures. No more considered a useful sign.
(5) Petechial hgs:
(i) In skin and conjunctivae [Overall incidence >50% of cases].
(ii) In typical hanging – No petechiae; face pale [because of complete occlusion
of blood to and from the brain]
(iii) When knot is under chin – Lower jaw protects neck from deep pressure by
the noose"Arterial flow continues; venous flow stops"Petechiae abundant;
congestion prominent
(iv) When knot is at one side, i.e. in front of one ear"subconjunctival hgs are one
sided
(6) Nostrils – bloody froth [due to rupture of engorged bv]
(7) Tongue:
(i) protruding; caught between the teeth. Protruded part is dark brown, even
black due to drying
(ii) swollen and blue, especially at the base
(8) Lips and mucus membranes of the mouth - blue
(9) Saliva:
(i) dribbling from the mouth; may be blood stained [rupture of engorged bv]
(ii) surest sign of antemortem hanging
(iii) Cause - (a) Stimulation of pterygopalatine ganglion (b) direct stimulation of
salivary glands by the ligature
(10) Hands – Clenched, especially in violent hangings
(11) Penis –
(i) engorged with blood [due to hypostasis]
(ii) may be semierect
(iii) Semen may be found at the tip
(12) Relaxation of sphincters – causes escape of urine and feces.
2. Internal
(1) Neck – Should be examined after removal of brain and viscera from the chest
and abdomen. This produces a bloodless field which prevents any artifactual
hemorrhages.
(2) Ligature mark:
(i) Tissues underneath the mark are dry, white and glistening.
(ii) There may be scattered hemorrhages caused by direct trauma.
(iii) Adjacent muscles may show occasional ecchymoses.
(3) Strap muscles – may be torn and may show hemorrhages.
(4) Carotid arteries:
(i) intima shows several horizontal splits with extravasation of blood in their
wall due to crushing and stretching [Amussat’s sign], much like ladder
tears in aorta seen in vehicular accidents [ch 18]. First described in 1843 by
Amussat.
(ii) More common in long drops as in judicial hanging
(iii) Rarely tears may be longitudinal.
(iv) May be combined with tears of media or adventitia.
(v) Sometimes dissection of the medial layer occurs with subsequent narrowing
of its lumen.
(vi) In patients who survive, such tears may lead to formation of thrombi and
subsequent cerebral ischemia and infarction.
(vii) Other conditions in which similar tears may be found are (a) blunt neck
trauma, (b) extreme overstretching (c) whiplash-injuries.
(5) Vertebral arteries – may show similar damage as in carotids with an even
higher frequency.
(6) Epiglottis and larynx – may show petechial hemorrhages
(7) Trachea –
(i) Congested
(ii) May be injured rarely
(iii) May show petechial hemorrhages
(8) Lungs:
(i) Congested, edematous and exude bloody serum on cut section.
(ii) May be pale sometimes. It has been asserted that lungs are congested if
constriction of lungs occurred at end of expiration and pale if it occurred at
end of inspiration. However there is no evidence for this assertion.
Moreover constriction of lung does not occur in an instant; hanging is a
process which continues for several minutes.
(iii) Subpleural ecchymoses
(9) Abdominal organs – congested
(10) Brain:
(i) may be normal, congested or pale.
(ii) May show subarachnoid hemorrhages
(11) Middle ears - hemorrhage
(12) Hyoid:
(i) May show fractures. They are anteroposterior compression fractures.
(ii) incidence – varies from 0-60%; average 15-20%.
(iii) Age – rare <30 y, because apices of greater cornu are cartilaginous before 30
y [ch 3].
(iv) Site – junction of inner 2/3rd and outer 1/3rd. Fractures of hyoid are also
found in ch alcoholics [battered alcoholic syndrome - ch 40]. Should be
kept in mind when doing an autopsy on an alcoholic.
(v) Demonstration of fractures - please see below under the heading “hyoid
bone fractures”.
(13) Thyroid:
(i) Superior horns may show fracture from pressure on thyrohyoid ligament.
More common >40 y.
(14) Vertebral column:
(i) Hemorrhages - beneath the area of the anterior longitudinal ligament of the
intervertebral disks in the lower thoracic and lumbar vertebrae [Simon sign,
Simon bleedings, Simon hemorrhages].
(ii) Appearance - look like dark red to violet horizontal lines between vertebral
bodies [Fig 19.11]; they are limited only to the area of the anterior ligament
of intervertebral disks and do not penetrate into the vertebral bodies.
(iii) Incidence - more frequent in (a) younger individuals (b) in complete
hanging and (c) in individuals with minimal degenerative changes in the
lumbosacral part of the spinal column.
(iv) Cause - overstretching of the spine because of free suspension of the body.
Causes stretching and tearing of small vessels within the disks. First
described in 1968 by the German forensic pathologist Axel Simon [born
1931].
(v) other cases in which similar hemorrhages are seen – Vehicular accidents,
falls from heights, drowning, hypothermia. Extremely rarely in natural
deaths.
E. Medicolegal Aspects of Hanging

1. Pressures required to obliterate neck structures

These are (i) Jugular veins"2 kg (ii) Carotid arteries"5 kg (iii) Trachea"15 kg
(iv) Vertebral arteries"30 kg (v) Vertebral venous plexus"undetermined, but
between 5 and 30 kg. [A] Pale face - If force applied to neck is > 30kg as
happens in complete hanging (when entire wt of body acts on neck), blood can
neither go towards head nor return from there. The result is a pale face. [B]
Congested face - If force applied to neck is between 2 kg and 30 kg (as happens
in strangulation), blood is able to go to face, but can not return, resulting in
intense congestion of face and bleeding from mouth, nostrils and ear (due to
rupture of small capillaries). The same is true of partial hanging, when only part
of the wt of body acts on the neck.

2. Partial hanging
Partial hanging is that specialized form of hanging in which some part of the
body is supported either by ground, or some object other than the neck [Fig
19.12].
Salient features:
(1) Point of suspension – in partial hanging is lower down eg (i) bedpost (ii)
chair (iii) door knob (iv) leg of table (v) railing of staircase
(2) Position of deceased – Deceased may be in (i) sitting (ii) kneeling or even
(iii) completely lying down position
(3) Distribution of the weight of the body – Weight of the body is distributed
on the ligature as well as on all points of body touching the ground. Thus
constricting force is less and congestive changes more marked.
3. Manner of hanging
Suicidal hanging is commonest. Accidental hanging is less common and
homicidal hanging still less common.
a. Accidental
(1) Children:
(i) climbing railings, trees, walls etc – falling from a high branch etc"clothing or
garment [chunni, muffler etc] gets entangled in a branch, nail or other
projecting object from wall"drawn tight round neck
(ii) during play - especially when imitating judicial hanging
(2) Infants – in cots with restraining vertical bars around it"try to crawl out,
move away or wriggle out of cot"fall out between the vertical bars"neck gets
caught between two vertical bars
(3) Sexual hanging [please see below]
(4) Stuntmen – exhibiting hanging as a stunt
(5) Suspension of chin against
(i) edge of a sofa or arm of chair
(ii) Staircase – victim slips"neck gets caught in one of the vertical bars on the
sides of staircase
(iii) Steering wheel – May happen during vehicular accidents [ch 18]
(iv) Tailboard of a lorry or cart.
(6) Workmen, masonry men etc – falling from scaffolding may get entangled
in ropes. Rarely while falling from ladder, neck may entangle against one of
its transverse rungs.

i. Sexual hanging
Sexual hanging [syn, Asphyxiaphilia, Asphyxiophilia, Autoerotic asphyxia,
Hypoxyphilia, Kotzwarrism, Masochistic hanging, Sexual asphyxia] is
accidental death caused by a self-induced decrease in oxygenation of blood
(hypoxia) produced most commonly by partial hanging.
Salient features:
(1) Reasons - Oxygen deprivation of the brain is thought to lead to an
enhancement of sexual orgasm for following reasons (i) .ed oxygenation and -
ed CO2 retention produces feelings of giddiness, lightheadedness, and
exhilaration, which heighten sexual response. (ii) Induction of erotic
hallucinations. (iii) partial asphyxia brings about -ed sympathetic arousal,
which in turn heightens orgasmic pleasure.
(2) Methods: (i) Partial hanging [a variant of suspension bondage] – Most
common method (a) Neck - is protected by a padding [usually a towel]
between the neck and ligature (b) Ligature - is passed round the neck in the
form of a running noose. Its free end is tied to a limb [wrist or ankles] or to a
fixed object. (c) Weight of the body is used to control pressure (d) Associated
paraphilias - (I) Masochism - [1] Subject ties up wrists and ankles together
with a chain, padlock, rope, string or wire. Sometimes noose is found around
waist and genitalia also. [2] May have blindfolded himself [3] Evidence of
self-mutilation on previous occasions - burns, cuts, puncture wounds etc on
the body [4] Clamps or pincers attached to genitalia or breasts (II)
Transvestism - [1] Found dressed up as a female, with bra, panties and sari (ch
25)]. [2] Bra may have been padded up to simulate full breasts [3] Sometimes
even sanitary pads, wigs and make up may be worn. (e) Sometimes found
naked or partially naked, with penis exposed through pants"Indicates penis
was being manipulated [Fig 19.14] (f) Erotic or pornographic literature, or
female nude photographs may be on the floor or elsewhere within view (g)
Evidence of recent emission of semen (h) There may be mirror in front to
watch the activities (i) A video camera may be there to make a photographic
 record (j) Mechanism of accidental death - If the noose touches carotid sinus,
consciousness is suddenly lost (Fig 8.5) and the victim is incompletely
suspended with legs on the ground. He may be found suspended close to an
object such as a chair or stool, that would have allowed him to sit upon and
release the constriction, after achievement of orgasm. (k) Evidence of previous
episodes on the neck - eg old scars (ii) Other methods involving asphyxia - (a)
chest compression, (b) inhalation of chemicals such as amyl acetate, carbon
tetrachloride, cocaine, chloroform,, ether, ethylene chloride, glue, ketamine,
nitrous oxide, paint thinners, propane, trichloroethylene or a volatile nitrite
[amyl nitrite]. A pad soaked with a sniffing chemical may be found nearby. (c)
plastic bags, masks or impervious bags over the face.,, These are secured
around the neck by an elastic band or a ligature to keep them in place. Interior
of bag may be smeared with any of the above chemicals. (d) submerging
under water (aqua eroticum),, (e) combination of several of these methods. (iii)
Non asphyxial methods - Electrical stimulation. Electrodes are applied to the
genitals or on abdominal wall usually with a low voltage supply from a battery
or transformer
(3) Why is it an accidental hanging - Death is not intended by the victim, but it
usually results accidentally when the “safety” mechanisms employed by the
deceased fail or when there is an overdose of chemical inhalation.
(4) Incidence – Western countries: 1-2/million population/yr. Much less in India.
(5) Sex - male: female ratio > 50:1.
(6) Scene of death: (i) Follow all protocols of a scene of death investigation [ch
1]. Following specific points are important (ii) Evidence of abnormal sexual
behavior, eg masochism, transvestism (iii) Evidence of previous occurrences
of similar events - (a) grooves in the rafter or door from ropes (b) verbal
communications with friends regarding nature of activities (c) evidence of
surfing net with sites related to sexual hanging (d) diaries (iv) Evidence to
protect neck - padding underneath ligature (v) No motive or other evidence of
suicide.
(7) Similar activities - Choking game [Please see below under accidental
strangulation].
(8) MLI: Differentiation from suicide – In insurance policies there is a clause
stating that no money would be paid in cases of suicide. Differentiation is not
always easy, especially when a strong reason for suicide appears to co-exist. In
 some cases, family members are so embarrassed that they are reluctant or
unwilling to provide enough data surrounding the circumstances in which the
patient was found, and the cause of death may be mislabeled as suicide.

b. Homicidal
Incidence - Extremely rare, because it is difficult for a single person to
overpower a man.
Lynching
Lynching is an extrajudicial execution carried out by a mob by hanging without
a fair trial.
Salient features:
(1) It is a form of homicidal hanging, since hanging was done without a fair
trial. A popular belief is that it was done when a black man raped a white
woman. However only about 1/4th of lynch victims were accused of rape or
attempted rape. Most blacks were lynched for outspokenness or other
presumed offenses against whites, or in the aftermath of race riots. Lynchings
took place most frequently in the Southern US from 1890 to the 1920s, with a
peak in 1892.
(2) One of the common methods was to hang the suspect from a tree by a rope
(3) PM findings would be same as those in homicidal hanging; signs of struggle
may be found.
c. Suicidal
Hanging is a common method of committing suicide.

4. Postmortem suspension
Postmortem suspension is when a person is first killed and then suspended to
simulate suicide [simulated hanging]. Some books use the word “postmortem
hanging” for this phenomenon. However since hanging signifies “death by
asphyxia”, this term should best be avoided.
Salient features:
(1) Ligature applied to the neck during supravital period will produce a ligature
mark
(2) Differentiating features of postmortem suspension from true suicidal
hanging [in contrast Table 1 gives differences w.r.t. antemortem hanging
which can be both suicidal and homicidal]. (i) Signs of dragging - to the place
of suspension (ii) When a dead body is suspended, the rope is usually tied first
around the neck and then around a beam, rafter or top of tree etc. then the rope
is pulled up. Both the support [beam etc] as well as rope would show evidence
of rope having dragged from below upwards. Fibres of rope would show
abrasions consistent with rope having pulled up. In true suicidal hanging, such
 abrasions would not be there. (iii) Beam paint - on rope (iv) Beam pain -
rubbed off the beam where rope was pulled up (v) Hands of victim - show
rope fibres in suicidal hanging, but not in pm suspension. May not be visible
with naked eye, but can be seen under the microscope after tape lifting [apply
adhesive tape to palm"lift it off"stick to a microscopic slide"observe under
microscope] (vi) Internal signs - not consistent with those of hanging, but with
the true cause of death [poisoning etc].

5. Judicial hanging
Judicial hanging is a method of execution in which a noose is tied round the
neck of condemned criminal, and he is made to drop between 1-5 m depending
on his weight.
Salient features:
(1) It is an official method of execution in India and several other countries
(2) Procedure – (a) The face of the victim is covered with a black mask (b)
hands tied behind back(c) Made to stand on a platform above trapdoors when
opens downwards when a lever is pushed. (d) On pushing the lever, the victim
falls equal to the length of the rope which lies loose (e) As the victim comes to
a sudden stop, his head is thrown in a direction opposite to where the knot was
placed. If it is placed submentally (the ideal position), the head would be
hyperextended, causing traumatic spondylolisthesis of axis [the so-called
“hangman’s fracture“; bilateral fracture of pars interarticularis of C2].
Depending on its severity, 3 types have been described (Fig 19.15). In
subaural position of the knot, typical hangman’s fractures are rare; fractures of
the base of skull are more common. Other fractures that have been described
in both placements of knots are bilateral fractures of pedicles or laminae of the
C1, C3 and C4, with associated dislocations, and fracture of odontoid process
of C2. Their frequency is lesser.
(3) Factors essential to cause quick death – In order to reduce the suffering of
the victim, it is desired that there be a quick death, or at least a rapid onset of
loss of consciousness. To achieve this, two most important factors are knot
positioning and the length of drop. (a) Position of knot – Submental is most
effective, but left subaural was used officially because it does not slip. (b)
Length of drop - Ideally it is between 1-5 m depending upon the weight of
the victim. If drop is too short (<1 m), asphyxiation would result; if it is too
long (>5 m), decapitation. Hence, in 1875, tables were proposed that regulated
the drop length in proportion to the individual’s weight. This list of drops was
then modified in 1886 by the Capital Sentences Committee concluding that for
an ‘efficient’ hanging the victim’s neck should be subjected to a force of 126
pounds.
(4) Cause of death - (a) Bilateral fracture of C2 with anterior subluxation (C2-
3 dislocation), resulting in fatal injury to the spinal cord [most commonly with
submental knot]. (b) Dislocation of atlanto-occipital joint with injury to
spinal cord [most commonly with left subaural knot] (c) Odontoid process of
C2 fracturing and causing pulping of spinal cord (d) Complete transection
of the cervical spine causing the neck to be lengthened considerably. In
proper judicial hanging there should be instantaneous and irreversible loss of
consciousness and irreversible apnea. Heart keeps beating for 15 minutes due
to autorhythmicity. Spasmodic involuntary muscular jerking is seen for the
 same period.
(5) PM findings - (a) Usual findings seen in hanging. In addition (b) Fractures
of base of skull and CV with trauma to spinal cord as mentioned earlier (c)
Intima of carotid shows transverse lacerations. Sometimes the arteries may
show complete tear (d) Injury to pharynx.

IV. STRANGULATION

Strangulation is that form of death which is caused (i) either by exclusion of air
from lungs, or oxygenated blood from the brain (ii) by means of a ligature round
the neck, (iii) the constricting force being anything other than the weight of the
body.

A. Classification
Strangulation is classified according to the type of ligature used (Table 2).
B. Cause of Death
(1) Same as that in hanging.
(2) However occlusion of carotid arteries is more common.
(3) In throttling, groping fingers may suddenly impinge upon carotid sinus
causing sudden death by vasovagal inhibition. Thus there may be a period of
partial asphyxia terminated suddenly by the onset of cardiac arrest.

C. PM Appearances [in classical ligature strangulation]

1. External
a. Ligature Mark
i. Examination
Must be done in (1) regular light (2) oblique light (3) UV light [to visualize faint
bruises made by soft materials.
ii. Features
(1) Regular features - please see Table 3
(2) Peculiar [additional] features –
(i) Effects of lateral displacement of blood from the squeezed area - (a)
 Reddening and congestion – especially above and below the ligature mark
(b) Preservation of mark during putrefaction
(ii) Ligature mark as a patterned abrasion – If a ligature with a pattern [eg chain
with links, plaited electric wire, spiral rope or woven belt] is used, a
patterned abrasion may form. It details should be noted and photographed,
as it is a vital clue in tracing the ligature
(iii) Abrasions around ligature mark – (a) may be vertical, linear, irregular or
crescentic. (b) May not be readily visible if the area is wet [due to
perspiration, application of wet cloth as ligature]. Body should be allowed
to dry and then examined again (c) Could be due to assailant’s fingernails
[more common in throttling] or victim’s own fingernails trying to remove
ligature. (d) Victims’ fingernails must be examined. May be fractured,
broken or may contain blood or tissue tags underneath. (e) Must be clipped
and sent for analysis in paper bags. DNA from blood or tissue tags may
reveal own DNA, or sometimes DNA of assailant, if he tugged at his skin.
(iv) Bruising of neck muscles – more common if (a) rough ligature is used (b)
there was movement of ligature over the skin, as in struggle
(v) Oblique ligature mark – Traditionally it is horizontal [Table 3], but may be
oblique if the victim was dragged by ligature, after he was strangled in a
recumbent position
(vi) Ligature mark interrupted at front – due to (a) victim’s fingers attempting to
pull the ligature away (b) presence of clothing
(vii) Ligature mark interrupted at back – due to (a) presence of clothing or long
hair [esp in females] between the ligature and skin (b) If assailant presses
from the front, or pulls from the back, using the ligature stretched between
two hands
(viii) If knot has been applied – Wider area of bruising at the site of knot
(ix) If hard ligature [eg cord, rope, wire] is used – Abrasions may be produced,
which become hard, yellow-brown and parchment like on drying. There
may be exudation of tissue fluid "forms a stiff film on drying
(x) If soft and yielding ligature [eg scarf or towel] is used – (a) only flushing of
skin or at most a slight depression may be seen (b) The marks may fade
soon after death. Thus in these cases, body should be examined soon after
death [importance of examination of body at the scene of crime itself] (c) If
mark is completely obscure – (1) Examine under UV light (2) dissect skin
 and muscles"presence of hemorrhages would reveal the position of ligature
mark
(xi) If a narrow ligature [eg cord, thin rope or wire] is used – The ligature is
forced deeply into the skin. After the ligature is removed"skin recoils due to
elasticity"Ligature mark may become narrower than the width of ligature
[cf stretchable ligature]
(xii) If a stretchable ligature [eg nylon, silk, terylene] is used – Ligature may be
broad, but by stretching becomes longer and thinner"ligature mark much
narrower than the width of ligature [cf narrow ligature]
(xiii) If a folded cloth [eg a rolled sari or dupatta] is used – There may be a great
difference between the appearance of ligature mark and the ligature
[because it is examined unfolded]
(xiv) If a complex ligature composed of several pieces knotted together is used –
Marks of knots may be produced at several points, which may be confusing
to an untrained mind
(xv) If two sticks are used [bansdola] – only those areas of neck will show
marks, where the sticks came into contact with skin
(xvi) If foot is used – (a) wide mark corresponding to width of foot (b) wide area
of bruising (c) fracture of laryngeal cartilages more common
(xvii) If ligature has been tightened pulling on the cross ends – (a) Mark more
prominent at site of cross-over (b) marks produced by two ends will be at
different levels (c) Cross-over mark may be at front, back or side depending
on relative positions of victim and assailant
(xviii) Multiple turns – (a) produce a complex mark, in which sometimes it may
be possible to count the number of turns (b) if folds of skin are caught
between multiple turns – pressure on capillaries may rupture them leading
to petechial hemorrhages. These confirm the antemortem nature of
strangulation. Vesicles containing fluid may also form
(xix) Effect of strong pressure – (a) Laceration of skin (b) fracture of cartilages
(xx) Effect of tissue edema – Ligature pressing on neck tissues"edema develops
around ligature, especially above"Ligature gets tightened further"more
edema"vicious cycle may continue even after death due to passive
transudation of tissue fluid"Ligature mark appears much deeper"Impression
to the untrained eye is that the ligature was applied very tightly [possibly
reflecting anger and rage of assailant], while in fact the ligature may not
have been applied so tightly.
b. Pseudostrangulation
Pseudostrangulation refers to a situation, where a ligature mark resembling a
strangulation mark [pseudoligature mark] is seen on the neck, but it is produced
by mechanisms other than antemortem pressure by a ligature.
Salient features:
(1) Causes: (i) Blanching of pm staining - by a tight collar or necktie etc [ch 9]
(ii) Decomposing bodies – with buttoned shirt at the neck, tight collars, or
other clothing round the neck. As body decomposes, tissue swells around the
tight fitting garment, producing a mark simulating strangulation mark. (iii)
Mummified bodies – May show similar marks (iv) Infants and children (a) if
they have short neck – Produced from skin folds due to bending of head (b)
hypothermia - [ch 22] (v) Short necked adult individuals – Same mechanism.
Much less commonly seen than in children.

c. Signs of Asphyxia
(1) Classical signs of asphyxia are seen [please see at the beginning of chapter].
The signs are marked if pressure applied >30 kg [please see below].
Additional features.
(2) Head, face and neck – congestion and petechial hemorrhages.

d. Other signs
(1) Abrasions and contusions on face – if there was struggle
(2) Effects of Pressure – [For principles, please see above under “Medicolegal
aspects of hanging"Pressures required to obliterate neck structures”]
(i) If pressure applied is <2 kg - no major structure is blocked. Death is due to
vasovagal shock. Most external and internal signs will be absent
(ii) If pressure applied is between 2-30 kg – Most common situation (a) Marked
congestion of face. (b) Bleeding from nose [epistaxis], mouth
[stomatorrhagia] and ears [otorrhagia] due to engorged capillaries [Fig
19.16]. (c) Examination of tympanic membrane [TM] with an otoscope – If
there is frank bleeding from ears, TM will be found ruptured. Source of
bleeding is middle ear. If no bleeding"TM would still be found congested.
(iii) If pressure applied >30 kg – Asphyxial signs are marked.
2. Internal
(1) Neck - Hemorrhages
(i) beneath the ligature mark under the skin
(ii) in the strap muscles
(iii) sides of tissues around larynx and trachea
(iv) in laryngeal structures
(2) If assailant kneeled on the chest – fracture of ribs
(3) If assailant kneeled on the abdomen – laceration of abdominal organs, eg
liver, spleen, rupture of intestines, gall bladder
(4) Lungs - show emphysematous bullae.

D. Medicolegal Questions [in case of ligature strangulation]

1. Whether death was caused by ligature strangulation?

(1) Characteristic PM signs of ligature strangulation would be present
(2) If ligature mark is invisible"use UV light
(3) In presence of putrefaction - Most signs of strangulation cannot be relied
upon. fractures of larynx and hyoid may be the only reliable characteristic
signs
(4) Mere presence of a ligature around the neck does not indicate strangulation,
as it may have been placed there after death to mislead the police.
2. If an infant was found strangulated due to umbilical cord, was it
homicidal or accidental?
Please see Table 4.

3. Whether the death was suicidal, homicidal or accidental?

a. Homicidal strangulation
(1) Strangulation is mostly homicidal, followed by suicidal and accidental in that
order.
Memory Aid 2: Manner of death: hanging and strangulation
Hanging is mostly suicidal; strangulation is mostly homicidal
(2) Differences from suicidal strangulation [Table 5].
(3) Incidence – much commoner than suicidal strangulation. One of the
common methods of homicide.
(4) Victims – Usually women. Motive is sexual assault [please see case studies –
Boston Strangler].
(5) Homicidal strangulation is sometimes associated with erotic feelings [lust
murder, ch 25].

b. Suicidal strangulation
(1) Incidence – rare
(2) Methods:
(i) Like a tourniquet using knots – Simplest and commonest. Ligature may be
tied simply like a tourniquet using conventional knots
(ii) Spanish Windlass technique - (a) Technique - A stick or a rod is introduced
underneath the ligature and the rod twisted to tighten noose.
c. Accidental strangulation
(1) Isadora Duncan syndrome - Long scarf, end of a sari or a dupatta
traditionally worn by women around their necks can get entangled within the
spokes of a moving cycle rickshaw and can cause quick death by accidental
strangulation.,, To prevent such deaths, dupattas etc must not be worn while
traveling in a cycle rickshaw. Improved designs of cycle rickshaw wheels with
protective covers have also been proposed. The syndrome is named after the
world famous American dancer Isadora Duncan [1877 – 1927], who died on
14 Sep 1929, when the long scarf, she was wearing, got caught in the wire
wheels of her Buggati car. She died on the spot. At autopsy she was found to
have sustained a fractured larynx and carotid artery injury.
(2) Seat belts - In severe accidents, especially involving roll-over of vehicles,
there may be “submarining” with sliding of the body under the lap belt if it is
not properly adjusted. Much more common in short individuals and those who
are incapacitated in some way.

E. Types of Strangulation
Classical strangulation is the ligature strangulation (described above). Other
types are as below:
1. Throttling (Manual strangulation)
Throttling is compression of neck by human hands. It is a form of strangulation
where human hands are used in place of ligature [Manual strangulation].
Salient features:
Cause of death – Occlusion of b.v. of the neck.
a. PM appearances
i. External
(1) Asphyxial signs – eg congestion etc on face. Develop within 15-30 sec of
pressure on neck, and would continue to -in intensity if pressure is maintained.
However fingers may slip and press carotid structures in which case reflex
cardiac arrest occurs, causing immediate death. Thus intensity of asphyxial
signs would vary in all cases.
(2) Tongue – Usually protruded. May nor may not be bitten.
(3) Neck – Shows bruises and abrasions (i) Bruises - (a) Mechanism - produced
by tips or the pads of fingers. Usually more force is used than is necessary to
 kill the victim. (b) Shape – (I) Initially - (1) If fingers are static - Oval, Round
and of the size of digits. Size "1-2 cm [Six penny bruises - ch 12] (2) If
fingers skid across skin surface [as during struggle] – longer irregular marks,
especially along the jaw margins (II) Later – in both cases size -es due to
continued bleeding (c) Situation and extent – depends upon (I) degree of
pressure exerted over throat (II) manner of grasping neck (III) relative size of
victim’s neck in comparison with the assailant’s hands (IV) relative positions
of the assailant and victim - (1) Grip from right hand from front [Fig 19.17] (i)
Thumb impression on right side of victim’s neck. (a) Situation - under the
lower jaw over the cornu of thyroid (ii) Several finger marks on the left side of
neck. (a) Situation – left side of neck, obliquely downwards and outwards and
one below the other. Sometimes grouped together; may not be distinguished
separately (2) Grip from left hand from front [Fig 19.17] - (i) Rare. Seen if the
assailant was left handed. Findings are mirror image of the above, i.e. thumb
impression on left side of victim’s neck etc.

ii. Internal
(1) S/c tissues and muscles of neck –
(i) compressed backwards against cervical vertebrae
(ii) engorgement at and above the level of compression
(2) Bruises and frank hemorrhages -
(i) Present in (a) dermis (b) superficial fascia (c) deep fascia (d) muscles,
especially those surrounding the larynx both anteriorly and posteriorly. (e)
neck tissues, especially those surrounding or adjacent to the bifurcation of
the common carotid artery (f) base of tongue (g) pharynx (h) tonsils (i)
Larynx - especially immediately beneath the vocal cords. Sometimes
accompanied by severe laryngeal swelling. May or may not be
accompanied by fracture of hyoid and laryngeal cartilages. (j) thyroid gland
- beneath the capsule and within the substance (k) Salivary glands - (I) Seen
in parotid, submaxillary and submandibular glands. (II) Site - Beneath the
capsule and within the substance. (l) Lymphatic glands in the neck,
especially in the anterior triangle (m) Tissues at back of neck - when
counter pressure has been used.
(ii) Correspondence between external and internal bruising - (a) Extent, severity
and situation of internal bruising - Usually matches with (I)the strength and
degree of pressure used. (II) the external injuries. (b) Sometimes bruising is
absent externally, although internally extensive bruising may be present (c)
Rarely may be absent both externally and internally, especially if the victim
was unconscious and amount of pressure was minimal. (d) Site of external
bruising may not correspond exactly with that of internal, because of
mobility of skin.
(3) Tearing of muscles - especially sternocleidomastoid
(4) Carotid arteries -
(i) Show intimal tears in 10-15% cases.
(ii) Site - at or near carotid sinus.
(5) Laryngeal cartilages.
(i) Epiglottis - very rarely shows fractures because of its protected position.
Surface however may show a shower of petechial hemorrhages, or frank
hemorrhage.
(ii) Thyroid cartilage - (a) Lamina [ala] - may show fractures, either vertically in
the midline at the junction of laminae or obliquely or spirally across the left
or right lamina, if pressure is much greater. For trauma to front of neck
please see ch 17. (b) Horns [cornuae]- fracture of superior horns are much
more common than that of laminae [Fig 19.18] because they are more
 vulnerable and fragile than inferior horns. Frequently only the right superior
horn is fractured, because it directly underlies the thumb. (c) Abnormality
in the thyroid cartilage can be taken for fracture, and a small cartilage
triticea within the lateral thyrohyoid ligament can be mixed up with a
broken part of the superior cornu. (d) Like hyoid fractures, in general
fractures of thyroid too are more common in older people [because of
calcification of thyroid cartilages] (e) Because of greater force required to
fracture them, thyroid cartilage fractures are more serious than those of
hyoid bone.
(iii) Cricoid cartilage - (a) may show fractures. (b) Almost exclusively fractured
in throttling. (c) its fractures are almost always associated with fatality. (d)
May fracture across the front, midline or laterally.
(iv) Fractures are especially common in old persons with calcified cartilages
(v) Demonstration of laryngeal fractures - best done by first stripping the larynx
of its attached muscles and ligaments.
(6) Trachea:
(i) Tracheal cartilages may be fractured rarely, especially if the victim is old
[having calcified cartilages]
(ii) Trachea may show frank lacerations.
(7) Hyoid bone - Of all forms of compression of neck, fracture of hyoid is
commonest in throttling. Occurs in 30-50% of cases, with inward driving of its
distal fragments [inward compression fracture.
(8) Lungs -
(i) Congested with subpleural petechial hemorrhages.
(ii) Pulmonary edema.
(iii) Blood stained fine froth in bronchi
(iv) Microscopy - Some areas overdistended with rupture of alveolar walls and
some areas are collapsed; hemorrhages in the interstices under the pleurae
(9) Brain - Congested. Petechial hemorrhages in the white matter. Subarachnoid
hemorrhages.
b. Medicolegal questions
i. Whether death was caused by throttling?
(1) PM findings - typical of throttling would be present
(2) If victim was first killed by throttling and then hanged -
(i) Suspended body shows extensive injuries to neck structures
(ii) Signs of violence on body
(iii) Signs of sexual assault and rape may be present on women victims.
ii. Can PM findings similar to those of throttling be produced by other causes?
Yes. In hard compression of neck eg air choke, blood choke [two common choke
holds], flying kicks, jumping on neck, karate chops and kicking or stamping.
These can in fact cause much greater damage [eg bilateral comminuted fractures
of larynx] than are usually seen in throttling.
iii. For how long must the pressure be applied to cause death?
For 2 min or more.
iv. Whether throttling was suicidal, homicidal or accidental?
(a) Suicidal throttling
(1) Suicidal throttling is not possible. Any attempt at suicidal throttling would
inevitably produce unconsciousness first. As unconsciousness sets in, fingers
relax.
(2) A person not realizing that he cannot throttle himself may first attempt
throttling failing which may use ligature. In such cases some fingernail marks
may be seen over the neck.
(b) Homicidal throttling
(1) Incidence - Because of non-requirement of any weapon whatsoever and
immediate availability of hands, homicidal throttling is quite common. In all
cases of fingernail marks and contusions over neck, the presumption must be
of homicidal throttling.
(2) Method of choice - for killing weak individuals who cannot resist eg infants,
children and women
(3) Healthy adults can be throttled easily when
(i) sleeping or unconscious
(ii) stunned
(iii) taken unawares
(iv) under influence of drinks or drugs or
(v) weakened by disease or poison
(4) If a normal healthy adult is throttled -
(i) Signs of struggle would be present on both victim and accused as well as at
 the scene of crime.
(ii) Examination of accused may show abrasions, bruising and bitemarks at face,
arms, back of hands, fingers etc.
(iii) Fingernail scrapings of the assailant should be taken to compare tissue type
of victim.
(5) Sexual assault and rape - victim is often throttled during sexual assault and
rape. Motive is usually not to kill but to stifle cries. If victim dies, the accused
cannot take plea of accidental throttling.
(6) Defending party - may often allege that accused was actually trying to save
the falling victim by applying his hands over the neck. This is highly
improbable.
(c) Accidental throttling
(1) Sudden application of one or both hands or momentary grip on another
person’s throat may occur during demonstration of affection, joke,
physiological experiments, playful activity and sports [eg wrestling]. It cause
death from cardiac inhibition, which results from compression of carotid
sinus.
(2) Presence of injuries
(i) Bruises on neck - death could not have died instantaneously, because
formation of bruise requires a beating heart.
(ii) fracture of hyoid or thyroid - death cannot be due to accidental throttling,
because a mere touch cannot produce these injuries
(iii) minor damage or absence of damage"indicates accidental throttling, but
rarely can be seen even in homicidal throttling.
v. How much force was used by assailant?
Extent of damage - to neck structures. -damage indicates -force"indicates intent
to injure if not to kill.
vi. How much time must the victim have taken to die?
Very difficult to ascertain from PM findings. If very little or no injuries are
present, death might have been quick indicating less survival period. Severe and
extensive injuries indicate longer survival.
vii. Could it have been a case of throttling in a person about to die from other
causes?
In throttling during perimortem period [ch 11], nail marks may appear much the
same. Thus it is difficult to say whether deceased was alive or dead at the time.
2. Palmar strangulation
Palmar strangulation is a type of strangulation, in which one palm is placed
horizontally across the mouth and nostrils, and the other palm placed
perpendicular across the first in such a way, that its heel presses upon the front of
neck.
Salient features:
(1) Mixed with smothering - There is an element of smothering also (please see
below). The lower palm smothers, while the upper strangulates.
(2) Motive - Generally used to stifle cries from the victim. The upper palm is
used mainly to reinforce the lower palm used to stifle cry. Strangulation may
not be the primary motive of assailant.
(3) Victim – Easier to accomplish if victim is intoxicated
(4) PM findings – Same as that in ligature strangulation, except ligature mark.

3. Mugging
Mugging [syn, arm lock, choke hold] is strangulation caused by holding the
neck of the victim in the bend of the elbow.
Salient features:
(1) Two types. (i) Air choke [syn, bar arm control, choke hold] – Pressure is
exerted on front of larynx (ii) Blood choke [syn, carotid restraint, carotid
sleeper, lateral vascular neck restraint, sleeper holds] – pressure on both sides
of neck.
(2) Attack - in both is made from behind
(3) Mugging by lower limbs – rare. Neck pressed by foot or knee. It may be
repeatedly stamped upon
(4) Cause of death - (i) asphyxia (ii) reflex cardiac arrest
(5) PM appearances: (i) those of ligature strangulation with a broad object, i.e.
minimal signs. (ii) Diffuse abrasion along the jaw margin – [due to friction of
forearm] (iii) Diffuse bruising – behind larynx and in strap muscles of the
neck (iv) fracture of hyoid or thyroid is rare (v) in repeated stampings by foot
– (a) crushing of larynx and trachea (b) frank bleeding in soft tissues and
muscles of the neck (c) swelling (d) intima of carotid damaged (e) damage to
vagus and phrenic nerves.
4. Garroting
Garroting is a method of killing by asphyxia, where the victim is attacked from
behind without warning, and his throat is constricted.
Salient features:
(1) When used as judicial Execution: (i) It was a form of judicial executing
once practiced in Spain and Turkey. Sometimes there may be an iron collar
around the neck which is tightened by a lever. (ii) In one variation there is a
sharp spike at the back of the execution chair. As the ligature is tightened, the
neck is forced against the spike which penetrates the spinal cord and
immediate kills victim.
(2) When used as a method of homicide: (i) Results in sudden loss of
consciousness and collapse. The assailant is then able to tie a ligature around
neck without resistance. Even a relatively weak assailant can kill a healthy
adult. (ii) When used - by robbers at lonely places to attack and rob travelers.

5. Bansdola
Bansdola (doing away with bamboos) is a form of strangulation, where
compression of neck is achieved by bamboos.
Salient features:
(1) Method – Three procedures are usually employed (i) One bamboo is placed
over the front of neck and the other at the back. Both ends are tied to achieve
compression of neck (ii) victim is forced against ground"Bamboo is placed
across the front of neck"Assailant stands with a foot on each end of the stick.
(iii) Victim is pinned against a wall. Bamboo placed across the front of his
neck and pressed hard towards the wall with both hands.
(2) What is used: (i) Bamboo - most commonl (ii) sometimes a supple branch of
a tree is also used
(3) PM findings: (i) Same as that in ligature strangulation. (ii) In place of
ligature mark, bruises on front of neck corresponding to the placement of
bamboos are seen (iii) If 2 sticks are used, similar bruises over back of beck
(iv) If used against chest, similar bruises on chest. Other findings of traumatic
asphyxia.

V. HYOID BONE FRACTURES

Hyoid bone fractures are commonly seen in compression of the neck, eg
hanging, strangulation and throttling. Lacerations of pharynx may occur
following fractures of hyoid bone. Hyoid bone fractures are of 2 types - inward
compression fractures and outward compression fractures.

A. Types of Hyoid Fractures

1. According to displacement of fractured ends
a. Inward (lateral) compression fractures
(1) Occur due to inward compressive force as occurs in throttling.
(2) Mechanism - Fingers of the grasping hand squeeze the greater horns towards
each other"posterior [distal] fragment is displaced inwards [Fig 19.19(a)].
(3) Fracture - may be unilateral or bilateral. May occur at 2 places on either side
(i) Just at the base of distal fragment
(ii) At the joint between the greater horn and body of hyoid. Great care must be
taken to ascertain it, because a natural joint may be confused with a
fracture.
(4) Periosteum - torn on the outer side of the bone which is overstretched. Not
torn on the inner side [Fig 19.19].
(5) Complete detachment of smaller fragment from the hyoid - may occur if
the compression is severe. The smaller fragment may seen to be lying
medially to the rest of the bone, if neck structures have not been disturbed
during dissection. This can best be done by an in situ examination of hyoid.
(6) Preservation of hyoid as exhibit - Ideally hyoid should be preserved as an
exhibit. After preservation, sealing and labeling, it should be handed over to
the IO.

b. Outward (Anteroposterior) compression fractures

(1) Outward fracture - In case of hanging, as ligature presses on the neck, the
hyoid is forced directly backwards"-es divergence of greater horns"Outward
displacement of posterior fragment occurs, with rupture of periosteum on the
inside [Fig 19.19(b)].
(2) Nature of fracture - Like inward compression fractures, it may be unilateral
or bilateral, and like it may occur at 2 places. Similarly complete detachment
of smaller fragment from the hyoid may occur if the compression is severe.
The smaller fragment may seen to be lying laterally to the rest of the bone.
B. Demonstration of Fractures
(1) Palpatory method:
(i) Hyoid body is grasped in one hand
(ii) Distal fragment [tip] is held between the finger and thumb of other hand
(iii) A gentle attempt is made of bend the distal fragment both on the inside and
outside
(iv) In case of inward compression fracture, it can be easily bent in an inward
direction [because of torn periosteum outside]; but outward movement is
limited to the normal position only [because of intact periosteum on inside].
Exactly the opposite happens in anteroposterior compression fractures.
(2) Toluidine blue with stereomicroscopy - 1% Toluidine blue soln is applied to
suspect areas, left for 15 s and cleaned off with pure water. Examine bone with
a stereomicroscope [5-18 times magnification]. fractured sites would appear
bluish.
(3) X-ray and CT - before start of autopsy are the best and most certain method
to ascertain fractures. If for some reason, could not be done before start of
autopsy, the thyrohyoid complex should be carefully dissected out and x-rayed
separately. The x-ray or CT plates should be preserved as evidence.

VI. SUFFOCATION
Suffocation is exclusion of air from lungs from any means other than ligature
[Fig 19.20].

A. Environmental Suffocation
Environmental suffocation is deprivation of oxygen due to lack of oxygen in
the environment.
Salient features:
(1) There may be deficiency of O2 in the environment, or it may be replaced by
an inert gas as N2. Replacement of O2 by a poisonous gas such as Cl2 or H2S
would not cause death primarily by asphyxia, but by poisonous effects.
(2) Conc of O2 in air is 21%. Its fall to 16% or less is dangerous. With 5% conc
consciousness is lost rapidly and death occurs within a few minutes.
1. Causes
(1) During play - children may get locked in large boxes, trunks, or old disused
refrigerators
(2) Glue sniffing [inhalant abuse]- [ch 46]. Smothering may also be involved
[please see below]
(3) In the vicinity of lime kilns and wells or excavations in chalk rock
(4) In confined spaces – eg deep tanks of a ship, fermenters, grain bins, sewers,
silos, tanning vats and unused wells, dusts, hazardous gases, fumes and vapors
accumulate and oxygen may become deficient. A person may be suffocated on
entering such a confined space
(5) Cabin failure of aircraft - at high altitudes
(6) Natural upheavals - eg CO2 produced as a result of limnic eruptions.
[please see ch 44 for details – under the heading “MLI of CO2”].
2. PM findings
(1) As in asphyxia. (2) Petechial hgs are however absent (3) Head and face –
pale

B. Smothering
Smothering is caused by closing the external respiratory orifices by hands or
other means [eg a pillow].
1. Accidental smothering
(1) Prevalence - Most common manner of smothering
(2) Circumstances causing AS-
(i) Accidental fall - in large quantity of semisolid or finely divided material eg
ashes, coal dust, grain, hay, mud, sand etc so that his mouth and nose are
obstructed. Victim may struggle and try to breathe"inhales some material in
air passages, and swallows some material in his stomach. PM examination
will show matching material in air passages, lung, esophagus and stomach.
Partially the death is due to choking also.
(ii) Autoerotic asphyxia - Please see sexual hanging above.
(iii) Children – playing with plastic bags over their faces. May get accidentally
suffocated. It is not necessary for the open end [mouth] of bag to be tied
around neck. Even with bag open, enough CO2 may accumulate to cause
CO2 narcosis. Even a flat plastic sheet may adhere to face due to
electrostatic forces and block mouth and nose. More efforts to breathe, or
trying to move sheet away can generate more electrostatic forces causing
sheet to stick harder
(iv) Epileptic or intoxicated person"buries his face in pillow or mattress
(v) Infants - (a) Infants covered with heavy bedding, blankets or sheets - may or
may not die of suffocation, depending upon the force with which bedding
etc obstructed the air passag es. (b) Infant not covered with heavy sheets,
but overturns his face in bed"buries it in soft pillow or mattress"2 situations
may occur now (I) complete blockage"Smothers immediately (II)
incomplete blockage"does not smothers immediately"gradually face
becomes more congested because it is dependent; furthermore blood traces,
edema fluid, mucus and saliva keep accumulating over the pillow"blockage
is complete"smothering occurs
(vi) Glue sniffing [inhalant abuse].
(vii) Newborns - Membranes covering the head during birth etc [ch 27].
(viii) Person sexually assaulting female"covers her face and mouth with hands or
pillow to stifle her cries"when the act is complete he finds that the female
has died of AS.

2. Homicidal smothering
(1) Possible when
(i) victim is incapacitated (a) from drink or drugs (b) by a blow to the head
(ii) victim is very young, weak or old
(2) In children – easily achieved by either covering face with pillow, or
pinching nostrils by one mouth and closing mouth with the other.

3. Suicidal smothering
(1) Suicidal smothering by hands - impossible
(2) Possible – by
(i) Burying face in a mattress
(ii) Lying against the bed clothing to obstruct nose and mouth
(iii) tying a polythene or similar bag over the head.
(iv) Usually seen in mentally retarded persons.
(3) Cut throat wounds – if trachea is completely cut and soft parts obstruct the
trachea, it is smothering.

4. Examination of suspect
(1) Saliva, blood, squamous epithelium, tissue cells on assailant’s hands or
 pillow and other smothering material etc used to cause blockage
(2) Other Struggle marks

5. Autopsy findings
(1) Slow deaths - All classical asphyxial signs and symptoms are severe, if death
occurs by slow asphyxia [more common]
(2) Rapid deaths - If death is rapid due to reflex cardiac arrest"asphyxial signs
may be absent. They are classically absent in plastic bag suffocation.
a. External
(1) Obstruction by Bed clothing, cushion, Pillow etc applied with skill may not
leave any external signs of violence, especially if the victim is too young or
old.
(2) Head and face:
(i) Pale
(ii) Plastic bag – may be found over face. It may contain (a) Moisture – in case
of plain plastic bag suffocation (b) inhalants – in case of inhalant abuse.
Chemical examination is vital
(3) Nose and mouth:
(i) Oozing of blood
(ii) Skin around nose and mouth is pale white due to application of pressure
(iii) Scratches, nail marks, lacerations around nose and mouth
(4) Congestion, petechiae"rare. May be present if victim fights and struggles for
breath
(5) Nasal cartilage"fractured
(6) Frenulum of upper lip"Lacerated
(7) Lips, gums, tongue:
(i) bruised, lacerated. In doubt, confirm by microscopy
(ii) Tongue - may be bitten and protruded
(8) Anterior teeth"broken.
b. Internal
(1) Back of throat – copious mucus
(2) Air passages:
(i) show blood stained frothy fluid, containing RBCs and desquamated
respiratory epithelial cells.
(ii) If person is buried alive, show earth and sand.
(3) Lungs – Congested, edematous, show petechiae, areas of hemorrhage and
collapse [atelectasis]. Some areas show emphysema
(4) Internal organs – deeply congested. Show petechiae.

C. Overlaying
Overlaying is accidental death by smothering caused by a larger individual
sleeping on top of a smaller individual, usually an infant.
Salient features:
(1) Occurrence - Most commonly it occurs when mother shares bed with an
infant and during sleep rolls over the infant and crushes him. In many cases,
the mother is found to be under the effect of drugs and alcohol.
(2) PM Findings - (i) Signs of asphyxia, (ii) flattening and paleness of face and
nose, (iii) nostrils filled with blood stained froth, (iv) pillows and garments [of
both mother and child] stained with such blood stained froth.

D. Gagging
Gagging is a form of asphyxia which results from closure of airways by forcing
a gag material [rolled up cloth, paper balls etc] in the mouth.
Salient features:
(1) Gag - The material which obstructs airways.
(2) Position- The gag must be pushed in the mouth sufficiently deeply, so that it
touches the posterior wall of the pharynx (complete gagging). In incomplete
gagging, when the gag is not pushed up to the back, oral secretions may cause
the gag to swell and cause death some time later.
(3) Manner - (i) Suicidal (ii) Homicidal – (a) Unwanted infants - may be killed
by this method [ch 27] (b) In adults - Robbers may stuff a cloth inside mouth
of a chowkidar to keep him silent. There is simultaneous tying of hands (to
prevent removal of gag) and legs (to prevent running away). The cloth may
gradually swell up and cause gagging. Strictly speaking it is not homicidal, as
the intention of robbers was only to keep him silent. Generally more than one
person is required to gag a healthy struggling adult individual [one needed to
restrain, and another to gag]. (iii) Accidental – (a) False dentures – may
impact throat during anesthesia (b) Dental procedures - Gagging [mostly
nonfatal] commonly occurs during dental procedures, such as making a
 maxillary impression. Causes (I) Tactile stimuli - dentist’s fingers or
instruments contacting the oral mucosa or even by (II) Non tactile stimuli -
Patient seeing the dentist or remembering a previous dental experience. (c)
Injuries to nose and mouth – Blood may seep to the back of the throat and may
clot, producing an “artificial gag” of clotted blood. [if it trickles down trachea,
it would be choking] (d) Breast pushed too far in the mouth of a suckling baby
(e) During sexual activities [Fellatio]
(4) Cause of death: (i) Asphyxia [most common] (ii) Reflex vagal inhibition
[rarely]
(5) PM appearances: (i) classical signs of asphyxia (ii) Cloth must be removed
and sent for forensic examination [fibre, manufacturer or laundry’s mark,
saliva etc].

E. Choking
Choking is a form of asphyxia caused by an obstruction within the air-passages.
Salient features:
(1) Manner of death - Choking is almost always accidental.
(2) Level of blockage – foreign body gets arrested at or just below the vocal
cords. May produce an inflammatory reaction with edema.
(3) Seen most commonly in – People whose power to swallow or masticate is
severely impaired, eg (i) very young (ii) very old (iii) psychiatric patients (iv)
sick and infirm
(4) Common circumstances – (i) laughing or crying simultaneously with food
intake (ii) ingestion of alcohol
(5) Objects causing choking – Any small object which can enter trachea can
 cause choking. Most common objects are (i) Balloon [when trying to inflate it]
(ii) Battery (iii) Button (iv) Cloth [esp after ENT operations, eg tonsillectomy]
(v) Coin (vi) Corn (vii) Cotton (viii) Dentures (artificial) (ix) Fish (live) [as
during some unorthodox treatments] (x) Fish bone (xi) Food [eg loaf, meat,
milk] (xii) Fruit stone (xiii) hairpin (xiv) Leaves (xv) Marbles (xvi) Mud (xvii)
nails [during biting](xviii) Onion (xix) Peanut butter, (xx) pen cap (xxi) Potato
(xxii) Rag (xxiii) Rice [Fig. 19.22] (xxiv) ring (xxv) Rubber balloons (xxvi)
Rubber teat (xxvii) Seed (xxviii) Tooth (broken, extracted by a dentist).
(6) Choking by vomit or regurgitated food - (i) during anesthesia (ii)
insensibility from any cause eg poisoning (iii) during rape or violent sexual
intercourse(iv) Head injury – irritation of brain causes vomiting, which may
be inhaled due to unconsciousness (v) during fit of epilepsy (vi) Infants –
usually regurgitate clotted milk after a meal and choke on it (vii) Tranquilizing
drugs – may suppress gag reflex and may cause choking especially psychiatric
patients
(7) Choking by Blood – (i) Facial injuries during blunt trauma as in a fall, fight,
vehicular accident etc [broken nose, dislodged teeth, laceration of lips and
gums] (ii) ENT operations [in Dr. Suresh Gupta vs. Government of NCT of
Delhi 2004, the patient choked during an ENT operation – ch 2].
(8) Choking by Gauze piece - during operations
(9) Natural diseases - (i) Diptheria (ii) growths in epiglottis larynx and
bronchus (iii) H. influenzae infection in children (iv) hemoptysis in pulmonary
tuberculosis (v) hemorrhage into trachea (vi) infectious mononucleosis (vii)
pharyngeal abscess (viii) rupture of aortic aneurysm in air passages and (ix) a
tuberculous gland eroding in a bronchus and prolapsing in its lumen.
(10) Inhalation of steam and ingestion of irritant substances
(11) Allergic reactions – (i) Drug reactions [eg penicillin] (ii) Insect bites [bees,
wasps, hornets (ch 38)]. May cause swelling of laryngeal mucosa and cause a
quick death by choking.
(12) Blow to the front of neck – may cause hemorrhage and severe laryngeal
edema resulting in choking. Sometimes death may occur due to reflex vagal
inhibition.
(13) Very rarely pins, safety pins, small bone pieces may be lodged in the air
passages for relatively long periods without causing any serious problems.
1. Course
If patient regurgitates object and survives, complications may develop after a
latent interval.
2. Mechanism of death
Death results from anoxic anoxia. There may be
(1) Complete obstruction of larynx
(2) Incomplete obstruction of larynx resulting in laryngeal spasm. Sometimes
laryngeal spasm passes off before hypoxia becomes fatal.
3. Cause of death
(1) Immediate – Asphyxia
(2) Late – Complications eg pneumonia, lung abscess, bronchiectasis.
4. PM findings
(1) Typical of asphyxia.
(2) Air passages – Larynx and finer branches of bronchi show pieces of food.
Air passages show excessive secretion of mucus in which food is embedded.
Mucosa is deeply congested.
(3) Microscopically – Lungs – intense interalveolar edema. Collection of
desquamated respiratory tract epithelium.
5. MLI
(1) Accidental – Most common
(2) Suicidal – rare. Victims are usually psychiatric patients [dementia,
psychosis] or prisoners. A foreign body is forcibly thrust inside the throat.
(3) Homicidal:
(i) Infants – Infanticide is practiced by stuffing a wad of paper or cloth into the
larynx [if it remains in mouth, it is gagging]
(ii) Adults – rarely employed because of resistance offered by a healthy
conscious adult. May be practiced in old frail persons, and persons suffering
from some debility, disease, paralysis or in drunk and intoxicated persons.
6. Café coronary
Café coronary [syn, bolus death] is a condition in which a healthy person who
begins a meal, suddenly collapses and dies without any further distress. The
syndrome was first described by Haugen in 1963, when he described it in 9
cases.
Salient features:
(1) Predisposing conditions: (i) Age - middle aged or elderly (ii) Gross
inebriation, or use of sedative drugs. (iii) Drugs – especially anticholinergic
and antidopaminergic drugs. They are known to interfere with swallowing
mechanisms through reduction of salivation, .ed esophageal motility, delayed
gastric emptying, and aggravation of gastroesophageal reflux. Drugs alone do
not - the risk of café coronary, but combined with old age and/or psychiatric
conditions, the risk is significantly -ed. Patients receiving high dosage of both
categories of drugs also have -ed risk of choking. They must be monitored
closely. (iv) Institutionalization - in long-term medical care facilities (v)
Natural diseases - most notably Parkinsonism, clinically significant
neuromuscular dysfunction, dementia or mental retardation (vi) Poorly
chewed food – One of the factors responsible for it is the individual’s dental
status. They either have several teeth missing, are edentulous or have artificial
dentures. Children who have inadequate dentition are known to choke on food
too [crèche coronary]. (vii) Quick gulping. Haugen called it “the obvious
lack of ordinary table manners”. Combination of two or more conditions make
the person more liable to café coronary.
(2) Size of food bolus – usually very large. It could be large size of bolus, which
impinges upon the sides of larynx and stimulates the vagus nerve.
(3) Incidence - Overall incidence is 0.66/100,000 population/y. It -es with age
beginning at about the fourth decade [30-40 y] of life. The peak incidence of
10-14/100,000/y occurs at the 7th decade [60-70 y].
(4) Overall male: female ratio is 1:1.6.
(5) Place of occurrence – Despite the name café coronary [Fr, coronary attack
occurring in a café or restaurant], only about 1/3rd cases occur in a restaurant.
Other places are private homes, nursing homes, or mental institutions. In 85%
 of cases, other people are present at the time of the fatal incident.
(6) Type of food - The type of food most often associated with fatal café
coronary is meat [74%]. Most often it is steak. Feces have been found in
mentally ill [coprophagic café coronary].
(7) Level of obstruction - supraglottic in 1/3rd; infraglottic in 2/3rd.
(8) Signs of choking – are absent both during life [clinically] and at autopsy
[pathologically].
(9) Cause of death – reflex vagal inhibition of the heart. Suddenness of death is
most marked.
(10) Mechanism – old age, gross inebriation and/or neuromuscular
incoordination causes malfunctioning of deglutition mechanism"food slips
within the larynx, bifurcation of trachea or within the bronchus"Gross
inebriation and/or neuromuscular disorder inhibit gag reflex"food continues to
remain in windpipe"stimulates recurrent laryngeal nerve, a branch of vagus
nerve" vagus nerve stimulated"Cardiac standstill.
a. PM appearances
(1) Larynx – A large piece of poorly chewed piece of food is found. Sometimes
nothing is found, as the obstructing piece of food has been removed by
bystanders.
(2) Food in finer branches of bronchi is typically absent, because death occurs
immediately and no forced inspirations occur.
(3) Findings typical of asphyxia are absent [Table 6].
F. Traumatic asphyxia
Traumatic asphyxia is a form of asphyxia where exclusion of air from lungs is
effected by mechanical fixation of chest in such a way that normal respiratory
movements are prevented. Also known as crush asphyxia. It is mostly
accidental, but may be homicidal and suicidal as well.
1. Causes
a. Accidental
(1) Riot crush - When large crowds gather at a small place, and due to some
disturbance (eg fire, explosion, electricity failure etc), everyone starts running
hither and thither in a completely disorganized way resulting in a stampede.
Chest of each individual is pressed violently by the mass of the crowd. Some
individuals may fall down, and others may trample on their chests (human
pile deaths).
(2) Restraint asphyxia - When a policeman forcibly restrains a criminal,
especially by pinning him on the ground in a prone position, with his hands
pinned backwards. The death may also be due to excited delirium syndrome
(ch 11).
(3) Falling of earth or stone – usually in a coal mine or during tunneling or in a
building collapse
(4) During car repair - Mechanic repairing car positioned underneath a
car"Jack slips"Vehicle falls on top of his chest
(5) Industrial accident – Machinery falling on victim’s chest
(6) During natural disasters - earthquakes and landslides
(7) During railway shunting of carriages – victim may be pressed between two
railway carriages
(8) Heavy tree or branch of tree falling on a person sleeping underneath
(9) Some snakes [Boas and pythons] kill by winding around chest, constricting it
[ch 38].
b. Homicidal
(1) Assailant jumps on or steps upon the chest of victim
(2) Jack-knifing – Victim’s thighs and knees are forcibly hyperflexed against
his own chest and abdomen, so he can’t breathe [indirect compression of
chest]
(3) Traumatic asphyxia by bansdola – Chest is squeezed forcibly between two
sticks placed across front and back of upper part of chest.
c. Suicidal
Victim allows a heavy weight to fall upon himself. Seen mostly in mentally ill.

2. PM appearances
a. External
(1) Face, lips, scalp - Swollen, congested.
(2) Head, neck, upper chest above the level of compression:
(i) Intense congestion, petechial and confluent hemorrhages and deep purple or
purple red cyanosis. This is due to retrograde displacement of blood from
the SVC into the subclavian veins and head and neck veins, due to sudden
compression of chest. The level of compression is often very clearly
marked, below which the skin is pale [Fig 19.23] or sometimes mildly
cyanosed.
(ii) The spread of blood to the veins of upper limbs is prevented by valves, but it
can easily go in the valveless veins of head and neck, where it can rupture
distal venules and capillaries"petechial hemorrhages of skin, eyelids,
conjunctivae, mucus membranes of mouth. Also bleeding from nose, mouth
and ears. May cause “blood blisters” underneath the sclera [due to
hemorrhages] which bulge through the eye.
(iii) The purple red color is both due to dilated bv as well as hemorrhages in the
tissues around them.
(iv) If patient recovers, the purple color gradually disappears in 10-14 days
without the color changes seen in bruises.
(3) Pallor - At the level of shirt collar or folds or creases in the garments, braces,
buttons etc.

b. Internal
(1) Fractures - of ribs, sternum, vertebrae, and other bones depending on how
the body was crushed.
(2) Brain - Congested. Shows petechial hemorrhages
(3) CVS - Right side of heart markedly distended. Subendocardial petechial
hemorrhages. All veins above aorta are markedly distended.
(4) Lungs - Dark, heavy. Show subpleural petechial hemorrhages.
(5) Internal organs - Congested.

G. Burking
During the years 1827-8, two Irish immigrants William Burke (1792-1829) and
William Hare (1792-1858) killed 17 persons by a special method now known
as Burking, and sold their corpses for dissection to Dr Robert Knox, a private
anatomy lecturer, who used to teach students from the Edinburgh Medical
School. They used to invite a beggar to their house, give him food and alcohol,
and when the victim was drunk, throw him on the ground. Burke used to sit on
the chest [traumatic asphyxia] and close victim’s nose and mouth with his hands
[smothering]. Hare used to pull the victim round the room by the feet.
(1) Burking is a method of homicidal asphyxia where two asphyxia methods –
smothering and traumatic asphyxia – are simultaneously used.
(2) Other combinations – are known eg
(i) traumatic asphyxia and strangulation,
(ii) smothering and strangulation etc; but traditionally they are not called
burking.
H. Positional Asphyxia
Positional asphyxia [syn, postural asphyxia] is exclusion of air from the lungs
due to abnormal position of the body.
Salient features:
(1) Causes: (i) When chest is prevented from expansion by internal pressure -
eg. body is placed in such a position that abdominal organs press upon the
diaphragm from below upwards. (ii) Falling in confined spaces - eg a
well"victim gets wedged between the walls [may be considered a case of
wedging also] (iii) Forcible flexion - of neck on the chest. (iv) Indirect
compression of chest - Body is in a jack-knife position, i.e. victim’s thighs and
knees are driven against his own chest. (v) Intoxicated person - Slides out of
bed"Head and adjoining region hang down from the edge, and remaining body
rests at a relatively upper level.
(2) Circumstances favoring positional asphyxia - Victim is incapacitated due
to some reason so that he cannot voluntarily make efforts to respire (i) strong
intoxication (ii) Unconsciousness due to trauma, stroke or other natural
disease.
1. PM findings
Same as that in traumatic asphyxia, except fractures and blunt injuries.
2. MLI
Almost always accidental. But may be homicidal, if assailant “doubles up”
victims body in a jack-knife position.

VII. DROWNING

Drowning is a form of asphyxia caused by aspiration of fluid into air-passages,

caused by complete or partial submersion in water or other fluid.
Salient features:
(1) Sp gr of body is 1.08. Other sp gr in increasing order are (i) Fat-0.92 (ii)
Brain-1.04 (iii) Soft organs-1.05 (iv) Muscle-1.08 (v) Bone-2.01. Natural
tendency of the body is thus to sink down.
(2) Complete submersion is not necessary; submersion of only nose and mouth
can cause drowning, as is seen in alcoholics passing out in shallow streams
and getting drowned.
(3) Current concepts - According to current thinking the term “drowning”
should include both fatal and nonfatal drowning. Accordingly a new definition
of drowning has been suggested. It states, “Drowning is the process of
 experiencing respiratory impairment from submersion/immersion in liquid.”
The definition includes cases of drowning in all kinds of liquid, except body
fluids [amniotic fluid, milk, saliva, vomitus].

A. Classification
1. Wet drowning
Wet drowning [syn, classical drowning, primary drowning] involves inhalation
of water into lungs.
Salient features:
(1) Enormous quantities of liquid is inhaled into lungs
(2) The victim suffers from severe chest pain.
(3) Fatal period - Death occurs within minutes of submersion.
(4) Cause of death – (i) Cardiac arrest (ii) ventricular fibrillation (iii)
Hyperkalemia.
2. Dry drowning
In dry drowning, there is no significant presence of liquid in the lungs.
Salient features:
(1) Mechanism: (i) Laryngospasm - Just a few drops of liquids enter the
larynx"elicit a violent laryngospasm"death due to asphyxia without entry of
water in lungs. (ii) Absorption of liquid in circulation – victim brought out of
water"resuscitated"water absorbed in hypertonic plasma.
(2) Incidence - About 10-15% of all drownings.
(3) Victimology – Commonly seen in (i) children (ii) adults under the influence
of alcohol, sedatives or hypnotics.
(4) Resuscitated victims display (i) panoramic views of past life (ii) pleasant
dreams with no distress.
(5) PM Appearances – Diagnosis is mainly of inference and exclusion as no
classical signs are there (i) Signs of asphyxia – prominent (ii) Trachea – may
be congested. May contain water (iii) lungs – virtually dry. Do not contain
water.

3. Near drowning and secondary drowning

a. Near drowning
Near Drowning is defined as initial survival at least beyond 24 hours of an
individual after asphyxiation due to submersion in fluid.
Salient features:
It is associated with secondary complications, which require further medical
management.
b. Secondary drowning
Secondary drowning is death following near drowning after a period of relative
wellbeing.
Salient features:
(1) Causes - (i) posthypoxic encephalopathy [most common], (ii) inadequate
alveolar gas exchange due to primary alveolar membrane dysfunction and (iii)
loss of surfactant.
(2) It can happen after immersion both in fresh and salt water.
(3) Incidence - 2-5% of all drownings.
4. Immersion syndrome
Immersion syndrome [syn hydrocution, submersion inhibition] is death
resulting from cardiac arrest due to vagal inhibition, subsequent to immersion in
liquid. Cardiac arrhythmias, particularly those associated with the long-QT
syndrome may be responsible in some cases. Molecular autopsy is required to
diagnose such conditions [please see ch 5].
Salient features:
(1) Incidence – 1-2% cases of drowning
(2) Causes: (i) icy cold water stimulating the nerve endings at the surface of the
body (ii) cold water entering ear drums, nasal passages, pharynx and larynx,
stimulating nerve endings at mucosal surfaces (iii) Water striking the
 epigastrium
(3) Circumstances: (i) Diving into the water feet first (ii) Diving with horizontal
entry in water [with consequent blow on the abdomen] (iii) ”Duck diving” by
the inexperienced [“Duck diving” is a surfing term in which the surfer pushes
the surfboard underwater.
(4) Aggravating factors: (i) Alcohol -s incidence because of (a) general
vasodilatation of skin (b) central effects on vasomotor center (ii) Emotional
tension – because nervous reflex circuits are more active [eg during suicidal
attempts]. Imp – Deprivation of oxygen may be a contributing factor in
virtually all types of drowning, especially as the time of immersion lengthens.

B. Causes of Death Associated with Drowning

(1) Asphyxia:
(i) Obstruction of airways by fluid. Associated causes are
(ii) Circulatory failure [due to myocardial anoxia] and
(iii) Respiratory failure [due to respiratory center anoxia]. Now it is thought
other factors also play a part
(2) Laryngeal spasm – due to entry of water into larynx
(3) Vagal inhibition – Please see under “immersion syndrome” above
(4) Injuries – due to body striking hard objects within water or head striking the
base of swimming pool etc. May cause (i) concussion (ii) Fracture dislocation
of cervical vertebrae (iii) Fracture of skull
(5) Cramps - occurring within water, disallowing victim to swim himself to
safety
(6) Exhaustion – due to continued struggle
(7) Long QT syndrome – rarely
(8) Ventricular fibrillation
(9) Hypoxemia and metabolic acidosis
(10) posthypoxic encephalopathy
(11) Resetting of hypothalamic thermostat at a lower temperature – For
details of last 4 causes, please see above under “pathophysiology”.
(12) Electrolyte disturbances – Rejected now.

C. Fatal Period
Four minutes in Fresh water and Six to Seven minutes in Sea water [Memory
Aid - 3].

D. PM Appearances [Wet Drowning]

Autopsy must be started as soon as possible, otherwise classical signs eg foam
and froth at mouth and in lungs, overdistension of lungs may become less
pronounced or may disappear altogether.
1. External
(1) Clothing - Wet. Small aquatic animals may be found trapped.
(2) Skin – (A) General - wet, cold, moist, pale [vascular contraction] (B) Cutis
anserina [CA] [syn, goose flesh, goose skin] – (i) Appearance – granular and
puckered (ii) Mechanism – spasm of erector pilae muscles, attached to hair
follicles. (iii) Conditions in which cutis anserina is seen (a) during life - when
skin comes in contact with cold water [drowning]. In India since water is
usually warm CA due to drowning is rarely seen. (b) after death - (I)
immediate onset - submersion of body in cold water immediately after death,
when muscles are still warm and irritable and have ATP supply intact [agonal
contraction] (II) Late onset - by rigor mortis of same muscles [postmortem
artifact ch 10]. (C) petechial hemorrhages - rarely
(3) Face – (a) color – cyanotic (b) conjunctiva – congested; show petechial
hemorrhages, especially in lower eyelids (c) pupils – dilated (d) Tongue –
swollen and protruded (e) Foam or froth – (i) Time of appearance - Appears
within 2 min of drowning (ii) Quantity – varies directly with the length of
submersion and violent respiratory efforts (iii) Characteristics - fine, white,
lathery foam at mouth and nostrils [one of the most characteristic external
signs of drowning; Fig 19.25]. (iv) Color - usually white, but may be blood
stained [from intrapulmonary bleeding] (v) More commonly seen in sea water
drowning (vi) shape - projects as a small balloon or mushroom like mass
[champignon de mousse], from mouth and nostrils (vii) On wiping –
reappears, especially when chest is compressed (viii) Bubbles - do not readily
collapse when touched with the point of a knife (ix) Other conditions where
froth is seen [pseudofoam]– (a) electrocution, (b) epilepsy, (c) opium
poisoning, (d) pulmonary edema, (e) putrefaction, (f) strangulation. Froth
from these conditions can be differentiated from that in drowning by the fact
that in drowning froth is finer, much more in volume and quantity and
 reappears on wiping. In addition, each condition will have its own specific
signs. For example, in putrefaction, the body will be bloated, discolored
greenish black and have foul smell. (x) Situations when foam is not seen in
drowning – (a) There were no violent respiratory efforts (b) Victim died
immediately of immersion syndrome (c) dry drowning, when water could not
enter lungs (d) Artificial respiration was performed, especially with respirator
(e) Putrefaction - Foam disappears when putrefaction sets in. But putrefaction
produces its own characteristic foam [pseudofoam].

(4) Body and natural orifices [mouth, nostrils, ears]: coated with algae
[including diatoms], grit, mud, sand, seaweed, silt and waterweed.
(5) PM staining - (a) Location – (I) Standing water [eg pond]- confined to head
 [Fig 19.25], neck and front of chest, lower arms and legs, because the body in
water floats face down and buttocks up, with legs and arms hanging down
[Fig 19.27] (II) Rapidly moving water [eg river]– PM staining may not
develop because of constant change in body’s position. (b) color – bright pink
[may often be confused with that seen in CO, but CO is not found in blood].
(6) Rigor mortis – appears early, especially when the victim struggles violently
just before death to save himself.
(7) Signs of vomiting, micturition, defecation and seminal emissions – as
these phenomena occur agonally.
(8) Hands – (a) show cadaveric spasm - Grass, gravel, leaves, moss, sticks,
twigs and weeds may be firmly grasped in the hands [“drowning man
clutching at the straw”]. It is the surest sign of antemortem drowning. (b)
Fingers – abraded (c) Nails – damaged. Show sand, mud and other foreign
material under the nails. (d) Washerwoman’s hands - (i) Appearance –
bleached (white), sodden, thickened and wrinkled (corrugated) [like the soggy
hands of a washerwoman]. Changes are seen both in hands and feet [Fig
19.26], but if shoes are worn, it may take twice as long for same changes to
appear. Washerwoman’s skin is merely a sign of immersion and is not a sign
of antemortem drowning. (ii) Mechanism - absorption of water into outer
layers of skin (iii) Progression : Exact calculation of time is not possible,
because seen early in warm water. Average durations are (A) 2-4
hours"wrinkling and soddening [sodden"thoroughly soaked, soggy, heavy] of
fingertips (B) 4-8 hours"bleaching of epidermis (C) 24 hours"entire hand
shows bleached, wrinkled and sodden appearance (D) 48 hours"Peeling of
cuticle from palm and sole (E) 3-4 days"Skin can be peeled off like a glove
(9) Scrotum and penis – May be retracted due to coming in contact with cold
water [etiology similar to that of cutis anserina]. This phenomenon has been
called “reaction phenomenon”.
(10) Injuries:
(i) Antemortem – (a) before drowning episode - Abrasions and contusions
produced before drowning episode [eg during struggle] may get masked
due to soggy skin. After skin is allowed to dry, they become visible. (b)
during drowning episode – injuries due to striking on sides and bottom of
wells, stones at bottom of lakes, rivers etc may be found
(ii) Postmortem – due to (a) damage by underwater flora or fauna [fish bites etc]
(b) propeller of boats – May be cut right into half (c) by breakers off shore
(d) against uneven surface or rocks at the bottom [Fig 19.27]
(11) Putrefactive changes – (a) Early - appear early after body is brought to the
surface; within a few hours after being brought out from water, the body may
start showing putrefactive changes. Skin may acquire a green or bronze color
or may be exceptionally dark, presenting the appearance of a “negro’s head”
[tête de nègre]. (b) Where not seen – changes such as greenish black
discoloration may not be seen over areas which are tightly wrapped in
clothing, shoes etc, or surfaces which are in close contact with each other [eg
arm pits, upper limbs, lower limbs if they are tied together].
2. Internal
a. Air passages
(1) Trachea and bronchi:
(i) full of foam, froth [Fig 19.28], water
(ii) May contain algae [including diatoms], grit, mud, sand, seaweed, silt and
waterweed, which would match with that present in water. Presence in
terminal bronchioles is more significant than presence in trachea, which
may be due to passive entry even in PM drowning.
(iii) May contain stomach contents – due to vomiting and subsequent aspiration
during the unconscious gasping phase of drowning
(2) Mucosa – congested.
b. Lungs
(1) Radiography – Chest may be radiographed before incision. Alternatively
only lungs may be dissected out and radiographed before sectioning.
(i) Pulmonary edema, seen as Kerley B-lines [short parallel lines at the lung
periphery seen on chest radiographs with interstitial pulmonary edema].
(ii) extravascular lung water
(iii) mud, silt etc can be seen. Silica is radiopaque
(2) Size -
(i) voluminous, overdistended. Medial aspect of each lung approaches the
midline.
(ii) may completely cover heart;
(iii) bulge out of chest as soon as sternum is removed [ballooning]. (B)
Ballooning is .ed in - (I) pulmonary diseases eg extensive pleural adhesions,
fibrosis etc.
(3) Weight – May be up to 1000 g each, especially in salt water drowning
[normal – app 400 g (appendix 4)].
(4) Surface – Shows rib markings [grooves]. Have a doughy feel and pit on
 pressure
(5) On section – watery, frothy, blood stained fluid oozes out of cut lung
surfaces.
(6) Acute pulmonary edema – Pathophysiology - (a) - in ambient hydrostatic
pressure (b) peripheral vasoconstriction from ambient cold (c) -ed pulmonary
blood flow resulting from exercise [struggle] "- pulmonary capillary
pressures"extravasation of fluid into the interstitium.
(7) Congestion:
(i) usually moderately congested.
(ii) may be pale. Mechanism of paleness- (I) forcing out of blood from lungs (II)
Compression of vessels in the inter-alveolar septa by the air and water
trapped in the alveoli.
(8) Paltauf’s hemorrhages [syn, Paltauf’s spots, signum Paltaufi]-
(i) Appearance - Shining, pale pink or bluish red hemorrhages, immediately
beneath the pleurae.
(ii) Size – minute or up to 3-5 cm in diameter
(iii) Incidence – 50%.
(iv) Location – lower lobes of lungs [most common]. May also be on interlobar
surfaces or anterior surfaces of entire lungs.
(v) Mechanism – Tearing of the interalveolar partitions due to -ed pressure
during forced expirations
(9) Petechial hemorrhages – Absent or extremely rare
(10) Appearances in fresh water and seawater drowning - Table 7. The
differences in appearances tend to become less clear as body remain in water
for longer period
(11) Histologically –
(i) Edema – protein rich edema fluid in interstitial spaces
(ii) Interstitial congestion
(iii) alveoli - (a) Acute dilatation of alveoli with extension, elongation and
thinning of the septa (b) alveolar walls are torn. Drowning water penetrates
alveolar walls to enter tissues and blood vessels [this is the basis of diatom
test]. (c) compression of alveolar capillaries (d) alveolar hemorrhages (e)
alveolar macrophages (f) May contain stomach contents [vomiting and
subsequent aspiration]
(12) Hydrostatic lung:
(i) Seen in PM drowning.
(ii) Due to sheer hydrostatic pressure water enters inside the lung and may
simulate true “drowning lung”.
(iii) A dead body immersed for 20 hours at a depth of 2 meters will show
“hydrostatic lung”.
(iv) Differentiating feature is absence of froth in trachea, bronchi and at mouth.
c. Heart and great vessels
(1) Rights side of heart –
(i) dilated.
(ii) Mechanism - Inhalation of water caused obstruction of pulmonary circulation
by obscure mechanisms"back pressure"dilatation of right side of heart.
(iii) Right side of heart and large veins contain dark fluid blood.
(2) Petechial hemorrhages - in subepicardial region posteriorly
(3) Aorta – intima is stained red.
d. Blood
Fluid - due to dilution by
(i) inhaled fluid and
(ii) release of plasminogen activator from damaged endothelium of pulmonary
capillaries.

e. Stomach and intestines

(1) Gastric mucosa – soft and heavy
(2) Water -
(i) Present in stomach in 3/4th and in intestines in 1/4th of all cases.
(ii) Amount should be measured and examined for foreign substances [naked
eye, microscopic]. Also chemically for composition
(iii) Diagnostic value – (a) If chemical and microscopic nature of water is same
as that of drowning medium, it could be a great confirmatory evidence of
drowning. But it could also be due to victim having drunk the same water
before drowning. (b) If the submersion medium was of a filthy or
disagreeable nature, eg contaminated with debris, feces or other undesirable
material, liquid manure or muddy water, then it is of great diagnostic value,
as such water is unlikely to be drunk voluntarily. (c) Water in intestines -
indicate peristaltic movements [a vital phenomenon], but this could again
be due to antemortem ingestion of water.
(iv) Water is absent – if person died due to immersion syndrome, syncope, shock
and in putrefaction.
(3) Foreign matter - May contain algae [including diatoms], grit, mud, sand,
seaweed, silt and waterweed, which would match with that present in water.
(4) Sehrt’s sign - Micro-ruptures of gastric mucosa [rupturae parvulae mucosae
curvaturae ventriculi minoris] due to overstretching of stomach due to
swallowed liquid. Named after German pathologist Sehrt Ernst [born 1879]
who first described them in 1932.
(5) Wydler’s sign - Entire gastric content is collected in a beaker and allowed to
stand for an hour. The contents divide into 3 layers — foam on the top, liquid
in the middle and a solid component at the bottom [Fig 19.29]. First described
in 1869 by Ferdinand Wydler in his book Zur Diagnose des
Ertrinkungstodes.
f. Brain
Swollen with flattening of gyri.
g. Temporal bone and middle ear
(1) Hemorrhages - in the petrous and mastoid regions of the temporal bone.
The hemorrhages are localized in the mucosa of the middle ear and mastoid
cells. Incidence – 50%.
(2) Mechanisms:
(i) - venous and capillary pressure - owing to respiratory efforts against a
closed glottis
(ii) penetration into the middle ear of inhaled liquid via the eustachian tube –
due to violent efforts at inhalation
(iii) barotrauma, i.e. -ed pressure.
(iv) Conditions in which temporal bone hemorrhages are seen – (a) CO
poisoning (b) drug overdose (c) Hanging (d) Strangulation (e) MI (f) Head
 injury. Thus they are not pathognomonic of drowning.
h. Paranasal sinuses
There is free liquid in the paranasal sinuses - most commonly in maxillary and
sphenoid [Sveshnikov’s Sign]. Named after Russian pathologist Sveˇšnikov
Vjacˇeslav Alexandrovicˇ [1918-1988], who first described it in 1965.
i. Spleen
(1) Small (<0.2% of body weight). Due to sympathetic stimulation with
vasoconstriction and contraction of the spleen capsule and trabeculae.
Contraction of the spleen during breath-hold apneas and diving has been
observed in humans. Victims of drowning tend to hold their breath"splenic
contraction.
(2) Drowning index [DI] -
D.I. =
Weight of both lungs and pleural effusion
Weight of spleen

Values are ≥14.1 in drowning and much below this figure in non-drowning
deaths.
(3) Sabinsky’s sign [splenodystrophia anemica] - Small, anemic spleen seen in
cases of mechanical asphyxia, especially in drowning. First described by
Russian pathologist Z J Sabinsky in 1865. He directly observed spleen in
animals being killed by asphyxia, and found that with the onset of asphyxia,
the spleen began to shrink.
j. Muscles
Bruising and rupture – especially of those around shoulder joint [due to violent
efforts].
k. Other organs
Congested.

3. Immunohistochemistry
Microtubule-associated protein 2 (MAP2) – .ed expression in cerebral neurons
[ch 5].

E. Laboratory Tests (of Drowning)

1. Diatoms
Diatoms were first discovered in lungs in a case of drowning by Hofmann in
1896.
a. Description
Diatoms (phylum Bacillariophyta) are microscopic, unicellular, radially or
axially symmetrical algae having a unique cell wall made of silica (frustule) (Fig
19.30).
(1) Pigments - They contain “chlorophyll-a” and carotenoid fucoxanthin.
(2) Habitat - (a) They live in both fresh water and sea water. (b) They also
occur on moist soil and rocks and in (c) atmosphere (d) The vary from place
to place, and there is seasonal variation at the same place.
(3) Size - ranges from 2µ to 2 mm. Most species are from 10-80µ. During
drowning diatoms of <20µ are able to pass through pulmonary circulation into
systemic circulation.
(4) Shape – Boat shaped, circular, crescentic, linear, oval, rectangular or
triangular. Diatom skeletons are readily recognizable as radially or axially
symmetrical structures.
(5) Number - About 200 genera and 100,000 species are known.
(6) Resistant to heat and acid – because of silica walls.
b. Principle
(1) Antemortem drowning (Fig 19.31): Person is respiring"Water enters lungs
along with diatoms" violent respiratory efforts cause rupture of alveolar
walls"diatoms <20µ pass through pulmonary veins and lymph channels"Reach
left ventricle"From here pumped to the entire body"diatoms reach peripheral
organs eg, bone, brain, liver, skeletal muscle, spleen etc, and can be
demonstrated there. Also found in body fluids eg bile and urine.
(2) Postmortem drowning: Person is NOT respiring"Water passively enters
lungs along with diatoms"No violent respiratory efforts"No rupture of alveolar
walls"diatoms found in lungs but NOT in peripheral organs. Diatoms can not
be demonstrated in peripheral organs.
(3) Time of drowning – Different species of diatoms are found in same body of
water in different seasons (summer, winter, rainy season etc).
(4) Site of drowning – In a free flowing body of water, different species of
diatoms are found at different places. By examining the species of diatoms,
one could opine, where exactly the person was drowned. This new field,
where legally relevant information can be derived from diatoms is known as
forensic diatomology.
c. Controversies
Diatoms may be found in bone marrow and organs due to mechanisms other than
drowning.
(1) Air borne diatoms – Diatoms are present in air too, which all persons keep
respiring during life. They can enter circulation through pulmonary capillaries
(2) Ingested diatoms – Diatoms are present in drinkable water such as from
wells and that which comes in tap water. They can enter circulation through
frank ulcers or micro abrasions in the GIT.
d. Methods of extraction
(1) Direct digestion of material:
(i) With corrosives [HNO3, H2SO4]
(ii) Enzymatic digestion with proteases such as proteinase-K - -es the yield, as
the method is less destructive. Even soft bodied algae and protozoa can be
recovered.
(iii) strong anionic detergents such as sodium dodecyl sulfate (SDS) and
hydrogen peroxide - advantages as in enzymatic digestion
(iv) simply heating soft tissues in a water bath overnight
(2) Indirect digestion of material –
(i) incinerate material in electric oven"dissolve the ashes with corrosives as
above
(3) Ultrasonic radiation - to solubilize tissue
(4) Direct microscopic examination:
(i) Lungs – Water is squeezed from lungs"squeezed water centrifuged"sediment
examined. Diatoms found in other tissues must be of same species as seen
here
(ii) Other tissues – microscopic examination shows optically empty sections.
(5) Membrane filtering method (blood samples) – Obsolete now.
e. Reference water samples
(1) About 2000 ml of water sample should be collected from the suspected site
of drowning and stored in the refrigerator as a reference sample.
(2) 15 mL of iodine soln is added to kill microorganisms
(3) Allowed to settle overnight
(4) Next day most of the top layer of water is poured off. Remainder centrifuged
to recover diatoms.
f. Technique
(1) Bone marrow of long bones - is highly reliable and suitable for
demonstration of diatoms. Femur and sternum are the most useful and least
 contaminated samples for this test; If not available for some reason tibia,
humerus, radius, ulna etc can be used.
(2) Removal of marrow:
(i) The bone is washed in distilled water
(ii) Periosteum removed
(iii) A piece of rectangular bone is removed with a sharp and clean knife
(iv) Marrow is curetted out from the gutter [Fig 19.32]

(3) Soft tissues – brain, kidney, liver are washed and 1x1 cm pieces cut from
deeper tissues.
(4) Digestion:
(i) 5 g of bone marrow or soft tissue is put in separate test tubes
(ii) Covered with 5 times the volume of Conc HNO3.
(iii) Left at room temp for 1-2 days
(iv) All organic tissues are dissolved but not diatoms as they have silica shells
(5) Centrifugation:
(i) Tube containing digested tissues is centrifuged
(ii) Supernatant acid poured off
(iii) Replaced with distilled water
(iv) The process repeated 2-3 times to dilute the acid
(6) Examination – Deposit examined under phase contrast microscope or dark
ground illumination. Diatoms examined. If they match those recovered from
water, antemortem drowning is established.
g. MLI
(1) Controversial cases - Diatom test is not conducted routinely. In
controversial cases, when a body is sent for 2nd postmortem examination, it is
usual for the 2nd pathologist to conduct diatom test.
(2) Diatom test assumes importance when only bones or isolated parts, eg a
limb is recovered from water. In such cases despite the fact that soft tissues
[lungs etc] are not available, death by antemortem drowning can still be
determined.
(3) Rarely when entire body is available but PM signs are ambiguous, diatom
test is employed.

2. Examination of blood
Principle: Blood tests used in the diagnosis of drowning depend on the fact that
if the person was respiring during drowning (antemortem drowning), water will
enter lungs, and through ruptured alveolar capillaries reach the left heart. The
blood in left heart will thus reflect several physical and chemical changes,
depending upon the constitution of water (Fig 19.33). Right heart would not
show corresponding changes. Objections to blood tests: In the presence of a
patent foramen ovale (seen in about 1/3rd of all people), blood in the two
chambers would mix and differences would not be seen.
a. Physical tests
(1) Specific gravity - In all cases of drowning, irrespective of the salinity, the
SG of the left atrial plasma is < SG of the right atrial plasma. Difference of
0·003 and above is significant.
(2) freezing point and electrical conductivity of blood in the left side of heart
would be different from that in the right side, due to hemodilution. First used
in 1902 by Carrara.
b. Chemical tests
(1) Chloride estimation (Gettler’s test)- Sea water contains 1940 mg% NaCl.
Human blood contains 340-370 mg%. Fresh water contains close to 0 mg%.
Drowning in sea water (having -Cl- than blood) will -chloride levels in left
heart. Drowning in fresh water (having .Cl- than blood) will .chloride levels
in left heart. Difference of Cl- levels in the two sides of heart should be >20
mg% to arrive at a diagnosis of drowning. First used in 1921 by Alexander
O. Gettler (1883-1968), Chief Medical Examiner of New York City.
(2) Magnesium - Sea water contains more Mg than in blood. Just like Chloride,
Mg+ also shows same differences. First used in 1944 by Moritz.
(3) Strontium - Same principle. Strontium levels in sea water are 8000 µg/L
compared to that in blood (30 µg/L). Fresh water contains virtually same
amount as that in blood. Strontium level - in the left heart in sea water
drowning. A difference of >20 µg/L denotes drowning in sea water.
(4) Other components - (a) Bromide - The bromide conc of sea water is 65–68
µg/mL, approximately 7500 to 10,000 times higher than that of river water or
 blood from normal healthy individuals. Has been used in diagnosis of
drowning. (b) Industrial waste – Chemical compounds discharged as industrial
waste [oils, hydrocarbons] into waterways may enter lungs during course of
drowning and may act as a diagnostic guide.

F. The Circumstances of Drowning

Manner of death cannot be interpreted from autopsy alone. History, scene of
crime examination, autopsy and toxicology examination all must be pieced
together to reach a conclusion.
1. Accidental drowning
Drowning accounts for more accidental deaths in children and adolescents than
all other causes except motor vehicle accidents. Causes – (1) accidental fall of
non-swimmer in water, (2) alcohol or drug use, (3) hypothermia (4) lack of
supervision, (5) Natural diseases, eg cardiac arrhythmias, (6) seizures (7) trauma
[before or during submersion].
2. Suicidal drowning
(1) Prevalence - Common in India, among women, in localities nearby water
reservoirs [Canal, Lake, River, Sea]
(2) Clothed or unclothed:
(i) Women suicides are generally body fully dressed [Nude female bodies often
indicate homicide]
(ii) In a non-swimmer, naked body suggests suicide (iii) Suicides usually remove
some of their outer clothing or shoes before leaping into water
(3) General behavior:
(i) Multiple suicidal methods – sometimes a person may resort to other suicidal
methods [cut throat, poisoning, stab] before drowning himself, either to
hasten death, or if the first method failed
(ii) Body found with heavy weights attached to it – homicide or suicide. But in
children homicide alone.
(iii) Nature of weights, whether tied by ligature for fixed in clothing or found in
the pockets are important
(iv) Sometimes suicides tie their hands or legs together. In such cases manner of
tying, knot of rope or ligature should be examined to determine if such
knots could be tied by the person himself [Forensic knot analysis - ch 30].
Complicated knots may be within a particular profession only [eg sailor’s
knot]
(4) Shallow water:
(i) Generally drowning in shallow water [from where victim could have easily
retrieved himself] indicates homicide.
(ii) Rarely mentally unsound, drunk or drugged persons may accidentally drown
in shallow water.
(iii) Still rarely suicides may drown themselves in shallow water; sometimes
 even by putting the head in a pail or cistern.
(5) Case study - English writer Virginia Woolf [1882 –1941] committed suicide
on 28 Mar 1941 by drowning. She put on her overcoat, filled its pockets with
stones, and walked into the River Ouse near her home and drowned herself.
Her body was found 3 weeks later, on 18 Apr 1941.
3. Homicidal drowning
(1) Homicidal drowning:
(i) Victim is forcibly pushed under water to drown him.
(ii) Infants and children can be easily pushed under water.
(iii) If the victim is an accomplished swimmer, a heavy weight may be tied to his
body.
(iv) An adult may first be made unconscious [eg by hitting him over the head].
(2) Postmortem submersion -Person is first killed by some other means
[poison, strangulation, head injury etc]"Dead body disposed off in water, in
the hope that police would think it was a case of accidental drowning [Table
9].
(3) Drowning in shallow water - eg ankle deep rivulet strongly suggests
homicide, although rarely it may be suicidal [please see above]. If head injury
is found, both accidental and homicidal drowning are possible
(i) Accidental - (a) with head injury - the victim slipped"sustained head
injury"lost consciousness"drowned in shallow water. (b) with or without
head injury - victim under influence of alcohol, drugs, or collapsed from
natural disease [MI, epilepsy]"drowned
(ii) Homicidal - (a) Victim’s head forcibly held under water by assailants till he
drowned (b) victim was struck on the head homicidally"lost
consciousness"dumped in water to drown. For differentiation, other features
must be looked for eg signs of struggle [torn clothes, scratches, bruises etc],
circumstantial evidence etc.
G. Duration of Submersion
(1) Temp - Body heat is lost about twice as rapidly in water than in air
(2) Putrefactive changes -
(i) 2 hours"Wrinkling of skin starts
(ii) 12 hours" Bleaching of cuticle
(iii) 24 hours"Bleaching, corrugation and soddening of cuticle becomes very
much pronounced
(iv) 48 hours"Cuticle begins to separate from palm of hand and sole of foot
(v) 3-4 days"Cuticle can be peeled off like a glove
(3) Rate of putrefactive changes:
(i) twice as slow in water as in air - as long as body remains in water [lesser
number of putrefactive microbes in water; no availability of air for
putrefactive processes] [Casper’s dictum – ch 9].
(ii) twice as fast as in air - when body is retrieved and exposed to open air
[excessive water soaked in tissues facilitates microbial activity].
(4) Time of floatation:
(i) Mechanism - As putrefaction advances, gases of decomposition make the sp
gr of body less than of water and it comes up.
(ii) Time of floatation is the period in which a body [untied with any weights]
would come up to the surface of water.
(iii) Time of floatation depends on (a) Salinity of water – In salt water bodies
float earlier (b) Sp gr of body – infants and obese persons float earlier
[more fat".sp gr] than thin and heavily framed persons
(iv) Position at the time of floatation - (a) Normally – spine uppermost (b) Obese
persons and women – face up. Due to fat and gas in breast and abdomen
(v) Place of floatation – (a) generally same as the place of drowning. Body does
not move much under water, unless there are strong currents (b) When body
comes up and is not discovered immediately, then it may move away
considerably.
(vi) Time period in India - floatation occurs in (a) 12-18 h in summer (b) 18-36 h
in winters.
(vii) In colder countries - the period is 2-7 days depending on temperature of
water.

20. Starvation

I. INTRODUCTION

Starvation is a severe reduction in nutrient, vitamin and energy intake that

occurs either from withholding of food or from administration of unsuitable
food.
Salient features:
(1) Types: (i) Acute starvation - withholding of food is sudden and complete.
(ii) Chronic starvation - withholding of food is gradual. Chronic
malnutrition, as occurs in poor, deprived sections of society.
(2) Inanition - Symptoms and effects of starvation.

II. CAUSES

A. According to Etiology
1. Circumstantial causes
(1) Poverty [most common cause in India]
(2) Fasting
(3) Accidental: (i) earthquakes (ii) famine [failure of crops, overpopulation,
war] (iii) landslides (iv) lost in desert or jungle (v) marooned on island (vi)
shipwrecks (vii) trapped in mines and pits etc.
2. Medical causes
(1) Ankylosis of jaw (2) Alcohol and drug addicts [partial starvation only. Food
is ignored due to overwhelming desire for drug. In alcoholics calories are
supplied by alcohol, so no food intake " protein malnutrition] (3) Anorexia
nervosa (4) Bulimia nervosa (5) cancer and stricture of esophagus (6) Coma
(7) Diabetes mellitus (8) Digestive diseases (9) Mental illness [Major
depressive disorder, paranoid schizophrenia, senile dementia].
3. Miscellaneous
(1) Eccentrics may refuse to eat food for no reason.
(2) Ignorance, witchcraft etc – parents either do not provide food, or do not
provide food of right kind.

B. According to Manner
1. Accidental starvation
Same as mentioned above [circumstantial causes].
2. Suicidal starvation
(1) Fasting - (i) political reasons [fast unto death] (ii) purely exhibition.
(2) Mentally ill and hysterical persons - often do not take food.
3. Homicidal starvation
Withholding of food from unwanted children, step children, illegitimate children,
child abuse, elderly people, feeble minded, jail inmates etc.
III. SYMPTOMS AND SIGNS

A. Acute Starvation
Starvation is an acute severe form of primary PEU [Protein-Energy
Undernutrition].
1. Clinical
a. 30-48 hours
(1) Feeling of hunger
(2) Pain in epigastrium, which is relieved by pressure.
b. 4-5 days
(1) General: (i) Temp – subnormal (ii) Voice – weak, whispering (iii)
Absorption of s/c fat and emaciation – (a) Cheeks - sunken (b) Eyes – sunken,
glistening. Pupils dilated (c) Bony prominences - become visible (d) Chest –
ribs prominent, concavities in intercostal spaces, [Fig 20.1] supraclavicular
fossae sunken (e) Abdomen - concave and scaphoid [boat shaped] [Fig 20.1]
(f) Limbs – thin, flaccid, loss of muscular power (g) Muscular weakness –
progressive, severe (h) Loss of wt – Marked. (iv) Odor – offensive, especially
towards death.
(2) Dermatologic: (i) Skin - dry, inelastic, pigmented, rough, thin, wrinkled.
Shows follicular hyperkeratosis and trophic skin changes (ii) Hair and nails –
brittle, dry, lusterless, hair loss.
(3) CVS: (i) Cardiac insufficiency (ii) Pulse – slow at rest; paroxysmal
tachycardia on exertion
(4) GIT: (i) Lips – cracked, dry (ii) Tongue – coated, dirty (iii) Thirst –
intolerable (iv) Saliva – Scanty, thick (v) Motility - Initially constipation.
Diarrhea and dysentery towards death.
(5) Genitourinary: Urine – acidosis, highly concentrated, scanty, turbid
(6) Intellect: (i) Generally clear till death (ii) In some cases – delusions and
hallucinations of sight and hearing.
c. >5 days
(1) 1st stage - Initially rapid mobilization of protein stores " converted by liver to
glucose to maintain energy supply to brain [which can utilize only glucose]
(2) 2nd stage – . in the utilization of proteins; shift to fat metabolism
(3) 3rd stage – As complete depletion of fat stores occur, metabolism is again
shifted to proteins.

2. Lab investigations
Same as in chronic starvation below.

B. Chronic Starvation
1. Clinical
Changes occur in a constant order (1) . ed resistance to infection " diarrhea,
dysentery, tuberculosis (2) - ing cachexia (3) Anemia (4) Edema – begins first in
lower limbs and feet (5) Fatigue, lethargy [mental and physical] (6)
Hypotension, peripheral vascular stasis (7) Loss of hunger, hunger pains, well-
being (8) Loss of wt – progressive; rapid in first 6 months (9) Mental faculties –
gross mental retardation, loss of self-respect (10) Pigmentation (11) Polyuria
(12) Temp ..
2. Lab investigations
(1) Blood:
(i) Alkaline phosphatase, Angiotensin Converting Enzyme [ACE], calcium,
chlorides, cholesterol, glucose, iron binding capacity [transferrin levels],
Mg, phosphate, Proteins, Sugar, T3 - .
(ii) Ketones [acetone], NPN, urea - -
(2) Urine – Ketones present, pH ..

IV. CAUSE OF DEATH

(1) Causes of death are: (i) Circulatory failure due to brown atrophy of heart (ii)
Exhaustion (iii) Intercurrent infections
(2) Contributing factors are: (i) Dehydration (ii) Hypothermia.

V. FATAL PERIOD

(1) In number of days:

(i) Both water and food are completely withdrawn " 10 days [both adults and
newborns]
(ii) Only food withdrawn " 60 days
(iii) Only water withdrawn " 10 days [happens rarely when a camper is lost in
desert, has good food supply but no water].
(2) By % loss of body reserves – Loss of
(i) 20% protein (ii) 40% total body wt and (iii) 80% fat is fatal.

A. Factors Influencing the Fatal Period

All following conditions [Table 1] can be understood by the fact that - ed fat
reserves and . ed expenditure mean more survival and vice versa.
VI. PM APPEARANCES

(1) General:
(i) Ascites [in 10% cases]
(ii) Edema - under the eyelids, cheeks and chin, inside the thigh and around
ankles
(iii) loss of s/c fat and emaciation – extreme. Gives rise to (a) sunken eyes and
cheeks, (b) bony prominences [eg clavicles, tips of shoulders, ribs, anterior
superior iliac spine] are more prominent. (c) Chest - ribs prominent,
concavities in intercostal spaces, supraclavicular fossae sunken (d)
Abdomen - concave and scaphoid (e) Limbs – thin, flaccid (f) Wt - . ed
more than 40%
(iv) Intercurrent diseases, superadded infections due to loss of vitality (e) Odor –
offensive, especially towards death
(2) Rigor mortis – sets in and disappears early
(3) Face – pale
(4) Dermatological:
(i) Skin – dry, inelastic, pigmented, rough, thin, wrinkled. Shows follicular
hyperkeratosis and trophic skin changes
(ii) hair and nails– brittle, dry, lusterless
(5) Fat:
(i) Complete absent from around internal organs, and in mesentery, omentum,
and s/c tissues. This is never seen in wasting diseases eg cachexia and
tuberculosis.
(ii) disappears late from – fat of female breast, around orbit
(iii) subepicardial fat – replaced by watery gelatinous material
(6) Muscular system:
(i) Muscles - atrophied and dark due to - in lipochrome
(ii) Fibres – (a) lose striations, (b) become more uniform due to granular
degeneration
(7) Skeletal system:
(i) Children - (a) Dental defects [eg caries, decalcification] (b) Rickets (c) Spinal
curvature
(ii) Adults - (a) Osteomalacia
(iii) in both – (a) Demineralization of bone (b) stress fractures
(8) Viscera [general]:
(i) Great . in size and wt of all organs, except brain [changes similar to those in
senility]
(9) Heart:
(i) small [due to brown atrophy]
(ii) chambers empty
(10) Lungs: (i) collapsed (ii) edematous (iii) pale (iv) on cut section – exude
very little blood, show hypostatic basal congestion
(11) GIT: (i) Lips – cracked, dry (ii) Tongue – coated, dirty (iii) stomach and
intestines show atrophy of all layers (iv) intestines – (a) walls appear like
tissue paper, very friable to touch and break easily (b) mucosa – shows
extensive non-specific ulceration as seen in ulcerative colitis (c) contents –
offensive watery fluid and gas (v) mucosa – stained with bile
(12) Liver: (i) atrophied (ii) shows necrosis due to protein deficiency
(13) Gall bladder – distended with bile [no food in duodenum " no
cholecystokinin " no contraction of GB].
(14) Spleen – shrunken
(15) Renal system: (i) kidneys – atrophied (ii) urinary bladder – empty [cf gall
bladder].
(16) Brain – wt retained [unlike other organs], pale, soft
(17) Blood: (i) Volume – marked reduced (ii) anemia – hypochromic microcytic
(18) Special investigations – Blood and urine findings same as given in ch
starvation above.

VII. D/D AT AUTOPSY

(1) Diseases which cause loss of wt - Addison’s disease, AIDS, anorexia

nervosa, chronic diarrhea, diabetes mellitus, food intolerance,
hyperthyroidism, malabsorption syndromes, malignancy, pernicious anemia,
progressive muscular atrophy, pyloric stenosis and tuberculosis.
Differentiation - (a) In none of the above diseases, marked absence of fat
[especially around orbits and from female breast] as in starvation would be
noted. (b) Specific findings of each disease would be evident
(2) Sometimes disease is both the cause and effect, setting up a vicious cycle, eg
TB " malnutrition " accentuation of TB. Primary cause of death may be given
as that which shows more marked features.

VIII. MEDICOLEGAL ASPECTS

Hunger strikes – Medicolegal issues arise when a political prisoner goes on a

hunger strike and the jailor requests the jail doctor to force-feed the prisoner in
order to save his life. (i) The current legal situation in India appears
ambiguous according to IPC (a) Force feeding - doctor may be sued for using
criminal force u/s 350, 352, IPC. (b) No force feeding - doctor may be sued for
abetment of suicide (u/s 306, IPC). (ii) Indian constitution – Article 21 ensures
right to life; there is no equivalent right to die. Since Indian Constitution is
supreme, force feeding of hunger-strikers is lawful in India. (iii) Criteria for
force feeding – appearance of ketones in urine (iv) World Medical Association
Guidelines – The situation is reverse. WMA has given guidelines to doctors in
its Declaration of Tokyo (adopted in 1975; amended in 2005) and Declaration
of Malta (adopted in 1991; amended in 1992). Both respect the autonomy of the
patient, and suggest that the doctor should NOT force feed in such cases.
Feeding is allowed, when patient has lapsed into coma.

21. Deaths Associated with

Anaesthesia
and Surgery

I. FATAL BLOOD CONCENTRATIONS

(1) Chloroform - Pl see ch 40

(2) Diethyl ether - 180 mg%
(3) Divinyl ether - 50 mg%
(4) Ethyl chloride - 40 mg%
(5) Halothane - 20 mg%
(6) Trichloroethylene - 50 mg%
Memory Aid 1: Fatal blood concentrations of anesthetics
It is useful to remember fatal blood concentrations of anesthetics in relation to that of alcohol, which is
500 mg%. Now remember following 2 mnemonics:
1. The following mnemonic outlines 3 imp anesthetics which have 1/10th of this concentration, i.e. 50
mg%.
Three can form diving ethics
Three can = trichloroethylene
Can form = chloroform
Diving ethics = divinyl ether
2. Hell = halothane. Hell should be worst. So it has lowest fatal concentration [20 mg%], i.e. 1/25th of that
of alcohol.

II. CAUSES OF DEATHS ASSOCIATED WITH ANAESTHESIA

AND SURGERY
Anesthesia may be general, or of some specified type. The causes of general
anesthetic and operative deaths are (Table 1):

A. Deaths Associated with Anesthesia

(1) Inexperience – Many deaths occur due to inexperience and failure to adopt
precautions when clearly indicated
(i) Inadequate depth of anesthesia – Intubation and bronchoscopy may cause
vagal inhibition if depth of anesthesia is inadequate
(ii) Inadequate ventilation – Hypoxia, sudden death due to heart failure
(iii) Post-operative respiratory obstructions – by tubing or swabs.
(iv) Breathing circuit disconnections
(v) Between staff
(vi) Haste
(vii) Distraction
(viii) Excessive pressure on airway – rupture of lungs
(ix) Positive pressure ventilation – converts a simple pneumothorax into tension
pneumothorax
(x) Intubation of esophagus instead of trachea
(2) Clinical factors -
(i) Underventilation
(ii) Low blood volume
(iii) Inadequate transfusion
(iv) Anoxia (causes cerebral damage)
(v) Inadvertent hypothermia
(vi) Hyperpyrexia
(vii) Inhalation of regurgitated material (vomit), especially during the post-
operative period
(3) Technical mishaps -
(i) Administration of incompatible blood
(ii) Infusion of wrong drug or fluid (a) sodium citrate for normal saline. They
are both colorless and have virtually similar labels. To avoid such errors,
use distinctive labels and keep in separate cupboards (b) Anesthetic of
greater strength than required (c) ether injected in error for a local
anesthetic. Label should be checked as well as odor to prevent such
incidents (d) Administration of adrenaline in error for cocaine
(iii) equipment failure
(iv) Inadvertent inhalation - of gauze and other swabs, dentures
(v) Mislabeling of Oxygen and anesthetic gases
(vi) Explosions and fires – Ignition of inflammable anesthetic vapor by an
electrical spark. Most dangerous inflammable mixtures are cyclopropane-
oxygen and ether-oxygen. The spark may arise from a faulty electrical
appliance, X-ray apparatus, static electricity or from a surgical diathermy
electrode.

Common adverse reactions associated with anesthetic agents

Malignant hyperpyrexia (Malignant Hyperthermia)
Malignant hyperpyrexia, malignant hyperthermia (MH) or malignant
hyperthermia syndrome (MHS) is a rare life-threatening condition triggered by
exposure to certain general anesthetics (specifically all volatile anesthetics),
nearly all gas anesthetics, and the neuromuscular blocking agent
succinylcholine.

III. INVESTIGATION OF DEATHS ASSOCIATED WITH

ANAESTHESIA AND SURGERY

A. Preliminary Investigations
1. Visit to the operation room
Check all equipment, preferably in consultation with an independent anesthetist
from a different hospital. Check all valves and containers to ensure that there
was correct mixing of percentages of gases.
2. History
(1) Obtain history of exposure to relevant and potentially toxic chemicals
during (a) the period prior to hospitalization(b) hospital stay (c) Preanesthetic
preparation (d) Anesthesia
(2) Obtain list – of relevant and potentially toxic chemicals associated with each
of these periods
(3) Thorough review of hospital chart
(4) Hold discussions with the surgical and anesthetic team.
3. Existing diseases
Some surgical conditions are high risk per se eg resection of the aortic aneurysm
and repair [surgeon may not be able to control bleeding]
4. Anesthesia
(1) Get information about anesthetic agents used
(2) Check if method of administration was correct
(3) Inadvertent wrong mixing of anesthetic agents may have occurred.
(4) Note duration of time the patient remained under anesthesia. Was it
excessive?
5. Equipment
(1) All equipment including containers, valves etc must be checked in
association with appropriate qualified personnel.
(2) Check is correct mixing of gases was ensured.

B. Autopsy
(1) Examine all devices in situ:
(i) Devices - attached to and inserted into the body must not be removed, either
by the operating surgeon or nurse before sending body for postmortem.
Common indwelling devices encountered are airways, chest tubes,
 indwelling catheters and needles, intravenous cannulae and wound drains.
(ii) Autopsy pathologist - should open cavities with devices in situ, to know
where the other end was reaching [eg intubation device may be in the
esophagus, thoracic drain pipe may be puncturing lung etc]. All devices
must be checked for patency also.
(iii) Fluids in each cavity - Note presence, smell and volume etc. Preserve for
analysis
(2) Examination of operation site – Must be thoroughly examined, although at
times it may be difficult because of surgical alterations of the anatomy as well
as because of the presence of hemorrhage, adhesions, sepsis and edema etc.
(3) Look out for artifactual findings - Sutures from stomach and intestine may
appear to have broken down. It could however be an autolytic change
(4) Surgical errors -
(i) Ligation of a wrong vessel, eg ligation of coronary artery, while implanting a
heart valve prosthesis.
(ii) Inadvertent ligation of ureter, bile duct
(iii) Perforation of large bv
(iv) Inadvertent removal of a vital organ
(5) Brain:
(i) Hippocampal gyrus and cerebellum - show hypoxic changes. The Ammon’s
horns [syn, Cornu Ammonis, CA, hippocampus] are particularly
vulnerable, especially the Sommer sector [region CA1] and to a slightly
less extent, the endfolium. The selective necrosis in the Sommer sector may
be identifiable macroscopically if the patient survives for more than a few
days.
(ii) Diffuse severe leukoencephalopathy of cerebral hemispheres with sparing of
immediate subcortical connecting fibres
(iii) Demyelination and obliteration of axon
(iv) Infarction of basal ganglia
(v) Damage is limited to white matter.

Samples to collect
(1) Blood - For grouping, cross matching etc. Collect blood of deceased,
transfused blood, empty and half empty blood bags etc
(2) For culture - exudates, pus
(3) Samples from all organs - Histopathology
(4) For toxicology - Both lungs must be tied and submitted for toxicological
examination [ch 5]. Other viscera as in standard toxicology death.
(i) Alveolar air - collection procedure as given in ch 5.
(ii) Gases from cavities, heart and blood vessels - Fill body cavity with
water"use a rubber dam to trap gases before cutting the organ.

IV. LEGAL ASPECTS OF ANESTHESIA

A. Legal Responsibilities of an Anesthetist

Role during illegal surgery:
(1) It is the duty of anesthetist to refuse anesthesia during illegal surgery [eg
illegal MTP, organ retrieval, amputation of healthy limbs for making beggars
etc].
(2) He cannot claim he did not know the nature of surgery because during
preanesthetic check-up he must have discovered it.
(3) He must bring it to the notice of legal authorities.
(4) If he administers anesthesia during illegal surgery he is a party to crime.

22. Deaths Due to Cold and Heat

I. COLD

Hypothermia is a condition in which core (rectal) temperature drops below 35.0

°C (95.0 °F). This is the minimum temperature required for normal metabolism
and body functions.

A. Stages of Hypothermia

B. Cause of Death
(1) Failure of vital centers - due to anoxia
(2) Cessation of heart function – due to atria1 and ventricular fibrillation.

C. Local Effects
Local effects are divided into two groups -
(1) those that occur without any freezing of the body tissues, e.g. chilblains
(pernio) and trench foot (immersion foot), and
(2) those that result from the freezing of the skin or a body part (generally the
fingers, toes, ears, nose and cheeks).

1. With tissue freezing

Frostbite
Frostbite (congelatio) is a cold-related injury characterized by freezing of
tissues.
Salient features:
(1) It occurs at temperatures below 0°C.
(2) Mechanism: (i) Ice crystals form in the skin and deeper tissues. (ii) These
 exert osmotic force, causing water to move from intracellular spaces. (iii)
This in turn, causes swelling of tissues (filling up of intercellular spaces with
fluid). (iv) At the same time there is cellular dehydration, hyperosmolarity,
denaturation of proteins and destruction of enzymes.
(3) Signs and Symptoms: Skin - numb and discolored; it is purple in most
severe cases. Blisters appear, which may become hemorrhagic. On touching
the skin, it does not feel like normal “bouncy” skin; instead it feels just like a
rock, block of ice or like a piece of chicken from the freezer.

2. Without tissue freezing

a. Trench foot (immersion foot)
Trench foot is a condition caused by prolonged exposure of the feet to damp,
unsanitary and cold conditions.
Salient features:
(1) The word “trench” refers to trench warfare, used in World War I, where many
soldiers suffered from this condition.
(2) Predisposing factors: (i) Temperature: 5-8°C. (ii) Dampness
(3) Signs and symptoms: (i) In uncomplicated cases, there is no permanent
injury. (ii) The affected feet become numb (iii) turn blue (cyanosis) or red
(erythrosis) and (iv) may swell. (v) Advanced condition involves blisters and
open sores, which lead to fungal infections; this is sometimes called tropical
ulcer [jungle rot] (vi) If left untreated, trench foot usually results in gangrene,
which may require amputation.
b. Chilblains
Also known as pernio and perniosis. There is redness and inflammation of
skin. Acral ulcers (ulcers affecting digits and toes) form. These are due to
constriction of capillary beds in the skin.
D. Causes of Hypothermia
LPG - Liquefied petroleum gas [syn, autogas, LPG] is now a commonly used
commercial vehicle fuel [it is different from CNG]. It consists of a mixture of
propane [C3H8] and butane [C4H10] which when moderately compressed turns
into a liquid at atmospheric temperature and then reverts back to a gas when the
pressure is sufficiently reduced. It is cheaper and more environmental friendly
than petrol or diesel. Motor vehicles can now be purchased to run on LPG or,
more commonly, they are converted from running on petrol or diesel. Its
operating temperature is extremely low. The boiling point is between -42° and
0°C, depending on the hydrocarbon mix. Owing to its rapid vaporization and
consequent lowering of temperature it can cause severe cold injuries if brought
into contact with the naked skin. Several cases of cold injury following skin
contact with LPG at filling stations have been described., Mostly the accident
occurs due to vapor leak between the gun nozzle and fuel tank.

E. PM Appearances
1. External
(1) Skin:
(i) PM staining is reddish. Mechanism - OxyHb cannot give up O2 because of
excessive cold [The oxygen dissociation curve of Hb shifts to the left side
at low temperatures] " Diffuse through skin " Causes reddish color
(ii) Even non dependent areas show pink, brown pink or violet patches with
indistinct blurred margins, especially over and around joints [eg knees,
elbows, hips]. Mechanism " These are hyperemic areas, which develop just
prior to death as the skin is pressed against snow or cold ground. Mental
confusion leads to uncoordinated movements eg crawling.
(iii) In some cases, skin may be completely white [“white death”]
(iv) Sometimes spots of bluish discoloration are seen on hands, elbows, knees
and feet [represent minor frostbite lesions].
(v) Histology – edema and hyperemia of dermis, foci of inflammatory cell
infiltration
(2) Generalized edema - Swelling of ears, hands noticeable. Mechanism - Cold
injury " capillaries are damaged " leaking of plasma into the tissue
(3) Cold stiffening [syn cold rigor]:
(i) Body fluids, fats and tissues are frozen, solidified and stiff due to extreme
cold, giving rise to a stiffened posture.
(ii) May be confused with rigor mortis
(iii) Differences from rigor – Table 3.
(iv) Freezing with subsequent hardening of s/c fat, especially in infants
sometimes makes the skin folds rigid, which may be mistaken for ligature
mark [pseudoligature mark - ch 19].
2. Internal
(1) Blood: (i) Bright red (ii) Intravascular hemolysis [seen after freezing of
blood]
(2) Skull – ice inside skull may cause separation of skull sutures.
(3) Brain – Cytotoxic cerebral edema [ch 17].
(4) Heart:
(i) Ice crystals present [also in bv and interstitial tissue spaces].
(ii) Right atrium and ventricle dilated.
(5) Lungs:
(i) Congested
(ii) Intra-alveolar, interstitial, and intrabronchial hemorrhages
(iii) Bronchopneumonia
(6) Stomach:
(i) Mucosa studded with numerous brown-black acute erosions.
(ii) Similar to those seen in stress.
(iii) First described by Wischnewski in 1895 [known as Wischnewski erosions,
points, spots or ulcers.].
(iv) Mechanism - (a) stress (b) -ed tissue amines, histamine and serotonin. (c) -
in capillary permeability (d) impairment of the blood flow in the GIT
mucosa (e) . in O2 dissociation.
(7) Pancreas:
(i) Fat necrosis [most constant finding]
(ii) Aseptic pancreatitis
(iii) Pancreatic hemorrhage.
(8) Adrenals – Lipid depletion from the adrenal cortex.
3. PM chemistry
(1) Blood - Glucose -ed
(2) Urine - - ed catecholamine [adrenalin, noradrenalin], histamine and serotonin
[quite valuable in diagnosing hypothermia]; - ed glucose
(3) Vitreous:
(i) - glucose [in nondiabetics].
(ii) -CO2. Glucose conc and total CO2 content vary inversely with temp.

F. ML Significance
1. Paradoxical undressing
(1) Def - Refers to a cold-exposed hypothermic person taking off his clothes just
before death. He is found dead in an extremely cold environment, but
paradoxically he is naked, with clothes strewn around.
(2) The phenomenon is rare
(3) It is a terminal event
(4) More common in old
(5) Hide and die syndrome - This may be seen sometimes. Characteristics are
 (a) Person may hide himself in corners, in cupboards, under piles, furniture or
other household goods (b) Naked or seminaked person is found amid a greatly
disturbed scene, with furniture pulled over and drawers and cupboards
emptied out. All disturbance is however at lower levels only. Tops of tables
are not disturbed. May lead a police officer to believe a criminal act has taken
place. Visit to scene of crime by an experienced pathologist is necessary.
(6) Appearance of the body implies a criminal act, especially rape, but no signs
of foul play are there.
(7) Mechanism – (a) Hypothermia " (I) . sympathetic activity of the skin, and (II)
Paralysis of the thermal regulatory mechanism " dilation of cutaneous bv " -
skin temperature " spurious feeling of warmth "Undressing. (b) Terminal
mental confusion, delirium and hallucinations.

II. HEAT
1. Heat edema
Heat edema [syn, Colombo flop, Deck ankles] is a very mild form of heat illness
which appears as dependent soft tissue swelling, usually in the lower extremities,
in a person lacking acclimatization.
2. Heat rash
Heat rash [syn lichen tropics, miliaria rubra, prickly heat] is another very mild
form of heat disorder characterized by rash on anterior surface of elbows,
posterior surface of knees, sternum, clavicle, waist, axillae. Palms and soles are
not affected.
3. Heat cramps
Heat cramps [syn, Cane cutter’s cramps, Fireman’s cramps, Miner’s cramps,
Stoker’s cramps] are severe muscle spasms resulting from a combination of
prolonged exercise, heavy sweating, and excessive water replacement in extreme
heat.
4. Heat syncope
Heat syncope [syn, heat collapse] is a condition resulting from intense peripheral
vasodilatation leading to peripheral pooling and hypotension.
5. Heat exhaustion
Heat exhaustion [syn, heat prostration] is a condition resulting from severe
dehydration after a huge amount of sweat has been lost.
6. Heatstroke
Heatstroke [syn, Coup de soleil (French, lit. stroke of the sun), heat
hyperpyrexia, siriasis, sunstroke, thermic fever] is the most serious heat disorder
characterized by a complete breakdown of thermoregulatory mechanism,
complete loss of sweating and temperature rising >41°C [106°F].
Salient features:
(1) Terms “sunstroke” and “thermic fever” are more often used when there has
been a direct exposure to the sun
(2) Pathophysiology - Heat " renal and splanchnic vasoconstriction with
concomitant peripheral vasodilatation " shunting blood to the periphery [to
dissipate heat] " If exposure to heat continues, the vasoconstriction needed to
keep the blood in the periphery fails " cutaneous blood flow . es " less heat
dissipation " hyperthermia " cerebral edema " ed ICP " .ed cerebral blood flow
" CNS dysfunction. Subarachnoid hemorrhages in some cases.
(3) Factors aggravating heatstroke: (i) absence of a full acclimatization (ii)
alcoholism (iii) drugs [major tranquillizers] (iv) dysentery with resulting
dehydration (v) heavy and impervious clothing (vi) humid atmosphere [at
100% humidity, even a relatively low temp of 32°C may lead to heatstroke]
(vii) infections (viii) muscular activity (ix) no breeze (x) obesity (xi) old age
(xii) toxic pyrexia [recent or present]
(4) Signs and symptoms – onset is sudden with sudden collapse and loss of
consciousness. (i) Prodromal symptoms - Cramps, dizziness, excessive thirst,
faintness, giddiness, headache, general weakness, lack of energy, mental
confusion, nausea & vomiting, purposeless movements, restlessness,
staggering gait (ii) Skin – dry, hot, flushed, cessation of all sweating (iii) Temp
– 42°C [108°F] is common; 45°C [113°F] has been recorded. When temp rises
> 42°C, vasodilatation occurs with . in blood volume " circulator collapse "
cardiac failure (iv) Respiration – rapid [>30/min], deep, Kussmaul type (v)
CVS – (a) BP . (b) Tachycardia; pulse >130/min. Becomes irregular later (vi)
CNS deficit – due to - ed temp (a) bizarre behavior (b) cerebellar dysfunction
(c) Clouding of senses (d) convulsions [generalized or Jacksonian] (e)
decerebrate rigidity (f) delirium (g) Eyes - fixed and dilated pupils, oculogyric
crisis (h) hallucinations (i) muscular twitching (j) opisthotonus (k) speech
difficulties (l) coma.
(5) Prognosis – bad; mortality is very high.
(6) Diagnosis - Based on classical triad of (i) - ed temperature (ii) dry skin (iii)
neurological deficit
(7) Differential diagnosis: (i) Falciparum malaria (ii) Datura poisoning
(8) Management: (i) Move individual to a cooler place (ii) loosen clothes or
undress (iii) allow air to circulate around the patient (iv) wrap individual in
wet towels or clothing (v) Place ice packs in areas with the greatest blood
supply [neck, under the arm and knees, groin] (vi) monitor body temp
constantly to guard against overcooling. If hyperpyrexia continues for > 4
hours, prognosis is bad. Even if the condition is not fatal, the patient may have
permanent neurological deficit. (vii) Monitor HR and RR (viii) IV fluids and
electrolytes (ix) Iced gastric lavage (x) Anti-convulsant [if convulsions] (xi)
After initial treatment, bed rest may be recommended for several days.
(9) Fatal period – 5 min-3 days

a. PM appearances [of heatstroke]

Not specific.
(1) Temp – remains high after death. PM caloricity may be seen.
(2) CNS:
(i) Brain – (a) congested and edematous. (b) Petechial hemorrhages seen in
white matter (c) cerebral hemispheres - (I) show - in weight, (II) flattening
of convolutions (III) Histopathology – [1] Chromatolytic changes [2]
Degeneration of neurons [least in globus pallidus] [3] Microglia – show
diffuse proliferation [4] Pyknotic nuclei [5] Swollen dendrites (d) Scattered
petechiae all over the brain, especially in the walls of 3rd ventricle and floor
of 4th ventricle. (e) Cerebellum – shows most striking and consistent
changes. (I) Purkinje layer – [1] shows edema [2] Purkinje cells – show
disintegration, swelling and reduction in number. [3] If survival is >24 h "
complete degeneration of Purkinje layer and gliosis. (II) Rarefaction of
granule cell layer (f) Hypothalamus – edema of nuclei
(ii) Meninges - congested.
(3) Heart:
(i) Dilatation of right auricle
(ii) Flabbiness of muscles
(iii) Myocardial degeneration
(iv) Petechial or confluent subepicardial and subendocardial petechial
 hemorrhages
(4) RS:
(i) Trachea and bronchi – contain frothy hemorrhagic fluid
(ii) Lungs – Congestion, Edema, hemorrhages, lobular pneumonia [if survival is
more]
(5) Liver:
(i) Centrilobular necrosis
(ii) Congestion
(6) Kidneys:
(i) Short survival - (a) -ed wt (b) Congestion (c) Edema
(ii) Longer survival - (a) Hemoglobinuric nephrosis (b) Tubular necrosis
(7) Adrenals:
(i) Cortical degeneration
(ii) Adrenal and pericapsular hemorrhages
(iii) Sinusoids – engorged
(8) Bone marrow: Degeneration of megakaryocytes [if survival >24h]
(9) General:
(i) Visceral hemorrhages - Mechanisms (a) - ed temperature " hepatic damage "
prothrombin depletion (b) thrombocytopenia and . plasma fibrinogen (c) -ed
capillary fragility due to anoxia
(ii) Disseminated intravascular coagulation.

23. Impotence and Sterility

I. INTRODUCTION

A. Impotence
(1) Impotence is inability of a person to perform sexual intercourse. Impotence
in male is better termed as Erectile Dysfunction (ED).
(2) Potentia copulandi – Power to copulate.
B. Sterility
(1) Sterility is inability to beget or conceive children (in the male and female
respectively).
(2) Infertility is a preferred term. It is used in relation to a couple unable to
beget children, and is defined as failure to conceive following twelve months
of unprotected and regular intercourse.
(3) A person can be impotent without being sterile or vice-versa. Both conditions
may co-exist too.

II. CAUSES OF IMPOTENCE IN THE MALE

A. Psychogenic
1. Generalized
(1) Age related decline in sexual arousability
(2) Generalized unresponsiveness
(3) Primary lack of sexual arousability
(4) Generalized inhibition
(5) Chronic disorder of sexual intimacy.
2. Situational
a. Partner related
(i) Lack of arousability in a specific relationship (ii) High central inhibition
owing to partner conflict or threat (iii) Lack of arousability owing to sexual
object preference (impotence quoad hoc)- Person is impotent towards one
particular woman (say wife), but not towards the rest. This may lead to
medicolegal problems. “Quoad hoc“ is a Latin phrase meaning “As to this” or
“with respect to this”. Thus “impotent quoad hoc” literally means “impotence
with respect to”.
b. Performance related
(1) Associated with other sexual dysfunction/s (eg, rapid ejaculation)
(2) Situational performance anxiety (eg, fear of failure).
c. Psychologic distress related or adjustment related
(1) Associated with negative mood state (eg, depression)
(2) Major life stress (eg, death of partner)
B. Organic
Memory Aid 1: Organic causes of impotence
I = Inflammatory (eg, Prostatitis)
M = Mechanical (eg, Peyronie’s disease)
P = Postsurgical (eg, Radical prostatectomy)
O = Occlusive (eg, Vascular Atherosclerosis)
T = Traumatic (eg, Pelvic fracture)
E = Endurance factors (eg, Chronic renal failure)
N = Neurogenic (eg, Multiple sclerosis)
C = Chemicals (eg, Drug induced - antihypertensive drugs)
E = Endocrine (eg, Diabetes mellitus)
For differences in emasculation and castration and effects of castration before
and after puberty, please see ch 11"Grievous hurt"Emasculation.

III. CAUSES OF IMPOTENCE IN THE FEMALE

[A] Impotence in the female is better termed as Female sexual dysfunction

[FSD]. The American Foundation of Urologic Disease (AFUD) Consensus Panel
in 2000, classified female sexual dysfunction in following 4 groups (1) Sexual
desire disorders - (i) Hypoactive sexual desire disorder (HSDD)- [syn frigidity]
Absence of desire for sexual activity (ii) Sexual aversion disorder - Phobic
aversion to and avoidance of sexual contact with a sexual partner (2) Sexual
arousal disorder - Inability to attain sufficient sexual excitement. (3) Orgasmic
disorder - No orgasm following sufficient sexual stimulation and arousal (4)
Sexual pain disorders: (i) Dyspareunia - Persistent genital pain associated with
sexual intercourse. (ii) Vaginismus - Persistent involuntary spasm of the
musculature of the outer third of the vagina that interferes with vaginal
penetration. (iii) Other sexual pain disorders (non-coital) - Genital pain induced
by non-coital sexual stimulation. In some of the above cases [eg orgasmic
disorders, dyspareunia], intercourse is physically possible; thus would not
amount to legal impotence. Husband cannot sue for nullity if wife suffers from
such conditions [Please also co-relate with male sexual dysfunction above]. [B]
Etiology of FSD – (1) Abnormalities of genitals – eg vaginal atresia (2) cancers
(3) Gynecologic problems (4) Long-term medical diseases (5) medications (6)
psychosocial difficulties, eg vaginismus (7) systemic ailments.

IV. CAUSES OF STERILITY IN THE MALE

(1) Congenital -
(i) Anorchia
(ii) Azoospermia and related conditions [Table 1] [could be acquired too].
(iii) Cryptorchidism
(iv) Congenital Absence of Vas Deferens
(v) Genetic abnormalities - (a) Karyotype anomalies including Klinefelter
syndrome (b) Y chromosome microdeletions (c) Kallmann syndrome (d)
mutations in genes involved in Hypothalamus–pituitary–gonadal axis (e)
Partial/Mild Androgen Insensitivity syndrome)
(2) Acquired -
(i) Acquired hypogonadotrophic hypogonadism or endocrine factors
(ii) Erectile, ejaculatory dysfunction
(iii) Exogenous factors [medications, cytotoxic drugs, irradiation, heat]
(iv) Obstruction, subobstruction of proximal and/or distal urogenital tract
(v) Post-inflammatory forms [orchitis, epididymitis]
(vi) Recurrent urogenital infections [prostatitis, prostatovesiculitis]
(vii) Surgeries that can damage vascularization of the testes
(viii) Systemic diseases [liver cirrhosis, renal failure]
(ix) Testis trauma
(3) Idiopathic -Unknown etiology [about 50%].
Quantity of seminal fluid in a single emission is 1.5 -6.8 ml [ch 23]. Of this
seminal vesicles contribute most [70%]; prostate [25%]; testes [4%], and
bulbourethral glands [1%].
Memory Aid 2: Quantity of semen
Some Professionals Test Bulb
Some – Seminal Vesicles
Professionals – Prostate
Test – Testes
Bulb – Bulbourethral glands
How much contributed
Seminal vesicles – seventy %
Prostate – Pacchis [Hindi for 25] %
Test – 4 letters, so 4% by testes
Bulb – Bulbourethral glands – Last letter “l” looks like 1, so 1% by Bulbourethral

V. CAUSES OF STERILITY IN THE FEMALE

(1) General -
(i) Extremes of age
(ii) Tobacco smoking
(iii) Sexually transmitted disease
(iv) Body weight and eating disorders
(v) Chemotherapy - Alkylating drugs [busulfan, chlorambucil, chlormethine,
cyclophosphamide, ifosfamide, elphalan, procarbazine]
(vi) Other general factors – Cannabis, Significant liver or kidney disease,
Thrombophilia (hypercoagulability or a prothrombotic state)
(2) Hypothalamic-pituitary:
(i) Hypothalamic dysfunction
(ii) Hyperprolactinemia
(3) Ovarian –
(i) Anovulation [anovulatory infertility]
(ii) .ed ovarian reserve [number of eggs that can be successfully recruited for a
possible pregnancy are .ed]
(iii) Gonadal dysgenesis [Turner syndrome]
(iv) Luteal dysfunction
(v) Ovarian cancer
(vi) Polycystic ovary syndrome
(vii) Premature menopause
(4) Tubal/peritoneal – (i) Endometriosis (ii) Pelvic adhesions (iii) PID, [usually
due to chlamydia] (iv) Tubal dysfunction (v) Tubal occlusion
(5) Uterine - (i) Asherman’s Syndrome (ii) Uterine fibroids [leiomyoma] (iii)
Uterine malformations
(6) Cervical - (i) Antisperm antibodies (ii) Cervical stenosis (iii) Non-receptive
cervical mucus
(7) Vaginal - (i) Vaginismus (ii) Vaginal obstruction
(8) Genetic -
(i) Intersex conditions [eg androgen insensitivity syndrome]
(ii) Mayer-Rokitansky-Küster-Hauser Syndrome [MRKH] - Primary amenorrhea
and an underdeveloped uterus. Incidence - 1 in 5,000 females.
(iii) Turner’s Syndrome.

VI. MEDICOLEGAL ASPECTS OF IMPOTENCE AND

STERILITY

A. Law Relating to Marriage in India

1. Hindu Marriage Act, 1955 [HMA]

a. Conditions of a valid hindu marriage
According to S.5 of the Hindu Marriage Act, 1955, (HMA) a total of five
conditions must be fulfilled for a proper legal Hindu marriage (i) No living
spouse - At the time of marriage, neither party must have a living spouse (ii) No
mental illness - At the time of marriage (a) neither party must be incapable of
giving a valid consent to it due to unsoundness of mind (b) though capable of
giving a valid consent, neither party must be suffering from a mental disorder of
such a kind and degree, so as to be unfit for marriage and procreation of children
(c) neither party must be subject to recurrent attacks of insanity. Earlier, there
was a 4th condition – epilepsy – also, but it has been repealed w.e.f. 29 Dec
1999. Currently if either party, or both are epileptic, it is a valid and legal
marriage [ch 28 – Civil responsibilities of the mentally ill]. (iii) Age - The
bridegroom must be above 21 years of age and bride of 18 years of age. (iv) No
prohibited relationship - Both parties must not be within degrees of prohibited
relationship (eg, father and daughter; mother and son; brother and sister; uncle
and niece; aunt and nephew), unless custom allows (v) No Sapindas - Both
parties must not be sapindas [a Sanskrit term meaning “people connected by
particles of one body”] of each other, unless custom allows [Sapinda relationship
extends as far as the third generation (inclusive) in the line of ascent of mother,
and fifth (inclusive) in the line of ascent through the father]. Table 2 summarizes
various conditions of a valid Hindu marriage and what happens when they are
not met with.

b. End of marriage
Under HMA, marriage can end in one of 3 ways -(i) Null and void (ii)
voidable (iii) divorce.
i. Null and void
(1) Rationale behind null and void marriages – Marriages are so morally
degrading that their continuance may be damaging to the society fabric. Thus
they are declared null and void ab initio (S.11 HMA), ie. they are never
 deemed to have taken place legally
(2) When null and void - if conditions (i) , (iv) and (v) above are not met with.
(3) So-called “wife” does not have any right to property, nor is she entitled to
alimony [support money given after divorce].
ii. Voidable
(1) Rationale behind voidable marriages - Law understands that under certain
conditions, one partner may have difficulties living with the other. But the
conditions may not be serious [or morally degrading] enough to cause it to
declare marriage null and void ab initio.
(2) However if the affected party applies for nullity of marriage, nullity may be
granted by the court. Partner is not entitled to alimony etc (S.12 HMA).
(3) Conditions (a) if the marriage has not been consummated (i.e. no
intercourse has taken place after marriage) owing to the impotence of the
other party. Consummation of marriage [also known as vera copula (L. vera,
true; copula, union) - Full sexual intercourse, Real union] is considered an
integral part of marriage (b) if the other party was of unsound mind (c) If the
consent of the other party was taken by force or fraud (d) if the wife, at the
time of marriage, was pregnant by some person other than the husband.
iii. Divorce
(1) Divorce is given after marriage is legally deemed to have taken place
[S.13(1), HMA].
(2) Wife is eligible for alimony.
(3) Grounds - 9 grounds. (A) Things which a spouse does to himself (i) Has
had voluntary sexual intercourse with any person other than his spouse (ii)
Ceases to be a Hindu by conversion to any other religion (iii) Renounces the
world by entering any religious order (B) Things which a person does to
spouse (i) Treats spouse with cruelty [repeated MTPs without husband’s
consent have been accepted by courts as causing “cruelty to husband” (ch 26)]
(ii) Deserts spouse for a continuous period of 2 years (C) Diseases (i) If the
spouse is incurably of unsound mind (ii) If he has been suffering from a
virulent and incurable form of leprosy (iii) If he has been suffering from
venereal disease in a communicable form [eg HIV, AIDS] (D) Others: If he
has not been heard of as being alive for a period of 7 years. In addition to the
above, certain additional grounds are available only to wives u/s 13(2), HMA.
These are: (a) If the husband has been guilty of rape, sodomy or bestiality (b)
 If the marriage of the girl was solemnized before she was 15 years of age, and
upon attaining that age, she repudiated the marriage. She can however
repudiate the marriage only till she is 18 years of age; not after attaining that
age.

2. Prohibition of Child Marriages Act, 2006

(1) Passed to overcome the shortcomings of Child Marriage Restraint Act, 1929.
(2) It received Presidential assent on 10 Jan 2007, and came into effect from 1
Nov 2007.
(3) It -ed punishment of marriage of girls<18 y and boys <21 y, and also made
such marriages voidable. Before 2007 such marriages were neither void, nor
voidable. Doctrine of Factum valet applied [what ought not to be done
becomes valid when done].

B. Questions of Impotence and Sterility

The question of impotence and sterility arises in both civil and criminal matters.
1. Civil
a. Marriage and its termination
(1) Impotence at the time of marriage"
(i) HMA - Marriage is voidable, i.e. if the affected party presents a suit in court
for nullity, the marriage is dissolved [S.12, HMA]. If no such suit is
presented, the marriage may continue.
(ii) SMA – Marriage is void [S.24, SMA]. For a successful suit of nullity, the
impotence should be incurable. If impotence is curable, nullity would not
be granted. In a British case S.v.S.(1962), the wife had vaginal atresia
preventing full intercourse. An artificial vagina could be constructed by
means of plastic surgery, but the husband asserted that it would not amount
to normal sexual intercourse (vera copula). He filed a suit for nullity of
marriage, but it was rejected.
(2) Impotence developing after marriage"Marriage is neither null & void, nor
voidable, nor divorce can be obtained. Divorce may however be sought for
causing cruelty to the partner (as not being able to perform sexual intercourse
may be taken as equivalent to treating the partner with cruelty).
(3) Sterility at the time of marriage"Marriage is neither null & void, nor
voidable, nor divorce may be obtained.
(4) Sterility developing after marriage" Same as (3) above.
b. Fecundatio ab extra
Fecundatio ab extra refers to conception occurring in a woman when the semen
was deposited on her thighs or on the vulva.
Salient features:
(1) Physiology - Impotent person"unable to penetrate vagina"semen deposited
on woman’s thighs or on the vulva"Spermatozoa travel up the genital
passage"pregnancy results
(2) If pregnancy results from fecundatio ab extra, marriage is not said to be
consummated; it can still be annulled on grounds of impotency.
c. Disputed paternity and legitimacy
A sterile male may dispute the paternity and legitimacy of his child [also see ch
24]. Please see ch 29 for solving disputed paternity.
d. Suits of adoption
e. Claim for damages
When loss of sexual function is claimed as the result of assault or accident.

2. Criminal
Rape and Unnatural offences

3. Both Civil and Criminal

Adultery
Adultery is sexual intercourse by a man M with a married woman W, without the
consent of her husband H. Punishment – 5y or fine or both. Wife is not
punishable [S.497, IPC].

VII. STERILIZATION

Sterilization is a procedure to make a person sterile, without interfering with the

potency. It is usually done by vasectomy in the males and tubal ligation in the
females.

A. Classification
1. According to intent
Whether the intent was to produce sterilization.
a. Direct
The operation was intended to produce sterilization
b. Indirect
Sterilization was an unintended result of an operation, eg removal of a bleeding
uterus to save life of a woman [syn, incidental].

2. According to sex
(1) Male sterilization
(2) Female sterilization

3. According to reversibility
a. Temporary [reversible] sterilization
Eg IUCD in females. But this is more appropriately called contraception, rather
than temporary sterilization. Most active research currently is on non-hormonal
male contraceptives.
b. Permanent [irreversible] sterilization
Eg hysterectomy.

4. According to consent
Whether the consent was present or not.
a. Voluntary
Voluntary or elective sterilization is done with the consent of the person. It is of
following types:
(1) Contraceptive – to limit the size of family [family planning]
(2) Eugenic – To prevent conception of children who are likely to be physically
or mentally defective. Done in order to improve race by preventing
transmission of hereditable anomalies, defects and diseases.
(3) Incidental [syn, indirect]– unintended result of a different operation or
(4) Therapeutic – to prevent danger to the life or health of woman during
unintended future pregnancy.
b. Compulsory
Compulsory or forced sterilization is done without the consent of the person,
usually on the order of the State.
Salient features:
(1) When done - Usually done on mental defectives or sex offenders
(2) Legal provisions – There is no legal provision for compulsory sterilization in
India. However during promulgation of Emergency between 1975 and 1977 a
number of persons were compulsorily sterilized in a vain attempt to check
rising population.

B. Methods
(1) Chemical [pharmacological] – There is no “sterilization pill” that causes
permanent inability to reproduce. Antiandrogens [Cyproterone acetate,
Leuprolide acetate, Medroxyprogesterone acetate] are used to reduce libido.
(2) Electrical - Electrocoagulation is used with a laparoscope to burn and block
the tubes. No longer recommended because of risk for internal burns during
the procedure and for ectopic pregnancy after the operation.
(3) Mechanical – A device (hinged or spring clips or a small ring or band made
of silicone rubber) is placed to close and seal each fallopian tube or spermatic
duct.
(4) Radiological – Radiological exposure of testes. Not recommended.
(5) Surgical -
(i) Females – Hysterectomy, Tubal ligation
(ii) Males – orchidectomy [syn, castration, frequently used for the sterilization of
animals, but rarely for humans], vasectomy.

C. Guiding Principles
(1) Consent –
(i) of subject - required. Person should be >18 y
(ii) of subject’s spouse – (a) Not legally required in India, but to avoid marital
discord later, it is advisable for doctor to have written consent of subject’s
spouse also [ch 2"consent of spouse]. (b) Countries requiring spousal
consent for sterilization - Brazil, Chile, Ecuador, Guatemala, Honduras,
Japan, Niger, Rwanda, Taiwan and Turkey. (c) Countries requiring that
spouse be informed - Finland, Hungary, and Switzerland.
(iii) Who cannot give consent - (a) Person <18y (b) Mentally unsound
(2) Legality in India – legal after informed consent
(3) Post vasectomy guidelines – Avoid intercourse for 3 months or until semen
examination shows absence of spermatozoa on 2 consecutive occasions.
Continuous monitoring for 3 months or longer if other methods [chemical,
 electrical, radiological] are used.

D. Medicolegal Aspects
(1) Wrongful birth and life suits:
(i) Wrongful birth suit - If a sterilization operation fails, a person may suffer the
“injury” of being born into the world and may claim damages. Such suits
are generally unsuccessful.
(ii) Wrongful life suit - It is an action brought by or on behalf of a deformed
child against the doctor [defendant], claiming that because of the
negligence of the defendant he or she has to endure a deformed and
unhappy existence. The child in a wrongful life claim does not allege that
the defendant’s negligence caused his or her deformity. Rather, the child
alleges that the defendant’s negligence, in failing adequately to inform the
parents of the risk of a deformed birth, caused his birth. That is, had there
been no negligence, the child would not have been born to experience the
pain and suffering attributable to the deformity. In other words, he or she
would have been better off not being born. [for a variation of wrongly life
suit (illegitimacy), please see ch 24].
(2) Couple may claim damages for the cost of unsuccessful procedure, pain and
suffering as a result of pregnancy, medical expenses of pregnancy, and the loss
of comfort.

VIII. THE DELHI ARTIFICIAL INSEMINATION (HUMAN)

ACT, 1995

The Delhi Artificial Insemination (human) Act, 1995 (Delhi Act no. 12 of
1996) was passed to provide for the regulation of donation, sale and supply of
human semen and ovum for the purpose of artificial insemination. Its main
provisions are (i) All semen banks in Delhi would have to be duly registered
(S.3) (ii) Registration shall be renewed every year (S.4) (iii) On receipt of
application for registration, the Supervisory Authority (Director of Health
Services, Govt of NCT of Delhi) shall, if satisfied, register the applicant and
issue him a certificate of registration (S.5) (iv) If semen bank is run without
registration, there is fine of `5000 on first offence. On second offence or
subsequent offence, there is imprisonment of 3 months or fine of `5000. (S.6) (v)
The semen bank before accepting semen for artificial insemination shall test the
donor for HIV 1 and 2 antibodies by using ELISA kit. Donor shall be allowed
to donate only when found HIV negative (S.10) (vi) The donated semen shall be
stored by cryopreservation in liquid nitrogen or any other safe method for a
minimum period of 3 months in order to exclude window period of HIV 1 and 2
(S.11) (vii) At the end of 3 months, a second ELISA test shall be done (S.12)
(viii) S.14 gives the duties of qualified medical practitioner and Government
hospitals performing artificial insemination. They will (a) keep complete
record of the bio-data including mark of identification of the donor and the
recipient of the semen or ovum; (b) test the recipient for HIV 1 and 2 and
sexually transmitted diseases before performing artificial insemination; (c) seek
the written consent of the husband and the wife, seeking artificial
insemination; (d) seek the written consent of the donor and the recipient and
their spouse, in case of requests of semen or ovum from specified
donor/recipient (e) not segregate the XX or XY chromosomes for artificial
insemination (f) maintain secrecy about the identity of the donor and the
recipient of the semen/ovum; (g) seek the written consent of the recipient for
using the semen on the basis or only one ELISA Test being negative where
facilities for cryopreservation and liquid nitrogen for semen are not available.

IX. ASSISTED REPRODUCTIVE TECHNOLOGY (ART)

(1) Assisted reproductive technology (ART) – Refers to the art and science of
getting gametes together. May be done by artificial or partially artificial
means. May or may not involve third party [eg IVF of parents’ own gametes].
(2) Third party reproduction - Use of oocytes [oocyte donation], sperm [sperm
donation], embryos [embryo donation], or uterus [surrogate motherhood] that
have been provided by a third person (donor) to enable an infertile individual
or couple (intended parent) to become parents. While the donors may be
known or anonymous to the intended recipients depending on the process of
recruitment, surrogates are usually known to the intended parents.
(3) Guidelines for ART in India – have been laid down by ICMR [National
Guidelines for Accreditation, Supervision and Regulation of ART Clinics in
India, 2005 (abbreviated hereafter as - NG, 2005)]. No punishments have been
mentioned. Not following guidelines may at most call for an action by MCI or
 SMC [ch 1].

A. Techniques
1. Artificial insemination
Artificial insemination (AI) is artificial introduction of semen into the
reproductive tract of a female to produce pregnancy.
a. Types
(1) Artificial Insemination Homologous (or Husband) [AIH] – semen of
husband is used
(2) Artificial Insemination Donor [AID] – semen of some person other than
husband is used
(3) Artificial Insemination Homologous and Donor [AIHD] – Pooled semen is
used in which semen of both husband and donor are mixed.
b. Medical aspects
(1) Donor –
(i) advised not to ejaculate for 2-3 days before providing the sample in order to -
the sperm count.
(ii) Tested for HIV, hepatitis B etc. Semen cannot be taken if donor suffering
from these diseases.
(2) Collection of semen –
(i) through masturbation
(ii) use of an electrical stimulator
(iii) use of a special condom [collection condom] to collect semen during
intercourse.
(3) Quarantine - The sperm is quarantined for a period of 6 months. Donor re-
tested prior to AI.
(4) Woman’s menstrual cycle - is closely observed, by tracking basal body
temperature and changes in vaginal mucus, or using ovulation kits,
ultrasounds or blood tests. The time of maximum fertility coincides with that
of ovulation. Ovum can survive for a maximum of up to 24 h without
fertilization after it leaves the ovary. Similarly spermatozoa survive for a
maximum of 24 h within female genital tract. The take an average of 6-24 h
for traveling from vagina to tubes. Because of uncertainly of ovulation.
c. Indications
(1) for AIH -
(i) Male factors - (a) Husband has an ED [impotency] (b) Husband has a
physical anomaly making him unable to deposit semen naturally
[elephantiasis, epispadias, hypospadias, hydrocele, penile and scrotal
tumors, retrograde ejaculation etc] (c) husband is dead, and his semen was
harvested after death [Posthumous assisted reproduction].
(ii) Female factors – Cervical stenosis, Persistent cervicitis, Scant or unreceptive
mucus.
(2) for AID -
(i) Husband is sterile
(ii) Husband suffers from hereditary disease
(iii) wife is allergic or iso-immunized to husband’s sperm
(iv) husband suffering from HIV or hepatitis B
(v) woman is unmarried or a widow
(vi) lesbian couples
(vii) Rh incompatibility [in olden times; not now].
(3) for AIHD – Husband has oligozoospermia. By mixing semen with that of
donor, sperm count is brought to normal with a possibility that husband’s
sperm would fertilize ovum.
d. Precautions
(1) Consent - of donor, recipient and their spouses is essential. As both donor
and recipient identities are shielded from each other, physician is the only link
between the two. It should be specifically stated that the physician has full
discretion to chose the best possible donor.
(2) Essential requisites of donor -
(i) Blood group - No Rh incompatibility. Should have same blood group as that
of husband
(ii) Family - Should have completed his own family
(iii) Health - Should be physically and mentally healthy. No familial, hereditary
disease or STD [HIV etc]. Chromosomal studies - should be done on him
for possible genetic defects
(iv) Physical characteristics, race etc - should match that of the husband of
recipient as closely as possible.
(v) Relationship with the couple - Should have no relation to either spouse.
(vi) Single donor’s semen should not be used to produce more than ten children.
More children in different families from same donor would ultimately - the
 possibility of consanguineous marriages.
(3) Couple-should be psychologically fit and emotionally stable
(4) Witness - must be present at the time of insemination
(5) Delivery - should not be done by the physician who performed AI. This
avoids the necessity of either falsifying the records or disclosing true paternity
in the records.
e. MLI
Please see ML aspects of ART below.
f. Complications
Please see complications of ART below.

2. Conventional in-vitro fertilization and embryo transfer [IVF-ET, test

tube babies]
(1) In vitro fertilization is the most common ART procedure. Mythological IVF
is well known. Gandhari bore 100 sons of Dhritarashtra without having any
biological relation with him. World’s first test tube baby Louise Brown was
born on 25 July 1978, in Oldham General Hospital, Greater Manchester, UK.
Done by Patrick Steptoe and Robert Edwards. Use of clomiphene citrate
and human chorionic gonadotrophin (hCG) enabled scientists to control and
time oocyte maturation. This converted IVF to a viable form of clinical
treatment. The world’s second and India’s first IVF baby, Kanupriya, alias
Durga, was born 67 days later on Oct 3, 1978. Done by Subhas Mukherjee in
Kolkata by an entirely different technique. Mukherjee was the first person in
the world to use (a) gonadotropins for ovarian stimulation prior to ovum pick-
up in an IVF treatment cycle; (b) the transvaginal route by colpotomy for
harvesting oocytes; and (c) freezing and thawing of human embryos before
transferring them into the uterus. Today there are an estimated 250 IVF clinics
in India.
(2) Procedure - Controlled ovarian hyperstimulation with exogenous
gonadotropins"oocyte retrieval via transvaginal ultrasonographic guided
aspiration"Fertilization of oocytes with sperm in culture"formation of
zygote"allowing zygote to develop for 3-5 days"Transcervical
Transfer of zygotes to uterine cavity under US guidance.

3. Surrogate motherhood
A surrogate mother is a woman who by contract agrees to bear a child for
someone else.
Salient features:
(1) There are two parties to the contract – “the commissioning couple” (who
makes the request) and the surrogate mother, who agrees to bear child on
behalf of “the commissioning couple” either for money (Commercial
surrogacy, paid surrogacy), or simply to help the couple out of love and
affection [Altruistic surrogacy], eg a woman agreeing to bear child for her
sister or even her daughter.
(2) Types - Surrogacy is of two types: (i) Traditional (Complete) surrogacy –
Female of the “commissioning couple” is unable to bear children (ovarian,
fallopian tube or uterine pathology). Sperm from the male of the
“commissioning couple” is used to impregnate the surrogate mother.
Impregnation is done via IUI (intrauterine insemination), or ICI (intracervical
insemination) which is performed at a fertility clinic [as in Baby M case –
please see below]. Rarely intercourse is used for sperm transfer. The couple
thus “buys an ovum” from the surrogate mother and also hires her uterus. The
surrogate mother returns the baby to the “commissioning couple” after
delivery. (ii) Gestational surrogacy (uterine surrogacy)– The female of the “the
commissioning couple” has a functioning ovary, but there is uterine
pathology, so she can not carry on the pregnancy in her own uterus. The
couple thus hires the uterus only. The baby is conceived in-vitro with the
sperm and egg of “the commissioning couple”, and transferred to the uterus of
the surrogate mother, who returns the baby the couple after delivery. (iii)
Ovarian surrogacy – A third form is also recognized by some. The female of
the “the commissioning couple” has a functioning uterus, but there is ovarian
pathology. She thus “buys only an ovum” from the surrogate mother.
Pregnancy is carried out in her own uterus. It is not traditionally considered a
case of surrogacy.
(3) Other classifications – Surrogacy can be classified in a number of other
ways depending upon how it is looked at. (i) International surrogacy [syn,
overseas surrogacy]- A surrogacy arrangement, involving an overseas country.
Assumes significance when one country recognizes surrogacy, but the other
does not [please see Jan Balaz and Susanne Anna Lohle case below]. (ii)
Same sex surrogacy [syn, Gay surrogacy]- Same sex male couple hires a
 surrogate mother; same sex female couple hires a sperm donor. In 1999,
Barrie and Tony Drewitt-Barlow became the first British same-sex couple to
be named on their children’s birth certificates. They hired a surrogate mother
in California [international surrogacy], who gave birth to twin brothers Aspen
and Saffron. Following a ruling by an American court, the twins became the
first British children to be registered as having two fathers and no mother. In
2003, they used the same egg donor and a different surrogate to have the 3rd
child, and in 2010 another surrogate to have twin boys Dallas and Jasper. They
now have five children – all surrogate babies. They set up the British
Surrogacy Centre in Essex, in Feb 2011.

4. Other techniques
(1) Embryo donation [ED]:
(i) A form of third party reproduction [please see above].
(ii) It is donation of surplus embryos remaining after one couple’s In vitro
fertilization, or IVF treatments, to another person or couple.
(iii) The embryos are typically donated after the woman for whom they were
originally created has successfully carried one or more pregnancies to term.
(iv) The resulting child is considered the child of the woman who carries it and
 gives birth, and not the child of the donor.
(v) Same principle is followed in oocyte [egg] donation.
(vi) No compensation is generally asked for. It is done on altruistic basis.
(2) Gamete intrafallopian transfer (GIFT) – First reported in 1984. After
collection of ovum as in conventional IVF, they are mixed with sperm and
transferred back into fallopian tube with the hope that they would form a
zygote. A fundamental problem with this procedure is that fertilization is not
confirmed unless the patient conceives. Therefore other techniques like ZIFT
and TEST were developed.
(3) Intracytoplasmic Sperm Injection [ICSI]:
(i) Procedure – (a) The ovum is injected with a single sperm, taken from the
husband’s sperm (after preparation in the lab). (b) A special needle is used
to go through the wall of the egg and the sperm is introduced into the
cytoplasm of the egg. (c) The fertilization is observed; if division occurs,
the embryos are transferred into the woman’s uterus.
(ii) Indications - (a) Cases who had vasectomy and surgical reversal failed. (b)
Past Infections which result in surgically intractable obstructions. (c) severe
problems in the seminal fluid [eg severe deficiency in number or motility of
the sperms or both]. (d) when the man has no sperms in the seminal fluid
but has sperms in his testicles, eg absence of vas deferens. One of the
techniques of sperm retrieval is used [please see below].
(iii) Advantages - Only a single sperm is required, and it does not even have to
be motile.
(4) Oocyte Donation [OD] or egg donation – Donors may be
(i) Anonymous - Donors unrelated to the recipients who do it for altruistic or
monetary reasons. They are typically recruited by egg donor agencies.
(ii) Designated donors - a friend or relative brought by the patients to serve as a
donor
(iii) Patients taking part in shared oocyte programmes. Women who go through
IVF donate unused eggs to others.
(5) Techniques of Sperm Retrieval – These techniques are for sperm retrieval
only. Must be followed by ICSI [please see above]
Techniques are (a) Microsurgical Epididymal Sperm Aspiration or MESA (b)
Percutaneous Epididymal Sperm Aspiration or PESA (c) Testicular
Microdissection (d) Testicular Perc-Biopsy (e) Testicular Sperm Aspiration or
 TESA (f) Testicular Sperm Extraction or TESE (I) Indications – Same as ICSI
above. The two procedures are used in combination
(6) Tubal Embryo Stage Transfer [TEST, embryo intrafallopian transfer, Tubal
Embryo Transfer, TET] – Same as ZIFT (please see below), except that here
pre-embryos are transferred on day 2 or 3 after fertilization. They are thus
more mature. Its advantage over ZIFT is that it allows for the assessment of
fertilization and embryo quality.
(7) Zygote Intrafallopian transfer (ZIFT) – Same as GIFT, except that
fertilization occurs outside the body and zygote is transferred back to the
woman. In both TEST and ZIFT, the embryos are placed in an environment
which is expected to be optimal for further development and implantation.
(8) Other miscellaneous procedures:
(i) Controlled ovarian hyperstimulation only [COHS]
(ii) direct intraperitoneal insemination [DIPI]
(iii) fallopian tube sperm perfusion [FSP]
(iv) intrauterine insemination [IUI]
(v) combination of IUI and DIPI and
(vi) peritoneal oocyte and sperm transfer.

B. Semen Banking
A semen bank [syn, sperm bank] is a facility that collects and stores human
sperm mainly from sperm donors, primarily for the purpose of achieving
pregnancies through AI.

C. ML Aspects of ART
There is no law on artificial insemination applicable in the entire country [The
Delhi Artificial Insemination (Human) Act, 1995 is applicable only in Delhi].
NG, 2005 [please see above] are only the nature of guidelines.
(1) Adultery:
(i) ART used for married woman with the consent of the husband does not
amount to adultery on part of the wife or the donor. AID without the
husband’s consent can, however, be a ground for divorce or judicial
separation [S.3.16.2, NG 2005]
(ii) u/s 497, IPC – sexual intercourse is an essential element in adultery. Since
 AID does not involve sexual intercourse, it does not amount to adultery. If
husband consents to AID through actual intercourse with a third party, it
cannot amount to adultery, since adultery can only be committed in the
absence of husband’s consent.
(2) Confidentiality - Any information about clients and donors must be kept
confidential. [S.3.2.3, NG 2005]
(3) Consummation of marriage – Conception by ART, even in cases of AIH,
does not amount to consummation of marriage, although the child conceived
may be biologically that of husband (thus marriage remains voidable)
[S.3.16.3, NG 2005]
(4) Damages – doctor can be sued for damages if
(i) He conducts AIH without husband’s consent or conducts AID without donor
or his wife’s consent
(ii) Recipient contracts a transmissible infection like HIV.
(5) Divorce and judicial separation – please see “Adultery” above.
(6) Incest – Risk of inadvertent admixture of gametes between closely related
couples is a distinct possibility because of confidentiality. It has been asserted
that it is doctor’s duty to check records and exclude possibility of close
relations, eg by checking surnames etc, but as surnames change after marriage,
such cross-checking on the part of doctor is impossible. Nevertheless in order
to avoid damage suits later, doctor should specifically include the exclusionary
clause in the contract making him free from such liabilities.
(7) Legitimacy - A child born through ART shall be presumed to be the
legitimate child of the couple. He shall have a legal right to parental support,
inheritance, and all other privileges of a child born to a couple through sexual
intercourse [S.3.12.1, NG 2005]. In legal documents, eg birth certificate,
school leaving certificate, passport etc, the name of the parents to whom he
was born will be entered, even if the child was genetically unrelated to them.
It is furthermore advisable for parents to adopt the child legally.
(8) Minimum age for ART - For a woman between 20 and 30 years, two years
of cohabitation/marriage without the use of a contraceptive, excepting in cases
where the man is infertile or the woman cannot physiologically conceive. For
a woman over 30 years, one year of cohabitation/marriage without use of
contraceptives. Normally, no ART procedure shall be used on a woman below
20 years [S.3.14.1, NG 2005]
(9) Nullity of marriage – please see consummation of marriage above
(10) Posthumous AIH - A child born to a woman artificially inseminated with
the stored sperms of her deceased husband must be considered to be a
legitimate child notwithstanding the existing law of presumptions u/s 112,
IEA Indian Evidence Act, which says that child born after 280 days of death
of husband is illegitimate [ch 24] [S.3.16.5, NG 2005].
(11) Rights of a Child Born through ART Technologies [S.3.12, NG 2005]:
(i) Children born through the use of donor gametes shall not have any right
whatsoever to know the identity (such as name, address, parentage, etc.) of
their genetic parent(s) [S.3.12.3, NG 2005]
(ii) In the case of a divorce during the gestation period the law as pertaining to a
normal conception would apply [S.3.12.4, NG 2005]
(12) Unmarried woman opting for AID – There is no law barring an unmarried
woman to AID. The child would inherit all property of the woman, if the
woman dies intestate. However it is advisable for her to make a will
immediately after birth of such a child and make him a beneficiary.

24. Virginity, Pregnancy and Delivery

I. VIRGINITY

A. Definitions
(1) A virgin (virgo intacta) [Latin virgo, “sexually inexperienced woman”] is a
female who has not experienced sexual intercourse.
(2) Defloration [Latin de, away; flore, flower. A poetic likening of the rupture of
hymen by sexual intercourse to the plucking of flowers] means loss of
virginity with associated rupture of hymen. Such a woman is called a
deflorate woman.
(3) Loss of virginity without associated rupture of hymen results not in a
deflorate woman, but a false virgin.
(4) Apta viro [please aptae viris] is a woman who is “fit for a husband” or “a
woman who has reached marriageable years”.
B. Normal Female Genital Anatomy
1. External
The labia majora (1) [L. labia, lip] [Fig 24.1] are two elongated folds of skin
projecting downwards and backwards from mons pubis (2) [Latin, “pubic
mound”. Also known as mons veneris [“mound of Venus”] or simply the mons].
It is a pad of fat lying in front of pubis. They meet in front at anterior
commissure (3) and at the back at posterior commissure (4) in front of the
anus (5) In a virgin the labia majora are thick, firm, elastic and rounded and lie
in apposition so as to completely close the vaginal orifice. (6) The labia minora
(8) are about 4 cm long; they are two soft, small, thin, pink and sensitive folds
just within the labia majora. Between Labia majora and the labia minora is a
groove called interlabial sulcus. (19) There are 2 such sulci-left and right. The
lower portions of labia minora fuse in the midline and form a fold called
fourchette (9) [Fr, “little fork”]. The depression between fourchette and the
vaginal orifice is called fossa navicularis (10) [L fossa, depression; navicula,
boat; a boat shaped depression]. Clitoris (11) [Gk, kleis, key; in reference to it
being key to female genitals] is a small button-like organ located near the
anterior junction of the labia minora, above the urethral opening (12) and
vagina. It is covered with a fold of skin that surrounds and protects it [clitoral
prepuce, clitoral hood, or preputium clitoridis). It develops as part of the labia
minora and is homologous with the foreskin (also called prepuce) in male
genitals. The frenulum (13) [also known as the Crus glandis clitoridis] is a small
fold of tissue on the under surface of clitoris, created by the two medial parts of
the labia minora. Urethral opening is 2.5 cm behind the clitoris and immediately
in front of the vaginal orifice. Vestibule (14) is a narrow triangular area which
extends from the clitoris above to the anterior margin of the hymen below, and
laterally to the labia minora.
Memory Aid 1: Female genital anatomy
Fossa navicularis is in Front of Fourchette; Vestibule is Ventral to Vagina.
It usually remains concealed by the labia. Vulva includes mons veneris [which
forms its anterior portion], labia major, labia minora, clitoris, vestibule, hymen
and urethral opening. The perineum (15) is a wedge shaped area between the
lower end of the posterior wall of vagina and the anterior anal wall. The cervical
canal is nearly at right angles to the vagina when bladder and rectum are empty.
Bartholin's glands (16) secrete a mucoid fluid, which drains in vagina through
Bartholin duct openings (17).

Hymen
Hymen [Fig 24.1, (7)] [Gk Hymenaios, God of marriage] is a fold of mucus
membrane about 1 mm thick, situated at the vaginal outlet.
Salient features:
(1) The average adult hymen consists of folds of membrane having an annular or
crescentic shape, the broadest part lying posteriorly
(2) Diameter of hymenal orifice in children – (i) 1 mm/y [eg 1 mm at 1 y;
2mm at 2 y and so on] till it reaches about 10 mm in a prepubertal girl. (ii)
>10mm diameter in a prepubertal girl indicates sexually abused girl. [Please
compare with hymenoscope ball sizes (ch 25)].

i. Types
Shown in Fig 24.2. Differences between fimbriated and ruptured hymen [Table
1].
ii. Rupture
Rupture of hymen during first sexual intercourse is known as defloration; such a
woman is termed a deflorate woman.
Salient features:
Causes other than sexual intercourse – (i) Accident – (a) Straddle injuries eg
(I) Fall on a projecting object (II) Slipping on fence, furniture, pole etc (III)
Playing at seesaw (b) Ch of accidental rupture - (I) Associated tearing of
perineum (II) periurethral tissues, labia and mons usually involved (III) Injuries
on other parts of the body are also seen, consistent with the history of accident
(IV) tears generally not associated with abrasions or bruising of hymenal
margins (c) Separation of thighs forcibly in children – generally will not rupture
hymen. But if separated too far with tear of perineum, hymen may
simultaneously be ruptured (d) Hymen does not usually rupture by (I) Dancing
(II) Jumping (III) riding (IV) vigorous exercise (ii) Bad hygiene - causes
irritation"scratching"torn hymen (iii) Foreign body – (a) Sola pith – Used by
prostitutes to dilate the vagina of very young girls to make them suitable for
sexual intercourse [aptae viris]. Sola is an Indian plant with stems containing
woody pith [sola pith]. It is sponge wood with great absorptive powers. A piece
of sola pith is inserted into the young girl’s vagina. The piece is as large as the
vagina can contain. The girl is asked to sit in a tub of water. The absorbent
sponge wood absorbs water and swells up, enlarging the vagina. The process is
repeated with bigger pieces of sola pith, till the vagina is roomy enough for
sexual intercourse. The hymen is torn in this process. (iv) Gynecological
examination (v) Masturbation – (a) especially with a large object (b) If
manipulation is limited to parts anterior to hymen, it may be spared (c)
Characteristics –(I) Clitoris and labia minora enlarged (II) Vaginal orifice dilated
(III) Vagina roomy (IV) hymen thickened and shows scratches (vi) Sanitary
tampons (vii) Surgical operation (viii) Ulceration – diphtheria, fungus, other
causes.

2. Internal
a. The vaginal passage
(1) Passage - The vaginal passage is a roughly cylindrical tube, about 7.5 cm
long.
(2) Walls - The tube’s anterior wall is shorter [6 cm], and posterior wall longer
[9 cm].
(3) Cavity - It is collapsed antero-posteriorly to form a crosswise slit. When
distended, it looks like a gourd, wider at the top.
(4) Width at the upper end - (i) 3-4 cm in nullipara and (ii) 6-7 cm in parous
women.
(5) Fornix -
(i) The fornices of the vagina (fornix vaginae) [Latin fornix, arch] are arch like
recesses around the cervix.
(ii) They are the deepest portions of the vagina, created by the vaginal portion of
cervix.
(iii) Number - There are four fornices in all - (a) the posterior fornix is the
largest recess, and lies behind the cervix. It is close to the rectouterine
pouch (b) the anterior fornix is shallower and lies close to the
vesicouterine pouch (c) The two lateral fornices lie on each side of the
cervix.
b. Relations
(1) Anteriorly – Bladder
(2) Laterally – Levator ani muscles
(3) Posteriorly – Perineal body and rectum
(4) Superiorly – Pouch of Douglas.

C. Signs of Virginity

1. Genital signs
(1) Hymen -
(i) Normal hymen is annular or crescentic in shape, but may be of other shapes
[Fig 24.2]
(ii) Thickness - 1 mm
(iii) Broadest part - lies posteriorly
(iv) May be very fleshy or cartilaginous sometimes [may result in false virgin]
(v) At 10 years of age, the tip of small finger can be passed through it; at
puberty, one finger can be passed [also see diameter of hymen above].
(2) Posterior commissure and fourchette – intact. They are usually torn after
violent and forcible sexual intercourse [ch 25] or childbirth. A single act of
intercourse does not cause much alteration in genitalia, except rupture of
hymen.

2. Extragenital signs
Breasts
(1) In a virgin - the breasts are firm, elastic and hemispherical. Nipple is small
 and undeveloped, surrounded by an areola which is pink in fair complexioned
women and dark brown in dark women.
(2) Breasts become large and flabby - by frequent handling, manipulation,
sexual intercourse, lactation and suckling
(3) Single act of coitus - does not enlarge breasts
(4) Milk – present only in lactating mothers. In some hormonal disorders, milk
may be seen even in virgins.

D. Medicolegal Aspects of Virginity

1. True virgin v False virgin
(1) Classically presence of an unruptured hymen was considered a sign of
virginity. But now it is known that this is not true. Because of the ancient and
classical association of intact hymen with virginity, any woman with an intact
hymen may be called a virgin by a layman or even an inexperienced doctor.
But if she has experienced sexual intercourse, she would be a false virgin [i.e.
one who appears a virgin on hymenal examination, but is not truly a virgin].
(2) True virgin is a woman who has never experienced sexual intercourse. Her
hymen may or may not be intact.
(3) False virgin is a woman who has experienced sexual intercourse, but her
hymen is intact.
(4) Principal signs of virginity - Table 3. Any single sign alone may not be
taken as a sure sign of virginity, but all signs taken together are virtually
diagnostic of virginity.
(5) Rupture of hymen – usually occurs at first intercourse.
(6) Causes of intact hymen even after 1st intercourse – If it is elastic, fleshy,
folded, loose, thick or tough. Such a hymen permits displacement, distortion
and stretching without rupture.
(7) Intact hymen has been seen in women having repeated sexual acts, women
presenting for delivery and even prostitutes [although in some prostitutes,
intact hymen may be due to hymenoplasty].
(8) Carunculae myrtiformes or Carunculae hymenales– In women used to
intercourse [eg married women, prostitutes etc] the hymen almost disappears
giving rise to just a few small, fleshy, minuscule, round projections or tags of
tissue at the periphery [hymenal ring].
2. Divorce
If the woman was not a virgin at the time of marriage, there is no provision
either for nullity or divorce under HMA 1955 [ch 23].
3. Defamation
A person may be charged for defamation [S.499, IPC] if he alleges loss of
virginity of a woman, and she is found to be a virgin on examination.
4. Rape
Allegations of rape may be proved if loss of virginity can be shown, keeping all
other factors in consideration.
5. Nullity of marriage
If a married woman wants her marriage to be declared null and void on account
of impotency of husband (S.12 of Hindu Marriage Act, 1955), she must prove
that she has been a virgin, and that her husband has been unable to consummate
marriage [please see medicolegal aspects of impotence and sterility in previous
chapter].

II. PREGNANCY

Pregnancy is the condition of having a developing embryo or fetus in the

female, when an ovum is fertilized by a spermatozoon.
Salient features:
Age – occurs between 14-45 y, but has been recorded beyond either extreme.

A. Diagnosis of Pregnancy

1. Signs of pregnancy in the living

a. Presumptive signs of pregnancy
Probability of pregnancy is about 25%.
i. Amenorrhea
(1) Earliest sign
(2) Other reasons for amenorrhea
(i) endocrine or local pathology, environmental and nutritional causes, severe
anemia, tuberculosis etc
(ii) fear or nervousness [due to illicit intercourse in an unmarried woman]
(iii) intense desire for pregnancy [in married women]
(3) Pregnancy during already existing amenorrhea – may occur
(i) in women who have never menstruated
(ii) during amenorrhea of lactation.
ii. Breast changes
Quite characteristic in primigravida but are of less value in multigravida
(1) Up to 8 weeks – tenseness and tingling in breasts
(2) After 2nd month -
(i) -in size
(ii) become nodular [due to hypertrophy of mammary alveoli]
(iii) Superficial veins - enlarged and more distinct
(iv) Nipples – deeply pigmented and more erectile
(v) Areola – becomes dark brown [it is pink in the virgin]. Montgomery’s
tubercles are seen. These are small rounded dark colored tubercles seen on
areola [represent enlarged sebaceous glands].
(3) 3rd month – Colostrum is secreted.
(i) It is a thin, yellowish fluid consisting of fat globules and large phagocytic
cells filled with droplets of fat.
(ii) It can be expressed from the breasts by gentle massage.
(4) 6th month - Striae [silvery lines] are seen on the breast due to stretching of
the skin. More prominent in primiparae.
iii. Fatigue
(1) Women in the first trimester of pregnancy experience significantly greater
fatigue; they spend more hours sleeping.
(2) Could be due to neuroactive steroids.
iv. Morning sickness
(1) Comprises of nausea and vomiting, seen usually in the morning. Passes off in
a few hours
(2) Appears by the end of 4 wks and ends by 12 weeks
(3) Varies greatly in severity.
v. Hyperpigmentation
(1) Incidence - Develops in up to 90% of women.
(2) Usually more accentuated in those with a darker complexion.
(3) Main changes are
(i) Linea nigra – [Latin, “black line”] Pigmentation of the midline of the
abdominal skin. Extends from pubis to beyond the umbilicus
(ii) Melasma gravidarum - Irregular brownish patches of varying size on the face
and neck. Also known as chloasma or mask of pregnancy.
(iii) Pigmentation of the areolae and genital skin may be accentuated.
(4) Etiology -
(i) Melanocyte-stimulating hormone which is -ed during pregnancy
(ii) Estrogen and progesterone also have melanocyte-stimulating effects.
(5) D/d - Oral contraceptives may cause similar pigmentation.
(6) These pigmentary changes usually disappear, or regress considerably, after
delivery.
vi. Quickening
(1) Quickening is slight fluttering movements felt by the mother from about 16th
-20th wks of pregnancy.
(2) Due to movements of the fetus.
vii. Sympathetic disturbances
Irritable temper, Perverted appetite, Salivation.
viii. Urinary disturbances
(1) During early weeks of pregnancy, the enlarging uterus exerts pressure on the
bladder"Frequent micturition.
(2) As pregnancy advances, uterus rises up into abdomen"Frequency returns to
normal
(3) Few weeks before term"head descends in pelvis"frequency -es once again.
ix. Vaginal changes
(1) Color change in the vulvovaginal mucosa - changes from rose color in the
nonpregnant state to pale violet in early pregnancy [Chadwick’s sign,
Jacquemier’s sign, Jacquemin’s sign]. First seen at 4th week as a result of
venous obstruction. Other changes at this period
(2) Anterior wall of vagina – flattens
(3) Vulval and vaginal tissues – become softer
(4) Secretion of mucus -es
(5) Vaginal pulsation - can be felt.
x. Vascular changes
Angiomas [vascular spiders], develop in about 65% of white women and 10%
of colored women. These are minute, red elevations on the skin, particularly
common on the face, neck, upper chest, and arms, with radicles branching out
from a central lesion. The condition is often designated as nevus, angioma, or
telangiectasis. Palmar erythema is seen in about 65% of white women and 33%
of colored women.

b. Probable signs of pregnancy

Probability of pregnancy is about 50%.
i. Enlargement of abdomen
(1) End of 12th wk [3rd m] – uterus fills up the pelvis
(2) >12th wk – uterus appears over the brim. This causes abdomen to show
visible enlargement in size [Table 4].
(3) end of 20th wk [5th m] – Uterus is midway between symphysis and umbilicus
(4) end of 6th m –
(i) Uterus at umbilicus
(ii) Striae gravidarum appear. (a) These are bluish or slightly pinkish, curved
irregular, depressed lines arranged more or less concentrically, sometimes
radially around umbilicus. (b) They gradually become broader and deeper
near inguinal ligament. (c) Locations - abdomen (most common; 48%),
breasts (25%), thighs (25%), hips (d) Etiology - Rupture of subcuticular
elastic fibres, due to gradual distension of abdomen. Hormonal changes also
play a role (e) Most women experience striae gravidarum during their first
pregnancy. Some who do not develop striae in their initial pregnancy
develop them in subsequent pregnancies. Some women do not develop
them at all. Genetics may play a role. (f) Progression - Become paler with
time. After 1 y, appear as white scars [linea albicantes]. These are irregular,
white or silvery s/c scars. They do not develop in all cases, and in some
cases they disappear after sometime.
(5) end of 7th m –
(i) Uterus midway between umbilicus and xiphisternum
(ii) umbilicus becomes level with the skin
(6) end of 8th m – at xiphoid cartilage
(7) 9th -10th m –
(i) Uterus descends in pelvis
(ii) falls forwards due to its weight.
ii. Uterus
Hegar’s sign [after German physician Alfred Hegar (1830–1914)]:
(1) Most valuable sign in early pregnancy.
(2) +ve at 6th wk [Table 4].
(3) How to elicit:
(i) One hand is placed on abdomen
(ii) Two fingers of the other in vagina.
(iii) Firm hard cervix is felt, and above it the elastic body of the uterus. Between
the two, the isthmus is felt as a soft compressible area.
iii. Cervix
(1) Goodell’s sign - Softening of the vaginal portion of the cervix from -ed
vascularization. Softening proceeds from below upwards. Starts at 2nd month
[8 weeks] and is well marked by 4th month. After American gynecologist
William Goodell [1829 – 1894].
(2) Shortening of cervix – towards last months of pregnancy
(3) Orifice – becomes circular instead of being transverse. Admits tip of finger to
greater depth.
iv. Braxton Hick’s sign
Intermittent painless contractions. Felt after 4th month [16 weeks]. Contractions
last about 1 minute followed by a relaxation period of 2-3 minutes. Present even
when the fetus is dead. After English obstetrician John Braxton Hicks [1823 –
1897].
v. Ballottement
Ballottement [Fr ballotter, to toss] is a palpatory technique for confirmation of
pregnancy, as the fetus can be tossed up and down like a ball within the uterus.
Salient features:
(1) Sign is +ve by 16-20 wks [Table 4].
(2) Fetus can be tossed up and down at this period - because (i) fetus is small
in relation to the amniotic fluid present, and (ii) the umbilical cord has
lengthened enough to allow free movement of fetus
(3) Demonstration - (i) External ballottement – (a) Sudden motion is given to
the abdominal wall covering the uterus (b) Rebound of the fetus can be felt in
a few seconds (ii) Internal [vaginal] ballottement - (a) two fingers inserted into
 the anterior fornix (b) sudden upward motion given (c) Fetus “tosses up” in
the liquor amnii, and after a moment drops back on the fingers, like a ball
bouncing back
(4) False –ve – When amniotic fluid is scanty.
vi. Ladin’s sign
Softening in the midline of the uterus anteriorly at the junction of the uterus and
cervix [6th wk].
vii. Osiander’s sign
Feeling of pulsations through the lateral fornices [8th wk]. After German
obstetrician Johann Friedrich Osiander [1787-1855].
viii. Palmer’s sign
Regular and rhythmic contractions of the uterus in early pregnancy [8 wks]. Two
fingers of right hand are put into the vagina and left hand is put on the lower
abdomen. Wait for 2-3 minutes"uterus becomes firm and then ill defined
according to its contractions and relaxation. The sign was important in pre
ultrasonography days; nowadays it is only of theoretical importance.
ix. Piskaçek’s sign
Asymmetrical enlargement of uterus, if there is lateral implantation. One half of
uterus is firmer than the other [8th wk]. After Austrian obstetrician Ludwig
Piskaçek [1854-1932].
x. Uterine soufflé
Uterine soufflé is a soft blowing murmur due to passage of blood through the
uterine vessels.
Salient features:
(1) Synchronous with mother’s pulse [please also see placental and funicular
souffle below, which are synchronous with fetal ht sounds]
(2) Heard by auscultation on either side of the uterus just above ingutinal
ligament
(3) +ve at the end of 16th wk
xi. Von Braun-Fernwald’s sign
Irregular softening and enlargement of the uterine fundus during early pregnancy
[5–8 wks]. After Austrian obstetrician Karl von Braun-Fernwald [1822–1891].
xii. Biological tests
Biological tests are based on the reaction of test animals to Human Chorionic
Gonadotropin (hCG) contained in the pregnant woman’s urine.
Salient features:
Prevalent before 1960s, but now completely taken over by immunological
tests.
xiii. Immunological tests
Based on ‘specific’ fetoplacental products, eg hCG.
(1) Advantages -
(i) Convenient and sensitive [accuracy 98%]
(ii) No animal is required
(iii) quicker [2 min]
(2) Sample taken – First voided urine in the morning. Contains highest levels of
hCG. Following immunological tests are available.

c. Positive signs of pregnancy

Probability of pregnancy is 100%.
i. Fetal movements
Felt by 24th wk by placing hands on abdomen.
ii. Fetal parts
Identified by 36th wk by abdominal palpation.
iii. Fetal heart sounds
(1) Time - First heard between 18-20 wks [Table 4].
(2) Nature -
(i) Sounds are similar to ticking of a watch placed under a pillow.
(ii) Not synchronous with mother’s pulse
(3) Rate -
(i) 20th wk – 160/min
(ii) 36th wk – 120/min
(4) Fetal ht sounds not heard in following cases -
(i) Dead fetus
(ii) In live fetus when (a) Examination done before 18 wks (b) Fat abdominal
wall (c) Excessive liquor amnii.
iv. Placental soufflé
(1) A soft murmur heard over the placental site.
(2) Synchronous with the fetal ht sounds [unlike uterine soufflé – please see
above].
v. Funic or umbilical soufflé
(1) A soft blowing murmur due to passage of blood in umbilical cord.
(2) Synchronous with the fetal ht sounds.
vi. Ultrasound
(1) Done by employing 3-dimensional scanning with Ultrasound
(2) Time -
(i) 6th wk – Gestational sac is seen as a white ring
(ii) 7th wk – Distinct echoes from the embryo within the gestational ring
(iii) 10th wk – Fetal heart beat becomes detectable
(iv) 11th wk – Earliest period when sex of baby may be determined. But accuracy
rate is very low
(v) 13th wk – Accuracy of determination of sex is between 99% to 100% if there
is no malformed external genitalia. Sex of unborn child cannot be disclosed
to any person [please see PCPNDT Act below].
(vi) 14th wk – Fetal head and thorax become detectable.
vii. X-ray
(1) Earliest detection – 12 wks. At 16 wks, can be detected with absolute
certainty [skull and spine are seen at this time]
(2) Shadows to be seen are -
(i) Crescentic or annular shadows of skull
(ii) A series of small dots in a linear arrangement along the line of vertebral
column [vertebrae]
(iii) A series of fine curved parallel lines [ribs]
(iv) Linear shadows of limbs
(3) X-ray examinations also useful in
(i) Fetal abnormality or death [ch 27]
(ii) Hydatidiform mole
(iii) Twin pregnancy.

2. Signs of pregnancy in the dead

(1) Uterus -
(i) Weight of a virgin uterus is"30-40 g
(ii) Adult uterus measures 3” # 2” # 1”. Divided into two parts – Body or corpus
[2”] and cervix uteri [1”].
(iii) In fetal life, cervix is considerably larger than the body
(iv) After parturition, the uterus nearly regains its usual size, weighing on an
average the same as the virgin uterus, but its cavity is larger than in the
nulliparous state.
(2) Ovary -
(i) The size of each adult ovary: 3 cm x 1.5 cm x 1 cm [uterus is about 2.5 times
bigger (in every dimension) than each ovary]
(ii) The weight of each ovary in a non pregnant state: 2-3.5 gm. In pregnancy
slightly heavier.

B. ML Aspects of Pregnancy

1. Capital sentence
If woman sentenced to death is pregnant, the High Court shall commute the
sentence to imprisonment for life [S.416, CrPC].

2. Gestation period
(1) Average period – Normal gestation period from LMP is 280 days [or 10
times the intermenstrual period, which is 28 days]. Since ovulation and
consequent fertilization occurs on the 14th day, the actual physical existence of
the fetus within the womb is 266 days. Please compare with S.112, IEA
below.
(2) Maximum period – Maximum period recorded in a reliable medical journal
 is 359 days [British Medical Journal].
(3) Minimum period with viability – A viable child means a child capable of
independent existence from its mother. Generally accepted period of viability
is 28 weeks [196 days] from LMP. Babies born earlier may survive, but suffer
from severe neurological deficits.

3. Posthumous child
It is a child born after the death of father, the mother having conceived by the
said father. Legal issues involved are:
(1) Compensation case against mother for slander
(2) Inheritance of property
(3) Legitimacy.

4. Pregnancy without being aware of it [unconscious pregnancy]

(1) May occur very rarely.
(2) Still more rarely, pregnancy may progress to full term without the woman
being aware of it, although she may be aware of the enlarging abdomen, which
might be thought to be due to some disease.

5. Pseudocyesis
Pseudocyesis, false pregnancy or hysterical pregnancy is the appearance of
clinical signs and symptoms associated with pregnancy when the female is not
pregnant.
Salient features:
(1) Etiology – Seen in younger women who intensely desire children or women
nearing menopause. Most women suffer from some form of psychological or
hormonal disorder.
(2) Signs and symptoms – All or most are presumptive and probable signs.
(i) Amenorrhea and breast changes may be there
(ii) woman may even feel fetal movements
(iii) -Abdominal size – due to (a) abnormal deposition of fat (b) tympanites
[excessive gas accumulation in the GIT] or (c) ascites
(iv) Pseudopregnancy may advance to full term and the woman may go into
false labor pains. These labor pains may cease suddenly when the patient is
told she is not pregnant.
(3) In case of doubt, clinical examination and ultrasound would reveal an empty
uterus. False pregnancy is very common in animals [particularly dogs and
mice]; in animals, it is called pseudopregnancy. Clinical signs seen are wt
gain, mammary enlargement, lactation and maternal behaviour.

6. Determination of period of pregnancy

(1) By counting days since LMP
(2) From quickening [for date please see above]
(3) McDonald’s rule - Applicable from 22-34 weeks age of gestation.
(i) Fetal age (in weeks) = fundal height in cm
(measured from symphysis pubis to top of uterus) #
8
7
(ii) Fetal age (in months) = fundal height in cm
(measured from symphysis pubis to top of uterus) #
2
7
(4) Naegele’s Rule - Expected date of confinement = 1st day of LMP +9 months
+ 7 days.

7. Sex Selection
a. The Pre-Conception and Pre-Natal Diagnostic Techniques (Prohibition of
Sex Selection) Act [PCPNDT], 1994
Salient features:
(1) It was enacted in 1994, and subsequently amended in 2002.
(2) Aims: (i) Pre-natal diagnostic techniques for determination of sex of fetus
were prohibited. Aim was to prevent female feticide (ii) Advertisement of pre-
natal diagnostic techniques for detection or determination of sex were
prohibited (iii) Pre-natal diagnostic techniques for detection of genetic
abnormalities were allowed.
(3) Some important definitions – Dealt with in Ch I. [A] Diagnostic
procedures and tests. 3 are defined (i) ”pre-natal diagnostic procedures”
means all gynecological or obstetrical or medical procedures such as
ultrasonography, fetoscopy, taking or removing samples of amniotic fluid,
chorionic villi, blood or any other tissue or fluid of a man, or of a woman for
being sent to a Genetic Laboratory or Genetic Clinic for conducting any type
 of analysis or pre-natal diagnostic tests for selection of sex before or after
conception [S.2i]. Genetic clinic is a place where such procedures are
performed [S.2d]. It includes a vehicle where ultrasound machines, or other
equipment capable of determining sex is kept. (ii) ”pre-natal diagnostic
techniques” includes all pre-natal diagnostic procedures + prenatal diagnostic
tests [S.2j]; (iii) ”pre-natal diagnostic test” means ultrasonography or any test
or analysis of amniotic fluid, chorionic villi, blood or any tissue or fluid of a
pregnant woman or conceptus conducted to detect genetic or metabolic
disorders or chromosomal abnormalities or congenital anomalies or
hemoglobinopathies or sex-linked diseases [S.2k]. Genetic laboratory is a
place where such tests are performed [S.2e]. It includes a vehicle as mentioned
above; [Taking of samples is “procedure”; analyzing it is “test”; both together
are “techniques”]. Ultrasonography is the ONLY diagnostic test, which is
included in both Prenatal diagnostic procedures and Prenatal diagnostic tests.
[B] Places – 3 are defined. (i) Genetic Counselling Centre is a place which
provides genetic counselling to patients [S.2c]. (ii) Genetic clinic and (iii)
genetic laboratory are mentioned above. All 3 must be registered with the
appropriate authority [s18]. In case of any violation, the registration will be
cancelled [S.20]. If the owner of these places want to institute an appeal
against the order, it must be done with 30 days to the State govt [if authority
was state level] and to the Central govt [if authority was center level] [S.21].
(4) Regulation of Genetic Counselling centers, genetic laboratories and
genetic clinics –Dealt with in Ch II [S.3 – only one section in this chapter]. (i)
No person can conduct a sex selection [S.3A] (ii) No person can sell any
ultrasound machine or imaging machine or scanner or any other equipment
capable of determining sex of fetus to any person or clinic etc not registered
under the Act [S.3B].
(5) Regulation of pre-natal diagnostic techniques [PNDT]–Dealt with in Ch
III [S.4-6]. (A) Prenatal Diagnostic Techniques can be conducted only for (i)
Chromosomal abnormalities (ii) Congenital Abnormalities (iii) Genetic
metabolic diseases (iv) Hemoglobinopathies (v) Sex-linked genetic diseases
(vi) Any other abnormalities or diseases as may be specified by the Central
Supervisory Board [S.4(2)]. [Memory aid 2- C2GHS]. [These are indications
of PNDT]. (B) Any one [or more] of the following conditions must be fulfilled
before the techniques can be carried out (i) Age of the pregnant woman >35 y
 (ii) pregnant woman has undergone ≥2 Spontaneous abortions or fetal loss (iii)
pregnant woman had been exposed to potentially Teratogenic agents such as
drugs, radiation, infections or chemicals (iv) pregnant woman has a Family
history of mental retardation or physical deformities such as spasticity or any
other genetic disease, and (v) any other condition as may be specified by the
Central Supervisory Board. The person undertaking the procedure must record
the fulfilling condition in writing [S.4(3)]. [Memory aid 3 - A Special
ToFfee]. [Since these are preconditions, ideally they should have come before
the indications.] (C) Informed consent – Prenatal diagnostic procedures can
only be conducted after a written informed consent [ch 2]. A copy of the
written consent is to be given to pregnant woman [S.5(1)]. (D) Prohibition of
communicating sex of fetus - Person conducting prenatal diagnostic
procedure cannot communicate sex of fetus to the pregnant woman concerned
or any other person by any means [S.5(2)]. (E) Determination of sex
prohibited - No person or clinic etc can determine the sex of a fetus or cause
selection of sex before or after conception [S.6].
(6) Penalties: (i) on Advertisement – of any of sex selection or sex
determination techniques; 3 y + `10,000 [S.22] (ii) on Sex selection or sex
determination - (a) To doctor – 1st conviction"3 y + `10,000. Subsequent
convictions"5 y + `50,000 [S.23(1)]. On conviction, name will be removed
from medical register for 5 y for 1st offence and permanently [professional
death sentence] on 2nd offence [S.23(2)] (b) To patient - 3 y + `50,000 for 1st
offence and 5 y + `100,000 for 2nd offence [S.23(3)]. If the woman was
compelled she will not be punished [S.23(4)], but the person compelling her
would be.

8. Superfecundation
Superfecundation is fertilization of two or more ova from the same menstrual
cycle in separate copulatory events.
Salient features:
(1) Monopaternal superfecundation [MS] – Multiple copulatory events are
performed by the same partner. When multiple pregnancies result from a
single copulatory event, it is known as twins, triplets etc. There is no
scientific way to differentiate between monopaternal superfecundation and
twinning.
(2) Multipaternal [Heteropaternal] superfecundation [HS]– Multiple
copulatory events are performed by different partners.
(i) If there are two partners [most common], it is known as dipaternal
superfecundation. Depending on number of partners, there can be
tripaternal, tetrapaternal, pentapaternal superfecundation etc. This is
common in animals but uncommon in man due to social taboos. The
frequency of HS among dizygotic twins whose parents were involved in
paternity suits is 2.4%. Before the era of DNA profiling, they could be
detected only by blood examination, and before blood examination era only
by external appearance, eg one black and one white baby born at birth
clearly indicated a case of superfecundation.
(3) Age of fetuses – is same. Development is parallel but not equal. Depends
upon relative blood supplies from separately formed placentae.
(4) Fate – one fetus may end up as fetus papyraceous or may end up in
vanishing twin syndrome [please see below].
(5) Incidence of multiple pregnancies:
(i) Determined by Hellin’s law [syn, Hellin-Zeleny law] – 1 in 89 pregnancies
ends in the birth of twins; one in 892 [7921], of triplets; one in 893
[704,969], of quadruplets.
(ii) Of all twin pregnancies, 70% are binovular twins.

9. Superfetation
Superfetation is fertilization of an ovum in the presence of an existing
pregnancy.
Salient features:
(1) Preconditions – Septate or double uterus facilitates superfetation, but is not
an absolute necessity.
(2) Age of fetuses – is different. Difference varies from 1-3 months
(3) Development of fetuses – different. Elder fetus can be determined by rule of
Haase [ch 3].
(4) Parturition – May be single or multiple. In a single parturition, two or more
fetuses in different stages of development may be born at the same time. In
multiple parturitions [very rare], full term fetuses are born at different periods.
An alternative explanation to multiple parturitions is that both fetuses started
life together as twins, but one of them did not develop normally either due to
 lack of proper blood supply, or because of some other cause. Once the
“dominating” twin is born, the other twin starts receiving proper blood supply,
matures in a few months and is born at a subsequent parturition.
(5) Fetus papyraceus [syn, Fetus compressus] -
(i) Def - A flattened, partly mummified twin fetus that dies early in pregnancy
and remains in the uterus until the term is completed.
(ii) Frequently discovered - during an ultrasound examination.
(iii) Fate - The fetus is compressed between the uterine wall and the amniotic sac
of the living twin. It is flattened like a paper or parchment and is mostly
mummified. May be incorporated into the placenta of the surviving twin
and, if large enough, visible at delivery.
(iv) Age at death – can be determined by its CR length.
(v) Occurrence - Common in superfetation, but may be seen in superfecundation
also.
(6) Vanishing twin syndrome -
(i) Def - Multifetal gestation with subsequent disappearance of one or more
fetuses. First described by Stoeckel in 1945.
(ii) Features - There may be (a) complete reabsorption of a fetus, (b) formation
of a fetus papyraceus, or (c) development of a subtle abnormality on the
placenta such as a cyst, subchorionic fibrin, or amorphous material.
(iii) Causes - (a) chromosomal abnormalities in the vanishing twin, (b) improper
cord implantation.
III. LEGITIMACY AND PATERNITY

A child is said to be legitimate, if it is born (i) during the continuation of a legal

marriage, or (ii) within 280 days of death of husband or (iii) within 280 days
after the dissolution of marriage by divorce [S.112, IEA].
Salient features:
(1) A legitimate child is entitled to inherit the property of his parents.
(2) The child is illegitimate (bastard) if the alleged father (i) is under the age of
puberty (ii) is physically incapable to beget children [eg due to illness,
congenital or acquired deformities, azoospermia, vasectomy etc] (iii) did not
have access to his wife when the child was begotten (iv) displays a blood
group or DNA profile, which is not compatible with that of child.
(3) Posthumous AIH - Child will be considered legitimate even if born >280
days after death of husband [ch 23].

A. When Does the Question of Legitimacy Arise?

The question of legitimacy arises in following situations:
1. Inheritance
Only a legitimate child can inherit the property of his father.
2. Affiliation cases
An affiliation (L filius, son) case refers to a legal dispute in which the paternity
of an illegitimate child is sought to be determined, and the obligation of
contributing to its support enforced.
Salient features:
(1) In India, affiliation cases are decided by S.125, CrPC. If paternity is proved,
a First Class Magistrate may order the father to pay a monthly allowance of
any sum for the maintenance of such child.
(2) Medical examination in affiliation cases – Same as that in suppositious
children [please see below].
3. Suppositious children
A suppositious (fictitious) child is one produced by a woman who claims it as
her own whereas in actual fact it is not her child.
Salient features:
(1) Difference from an affiliation case [please see Table 7]
(2) Common situations where suppositious children are produced
(i) A woman may feign pregnancy and delivery and later produce a living child
as her own
(ii) A woman may substitute a male child for a female child
(iii) A woman may substitute a living child for an aborted child
(3) Reasons for producing a suppositious child -
(i) Blackmail
(ii) Bringing a charge of breech of promise of marriage against a man
(iii) Claiming property
(iv) Obtaining money
(4) Medical examination in suppositious children -
(i) Examine for signs and pregnancy and delivery. (a) If absent, the child is
suppositious (b) if present, date of delivery should be calculated from signs.
It must be compatible with the age of child produced.
(ii) Blood group examination of mother, child and alleged father
(iii) If blood examination proved inconclusive, DNA profiling. Please see also
ch 29.
4. Disputed paternity
Paternity is said to be disputed, when the alleged father denies being the father
of a child. Paternity is disputed in suppositious children and affiliation cases
[also see ch 23]. Please see ch 29 for solving disputed paternity.
5. Posthumous births
A birth is said to be posthumous when the alleged father is dead. If the family of
the dead man refuses to accept the child, the case becomes similar to that of
disputed paternity.
6. Wrongful life
It is a variation of wrongful life suit [ch 23]. Here a normal, healthy child sues
his parents for his illegitimacy. In Zepeda v. Zepeda, 41 Ill. App. 2d 240, 190
N.E.2d 849, 851 (1963), a healthy illegitimate child brought an action against his
father, claiming injury by virtue of his illegitimate status. The court rejected the
claim, one of its reasonings being fear of a flood of litigation.

IV. DELIVERY

Delivery is natural or assisted expulsion of the child at full term.

A. Signs of Recent Delivery in the Living

Signs given below are more typical of a full term delivery than of a premature
delivery.
1. General indisposition
(1) Woman is pale, exhausted and ill looking with
(2) -pulse and slight fever for first 2-3 days.
2. Breast changes
(1) Breasts:
(i) Full, enlarged, tender with a knotty feeling
(ii) Superficial veins prominent
(iii) Colostrum or milk may be expressed by compression
(2) Areola: dark, Montgomery tubercles [areolar glands] present
(3) Nipples - enlarged
3. Abdominal changes
Abdominal walls are (i) pendulous, (ii) wrinkled and show (iii) linea albicantes
[for details, please see above] and (iv) linea nigra (v) In case of c/s - Abdomen
shall show incision or scar.
4. Perineal changes
(1) Sometimes lacerated
(2) From age of laceration, date of delivery may be calculated.
5. Uterus
a. Morphology
(1) Immediately after delivery –
(i) Feel - Contracted and retracted body of uterus feels like hard muscular tumor
(ii) Upper border – lies 3 cm below umbilicus
(iii) Diminishes in size – at a rate of 1.5 cm/day
(2) 1wk - Upper border – Midway between umbilicus and pubis
(3) 2wks - Descends into pelvis [becomes a pelvic organ]
(4) 9wks – Returns to normal condition.
b. Contractions
Intermittent uterine contractions present for first 4-5 days.
6. Cervix
(1) Immediately after delivery -
(i) Cervix soft and dilated
(ii) Edges torn and lacerated transversely
(2) 24 hours -
(i) Internal os begins to close
(ii) External os is soft and patent and admits 2 fingers
(3) End of 1 week – one finger is admitted with difficulty
(4) End of 2 weeks – external os is closed.
7. Labia
(1) Bruised (2) Swollen and tender (3) lacerated [sometimes].
8. Vagina
(1) Smooth walled. Rugae begin to appear by 3rd wk.
(2) Capacious and relaxed
(3) Shows recent tears, which heal by 7th day.
9. Lochia
Lochia [Gk. Lokhos, childbirth] is a discharge from uterus which lasts for 2-3
weeks.
Salient features:
(1) Stages – 3 stages are seen. All have peculiar, sour odor.
(i) Lochia rubra – (a) Duration - Lasts first 4-5 days. (b) Nature - bloody (c)
Color - bright red (d) Quantity discharged – 250 mL [total] (e) Contents -
Blood clots, decidual cells, fetal membranes [shreds], lanugo, meconium,
vernix caseosa
(ii) Lochia serosa – (a) Duration - lasts 4 days [from 6th -9th day of delivery]. (b)
Nature – serous, watery; (c) color – pale (d) Contents – Blood cells [less
RBCs, but more WBCs], Cervical mucus, Microorganisms [anaerobic
Streptococci, Staphylococci], Wound exudates
(iii) Lochia alba - (a) Duration - from 10th -21st day. (b) Nature – scanty, thick,
turbid; (c) color – initially yellowish gray; later whitish. (d) contents –
cholesterol crystals, decidual cells, fatty and granular epithelial cells,
leucocytes, microorganisms, mucus,
10. Lab tests
Blood and urine continue giving +ve pregnancy tests for 7-10 days

B. Signs of Recent Delivery in the Dead

(1) All local signs mentioned above [except essentially “live” signs eg
intermittent contractions of uterus]
(2) Uterus [Table 8]- Additional changes are as follows
(i) Immediately after delivery – (a) flabby. (b) Cavity – almost obliterated by
apposition of anterior and posterior walls
(ii) 2-3 days after delivery – (a) Length – 17.5 cm (b) Breadth – 10 cm
(3) Placental site - Immediately after delivery – Placental site appears as an
irregular, nodular, elevated area. Covered with clotted blood, lymph and
portions of decidua. Size
(4) Peritoneum covering of lower uterus – Immediate till few days – arranged
in folds. These folds disappear after a few days.
(5) Ovaries, fallopian tubes –
(i) Congested immediately after delivery. Become normal if a few days.
(ii) Corpus luteum – quite large. Found in one of the ovaries
(6) Urinary bladder – Immediately after delivery – edema and hyperemia.
Sometimes submucous extravasation of blood.

C. Signs of Remote Delivery in the Living

Generally a single full term delivery leaves permanent signs on the body of
mother. A premature delivery may show little or rarely no marks.
(1) Abdomen – abdominal wall is lax. Shows multiple white scars on lateral
aspects. Linear nigra present
(2) Breasts –
(i) Lax, pendulous, soft, wrinkled [if baby was nursed]. Show linea albicantes.
(ii) Nipples – enlarged
(iii) Areolae – dark
(iv) Montgomery tubercles - present
(3) Vulva – partially gaping, labia do not oppose orifice completely
(4) Vagina – partially open, vaginal rugae are absent, walls are relaxed
(5) Perineum – may show a scar of an old tear
(6) Cervix - Table 9.

D. Signs of Remote Delivery in the Dead

Uterus and cervix – Table 9.
E. ML Aspects of Delivery
(1) Abortion – It may be alleged that the woman aborted illegally, while it might
have been a premature delivery
(2) Amniotic fluid embolism - Please see ch 26.
(3) Blackmail – A lady may produce a suppositious child and claim it to be
fathered by a man whom she blackmails [please see above under “disputed
paternity”]. Signs of recent delivery must be present on the woman. The DNA
of child must match with that of mother and claimed father.
(4) Chastity – A person may claim that his wife is not chaste and has had sexual
relations before, and has delivered a child fathered by someone else. Signs of
remote delivery must be present on the female.
(5) Concealment of birth – Woman may be accused to concealment of birth by
secret disposal of dead body (u/s 318, IPC), while in fact, she never delivered.
(6) Divorce – (a) After marriage - Delivery of a child fathered by someone other
than the husband after marriage is a ground for divorce. (b) Before marriage -
Delivery before marriage is not a ground for divorce even if fathered by
someone else than husband. (c) Pregnant at the time of marriage - If at the
time of marriage the woman was pregnant by someone other than the husband,
it is a voidable marriage. [please see ch 23 – impotence and sterility].
(7) Feigned delivery – Woman may feign delivery in order to get leave from
office, or to escape capital sentence.
(8) Infanticide – woman may have been accused of infanticide, while in fact she
never delivered.
(9) Legitimacy – A child is legitimate, if he is delivered within 280 days after
the dissolution of marriage (S.112, IEA).
(10) Nullity of marriage – Delivery of child before marriage is not a ground for
nullity of marriage.
(11) Precipitate labor - please see ch 27.
(12) Water births - Water birth is a method of delivery, which involves partial
immersion of mother and delivery of child in warm water. Proponents believe
that this method is safe and provides many benefits for both mother and infant,
including pain relief and a less traumatic birth experience for the baby.
However, critics argue that the procedure introduces unnecessary risks to the
 infant such as infection and water inhalation.

25. Sexual Offences

I. INTRODUCTION

Sexual offences are criminal forms of human sexual behavior. A sex offender is
one who commits a sexual offence.

II. CLASSIFICATION

Sexual offences may be classified as below:

(I) Natural sexual offences (Offences involving natural penile-vaginal
penetration) (A) Violent – Done without consent e.g. rape (B) Non violent –
done with consent e.g. incest, adultery (II) Unnatural sexual offences
(Offences involving penetrations other than penile-vaginal)
(A) Sodomy (B) Buccal coitus (C) Tribadism
(III) Sexual perversions (sexual psychiatric disorders. Classified by DSM-5 as
paraphilic disorders) (A) Pedophilia (sexual intercourse with children); (B)
Exhibitionism; (C) Voyeurism; (D) Sadism; (E) Masochism; (F)
Frotteurism; (G) Necrophilia; (H) Undinism; (I) Miscellaneous [please see
below]

III. RAPE

Rape (Latin rapio; seize, snatch) is an assault by a person involving sexual

intercourse with another person without that person’s consent. Historical -
Instances of rape occur in Greek and Roman mythology. In Greek mythology,
Phoebe and Hilaeira, the daughters of Leucippus were forcibly abducted and
raped by the twin brothers Castor and Pollux [Fig. 25.1]. In Roman
mythology, the rape of Lucretia was a starting point of events that led to
overthrow of Roman Monarchy and establishment of Roman Republic. As a
direct result of rape, Lucretia committed suicide.

A. Legal Provisions Regarding Rape in India

1. Provisions in IPC
a. S.166A, IPC
If a police officer fails to record FIR u/s154(1) CrPC of a victim of rape [and
also of vitriolage (S.326A, 326B IPC), outraging the modesty of woman (S.354
IPC, S.509, IPC), disrobing a woman (S.354B, IPC), trafficking a person
(S.370, IPC) and exploitation of a trafficked person (S.370A, IPC)], he shall be
fined and given rigorous imprisonment for a minimum of 6 months and up to 2
years.
b. S.166B, IPC
If any hospital, whether Govt or private does not provide immediate first-aid or
treatment free of cost to any victim of rape [or vitriolage] u/s357C CrPC [Pl
see below], the in-charge of hospital would get a punishment for 1 y or fine or
both [Same punishment is also given if free medical aid is not provided to
victims of vitriolage (S326A IPC). Pl see ch 11].
c. S.228A, IPC
Whoever prints or publishes the name or any matter which may make known the
identity of victim of rape shall be punished with imprisonment of up to 2 years
and fine. Publication is possible only under following circumstances (i) a police
officer publishes name for investigation, or (ii) victim (>18 years) authorizes in
writing, or (iii) if victim is dead, minor or of unsound mind, next of kin has
authorized in writing.
d. S.327, 329 (causing hurt, Grievous hurt, to constrain to an illegal act)
e. S.328 (Causing hurt by means of poison, with intent to commit an offence
– Drug Facilitated Sexual Assault)
Please see ch 31.
f. S.375, IPC (Definition of rape)
The definition of rape was changed radically after the infamous Delhi gang rape
case of 2012. A committee was made under the chairmanship of former Chief
Justice JS Verma with the task of reforming and invigorating anti-rape law. The
comprehensive 630 page report was completed in 29 days and lauded both
nationally and internationally. This eventually led to the passing of The Criminal
Law (Amendment) Act, 2013 [CLAA 2013]. It came into force on Feb 3, 2013.
Currently the definition is as follows:
Definition of rape - A man is said to commit “rape” if he:
(a) penetrates his penis, to any extent, into the vagina, mouth, urethra or anus
of a woman or makes her to do so with him or any other person; or (b) inserts,
to any extent, any object or a part of the body, not being the penis, into the
vagina, the urethra or anus of a woman or makes her to do so with him or any
other person; or (c) manipulates any part of the body of a woman so as to cause
penetration into the vagina, urethra, anus or any part of body of such
woman or makes her to do so with him or any other person; or (d) applies his
mouth to the vagina, anus, urethra of a woman or makes her to do so with him or
any other person, under the circumstances falling under any of the following
seven descriptions:
Memory Aid 1: 4 acts required for rape
1. 4 acts required for rape can be remembered by PIMA
(a) Penetrates [Penis] (b) Inserts [any object, part of body] (c) Manipulates [woman] (d) Applies [mouth]
2. 4 places where insertion is mentioned [from top] – mouth, urethra, vagina, anus. 4 acts and 4
penetration places give a total of 16 possible combinations [Table 1]
3. Mouth specifically mentioned only in (a). Not included in (b) and (d). Implied in (c). Understandable
why it is not included in (d), because that act would amount to just kissing – a less serious offence than
rape.
4. In (c) assailant is not manipulating the inserting object, but rather the object (woman) where insertion
occurs.
(1) Against her will
(2) Without her consent
(3) With her consent, when her consent has been obtained (a) by putting her or
(b) any person in whom she is interested in fear of death or of hurt
(4) With her consent, when the man knows that he is not her husband, and that
 her consent is given because she believes that he is another man to whom she
is or believes herself to be lawfully married
(5) With her consent, when, at the time of giving such consent, (a) by reason of
unsoundness of mind or (b) intoxication or (c) the administration by him
personally or through another of any stupefying or unwholesome substance,
she is unable to understand the nature and consequences of that to which she
gives consent
(6) With or without her consent, when she is under 18 years of age [statutory
rape]
(7) When she is unable to communicate consent [Note - The age of consent was
changed from 16 y to 18 y by CLAA 2013. Condition
(8) was also added by the same amendment].
Explanation 1: For the purposes of this section, “vagina” shall also include
labia majora [added by CLAA 2013. This effectively means that even touching
of penis with vulva amounts to rape].
Explanation 2: Consent means an unequivocal voluntary agreement when the
woman by words, gestures or any form of verbal or non-verbal communication,
communicates willingness to participate in the specific sexual act, provided that
a woman who does not physically resist to the act of penetration shall not by the
reason only of that fact, be regarded as consenting to the sexual activity [added
by CLAA 2013].
Exception 1: A medical procedure or intervention shall not constitute rape.
[added by CLAA 2013].
Exception 2: Sexual intercourse by a man with his own wife (even without her
consent) is not rape, if she is > 15 years of age. If she is < 15 years, sexual
intercourse with or without consent is rape (marital rape).
Memory Aid 2: Explanations and Exceptions to S.375 IPC
Vice Chancellor Medicates Wife
Explanations:
Vagina includes labia majora
Consent means an unequivocal voluntary agreement
Exceptions:
Medical procedure is not rape
Wife >15 y cannot be legally raped by husband
i. Comments
(a) penetrates his penis, to any extent, into the vagina, mouth, urethra or anus
of a woman or makes her to do so with him or any other person. Ex - (1) “Z”
draws a loaded gun and threatens woman “W” to kill her if she does not allow
penetration of penis of man “M” into her vagina [or mouth, urethra or anus] "
under fear of injury or death, she allows this " “Z” has raped “W”. “M” has not
raped “W”, if he was under similar threat. However if “Z” and “M” were
working in collusion, then both have raped her. (b) inserts, to any extent, any
object or a part of the body, not being the penis, into the vagina, the urethra or
anus of a woman or makes her to do so with him or any other person. Ex - (1)
“Z” inserts his finger into the vagina [or urethra or anus] of a woman “W” " Z
has raped W. (2) “Z” inserts a pencil into the vagina [or urethra or anus] of a
woman “W” " Z has raped W. Earlier to 2013 amendments, both these situations
were not rape; Z could at most be prosecuted u/s 354 IPC. (3) “Z” inserts his
finger or pencil into the mouth of a woman “W” " Z has not raped W, as mouth
has been left out of this clause. (4) “Z”, a medical doctor, after taking
informed consent from woman “W” performs a PV examination on her " Her
husband alleges rape " Z has not raped W. Exception 1 excludes medical
procedures from definitions of rape. (c) manipulates any part of the body of a
woman so as to cause penetration into the vagina, urethra, anus or any part
of body of such woman or makes her to do so with him or any other person. Ex
– “Z” pushes a woman “W” from behind [or causes her to trip over] so that she
falls " A stick lying on the ground penetrates her vagina [or urethra, anus or any
part of her body] " “Z” has raped “W”. This is a very far reaching clause and
it remains to be seen how courts interpret this clause. Importantly, here “Z” does
not manipulate the inserting object; but rather the woman so that insertion
occurs. A seriously doubtful portion of the clause is “any part of body of such
woman”. If in the above example, the stick penetrates her eye [or ear, mouth
etc], yet it would be rape. This obviously is absurd, and quite probably courts
would not interpret such situations to be rape. (d) applies his mouth to the
vagina, anus, urethra of a woman or makes her to do so with him or any other
person. Ex - (1) “Z” licks the vagina [or urethra or anus] of a woman “W” " Z
has raped W (2) “Z” threatens woman “W” to allow man “M” to lick her
vagina [or urethra or anus] " Under fear of injury or death, she does so " Z has
raped W. Situation regarding M’s culpability is same as above [“penetrates”
clause]. (3) “Z” forcibly applies his mouth over the mouth of a woman “W” " Z
has not raped W, as mouth is not included in this clause. Z can however be
prosecuted u/s 354 IPC.
ii. Difference between will and consent
(1) Will and consent - “Will” is a psychological desire; “consent” is a legal
concept [pl see S.90, IPC (ch 2)]. Illustrations
(i) Mother tells child to eat spinach"Child says "no" because he does not like the
taste [he has no "will" or desire to eat]"Mother asks him to go out of house
as punishment"Not wanting to take punishment, child reluctantly agrees"He
has consented for eating spinach, but the consent is taken by inducing "fear
of injury" so it is invalid. Child eats spinach, but it is against his will and
without his consent
(ii) Mother tells child to eat spinach"Child says "no" [as above]"Mother says he
will not grow well if he does not eat spinach"child eats spinach because he
wants to grow, but he eats unwillingly. Consent is not taken by fear of
injury, or under a misconception of fact, so it is valid. Will is absent,
consent is present. [“Medicine to an ailing child” may be substituted in
place of spinach]
(iii) Mother tells child to eat chocolate"Child loves chocolates. He eats readily.
Both "will" and "consent" are present.
(iv) Teacher asks student to attend his class"student does not want to attend,
because class is boring"teacher says he will not let him sit in examinations
if his attendance is short"student attends class reluctantly "consent not
valid, as obtained by fear. Both will and consent are absent.
(2) When both will and consent are absent in rape – Most common situation.
Example: Accused seizes woman in bushes and has forcible intercourse with
her.
iii. Explanations of S.375, IPC
(1) Against her will - Example: teacher promises to pass weak student, if she
has sex with him. She agrees “unwillingly”. Consent present [because all
requirements of S.90, IPC (ch 2) are fulfilled]. But will is absent"Rape.
(2) Without her consent - Example: doctor says to illiterate patient that sexual
intercourse with him is the only treatment available. She agrees willingly
[because she wants treatment. Will is additionally indicated because she may
even visit his clinic daily for this “treatment” and may even pay doctor for it].
Will present; Consent absent [because taken “under a misconception of
 fact”]"Rape.
(3) With her consent, when her consent has been obtained (a) by putting her
or (b) any person in whom she is interested in fear of death or of hurt -
Man tells woman he would maim her if she does not have intercourse with
her"She agrees"Rape.
(4) With her consent, when the man knows that he is not her husband, and
that her consent is given because she believes that he is another man to
whom she is or believes herself to be lawfully married - (a) Man (M) enters
friend (F’s) house to meet him" House is in dark" F’s wife thinks F has come"
offers intercourse"M agrees"both have intercourse (woman even assisting him
in the act) "Rape [NB. Here man does not deceive woman. She is mistaken on
her own. A similar situation may occur in case of a blind woman. If man
deceives woman, he is liable u/s 493 IPC for which punishment is greater
(10y)].
(5) With her consent, when, at the time of giving such consent, (a) by reason
of unsoundness of mind or (b) intoxication or (c) the administration by
him personally or through another of any stupefying or unwholesome
substance, she is unable to understand the nature and consequences of
that to which she gives consent - Man asks insane girl to have sex with him.
She agrees"Rape.
(6) With or without her consent, when she is under 18 years of age - Girl
suggests to boy friend that they should have sex"He agrees"Girl is <18
years"Rape.
(7) When she is unable to communicate consent - Boy has had voluntary sex
act with his girl friend several times " Thus consent is taken for granted by
him One day he finds her sleeping [or unconscious] has intercourse with her
presuming consent rape, because she was unable to communicated her consent
at this particular time.
Explanation 1: For the purposes of this section, “vagina” shall also include labia
majora [meaning of “vagina”] - Man seizes woman in bushes and tries to have
intercourse with her forcibly. As soon as penis touches vulva, he loses erection
because of fear"Rape. [slightest penetration – even touching of penis with vulva
is rape. Ejaculation not necessary. Pl also see below under Medicolegal questions
relating to rape" Penetration level sufficient to constitute rape].
Explanation 2: Meaning of consent - Consent should be explicit and not implicit.
Ex - Man “M” asks a woman “W” in a lonely place if he can have sex with
her"She keeps quiet" M thinks her silence is an indication of consent"he has sex
with her during which period also she is quiet"This is rape
Exception 1: A medical procedure or intervention shall not constitute rape - Woman
comes to a doctor for antenatal check-up. After taking informed consent, the
doctor conducts a PV examination. Since it is a medical procedure, it is not rape,
although insertion of finger in vagina is rape.
Exception 2: Sexual intercourse by a man with his own wife (even without her
consent) is not rape, if she is > 15 years of age. If she is < 15 years, sexual
intercourse with or without consent is rape - (a) man asks legally married wife
to have sex" she says no"He ties her to bed and has forcible sexual intercourse
with her"NOT rape [In India, woman is deemed to have given unconditional
consent for sexual intercourse to her husband at the time of marriage. This is not
so in several western countries, where both husband and wife must take consent
from the other before having sex] (b) Wife <15 years" Requests husband to have
sex with her" they have sex" Rape.

g. S.376(1) and S.376(2), IPC (Punishment for rape)

S.376 (1) : Punishment for rape: Whoever commits rape shall be punished with
imprisonment [simple or rigorous (with hard labor)] for more than 7 years (up
to life) +fine.
S.376 (2) : Added by The Criminal Law (Amendment) Act 1983, and modified
further by The Criminal Law (Amendment) Act 2013 [CLAA 2013]. Defines
and punishes 14 serious forms of rape. Punishment in all 14 cases is rigorous
imprisonment for more than 10 years and up to imprisonment for life
[which shall mean imprisonment for the remainder of that person’s natural
life]+Fine. The forms are [with memory aids]: (a) a police officer commits
rape (i) within the limits of his jurisdiction, or (ii) in the premises of any police
station, or (iii) on a woman in his custody. (b) a public servant [Memory aid 3],
takes advantage of his official position and commits rape on a woman working
under him. (c) a member of the armed forces [Memory aid 4] deployed in an
area by the Central or a State Government commits rape in such area. (d) a
person on the management or on the staff of a jail, remand home or other place
of custody, or of a women’s or children’s institution [Memory aid 5],
commits rape on any inmate of such jail, remand home, place or institution
[custodial rape]. (e) a person on the management or on the staff of a hospital
commits rape on a woman in that hospital. (f) a relative, guardian or teacher
of, or a person in a position of trust or authority towards the woman, commits
rape on such woman. Family or father figure [Memory aid 6]. (g) a person
commits rape during communal or sectarian violence. (h) a person commits
rape on a woman knowing her to be pregnant. (i) a person commits rape on a
woman <16 y [before CLAA 2013, this age was 12 y]. (j) a person commits rape,
on a woman incapable of giving consent. (k) a person in a position of control
or dominance over a woman, commits rape on such woman. - Kontrol
[Memory aid 7]. (l) a person commits rape on a woman suffering from mental
or physical disability. Lunatic [Memory aid 8. (m) a person while committing
rape causes grievous bodily harm or maims or disfigures or endangers the
life of a woman [Memory aid 9]. (n) a person commits rape repeatedly on the
same woman. Number of times [Memory aid 10].
S.376 A, B, C, D, E
CLAA 2013 has modified S.376 A,B,C and D and has added S.376E, which did
not exist earlier.
(1) S.376A, IPC - Punishment for causing death or resulting in persistent
vegetative state [PVS] of victim - Whoever, commits an offence u/s 376(1)
and 376(2) and in the course of such commission inflicts an injury which
causes the death of the woman or causes the woman to be in PVS, shall be
punished with minimum rigorous imprisonment of 20 y, which may extend
to imprisonment for life [which shall mean imprisonment for the remainder of
that person’s natural life] or with death. Memory aid 11 - Aruna Shanbaug
case.
(2) S.376B, IPC - Sexual intercourse by husband upon his wife during
separation - Wife living separately from husband (i) under a decree of
separation [u/s 10 of Hindu Marriage Act, 1955, wife may request court to
allow her to live separately from husband] or (ii) otherwise. In either case,
husband goes to her premises and has intercourse without her
consent"punishment is imprisonment (simple or rigorous) of >2 yrs; may
extend to 7 y+ fine. Memory aid 12 - Bride.
(3) S.376C, IPC - Sexual intercourse by a person in authority - Whoever,
being (a) in a position of authority or in a fiduciary relationship [Pl see ch
2"Duties of a medical practitioner"Fiduciary duty]; or (b) a public servant; or
 (c) superintendent or manager of a jail, remand home or other place of custody
established by or under any law for the time being in force, or a women’s or
children’s institution; or (d) on the management of a hospital or being on the
staff of a hospital, abuses such position or fiduciary relationship to induce or
seduce any woman either in his custody or under his charge or present in the
premises to have sexual intercourse with him, such sexual intercourse not
amounting to the offence of rape, shall be punished with >5 y imprisonment of
either description; may extend to 10 y, and shall also be liable to fine.
Reasoning"It is easy to obtain consent from woman, because these are
positions of authority. Memory aid 13 - Custodial; Control.
(4) 376D, IPC - Gang rape - Where a woman is raped by one or more persons
constituting a group or acting in furtherance of a common intention, each of
those persons shall be deemed to have committed the offence of rape.
Punishment is >20 y rigorous imprisonment. It may extend to life [which
shall mean imprisonment for the remainder of that person’s natural life]. There
will also be fine, which shall be just and reasonable to meet the medical
expenses and rehabilitation of the victim, and shall be paid to the victim.
Ex: If four persons each restrain one limb of a woman and actual intercourse is
done by the fifth person, all 5 are deemed to have gang raped her. If one of the
persons in the gang is a woman, she is not liable according to Supreme court.
Before CLAA 2013, gang rape was mentioned u/s 376(2) (g) .
(5) 376E, IPC - Punishment for repeat offenders [Memory aid 14] -Whoever
has been previously convicted of an offence punishable u/s 376, 376A or
376D and is subsequently convicted of an offence punishable under any of the
said sections shall be punished with imprisonment for life which shall mean
imprisonment for the remainder of that person’s natural life, or with death.
(Memory Aid 15) D E A th penalty is only given in A and E.
Tables 2, 3 and 4 summarize the special situations relating to rape.
h. S.493, IPC
Cohabitation caused by a man deceitfully inducing a belief of lawful marriage is
punishment 10 y+fine. This section appears similar to S.375(4) above, but has
subtle differences. IN S.493 man uses deceit to make woman believe he is her
husband. In S.375(4). she is deceived on her own. Ex (a) Boy ‘B’ is legally
married to girl ‘G’ in childhood [Under Hindu Marriage Act, 1955, boy should
be > 21 y and girl >18 y. But if marriage is solemnized against these conditions,
the marriage is valid – ch 23]. Soon thereafter B goes to a different country to
study. He lives with his friend ‘F’ and tells about his marriage. Several years
later, ‘F’ goes to that village and tells girl ‘G’ that he is her husband. She can not
recognize him as many years have passed, and has sex with him"Punishment u/s
493.
i. S.498, IPC
Enticing or taking away or detaining with criminal intent a married
woman"punishment 2 y+ fine. He may have taken away woman with intention
to rape, but even if he has not actually raped the woman, this section comes into
play.

2. Provisions in CrPC
a. S.26(a), CrPC
All rape cases should be tried as far as practicable by a Court presided over by a
woman.
b. S.53A, CrPC
Medical examination of accused – Please see below under “examination of
accused”.
c. S.154, CrPC
(1) S.154(1), CrPC - If information of offence is given by a woman against
whom an offence of rape [also offences of vitriolage (S.326A and 326B,
IPC), outraging modesty of woman (s354 IPC), sexual harassment (354A
IPC), attempt to disrobe(S.354B, IPC), voyeurism (S.354C, IPC), stalking
(S.354D, IPC), insulting modesty of woman (S.509, IPC)] has been
attempted or committed, then such information shall be recorded by a
woman police officer or any woman officer [Pl see ch 1 for more on S.154,
CrPC].
(2) S.154(1)(a), CrPC - In case the affected person is temporarily or
permanently mentally or physically disabled, then police officer will record
complaint at the residence of the affected person or at some other convenient
place of affected person’s choice in the presence of an interpreter or a special
educator
(3) S.154(1)(b), CrPC - Such recording of statement shall be videographed [All
3 provisions mentioned above added in 2013 by CLAA. Pl also see ch 1].
d. S.157(1) (b), CrPC
Investigation in relation to an offence of rape - Recording of statement of the
victim shall be conducted (i) at the residence of the victim or in the place of her
choice and (ii) as far as practicable by a woman police officer (iii) in the
presence of her parents or guardian or near relatives or social worker of the
locality.
e. S.164 (5-A), CrPC
(1) In case of offences of rape [also offences of sexual harassment (S.354 and
354A, IPC), attempt to disrobe (S.354B, IPC), voyeurism (S.354C, IPC),
stalking (S.354D, IPC), insulting modesty of woman (S.509, IPC)], a judicial
magistrate shall record the statement of the person against whom such
offence has been committed.
(2) If affected person is temporarily or permanently mentally or physically
disabled, the magistrate shall take the help of an interpreter or a special
educator in recording the statement, and such recording shall be
videographed. Such statement by the disabled person shall also be considered
a statement in-lieu of examination-in-chief [ch 1], when the case finally goes
to court.
f. S.164A, CrPC
Medical examination of victim – Please see below under “examination of
victim”.
g. S.173(1A), CrPC
Investigation in relation to rape of a child may be completed within three months
from the date on which the information was recorded by the officer-in-charge of
the police station.
h. S.176(1A)(b), CrPC
Please see ch 1.
i. S.198(6), CrPC
No court can take cognizance of marital rape, if the wife is <18 y, if >1 y has
elapsed from the date of commission of offence [limitation period].
j. S.273, CrPC
If evidence of a suspected victim of rape or any other sexual offence is being
recorded and if her age is <18 y, the court may take appropriate measures to
ensure that such victim is not confronted with the accused, while at the same
time ensuring the right of cross-examination of the accused [added by CLAA
2013].
k. S.309(1), CrPC
When the inquiry or trial relates to an offence under S.376 to 376-D, IPC, it
shall, as far as possible, be completed within a period of two months from the
date of filing of the charge sheet.
l. S.327(2), CrPC and 327(3), CrPC
(1) in camera trial – The enquiry into and trial of rape of an offence u/s 376 and
376A to 376 E of IPC shall be conducted in camera [from L. camera “vaulted
room” - thus in a judge’s room; in secret; in empty court] [S.327(2), CrPC].
Another in camera procedure is in relation to a mentally ill person [ch 28].
(2) When another person can attend – If either party wants any particular
person to be present, it may request the judge and he may allow
(3) Proceedings not to be published without permission of court [S.327(3),
CrPC] (this is different from S.228A, IPC, where name of victim revealing
her identity cannot be published).
m. S.357B, CrPC
Additional compensation - In case a crime u/s376D IPC has been committed
[i.e. gang rape], the State would pay compensation to the victim for
rehabilitation, over and above the fine which is to be paid by the convicted
person. [added by CLAA 2013].
n. S.357C, CrPC
All hospitals, whether Govt or private must provide immediate first-aid or
medical treatment free of cost to any victim of rape [The law of free medical
aid also applies to victims of vitriolage (S.326A, IPC). Pl see ch 11]. [added by
CLAA 2013].

3. Provisions in IEA
a. S.54, IEA
(1) Previous bad character not relevant, except in reply — In criminal
proceedings, the fact that the accused person has a bad character is irrelevant,
unless evidence has been given that he has a good character, in which case it
becomes relevant. Explanation 1—This section does not apply to cases in
which the bad character of any person is itself a fact in issue. Explanation 2
—A previous conviction is relevant as evidence of bad character.
(2) Illustration – If a person [A] is accused of rape, it does not help the
prosecution to show that A was a person of bad character. However, if A has
already produced evidence that he has a good character, then prosecution can
produce evidence to show he has a bad character.
Memory Aid 16: Important sections of IEA
1. S.45 " Definition of expert witness [ch 1]
Transpose the digits of above
2. S.54 " Previous bad character not relevant, except in reply
Add 101 to both the above sections:
45+101 " 146
54+101 " 155
3. S.146 Questions regarding general immoral character of victim cannot be asked
4. S.155(4) – In cases of rape, it may be shown that the prosecutrix (victim) was of generally immoral
character [Now removed]

b. S.114A, IEA (Burden of proving consent is on man)

(1) Man “M” is accused of raping woman “W” u/s 376(2)(a) till 376(2)(n) "
Sexual intercourse between “M” and “W” has been established (e.g. vaginal
swab of “W” shows DNA of “M”) " question is of consent only "“M” asserts
that “W” had consented, but “W” says she had not consented"court will
presume her statement " If “M” wants to defend himself, he must prove that
woman had consented. How he does it is his problem. [S.114A, IEA is thus
also known as “presumption of lack of consent”].
Memory Aid 17: 4 most important sections for rape
Remember 114 [114A IEA]
Now 114×2 " 228 [228A IPC]
Add 99 " 327 [327(2) and (3) CrPC]
Add 30 " 357B and 357C CrPC

(2) S.114A, IEA is the embodiment of a fundamental principle in law known as

the “doctrine of adverse inference”. Simply stated, the adverse inference
doctrine or rule states that when a party has relevant evidence within his
control which he fails to produce, that failure gives rise to an inference that the
evidence is unfavorable to him. It is also known as empty chair doctrine or
adverse interest rule.

c. S.146, IEA
In cases of rape or attempt of rape, where the question of consent is an issue, it is
not permissible to adduce evidence or to put questions in the cross-examination
of the victim as to her general immoral character, or her previous sexual
experience with any person for proving such consent or the quality of consent.
d. S.155(4), IEA
(1) This has been removed in 2002. Earlier it stated, “When a man is prosecuted
for rape or an attempt to ravish, it may be shown that the prosecutrix (victim)
was of generally immoral character.”
(2) This was highly criticized by women’s groups, leading to its removal.
Reasoning same as in S.146, IEA above.

B. Types of Rape
Statutory rape
Sexual intercourse with a girl <18 y, with or without consent. Before Feb 3,
2013, it was 16 y. CLAA 2013 changed it to 18 y.

C. Consent
1. Age of consent
(1) Age of consent for allowing physical examination is 12 years.
(2) Age at which girl can give valid consent for sexual intercourse is 18 years.
(3) Age at which girl can authorize press to publish her name and picture is 18
years (S.228A, IPC).
2. When consent is not valid
According to S.90, IPC, consent (as is intended by any section of IPC) is not
valid when it is given (1) under fear of injury or (2) under a misconception of
fact (3) mentally unsound (4) intoxicated person and (5) child <12 y. The last
condition stands modified to 18y, since S.375 specifically raises it for rape.
3. Consent from intoxicated woman
Girl was administered some intoxicating substance and then raped. When
brought to the medical officer she was still drunk. Consent unobtainable;
relatives not traceable. How to obtain consent? Doctor must immediately
examine u/s 92, IPC"Examination for girl’s benefit. She may have got STD or
unwanted pregnancy.
4. Rape and arousal
It has been suggested that if arousal occurs during rape, it indicates consent. This
is not true. Arousal has been known to occur even in non-consensual and
forced sex, as the main function of arousal is lubrication, which in turn
protects female genitals from injury.
D. Important Terms
(1) Carnal knowledge - (L. carnis, flesh) Sexual intercourse
(2) Sexual battery - Non-consensual touching of the intimate parts of another.

E. Examination of the Victim

1. Objectives
(1) Record - all injuries
(2) Corroboration of victim’s story:
(i) Whether there is evidence of recent sexual intercourse as alleged
(ii) Whether there is evidence of previous sexual intercourse
(iii) Do the physical signs confirm the use of physical force or of stupefying
drugs as alleged
(iv) Whether the physical findings are consistent with history
(3) Collection and preservation of trace evidence from victim’s body [may
assist in identification of assailant, eg saliva, hair, DNA profile from semen
etc]. All trace evidence must be properly packed, sealed, labeled and then sent
to the laboratory to maintain chain of custody [ch 1]
(4) Treatment of the victim [of physical and psychological damage]
(5) Examination of scene of offence – if desirable. Leaves, grass, mud etc
entangled in victim’s hair, clothes body etc may have to be matched with that
present at the scene.
2. Precautions
(1) For the police – Should advise victim not to change clothes, bathe, or
douche prior to physical examination
(2) For the doctor – Preferably visit the scene of crime to collect additional
trace evidence (blood and urine stains, seminal stains)
(3) For both – Examination should be carried out without delay. Signs of sexual
assault may fade rapidly with passage of time (a) Minor injuries may fade
rapidly (b) swelling and tenderness of vulva may disappear (c) spermatozoa
may not be detectable.
3. Preliminaries and general procedure
(1) Requisition from:
(i) Any police officer [SI requirement, (as in case of accused examination) not
here] can ask a govt doctor to examine the victim, and if such govt doctor is
not available any doctor [16 km clause, (as in case of accused examination)
 not here]. Victim’s consent is necessary. Victim must be produced before
the doctor within 24 hours of receiving information of rape [S.164A(1),
CrPC]. This requirement is not there for accused of rape.
(ii) Court
(2) Consent:
(i) Written and witnessed consent of the woman must be taken. If requisition
from police is there, but no consent from woman, examination can not be
done [S.164A(4), CrPC]
(ii) Court order"examination can be done without consent [if victim of rape does
not consent for examination, police official must be advised to get a court
order – ch 2]
(iii) Consent for additional procedures – For (a) collection of specimens (b)
taking photographs (c) treatment (d) release of information to the press,
specific consent must be taken.
Memory Aid 18: Important components of medical examination of rape victim [S.164A, CrPC]
T I GER CAUGHT IMMEDIATELY
1. T – Time within Twenty four hours [S.164A(1), CrPC]
2. G – Govt Hospital. In Emergency, i.e. when no Govt doctor available, any other doctor [S.164A(1),
CrPC]
3. R – Report must have 6 components [S.164A(2), CrPC]
4. R – R for each conclusion to be given [S.164A(3), CrPC]
5. C – Consent to be recorded [S.164A(4), CrPC, S.164A(7), CrPC]
6. T – Time of commencement and completion of examination to be recorded [S.164A(5), CrPC]
7. Immediate – Immediate handing over of the report [S.164A(6), CrPC]

(iv) Consent for information to police - No consent is required for release of

information to police. That is why an informed consent is necessary before
examination, whereby the doctor informs the patient specifically that he
would be informing the police about the event and handing over all
evidences to them. If the victim gives consent only for physical
examination, but not for information to police, the doctor should record it
in writing, get signatures from the victim, and refrain from proceeding
with the examination. Agreeing to her request may make him liable to be
prosecuted u/s 201 IPC [causing disappearance of evidence of offence].
An analogy may make is clearer. It is possible that the victim gives consent
only for general physical examination and not for anything which she
 considers “invasion of privacy”, eg. PV examination and taking of
vaginal swabs [qualified consent, restricted consent]. In such cases, if
doctor proceeds with restricted examination, he may be sued u/s 201 IPC
for causing disappearance of evidence of offence.
(v) Examination without consent"Doctor can be charged u/s 354, IPC (outraging
the modesty of a woman). Ex. 14 year old girl has voluntary intercourse
with her boy friend"Statutory rape"Police wants to prosecute boy"produces
girl before doctor for medical examination"girl refuses consent [person >12
years can refuse consent]"examination can not proceed. Only court order
can be used to force her to submit to examination.
(vi) Consent of parents or guardians is taken"(a) If girl is <12 years (b) mental
illness, unsound mind, cognitive disorders (c) acute drug or alcohol
intoxication (d) shock due to acute trauma (e) Acute medical conditions
leading to unconsciousness
(vii) Conflict of consent – please see ch 2.
(viii) Report to be declared null and void in absence of consent – If woman’s
consent is not there, examination would be unlawful [S.164A(7), CrPC]
(3) Time - The exact time of commencement and completion of examination
must be noted in the report [S.164A(5), CrPC]. This would indicate the
interval between the alleged time of incidence and examination.
(4) Identification:
(i) Police officer accompanying the victim should identify her. His name and
number must be recorded
(ii) Two identification marks recorded
(5) Presence of a female chaperone – is a must during examination, otherwise
there may be allegations on the doctor himself [u/s 354, IPC – Outraging the
modesty of a woman]. Ideally there should be a nurse [from doctor’s side] and
a female attendant [from victim’s side] or a female police officer
(6) Information about victim [Legally necessary]:
(i) The name and address of the woman and of the person by whom she was
brought [S.164A(2) (i), CrPC]
(ii) The age of the woman [S.164A(2) (ii), CrPC]
(iii) General mental condition of the woman (This is an additional requirement –
as compared with S.53A) [S.164A(2)(v), CrPC]
(iv) Other relevant particulars in reasonable detail [S.164A(2)(vi), CrPC].
 Detailed mention of these are not made in law, but the following
information is implied.
Memory Aid 19: 6 components of report of rape victim [S.164A(2), CrPC]
First 2 are preliminaries and easy to remember
1. Name, address [S.164A(2)(i), CrPC]
2. Age [S.164A(2)(ii), CrPC]
For rest 4 – DIMM
3. Description of material taken for DNA [S.164A(2)(iii), CrPC]
4. Injury marks [S.164A(2)(iv), CrPC]
5. Mental condition of victim [S.164A(2)(v), CrPC]
6. Material particulars (any other) [S.164A(2)(vi), CrPC]

(7) Information about victim [Other] – Partially implied by [S.164A(2)

(vi), CrPC]. Thus highly desirable to record (i) Parents’ name (ii) Marital
status (iii) Occupation (iv) Height and weight (v) Physical development
[indicates if she was capable of struggle]. In case of children note additionally
the development of breasts and genitalia (vi) Place of examination (vii)
Previous history - (a) Menstrual history (b) Operations [Gynecologic, Pelvic]
(c) Pregnancies (d) Sexual experience (e) Vaginal discharge (f) Venereal
disease etc (viii) Requisitioning authority [police, court etc]
(8) Statements of the victim [history]– All relevant statements must be
recorded. Degree of agreement between various statements goes in her favor;
disagreement or contradiction goes against her. Note especially
(i) Whether she knew the accused
(ii) If anything was given to her to eat, drink or smoke before the act. Could she
make out if it was alcohol or some intoxicating drug [possibility of drug
facilitated sexual assault]
(iii) Whether she [or any of her relatives and friends] was put under any threat
[physical or psychological]. If physical threat, what restraints or weapons
were used?
(iv) Did she call for help?
(v) Date and time of alleged offence
(vi) Place of offence – whether indoor or outdoors; was the weather wet or dry
(vii) Did she have recent consensual intercourse? If yes, when? [more pertinent
in married victims]
(viii) Number of alleged assailants (gang rape) [In case of too many assailants,
 she might suffer fractures, or complain of severe abdominal pain due to
weight of too many men atop her]
(ix) Did she struggle or was she too afraid to put up resistance
(x) Which injuries is she aware of [their location etc. This may not be too
obvious to the doctor otherwise]
(xi) Did she feel any pain during or after the incident? [pain on walking,
micturition or defecation is often present]
(xii) Did ejaculation take place? If yes, was it within her body [vagina, anal
canal etc] or outside. If occurred outside, did she notice the appearance of
discharge
(xiii) Was there any bleeding from the part penetrated [vagina, anal canal, oral
cavity etc]
(xiv) Did she scratch or bite the assailant, or use some other weapon on them
[would help correlate injuries on the accused]
(xv) What was the relative positions of the victim and accused during the act
(xvi) Type of sexual acts [eg oral, vaginal, anal, between the thighs etc]
(xvii) Number of sexual acts performed by each assailant
(xviii) Did they use condoms or lubricants [if condoms were used, absence of
spermatozoa may be accounted for. If lubricants were used, they may
specifically be tested for in vaginal swabs]
(xix) Was she using sanitary pads or tampons? If yes, did she dispose them of
after the incident?
(xx) Did she lose consciousness during or after the act
(xxi) Events after the sexual assault - (a) Changed or washed private parts or
clothing (b) Took bath or douche (c) Defecated or urinated after assault; or
washed mouth [brushed] after oral intercourse (d) Did she comb hair (e)
Did she take any sedatives or alcohol after the incident (f) Did she take any
medication on her own after the incident
(xxii) Time period between sexual assault and police complaint. If there is any
delay, what were the reasons?
(xxiii) General demeanor – as she narrates her story [whether aggressive,
agitated, angry, calm, co-operative, dazed, disheveled, distressed, excited,
intoxicated, shocked, tearful or withdrawn].
4. Physical examination
(1) Time – should be done as early as possible after assault, as some signs eg
 swelling and edema of clitoris, labia, vaginal introitus etc may fade within 1-2
hours.
(2) Undressing the victim – Doctor should make no attempt to undress the
victim. She should be asked to undress herself
(3) Second examination - If the woman is in menstrual period, a second
examination should be conducted after stoppage of menstruation.
a. Clothes
(1) Find out if clothes worn at the time of examination are the same as those
worn at the time of assault [If they are different, examination of clothes may
not be of much use]
(2) Removal of clothes – In layers
(i) Outer clothing (a) Patient stands on a large clean sheet of paper and takes off
her outer clothing. Anything that falls eg buttons, earth, fibers, grass,
gravel, hair, leaves, mud, sand, seeds etc can thus be collected on the paper.
The paper is folded and sent for examination. (b) Examination - Clothing
is examined [for tears, soiling, loss of buttons] and then sent for laboratory
examination separately [To detect stains eg blood, earth, feces, grass,
grease, mud, saliva, semen, tears, urine etc. Physical, chemical and
biological examination of these trace materials is done in the laboratory.
DNA profile of the accused can also be made from blood, semen or saliva
stains. Hair, fibers, buttons etc can be compared with those of the accused].
(c) Drying - Clothes should always be dried before sending to laboratory
[Sending clothes with wet blood and seminal stains etc would encourage
growth of fungus, destroying vital evidence] (d) Packing – Clothes should
never be packed in polythene bags [they would tend to preserve moisture
and encourage grown of fungus]. They should always be sent in clean paper
bags.
(ii) Inner clothing [panties, bra etc] – Same procedure is adopted. A different
paper is used
(iii) Other clothing – Other minor pieces of clothing and related material [eg
handkerchief, vulval pads, vaginal tampons etc] must not be overlooked.
Sometimes victim uses handkerchief to clean her genitals. Pads and
tampons may show seminal stains.
(3) Examination of clothes:
(i) Stains – are examined both by naked eye as well as lab examination.
 Significance of various stains: Seminal stains – strongly point towards
sexual assault. Besides clothing, they may also be found at the scene of
crime [eg bedding, carpets, car seats etc]. Seminal stains on undergarments
and outer garments do not necessarily indicate ejaculation outside the
vagina. They may drip out of private parts due to movements of the victim.
Movements of victim may also cause semen to drip from the private parts
to virtually any other place, which the victim visited.
(ii) Trace evidence – finding of grass, leaves, mud, sand etc on clothings may
support the victim’s assertion about the place where the assault occurred.
b. General examination
(1) Prerequisites:
(i) Lighting - Examination must be done in (a) well illuminated room and then
additionally (b) under UV light also [invisible or faint seminal stains will
show up as fluorescent bluish white stains under UV light [because of
choline]. Please see below under seminal fluid-physical examination also]
(ii) Photographic record – (a) External – All injuries howsoever minor; broken
fingernails, torn clothes, seminal stains etc (b) Internal – Pictures of vaginal
vault and cervix with a photocolposcope or video colposcope [Colposcopes
with an arrangement for photography]. Useful for production in court later.
(iii) Labeled diagrams – of all injuries should be made. Sizes of all injuries and
their relative positions from one another should be recorded.
(2) Eyes:
(i) Redness and swelling of eyelids, conjunctival congestion – indicate constant
crying
(ii) Pupils - constricted or dilated [indicate intoxication, head injury];
(iii) Petechial hemorrhages - On conjunctiva [also eyelids, and elsewhere] –
indicate attempt by accused to smother in order to stifle cries
(3) Pulse and respiratory rate – may be - due to emotional stress or major
trauma
(4) Gait – Guarded gait due to pain. Victim walks with legs apart and slow paces
(5) Examination for drunkenness – If victim appears drunk, examine for
drunkenness [please see ch 40].
(6) Marks of violence – May or may not be present. [A] When present – (I)
Determine age of injuries – to correspond with allege time of offence (II)
Observe nature and site - Areas of tenderness, bite marks, bruises, lacerations,
 scratches etc must be searched for on the entire body. Describe their size,
shape, extent, special characteristics [eg bruises showing restraints on arms
and legs], area on which present and possible age. Try to correspond with
victim’s description of assault. Injuries around special locations may indicate
specific activities by accused. From above downwards these signs may be (i)
around mouth and throat – Attempts to prevent victim from calling for help
(ii) Lips – due to blows, rough handling, attempts to kiss and bite (iii)
Shoulders and Back – due to pressure to pin down victim on ground (iv)
Wrists and arms – due to attempts to seize victim (v) Nails – Damaged, broken
or avulsed nails [due to victim scratching assailant]. Collect debris from under
the nails. Examine for epidermal cells, blood, hair, fibers etc. DNA profile
may be prepared. This may be matched to the suspect and his clothes etc.
[same procedure is performed in throttling"ch 19]. (vi) Breasts – due to
manual squeezing, manipulation, rough handling. Love bites may be present
[ch 3] (vii) Nipples – may be completely bitten off [class IV bites, ch 3] (viii)
Thighs and buttocks – due to attempts to separate thighs or buttocks for
penetration. Both inner and outer side of thighs may be scratched, bruised or
lacerated.
Rarely even incised wounds may be seen on thighs due to application of knife in
order to forcibly separate thighs, while the victim attempts to adduct thighs
together [this is a rare example of defense wounds on thighs. Generally they
are found on hands [ch 12]. [B] When absent – Accused often takes the plea
of absent marks of violence as indicative of consent. Marks of violence absent
even in the absence of consent due to (i) fear of injury, death"submission by
the victim (ii) Incapacitation caused to victim by (a) throat grips (b) strong
neck holds (c) severe blow on the head (iii) force used is insufficient to cause
injury (iv) Too early examination. Bruises may not be noticed for up to 48 h
following assault (v) Too delayed examination – due to late reporting. Marks
of minor injuries would fade or heal. (vi) Description of marks of injury – is a
legal necessity [S.164A(2) (iv), CrPC]
(7) Bite marks – They may comprise of true bites or just love bites [ch 3, 12].
[A] True bites – Class II, III and IV bite marks [ch 3]. [B] Love bites - (i)
Class I bites (ii) Etiology - strong continuous suction kisses during passionate
sexual intercourse (iii) Pathogenesis - Negative pressure produced by
suction"rupture of small vessels from .ed air pressure"Intradermal petechial
 hemorrhages (iv) Appearance - (a) discoid or elliptical patterned bruises [1-2
cm] or (b) a shower of petechial hemorrhages which may be confluent, or (c)
both (d) Sometimes the shape of upper and lower lips is reproduced (v) Site –
wherever the victim is kissed with strong suction. Commonly on face, neck,
shoulders, breasts, nipples, chest wall. Less commonly at lower abdomen,
upper part of thighs.
(8) Petechiae on face or conjunctiva – May indicate
(i) intentional attempts to make victim unconscious to silence her or
(ii) unintentional partial asphyxia caused during forcible restraint.

c. Local examination
Local examination of genitalia is most crucial
(1) Position:
(i) Victim placed in lithotomy position [legs drawn up and widely open] in good
light.
(ii) Application of local anesthetics [eg cocaine] may become necessary if too
 much pain is felt on separation of thighs.
Memory Aid 20: Ano-genital injuries in rape
TEARS (Tears, Ecchymoses, Abrasions, Redness, Swelling)

(2) Methods of examination:

(i) Direct visual inspection
(ii) Colposcopy – Better [ch 26]
(iii) Toluidine-blue [Tb] contrast application – (a) Best. (b) Reveals
microinjuries, not revealed even by colposcopy (c) Procedure - (I) Take
vulval swabs for forensic analysis before application of stain (II) Toluidine
blue (1%) is then painted on the posterior fourchette, using a swab, before
any instrumentation. (III) After a few seconds, the residual stain is removed
with lubricating jelly and gauze. (IV) The patient may experience some
stinging at the application site. [toluidine blue is also used to detect
microfractures of the hyoid and thyroid – ch 19]. Please co-relate all
injuries [Normal female genital anatomy] in
ch 24.
(3) Clitoris – red, swollen, edematous. D/d - May be due to uncleanliness and
consequent scratching, masturbation.
(4) Labia:
(i) Finger nail abrasions, bruises, reddening, lacerations, soiling etc should be
noted on major and minor labia. These are due to attempts of the assailant
to draw apart labia.
(ii) Thin tears in the folds of skin between the labia majora and minora are seen
sometimes. These are due to labia minora being inverted towards the
vaginal orifice, causing stretching of their junction with the labia majora.
(5) Hymen:
(i) In case of virgins tears usually occur posteriorly at 6 O’ clock position, or
posterolaterally [5 O’ clock, 7 O’ clock], or less commonly still more
laterally [4 O’ clock, 8 O’ clock] [Fig 25.3]. Abrasion collars in firearm
wounds are also described by referring to clock positions – ch 13].
(ii) Reasons why tears occur more commonly in posterior structures
[fourchette, posterior commissure, perineum etc], rather than anterior
structures [vestibule, clitoris, anterior commissure, mons etc] - (a) the
anatomic site of fixation to the perineal body lies posteriorly; consequently
the tissues are at greatest stress in this location when forceful stretching
 occurs. (b) Anteriorly periurethral tissues buttress the hymen. There is no
such support posteriorly.
(iii) In case of already ruptured hymen [as in married women] there may only be
abrasions and bruising of hymen.

(6) Method of hymenal examination -

(i) Conventional method using Glaister-Keene rods - These are glass or plastic
rods bent at about 150° one end. They have a small spherical head at one
end. So called because first made by John Glaister in Pyrex glass. They
can be fitted with a light, which travels even through the bend by total
internal reflection. Before insertion, the rod should be at body temperature.
The spherical glass head is gently passed through the hymenal aperture and
then eased forwards, when the hymenal edges become slightly everted. By
slowly rotating the sphere, around which the edges are deployed hymenal
tears can easily be seen. This method does not cause any pain or injury.
(ii) Foley’s catheter or an inflatable balloon – Same as above, except that a
Foley’s catheter can be used. Easily available in all hospitals. Glaister-
Keene rods are not easy to get, and may have to be order-made.
(iii) Conical measures [Fig. 25.4] - These are wooden cones similar to the ones
used for measuring circumference of heart valves [ch 5].
(iv) Hymenoscope - This is a refinement of Glaister-Keene rods mentioned
above. While GK rods have a source of light at the rear, hymenoscope has
 a source of light within the ball (2) [Fig. 25.5]. A urethroscope light bulb
(1) is screwed into the cavity of the rod (3) and projects into the ball. Wires
(4) are led from the light bulb, through the rod to an ordinary pocket
battery. Secondly clear plastic material is used instead of glass. Thirdly, the
ball and the rod are hollow, and the ball can be unscrewed from the rod. The
ball is constructed in two parts which are then joined. A series of
interchangeable balls, graded in size can easily be made (5). One with
diameter of 3/4 inch (18 mm) is best for general use, but is too large for
virgins and children, and too small for women who have had frequent
sexual intercourse. A ball with 1/2 inch (12.5 mm) diameter is good for
virgins and with 1 inch (25 mm) diameter for married women. The rod has
an external diameter of 4/10 inches (10 mm) and an internal diameter of
2/10 inches (5 mm). The instrument can be easily made by an electrician. It
is simple, light in weight, not fragile, and easily cleaned with soap and
water followed by spirit. The long flex is useful in allowing the battery to
be out of the examination field (eg it can be in the pocket).
(v) Through rectum - Pass a finger into the rectum"push posterior vaginal wall
forwards and downwards"This pushes the hymen forwards which can now
easily be seen lying against the posterior vaginal wall. Procedure may be
painful in simultaneous rectal assault.
(7) Character and extent of hymenal injuries would depend upon:
(i) Amount of force used
(ii) Disproportion between male organ and vaginal introitus
(iii) Extent of penetration
(iv) Nature of hymen [taut, elastic, tough, deep seated, fimbriate etc]
(8) Age of Hymenal tears:
(i) Immediately after the act – margins of torn hymen are red, sharp and bleed on
touch. The tissues round them are tender
(ii) 3-4 days – edges of tears are congested and swollen
(iii) 7 days – complete healing takes place, but the torn parts do not unite.
Appear as V-shaped defects
(iv) Several months – V-shaped
(9) Fossa navicularis – May show small tears 1-2 mm in size. Caused by
excessive stretching. It disappears after repeated sex acts; thus may not be
seen in married women
(10) Fourchette – Fragile. May show similar tears as fossa navicularis.
Generally torn at the first intercourse; thus an imp sign in virgins but not in
 married women.
(11) Vaginal introitus – slightly edematous. Shows abrasions, bruises.
(12) Vaginal canal:
(i) Use a vaginal speculum for examination
(ii) Look for abrasions, bruises, lacerations. Tears may extend up rectum
[rectovaginal fistula] or bladder [vesicovaginal fistula].
(iii) Bruising - (a) site – most common is anterior vaginal wall [lower 1/3rd] and
posterior vaginal wall [upper 1/3rd]. Bruising of this nature is more
consistent with penetration of penis than with digital penetration. (b) color –
(I) Immediate – dark red (II) 24 h – deep red or purple.
(iv) In consensual intercourse, since there is preliminary stimulation and
consequent lubrication, injuries are not seen.
(v) Lacerations – May rarely be present even in consensual intercourse if (a)
there is marked disproportion between penis and vagina (b) If the
copulation is very active, enthusiastic and forceful (c) when there has been
a complete abstinence from intercourse for a considerable length of time
(vi) If there are no fresh injuries, assess the following: (a) Number of fingers that
can be introduced through the hymenal orifice. (I) This allows the examiner
to assess elasticity of hymen and to determine the degree of penetration
which would be possible without its rupture. (II) In most young women, a
finger may be passed into vagina through an intact annular hymen, which is
felt as a constricting ring round the tip of finger. (III) If two fingers may be
passed easily, sexual intercourse is possible without hymenal rupture. (b)
The areas and degree of tenderness complained of by the patient (c) Laxity
of vaginal orifice - Indicates previous penetration (d) Length of vagina into
the posterior fornix - Elongation indicates previous repeated sexual
intercourse
(13) Vaginal vault:
(i) May vary from minimal mucosal trauma to extensive lacerations. The latter
may occur when there is marked disproportion between penis and vagina
[eg rape on young girls] or if a sexual pervert penetrated some instruments.
(ii) Lacerations are usually seen in posterior fornix of the right side of the vault
and less frequently on the left side.
(iii) Not seen in the anterior fornix.
(14) Cervix – Examination of cervix is best done with a colposcope. It is a
 stereoscopic binocular field microscope with a long focal length and powerful
light source and permits a magnification between 2 to 40 times. Video
colposcopes allow digital image capture. Abrasions of cervix are mostly seen
in digital rather than penile penetration. Abrasions must be differentiated from
erosions [Table 5]. Cervical erosions do not occur due to penetration.

(15) Posterior commissure – rupture may be seen, but is more common in

young virgins because of disproportion between male organ and female
vagina.
(16) Perineum – torn, especially in young children.
(17) Genital injuries may be absent due to
(i) Genitals only touched or rubbed with penis
(ii) Elasticity of genitalia and hymen in a post-pubertal female
(iii) Victim sexually experienced; roomy vagina
(iv) Use of lubricants.
(18) Presence of genital injuries – eg abrasion, bruises or lacerations are
consistent with intercourse with a consenting woman and do not necessarily
indicate rape. Local genital injuries and genital bleeding in a newly married
bride are well-accepted phenomena.
(19) Back and buttocks – Grass, leaves, mud etc on back or buttocks would
confirm sexual assault taking place outside in specific areas
(20) Anal canal – Tears if anal penetration occurred.
(21) 2nd examination – of the victim must be done a day after the first, as some
 bruises, especially those in the lower vagina may take some time to come up
to the surface [delayed bruising (ch 12)].

d. Hair
(1) Scalp hair:
(i) Note general condition – Disheveled, tangled, torn
(ii) Look for entangled grass, leaves, sand, soil etc. Can reveal place of assault.
(iii) Blood indicates local lacerations etc.
(iv) Comb and send any trace evidence that falls out
(v) Collect hair from front, top, back, left and right side
(2) Pubic hair:
(i) Should be combed out
(ii) May reveal non matching male pubic hair; foreign material
(iii) If matted, clip them with scissors. Send for DNA; matting may be due to
dried semen
(iv) In case of deceased – pull 15-20 hair with forceps [makes available root
characteristics for comparison]
(v) In case of living victim – cut; don’t pull
(vi) Areas to collect from – pubic region, vulva
(3) Preservation and maintenance of chain of custody – Vital for legal
validity [ch 1]. Pack, seal, label and sent to lab.

e. Finger nails
(1) Fingernail scrapings – Take from beneath each nail. Send all ten fingernail
scrapings in separate envelop marking each finger and side of hand. Skin,
blood, cloth fibers, hair etc of assailant may be found on microscopic
examination. DNA profiling from these materials can reveal identity
(2) Fingernail clippings – Take [of all ten nails] with a nail cutter. Send each in
a separate envelop with nail cutter separately. Nail cutter should be new and
unused before.

f. Seminal stains
Steps should be followed in strict sequence
(1) If pubic hair are matted – Nip away with scissors entire matted hair as
close to skin as possible. Moisten them with normal saline for half an hour and
examine under microscope. If examination not possible, place in a small paper
envelop, seal, label and hand over to police to be sent over to forensic biology
section for examination.
(2) Swabs from outside areas:
(i) Before starting local examination take swabs from (a) vaginal area [outside]
(b) Perineum (c) Pubic area (d) Inner side of thighs (e) Any other suspected
area [buttocks, abdomen, hands, breasts, face], which can be discovered by
taking the patient in dark and examining entire body area by UV light.
Seminal stains would fluoresce bluish white.
(ii) Use a normal throat swab moistened with normal saline.
(iii) Take four swabs [from all areas contaminated with semen] with cotton
moistened with saline. (a) Prepare smears with the first– on a glass slide
immediately, and dry (I) fix - by heat or chemically [Fixatives that can be
used are (1) commercial spray fixative (2) equal quantities of absolute
alcohol and ether (3) methanol]. Fixation is a process by which biological
tissues [eg spermatozoa] are preserved from decay by preventing autolysis,
putrefaction and fungal growth etc. It also .es the mechanical strength and
stability of tissues. (II) Label slides – using a diamond pencil. Write
 patient’s name and MLC number. (III) Examine for spermatozoa, or hand
over to police to be sent over to suitable department [forensic biology]. (IV)
If very few sperms are seen, record location on X and Y axis, by a
specialized microscope. Defense may want a re-examination of slide by its
own expert (V) After examination, preserve slide for possible production in
court (b) Dip the second swab in a small quantity of saline"examine for
presence and motility of sperms (c) Dry the other two. Send one for
chemical [eg acid phosphatase], immunological, TLC or other methods of
analysis [please see below] and other for DNA profiling.
(iv) If seminal stains have dried out - scrape with a blunt knife, seal, document
and send entire flake for chemical and biological examination.
(3) Tampons – if present, remove and send for examination
(4) Vaginal aspirates [VA]:
(i) Instill 5 ml of normal saline in posterior fornix.
(ii) Aspirate by means of a blunt end pipette or a flexible plastic pipette.
Preferably concentrate by centrifugation at 2,000 g for 15 min. Collect
cellular pellet.
(iii) Alternatively take some mucus on a glass rod or wooden spatula from upper
vagina [less preferable].
(iv) Immediately place onto a clean, prewarmed microscope slide, and examine
for motile spermatozoa under a phase contrast microscope.
(v) Store at -80°C, if examination cannot be done immediately.
(vi) If VA cannot be taken for some reason, take a vaginal swab as below, insert
in a small amount of normal saline and examine.
(5) Vaginal swabs from inside:
(i) Swabs to be taken after taking vaginal aspirates, but before any digital
examination
(ii) Low vaginal swab – Take after examination of hymen
(iii) High vaginal swab – (a) insert a small vaginal speculum, and take under
direct vision through speculum (b) In case of small children or gross
injuries – use local anesthetic before inserting vaginal speculum; rarely GA
may be required
(iv) Take 4 swabs and deal as with “swabs from outside areas”.
(v) If there has been penetration, but offender had vasectomy, or did not
ejaculate - Non-sperm male cells [from penile shaft] may be present [if
 condom was not used]. These are identified by Y-chromosome specific
DNA probes [Fluorescence in situ hybridization or FISH; please see
below]. The cells can be amplified by PCR and a DNA profile made [ch
29].
(6) Cervical swabs:
(i) From within the cervical canal.
(ii) Take in all cases, especially if offence was committed >48 h previously.
(iii) Gives better results than vaginal swabs.
(iv) Take 4 swabs and deal as with “swabs from outside areas”.
(7) From other objects – eg condoms etc found at scene [please see below
under “seminal fluid"collection of material].
(8) Interpretation:
(i) Detection of at least one motile spermatozoa denotes sexual assault within
last 24 h.
(ii) Detection of at least one intact non-motile spermatozoa confirms sexual
assault, but timing cannot be ascertained
(iii) Finding of broken spermatozoa [eg separate heads and tails] - Not
conclusive, as these appearances can be mimicked by several artifacts.
(9) Description of material taken for DNA profiling – is a legal necessity
[S.164A(2) (iii), CrPC].

g. Blood stains
(1) Note presence or absence of blood stains around genitals and on legs
(2) Determine if these could be due to menstruation
(3) Profuse bleeding from vagina may wash out seminal fluid and spermatozoa
may not be found. Despite this fact, a vaginal swab should be taken and slide
made.

h. Venereal disease
(1) Common VDs and microorganisms associated with them, and which may be
seen after rape are:
(i) Bacterial - (a) Chancroid [Haemophilus ducreyi] (b) Chlamydia [Chlamydia
trachomatis] (c) Granuloma inguinale [Klebsiella granulomatis] (d)
Gonorrhea [N gonorrhoeae] (e) Syphilis [T pallidum]
(ii) Fungal - Candidiasis [yeast infection]
(iii) Viral - (a) Herpes simplex (b) HIV (c) HPV [Human papillomavirus] (d)
Molluscum contagiosum [molluscum contagiosum virus MCV] (e) Viral
hepatitis [Hepatitis B virus]
(iv) Parasites - (a) Crab louse or “pubic lice” [Pthirus pubis] (b) Scabies
[Sarcoptes scabiei]
(v) Protozoal - Trichomoniasis [Trichomonas vaginalis].
(2) General cleanliness – of the victim should be noted. In unclean women,
irritation and resultant abrasions may be there due to self-scratching.
(3) Inflammation – Due to most of above VDs. Erythema may be due to general
uncleanliness. Must be differentiated
(4) Discharge – may be due to gonorrhea, syphilis or several other VDs. Collect
swab for microscopy and culture.

i. Lab Examination
(1) Blood and urine:
(i) for date rape drugs and therapeutic medications.
(ii) for pregnancy tests – in late arrivals
(2) Vaginal swab – Should be collected by introducing sterile dry cotton swab
into the posterior vault of the vagina or preferably into the cervical canal.
(i) Look for spermatozoa [please see below – seminal fluid – microscopic
examination].
(ii) If condom use has been alleged by victim, test for lubricants and other
materials found on condom. (a) Lubricants - (I) A polydimethylsiloxane
(PDMS) liquid as lubricant is used by many condom manufacturers.
Detected by Fourier transform infrared spectroscopy [FTIR]. (II) Corn
starch, Lycopodium, silica, and talc can also be observed microscopically.
(b) Spermicides – (I) Nonoxynol-9 as spermicidal jelly – detected by FTIR.

j. Fingerprints of assailant
On body of victim may be recovered with proper techniques [ch 3].

5. Psychiatric examination
(1) Whether well-oriented in time, place and person [for relevant questions to
determine this, please see ch 1]
(2) whether amnesic, sleepy [drug facilitated sexual assault]
(3) Unduly afraid, depressed
(4) harboring any suicidal tendencies
(5) Any signs of post traumatic stress disorder [PTSD]. 24 hour vigil should
be ordered if victim is likely to harm herself out of depression or guilt.

6. Opinion
The opinion is given in one to the following ways
(1) There is evidence of recent sexual intercourse – When recent injuries to
genitals and other body parts are found and motile spermatozoa are recovered
from vagina
(2) There is evidence of remote sexual intercourse – When partially healed
injuries to genitals and other body parts are found and non-motile spermatozoa
are recovered from vagina [typically occurs when victim reports late to the
police]
(3) There is evidence of recent penetration – When there are local recent
injuries to genitals, but no spermatozoa are recovered. [typically occurs when
penetration is by vasectomized person, by a person wearing a condom, with a
finger, dildo, pencil, stick or some other similar object].
(4) There is evidence of remote penetration – When there are local partially
healed injuries to genitals, and no spermatozoa are recovered.
(5) There is evidence of recent sexual assault – When there are recent
injuries/bite marks etc on face, cheeks, neck, breasts, nipples, thighs etc, but
injuries to genitals are absent [typically occurs when help arrives before actual
penetration occurs]
(6) There is evidence of remote sexual assault – When there are partially
healed injuries on face, cheeks, neck, breasts, thighs etc; injuries to genitals
are absent.
(7) There is no evidence of vaginal penetration, but the possibility cannot be
ruled out – When there are no injuries, and no spermatozoa are recovered
from vaginal canal.
(8) There is evidence of recent oral/anal intercourse – When recent injuries
are noted and motile spermatozoa are recovered from these areas.
(9) There is evidence of remote oral/anal intercourse – When partially healed
injuries are noted, and non-motile spermatozoa are recovered from these areas.
(10) There is evidence of recent/remote oral/anal penetration – When
 recent/partially healed injuries are found and spermatozoa are not recovered.
(11) There is no evidence of oral/anal penetration, but the possibility can not
be ruled out – When there are no injuries, and no spermatozoa are recovered
from oral cavity/anal canal.
(12) Reasons to be stated - The report must state precisely the reasons for each
conclusion arrived at [S.164A(3), CrPC].

7. Handing over of report

Doctor must immediately give the report to the investigating officer, who must
then forward it to the magistrate immediately [S.164A(6), CrPC].

F. Examination of Victim in Special Cases

1. Rape on children and virgins

Findings are same as above. Following additional points must be kept in mind
because of gross disproportion between size of male organ and vaginal introitus.
In general younger the child, greater the disproportion between genitals and
greater the local injuries.
(1) Gait – Child walks with great difficulty due to pain
(2) Signs of general violence – are typically absent as a child neither has any
idea of what is happening, nor is capable of any resistance.
(3) Thighs – Attempt to separate thighs may cause child to cry because of great
pain. Local anesthetic should be applied in such cases.
(4) Labia - must be separated with gentle traction as they may be extremely
tender.
(5) Hymenal tears:
(i) Hymen is deeply situated in children
(ii) Rupture of hymen is the main evidence.
(iii) Salient features (a) injuries are more severe than those in the adults (b)
Multiple hymenal lacerations (c) hymen may be entirely destroyed
(iv) Tear caused by acts other than rape – eg by digital penetration or by tampons
would be old; would not bleed on touch.
(6) Vaginal canal:
(i) Abrasions, bruises and lacerations would be more severe because of
disproportion.
(ii) Lacerations of anterior and posterior vaginal walls. Anterior tears may
involve the bladder and posterior tears, the anorectal canal.
(iii) Clots of blood – may be found within the vagina. Blood may be oozing from
the vaginal canal.
(iv) Mucopurulent discharge from vagina – if parents have brought child late and
she had acquired infection.
(v) If vagina is very small, accused would place the penis either within the vulva
or between the thighs. In such cases injuries to vagina would be absent.
(7) Vaginal vault – shows extensive lacerations. There may be vaginal
herniation of abdominal viscera.
(8) Fourchette – fragile, tears during first intercourse. Very important sign in
virgins.
(9) Posterior commissure – rupture is more common, because of disparity
between male organ and vaginal canal
(10) Perineal body – may be torn.

2. Rape on deflorate women

(1) Changes seen in deflorate women
(i) Hymen - completely destroyed
(ii) vaginal orifice – dilated
(iii) mucus membrane – wrinkled and thickened. These changes are seen even
without childbirth.
(2) Complete penetration in such women may occur without any evidence except
presence of seminal fluid. Absence of injuries in such women does not rule
out penetration.
(3) Local injuries may be seen:
(i) If excessive violence was used
(ii) Victim offered resistance
(4) Injuries on other parts of the body – eg breasts, lips, inside of thighs,
buttocks etc are indicative of rape. Such injuries are unlikely to occur in a
consenting woman.

3. Rape on pregnant women

(1) Injuries to abdomen are more severe because of its prominence
(2) Breasts are tender and may show greater injury
(3) Injuries to fetus may be there. May result in abortion.

4. Rape on postmenopausal and elderly women

Findings are same as above. Following additional points must be kept in mind
(1) Reporting - Alterations in mental status, dependence on others, and physical
restrictions can prevent reporting.
(2) Vaginal canal –
(i) Abrasions, bruises and lacerations would be more severe because of atrophic
post-menopausal vagina.
(3) Perineal trauma – would be more for the same reasons as above.

G. Examination of the Accused

(1) Procedure similar as in case of victim.
(2) Better done:
(i) after examination of victim – (a) evidence evaluation in victim is more vital
as it may be lost quickly [eg motility of spermatozoa may be lost soon] (b)
confirmation of injuries, which she states to have inflicted on the accused
(c) Victim needs psychological support. Earlier examination allows earlier
psychological referral
(ii) by the same doctor who examined victim – better co-relation of injuries in
both [scratch marks on accused co-related with broken nails in victims; bite
marks on accused co-related with teeth of victim etc; more severe genital
injuries in victim co-related with disproportionately large size of male
organ]

1. Preliminaries
(1) If brought by general public - Inform police. Label case as MLC [ch 11]
(2) If brought by police - should be identified by the escorting police officer.
Two identification marks must be recorded on the MLC.
(3) Consent:
(i) If not arrested [eg when brought by mob]- Should be taken. If not given, wait
till police arrives and arrests him formally
(ii) If arrested – (a) can be done without consent u/S.53ACrPC (b) Request to
be made by SI and above - In case of suspected rape, a police officer of
the rank of sub-inspector (SI) can ask a govt doctor to examine the accused,
 and if such govt doctor is not available any doctor within a radius of 16 km
from the place of offence. If accused does not give consent, doctor can use
reasonable force to examine him (no consent necessary). (c) What doctor
must note - The doctor must include following particulars in his report (I)
The name and address of the accused and of the person by whom he was
brought [S.53A(2) (i), CrPC] (II) the age of the accused [S.53A(2) (ii)
CrPC] (III) marks of injury [S.53A(2) (iii), CrPC] (IV) Description of
material taken for DNA profiling [S.53A(2) (iv), CrPC] (V) Other relevant
particulars in reasonable detail [S.53A(2) (v), CrPC] (VI) Reasons - The
report must state precisely the reasons for each conclusion arrived at
[S.53A(3), CrPC] (VII) Time - The exact time of commencement and
completion of examination must be noted in the report [S.53A(4), CrPC]
(4) Note - Date, month and place of examination
(5) The examination must be begun without delay, as the signs proving act may
disappear rapidly.
(6) General medical history:
(i) past illnesses, serious accidents and surgical operations.
(ii) H/o medication, consumption of alcoholic and other intoxicating agents.
(7) Last few activities -
(i) history of any sexual act indulged in last 24 h.
(ii) when was last bath taken
(iii) when did he change his clothes last
(iv) if there are injuries [fresh or old] on the body, what explanation does he have
for them.

2. General examination
(1) General behavior and mental state - whether angry, excited, fearful, guilty
looking, inhibited.
(2) Clothes - note
(i) blood and semen stains
(ii) cosmetic traces [eg face powder, lipstick stains]
(iii) physiological stains - mucus, saliva, tears, milk etc
(iv) presence of hair, fibers and foreign matter [eg dust, mud, grass, soil, sand]
and whether the same matches with that found on victim’s clothes.
(v) tears and loss of buttons.
(vi) Trousers - (a) Soiling - Do the trousers show any soiling with mud and grass
at the level of knees. The soiling may be at a level above knees as trousers
may have been lowered to expose genitals. (b) Zip fly - preserve any hair,
fiber etc caught in between, as it may be from victim. There may be blood
and seminal stains on the inside of trouser fly
(vii) Underwear - does it show any tears; underwear cord fastened, unfastened or
loosely fastened. Presence of blood and seminal stains
(viii) Preserve all clothes, seal and send for examination.
(3) Female hair:
(i) Besides noting their presence on clothes [as above], note their presence also
on face, body, penis, prepuce and pubic hair of the accused.
(ii) Pubic hair may have to be combed to separate female hair lying loosely
entangled.
(iii) Preserve for cross matching with victim
(4) Shoes - note particles of earth or any other foreign matter trapped between
the uppers and soles at the welt of shoes. Foreign material on clothes and
shoes can help establish the place of occurrence. May help to corroborate or
refute victim’s story.
(5) Whether appears to be under influence of alcohol or other intoxicating
drugs. If yes conduct examination for drunkenness simultaneously [ch 40]
(6) Comparison of characteristics with that of victim - Note age, development
of genital organs and physical powers. Compare each with that of victim and
determine if the incompatibility can explain injuries, possibilities of
overpowering etc.
(7) Hair - if disheveled, disorderly, contaminated with soil etc. If bunches of hair
are missing
(8) Injuries:
(i) Note injuries eg abrasions, bruises, lacerations, teeth bite marks, over face,
neck, hands, chest, abdomen, genitals and thighs.
(ii) Establish if they could be as a result of resistance offered by victim.
(iii) Determine their age and note if consistent with time of occurrence of
incident.
(9) Nails - should be scraped, and scrapings examined for blood, epithelial cells,
fibres etc.
(10) Pubic hair:
(i) Present or shaved.
(ii) If present note if matted due to emission of semen.
(iii) Cut away about 10-15 at the base for matching with those found on victim
(11) Venereal diseases [VD]- Note all signs of any VD. Prophylactic treatment
of patient may be started. If victim has reported late and shows same VD, it is
a corroborating symptom. Significantly VD may be transmitted both from
accused and victim to each other.

3. Examination of genitals
(1) Development of genitals - to be noted. Conduct an examination for erectile
dysfunction [impotency] also [ch 23]
(2) Injuries on the body - abrasions, bruises, lacerations all over the body
especially to local parts
(3) Local injuries:
(i) Abrasions, bruises, lacerations of the shaft of penis, prepuce, scrotum, inside
of thighs.
(ii) Forceful penetration, produces injuries to frenulum of prepuce in the
uncircumcised.
(iii) Abrasion of glans is seen in both circumcised and uncircumcised.
(iv) Such injuries are common in young children and virgins with narrow
 introitus, because of disparity in size.
(v) When disparity in size is not there, patchy redness of glans, especially around
the rim is more common.
(vi) Dried blood and seminal stains may be present on the shaft of penis,
scrotum, inside of thighs and adjoining skin
(4) Smegma - Smegma [Gk smegma, soap] is a cheesy secretion which collects
under the foreskin of the glans it requires about 24 hours to collect and is
usually rubbed off during complete penetration, as the foreskin is pressed
backward during intercourse.
(i) Retract the foreskin and record the presence of absence of smegma.
(5) Examination of penis and glans for vaginal cells:
(i) Suspect’s penis is washed with saline"material stained with Papanicolaou’s
stain"vaginal and cervical cells are stained"indicate that penis was in
contact with female genital tract. Barr bodies in the cells indicate cells of
female origin. A DNA profile can be made from female cells using PCR [ch
29], which can establish the identity of the victim.
(ii) Suspect’s penis is cleaned with a filter paper"Expose filter paper to vapors of
Lugol’s iodine"If vaginal epithelial cells are present, paper turns brown,
because of the presence of glycogen in vaginal cells. This test is +ve up to
4th day.
4. Specimens to be collected
(1) Blood - for grouping
(2) Head hair - May have to be matched with those found on victim’s hand,
clothes and at the scene.
(3) Pubic hair:
(i) Combings [for sample of victim’s hair].
(ii) Cut pubic hair [for sample of accused’s hair]. Of great value if they are
matted, because they indicate emission. Avulsed pubic hair must not be
taken. It is a painful procedure and serve no additional purpose.
(4) Loose hair - anywhere on the body
(5) Swabs - from urethral orifice, coronal sulcus, prepuce, penile shaft, scrotum,
pubic area and inner aspects of thighs. They may reveal infecting organisms,
blood, leucorrheal stains, vaginal cells etc which may be cross-matched with
that found on victim
(6) Nail scrapings - victim’s skin underneath show struggle with the victim.

5. Opinion
The opinion is given in one to the following ways:
a. On the question of having performed the act
(1) Findings are suggestive of subject having been involved in a recent non-
consensual sexual act [if there are gross injuries on body and genitals +
smegma is not present under the glans + there is presence of vaginal cells on
the penile shaft]
(2) Findings are suggestive of subject having been involved in a recent sexual
act [if there are no injuries on body + smegma is not present under the glans +
there is presence of vaginal cells on the penile shaft]
(3) Findings are suggestive of subject having attempted a non-consensual sexual
act. There is nothing to suggest penetration of the penis in the vaginal tract.
However a superficial touching of penis with female genital organs cannot be
ruled out [if there are gross injuries on body and genitals + smegma is present
under the glans + there are no vaginal cells on the penile shaft]
(4) There is nothing to suggest that the subject performed a recent sexual act,
consensual or non-consensual [if there are no injuries on body and genitals +
smegma is present under the glans + there are no vaginal cells on the penile
 shaft].
b. On the question of ED
Please see ch 23.

6. Handing over of report

Doctor must immediately give the report to the investigating officer, who must
then forward it to the magistrate immediately [S.53A(5), CrPC].

H. Medicolegal Questions Relating to Rape

1. Can a female rape a male?

Legally this is not possible in India? In western countries (eg Canada, France) it
is possible. In India in similar circumstances, at most female can be charged
under S.350, IPC (criminal force). Punishment 3 months and/or `500 fine (S.352,
IPC).

2. Is emission necessary to constitute an offence of rape?

No.

3. How much penetration is sufficient to constitute rape?

Even touching of penis with vulva would legally constitute rape.

4. Age of the accused

(1) India - Charge of rape cannot be brought against a child <7 years of age
(S.82, IPC). Please also see ch 3 – Criminal responsibility.
(2) Under common law [ch 1] of England:
(i) A boy <14 y cannot commit rape [R v. Phillips (1839) 8 C&P 736; R v Waite
[1892] 2 Q B 600].
(ii) This rule has now been abolished by s1 of the Sexual Offences Act 1993.

5. Age of the victim

Females of all ages have been raped (from newborns to over 90 years). Children
are more commonly raped because
(1) in India, there is a false belief that having sexual intercourse with a virgin girl
can cure venereal disease. So many persons attempt intercourse with very
 young girls, who are bound to be virgins
(2) children offer less resistance.

6. Rape during sleep, under narcotics or hypnosis

(1) Administration of narcotics – Rape is possible (please see DFSA above)
(2) During anesthesia:
(i) Rape is certainly possible. Doctors have been charged. On emerging from
light anesthesia, patients [especially neurotic] may have hallucinations or
dreams of an erotic or fearful nature. Such patients may genuinely believe
that the doctor had sexual intercourse with them while they were
unconscious.
(ii) Putting a woman under the influence of chloroform is very difficult [ch 40].
(iii) there is no drug which can produce immediate unconsciousness when placed
over the face of the person [ch 40].
(3) Sleep – impossible to have sexual intercourse with a woman in her sleep
(4) Hypnosis – No one can be hypnotized against his/her consent. Thus woman
must understand fully the consequences before giving consent for hypnosis.
However consent for hypnosis is not consent for sexual intercourse, and thus
sexual intercourse without consent under hypnosis is rape.

7. Rape and resistance

If the victim does not have injuries, it may be believed that she did not apply
resistance to the maximum and thus she had consented. This is not necessarily
true. Lack of resistance can be due to
(1) terror
(2) feeling of helplessness
(3) when a loved one has been put under threat
(4) she was tied
(5) her own clothes obstructed movement
(6) multiple assailants
(7) weak woman. However cases have occurred when a woman consented for
intercourse to obtain some reward, which was not given afterwards.
Consequently she denied having given consent. Please see S.114A, IEA above
for details.
8. Impersonation
Rape by impersonation of husband is possible
(1) Dark - If woman is lying in the dark, and accused secretly enters. Woman
may think he is the husband
(2) Identical twin – may impersonate his brother
(3) Long absence - Marriage at young age after which husband went abroad.
Somebody else returns after some years claiming to be her husband.

9. Rape by fraud or misrepresentation

Sexual intercourse by fraud or misrepresentation is rape
(1) Doctor tells patient sexual intercourse with him is necessary for treatment
(2) Music teacher tells student, it is necessary for improving her voice.

10. Intercourse other than penile-vaginal intercourse

S.375. IPC now includes all kinds of illegal penetration [by penis, any part of
the body, by any object, eg pencil] under rape. The part penetrated may be
vagina, anus, urethra, tightly closed thighs, axilla, or any part of woman’s body
[pl see S.375, IPC above]. However anal or oral intercourse even with a legally
married wife is illegal u/s377 IPC.

I. MLI of rape
Rape is a cognizable offence

G. Child Sexual abuse

Child sexual abuse [syn child molestation, sexual exploitation] is using the child
as an object for sexual satisfaction.

IV. INDECENT ASSAULT

Indecent assault is any unwanted sexual behaviour or touching which is forced

upon people against their will [ex - touching arms, shoulders, breasts, buttocks
etc of a female colleague against her will].

A. Legal Aspects of Indecent Assault

294, 354, 509, [IPC Sections].

B. Sexual Harassment
Sexual harassment, is intimidation of a sexual nature, or inappropriate promise
of rewards in exchange for sexual favors.

1. Legal aspects

a. Vishaka judgment (1997)

In India, the first major case of sexual harassment occurred in the state of
Rajasthan in Sep 1992. A female social worker tried to stop the wedding of an
infant girl, less than a year old in her village, Bhateri, about 45 km from Jaipur.
Outraged by this, five men from the upper-caste family of the infant decided to
“teach her a lesson” and gang-raped her repeatedly in the presence of her
husband. In its landmark judgment, Vishaka v. State of Rajasthan, A.I.R. 1997
S.C. 3011, the Supreme Court of India, for the first time laid down guidelines
defining what exactly is sexual harassment at the work place, and what should be
done to deal with it.

b. S.354A, IPC
S.354A, IPC (added in 2013) defines sexual harassment and its punishment.
(1) Definition - A man doing any of the following 4 acts commits the offence of
sexual harassment.
(i) physical contact and advances involving unwelcome and explicit sexual
overtures; or
(ii) a demand or request for sexual favors; or
(iii) showing pornography against the will of a woman; or
(iv) making sexually colored remarks [S.354A(1), IPC]
(2) Punishment -
(i) For first 3 acts mentioned above"Rigorous imprisonment up to 3y or fine or
both [S.354A(2), IPC]
(ii) For 4th act mentioned above" Imprisonment [simple or rigorous] up to 1 y or
fine or both [S.354A(3), IPC].

V. SEXUAL PERVERSIONS
Sexual perversions or paraphilias are sexual behaviors that involve unusual
objects (eg animals, dead people) and activities (eg exhibitionism, voyeurism). If
not fulfilled they can cause clinically significant distress [DSM-5]. Most
common paraphilias include exhibitionism, fetishism, frotteurism, pedophilia,
sexual masochism, sexual sadism, transvestic fetishism and voyeurism.

A. Buccal Coitus
please see Fellatio.

B. Eonism
Please see transvestism below.

C. Exhibitionism
Exhibitionism is obtaining sexual arousal by exposing genitals to an
unsuspecting stranger.
Salient features:
(1) May or may not be accompanied by masturbatory acts
(2) Prevalence – 2nd most common paraphilia after sadomasochism
(3) Perpetrator – mostly males, although female exhibitionists are also known
(4) Victims [to whom genitals are displayed] – children, persons of opposite sex
(5) Etiology:
(i) Majority suffer from psychotic disorders - (a) Alcoholism (b) Epilepsy (c)
GPI (d) OCD (e) Psychopathic personalities (f) Senile dementia
(ii) Monoamine excess – especially dopamine. Patients being treated for
Parkinsonism with carbidopa/levodopa [metabolic precursor of dopamine]
and pergolide [direct dopamine agonist] show -ed tendency of
exhibitionism. On discontinuing medications, these tendencies subside.
(6) Legal aspects – punishable u/s S.268 IPC - Public nuisance; S.290, IPC -
Punishment for public nuisance in cases not otherwise provided for [fine of
`200]; S.294, IPC - Obscene acts and songs [3 m or fine or both]; S.509, IPC
- Word, gesture or act intended to insult the modesty of a woman [1 y or fine,
or both].
(7) DSM-5 [ch 28] assigns code 302.4 to exhibitionistic disorder.
D. Fetishism
Fetishism is obtaining sexual arousal using or thinking about an inanimate
object or part of the body.
Salient features:
(1) The inanimate object [fetish] - is generally a piece of cloth [eg bra,
handkerchief, panties, petticoat, stocking or undergarments] or even shoe or
sandal of the opposite sex. Sometimes it may be a flower or garland worn by
the female. A picture of fetish may also suffice.
(2) Acts that produce orgasm:
(i) Fetish is usually stolen and genitals are rubbed with it till ejaculation occurs.
(ii) Shoe may serve as an artificial vagina for such fetishists.
(iii) Looking at the fetish may have the same effect.
(iv) Sometimes just the act of stealing a fetish produces an orgasm.
(3) Sex – almost exclusively seen in males.
(4) MLI:
(i) Fetishist may commit theft, robbery etc to obtain fetish and may get caught
for theft.
(ii) Women may be attacked to get the fetish. This may rarely be accompanied
by rape or sexual assault.

E. Frotteurism
Frotteurism [French frotter, to rub] is obtaining sexual arousal and gratification
by rubbing one’s genitals against others in crowds and public places.
Salient features:
(1) Offenders generally are unable to perform normal sexual acts, and would
have a premature ejaculation if they attempted it.
(2) Co-morbidity - Often seen with other paraphilias such as exhibitionism,
voyeurism etc
(3) Legal aspects:
(i) S.354, IPC [assault or criminal force to woman with intent to outrage her
modesty]
(ii) All IPC sections discussed under exhibitionism are applicable also.
F. Lesbianism
Lesbianism [syn tribadism] is sex between two women. The term comes from
the name of an island, the Isle of Lesbos, mentioned in Greek mythology, where
women used to practice homosexuality.
Salient features:
(1) Active partner [often a transsexual or transvestite] is called a butch or dyke;
passive partner known as femme.
(2) The active partner uses a dildo either strapped around waste, or manipulated
by hand. It is punishable u/s377, IPC.

G. Lust Murder
Lust murder [syn erotophonophilia] is homicide in which the offender gets
erotic satisfaction by killing.
Salient features:
(1) Considered an extreme form of sadism.
(2) Sex - Most lust murderers are males, but female lust murderers are known.
(3) Manifests by:
(i) Murder - during sexual intercourse.
(ii) Mutilation – of victim’s sexual organs, cutting or stabbing of breasts, lower
abdomen evisceration. Usually takes place postmortem, but may occur
before death also. May be accompanied by sucking, licking or mouthing of
wounds, drinking of blood [vampirism]
(iii) May include other activities - (a) removing clothing from the body, (b)
posing and propping of the body in different positions, generally sexual
ones, (c) insertion of objects into bodily orifices, (d) Masturbating over
dead body (e) necrophilia and necrophagia
(iv) Murder after rape, plainly to prevent victim from going to police, or due to
anger, jealousy or revenge is not lust murder.
(4) Fantasies - are a key component in lust murders. These may be fueled by
pornography and facilitated by alcohol.
(5) Most common among - serial killers. They chose a victim with a specific
trait [offender’s Ideal Victim Type (IVT)]. Once the offender has found in
IVT, he might engage in stalking [following victim everywhere] or other
predatory behaviors before acting out his fantasy on his victim.
(6) Periodic outbursts - are often seen. Due to offender’s recurring compulsion
or sudden outbursts of sexual desire. Behavior is normal during two outbreaks.

H. Masochism
Masochism [syn, passive algolagnia] is sexual arousal through pain inflicted on
onself through another person, usually a partner of the opposite sex. Named after
an Austrian novelist Leopold Sacher Masoch (1836-1895), who suffered from
this perversion. Stimulant for his work was being whipped by his wife.
Salient features:
(1) This condition is opposite of sadism. The term algolagnia [Gk, algos, pain;
lagneia, lust] includes both sadism or masochism.
(2) Epidemiology:
(i) Sex – Mostly found in males. About 1 in 20 of all masochists are female.
Masochist females willingly expose themselves to the risks of severe bodily
injury at the hands of their sexual partners.
(ii) Found in all age groups and in all socioeconomic strata.
(3) Characteristics:
(i) Masochists get pleasure from being abused, beaten, degraded, dominated,
enslaved, humiliated or tortured by their sexual partner.
(ii) Tend to place themselves repeatedly in self-defeating situations.
(iii) Painful stimuli may entirely replace the ordinary sex stimuli.
(4) Combinations – Both sadism and masochism are rarely found in a pure
state. Usually found together in combination, with one trait dominant over
other [sadomasochism].
(5) Bondage - is the tying, binding, or restraining of a person for the sexual
pleasure of both parties involved. Rope, cuffs, bondage tape, self-adhesive
bandages, or other restraints are used for this purpose. Giving and receiving
pain occupies their sexual life of such partners so much that sexual intercourse
may never be indulged into.

I. Masturbation
Masturbation [syn ipsation, onanism] is deliberate self-stimulation resulting in
sexual climax.
Salient features:
(1) mild masturbatory exercise in both men and women are part of normal
physiological response and are considered completely normal and even
healthy activities
(2) Technique:
(i) Males - manual, rubbing genital parts against bed or other objects.
(ii) Females - (a) Manual – (I) Moving a finger gently and rhythmically over
clitoris or labia minora (II) Application of steady pressure over these parts
with several fingers or whole hand (b) Other – Bananas, dildos [artificial
masculine genital parts, made of plastic or rubber], electrical vibrators,
fingers, glass tubes, hollow articles [eg test tubes, bottles], metallic bars and
wooden rods. Also rubbing genitalia against pillows, bed or some other
similar object
(3) Anal and urethral insertions – also seen, but rare
(4) Legal aspects:
(i) Privately done - Not an offence
(ii) Publicly performed – Punishable u/s S.268, S.290, S.294 and S.509, IPC [for
details, please see exhibitionism above].

J. Mixoscopia
Observing the sex performance of other couples.

K. Necrophilia
(1) Necrophilia [Gk nekros, corpse; philia, love] Intercourse with dead people.
(2) Necrophagia [Gk phagos, to eat][syn, anthropophagy] is eating their flesh
for sexual gratification.
(3) Etiology: (i) genetic (ii) temporal lobe anomalies (iii) head trauma during
infancy (iv) sexual inadequacy with living (v) drugs and alcoholism (vi)
sexual abuse during childhood (vii) unconscious suppressed hostility towards
females (viii) helplessness and resistlessness of the victim [exercising sexual
power over corpses] (ix) Castration anxiety
(4) Characteristics:
(i) May have sadistic tendencies [necrosadism]. May mutilate corpse after
intercourse.
(ii) Decomposition, foul smell and coolness act as stimulants
(5) MLI – punishable u/s297, IPC - Offering any indignity to any human
corpse. Punishment [1 y or fine or both] [please also see ch 5].

L. Oedipus complex
Intended sex between mother and son.

M. Pyromania
Getting sexual stimulation by seeing flames and destruction of a building. It is a
psychosexual disorder.

N. Sadism
Sexual arousal through inflicting pain on another person. From French author
Marquis de Sade (1740-1814), who wrote books in which the characters
suffered from this condition. Also known as algolagnia.
Salient features:
(1) Seen more commonly in men
(2) Often seen in association with masochism [sadomasochism, which is the
commonest paraphilia].
(3) Etiology:
(i) Psychotic disorders – sociopathic, schizoid or other personality abnormalities
(ii) Organic brain abnormalities and damage – gliomas, temporal horn dilatation
(iii) Endocrine abnormalities
(iv) Early experiences - of brutality in relation to sex
(v) family background
(vi) substance abuse.
(4) Methods employed:
(i) Beating [may cause fractures, rupture of internal organs]
(ii) Biting [eg cheeks, breasts, nipples]
(iii) Bondage –tying up or otherwise restraining [syn sexual bondage]
(iv) Burning skin by cigarettes, lighters, hot wax
(v) Inserting bottles, candles or sticks in anus or vagina
(vi) Producing cuts
(vii) Whipping etc
(5) MLI – Generally done in association with a consenting masochist. If done
 forcibly without consent, person may be charged with S.323, 324, 325 and
326 IPC [ch 11]. Even consensual acts have been successfully prosecuted in
foreign countries, because sadomasochism per se is illegal.

O. Sexual oralism
Sexual oralism is obtaining sexual pleasure from application of mouth to the
sexual organs.
Salient features:
Seen in both homosexuals and heterosexuals

Types

a. Anilingus
Oral stimulation of the anus. Active and passive agents may be of either sex.

b. Cunnilingus
Cunnilingus [syn, mouth job] is oral stimulation of female sexual organs
[clitoris, vagina etc].
Salient features:
(1) It can be done by a person of either sex, a child or even an animal.
(2) Risks - If female is pregnant, may accidentally cause air embolism [suction
of air through uterine veins].

c. Fellatio
Fellatio [syn, blow job, buccal coitus, Coitus per os, fellation, intercourse
through mouth, irrumation, Sin of Gomorrah (for origin, please see sodomy
below)] is oral stimulation of male sexual organs [penis and occasionally
scrotum].
Salient features:
(1) Like cunnilingus it can be done by a person of either sex, a child or even a
trained animal.
(2) Risks - May cause accidental gagging of the fellator [Please see ch 19].
(3) Lesions caused by fellatio:
(i) Oral submucosal hemorrhages - secondary to repetitive negative pressure and
blunt trauma associated with fellatio. May be an incidental finding in
 sexually active adults and in children suffering from sexual abuse. Appear
as erythematous, petechial, or ecchymotic macules or patches at the
junction of the hard and soft palate. May appear bilaterally or as single
lesions extending across the midline. The lesions do not blanch with
pressure, are asymptomatic, and non-ulcerated. The uvula and structures of
the oropharynx are typically spared.
(ii) STDs including HIV.

P. Sodomy
Please see below.

Q. Transvestism
Transvestism [Latin trans, opposite; vestere, clothing] is sexual arousal from
dressing in the clothes of the opposite sex.
Salient features:
(1) There is often a desire to be identified with the opposite sex. Also known as
cross dressing, eonism [After French diplomat Chevalier d’Éon [1728-1810]
who had this disorder], fetishistic transvestism or transvestic fetishism. The
sufferer is known as a transvestite.
(2) Epidemiology:
(i) Prevalence – 3rd most common paraphilia after sadomasochism and
exhibitionism.
(ii) Age – Most develop the disorder by late adolescence
(iii) Sex – mostly seen in males. Very few cases of female transvestites are
known.
(iv) Associations – Generally associated with (a) autoerotic asphyxia [ch 19], (b)
bondage and (c) sadomasochism. A small percentage are homosexuals.
(3) MLI:
(i) suicide by transvestites may appear like cases of autoerotic asphyxia.
(ii) May be punishable u/s290, IPC - Punishment for public nuisance in cases
not otherwise provided for [fine of `200], eg a man loitering around
wearing a bra etc may be considered to cause public nuisance.
(4) DSM-5 [ch 28] assigns code 302.3 to transvestism.
R. Triolism
Intercourse between three people, either two females and a male or two males
and a female. Another variation is when a person shares his wife/girl friend with
another, and observes the act from a hidden place. Also known by various other
names such as Triolism and Ménage a trois.

S. Undinism
Same as Urolagnia.

T. Uranism
Uranism is a general term given to the perversion of sexual instincts. Sexual
gratification by fingering, fondling, licking also goes under the name Uranism.
Not to be confused with Urolagnia.

U. Urolagnia
Sexual excitation at the sight of urine, or people urinating. Also known as
undinism and urophilia.

V. Voyeurism
Same as Peeping Tom; sexual arousal by observing nude individuals without
their knowledge.
Salient features:
(1) Legal definition - Watching or capturing the image of a woman engaging in
a private act in circumstances where she would usually have the expectation of
not being observed either by the perpetrator or by any other person at the
behest of the perpetrator or disseminates such image [S.354C, IPC].
(2) Punishment -
(i) On first conviction - Imprisonment [simple or rigorous] of minimum 1 y.
May extend to 3 y. Also fine [any amount]
(ii) On second or subsequent conviction - Imprisonment [simple or rigorous]
of minimum 3 y. May extend to 7 y. Also fine [any amount]. There are 2
explanations to this section. Explanation 1 - For the purpose of this
section, “private act” includes an act of watching carried out in a place
which, in the circumstances, would reasonably be expected to provide
 privacy and where the victim’s genitals, posterior or breasts are exposed or
covered only in underwear; or the victim is using a lavatory; or the victim is
doing a sexual act that is not of a kind ordinarily done in public.
Explanation 2 - Where the victim consents to the capture of the images or
any act, but not to their dissemination to third persons and where such
image or act is disseminated, such dissemination shall be considered an
offence under this section [S.354C, IPC].
(3) DSM-5 [ch 28] assigns code 302.82 to voyeurism.

VI. SODOMY

Sodomy [syn, buggery, Greek love] is anal intercourse between two men
[homosexual] or a man and a woman [heterosexual].
Salient features:
(1) The practice was prevalent in ancient Greece [Greek love]
(2) Gerontophilia [sex with old] and pederasty [sex with young] includes acts of
sodomy [please see below].
(3) Partners:
(i) Active agent is one who penetrates; passive, the one who is penetrated.
(ii) When passive agent is a child [usually a boy], he is known as a catamite.
Sodomite is one who practices sodomy. There may be both active and
passive sodomites.
(iii) Both active and passive agents may interchange, even if one of the partners
is a female. She uses a dildo to penetrate when acting as an active partner.
(4) Constituents of offence:
(i) Any degree of penetration, or even an attempt at penetration into the anal
margin
(ii) Ejaculation is not necessary
(5) Prevalence:
(i) Frequent among people living in hostels, military barracks, prisoners and
sailors etc because they are isolated from women from long periods
(ii) Socioeconomic status - seen among all levels
(iii) Often resorted to, when the attacker discovers that the woman is
menstruating [Aruna Shaunbaug case - ch 2].
A. Male Prostitutes
In India some eunuchs act as male prostitutes to earn livelihood. They act as
passive agents in sodomy. They grow long hair, wear lipsticks and female
ornaments, dress like women and develop mannerisms similar to women. They
cannot offer vaginal intercourse. Mostly they would satisfy customers by
axillary, intercrural or oral intercourse or masturbation. Two types exist:

1. Hijrahs
(1) These are males who have been castrated [removal of testis] and emasculated
before puberty.
(2) They keep adding to their tribes by abducting young boys and castrating
them. When the wound heals, the scar invaginates and comes to resemble
those of females, although the depth is not that of normal vagina.
(3) Being castrated before puberty, female characteristics such as female voice,
feminine distribution of fat and hair, and development of breasts are common.
(4) They intentionally wear feminine attire and behave in a feminine way, in
order to act as a perfect female substitute for prostitution.
(5) But they are biological males; their buccal smears show male sex chromatins.

2. Zenanas
(1) These are males whose genitals are intact.
(2) They simply wear female attire and behave like females.
(3) They live separately from hijrahs
(4) Both hijrahs and zenanas maintain a line of separation between themselves
and the female prostitutes.

B. Examination of the Passive Agent

Examination is conducted on same general lines as that of victim of rape.
Findings may disappear within 1-2 days so immediate examination is a must.
Only hematoma and lacerations are visible for several days - hematoma for 7-10
days and lacerations for 2-3 weeks.

1. Preliminaries
(1) Consent - informed consent must be taken. If <12 y, consent of parents or
guardian
(2) Profession - is it his profession to act as a habitual passive agent
(3) General history - hemorrhoids, anal fissures etc. Victim would complain of
pain during walking, defecation and anal examination.
(4) History relating to bowel movements: (i) any surgical operation (ii) bowel
habits (iii) instrumentation of the bowel (iv) previous constipation (v) use of
enema, laxatives and suppositories (vi) previous acts of anal intercourse, their
frequency, i.e. whether the victim was a habitual agent (vii) last act of anal
intercourse
(5) History relating to current act:
(i) Date, time and place of alleged act
(ii) Bleeding or any other discharge - at the time of act; afterwards.
(iii) Defecation after the alleged act
(iv) Degree of penetration
(v) If any struggle or resistance was offered, or was the act consensual
(vi) Pain experienced - at the time of act; subsequently
(vii) Position in which act was performed
(viii) Use of lubricant
(ix) Whether bathed or washed anal area after the act
(x) Whether changed clothes or not
(xi) Whether ejaculation occurred or not

2. Examination of clothes
Please see above “examination of rape victim" examination of clothes”. Fecal
stains should especially be searched for as incontinence may be a symptom.

3. General examination
(1) Mental state - Note if child is tense, fearful, crying or relaxed. Mild
sedation is advisable if child tense.
(2) Genital examination - for injuries [eg abrasions, bruises, lacerations,
teethbite marks] is done as in case of rape victim. Look specifically for
scratches around buttock and anal region.

4. Anal examination
(1) Position:
(i) Older children are examined under a powerful light in the knee-elbow
 position by pulling the glutei to both sides. The anus is readily visualized in
this way. Lesions observed are indicated on a diagram according to clock
quadrant [as in hymen above, Fig 25.3].
(ii) Because knee-elbow position is difficult to get in younger children and may
cause some victims unusual embarrassment or recall memories of prior
abuse, left lateral position relaxing the glutei and knees with the head on a
pillow may be employed in a very young child. Knees may be drawn as far
towards the chest as possible [lateral decubitus] (iii) In case of female
victim there should be a female chaperone.
(2) Normal anal orifice:
(i) Normal orifice is slit like, and runs anteroposteriorly.
(ii) Surrounding skin shows marked natural folds due to the action of
Corrugator Cutis Ani muscle.
(3) Local swabs - Take swabs from anal verge, skin of perineum, from inside the
anal canal and rectum. May show lubricant matter, seminal fluid or organisms
of venereal diseases on culture, all of which are positive proof of anal
penetration.
(4) Proctoscopy - Pass a small unlubricated proctoscope "inspect lower rectum
and anal canal for injuries or mucosal abnormality"take swabs from lower
rectum and anal canal
(5) Lesions:
(i) marked in children because of great disproportion in size between anal orifice
of victim and penis of accused.
(ii) Lesions may be produced if penis or any similar objects [fingers, dildos etc]
are introduced
(iii) if a moderate sized penis is introduced with care and if adequate lubricants
have been used, there may be no injury. This is partially because of anal
dilation and partially due to lubricants.
a. Findings in a first time or occasional passive agent
(1) Buttocks - Note fresh or healed lesions, dried secretions, ecchymoses,
rashes, STD lesions, handprints or fingerprints.
(2) Perianal skin - Examine for presence of inflammation. Record findings of
dried secretions, bruising, tears, lacerations, fissures, tears, or lacerations that
are located on the external surface, internal to the sphincter, or extend across
the pectinate line, which is the juncture between the anal mucosa and the anal
epithelium.
(3) Anal orifice [Fig 25.11]: (i) irritable (ii) mucosal rim - prolapsed (iii) tender
to touch (iv) see how it admits index finger - (a) only one finger is admitted
without discomfort - normal (b) only one finger is admitted with discomfort -
full act has not taken place (c) two fingers are admitted with slight discomfort
- full act might have taken place.
(4) Anal laxity:
(i) Note dilation and loss of elasticity [loss of normal anal tone].
(ii) Estimate or measure the diameter of any anal dilatation.
(iii) Lateral buttock traction test [syn, ‘O’ sign, reflex relaxation of the anus]
- Procedure - (a) The buttocks are spread by the thumbs of both hands [Fig
25.11] causing enough lateral traction to separate the buttocks, and visualize
the anus. (b) Anus dilates slightly in a habitual catamite [positive lateral
buttock traction test]. Dilation of >15 mm is significant, and up to 40-50
mm [4-5 cm] may occur in a habitual catamite. Rectum can be seen
through it. (c) Anus contracts slightly in normal persons [negative lateral
buttock traction test].
(5) Blood stains - around anus, on perineum and on clothes. If occult blood is
suspected, perform a guaiacum [or any other presumptive] test for blood [ch
29].
(6) Fecal matter - around anus, if there has been incontinence
(7) Hematoma - Frequently seen (i) as a localized swelling, or (ii) as a diffuse
swelling around anal margins. There may be obliteration of normal anal skin
folds
(8) Abrasions:
(i) scratch abrasions varying in number.
(ii) Extend from anal margin into the anus itself.
(iii) May be present at any side around the anus.
(iv) If specks of blood are adherent, it suggests recent act
(9) Anal canal - look for any foreign bodies
(10) Lacerations of anal canal:
(i) Seen if violence has been used, especially if the victim is young
(ii) rare in adults
(iii) best seen by pulling the skin outwards [Fig 25.11].
(iv) Cause - overstretching of skin
(v) Appearance - (a) seen as large fissures. (b) Triangular or wedge shaped. (c)
Generally single and seen at the posterior part of the anus. (d) Base is
directed externally at anal ring. (e) Apex upwards and inwards. (f) may
involve only external skin or may extend within the anal canal to the
mucocutaneous junction.
(11) Laceration of sphincter ani:
(i) Seen if violence has been used, especially if the victim is young
(ii) Rare in adults
(12) Anal prolapse
b. Findings in a habitual agent
(1) Anal hair - shaved
(2) Anal orifice - is dilated, inelastic, lax and overstretched. Elastic anus (i.e.
one capable of dilation) does not indicate habitual agent.
(3) Anal margin and skin around anus:
(i) Smooth and thickened extending into the anal canal up to the mucocutaneous
junction, and sometimes into the upper anal canal.
(ii) Epithelization of anal mucosa
(iii) There may be anal fissures and scars
(iv) May reveal hemorrhoids
(4) Anal muscles - tone is lost. Anal reflex [contraction of the anal sphincter on
irritation of the anal skin] is delayed.
(5) Funnel shaped anus - is rare, and is usually an anatomical variation.
However slight depression of buttocks towards anus may be seen [due to
absorption of fat]
(6) Lateral buttock traction test: Please see above.
(7) Anal mucosa - absence of fine wrinkles
(8) Venereal disease - Anal condyloma of venereal disease [condylomata
acuminata] and signs of and anal neoplasia may be present.
C. Examination of the Active Agent
Examination is conducted on same general lines as that of accused of rape.

1. Preliminaries
(1) Consent - Must be taken. If arrested, may be examined without consent u/s
53, CrPC [ch 11]
(2) History - Active agent is usually the accused. His version of details of the
event must be recorded.

2. Examination of clothes
(1) Disheveled and torn - if passive agent resisted
(2) May show seminal and fecal stains.

3. General examination
(1) Injuries consistent with resistance and struggle faced - eg abrasions, bruises,
teeth bite marks.
(2) Blood and seminal stains on the body.

4. Local examination
(1) Penis:
(i) May be elongated and constricted at some distance from the glans.
(ii) Urethra may be twisted.
(iii) Redness and swelling due to friction and irritation
(iv) Traces of fecal matter and lubricant
(v) Peculiar smell of feces and anal glands
(vi) Abrasions on prepuce, glans penis
(vii) Tearing of frenulum
(viii) Coronal sulcus - shows fecal soiling, blood, foreign hair
(2) Urethra:
(i) Urethral swabs - Smears should be taken from the external meatus after
applying pressure on the undersurface of the penis along the urethra. May
show fecal material
(ii) Culture - May show organisms [eg gonococci] similar to those found on the
anal verge swabs from passive agent [corroborates penetration]
D. Specimens to be Collected
In both active and passive agents. The agents may have interchanged roles if it
was a consensual act.
(1) Fluids:
(i) Blood - for venereal diseases, testing for HIV
(ii) Urine
(2) Nail scrapings
(3) Hair - (i) head hair (ii) pubic hair (iii) loose hair and fibres anywhere on
body
(4) Swabs: (i) from any soiled areas of skin (ii) from anal, perianal and lower
rectal area [from suspect passive agent] (iii) from shafts of penis, coronal
sulcus and glans [from suspect active agent].

VII. SEMINAL FLUID

A. Collection of Material
(1) Fluid and dried semen from vaginal canal and body surface: Please see
above under “Examination of victim”
(2) From condoms – use throat swab
(3) From cloth – eg panties, undergarments, rugs, carpets, sari, salwar etc. Cut
out the stained portion. Dry (to prevent fungal contamination) and preserve
(4) From smooth impervious surface – eg cement and wooden floor etc.
Scrape with the tip of knife and preserve in an envelop.

B. Physical Examination
(1) Appearance – Dry seminal stains are grayish white in color, and show an
irregular map like outline
(2) Feel – Cloth is stiff as if starched
(3) Odor – Characteristic
(4) Under UV light – Shows bluish-white fluorescence [not specific, as other
albuminous substances also fluoresce, eg nasal and leucorrheal discharge,
detergents]. Fluorescence absent in a semen +ve sample
(i) Presence of blood along with
(ii) Stain soaked in water.

C. Chemical Examination

1. Acid phosphatase test

Method of detection: (i) Reagent is prepared by adding α-naphthyl phosphate
and Brentamine Fast Blue B (ii) suspected stain is touched with a cotton swab
moistened with sterile water (iii) reagent added to swab (iv) development of
intense purple color within 2 min is +ve for semen. Any color developing after
this is –ve.

2. Ammonium molybdate
Seminal fluid contains free phosphate. The presence of free phosphate in acidic
solution can be detected by adding ammonium molybdate solution. In the
presence of nitric acid, yellow colored ammonium molybdophosphate is
formed after a few minutes. This test is obsolete now.

3. Barberio’s test [1911]

Add saturated aqueous or alcoholic soln of picric acid to spermatic fluid. Yellow
needle shaped rhombic crystals of spermine picrate are formed [Fig 25.12].
Reaction depends on presence of spermine, which comes from prostate. See
also Puranen’s test.
4. Chromatography
(1) Choline is detected by chromatographic methods [paper chromatography,
TLC].
(2) Choline and spermine are present in a unique ratio only in semen. This can
be determined by TLC. 1 µL of semen can be detected by this method.

5. Creatine phosphokinase
Creatine Phosphokinase (CPK) [syn, Creatine kinase (CK), phospho-creatine
kinase] acts as an energy reservoir and is expressed by several cells and tissues
including spermatozoa that use large amounts of energy.
Salient features:
(1) CPK is found both in spermatozoa and seminal plasma. The CPK activity of
sperm is 2.0 # 10–6 IU/106 spermatozoa. CPK activity of seminal plasma is
 660 IU/L.
(2) The enzyme is stable and can be demonstrated even in several month old
stains.
(3) Since CPK is present in several other cells [skeletal muscle, smooth muscle,
brain, retinal photoreceptor cells, hair cells of the inner ear], it is only a
presumptive test.

6. Florence test [1896]

(1) Florence test depends on the presence of choline in semen, which comes
from seminal vesicles. Choline is responsible for seminal stains fluorescing
bluish white under UV light.
(2) Procedure - To the suspect material a drop of Florence reagent
(KI+I2+H2O) is added
(3) Crystals - If semen is present dark brown rhombic [or lance-like] crystals of
choline iodide appear. They resemble haemin crystals, but can be
differentiated. CI crystals are larger and arranged in clusters, rosettes, crosses
etc.
(4) Specificity - Florence test is not specific for semen; several substances of
animal and vegetable origin give +ve test. Crystals very similar to choline
crystals can be made from noncoital postmortem vaginal swabs.

7. Immunological methods

a. Mab 4E6
Some seminal plasma proteins are absorbed to the spermatozoa surface [sperm-
coating antigens]. These components can be detected both on spermatozoa and
in the ejaculated fluid using Monoclonal antibodies (Mab). The antibody Mab
4E6 recognizes a sperm coating antigen 4E6 which is secreted by the epithelial
cells of the ejaculatory duct and binds to the surface of spermatozoa. Advantages
of using Mab 4E6 -
(1) Specific to human seminal plasma only [not found in animals]
(2) found in azoospermic patients as well.

b. SVSA
SVSA (seminal vesicle-specific antigen) protein is produced by seminal vesicles
and is present even in aspermic individuals. It is a substrate of p30. It can be
detected by using a Monoclonal Mouse anti-Human-Sperm antibody no. 5
(MHS-5). Advantages of using MHS-5 -
(1) Stability - It is fairly stable, and has been demonstrated even 48 h after
intercourse in vaginal swabs.
(2) High specificity - Only primate semen shows cross reactions.

8. Prostate Specific Antigen (PSA, P30)

Prostate Specific Antigen (PSA) is a glycoprotein produced by prostatic
epithelial cells.
Salient features:
(1) Detection of PSA [syn. p30 (so called because its mol wt is 30 kilodaltons)]
is strongly indicative of semen.
(2) Also useful if the offender has azoospermia, or has undergone a vasectomy
operation.
(3) Initially believed to be prostate specific, PSA is now known to be present, in
lower concentrations, in various body fluids, including urine, serum, breast
milk and amniotic fluid. Conc in semen is much higher.

9. Puranen’s test [1936]

Detects spermine like Barberio’s test. Dinitrona-phtholsulfonic acid [syn,
Naphtholgelb S, Naphthol Yellow S] is used instead of picric acid. Characteristic
orange microcrystals indicate semen.

10. Other methods

(1) Glyoxalase 1 (GLO 1). It is a genetic marker found in semen and in several
other body fluids and tissues namely RBCs, hair roots, lymphatic tissues, and
dental pulp.
(2) Oxytocinase
(3) Peptidase A
(4) Phosphoglucomutase
(5) Semenogelin I and II [SgI, SgII], are proteins originating in the seminal
vesicles and a substrate for p30, is a useful marker for the identification of
semen.
(6) Single photon fluorometry
(7) Sperm specific lactate dehydrogenase [LDH-C4; LDH-X]
(8) Trace metals in seminal plasma – Vaginal swabs may be tested for
following trace metals. Normal levels in human seminal plasma are (a)
Aluminum 46 µg/dL (b) Cadmium 12 µg/dL (c) Cobalt 31 µg/dL (d) copper
46 µg/dL (e) Lead 31 µg/dL (f) Manganese 7 µg/dL (g) Nickel 106 µg/dL and
(h) zinc 190 µg/dL.
Memory Aid 21: Tests for Semen
1. Barber creates glistening lucid hair
2. Semen p a sses f r o m pr o state
Barber – Barberio’s test
Creat es – Creatinine phosphokinase
Glistening - glyoxalase
Lucid - leucine aminopeptidase
Ha i r - Immunological
Semen - Semenogelin I and II
P eptidase A, PGM
Acid phosphatase
S
S
E
S
Florence, FISH
RNA based assays
Oxytocinase
Ga M ma Glutamyl transpeptidase [GGT]
PSA, Puranen’s test
r
o
Sperm specific LDH
Trace metals
Ammonium molybdate
Chroma Tography
E

D. Techniques using Fluorescence

Fluorescent techniques which detect some specific component of sperm [DNA
sequence, sperm antigens] are as specific as detection of a sperm itself, but far
easier.

1. Fluorescent in situ hybridization (FISH)

FISH (fluorescent in situ hybridization) is a cytogenetic technique used to
detect and localize the presence of specific DNA sequences on chromosomes.
Fluorescent probes are used that bind to specific DNA sequences eg those from
Y-chromosome only.

2. Immunofluorescence
Several fluorescent dyes, each with their own ideal performance parameters,
have been introduced for use in immunofluorescence.

a. SpermPaint
SpermPaint, is an immunofluorescent technique that uses two mouse
monoclonal antibodies, each coupled to an Alexa 488 dye, to fluorescently
label the equatorial segment of the sperm head and the sperm tails within a
given sample.

b. SPERM HY-LITER
SPERM HY-LITERTM (by Independent Forensics of Illinois, Lombard, IL) is a
novel kit similar to SpermPaint. It contains a proprietary human sperm–
specific mouse monoclonal antibody, combined with a fluorescent Alexa 488
dye so that the entire head of the sperm cells fluoresces when viewed under a
microscope.

E. Microscopic Examination
Detection of spermatozoa on microscopy is the confirmatory test for semen.
Salient features:
(1) Problems associated with microscopy: (i) it is of no use in azoospermia
[found in 10–15% cases dealt with by the Forensic Science Service],
vasectomized accused, or if condom has been used (ii) difficult to visualize
intact spermatozoa in stain samples, particularly where semen adheres to
clothes (iii) sperm can disintegrate if the stain is washed or comes into contact
with another object.
(2) Procedure – Specimens may be a swab from vaginal canal, or other material
(eg fabric stained with semen). Procedure is slightly different for each.

1. Swab from vaginal canal

(1) Both dry and wet specimens are examined.
(2) In a dry specimen, the vaginal swab is smeared on a glass slide, stained and
then examined for spermatozoa. Sperm motility cannot be seen by this
method. At least one intact spermatozoa must be visible to confirm emission.
It is because both sperm head and tail may be mimicked by a number of other
artifacts. Look for microorganisms for venereal disease [details above]. If
present send wet specimen for culture. If accused is infected with the same
organism, it forms a corroborative evidence.
(3) Wet specimens are used for sperm motility
(i) Procedure - (a) Moist swab (or a drop of mucus removed from vagina) may
be touched with a glass slide (b) Dilute with a drop of normal saline and
look for motile sperms.
(ii) Interpretations - (a) Motile sperms – (I) In vaginal samples are found up to
24 hours [100% are motile up to 3 hours; 50% are motile by 8 hrs; 10% are
motile by 24 hrs] (II) in endocervix up to 6 days. (b) Non motile sperm
heads are detected in the living (i) up to 7 days in the vaginal cavity, (ii) 2-3
days in the anus and rectum, and (iii) 24 hours in the mouth.

2. Stained fabric or other material with dried stains

(1) The specimen is allowed to moisten with a few drops of 1% HCl or 3%
acetic acid in a watch glass.
(2) Keep for 1 hr if stain if fresh; 4 hrs if old.
(3) Maximum concentration of sperms is in the central portion of stain.
(4) Prepare a film by rubbing the moistened portion of fabric on a slide.
(5) Dry in air without heat or fix for 1 minute in methyl or ethyl alcohol.
(6) Stains used for spermatozoa
(i) Baecchi Stain - A combination of methylene blue and acid fuchsin. Stains
sperm heads pink, and nuclei blue. Developed by Baecchi in 1909. (ii)
Christmas tree stain [syn, Kernechtrot-Picroindigocarmine Stain,
KPIC]. Most commonly used. Consists of two dyes. Nuclear Fast Red dye
[Kernechtrot Solution] stains nucleus red and Picroindigocarmine (PIC)
stains most other cellular material (e.g. epithelial cells) various shades of
green [Appearance is much like red ornaments on a green Christmas tree]
(iii) Methylene blue for 30 min and counterstain with eosin for 2 min or
(iv) Haemalum [soln of hematoxylin and alum] 5 min and counterstain
with eosin for 2 min [Fig. 25.14]. [Note to editor – Please check the
number of figure number manually, because computer file is not being
accepted]
(7) For all stains, anterior 2/3rd of head (occupied by acrosome) is unstained or
very faintly stained; only the posterior 1/3rd occupied by nucleus is stained.
(8) Older stains – are less likely to reveal intact spermatozoa
(9) Note co-ordinates – If only one or two sperm heads are found, their co-
ordinates should be noted and entered in the report. MLC number or PM
number must be etched on the glass slide with a glass marking pencil.
 26. Abortion

I. INTRODUCTION

[A] Legal definition: Abortion (miscarriage) is premature expulsion of fetus

from the mother’s womb at any time of pregnancy, before full term of
pregnancy is completed (S.312, IPC). In medicolegal practice, periods during
gestation are not indicated in calendar months [as they vary]. They are always
indicated in lunar months [each lunar month = 28 d], or weeks [called
postmenstrual weeks or PMW], or days. Thus in medicolegal language, normal
pregnancy lasts 10 lunar months, 40 weeks or 280 days. All periods are counted
from LMP. Since ovulation occurs 14 days after LMP, actual physical existence
of fetus within the womb is only 266 days. [Fig 26.1].

[B] Medical definition: Abortion is premature expulsion of fetus from the

mother’s womb before the age of viability (28 weeks). After this period, it is
stillbirth.

II. IMPORTANT TERMS

(1) Preembryo - Conception till the end of 5 post-menstrual week [PMW].

(2) Embryo – Start of 6th till end of 9th PMW.
Memory Aid 1: Stages in fetal life
• Remember the mnemonic from ch 3 for ossification of radius [2 " 5 " 6 " 9].
• Now replace 2 with 0 [0 " 5 " 6 " 9].
• 0-5 PMW " Preembryo [First 7 days of this stage is sometimes referred to as a “Developing
ovum”. This is time when implantation occurs.
• 6-9 PMW " Embryo
• 10 PMW - delivery " Fetus
(3) Fetus – Start of 10th PMW until delivery.

III. CLASSIFICATION OF ABORTION

[A] Clinical classification: (1) Complete- Expulsion of all products of

conception (2) Incomplete - Expulsion of some products of conception (3)
Induced- Termination of pregnancy for medical or elective reasons (4)
Inevitable - Vaginal bleeding or rupture of the membranes accompanied by
dilation of the cervix (cf threatened) (5) Missed- Undetected death of an embryo
or a fetus that is not expelled and that causes no bleeding (also called blighted
ovum, anembryonic pregnancy, or intrauterine embryonic demise) (6)
Recurrent or habitual- Three or more consecutive spontaneous abortions (7)
Septic- Serious infection of the uterine contents during or shortly before or after
an abortion (8) Spontaneous - Non induced abortion (9) Therapeutic -
Termination of pregnancy because the woman’s life or health is endangered or
because the fetus is dead or has malformations incompatible with life (10)
Threatened - Vaginal bleeding occurring before 20 wk gestation without
cervical dilation, indicating that spontaneous abortion may occur (cf inevitable)
[B] According to method induced (1) Natural - (a) Spontaneous (b) accidental
(2) Artificial – (a) Therapeutic or Justifiable (safe. Conducted by qualified
personnel) (b) criminal (unsafe. Conducted by quacks, by unrecognized methods
in unhygienic surroundings) [C] According to time period (1) Early - before 12
wk gestation (2) Late - after 12 wk gestation.

IV. NATURAL ABORTION

A. Epidemiology
(1) Incidence - 15% among clinically recognized pregnancies. 2-3 times higher
among very early and unrecognized pregnancies
(2) Past obstetric history - incidence higher among women with prior abortions
(3) Maternal age – Incidence -s with maternal age from 12% in women < 20
years to over 50% in women > 45 years
(4) Fetal age – Most common at 2-3 months.
B. Causes

1. Embryonic factors
(1) Chromosomal abnormalities - Cause of majority of early abortions.
Autosomal trisomies are most common (51.9%). Due to meiotic nondisjunction
during gametogenesis in normal parents. (2) Abnormal germ cells (3) defective
implantation (4) defects in the developing placenta or embryo (5) accidental
injuries to the fetus (6) Anembryonic pregnancy (7) Empty gestational sacs -
or “blighted ova” represent pregnancy failures with subsequent embryonic
resorption. (8) Low implantation of zygote. (9) Disease of decidua or placenta.

2. Parental factors
(1) One parent is the carrier of a balanced translocation - Chromosome
translocation is caused by rearrangement of parts between nonhomologous
chromosomes. When there is equal exchange of material it is balanced; when
unequal, resulting in missing genes it is unbalanced. (2) Infections (3) cigarette
smoking (4) diabetes mellitus (5) emotional disturbances (6) hormonal
deficiency (7) hypertension (8) nephritis (9) Rh incompatibility (10) sudden
shock (11) syphilis (12) toxicity [arsenic, lead, other heavy metals, cantharides,
drugs, ethanol, occupational exposure to benzene, gasoline, H2S] (13) uterine
anomalies - malformed uterus, retroverted uterus, submucous uterine fibroid,
uterine hypoplasia.

V. THERAPEUTIC VS. CRIMINAL ABORTION

[A] Therapeutic abortion is that which is done to save the life of woman. It is
done by qualified personnel. [B] Criminal abortion is unlawful expulsion of
products of conception from the uterus, i.e. outside of the provisions of MTP Act
1971. It may include (1) abortion by unqualified personnel (2) abortion for
indications other than those mentioned in the Act and (3) abortion after 20 weeks
of pregnancy (excluding those conducted to save the life of woman). Criminal
abortions come to light when the woman dies or some one gives information to
the police. (4) Abortionists are traditionally divided into three categories (i)
Expert or medically qualified (ii) Semi-skilled – nurses, midwives, chemists
etc who have rudimentary knowledge of human anatomy and (iii) unskilled.

VI. LEGAL ASPECTS OF ABORTION

A. S.312, IPC
(1) Scope - Abortion can only be done to save the life of a woman. Abortion
done for any other purpose would attract this section
(2) Consent of the woman should be there
(3) Woman herself is punishable under this section, if she performs abortion on
herself
(4) Punishment – (a) Before quickening - Imprisonment of 3 y or fine or both (b)
After quickening - Imprisonment of 7 y + Fine.

B. S.313, IPC
(1) All aspects remain same as above, except that
(2) Consent of the woman is not there
(3) Punishment – Imprisonment of 10 y + Fine [whether quickening has occurred
or not]

C. S.314, IPC
(1) All aspects remain same as in S.312, except that
(2) Death of the woman occurs
(3) Punishment – (a) If consent of woman was there - Imprisonment of 10 y +
Fine. (b) If consent of woman was not there – Life imprisonment + Fine.
(4) It is no defense to the abortionist that he did not know that his act could
cause death. Table 1 summarizes these three sections.
D. S.315, IPC
(1) Scope – The act must be done (a) with intent to prevent child being born
alive or (b) to cause it to die after birth (c) If act is done to save the life of
woman, than this section is not attracted
(2) Punishment – Imprisonment of 10 y or fine or both
(3) Difference from previous sections - Here the length of pregnancy is typically
> 28 weeks (age of viability) [Fig 26.2].
E. S.316, IPC
(1) Scope – Primary aim was to kill mother, but death of her quick unborn child
is caused. She remains unharmed
(2) Punishment – Imprisonment of 10 y or fine or both.

F. S.511, IPC
Failed attempt – In all the above sections, if the persons fails in his attempt to
cause abortion, he would still be punishable with half of the imprisonment
prescribed under that section.

VII. THE MEDICAL TERMINATION OF PREGNANCY ACT,

1971

A. Indications
Listed u/s 3 of MTP Act, 1971. For convenience of study, they are grouped
under following headings. The law nowhere mentions these headings (1)
Therapeutic – When the continuance of the pregnancy would involve a risk to
the life of the pregnant woman or of grave injury to her physical or mental health
[S.3(2)(i)]. (2) Eugenic - There is a substantial risk that if the child were born, it
would suffer from such physical or mental abnormalities as to be seriously
handicapped [S.3(2)(ii)]. This may occur (A) Diseases - If during the first 3
months the pregnant woman suffers from (i) Chickenpox (ii) German measles
(iii) Smallpox (iv) Toxoplasmosis (v) Viral hepatitis (vi) Viral infections (B)
Drugs - If the pregnant woman is treated with (i) Aminopterin (ii) Antimitotic
drugs (iii) Cortisone (iv) Thalidomide [of historical imp only] etc, or if she takes
(v) antidepressants or (vi) hallucinogens (C) X-rays – If mother is treated with
X-rays or radioisotopes (D) Heritable mental illness – If both parents are
suffering from a heritable mental illness [eg if one parent has
schizophrenia"chances of child developing it are 10-12%. Both parents have
schizophrenia"chances are 40%]. (3) Humanitarian - When pregnancy is
caused by rape [S.3(2), Explanation 1]. (4) Social - (A) When pregnancy has
resulted from failure of contraceptive methods in case of a married woman
[S.3(2), Explanation 2]. (B) When social or economic environment, actual or
reasonably expected may result in injury to mother’s health [S.3(3)].
Memory Aid 2: Indications of MTP
SETH – Social, Eugenic, Therapeutic, Humanitarian

B. Other Salient Features

(1) Under the MTP Act -
(i) MTP rules were formed in 1975 [as mandated by S.6 of MTP Act, 1971].
Repealed in 2003, via rule 10 of MTP rules 2003; the new rules are called
MTP rules 2003]
(ii) MTP regulations were formed in 2003 [as mandated by S.7 of MTP Act,
1971]. (1) Conflict with IPC - If a physician performs an abortion under
the provisions of this Act, then even if he violates any section of IPC [eg
S.312-326], he will not be guilty of any offence [S.3(1)]
(2) Consent -
(i) Pregnant woman <18 y or mentally ill – written consent of guardian required
[S.3(4)(a)]
(ii) Pregnant woman ≥18 y - can give consent [S.3(4)(b)]
(iii) Consent of husband – not legally required. However if woman repeatedly
undergoes MTP without consulting or informing her husband, he can get a
divorce under “cruelty clause” [ch 23] as it may amount to “cruelty to
husband”.
(3) Who can terminate pregnancy [rule 4 of MTP Rules, 2003] – Any one
who has following experience and qualifications
(i) 6 months house job in G&O
(ii) 1 y experience in the department of G&O
(iii) Holds MD or diploma in G&O
(iv) If registered as a doctor before 1971 [i.e. commencement of the Act], must
have experience of 3 y in practice of G&O [such cases are rare now due to
passage of time]
(v) Has assisted in performance of 25 MTPs of which at least 5 must have been
performed independently [with this experience, doctor can terminate
pregnancy only up to 12 wks].
(4) Up to what period pregnancy may be terminated -
(i) Up to 12 wks – Opinion regarding existence of indications may be expressed
 by 1 doctor [S.3(2)(a)]
(ii) 12-20 wks – Opinion must be 2 doctors or more [S.3(2)(b)].
(iii) >20 wks – please see below.
(5) Where pregnancy may be terminated –
(i) In a hospital established or maintained by Govt [S.4(a), MTP Act 1971]
(ii) In a place approved for MTP by (a) Govt or (b) District Level Committee
[DLC] constituted by Govt [S.4(b), MTP Act 1971]
(6) Emergency provisions – If MTP is required to save the life of a woman
(7) Pregnancy caused by rape, woman has not lodged complaint with police,
wants MTP -
(i) MTP can be done
(ii) Doctor must report the matter to police, preserve the products of conception
and hand it over to police for DNA profiling. Please see ch 24.

VIII. METHODS OF PROCURING CRIMINAL ABORTION

Methods differ according to different periods of pregnancy. They become more

drastic as pregnancy advances.
(1) Up to the end of 1st month – When woman has not missed a period, but
believes she may have become pregnant (i) Violent exercise (ii) hot baths (iii)
purgatives
(2) After missing the first period up to the end of 2nd month – Suspicion
becomes a surety now. More drastic measures are adopted (i) Abortifacient
drugs
(3) After 2nd month till parturition – Methods become more drastic; woman
may resort to mechanical interference.
Memory Aid 3: Methods of Criminal Abortion
Criminal abortion violates local mores
Abortifacient drugs
Violence
Local methods
Miscellaneous

A. Abortifacient Drugs

1. Drugs acting directly on the uterus

a. Ecbolics
Ecbolics [Gk ec, away from; ballein, throw] are drugs that increase uterine
contractions.
Salient features:
(1) Actions - -contractions, but do not relax or dilate the cervical canal and
external os, necessary to expel the fetus. Thus dangerous to use.
(2) Drugs used: (i) Apiol – Active principle of common parsley [Petroselinum
sativum] (ii) Ergot - (a) Most common ecbolic (b) Side effects – arterial spasm
and gangrene of extremities (c) Frequently fails during earlier months of
pregnancy (iii) Goldenseal [Orange-root, Orangeroot; Hydrastis canadensis]-
(a) perennial herb (b) Acts both as oxytocic [due to hydrastine and
hydrastinine] and emmenagogue. It is a stronger ecbolic than emmenagogue
(iv) Hormone preparations – Synthetic estrogens (v) Lead - Taken in the form
of pills made from diachylon [lead oleate] or lead plaster (vi) Pituitary extract
- (a) No effect when given by mouth; effective only by injection (b) Effect is
significant only near term (vii) Quinine - was in popular demand among
young service women during the 2nd WW for abortions. Caused serious
toxicity. (viii) Savin [Juniperus sabina] – useless in small doses (ix)
Miscellaneous - (a) Decoctions of cotton root bark (b) Nitrobenzol (c)
Picrotoxin (d) strychnine.

b. Emmenagogues
Emmenagogues are drugs which increase the menstrual flow.
Salient features:
Two types:
(1) Direct – which directly stimulate the uterus [used more often for criminal
abortion]. Ex – Aloes, Anemone, Apiol, Asarum arabicum, Borax, Broom,
Cantharides, Caulophyllin, Cimicifuga, Grains of paradise, Hellebore [white
and black], Juniper, KmnO4, Laburnum, Male fern, Manganese dioxide,
Mentha pulegium, Myrrh, Nutmeg [ch 46], Pennyroyal, Polygala, Pulsatilla,
Racemosa, Rue, Saffron, Sanguinarin, Santonin, Savin, Senecio, Senega,
Squills, Tansy, Thuja and Yew leaves.
(2) Indirect – which correct anaemia, or disturbed pelvic circulation, etc. [used
more often for treatment of amenorrhoea as folk medicine]. Ex – Tonics and
 hematinics eg iron.

2. Irritants of the genitourinary tract

(1) Applied locally - they produce reflex uterine contractions.
(2) Taken systemically - produce inflammation of kidneys.
(3) Ex (i) cantharides (ii) Oil of pennyroyal (iii) Oil of tansy (iv) Potassium
permanganate crystals, solution or tablets [100-300 mg]. (a) May cause acute
local punched out ulcers with raised edges and granular black base. (b) May
erode arterial vessels and cause severe hemorrhage.

3. Irritants of the GIT

(1) Any substance which produces irritation of colon, may produce hyperemia
and contractions of uterus also
(2) Emetics – Tartar emetic
(3) Saline cathartics [MgSO4]
(4) Strong purgatives - (i) Aloes (ii) Calomel (iii) Castor oil (iv) Colocynth (v)
Croton oil (vi) Elaterium [syn, elaterin. Plant extract from the juice of the fruit
of Ecballium Elaterium, the squirting cucumber] (vii) Gamboge [resin from
various species of trees of the family Guttiferae] (viii) Jalap (ix)
Phenolphthalein (x) Podophyllum (xi) Rhubarb (xii) Scammony [Convolvulus
scammonia] (xiii) Senna.

4. Local application of irritants

(1) Corrosives – eg carbolic acid, oxalic acid etc
(2) Irritants – All of the above may be applied locally also

5. Systemic poisons
Rationale is that at sublethal doses, the drug may be lethal to fetus which is
much more susceptible
(1) Inorganic irritants - eg salts of antimony, copper, iron, lead and mercury.
(2) Organic irritants - Barks [eg of plumbago rosea], cantharides,
Caryophyllus, juices [eg of calotropis], methi, saffron, seeds [eg of carrot,
Moringa (a flowering plant)] and unripe fruits [eg of papaya, pineapple etc].

B. Violence
Violence may cause abortion by (1) producing congestion of pelvic organs (2)
producing hemorrhages between uterus and membranes (3) dislocation of
placenta.

1. Direct violence
Force is directly applied over lower part of abdomen by following methods (1)
Kicks and blows (2) Kneading (produces severe pressure on the abdomen) (3)
Massage of uterus through the abdominal wall (4) Tight lacing (wearing a
tightly-laced corset).
a. Cupping
(1) This is a special method of direct local violence used in advanced pregnancy.
(2) Method - A wick is placed over hypogastrium and lighted A mug is placed
over it, mouth downwards Lighted wick consumes oxygen producing partial
vacuum mug is pulled upwards mug sticks to the hypogastrium due to partial
pressure forcible pulling separates placenta.

2. Indirect violence
Force is indirectly applied over lower part of abdomen by such activities as (1)
Carrying or lifting heavy weights (2) Cycling (3) Driving over rough roads (4)
Horse riding (5) Jumping from a height and running upstairs and downstairs

C. Local Methods
A tenaculum is often used in following procedures to steady the cervix and
uterus. Its marks are often found on the uterus during examination.

1. Abortion pastes
(1) Iodine containing pastes:
(i) Utus paste - A mixture of soap, myrrh resinoid and potassium iodide. Iodide
acts as an irritant causing abortion.
(ii) Interruptin - contains elemental iodine. The risks were the same as with
“Utus paste”
(iii) Fetex Paste (brand name) contains benzoin, iodine, thymol, potassium
iodide and saponified vegetable oil paste.
(2) Lead containing pastes - Diachylon - contains lead salts (e.g. lead oleate)
and oil.
2. Abortion stick
Abortion stick is a thin wood or bamboo stick about 12-18 cm long [Fig 26.3].
Salient features:
(1) Construction: (i) Traditional stick - At one end of the stick, a piece of cloth
or cotton wool is wrapped, which is soaked with one or more irritants eg,
Abrus precatorius, arsenic sulfate, arsenious oxide, asafetida (Ferula
asafetida), marking nut juice, mercuric chloride, red lead etc. (ii) Variation –
Instead of stick, a twig of some irritant plant may be used, eg Calotropis,
Cerbera thevetia, Nerium odorum, Plumbago rosea or zeylanica
(2) Method of use - Introduced into the uterus and retained there till uterine
contractions begin.

3. Air insufflation
Air is introduced into the uterus through vagina by means of douche tips,
orogenital contact, pumps and syringes in a false belief that air would dislocate
placenta causing abortion. This rarely happens. May cause death by air
embolism.

4. Curettage
More like a professional D&C. Done only by experienced criminal abortionists.

5. Dilation of the cervix

Dilation of cervix expels the contents of the uterus. Generally used after 8 wks
of pregnancy. Methods used are:
(1) Laminaria tent [syn, Laminaria stick, sea tangle tent]:
(i) A cone [tent] or thin rod of dried Laminaria digitata [large seaweeds
belonging to the brown algae group].
(ii) Availability - in a box containing 6 laminaria sticks in liquid. Each one is 8
cm in length; diameters measure 3, 4 and 8 mm. A white thread is attached
to one end for easy removal.
(iii) Laminaria sticks are inserted into the cervix" over the course of several
hours, they slowly absorb water and expand.
(iv) Introduction of several thin sticks was considered preferable to one with a
larger diameter. The latter became so tight with expansion that its removal
could become impossible, even with threads.
(v) Causes dilation of cervix and expulsion of uterine contents.
(vi) Also contains iodine, which is a uterine irritant.
(2) Slippery elm bark - It is the inner bark of Ulmus fulva, a tree which grows
in Central and North America. Contains mucilage. Pieces of bark are inserted
into the cervical canal. Absorbs water and swells to a slippery jelly. Dilates the
cervix. Acts as a mechanical irritant and lubricant also.
(3) Miscellaneous methods – Introduction in the cervix of (i) Pessaries (ii)
sponge and leaving them there.

6. Electricity
(1) Placement of poles: Generally +ve pole over the lumbosacral region; -ve
over the cervix [or posterior vaginal cul-de-sac], but can be done other way
round also
(2) Low voltage current is passed"Uterus contracts and expels contents.
7. Gum elastic bougies
(1) In more advanced pregnancies gum elastic bougies, catheters or balloons
are introduced through the cervix into the uterus [Fig 26.3].
(2) Mechanism - irritation of the uterus.
(3) Complication -Sepsis.

8. Rupturing of the membranes

(1) Method - Rupture of membranes is done by introduction of an instrument
into the cavity of the uterus eg a cannula, catheter, crochet needle, curtain rod,
douche, gloss rod, hairpin, knitting needle, nail, pen, pencil, penholder, probe,
screwdriver, stick, umbrella rib, uterine sound, wire etc.
(2) Who can do - abortionist, woman herself
(3) Mechanism - rupture of membranes"escape of liquor amnii"induction of
abortion
(4) Time of abortion - within a few hours to 3 days. May be delayed for several
weeks.
(5) Complications:
(i) Perforation of vaginal or uterine walls
(ii) breakage of instruments of parts of instruments within the uterine cavity
(iii) Infection.

9. Syringe aspiration
Large syring is taken"a catheter or plastic tubing is attached to it"introduced
within the uterus"suction applied"-ve pressure ruptures chorionic sac"
precipitates abortion.

10. Syringing
(1) Instruments used:
(i) Ordinary enema syringe [Fig 26.3]. May be used for douches of hot or cold
water, which are projected with considerable force towards the uterine os.
(ii) Higginson’s syringe [Fig 26.3]. One end is dipped into the solution, and the
other into the uterus. Repeated compression of bulb pushes fluid into the
uterus. If there is imperfect filling of the bulb, a mixture of air and fluid is
forced into the uterine cavity at a pressure higher than that in uterine veins.
(2) Injection material - Any irritant fluid, eg soln of irritating chemicals in
water, eg acids [inorganic], alum, cresol, formalin, KMnO4, lysol, Metallic
irritants [Arsenic compounds, Hg compounds eg corrosive sublimate, lead
compounds], soap, turpentine etc.
(3) Used by - woman herself or an unskilled or semi-skilled abortionist.
(4) Mechanism - The fluid detaches amniotic sac and placenta from the uterine
walls"uterine contraction "Abortion.
(5) Complications:
(i) Air embolism - ch 11.
(ii) Extensive local tissue destruction"fatal hemorrhage, infection.
(iii) systemic absorption of irritant substances "causing toxemia, shock and
death.
(iv) Vagal inhibition - May cause sudden death. Causes are (a) Sudden and rough
insertion of instruments in the uterus (b) rapid injection of unduly hot or
cold liquids.

D. Miscellaneous Methods
(1) Alternate hip baths in very hot and cold water
(2) Partial abortion by untrained abortionist; completed by a trained doctor
because it becomes threatened -
(i) Abortionist ruptures membranes and sends patient to doctor
(ii) Woman applied some corrosive substance to vagina (eg KmnO4) to produce
ulceration and bleeding; visits a doctor who completes abortion
(iii) Woman complains that her uterus is displaced; unsuspecting doctor passes a
sound resulting in abortion.

IX. THERAPEUTIC METHODS TO PROCURE (SAFE)

ABORTION

(1) Manual Vacuum Aspiration

(2) Dilatation and Suction Curettage
(3) Dilatation and Evacuation
(4) Other Surgical Methods
(i) Dilatation and extraction (D & X)
(ii) Induction
(iii) Hysterotomy

X. EVIDENCE OF CRIMINAL ABORTION

A. In the Living
Signs of recent abortion – same as those of recent delivery.

B. In the Dead
Following points must be proved to convict the abortionist
(1) that the dead woman was pregnant
(2) that the accused was responsible for the act which resulted in abortion
(3) that the accused intended illegal abortion
(4) that death was due to abortion.

1. PM findings
(1) Depend upon
(i) mode of abortion practiced
(ii) time elapsed between abortion and death. In sudden deaths woman may be
found dead in a posture consistent with recent abortion, eg lower garments
pushed up, legs spread wide apart, syringe or other instrument within
genital canal, apparatus and paraphernalia strewn around.
(iii) Time elapsed between death and PM examination
(2) In all cases of criminal abortion, female genitalia must be excised out of the
body and examined [ch 5]
(3) Maintain a full photographic record of all procedures conducted and findings.

a. Abortion by drugs
(1) Local examination of genitals – corrosion, erosions, inflammation of vulva,
vagina, cervix etc indicate local application of corrosives and irritants.
Preserve vaginal and vulval washings. Match with those found at the scene
[please see above].
(2) GIT –
(i) look for signs of congestion, inflammation, irritant poisoning
(ii) If present – (a) indicate administration of GIT irritants. (b) Examine entire
GIT carefully. (c) Preserve entire GIT contents for chemical analysis
(3) Urinary tract -
(i) Look for signs of congestion, inflammation, irritant poisoning
(ii) If present – (a) indicate administration of cantharides, turpentine.

b. Instrumental abortion
(1) Air embolism
(2) Infection:
(i) Seen in delayed deaths. Indicates instrumental abortion.
(ii) Vagina - walls may show pus. There may be frank discharge
(iii) Uterus - (a) Uterine sepsis usually involves endometrium, especially the
placental site and pieces of retained products (b) Myometrium, tubes,
adjacent pelvic organs [eg ovaries], peritoneum"infected.
(iv) Infection is rare in natural abortion.
(3) Injuries:
(i) Site - on vagina, cervix, uterus. Sometimes on abdomen also. There may be
abrasions, bruising, foreign bodies, hemorrhage, inflammation, lacerations,
perforations, punctures, ruptures etc. Bleeding in peritoneal cavity indicates
puncture through and through the genital tract. In the vagina, injuries are
present in the walls and especially in the posterior fornix.
(ii) Extent - Damage is more in unskilled or semi-skilled hands and also during
attempts at self abortion. All organs constituting genital canal [vagina,
cervix, uterus] may show perforations of various sizes and shapes. The size
of perforations may vary from a small ragged pinpoint to a much larger tear
of oval, round, stellate or irregular shape. Perforation of uterus indicates
penetration into the abdominal cavity and abdominal injuries must
specifically be searched for. Perforations, tears etc may be found on
bladder, intestines [small and large including rectum], mesentery and
omentum. If very long instruments [eg cycle spokes] are used, even
diaphragm may be pierced causing injuries to lungs and heart.
(iii) Nature - of injuries reveal type of instrument used eg pointed, blunt,
penetrating etc.
(4) Materials to be preserved:
(i) Fetal blood and tissues - DNA profiling would establish maternity and if
 required paternity, especially if suspected father was the once who
conducted criminal abortion.
(ii) Fluid from cut surface of lung and pulmonary blood - for fatty acid
estimation and for phenolic derivatives depending on the agent used.
(iii) Foreign bodies - if recovered from anywhere especially within the genital
canal or uterus, it must be preserved and sent for analysis. Sometimes rags
soaked in irritant solutions may be recovered. Sometimes they are inserted
there merely to stop post-abortion bleeding.
(iv) Instruments of abortion - (a) for toxicology [eg abortion stick] (b) for
microbiology (c) for typing of blood, and whether it matches that of mother,
fetus or both.
(v) Maternal Blood - (a) For toxicology and microbiology (b) for typing and
matching with that found at the scene and on the instruments
(vi) Scene of crime - All suspect material found at the scene of crime, eg barks,
bottles, containers, nozzles, syringes, tubes, twigs of plants etc. Material
expelled from uterus.
(vii) Tissue - from vagina, uterus, cervical canal, ovaries and all major internal
organs for histopathology.
(viii) Washings - from vagina, cervix, uterine cavity. For toxicology and
microbiology. Alternatively entire genital system may be sent frozen for
toxicology.

c. Abortion by syringing
Same as in instrumental abortion. Additional findings are
(1) Clothes - may be soiled with fluid
(2) Genital canal - may show corrosion or tissue damage due to use of
antiseptics, irritants or corrosives.
(3) Fluid - dark red fluid found between uterine walls and fetal membranes with
partial detachment of placenta. If soap has been used, fluid may be foamy.
(4) Venous system - Uterine, ovarian and pelvic veins and all veins extending
from the sides of the uterus up to the right heart, coronary vessels, superior
and inferior vena cavae and pulmonary conus may show bubbles of gas and
slimy fluid. Veins may be “ballooned out”. May show segmentation and may
have a “beaded” appearance. On touching, have a characteristic elastic feel.
Mechanism of entry - As fluid is pushed into the uterus under pressure, it
 enters dilated uterine sinusoids along with air.

2. Collection of material
Same as in living and as noted above.

XI. CAUSES OF DEATH IN CRIMINAL ABORTION

A. Immediate Deaths
Occur within minutes.
(1) Embolism [air, amniotic fluid, fat]
(2) Hemorrhage
(3) Poisoning [if poison was used to procure abortion]
(4) Vagal inhibition.

1. Amniotic fluid embolism

Amniotic fluid embolism (AFE) is condition in which amniotic fluid, fetal cells,
hair, or other debris enters the mother’s blood stream via the placental bed.
Presence of fetal debris in the pulmonary blood vessels of a mother who had
died suddenly in labor was first described by Meyer in 1926. In 1941, Steiner
and Luschbaugh were the first to attribute sudden death during labor to AFE.
Salient features:
(1) Occurrence - It occurs not only during (i) criminal abortion, but also during
(ii) first and second trimester abortions (iii) abdominal trauma (iv)
Amniocentesis (v) normal labor and delivery (vi) immediately postpartum
(2) Risk factors – (i) -ed maternal age (ii) augmented labor (iii) cervical
laceration (iv) cesarean delivery (v) Diabetes (vi) fetal macrosomia (vii)
induction and augmentation of labor (viii) placenta previa or abruption (ix)
Strong uterine contractions (x) uterine rupture, and(xi) vacuum, and forceps
deliveries.
(3) Incidence - 1 in 8000 to 80,000 deliveries. In 50% of cases, death occurs
within 1st hour of criminal abortion. In late deaths, DIC occurs
(4) Etiology –
(i) Mechanical blockage - pelvic trauma [inc rupture of uterus] due to
instrumental interference of criminal abortion opens up venous sinuses in
 the placental bed"Amniotic fluid [along with a fetal debris] enters venous
sinuses"causes pulmonary microvascular obstruction.
(ii) Anaphylactoid syndrome of pregnancy – amniotic fluid constituents in
circulation"release of various primary or secondary endogenous mediators
[arachidonic acid metabolites, bradykinin, endothelin, histamine,
leukotrienes]"severe transient vasospasm of pulmonary vasculature,
pulmonary hypertension, hypoxia, right heart failure, sudden death.
(5) Clinical features – (i) altered mental status (ii) DIC (iii) shortness of breath
(iv) sudden cardiovascular collapse (v) maternal death
(6) Lab diagnosis – (i) -Fibrin split products (ii) .Fibrinogen (iii) Prolonged
partial thromboplastic and prothrombin times (iv) thrombocytopenia
(7) Postmortem diagnosis – [A] Examination of dead body (i) Examination of
uterus – May reveal entrance site of emboli. (ii) Histopathology - (a)
Demonstration of (I) Amniotic and Chorionic cells (II) Fat globules (III) Fetal
squames (IV) Lanugo hair (V) Meconium (VI) Mucin and (VII) Vernix in
pulmonary vasculature and in uterine veins. (b) Stains used are (I) Alcian Blue
- detects mucin (II) H&E - routine staining (III) Attwood’s stain - stains the
keratin red and the mucus turquoise blue (IV) Lendrum stain contains
Phloxine-Tartrazine. Detects squames by staining them red (V) Mucicarmine
(VI) Sudan Black or Oil Red - Detects vernix caseosa. (c) Squamous debris
may persist for some weeks after the embolic event, and it is worth looking for
even in late deaths. (d) DIC - (I) deposition of fibrin microthrombi
[demonstrated with Martius Scarlet Blue] and extensive bleeding in internal
organs.

2. Vagal inhibition
The cervix and lower uterine segment are richly supplied with parasympathetics.
Touching by instruments, irritants, or hot and cold fluids, especially in a nervous
mother may prove instantaneously fatal. Anesthetization may contribute to rapid
death.

B. Delayed Deaths
Occur with 2-3 days [Fig 26.4]. (1) Local infection (2) Peritonitis (3) Pyemia (4)
Septicemia (5) tetanus (6) Toxemia.
C. Remote Deaths
Occur after weeks. (1) Bacterial endocarditis (2) Jaundice (3) Pulmonary
embolism (4) Renal failure.

XII. ML ASPECTS OF ABORTION

A. Fabricated Abortion
Fabricated abortion is false and malicious claim of an abortion by producing a
dead animal fetus. Women who have suffered trauma due to motor-vehicle
accidents, or physical assault may try to exaggerate the offence [to get more
compensation] by alleging that the trauma caused her to abort. A dead animal
fetus, or even a dead human fetus, acquired from a hospital may be produced to
support claim. Detailed examination of fetus and DNA profiling is necessary.

B. Trauma and Abortion

(1) If trauma is caused to the pregnant mother [eg motor vehicular accident, fall
from height, intentional blow], abortion may be induced. In such cases it
becomes necessary for the doctor to determine if trauma indeed resulted in
abortion. If intention was to kill mother and abortion was caused instead, it
would attract S.316, IPC.
(2) Difficulties in establishing a causal relationship between trauma and
abortion -
(i) Abortion may already be in progress when trauma occurred and it merely
hastened the process
(ii) Embryonic injury caused by trauma may not result in an abortion for several
weeks or even months.
(3) Criteria suggesting a causal relationship -
(i) Fetus and placenta should be normal before trauma
(ii) Factors known to cause abortion should be absent. These include (a) Chronic
infections in the mother [eg syphilis, toxoplasmosis] (b) Exposure to
abortifacients [folic acid antagonists, lead, X-rays] (c) Physical attempt to
induce abortion (d) Repeated h/o abortions without any cause (e) Uterine
abnormalities [eg congenital defect of uterine development, endometrial
polyps, incompetent cervical os, leiomyomas]
(iii) Abortion should occur within 24 h of trauma
(iv) The physical development of fetus and placenta should be compatible with
 the period of pregnancy at the time of trauma
(v) There should be an adherent clot or a depression on the placental surface.
(vi) Injuries to the fetus should be compatible with the time period of trauma.

C. Miscellaneous
(1) If abortion is due to occupational exposure to poisons [benzene, gasoline,
H2S], employer is liable for compensation. Many toxic agents causing
abortions [including 3 mentioned above] are included in Schedule III of
Workmens’ Compensation Act 1923 [WCA 1923] [ch 2].
(2) Wrongful life suits [please see ch 23].

XIII. DOCTOR’S DUTIES IN CASES OF CRIMINAL

ABORTION

(1) History taking – Must encourage the patient to give correct history. If she is
hesitant, should not force her to make a statement
(2) Consultation - with obstetrician
(3) Treat her - to the best of his ability. Should not view her as a criminal
(4) Maintain proper day-to-day records
(5) Preservation of evidence – (i) All soiled clothes (ii) Any foreign material
collected from the genital tract [abortifacient drugs, abortion sticks, syringes,
twigs etc] should be preserved and handed over to police
(6) Professional secrecy – must be maintained
(7) Arrange for dying declaration – if patient is serious
(8) In case of death – death certificate should not be issued. The body must be
sent for postmortem.
 27. Infant Deaths Including Battered
Baby Syndrome

I. INTRODUCTION

A. Infanticide
Infanticide is unlawful destruction of a child under the age of one year by
anyone. Infanticide does not include the death of fetus during labor, or when it is
destroyed by craniotomy or decapitation.

B. Feticide
Feticide is the killing of fetus at any time prior to birth (Main instances – MTP,
prenatal sex determination followed by selective abortion of female fetuses).

C. Neonaticide
Neonaticide is killing of an infant within 24 hours of birth. The term was first
coined by Resnick in 1970. The term is paradoxical, because although the term
“neonate” in obstetrics is used to denote an infant up to 28 days after birth, the
term neonaticide in psychiatry and forensic medicine is used for killing of an
infant within 24 hours of birth.

II. STILLBIRTH

A stillborn child is one which is born after 28th week of pregnancy and which
did not breathe or show any other signs of life at any time after being completely
born [WHO]. In the UK, according to the Still-Birth (Definition) Act 1992, this
period is reduced to 24 weeks.
Salient features:
(1) The child was alive in utero but dies during the process of birth.
(2) Stillbirths occur more frequently among illegitimate and immature male
children in primiparae.
(3) Incidence – 5%
(4) Causes – (i) Anoxia (ii) Birth trauma [especially intracranial hemorrhage due
to excessive moulding] (iii) Congenital defects (iv) Erythroblastosis fetalis (v)
Placental abnormalities (vi) Prematurity (vii) Toxemia of pregnancy.

III. DEAD BIRTH

A dead born child is one, which has died in utero, and shows one of the
following signs after it is completely born (1) maceration (2) rigor mortis (3)
putrefaction (4) adipocere (5) mummification [Table 2].
A. Maceration
Maceration (Latin macerare, to soften by soaking) is degenerative change
occurring in a fetus retained in utero after death. It occurs due to the softening
effect of soaking on solid tissues (pulpy fetus).
Salient features:
(1) The earliest sign of maceration is skin slippage (12 hours after IUD) [Fig
27.1]. The epidermis can be easily separated from the dermis by applying
oblique pressure. Loss of the epidermis exposes a red, shiny, moist dermal
surface, particularly noticeable over bony prominences.
(2) 24 hours"fluid-filled bullae are formed between dermis and epidermis [Skin
blebs].
(3) 48 hours"(i) Sweetish, disagreeable odor (ii) internal fetal organs and
connective tissue show increasing purple discoloration due to hemolysis and
breakdown of red cells. (iii) Dark, red-stained fluid accumulates in the serous
cavities. This should be distinguished from serous effusions acquired
antemortem. (iv) Proteolytic digestion by kallikrein contributes to - vascular
permeability. (v) Similar color changes are observed in the amniotic fluid,
which has a deep dark red appearance (“tobacco juice”), or in the event of
passage of meconium, a thick brown appearance. (vi) The volume of the
amniotic fluid .s following fetal death, and the level of α-fetoprotein in it may
be -ed because of concentration effect and -ed fetal skin permeability. (vii)
Autolysis of connective tissue - contributes to laxity of joints and lack of
definition of cut surface margins of the solid organs. Body is soft, flaccid and
flattens out when placed on a level surface. (viii) Bones are flexible and
readily detached from soft parts. (ix) Joints become abnormally mobile. (x)
Abdominal organs may show green discoloration due to leakage of bile
pigments from the gallbladder.
(4) 3 to 4 days" (i) Fetal epidermis loses integrity. (ii) Umbilical cord is red,
soft and smooth
(5) 5th day"S/c edema up to 5 mm.
(6) >1 week" (i) Meconium released into the abdominal cavity through the
dissolving bowel wall. (ii) Protruding autolyzed liver mass produces an
abnormal ultrasonographic appearance. May be mistaken for omphalocele.
(iii) Dystrophic calcification may develop in the autolyzed liver tissue. (iv)
fluid accumulation may mimic hydrops fetalis. (v) fluid accumulation at the
nape of the neck may be mistaken for a cystic hygroma or occipital
 encephalocele. (vi) distortion of skull occurs during vaginal delivery. May
lead to an erroneous diagnosis of hydrocephalus. (vii) Squeezing of the
autolyzed brain tissue into the spinal cord and along the spinal nerve roots into
the retropleural and retroperitoneal areas may produce tumorous masses of
neural tissue. May be mistaken for a neurogenic neoplasm. (viii) further
changes in color occur, from purple to brown discoloration.
(7) Several weeks - (i) a fading of color to yellow–gray occurs. (ii) Progressive
loss of fluid from the fetus eventually results in the formation of “fetus
papyraceous.” (iii) Dehydration results in shrinkage and compaction of tissues
and organs. (iv) Very occasionally an extrauterine pregnancy may be retained
for years forming so-called lithopedion (Greek lithos, stone, paidion, small
child), a calcified fetus retained in the abdominal cavity.
B. Rigor Mortis, Putrefaction, Adipocere and Mummification
Rigor mortis is a usual change after death. Putrefaction occurs if air enters the
liquor amnii after death. Adipocere would occur if sufficient liquor amnii is
there. Mummification would occur if all liquor amnii has drained out.

C. Radiological Signs of IU Deaths

The radiological sign of fetal death help to diagnose IU deaths, when the baby is
still in utero. They are in essence a study of the processes of maceration.

1. Robert’s sign (1944)

Earliest sign to appear. 12 hours after death. Air in aorta, pulmonary vessels
or abdomen.
2. Spalding’s sign (1922)
Appears 2 days after death. Overlapping of fetal skull bones seen on x-ray (or
ultrasound) examination. Due to shrinkage of cerebrum after intrauterine death.
[D/d. May also be positive (i) during or just prior to labor (ii) scanty liquor amnii
and diminished fetal vitality (iii) microcephaly (iv) craniostenosis.]
3. Deuel’s halo sign (1947)
3 days after death. Separation of the subcutaneous fat of the fetal scalp from the
cranial bones. Seen as a halo on radiography and USG. First described by Deuel
in 1947.

IV. VIABILITY OF THE FETUS

Viability is the ability of a fetus to survive outside the uterus.

Salient features:
(1) Indian Law - Age of viability has not been defined in Indian law.
(2) English law - Age of viability is 28 weeks [s1(2) Infant Life (Preservation)
Act, 1929 of UK]. Since India does not have explicit law on viability, by
derivation, 28 weeks may be taken as age of viability in India too. Some
books wrongly mention it as 210 days. If that fact is accepted, the definition
of stillbirth would have to be changed, which asserts that a stillborn child is
one which is born after 28th week of pregnancy [age of viability]. According
to the wrong “210 day viability standard”, babies born between 196 days
 and 210 days would not be viable, yet would be called stillborn. A classical
criteria of stillborn child is that it is “capable of being born alive.”
(3) Physiology - at age of viability pulmonary surfactant appears in the alveoli
of lungs ".es surface tension of alveoli"alveoli become able to inflate.
(4) Pathology - (i) When the pulmonary surfactant is deficient, Infant
respiratory distress syndrome [IRDS, neonatal respiratory distress
syndrome, earlier called hyaline membrane disease (HMD)] may result.
Pulmonary surfactant is rich in lecithin [syn, disaturated phosphatidylcholine,
dipalmitoyl phosphatidylcholine]. For composition, please see ch 19. (ii)
Lecithin synthesis - by type II alveolar cells -es dramatically as the lung
matures. Lecithin levels are expressed as a ratio against sphingomyelin, a non-
pulmonary lipid whose concentration is relatively constant in amniotic fluid
Memory Aid 1: Lecithin levels and lung maturity
L - lung, lecithin

L/S > 2 is rarely associated with IRDS. L/S < 2 indicates -ed risk of IRDS. (iii)
pathogenesis of hyaline membrane - .ed surfactant ".ed lung
compliance"hypoventilation"hypoxemia + CO2 retention" acidosis"pulmonary
vasoconstriction"pulmonary hypoperfusion"epithelial and endothelial damage"
plasma leak into alveoli"fibrin + necrotic cells [hyaline membrane].

V. LIVE BIRTH

[A] Legal definition of live birth in Indian criminal law - A child is “live
born”, if any part of that child has been brought forth, even though the child may
not have breathed or been completely born [Explanation 3 of S.299, IPC]. [B]
Legal definition of live birth in Indian civil law - “live-birth” means the
complete expulsion of fetus from its mother, irrespective of the duration of
pregnancy, and who after such expulsion breathes or shows any other evidence
of life [S.2(d) of The Registration of Births And Deaths Act, 1969]. Possible
evidences of life are (1) Cry. (2) Movement of body or limbs. Muscle twitching
is not safe to take as evidence of life as muscles may twitch for sometime after
death.

A. Signs of Live Birth

1. Shape of the chest
(1) Before respiration – (i) Chest is flat. (ii) Circumference 1-2 cm less than
that of abdomen at the level of umbilicus
(2) After respiration – (i) Chest expands. (ii) Drum shaped.

2. Position of diaphragm
(1) Before respiration – at the level of 4th or 5th rib.
(2) After respiration – at the level of 6th or 7th rib.
Memory Aid 2: Position of diaphragm before and after respiration
Remember 4, 5, 6, 7

(3) Precautions - (i) Abdomen must be opened before thorax - Highest point of
diaphragm must be noted. If thorax is opened first, air can enter thorax and
push diaphragm to a lower level giving a false indication of live birth.
Converse cannot happen, i.e. diaphragm going up on opening abdomen,
because lungs would prevent it. (ii) In putrefaction - gases may spuriously
alter position of diaphragm.

3. Lungs
Breathing causes significant and permanent changes in the lungs [Table 3]. Their
extent depends upon the period and strength of respiration.
a. Volume
Please see Table 3.
b. Margins
Please see Table 3.
c. Consistency
Crepitant after respiration, but also crepitant after putrefaction and after artificial
respiration. Please also see Table 3.
d. Color and expansion of air vesicles
(1) Before respiration – On section, interior of lung is uniform in color and
texture.
(2) After respiration -
(i) Alveoli are distended with air, initially at anterior surfaces and margins, and
then in the remaining portions.
(ii) With expansion, the air vesicles are slightly raised above the surface "seen as
 angular or polygonal areas on the surface of lungs.
(iii) As blood becomes oxygenated in the expanded areas, the entire surface has
a mosaic, mottled or marbled appearance. Aerated and expanded areas
appear rose-colored and these areas alternate with the collapsed unaerated
dark bluish areas.
(3) Precautions -
(i) Exposure to air of unexpanded lungs - may brighten color, but air cells
would not be distended
(ii) Artificially inflated lungs - Mottling may be absent. On cut section, the
exposed surface with exude little blood, but no froth. Please also see Table
3.
e. Gas
(1) Respired lungs – If lungs are dipped in water, part of air within the bronchi
and alveoli will be expelled and will rise to the surface as a stream of minute
dots.
(2) Gas due to putrefaction – Bubbles of gas, instead of being within the
alveoli, are under the pleura and within the substance of lungs [interstitial
blebbing]. The bubbles underneath the pleura can be moved from place to
place by stroking with a finger.
f. Blood in the lung beds
Blood within the lungs after respiration is twice than that present before
respiration [Table 3].
g. Weight of lungs
i. Fodéré’s test [syn, Static test]
(1) Procedure - Lungs are ligated across their hila, separated and weighed.
(2) Wt of both lungs combined - (i) before respiration - 35 g (ii) after
respiration - 70 g
(3) The -in weight is due to -ed flow of blood [Table 3].
ii. Ploucquet’s test
(1) Wt of lungs is calculated as a ratio of infant’s total weight to even out
differences due to wt of infants
(2) Wt of both lungs combined -
(i) before respiration – 1/70th of body wt
(ii) after respiration – 1/35th of body wt. Takes into account differences in lung
weights on account of different weights of body. Named after Wilhelm
 Gottfried Ploucquet [1774-1814] of Tübingen.
Memory Aid 3: Foderê and Ploucquet’s tests
Remember 35 and 70. These numerals just get transposed in the two tests. It is because of the coincidental
fact that the wt of newborn is roughly 2450 g [35x70]. Thus wt of both lungs before respiration [35g] turn
out to be 1/70th of BW and after respiration [70g] turn out to be 1/35th.
h. Hydrostatic test (Raygat’s test)
i. Principle
Upon breathing, both wt and vol of lungs are -ed. Wt is -ed due to inflow of
blood and vol due to inflow of air. The - in vol is much more than - in wt due to
which specific gravity of lungs is .ed.
Salient features:
(1) Sp gr of lungs – (i) Before respiration "1.04-1.05 (ii) After respiration "0.94
(2) Procedure - Hydrostatic test is performed in following four stages: (i) Stage
1 - Whole thoracic pluck consisting of both lungs and heart are placed in a
bucket of water. If the pluck floats"indicates air in lungs"indicates that the
infant may have born alive. If the pluck sinks, move to second stage. A piece
of liver is also sunk in water as control. It must sink in normal conditions. If it
floats, it may indicate putrefaction, making the test of dubious value. (ii) Stage
2 -Each brochus is tied, and lungs severed above the ligature. Each lung is
then placed separately in water. If either lung floats, it indicates that the infant
may have born alive. If either lung sinks, move to third stage. (iii) Stage 3 -
Cut each lung in 12-20 pieces (a) Roll a piece of lung gently between a finger
and thumb near the ear and see if there is a crackling crepitant noise. (b) Dip
 each piece under water and squeeze between thumb and finger and see if any
bubbles are escaping (c) observe if they float independently. For moving to the
next stage same criteria applies as above (iv) Stage 4 - Each piece is now
taken out of water, wrapped in a piece of cloth and squeezed by putting a
weight. This is an important step as it is supposed to remove the expiratory
reserve volume air, and tidal air. Residual air still remains within the alveoli,
which can not be taken out by any means. This residual air is responsible for
keeping the lungs afloat in infants who have been born alive and respired. If
the lungs were floating in earlier stages due to artefacts (such as gases
introdued by artificial respiration), the pieces of lung would not continue to
float till the last stage.
ii. Fallacies
There are two major fallacies of this test.
(a) Child respired after birth yet lungs sink
Causes:
(1) Absorption of air – Circulation continued after stoppage of respiration for
sometime"air from lungs is absorbed in circulation"No air remains in lungs.
(2) Atelectasis (non expansion) of lungs. Sequence of events is Feeble
respiration"Air does not enter lungs, but remains up to tracheal and bronchial
level"Oxygenation of blood occurs through tracheal and bronchial
mucosa"Lungs remains unexpanded, but children was alive.
(3) Alveolar duct membrane - Causing obstruction to entry of air in alveoli
(4) Diseases - (i) Acute edema (ii) Congenital syphilis (iii) Pneumonia
(5) Feeble respiration – More air is expelled from the lungs during expiration,
than what is inhaled during inspiration.
(b) Child did not respire after birth yet lungs float
Causes:
(1) Artificial respiration - given via a tube, catheter or cannula passed into the
trachea or by mouth to mouth respiration. Lungs are inflated partially. In case
of mouth to mouth respiration, air may be found in stomach too.
(2) Putrefaction - Putrefactive gases will make the lungs float. Distinctive
features
(i) Body - shows signs of decomposition
(ii) Lungs - (a) soft and greenish (b) Bubbles of gas - (I) large bubbles seen on
lung surface. (II) Unequal in size. (III) Project considerably from the
 surface. (IV) Gas within them can be pushed readily from place to place.
(V) Collapse on pricking.
(3) Respiration within the womb [vagitus uterinus]- Fetus may respire within
the womb if membranes have ruptured, but may die from natural causes
within the birth canal and may not breathe once completely born.
(4) Respiration within the Vagina [vagitus vaginalis] - Similar to above.
Respiration occurs within vagina, but not when completely born.
iii. Hydrostatic test is not necessary in following conditions
(1) One is sure fetus was born dead - Fetus is
(i) Born before age of viability [28 wks]
(ii) Macerated or mummified
(iii) Monster [eg anencephalic]
(iv) Bruising on lungs - indicating efforts at artificial respiration.
(2) One is sure fetus was born alive -
(i) Stomach - contains milk
(ii) Umbilical cord - has separated and a scar has formed.

i. Radiography of lungs
May reveal air within them.

j. Microscopic examination of the lungs

(1) Value - is limited. Cannot provide clear evidence of extrauterine respiration,
if child has lived only for a few minutes.
(2) Procedure -
(i) Removal - Thoracic contents are removed intact by cuts with a scalpel by a
“no touch” technique first described by Osborn [Pathologist and Medical
Superintendent, Derbyshire Royal Infirmary] in 1953. The technique aims
to eliminate artifacts.
(ii) Fixation - for 48 h
(iii) Sections - taken from the whole lung
(3) Appearances -
(i) at 4 months pregnancy - Parenchyma of the lung shows gland like structure
with cuboidal or columnar lining
(ii) at 5th month - air cells are filled with amniotic fluid
(iii) at full term - (a) thin walled adult type alveolus is formed. (b) Completely
 atelectatic, but many of its terminal bronchioles and vesicles are partly
expanded by amniotic fluid. (c) Fetus makes some respiratory movements
near full term, which fill its alveoli with amniotic fluid. This material is not
stained with H&E giving a spurious impression that air is present in lungs.
As respiration takes place, further expansion of alveoli occurs. Fluid present
in alveoli is partly absorbed back into the pulmonary circulation and partly
expelled through the bronchi. (d) Tardieu’s spots - are no indication of live
birth. They may be seen in stillbirth, live birth and in bronchopneumonia.

k. Tests for fetal lung maturity

Presence of creatine, lecithin and fat cells.

4. Changes in stomach and intestines

a. Air in stomach and intestines

(1) Breslau’s second life test; stomach bowel test [Fig. 27.3] - Stomach and
intestines are removed after tying double ligatures at each end, and put in
water. They float if respiration had taken place; otherwise they sink
(2) Principle - Air is swallowed into the stomach and intestines during
respiration, making them buoyant
(3) False +ve –
(i) Resuscitation attempts
(ii) Bacterial gas formation [putrefaction]
(4) Survival period – can be calculated: (i) Immediate after birth – gas in
stomach. Sometimes may take up to 15 min. In such cases, stomach bowel test
may be –ve even in live births, if death takes place before this period. (ii) 1-2
h – Gas reaches small intestines (iii) 5-6 h – colon (iv) 12 h - Rectum.
(5) Drawbacks and Fallacies –
(i) Useless in putrefaction
(ii) Air may be swallowed by the child in attempting to free the air passages of
fluid obstructions in cases of stillbirth.

b. Other material
(1) Other material present in the stomach may be (i) Amniotic fluid (ii) Blood
[maternal] (iii) meconium (iv) milk (v) Mucus and Mucins [glycoproteins in
 mucus] (vi) Saliva.
(2) Presence of milk is the only surest indication that the child was born alive.
(3) All the other indicate swallowing movements within the uterus or during
passage through the birth canal. No reliance may be made on them.

5. Changes in the middle ear

(1) Wreden’s test –
(i) Regular procedure – Skull cap is removed and base of skull submerged in
water. Petrous part of temporal bone [which forms roof of the middle ear] is
opened. If a bubble of air escapes from middle ear, the child was born alive.
(ii) Simpler method – Dip ears in water. Puncture tympanic membrane"Bubble
of air escapes" Live birth. Both procedures reveal presence of air in middle
ear.
(2) Principle - During embryonic life, the middle ear contains gelatinous tissue.
During efforts of breathing, the sphincter at the pharyngeal end of Eustachian
tube relaxes and some air enters the middle ear. Named after Roberto
Wreden of St. Petersburgh. Sometimes wrongly spelt as “Wredin’s test”. Also
recommended by H. Schmaltz in 1877.
(3) Reliability – Very low.

6. Other signs of live birth

Many of these also help in determination of time of survival.

a. Blood
(1) Nucleated RBC"disappear in 24 h
(2) Fetal Hb [synthesized mainly in liver]"(i) Before birth"80-90% (ii) 3rd
month"7-8% (iii) 6 m"disappears completely.

b. Meconium
(1) Characteristics: (i) It is a green viscid substance consisting of thickened bile
and mucus (ii) Stains are brownish green (iii) Stiffen the cloth (iv) Reaction is
acidic
(2) Expulsion -
(i) Completely excreted from the large intestine in 24-48 h after normal birth
(ii) May be completely excreted before birth in (a) breech presentation (b) severe
 anoxia.

c. Caput succedaneum
Caput succedaneum [CS] is an area of soft swelling that forms in the scalp over
the presenting part of the head in vertex presentations [Fig 27.2].
Salient features:
(1) Causes - (i) Juxtaposition of scalp to the opening of the dilated cervix during
labor, especially during prolonged or difficult delivery. (ii) Vacuum extraction.
(2) Mechanism – rigid cervical ring [or ring of extractor] presses on presenting
part [scalp] ".ed venous return"Localized area of congestion and edema
(3) Swelling – (i) Site (a) vertex presentations - Most commonly occurs
asymmetrically over the parietal region (b) Breech – over buttocks, scrotum,
labia (ii) crosses suture lines and is soft (iii) Thickness is 3-4 times the normal
thickness of scalp
(4) Fate – starts diminishing soon after birth. Completely disappears in a week.
(5) D/D – Cephalhematoma [Fig 27.2; Table 4].
d. Skin
(1) Initially -
(i) Skin is bright red.
(ii) Vernix caseosa covers skin mostly in axilla, inguinal region, folds of neck,
buttocks.
(iii) Rarely absent. It may also have been washed away
(2) 2 days – darker, brick red.
(3) 3rd day –
(i) Yellow due to physiological jaundice [due to relative insufficiency of
enzymes required for conjugation and excretion of bilirubin].
(ii) Skin of abdomen exfoliates during first 3 days after birth
(4) 7 days – color is normal.

e. Umbilical cord
i. Changes in umbilical cord proper
(1) 2h – Blood clots in the cut end
(2) 12-24h [Mnemonic 1 d]– Cord attached to the child shrinks and dries [no
 relation with live birth; seen in deadborn and stillborn also].
(3) 36-48h [Mnemonic 2 d]– An inflammatory ring forms at the base of stump.
(4) 2-3 d [Mnemonic 3 d]– Cord m ummifies [No relation to live birth; seen in
deadborn and stillborn also].
(5) 5-6 d – Cord falls off, leaving an ulcer
(6) 10-12 d – Ulcer heals, leaving a scar.
Memory Aid 4: Changes in umbilical cord
1, 2, 3, 4, 5-6"SIM Falls
(1) 1d"Shrinks
(2) 2d"Inflammatory ring
(3) 3d"Mummifies
4 d"Nothing happens
(4) 5-6d"Falls
(5) Healing occurs in twice as much time"10-12 d [twice of 5-6d]

ii. Vascular changes

(1) 10h–3d – UA closes [Table 5]
(2) 3-5 d – Left UV closes [Table 5].

iii. Signs of human interference

(1) Whether ligature has been applied or not [generally indicates live birth].
(2) Whether cut by scissors [sharp edges] or torn [ragged edges]. Latter indicates
self delivery or unskilled delivery.
(3) Note length of remaining cord.

f. Placenta
If placenta found with the body, it must be examined. Placental dimensions at
full term [ch 26]. Umbilical cord dimensions at full term [ch 3].

g. Circulation
Various circulatory structures close at fixed intervals [Table 5].
Memory Aid 5: Order of closure of fetal structures
A very very artistic forum
Artery (umbilical)"Vein (left umbilical)"Venosus"Arteriosus"Foramen ovale
Memory Aid 6: Umbilical vein
Q. Which vein is left?
A. Left is left [Right begins to obliterate at 4th wk and disappears by 7th wk]
Memory Aid 7: Umbilical artery
Umb il i cal artery is branch of iliac i nternal

Sometimes fossa ovalis can take longer to close, and sometimes remains open
throughout life [morbus ceruleus]. Patent foramen ovale is detectable in about
30% of general population.

h. Miscellaneous
Subdural hematoma – Although rare, but if present, indicates live birth. Due to
molding [ch 17].

VI. CAUSES OF DEATH

i. Precipitate Labor
Precipitate labor is the expulsion of fetus within less than 3 h of commencement
of contractions.
Salient features:
(1) All three stages of labor are merged in one
(2) Delivery occurs suddenly and rapidly even without the knowledge of mother
(3) Delivery may occur even unconsciously during (i) Anesthesia (ii) apoplexy
(iii) asphyxia (iv) coma (v) Deep drunkenness (vi) delirium (vii) eclamptic
convulsions (viii) fits (ix) Hypnosis (x) hysteria (xi) Influence of narcotic or
intoxicating drugs (xii) sleep (xiii) syncope. Such conditions are thought to
bring about deep lethargy and complete loss of sensation, preventing the
mother to sense the ongoing parturition.
(4) Risk factors are
(i) Multipara [extremely rare in primi]
(ii) Placental abruption
(iii) Roomy pelvis
(iv) Small premature baby. In babies weighing >2500 g, incidence is 3%.
(v) Mother not being able to distinguish the sense of fullness produced by the
descent of child from the feeling of bulky evacuation.
(5) Associated with - an -ed risk for maternal complications
(i) cervical and grade 3 perineal tears
(ii) need for packed-cells transfusions
(iii) post-partum hemorrhage
(iv) retained placenta
(6) Child may die from -
(i) Suffocation - if falls into lavatory pan containing feces
(ii) Drowning - if falls into a pan containing water [ch 19"Death of newborn
infants]
(iii) Head injury - with fracture of skull and intracranial hemorrhages [bilateral
SDH]. (a) Bones involved – (I) one or both parietal bones; (II) fracture may
radiate into the frontal and squamous portion of temporal bone (b)
Especially likely to occur (I) if mother was standing (II) There was hard
floor beneath. The cord is torn more commonly at the fetal end than at the
maternal end, but is rarely torn at the middle.
(iv) Hemorrhage - from torn end of the cord.
(7) PM findings -
(i) Placenta – is attached to newborn
(ii) Umbilical cord – lacerated, torn [details as above].
(iii) Hair and injured scalp – show grass, gravel, mud, sand.
(iv) Head - (a) Caput succedaneum and moulding of head - absent (b) fracture of
skull. (c) IC hemorrhages [please see above].
(v) Air passages and lungs – contain blood, meconium, vaginal mucus, mud,
gravel, sand, grass, urine, feces etc depending on where the child fell or
drowned.
(8) MLI -
(i) Infanticide - Plea of precipitate labor is sometimes raised in cases of
infanticide.
(ii) False allegation - Alternatively in a true precipitate labor case, mother may
be accused of infanticide. Differentiation in Table 6.

Criminal

a. Acts of commission
Acts of commission are acts done to cause death, eg suffocating the child.
Salient features:
Since the child was unwanted, there may have been attempts at criminal
abortion, attempts at self delivery [to cause immediate destruction] etc. These
may cause multiple circumferential abrasions around the whole surface of the
neck [due to fingernails].

i. Asphyxia
(a) Drowning
(1) Rare form of child murder
(2) Child may be thrown in tank, well or other reservoir of water [antemortem
drowning], or first killed and then thrown similarly [postmortem
submersion].
(3) Woman in parturition - may sit in a large tub of water and directly deliver
the baby in water"child delivered underneath water"dies of drowning before
any respiration takes place"Signs of asphyxia not evident
(4) Drowning in milk - At one time, in Varanasi and other neighboring places,
submersion of child’s face into a cauldron of warm milk used to be a common
mode of infanticide.
(5) Precipitate delivery"there may be mixture of urine, blood, meconium and
water in the infant’s air passages [please see above].
(b) Strangulation
(1) Manual strangulation [throttling] - nail marks may be found on child, but
they may also be due to frantic efforts of mother to deliver herself.
(2) Ligature strangulation - Ligature may be found in situ. Sometimes
umbilical cord may be used as a ligature material to mimic natural accident.
(c) Suffocation
(1) Methods:
(i) Smothering - (a) Closure of child’s nose with fingers and pushing up lower
jaw to occlude mouth. (b) Placing pillow or towel over infant’s face (c)
Pushing infant’s face down into bed clothing or against breast
(ii) Gagging - Forcing cotton-wool, mud, rag etc into the mouth.
(2) Autopsy - Force needed is so small, that no evidence of struggle or trauma
etc may be present. Only associated signs eg presence of cotton wool etc may
give away method of murder. If these have been removed, there may be no
clue left.

ii. Burning
(1) Rare form of child murder
(2) Application of dry heat, or more commonly immersing child in a cauldron of
boiling water. Usual plea is that child accidentally spilled hot water over him,
which was placed near him for bath.

iii. Fracture and dislocation of cervical vertebrae

Caused by twisting the neck.
iv. Poisons
Rarely poisoned milk may be given or poison may be injected or instilled in the
eye.

v. Trauma
(a) Head injury
(1) Inflicted by:
(i) Dashing the head against a wall or floor by holding feet [rare] - Bruising of
ankles and feet, where feet were gripped may be seen.
(ii) Blows on head with blunt weapon
(iii) Head pressed forcibly - under the leg of a bedstead [charpoy]
(2) Injuries produced:
(i) Contusions, lacerations - of scalp, brain.
(ii) Fractures of skull– comminuted, depressed. D/d – injuries produced by
forceps delivery [as above].
(iii) EDH in neonates - [ch 17] (iv) SDH, SAH.
(b) Injury to other organs
Abdominal injury, crushing of testes, thrusting of needle within brain through
fontanelles. Cut throat, incised wounds, stabs etc may be seen
(c) Throwing from height
Uncommon, but well-known method.

b. Acts of omission
Acts of omission are acts intended to overlook basic needs of the child, eg not
giving food to child.
Salient features:
(1) Examples of acts of omission – Failure to
(i) Clear the air passages – these may be obstructed by amniotic fluid or mucus
(ii) Protect child – from heat or cold
(iii) Provide proper assistance – during labor. May cause death by suffocation or
head injury
(iv) Supply child with proper food
(v) Tie the cord – after it is cut. May cause death by hemorrhage
(2) Person in-charge of the infant [mother, father, guardian etc] can be charged
 u/s 302, IPC if they fail to take care of child and allow him to die.

i. Abandoning of infants
(1) An abandoned child is called a foundling
(2) If father, mother or guardian of a child <12 y exposes or abandons him"7y
imprisonment or fine or both [S.317, IPC]
(3) If death of such exposed child occurs, parent or guardian would be punished
for murder or culpable homicide, as the case may be.

ii. Concealment of birth by secret disposal of dead body

Whoever intentionally conceals or endeavors to conceal birth of a child by
secretly burying or otherwise disposing of the dead body of a child whether such
child died before, after or during its birth, is punished with 2 y imprisonment or
fine or both [S.318, IPC].

VII. CHILD ABUSE

Child abuse is the physical, sexual or emotional mistreatment or neglect of a

child.
Salient features:
(1) Child abuse can occur in a child’s home, or in the organizations, schools or
communities the child interacts with.
(2) Five categories of child abuse: (A) Child neglect (B) Emotional and
psychological abuse (C) child sexual abuse and (D) physical abuse (E)
Intentional poisoning [chemical abuse].

A. Physical Abuse
Physical aggression directed at a child by an adult. Further divided into those
caused by mechanical trauma, and other forms of abuse [asphyxiation, burns and
scalds, drowning and subtle abuse].

1. Mechanical trauma

a. Battered baby syndrome

Battered baby syndrome [syn. BBS, Battered child syndrome, Caffey’s
syndrome, Caffey-Kempe syndrome, Maltreatment syndrome, Non Accidental
Injury of Childhood (NAIC), parent-infant traumatic stress syndrome (PITS),
Tardieu’s syndrome] is a clinical condition in which young children usually
under 3 years of age are beaten repeatedly over the most trivial provocation. The
children are often unwanted (female, mentally deficient, disabled, stepchildren).
Salient features:
(1) Lack of provocation - Beating is completely excusable. Provocation is
always trivial
(2) Precipitating factors – Often child’s irritating actions eg crying, refusal to
be quiet, persistent soiling of napkins etc
(3) Deprivation of nutrition, care and affection is present
(4) Delay - There is often delay between onset of injuries and medical attention
sought. It is sought, only when the child becomes critical and parents lose
nerve. The explanation is lack of money.
(5) Cerebral palsy - 10-15% cases of cerebral palsy may be the result of the
battered baby syndrome.

i. Epidemiological features
(1) Age – usually <3 years. But can occur at any age
(2) Sex – slightly more in males
(3) Status of child in family – unwanted, disabled, stepchild, failure of
contraception, pregnancy before marriage
(4) Socioeconomic factors of parents – (i) Age - Young [20-30 y] (ii) Family –
isolated (iii) Guilt amnesia (iv) Have criminal records (v) .educated, .IQ,
.socioeconomic class (vi) Psychiatric problems (vii) Socially unstable (viii)
Unemployed (ix) Parents themselves brought up in (a) disharmonious families
(b) families having long standing emotional or financial problems (c) chaotic,
violent family (d) They were themselves battered children (e) Wife often
battered by husband, with battering continuing during pregnancy (f) unhappy
childhood experiences.

ii. History
(1) Incompatible with injuries. Repeated trauma over time is the hallmark of
BBS. This causes abrasions, bruises, burns, fractures and other injuries of
 different ages. The classical explanation offered by parent is that the child fell
down the stairs. If that were the case, the age of all injuries would be the same
(2) Parents change history as they go to different doctors; even with the same
doctors, their history may have serious contradictions.

iii. Injuries
Injuries are due to direct manual violence [commonest].

(a) External injuries

(1) Tear of the frenulum – the most typical injury. Laceration of mucosa of
upper lip is also seen. Laceration may be so large as to cause separation of
inner surface of lips from base of gums. Typically caused by (a) efforts to
silence screaming (b) blow on the face (c) may also be produced by trying to
suffocate child [please see below].
(2) Soft tissue injuries –
(i) Types, site and shape – Almost anywhere on the body (a) Abrasions – on
 back. Caused by dragging (b) Bite marks [ch 3] – on cheek, neck, back (c)
Bruises (I) on either side of chest, behind the axillae, down the anterior
chest wall and around the large joints eg elbow and joint"Indicate places
where child was gripped strongly [Six penny bruises - ch 12] (II) on
buttocks and thighs – caused by belts, canes, common household objects eg
wooden ladles, hair brushes, pieces of wood, straps etc (d) Graze abrasions
- on back"Indicate dragging (e) Knuckle punches – on the back. Show as
rows of 3-4 round bruises [represent metacarpals of the offending fist] (f)
Lacerations – beating by hard blunt objects, eg canes and sticks (g) Pinch
marks – on face, neck, back, buttocks, thighs. Appear as butterfly shaped
bruises with one wing caused by thumb larger than the other caused by
opposing finger (h) slap marks – show as clear bruises [or as lines of
petechial hgs] resembling fingers [of the slap] on cheeks, neck and back. (i)
Scalp injuries – very characteristic. Caused by vigorous pulling on scalp
hair (I) Subgaleal hematoma (II) Traumatic alopecia – bald patches on scalp
(ii) Cause - rough handling, beating, kicking or throwing the infant around.
(iii) Age - Typically the injuries are of different ages, as they are inflicted at
different points in time.
(3) Eyes - (i) Black eye (ii) Hemorrhages [Retinal, Subconjunctival, Subhyaloid,
Vitreous] (iii) Lens displacement (iv) Retinal separation.
(b) Internal injuries
Extensive internal injuries may be present with minimal or no external signs of
injury.
1st. Skeletal injuries
(1) Lesions due to direct beating -
(i) Skull fractures, especially in occipito-parietal area. They are depressed,
 multiple and wide
(ii) Transverse and spiral fractures of long bones, especially due to twisting of
arms and legs etc.
(2) Traction lesions - These injuries result from jerking of shaking a child’s
limbs. May also result if, say, a toy is jerked away from a child’s hands.
Injuries of the periosteum of long bones are seen without fractures.
(i) Periosteal hematomas (a) If fresh – periosteum bulging with blood seen (b) If
old – Seen radiologically as an extra line of opacity running alongside the
affected length of bone. Due to calcification of bleeding which occurred
under the periosteum.
(ii) Periosteal shearing – because periosteum is easily stripped off in infants
(iii) Epiphyseal separation – seen radiologically as small fragments separated
from the main bone
(iv) Avulsion of metaphysis or chipping of the edges of metaphysis. These are
known as corner fractures and bucket handle fractures. Bucket handle
fracture is essentially the same as corner fracture, but this term is used
where the loose bone is rather wide at the distal end, making it end in a
crescent shape [Fig. 27.5].
(3) Anteroposterior compression of chest - Fractures of ribs in midaxillary line
(4) Side-to-side compression of chest -
(i) Fractures at the costochondral junctions
(ii) Fractures along posterior angles of ribs. After 1-2 wks, callus forms. On X-
rays these are seen as a “string of beads” [syn, rosary bead appearance]
in the paravertebral gutter [Nobbing fractures] [Fig. 27.6].
2nd. Visceral injuries
(1) Brain and meninges - SDH – Found in about 40% of fatal cases
(2) Lungs - Posttraumatic pulmonary pseudocysts [PTPPCs] – ch 17"Lung
 injuries.
(3) Liver - Bursting injuries – Another name for lacerations. Crushing or
compressing force on abdomen, as by fists
(4) Spleen - Bursting injuries – cause same as in liver
(5) Hollow viscera -
(i) Stomach, intestines and urinary bladder – may be ruptured, especially if
compressing force [fists etc] was applied when the viscera were distended
(ii) Second part of duodenum and jejunum – may be completely transected
(iii) Tearing of mesentery – may cause complete disruption of the small intestine.

iv. Diagnosis
(a) In the living
Can be done by
(1) Time taken to seek medical advice
(2) nature of injuries
(3) recurrence of injuries
(4) Imaging studies (i) X-rays of the entire body [babygram] (ii) MRI (iii)
Technetium 99m (99mTc) methylene diphosphonate (MDP) bone scintigraphy.
(iv) Fluorine 18–labeled sodium fluoride (18F-NaF) positron emission
tomography [PET].
(b) In the dead
(1) Imaging studies [as in the living] - before autopsy. Detects (i) old fractures
 (ii) Epiphyseal and metaphyseal injuries in various stages of healing
(2) Autopsy – shows external and internal injuries as mentioned above
(3) Cause of death –
(i) Head injury [most common]
(ii) Rupture of abdominal organ [2nd most common].

v. D/d
D/b stands for “Differentiate by”.
(1) Acute abdomen will occur in (a) Intrinsic gastrointestinal disease (eg.
peritonitis, obstruction, inflammatory bowel disease, Meckel’s diverticulum)
[D/b Radiographs, stool tests] (b) Intrinsic urinary tract disease (infection,
stone) [D/b Culture, ultrasound, intravenous pyelogram] (c) Genital problems
(e.g., torsion of spermatic cord, ovarian cyst) [D/b History, physical
examination, ultrasound, radiograph, laparoscopy] (d) sickle cell crisis [D/b
Angiography, sickle cell studies]
(2) Bruising will occur in (a) Hemophilia [D/b Prothrombin time, partial
prothromboplastin time] (b) Von Willebrand’s disease [D/b Von Willebrand’s
panel] (c) Henoch Schonlein purpura [D/b Typical distribution of lesions] (d)
Purpura fulminans [D/b Ruling out sepsis] (e) Ehlers-Danlos syndrome [D/b
Hyperextensibility] (f) Mongolian spot - Not a true bruise [see ch 12 for
details]
(3) Fractures will occur in (a) Osteogenesis imperfecta [D/b Radiology and blue
sclerae] (b) Rickets [D/b Nutritional history] (c) Birth trauma [D/b Birth
history] (d) Hypophosphatasia [D/b Decreased alkaline phosphatase] (e)
Leukemia [D/b Complete blood count, bone marrow] (f) Neuroblastoma [D/b
Bone marrow, biopsy] (g) osteomyelitis or septic arthritis [D/b History]
(4) Local erythema or bullae will occur in (a) Bacterial Cellulitis, Pyoderma
gangrenosum and Staphylococcal impetigo [D/b Culture, Gram stain] (b)
Herpes, zoster or simplex [D/b Scraping, culture] (c) Epidermolysis bullosa
[D/b Skin biopsy] (d) Contact dermatitis, allergic or irritant [D/b Clinical
characteristics]
(5) Metaphyseal lesions, epiphyseal lesions, or both are seen in (a) Scurvy
[D/b Nutritional history](b) Menkes syndrome [D/b .copper, .ceruloplasmin]
(c) Syphilis [D/b serology] (d) ”Little League” elbow [D/b History] (e) Birth
trauma [D/b History]
(6) Physiological striae - Linear red to purple marks may occur in teenagers due
to sudden growth spurt.

vi. Investigation
Family history – Record any previous infant deaths in similar circumstances. A
similar previous death strongly goes in favor of child abuse.

b. Shaken baby syndrome (SBS)

Shaken baby syndrome [SBS, infantile whiplash syndrome, whiplash Shaken
Infant Syndrome] refers to a constellation of signs and symptoms resulting from
violent shaking of the head of an infant or small child.

VIII. SUDDEN INFANT DEATH SYNDROME (SIDS)

Sudden Infant Death Syndrome [syn. cot death, crib death, SIDS, sudden
unexplained infant death, SUID] is defined as the sudden death of a seemingly
healthy infant [age <1y], whose death remains unexplained even after (i)
thorough case investigation (ii) death scene examination (iii) review of clinical
history (iv) complete autopsy and (v) serological, toxicological,
histopathological and microbiological examinations.
Salient features:
(1) History – typically child is quite well, when put to bed, or may only have a
minor URI [common cold, sneezing] or minor GIT disturbances
(2) Simultaneous sudden infant death syndrome [SSIDS] – Unexplained
death of 2 or more infants takes place within 24 h.

A. Theories of Causation
No one is sure why SIDS occurs, but there are several theories. Death may result
from a number of causes, which combine and act via a common pathway of
cardiorespiratory failure, while the child is passing through a vulnerable period
of development. The main theories are:
(1) Allergies -
(i) Cow’s milk protein allergy
(ii) House mite allergy
(2) Critical Diaphragm Failure [CDF] - Respiratory failure caused by CDF.
Four principal risk factors contributing to CDF are
(i) undeveloped respiratory muscles
(ii) non-lethal infections
(iii) prone resting position
(iv) REM sleep. Even relatively minor infections can cause an acute and
significant reduction in diaphragm force generation capacity that in
conjunction with other risk factors precipitate CDF.
(3) Deficiencies – of (i) Antibodies (ii) Biotin (iii) Calcium, magnesium,
selenium (iv) gamma globulins [hypogammaglobulinemia] (v) Vitamins
B,C,D,E.
(4) During pregnancy – certain factors were present that inhibited fetal
circulation [eg cocaine use (ch 41] "damage of fetal brain"medulla could not
control breathing properly
(5) Genetic:
(i) Brainstem abnormality of the serotonergic system – giving rise to defective
respiratory and autonomic responses.
(ii) Cardiac channelopathies – Genes coding for faulty ion channels or ion
channel-associated proteins"(a) long QT syndrome, (b) short QT syndrome
(c) Brugada syndrome (d) catecholaminergic polymorphic ventricular
tachycardia.
(iii) Faulty Interleukin-1 receptor antagonist (IL-1RA) protein – IL-1RA
modulates a variety of interleukin 1 related immune and inflammatory
responses, and is encoded by the IL1RN gene. There are 3 known variants –
Allele 1 is normal. Alleles 2 and 3 are associated with -ed risk of SIDS.
(iv) Left ventricular hypertrabeculation – This condition is characterized by a
highly trabeculated, “spongy” myocardium"causes heart failure,
arrhythmia, thromboembolic events. A wide variety of mutations are
responsible for hypertrabeculation.
(v) MAO-A molecular polymorphisms.
(6) Hormonal - Deficiency of parathyroid.
(7) Infections - Respiratory [bacterial - S. aureus; viral]
(8) Inflammatory reactions – In a small group of SIDS cases very high
cytokine [IL-1ß, IL-6, TNFα] concentrations are seen [“cytokine storm”]. May
be a possible explanation for SIDS.
(9) Obstruction of airways - (i) Anatomical abnormalities (ii) Nasal edema (iii)
Nasal obstruction or inflammation or both (iv) Excessive mucus in respiratory
passages (v) Flaccid pharynx in hypotonic babies (vi) Faulty neck posture (vii)
Laryngeal spasm
(10) Prone sleep position – Children who are made to sleep in prone position
have 3 times - risk. Parents are now advised a supine sleep position for infants.
Following factors may trigger death in this position
(i) Asphyxia due to airway compression
(ii) Rebreathing of exhaled gases in the face-down position
(iii) Impaired heat loss with subsequent hyperthermia when the face is pressed
against bedding
(iv) impaired cardiorespiratory regulation related to heat stress
(v) More bacterial growth – There is heavier growths of S. aureus and E. coli in
nasal samples from infants who sleep on their stomachs, compared with
babies who sleep on their backs.
(11) Sharing of beds - Approximately 50% of sudden infant deaths occur when
infants are sharing a bed with another person [co-sleeping].
(12) Sleep apnea – Prolonged sleep apnea in certain infants"hypoxia"death.
Infant is at the highest risk for SIDS during sleep [reason for calling it cot
death or crib death].
(13) Sleep-induced arrhythmias
(14) Toxic - Mattress related – Most mattresses contain P, As, or Sb compounds
as fire retardants"warmth and perspiration of the sleeping infant"infection by
microorganisms [esp the fungus Scopulariopsis brevicaulis]"generating
phosphines, arsines and stibines from materials containing P, As, or Sb"
Poisoning to death.
(15) Miscellaneous -
(i) Adrenal insufficiency
(ii) Conduction system anomalies
(iii) Deficient liver enzymes
(iv) Gastroesophageal reflux"bradycardia
(v) Hyperthermia
(vi) Hypothermia
(vii) Impaired glial-neuronal interactions in the cardio-respiratory centre of the
brainstem"stoppage of heart and respiration.
(viii) Metabolic disorders
(ix) Neurogenic shock
(x) Sodium overload in feeds
(xi) Suffocation by bedclothes and pillows.

B. Epidemiological Features
(1) Incidence – 0.6/1000 live births
(2) Age – Peak incidence at 2-4 months
(3) Sex - male predominance
(4) Geographical distribution - Worldwide
(5) Environmental – Exposure to cigarette smoke or use drugs of abuse while in
the womb [ch 46] or after being born.
(6) Child related:
(i) Birth weight - Risk is higher in preterm infants or those born with low birth
weight
(ii) Immunizations - (a) General - SIDS cases are immunized less frequently and
later than controls. Early and more frequent immunizations may reduce the
risk of SIDS. (b) Hexavalent vaccines – Some workers have found an -ed
risk of SIDS in children receiving hexavalent vaccines [diphtheria, tetanus,
acellular pertussis, Haemophilus influenzae type B, poliovirus and hepatitis
B (DTaP-Hib-IPV-HepB)]. These were introduced in Europe in 2000.
(iii) Multiple birth babies –incidence is 3 times in members of a twin pair and
still more in triplets. Could be because multiple birth babies are generally
premature and of low birth weight
(7) Parent related -
(i) Age of mother - - risk to those born to young mothers.
(ii) Alcoholic mother – Incidence of SIDS is -in children having alcohol-
consuming mothers than in those non-alcohol-consuming mothers.
Furthermore even in alcohol-consuming mothers, the incidence -es
significantly on weekends and New Year, when there is -ed consumption of
alcohol. It is hypothesized that alcohol impairs parental capacity to care for
their children.
(8) Socioeconomic – occurs more in poor families
(9) Time of death – Death always occurs during sleep. At all times of night,
with a moderate -in the early morning hours
(10) Season – More common in winters
(11) Latitude – More prevalent in countries with higher latitudes
(12) Miscellaneous factors – Risk is -ed in following conditions
(i) Having a brother or sister who had SIDS (ii) Heads covered with bedclothes.
(iii) Late or no prenatal care (iv) Premature birth (v) Short time period
between pregnancies (vi) Soft bedding in the crib.

C. Symptoms
Almost all SIDS deaths occur without any warning or symptoms when the infant
is thought to be sleeping.

D. Autopsy
All changes are not seen in any given individual case.
(1) Face -
(i) Facial pallor
(ii) No petechial hemorrhages in face or eyes
(2) Hands –
(i) Clenched
(ii) Contain fibres from bed clothes
(3) Definite pathology – found in about 15% brought as SIDS, eg (i) Congenital
heart disease (ii) Down’s syndrome (iii) Pneumonia (iv) tracheobronchitis. But
by definition, once significant pathology is discovered, they no more remain
cases of SIDS, and autopsy report should not mention this term. The term
SIDS should be entered as a cause of death, only when either no findings are
discovered, or very minor findings insufficient to explain death.
(4) Milk or blood stained froth – in child’s nostrils, mouth or bedding
(5) Respiratory passages – (i) froth (ii) milky vomit (iii) shedding of individual
tracheobronchial epithelial cells
(6) Inflammatory signs - (i) Laryngitis (ii) Tracheitis (iii) Bronchitis (iv)
Bronchiolitis (v) Pneumonitis (vi) pleuritis, either individually or in various
combinations
(7) Lungs – (i) Surface - Patchy or uniform purplish discoloration (ii)
Consistency – firm (iii) wt--ed (iv) pathology – congestion, edema
(8) Petechial hemorrhages – on visceral surfaces of heart, lungs and thymus.
 Most common finding [seen in about 75% cases)]. Could be due to terminal
inspiratory efforts against a closed glottis.
(9) Histopathology –
(i) Bronchi – peribronchiolar cell infiltration
(ii) Lungs - (a) patchy alveolar collapse (b) Alveolar walls - thickened (c)
aggregations of (I) platelets (II) neutrophil polymorphonuclear granulocytes
and (III) lymphocytes (IV) monocytes in the lung capillaries. Indicative of
early inflammation In about 1/5th cases, inflammatory cells are also found
in alveolar spaces [localized areas of bronchopneumonia] (d) capillary
thrombosis [producing ischemia during life].
(iii) Brain - (a) brainstem - bilateral hypoplasia of the arcuate nucleus.
(iv) Heart - (a) Conduction system - resorptive degeneration.
(10) Biochemical - -ed levels of cytokines [IL-1ß, IL-6, TNFα] in blood and
CSF.
(11) Genetic testing to exclude genetic disorders.

E. ML Importance
(1) Infanticide – May be misdiagnosed as SIDS due to lack of evidence.
Meadow’s dictum states that “one sudden infant death is a tragedy, two is
suspicious and three is murder, until proved otherwise”.
(2) SIDS infants as organ donors – A lot of confusion existed earlier regarding
the validity of using heart and other organs from SIDS infants because of
unclear etiology. Studies have now proved that heart and other organs from
SIDS infants can be transplanted in other infants with no -ed incidence of
death in recipients.
(3) Civil and Criminal cases involving SIDS – have generally failed in courts,
because courts recognize that this is a natural phenomemon.

28. Forensic Psychiatry

I. INTRODUCTION

[A] Psychiatry - Deals with the study diagnosis and treatment of mental illness.
[B] Forensic Psychiatry - Application of psychiatry for the purposes of law and
administration of justice. [C] Mental Health Act, 1987 (MHA)- Law passed by
the govt of India in 1987 relating to treatment and care of mentally ill persons.
This Act does not mention the words insane, insanity, lunatic and lunacy
anywhere. Instead the term ‘mentally ill person’ is mentioned and defined. These
terms should best be avoided. According to S.2(l) of MHA, a mentally ill person
is one who is in need of treatment, by reason of any mental disorder other than
mental retardation.

II. KEY TERMS IN FORENSIC PSYCHIATRY

A. Abreaction
Abreaction is reviving and bringing into consciousness traumatic experiences of
the past, which the patient has repressed subconsciously.

B. Actus Reus (guilty action)

Actus reus refers to criminal act. See also mens rea.

C. Affect
A term related to mood, feeling or emotion. It is described as mood, or inner
feelings at a particular moment. If mood is emotional ‘climate’ [more pervasive
and sustained], affect is emotional ‘weather’ [more fluctuating changes].

D. Affective Disorder
A disorder in which affect is disturbed (e.g. bipolar disorders, depression).

E. Amnesia
Amnesia is loss of memory. May be seen in head injury. Retrograde amnesia -
Extends backwards in time from the point of head injury. Anterograde amnesia
– Extends forwards in time from the point of head injury.
F. Compos Mentis
Having a sound mind [from Latin, composed mind]. For recording certain
statements eg dying declaration, making a valid will, it must be certified that the
declarant was compos mentis.

G. Confabulation
Confabulation refers to false answers given by amnesia patients without a
deliberate attempt to mislead. Typically seen in Korsakoff’s psychosis [please
see ch 40]. Confabulation is different from lying, but may be very difficult to
differentiate from it.

H. Delirium
Delirium [Latin de lira; “out of the furrow”, “off the track”] is a common and
severe neuropsychiatric syndrome with core features of (1) acute onset (2)
fluctuating course (3) attentional deficits and (4) reduced clarity of awareness of
the environment.
Salient features:
(1) Commonest organic mental disorder seen in clinical practice. 5-15% of
all medical and surgical inpatients develop delirium. This percentage is higher
in postoperative patients.
(2) Earlier known as acute brain syndrome, acute confusional state, acute
organic reaction, metabolic encephalopathy and toxic psychosis.
(3) Causes: (i) Medical conditions - [especially when there is continuous - temp]
e.g. CNS infections. Also in head trauma (ii) Toxic substances e.g. datura
(4) MLI: (i) person may become impulsive, violent and may commit homicide
or suicide (ii) A person in delirium is not responsible for his acts (iii) Wills
made in delirium are not valid.

I. Delusion
Delusion is a false belief in (i) something which is not a fact, and (ii) which
persists even after its falsity has been clearly demonstrated, and (iii) which is not
widely prevalent in persons of similar socioeconomic and educational status.
Dislikes, hatred and prejudices however ill-found are not insane delusions.
1. Types of delusions
(1) Delusional Misidentification Syndromes - include four types of
syndromes:
(i) Capgras syndrome (Delusion of doubles, Illusion des sosies) - Person holds a
delusion that a friend, spouse, parent, or other close family member has
been replaced by an identical-looking impostor [stranger]. Familiar person
is thus seen as a stranger.
(ii) The syndrome of subjective doubles - The patient’s own self is perceived as
being replaced by a double.
(iii) The syndrome of intermetamorphosis - Familiar persons are believed to
have exchanged identities [no stranger is involved]. A person misidentifies
his wife as his deceased mother and, later, as his living sister.
(iv) Fregoli syndrome (Illusion de Fregoli, The Fregoli delusion, the delusion
of doubles) – Delusional belief that one or more familiar persons, usually
persecutors following the patient, repeatedly change their appearance.
Memory Aid 1: Fregoli Syndrome
In Fregoli syndrome, person thinks that familiar persons follow him and change their figure [appearance].

(2) Erotomania - One believes that another person, usually someone of higher
status, is in love with him or her [de Clérambault’s syndrome]. The
affected individual attempts to contact the other person (through phone calls,
letters, gifts, and sometimes stalking).
(3) Grandeur (syn. Inflated self-esteem and self-image)- The affected person
thinks that he is very rich, while in reality he may be a pauper.
(4) Hypochondriacal (syn. Somatic) – The person believes he is ill, although he
is perfectly healthy
(5) Infidelity (syn. Jealousy) – Person thinks that his wife is unfaithful to him
while she is chaste. Also known as morbid jealousy, delusional jealousy,
sexual jealousy, Othello syndrome or Othello psychosis. (In the
Shakespearean play ‘Othello’, the main character Othello thinks that his wife
Desdemona is infidel and strangles her. He then kills himself with a sword!).
The syndrome may appear by itself or in the course of paranoid schizophrenia,
alcoholism, or cocaine addiction.
(6) Influence – Also known as
C
lérambault-Kandinsky syndrome [Memory Aid 2]. The person complains that
his actions, feelings and thoughts are being
C
ontrolled or influenced by some outside agency – sometimes even with the help
of hypnosis, telepathy etc.
(7) Nihilistic – The person feels he does not exist [Cotard syndrome].
Memory Aid 3: Cotard Syndrome
In Cotar d syndrome, person thinks he is dead

(8) Persecution (paranoia) - The person thinks that people around him are trying
to kill him [most common type of delusion]. The affected individual is
frequently highly litigious.
(9) Reference – The person believes that everyone is looking at him or talking
about him, or that items in newspapers or radio are referring to him
(10) Self-reproach – The person blames himself for past failures and misdeeds
which are of no significance
(11) Miscellaneous: delusions of jealousy, religion etc.

2. Medicolegal importance of delusions

(1) Criminal responsibility [CR]– To determine CR, the delusions must be
presumed to be real, and then it must be determined if the act done was
criminal or not [for details, please see below - McNaghten rule " examples].
(2) Testamentary capacity – A person affected by an insane delusion can make
a valid will, if the delusion is not related in any way with the disposal of
property or the persons affected by will.

J. Fugue
Fugue (pronounced - Fyoog) is a state of altered awareness during which the
affected person forgets his identity, assumes a new identity, leaves home and
wanders. It occurs in depressive illness, epilepsy, hysteria and schizophrenia.

K. Hallucination
Hallucination is a false sense perception without any external object or stimulus
to produce it.
Salient features:
(1) Hypnagogic hallucination – is a vivid dreamlike hallucination which occurs
as one is falling asleep. The opposite is hypnopompic hallucination, which
occurs as one is waking up. [g " p]. don’t indicate pathology.
(2) Pseudohallucination - is one in which the patient knows the stimulus is in
the mind.
(3) Types - They can occur in any sensory modality: (i) Auditory – Also known
as Paracusia. Person hears voices and imagines that someone is speaking to
him, when no one is present. (ii) Command hallucinations – Also known as
command automatism [please also see automatism below]. Patient is ordered
by hallucinatory voices to do unwanted and undesirable things. May even
commit suicide or homicide at the order of such imaginary voices. Found
closely in association with delusions of influence [please see above] (iii)
Gustatory – Feeling of tastes when no substance is in mouth (iv) Olfactory –
perceiving smells, when none is there. Also known as phantosmia (v)
Psychomotor –Person has feeling of movement of some part of the body,
where there is none. (vi) Tactile – Also known as haptic hallucinations. One
may feel as if insects are crawling underneath the skin, while there are none.
Seen in chronic cocaine abuse (vii) Visual – Person may see something, which
does not exist (God, imaginary object, fearful and attacking animal, snakes
etc).

L. Illusion
Illusion is a false interpretation by the senses of an external object or stimulus
which has a real existence. Ex. (i) A rope is hanging from a tree and the person
perceives it to be a snake. There is a real stimulus (rope), which is false
perceived as snake. In hallucinations, a person may see snakes hanging from the
tree, where even the rope is not there. A normal person may have illusions but on
proper explanation, he will realize his mistake (as when another person goes and
touches the rope to tell him it is not snake). But a mentally ill person may insist
it is a snake. (ii) Stem of a tree " patient thinks it is a ghost standing (iii) Birds
singing " patient thinks some person is speaking about him (iv) Person comes
with a dog to meet him " Patient thinks he has brought a lion to kill him.
M. Impulse
An impulse is a sudden and irresistible urge, compelling a person to perform
some action without motive or forethought.
(1) Types:
(i) Dipsomania – An irresistible desire to consume alcohol
(ii) Kleptomania – An irresistible desire to steal (stolen objects may be of little
value)
(iii) Mutilomania - An irresistible desire to mutilate
(iv) Pyromania - An irresistible desire to set buildings on fire
(v) Sexual impulses - An irresistible desire to perform a perverted sexual act
(vi) Suicidal and homicidal impulses - An irresistible desire to commit suicide
or homicide
(vii) Trichotillomania - An irresistible desire to pull out body hair.
(2) ML aspects – In India person is criminally responsible, because he knows
what he is doing [please see M’naghten rule and S.84, IPC below]. Under
the more advanced irresistible impulse test [not followed in India], person is
not criminally responsible.

N. Lucid Interval
Lucid interval (L. lucidus, clear) is a period of clarity of thought between two
subsequent bouts of mental illness [Fig 28.2].
Salient features:
(1) Most commonly seen in bipolar disorders [between two subsequent manic
attacks].
(2) It is also seen in head injury, where it refers to a period of consciousness
between two successive periods of unconsciousness [ch 17; Table 1].
(3) MLI – The person is responsible for all civil and criminal acts done during
lucid interval, eg making a will, entering into a contract (civil), committing a
murder (criminal).
O. Mania
Mania is one of the episodes of bipolar (manic-depressive) disorder (the other
being depressive), characterized by an elevated, or irritable mood state, an
increase in energy, decreased need for sleep and impaired judgment.

P. Mens Rea (guilty mind)

Mens rea refers to criminal intent.
Salient features:
Legally speaking, crime = mens rea + actus reus. If either actus reus or mens
rea is absent, crime does not take place legally.

Q. Oligophrenia
Oligophrenia is another name for feeblemindedness, mental subnormality or
mental retardation.
Salient features:
1. Older system of classifying oligophrenia used terms like idiot, imbecile and
moron. Because of stigma attached to such terms, this classification is not
 used now. Both older and modern classifications are compared in Table 2.

Memory Aid 4: Modern and older classification of subnormal IQs

P S M2 "Profound, Severe, Moderate, Mild
I I M , Bangalore"Idiot, Imbecile, Moron, Borderline
Memory Aid 5: Imbecile
Mental age of an imbecile [several and moderate intellectual disability] is below the age of criminal
responsibility [7 y]

2. Classification of individuals with higher IQs was given by Lewis Terman

(1877-1956) [Table 3].
R. Oneiroid States (Oneirophrenia)
Oneirophrenia is a hallucinatory dream-like state [Gk ‘oneiros’ (dream);
‘phrenos’ (mind)]. Shares some characteristics with simple schizophrenia (e.g
confusional state and clouding of consciousness). Causes - prolonged sleep
deprivation, drugs (e.g. ibogaine).

S. Phobia
A phobia (Gk: phobos, fear) is an irrational, intense and persistent fear of certain
situations, activities, things, animals, or people. The main symptom is the
excessive and unreasonable desire to avoid the feared stimulus. The fear is
beyond one’s control, and interferes with daily activities. Phobias may develop
to almost any object or situation. Some important phobias are: (i) Acrophobia,
Altophobia – fear of heights. (ii) Agoraphobia – fear of large open places (from
where escape is impossible) (iii) Aviophobia – fear of flying. (iv) Claustrophobia
– fear of confined spaces. (v) Hemophobia – fear of blood. (vi) Mysophobia –
fear of germs, contamination or dirt. (vii) Nosophobia – fear of contracting a
disease. (viii) Xenophobia – fear of strangers, foreigners, or aliens.

T. Psychosis
Psychosis [Gk psyche, mind; osis, disease] is an abnormal condition of the mind,
when there is a loss of contact with reality. People suffering from psychosis are
described as psychotic. Neurosis is now no more used as a diagnostic term, but
when it was used, it was usual to differentiate it from psychosis (Table 4).

III. THE MENTAL HEALTH ACT, 1987

The Mental Health Act was passed by the Indian Parliament in 1987. The aims
and objectives were to consolidate and amend the law relating to mentally ill
persons, their better treatment and care, better management of their property, and
their overall better protection. It is a social welfare legislation. It repealed the
Indian Lunacy Act, 1912. It changed certain objectionable and stigmatic terms
into more acceptable terms (Table 5).
Salient features:
(1) Mentally ill person is defined as a person who is in need of treatment by
reason of any mental disorder other than mental retardation [S.2(l)]
(2) License – (a) Establishment and maintenance of psychiatric hospitals or
psychiatric nursing homes can only be with license [S.6], which has to be
renewed every 5 years [S.94.] (b) The license will be revoked if the hospital is
not maintained according to provisions of the Act [S.11] (c) if hospital is run
without license, the penalty is imprisonment of 3 months and/or fine of `200
for first offence, 6 m and/or `1000 for second offence and if hospital is
continued to run without license even after that, a penalty of `100 per day
[S.82]
(3) Regular inspection of psychiatric hospitals by Inspecting Officers – In
order to know that psychiatric hospitals are working well and in accordance
with the Act, the State Government or licensing authority will appoint an
‘Inspecting Officer’ who at any time can enter and inspect any psychiatric
hospital, inspect its records and talk to patients in private. If working of
hospital not found satisfactory, he will report to the licensing authority who
will take appropriate action [S.13]
(4) Appointment of visitors and monthly inspection by them - For every
psychiatric hospital, the Govt shall appoint 5 or more visitors (of these at least
one should be a medical officer, preferably a psychiatrist, two should be
social workers and two others) [S.37]. Every month three or more visitors
 will make a joint inspection of every part of the psychiatric hospital and
examine every minor admitted as a voluntary patient, and preferably every
other mentally ill person admitted [S.38]. Regular visits by inspecting officers
and visitors ensure that psychiatric hospitals are run smoothly.
(5) Proper admission and discharge of patients – Please see below under
‘restraint of the mentally ill’
(6) Penalty for improper reception of mentally ill person – If a mentally
person is improperly admitted or detained in a psychiatric hospital, the
punishment is imprisonment up to 2 years or with `1000 fine or both [S.83].

IV. RESTRAINT OF THE MENTALLY ILL

Restraint of the mentally ill refers to lawful restraint of a mentally ill person
[MIP], who is a danger to himself or others. It can be (A) Immediate restraint or
(B) Admission in a psychiatric hospital.

A. Immediate Restraint
Immediate restraint means taking a mentally unsound person into immediate
control whose illness has exacerbated acutely, or who has suddenly become
violent. There is no specific provision in MHA 1987 for immediate restraint. It is
done U/s 81, IPC [act done to prevent other harm].
Salient features:
(1) Conditions when immediate restraint is required - Illnesses where a
person (i) may become dangerous to himself or (ii) to others (iii) may
wastefully spend his own property or (iv) that of others.
(2) Such illnesses are: (i) Delirium tremens (ii) mania (iii) Organic delirium
(3) Purpose: (i) To prevent such injury to himself, others and to the property (ii)
To prevent wasteful expenditure of his own or others’ property.
(4) Prerequisites – informed consent of guardian must be obtained. If consent
not obtainable for any reason, person can be restrained without consent, but
only as long as danger exists.
(5) Method – by safely locking up in a room under immediate personal care of
attendants.
B. Admission in a Psychiatric Hospital
Elaborate procedures for admission in a psychiatric hospital have been made so
no person may exploit the law. If a person is aggrieved over an unfavorable will
made by a relative, he may try to prove him mentally ill by getting him admitted
to a psychiatric hospital. A criminal may himself get admitted in order to claim
benefit of S.84, IPC.

1. Admission on a voluntary basis

(1) Major – Any person >18 y who considers himself a mentally ill person
[MIP] and desires to be admitted to any psychiatric nursing home for
treatment, may request the doctor in charge for being admitted as a voluntary
patient [S.15].
(2) Minor – In case of persons <18 y, request is made by guardian [S.16].
(3) Procedure – The doctor in-charge shall make such inquiry [examination etc]
as he may deem fit within 24 h and if satisfied that the applicant or minor
requires treatment he may admit him [S.17].
(4) Comments – A straightforward procedure. The possibility of patient
malingering illness is prevented by doctor himself examining such person.
Very few patients are admitted under this law.

2. Admission under special circumstances [application by relative or friend]

If mentally ill person [MIP] is unable to express his willingness for admission
(i) Patient may be admitted for up to 90 days on an application by relative or
friend [S.19(1)] (ii) Application should be on prescribed form (iii) It should be
accompanied by certificates from 2 medical practitioners [allopath, homeopath,
or ayurveda (S.2k)], one of whom should be a Govt doctor (iv) each doctor
should have examined the MIP separately within 10 days prior to application
[S.30]. (v) If above certificates are not attached, the doctor in charge may
appoint 2 doctors working in the hospital to examine him [S.19(2)].

3. Reception order on application

(1) Reception order [RO]– means a magisterial order for MIP to be “received”,
admitted and kept in hospital.
(2) Application by doctor in charge – If doctor thinks that treatment is needed
for >6 m or detention is needed for patient’s own safety and that of others, he
 would make an application to magistrate for a reception order [S.20(2)].
(3) Application by husband, wife or relative:
(i) Husband or wife of patient can make an application to magistrate.
(ii) If there is no husband or wife or if they are ill or absent or can not make an
application for whatever reason, any relative of patient can make an
application [S.20(3)].
(iii) He must state why the husband or wife is not making the application. He
should also indicate his relationship with the patient, and the circumstances
under which the application is being made [S.20(4)].
(iv) All persons making application under this provision [husband, wife, relative]
must be >18 y and must have seen the patient within 14 days of making
application [S.20(5)].
(v) The application must be in prescribed form and must be accompanied by
certificates from 2 medical practitioners, one of whom must be a Govt
doctor [S.20(6)].
(vi) Each medical practitioner should examine the patient independently
[S.21(a)]
(vii) The certificate should state that the MIP is suffering from mental disorder
of such a nature and degree that his treatment in the psychiatric hospital is
required and that such detention is necessary in the interests of the health
and personal safety of patient or for the protection of others [S.21(b) ].
(4) Procedure:
(i) When application is made by doctor – Magistrate would pass an RO, if he is
satisfied [S.22(1)]
(ii) When application is made by husband, wife or relative – (a) magistrate
would consider statements made in application and also the medical
certificates [S.22(2)] (b) he may personally examine Alleged Mentally Ill
Person (AMIP) [S.22(3)] (c) If he is satisfied that the patient needs
treatment, he would immediately pass RO; if not, he shall fix a date for
further consideration [S.22(4)] (d) He will give notice of date fixed to the
applicant, and to any other relevant person [S.22(5)] (e) Till the application
is disposed, magistrate would pass order for proper care and custody of
AMIP [S.22(6)] (f) On the date fixed for disposal of application, the
magistrate would consider the application in camera, in presence of (i) the
applicant (II) AMIP himself (III) a representative appointed by AMIP (IV)
 any other person whom magistrate thinks is fit to be there [eg a doctor, a
neighbor, friend etc]. After listening to all parties, the magistrate may either
pass an RO [no time limit of detention] or dismiss the application. The
magistrate would decide whether the cost of such enquiry would be charged
from applicant or from the mentally ill person [S.22(7)]. (g) If application is
dismissed, the magistrate shall record reasons for dismissal and shall give a
copy to the applicant [S.22(8)].

4. Reception order on production of mentally ill person before Magistrate

a. Wandering or dangerous mentally ill person

(1) Detention - An police officer in charge of a police station may detain any
wandering mentally ill person (WMIP) [who is wandering aimlessly] or
dangerous mentally ill person (DMIP) [who is dangerous to himself or others
due to his violent behavior][S.23(1)].
(2) Information - The Police officer would immediately inform him why he is
being detained. If WMIP or DMIP is incapable of understanding, their
relatives or friends must be informed [S.23(2)].
(3) Production before magistrate - Such WMIP or DMIP must be produced
before a magistrate within 24 h of detention. The period of journey is not
included [S.23(3)].
(4) Procedure:
(i) In respect of examination - Magistrate shall (a) examine the person personally
(b) cause him to be examined by a doctor and (c) make any other relevant
enquiries [S.24(1)].
(ii) In respect of admission – Doctor must certify the person to be mentally ill. If
he feels that patient may be malingering and needs sustained observation or
there is some other difficulty in on-the-spot diagnosis, he may say so to the
magistrate and he would pass a temporary order for detention for
observation of a period of up to 10 days [S.28(1)]. If diagnosis cannot be
made during that period, two more such orders can be passed. The doctor
must make a diagnosis within 30 days [S.28(2)]. If after medical certificate
from doctor the magistrate is satisfied of the need of his treatment or for
protection of himself or others (a) he may make an RO. (b) If any relative
or friend wants him to be admitted to a particular licensed psychiatric
 hospital and agrees to bear cost, and doctor in-charge of that hospital
consents, an RO for that particular hospital is made. (c) If relative or friends
furnishes a bond ensuring that WMIP or DMIP would neither injure himself
nor others, and agrees to keep him, the magistrate, instead of making an
RO, would hand over such person to the relative or friend [S.24(2)].

b. Cruelly treated mentally ill person

(1) Information to magistrate:
(i) Police officer – may inform magistrate if an MIP is in the custody of relative
or guardian, and is being cruelly treated by him [cruelly treated mentally ill
person, CTMIP] [S.25(1)].
(ii) Any private person – can similarly inform magistrate [S.25(2)].
(2) Procedure:
(i) The magistrate would call CTMIP, relative who is cruelly treating him and
person who is legally bound to maintain such CTMIP [S.25(3)].
(ii) Magistrate would order the person who is legally bound to maintain such
CTMIP to take his proper care. If he willfully neglects to comply with the
order, he can be fined up to `2,000 [S.25(4)].
(iii) If it appears to magistrate that despite fine etc, the CTMIP would not be
properly looked after, he would make an RO, under same procedural
guidelines as with WMIP and DMIP above [S.25(5)].
(3) Powers of Police Commissioner [PC]– In an area where PC has been
appointed, he would discharge all powers and functions of magistrate in
respect of WMIP, DMIP and CTMIP [S.36].

C. Discharge of a Mentally Ill Person

(1) Voluntary patient:
(i) If patient, or minor was admitted voluntarily, normally he should be
discharged within 24 h of a discharge request [S.18(1)]
(ii) If minor during admission attains majority, the doctor would intimate him of
this fact, and if no application from him for continuation of admission is
received within 1 month of such intimation, he would be discharged
[S.18(2)]
(iii) If doctor thinks more treatment is required, he would make a Board of 2
doctors within 72 h of receipt of application of discharge and seek its
 opinion. If Board recommends continuation of treatment, the patient can be
kept for 90 days against his will [S.18(3)].
(2) When admission was on application by relative or friend:
(i) Mentally ill person himself, or any of his relative or friend may apply to
Magistrate for discharge.
(ii) Magistrate would give a notice to the person on whose application patient
was admitted (iii) On hearing all parties he would either allow or dismiss
application [S.19(3)]
(3) Powers of officer-in-charge of a psychiatric hospital:
(i) He can discharge any patient other than a voluntary patient on the
recommendation of 2 doctors, 1 of whom should preferably be a
psychiatrist. But a mentally ill prisoner cannot be so discharged [S.40(1)]
(ii) A copy of discharge order must be sent to such authority [eg magistrate] on
whose reception order the patient was admitted [S.40(2)].
(4) Discharge of mentally ill persons on application – A mentally ill person
detained under RO made on application shall be discharged if the person on
whose application the admission order was made, applies in writing to the
medical officer in-charge. However if the medical officer certifies in writing
that the person is dangerous and unfit to be at large, he cannot be discharged
[S.41].
(5) Discharge of a person on his own request – Any MIP (not being a mentally
ill prisoner) who feels he has recovered from his illness may make an
application to a magistrate. He must attach a certificate from the medical
officer in-charge of the hospital where he undergoing treatment, or from any
other psychiatrist. Magistrate may pass an order for his discharge if he deems
fit [S.43].
(6) Person detained on reception order – Subsequently found by judicial
inquisition to be of sound mind, he shall be discharged [S.44].

V. MENTAL ILLNESS AND RESPONSIBILITY

Responsibility means legal liability of a person for his actions. It can be in civil
or criminal matters. Law presumes that every person is mentally sound until
proved otherwise.
A. Civil Responsibility

1. Competence as a witness
(1) Generally speaking a mentally ill cannot testify
(2) However he can testify under following special circumstances:
(i) Understanding not affected - if he can understand the questions put to him
and give rational answers to them [S.118 IEA]
(ii) During lucid interval
(iii) Understands obligations of an oath
(iv) Understands the necessity of telling the truth
(v) if able to tell coherently what he has seen.

2. Consent
(1) Consent to any act mentioned in IPC [eg hurt, medical examination, sexual
intercourse, surgery etc] - Not valid, because the mentally ill does not
understand the nature and consequences of the act [S.90, IPC - please also see
ch 2].
(2) MTP – consent invalid [ch 26].

3. Contracts
(1) Only a person of sound mind is competent to contract [S.11 Indian Contract
Act, 1872].
(2) When is a person said to have sound mind:
(i) If at the time when he makes the contract, he is capable of understanding it
and of forming a rational judgment as to its effect upon his interests [S.12
Indian Contract Act, 1872].
(ii) If other party can show it did not know the mental condition of the other
party, and the contract was fair " Contract may be held valid
(3) If mental illness develops after contract is signed – Contract is valid, until
and unless mental illness makes the other party unable to perform service
relevant to contract.
(4) Contract can be made during lucid interval [S.12 Indian Contract Act, 1872].
(5) A sane man, who is delirious from fever or who is so drunk that he cannot
understand the terms of a contract or form a rational judgment as to its effect
on his interests, cannot contract whilst such delirium or drunkenness lasts
 [S.12 Indian Contract Act, 1872].

4. Government service
A mentally ill person cannot enter a govt service.

5. Inheritance
Mentally ill person cannot be disqualified from inheritance to any property
[S.28, Hindu Succession Act 1956]. However S.25 of HAS 1956 disqualifies a
murderer [or an abettor of a murder] from inheritance. The situation is less clear
if a mentally ill person commits murder.

6. Management of property and affairs of mentally ill

This is guided by chapter VI of the MHA [S.50-S.77]
(1) Application [S.50]:
(i) If a person has become incapable of managing his property due to mental
unsoundness, an application for holding an enquiry into his mental
condition [judicial inquisition] may be made to the District Court [DC] by
(a) any of his relatives [not friend or unrelated person].
(ii) Alleged mentally ill person is personally examined either by the presiding
officer of the court. Court may call any other person [psychiatrist] for
opinion and report.
(2) Findings given after inquisition [S.51]:
(i) Whether the person is indeed mentally ill
(ii) if yes, can he take care of (a) himself (b) his property (c) neither. This fact
must be clearly stated by the doctor in his certificate.
(3) Appointment of guardian – if person incapable of taking care of himself, a
guardian is appointed [S.53].
(4) Appointment of manager by Court– if person is found incapable of taking
care of his property, a manager is appointed to take care of his property [S.54].
(5) Appointment and remuneration of guardians [S.57 MHA 1987]: Legal
heirs of mentally ill person cannot ordinarily be appointed guardians or
managers.
(6) Duties of guardian or manager [S.58]:
(i) To take care of mentally ill persons and those persons dependent on him
(ii) To take care of his property.
(7) Powers of manager [S.59]:
(i) Has all powers in relation to property, as the mentally ill person would have
had, if he was not ill
(ii) Sale, mortgage, lease of property for purposes of settlement of debts -
Manager can pay all debts and liabilities of the mentally ill persons by
mortgaging or selling any of the immoveable property of the mentally ill,
after making an application to the DC and taking permission from it.
(8) Admission to a psychiatric hospital – If District court thinks that the
condition of mentally ill person is such that he must be admitted in a
psychiatric hospital, an order is made to that effect. The detention would be till
such period the order is revoked [S.26].
(9) Cessation of mental illness [S.75]:
(i) If DC is informed that the person who was found to be mentally ill, is now
free from such illness, it may direct a subordinate court to inquire into the
matter.
(ii) A second inquiry is held following the same procedures. If person found to
the mentally sound, all actions taken regarding him would be set aside [eg
removal of guardians and managers etc].

7. Marriage
Condition (ii) of a valid Hindu marriage states that neither party must be
mentally ill at the time of marriage. If any party is mentally ill, the marriage is
voidable [for details, please see ch 23].

8. Partnerships
Mental illness of a partner does not automatically dissolve the partnership until
court is moved for its dissolution.

9. Testamentary capacity
Testamentary capacity is a person’s legal and mental ability to make or alter a
valid will.
Salient features:
(1) Definition of a will: (i) Any testamentary document [S.31, IPC] (ii) legal
declaration of the intention of a testator with respect to his property which he
desires to be carried into effect after his death [S.2(h) Indian Succession Act,
 1925]
(2) Person executing a will is a testator [male] or testatrix [female].
(3) Holographic will - It is a will that has been entirely handwritten and signed
by the testator. Normally, a will must be signed by witnesses attesting to the
validity of the testator’s signature and intent, but holographic wills that have
not been witnessed are treated equal to witnessed wills. They need not be
signed or attested [S.66(2) (a) Indian Succession Act, 1925]
(4) Requirements of a valid will: (i) It must be properly written or typed and
properly witnessed and signed by testator as well as at least 2 witnesses. (ii)
Age - Testator must be major [>18 years] (iii) Sound mind - He must be of
sound mind at the time of making the will [compos mentis]. A person is said
to possess a sound mind if he has (a) a capacity of recollecting memories and
recognizing his relatives and friends, (b) understanding their relations to him
and (c) judging his obligations to all. (iv) Testator should not be under (a)
undue force and (b) undue influence (v) There should be no dishonest
representation of facts
(5) Physical examination – (a) Specifically exclude influence of drug or drink,
excruciating pain etc (b) Conditions which do not disqualify (I) agraphia
[failure to communicate through writing] (II) alexia [failure to understand by
reading] (III) blindness, deafness, dumbness if person can communicate
properly through signs or writing (IV) diseases not affecting mind (V)
eccentricity [having unusual likes, dislikes and habits] (VI) Extreme age (VII)
feeble health (VIII) motor or sensory aphasia (IX) physical infirmity
(6) Sound mind – Doctor can certify soundness of mind after (i) history (ii)
Whether well-oriented in time, place and person (iii) psychiatric and
psychological examination including intelligence testing.
In particular determine and ask (a) questions about his family, relatives, friends,
business and social partners, their number, his degree of contact with them,
whether he can recognize them through pictures, his opinions about all of
them. (b) Does he appear to have delusions about anyone? (c) Extent, nature
and value of his properties, and manner of its distribution desired by him (d)
In an unjust or unusual distribution is being made, find out if it is intentional
and if there are any reasons for doing so (e) Can he repeat the main provisions
of his will (f) Power of concentration – by asking simple arithmetic sums (g)
To determine undue pressure or influence – Ask all persons to leave room and
 question him in isolation (h) Presence of any mental strain. (i) Impairment of
memory (iv) Lab investigations.
(7) Delirium and will – please see MLI of delirium above.
(8) Delusions and will – please see MLI of delusions above.
(9) Drunkenness and will – invalid if he did not understand what he was doing
(10) Lucid interval and will – Will is valid made during lucid interval
(11) Suicide after making a will – Will is valid, if suicide was not as a result of
mental disorder.
(12) Wills in extremis – Wills made by a dying person. Valid [cf ch 1 " dying
declaration].
(13) Nuncupative Will - A verbal will; a “deathbed” will. Valid, but shall be
null at the expiration of one month after the testator, being still alive [S.662.
(h) Indian Succession Act, 1925]
(14) Video taped (filmed) will – Indian law is silent on this. However such
video wills are seen as a good supplement to a valid will as they may serve to
demonstrate mental competence.

B. Criminal Responsibility
[A] A person may plead mental illness to avoid (1)Inquiry [S.328, CrPC] (2)
Trial [S.329, CrPC]. (3) Conviction [S.84, IPC] (4) Capital punishment. None
of these can proceed in the presence of mental illness. [B] Legal tests of
insanity – Insanity [or more correctly mental illness] has different medical and
legal definitions. Several tests have been adopted over the years to judge the
criminal responsibility of the mentally ill.

1. McNaghten rule (1843)

McNaghten [M’Naghten] rule - An accused person is not legally responsible
for his crime if it is clearly proved that (i) at the time of committing the crime, he
was suffering from such a defect of reason from disease of mind (ii) that he did
not know the nature and quality of the act he was doing (iii) or that what he was
doing was wrong.
Also known as ‘right or wrong test‘.
(1) Facts of the case - Daniel M’Naghten (1813 – 1865), a Scottish
woodworker was suffering from paranoid schizophrenia [his chief symptoms -
delusions and hallucinations]. He believed that spies sent by Tory party – the
 party in power in Britain at that time – were following him, and hatching a
conspiracy against him (delusions of persecution), and accusing him of several
crimes (auditory hallucinations). On 20 Jan, 1843, he decided to kill Tory
prime minister, Robert Peel, but by mistake shot his private secretary Edward
Drummond. He died 5 days later [Other imp forensic case involving British
Prime Minister - ch 42].
(2) Trial and Judgment – M’Naghten was found not guilty on grounds of
insanity. Not sent to jail, but to Bethlem Mental Hospital for life.
(3) Reasoning - There was agreement on both sides that M’Naghten suffered
from delusions of persecution. Ten physicians [1 for prosecution and 9 for
defense] found him mentally ill. M’Naghten’s delusions had led to a
breakdown of moral sense and loss of self-control, which had left him in a
state where he was no longer a “reasonable and responsible being”. He could
not differentiate right from wrong.
(4) Significance and Outcome – The verdict led to an unprecedented outcry in
parliament, press and public. Queen Victoria (1819–1901), who had herself
been the target of assassination attempts, wrote to the prime minister
expressing her concern at the verdict and the House of Lords revived an
ancient right to put questions to judges. Lord Chancellor Lord Lyndhurst put
before 12 judges, 5 hypothetical questions. The answers given to the House of
Lords on 19 June 1843 formed the basis of M’Naghten rule. M’Naghten rule
dominated the law on criminal responsibility in many countries throughout the
British Commonwealth for over 100 years, till it was set aside by Durham
rule. In India, M’Naghten rule has been incorporated in S.84, IPC.
(5) Criticisms: (i) It concentrates only on the cognitive aspect [Fig 28.3]. It does
not take into consideration the volitional aspect or the issue of control [major
criticism]. A mutilomaniac knows that what he is doing is wrong, but still
cannot control himself from mutilating a man, because of lack of control. By
M’Naghten rule, he is guilty. But actually should not be.
(6) Examples – The question to be asked is “if delusions were real, was the
person entitled to kill”? If he was, he is exempt from punishment, if he was
not, he is not exempt
(i) Exempt from punishment under following circumstances – Under an insane
delusion, the accused thought that (a) Person in front of him is attempting to
kill him (b) Person in front of him is a wild animal going to attack him (c)
 He is the state executioner
(ii) Not exempt from punishment under following circumstances - Under an
insane delusion, the accused thought that (a) person in front of him was
causing his character assassination (b) Some person was having affair with
his wife (c) Some person had stolen money from his house. Under all these
conditions – even if they occurred actually – a person must complain to
police and not take law in his own hands [MLI of delusions].

2. Irresistible impulse test (1887)

(1) First formulated by the Alabama Supreme Court in the 1887 case of Parsons
v. State [Parsons v. State, 81 Ala. 577, 2 So. 854 (1887)].
(2) Attempted to answer the major criticism of M’Naghten rule, that it does not
take into consideration the volitional aspect.
(3) It states – An accused person is not criminally responsible, even if he knows
the nature and quality of his act and knows that it is wrong, if he is incapable
of restraining himself from committing the act, because the free agency of his
will has been destroyed by mental disease.
(4) Not followed in India.
(5) Acts done under irresistible impulses like dipsomania, kleptomania,
mutilomania and pyromania are not punishable [please also see above under
the heading “impulse”].
3. Durham’s rule (1954)
Durham’s rule [syn, ‘product test’] states that an accused person is not
criminally responsible, if his unlawful act is the product of mental disease of
mental defect. [Memory Aid 6] It was formulated in Durham v. U.S. 214 F.2d
862.

4. Currens rule (1961)

Currens rule states that an accused person is not criminally responsible if at the
time of committing the act, the defendant, as a result of mental disease or defect,
lacked substantial c apacity to conform his conduct to the requirements of the
law which he is alleged to have violated. [Memory Aid 7] It was based on
United States of America, v. Donald Kenneth Currens, Appellant, 290 F.2d 751
(3rd Cir. 1961).

5. American Law Institute (ALI) Test (1962)

American Law Institute (“ALI”), published its Model Penal Code in 1962.
S4.01 of this Code forms the ALI test [Table 6].

6. Other solutions
Above tests of insanity are “All or none” tests. Either a person is guilty or not
guilty. Other “midway” solutions have been suggested as below.

a. Doctrine of diminished responsibility

Doctrine of diminished responsibility states that a person is not fully responsible
for his actions, but only partially, if by virtue of his unsoundness of mind, he did
not premeditate, deliberate or formed a specific intent to kill.
Salient features:
(1) Partial defense - It is a partial defense available to the accused. In India,
S.84 is an ‘all or none’ law, i.e. either is person is fully responsible or not
responsible at all for his actions. Some countries, most notably Scotland,
provide a middle path also – the doctrine of diminished responsibility –
whereby he is neither fully responsible, nor acquitted. Instead he is charged
for a lesser offence - ‘voluntary manslaughter’ [ch 11]. Mental diseases –
This defense requires evidence of a state of mind bordering upon, but not
amounting to complete insanity. (i) Mental diseases most commonly
qualifying for this defense - Arrested development of mental faculties,
depressions, injuries to head, obsessions, paranoia and psychopathic
personalities (ii) Mental diseases or states which do not qualify for this
defense - Bad temper, drug use, hatred, jealousy, low intelligence, mild
character defects, political fanatism, poor judgment, racial murders and
unfavorable personal feelings
(2) Countries: England - S.2 of Homicide Act 1957 provides this defense.

b. Guilty but mentally ill [GBMI]

If the court returns a verdict of GBMI, it must impose sentence, but it can only
be executed after the defendant has been given psychiatric treatment and
discharged. He then serves the remainder of the sentence.

VI. MEDICOLEGAL ASPECTS OF MENTAL UNSOUNDNESS

A. Inquiry and Trial of Mentally Unsound Persons

CrPC
(1) S.328, CrPC - Inquiry being held against a person " He claims unsoundness
 of mind " Magistrate will inquire into such soundness " He is found to be
mentally unsound " Inquiry will be postponed and person released. Because he
is incapable of making his defense.
(2) S.329, CrPC - Trial going on against a person " He is found to be mentally
unsound " Trial will be postponed and person released. Reason same as above.
(3) S.330, CrPC - Person undergoing inquiry or trial" found to be mentally
unsound " He shall be released on bail. Sufficient security being given by
relatives or friends that he shall be properly looked after, and not cause injury
to himself or others. If bail cannot be given, he will be detained in safe
custody of a proper place [name of place is not mentioned, but S.336, CrPC
implies, it could be jail also]. If a person is declared mentally unsound u/s 328,
329 or 330 CrPC, and at any stage it is claimed that accused has become
mentally sound, proceedings will be according to S.332, CrPC.
(4) S.331, CrPC - Person had earlier been released u/s 328 or 329, CrPC "
becomes normal " Inquiry or trial will start.
(5) S.332, CrPC:
(i) Person undergoing inquiry or trial " Claims mental unsoundness " brought
before magistrate" Magistrate finds him mentally sound " Trial will proceed
(ii) Person already found mentally unsound u/s 328, 329 or 330, CrPC " It is
claimed he has become mentally unsound " He will be brought before
magistrate " magistrate will decide whether accused is mentally fit or not.
(6) S.335, CrPC - Person committed a crime " given benefit of S.84, IPC
[NGRI] " Court will order safe custody of such person in a proper place.
[name of place is not mentioned, but S.336, CrPC implies, it could be jail
also]. Such person can also be delivered to a relative or friend, if an
undertaking is given that he will be prevented from doing injury to himself or
any other person.

B. Mental Unsoundness and Murder

(1) A murderer may allege mental unsoundness in order to get benefit of S.84,
IPC. If opinion is sought from doctor regarding mental unsoundness of a
murderer, he must administer him a full battery of psychological and
psychiatric tests.
(2) In addition he must make note of following facts
(i) History – of accused and his family regarding mental illness. Does it appear
 to have arisen suddenly after murder, or were there documented visits to
doctor earlier
(ii) Accomplices – not present
(iii) Prearrangement, Preparation, Preplanning – absent in mental illness
(iv) Motive – There should be no motive in mental illness
(v) Victims – may be multiple in mental illness. Some may be his own relatives
and friends
(vi) Conduct of accused at the time crime – No secrecy involved
(vii) Conduct of accused after crime – mentally unsound person would not
destroy pieces of evidence, and would notify even the police
(3) Procedures regarding enquiry and trial – guided by S.328-339, CrPC as
above.

C. Automatism
Automatism [from Gk, automatismos, self-action] is mechanical, repetitive,
undirected behavior that is not consciously controlled.
Salient features:
(1) Also called automatic behavior.
(2) Classification – May be classified into
(i) insane automatism [associated with psychiatric disease] and
(ii) sane automatism [not associated with psychiatric disease].
(3) Etiology:
(i) Cerebral disease (ii) Epilepsy (iii) Hypoglycemia (iv) hysterical states (v)
psychomotor epilepsy (vi) sleepwalking (vii) Toxic [drug automatism] -
Drug automatism is repeated intake of a drug because of drug induced
drowsiness and amnesia. (viii) Trauma [eg concussion, posttraumatic
automatism]
(4) Types of automatism:
(i) Ambulatory automatism - aimless wandering or moving about [fugue,
poriomania]
(ii) Command automatism – please see command hallucinations above.
(iii) Mimetic automatisms - consist of facial expressions [grimacing, smiling,
pouting]
(5) Medicolegal aspects – Indian law does not have any special provision for
 automatism. He can get benefit of S.84, IPC, if he can show he was not aware
of the act.

D. Somnambulism
Somnambulism [sleepwalking], is a sleep disorder in which the sufferer
performs activities that are usually done during a state of full consciousness.
Salient features:
(1) Activities during somnambulism may be as benign as sitting up in bed,
walking to the bathroom, and cleaning, or as hazardous as cooking, driving,
extremely violent gestures, grabbing at hallucinated objects, suicide or even
homicide. Activities are similar to automatism. Even during hazardous
activities, he rarely injures himself
(2) Somnambulism belongs to the parasomnia family of disorders, which
involves a number of abnormal and unnatural behaviors during sleep eg sleep
terrors, bruxism (teeth grinding) and restless legs syndrome
(3) Etiology – acute anxiety, stress, concealed mental conflict
(4) Sleepwalkers arise from the slow wave sleep (SWS) stage [Stage 3 sleep] in
a state of low consciousness and perform activities as if they are awake.
(5) Psychological profile – such patients are usually
(i) Socially well behaved
(ii) Unaggressive
(iii) Well adjusted in life.

E. Somnolentia
Somnolentia, semisomnolence or sleep drunkenness a condition of prolonged
transition from sleep to waking, with partial alertness, disorientation,
drowsiness, poor coordination, and sometimes excited or violent behavior.
Salient features:
(1) Patient may commit a crime, when suddenly aroused during sleep, especially
when he was dreaming
(2) Not criminally responsible.

F. Miscellaneous
1. Hypnotism
Hypnosis is a trance state characterized by extreme suggestibility, relaxation and
heightened imagination. Also known as mesmerism, because first suggested by
German physician Franz Anton Mesmer [1734 –1815]. MLI: (i) Crime
[murder etc] under hypnosis is possible, but the perpetrator cannot take the
defense that he was under hypnosis. No one can be hypnotized against his will,
and it is presumed that when a subject consented for being hypnotized, he knew
of all consequences.
2. Kidnapping from lawful guardianship
Taking away a person of unsound mind away from a guardian without his
consent is punishable u/s S.361, IPC [ch 3].
3. Self-inflicted injuries
Mentally ill persons may inflict injuries on their bodies [ch 12]. They must be
restrained, otherwise doctors and paramedical staff may be sued for negligence.

29. Blood and Biological Stains

I. BLOOD

A. Examination of Suspected Blood Stains

1. Whether the given stain is blood or not?

a. Presumptive tests
A presumptive test has a high sensitivity but low specificity.
Salient features:
(1) If a presumptive test is -ve, one is almost sure blood is absent [because of
high sensitivity. Blood can be detected in samples with 105-fold dilutions or
more. But if the test is +ve, confirmatory tests need to be done [because of low
specificity].
(2) Principle: (i) Heme group of Hb has a peroxidase like activity, i.e. it can
split off a nascent oxygen from an oxidant [usually 3% H2O2]. H2O2
peroxidase
H2O+[O] (ii) The nascent oxygen can either (a) change the color of a chromogen
or (b) cause a substance to emit light. Based on this, presumptive tests are
divided into two – [A] color tests [B] Chemiluminescent and Fluorescent tests.
Most frequently used reagents are phenolphthalein and luminol tests.

i. Color tests
(1) False +ve – Color reaction with a substance other than blood.
(i) Chemical oxidants
(ii) Plant materials – eg horseradish contain peroxidases"false +ve results.
(iii) Materials of animal origin [including human], which are not blood but may
contain contaminating traces of blood.
(2) False -ve – No color reaction with blood.
(i) Extremely low blood dilutions - tetramethylbenzidine [1:400,000]; o-tolidine
and leucomalachite green [1:200,000]; phenolphthalein [1:2000]. Washing,
rain, heat and time may reduce the conc of blood in the sample.
(ii) Contamination with reducing agents – (a) several detergents and foods (b)
ascorbic acid. Lesser contaminants are required in lower blood dilutions [to
elicit false -ve]; thus both factors present together elicit false –ve easily.
(3) Chromogens – Over 20 have been used. 6 common ones are discussed
below.
(a) Benzidine [Adler test]
(1) Historical - Originally described by Adler in 1904
(2) Procedure:
(i) Take stained material"cut out a small piece of stain or tease out some fibers
containing stain"Place them on a porcelain tile"Add a drop of saturated soln
of benzidine in glacial acetic acid"A dark blue color indicates a chemical
oxidant and the test should be considered inconclusive. If there is no color
change"Add a drop of 3% H2O2"If blood is present, a dark blue color is
produced immediately"may eventually turn to brown.
(ii) Alternatively swab the suspected blood stain with clean filter paper or a
swab, which may be moistened if necessary with deionized water, ethanol
or saline and proceed as above.
(3) +ve reaction – given by even (a) very old blood stains, (b) stains that have
been exposed to heat or cold, (c) stains that have been treated with cleaning
 agents (d) Very dilute blood stains [up to a dilution of 1:300,000]
(4) Weak reaction given by – bacteria, formalin, milk, oxidizing agents, pus,
rust, saliva and certain vegetable and animal juices
(5) Current status - Was once considered one of the best presumptive tests, but
because of proven carcinogenicity of benzidine, was replaced by o-tolidine
test.
(b) Phenolphthalein [Kastle-Meyer test]
(1) First described by Kastle and Shedd in 1901, for the detection of plant
peroxidases. In 1903, Meyer used it for the determination of peroxidase in
blood and pus.
(2) Procedure – Make stain extract with distilled water"add 20 drops of
phenolphthalein reagent [phenolphthalein 2 g + NaOH 20 g + Zn + Distilled
H2O 100 ml]"add 2 drops of H2O2"If blood present, a characteristic pink
color develops immediately.
(3) Comparison with benzidine – Specificity more than that of benzidine, but
sensitivity is lesser.
(4) Disadvantages -
(i) Amount of recoverable DNA - is reduced when this test is used.
(ii) False +ve – with traces of Cu. They are not really considered false +ve in
true sense, because the color produced is not the characteristic pink, but
some other color.
(c) O-tolidine test [Kohn test]
(1) Reaction is similar to that of benzidine and is conducted under acidic
conditions
(2) Produces blue color resembling benzidine
(3) Not to be confused with o-tol
u
idine test [please note extra “u”] which is a test for chloride ions in water (as in
swimming pool water) and not for blood.
Memory Aid 1: O-toluidine test
Under Water - Test with an “u” [tol Uidine] is used for Water chloride.
(d) Leucomalachite green [LMG]
(1) Also referred to as McPhail’s Reagent [Hemident]
(2) Procedure -
(i) Take stained material as in benzidine test.
(ii) Apply 1-2 drops of the LMG reagent.
(iii) Other steps are similar as in benzidine test
(iv) An immediate blue-green color change indicates blood.
(3) Disadvantages -
(i) Use of LMG obstructs DNA recovery from stain.
(ii) Sensitivity is 10 times less than that of Luminol.
(e) Tetramethylbenzidine [TMB]
All steps are same as in LMG test, except that the reagent used is TMB. Color
change is blue-green.

(f) Guaiacum test

(1) Reagent used - α-guaiaconic acid, a phenolic compound, that is extracted
from the wood resin of Guaiacum trees, which grow in subtropical and
tropical regions of the Americas.
(2) All steps are same as in LMG test, except that the reagent used is Guaiacum.
Color change is deep blue.
Memory Aid 2: Presumptive tests for blood
1. Benzidine is Blue
2. Phenolphthalein is Pink
3. Leucomalachite is blue Green because Leaves are bold Green
4. All other colors are blue or blue green.
5. Guaiacum is not green. Thus it has to be blue.
6. Blue Green is in TMB and LMG

ii. Chemiluminescent and fluorescent tests

Salient features:
(1) Luminol is the luminescent dye and Fluorescin, the fluorescent dye that is
used for determination of blood.
(2) Done in dark room - Blood stains which are normally invisible to eye shine
in the dark.
(3) Advantages –
(i) They can be sprayed over large suspect areas
(ii) Patterns eg bloody footprints, fingerprints, splatters etc can be made out
(iii) Can be sprayed in inaccessible nooks and corners and crevices of a room, or
 in a vehicle etc to know where exactly stains are present
(iv) Can determine blood at crime scenes, even if they are thoroughly cleaned
and washed.
(4) Disadvantages - if sample is very little, the spraying of these reagents causes
dilution. This may cause problems later if DNA profiling has to be done.
(a) Luminol test
(1) Luminol gets oxidized in presence of Hb and H2O2"Luminesces with a blue-
white light.
(2) Advantages - (i) Considered the best overall presumptive blood test because
it has the greatest sensitivity and specificity of all. Sensitivity is 20 times more
than other tests – Greatest advantage. Hb has been detected in 1:10 million
dilutions. Bloodstains have been detected under 8 layers of paint. (ii) does not
destroy the DNA, (iii) Can be reapplied (iv) easy to use, (v) non-toxic, (vi)
Detection up to 7 wks [minimum] (vii) most resistant of all presumptive tests
to the possible influence of contaminants [eg detergents etc].
(3) Drawbacks -
(i) Operators must work in dark, making manipulations difficult.
(ii) Identification relies on one’s eyes becoming accustomed to the dark.
(iii) The reaction is short-lived [30 s].
(iv) Cannot differentiate between human and animal blood.
(v) Not specific for hemoglobin
(vi) Interferes with later determination of enzyme and protein genetic marker
systems [especially Erythrocyte Acid Phosphatase (EAP), Esterase D
(EsD), Peptidase A (PEP A) and adenylate kinase [AK] (vii) luminol is
suspected to be a mutagen.
(b) Fluorescein test
(1) Test first suggested in 1910 by Fleig.
(2) Fluorescin is the reduced form of fluorescein. Fluorescin is the prepared
reagent for analysis; on oxidation by heme it forms Fluorescein – which
fluoresces [Fluorescin/Fluorescein system]. Fluorescin sprayed stains are
exposed to light in the range of 425-485 nm [usually] using an alternate
source device [this is not necessary with luminol, which works on
chemiluminescence].
b. Confirmatory tests
Hb molecules are detected. An average RBC contains about 280 million
molecules of Hb. An ideal test [which does not exist] must be able to detect a
single molecule.

i. Microcrystal assays
(1) In microcrystal assays, blood crusts from a bloodstain are treated chemically
to convert heme into heme derivatives, which form crystals with distinctive
morphologies.
(2) The crystal morphology is examined with a microscope
(3) Drawback –Although specificity is high, sensitivity is very low.
(a) Hemin [Teichmann] crystal test
Described in 1853 by Ludwig Teichmann of Poland.
(1) Procedure –
(i) Place suspected stain or material on a glass slide
(ii) Add a small crystal of NaCl and glacial acetic acid [2-3 drops]
(iii) Cover with a cover slip
(iv) Apply little heat with a flame placed below the slide
(v) Cool and examine under microscope
(vi) If blood is present, faint yellowish-red to brownish-black rhombic crystals of
hemin [Ferriprotoporphyrin chloride (syn, hematin chloride)] are seen.
They are arranged singly or in clusters.
(vii) Confirmation of the nature of crystals - add a drop of H2O2 under the cover
slip"bubbles of gas are seen.
(2) False negative –
(i) Old stain
(ii) Fabric washed or treated with chemicals
(iii) Defective chemicals used [moisture in acid]
(iv) Wrong application of test [addition of too much NaCl, overheating].
(3) False positive - None.
(b) Hemochromogen [Takayama] crystal test
Described in 1912 by Masaeo Takayama of Japan.
(1) Procedure -
(i) Place suspected stain or material on a glass slide
(ii) Add 2-3 drops of Takayama reagent [Water: Saturated glucose soln: NaOH
(10%): pyridine = 2:1:1:1]
(iii) Cover with a cover slip
(iv) If blood is present, pink feathery crystals of hemochromogen [Pyridine
ferroprotoporphyrin (syn, reduced alkaline hematin)] arranged in clusters or
sheaves appear within 5 min [Fig 29.1]. However to be sure that the
suspected stain is not blood, one must wait for 30 min. If crystals do not
form up to this period, the test is declared negative
(v) Slide warming [up to 37°C in an incubator, especially in cold weather]
hastens the reaction, but is not necessary as in Teichmann test.
(2) Advantages -
(i) Hemo chromogen crystal test is more reliable [with memory aid 3].
(ii) Gives good results even with old stains
(iii) Heating is not necessary.
(c) Wagenaar test
Also called acetone-chlor-hemin test. Developed in 1935. Suspected bloodstain
+ Few drops of acetone + one drop of dilute HCl. If hemoglobin is present,
characteristic crystals form, which are observed under a microscope.

ii. Microscopic examination

(1) Presence of RBCs etc -
(i) Suspected stain extracted with Vibert’s fluid [or any of the solvents
mentioned above]" Examined under microscope"presence of cellular
materials [RBC, WBC and platelets] confirms blood. In a dried stain, all
cellular material becomes unrecognizable [cells are broken down]. In such a
case, other confirmatory tests are employed
(ii) Intact RBCs seen only in (a) fresh wet stains (b) in blood clots
(2) Identification:
(i) Mammals – biconcave, circular, non-nucleated. Exceptions - camel and yak –
RBCs are biconvex, elliptical, non-nucleated.,
(ii) Mammals showing nucleated RBCs [nRBCs] - Small numbers of nRBCs are
seen in (a) alpacas [0-3/100] and (b) some breeds of dogs [Miniature
Schnauzers and Dachshunds] (c) Humans (I) Newborns (II) in certain
diseases and poisonings [lead poisoning (plumbism); Bone marrow
 neoplasia, Pernicious anemia]
(iii) Other animals – in amphibia, birds, fish, reptiles – biconvex, oval,
nucleated.

iii. Spectroscopic Examination

(1) It is essentially absorption spectroscopy [for principle, please see ch 31].
(2) Most delicate and reliable test for detecting the presence of blood in both
recent and old stains
(3) Quantity required is <0.1 mg

2. If the stain is blood, whether it belongs to a human or not (species

origin)?
Currently done by (1) immunological, (2) enzymological or (3) DNA tests.

Immunological

Principle [of immunological tests]

(1) Human serum contains proteins in colloidal suspension
(2) If it is injected in animals, they would be immunized against these proteins
and produce antibodies [precipitins]. The serum is called antihuman precipitin
serum
(3) If human serum is brought in contact with the serum of immunized animal
[diluted up to 1:1000], the two would react forming a visible precipitate
[within a minute].
3. Human leukocyte antigen (white cell antigens, HLA typing)
Human Leucocyte Antigens are a group of highly polymorphic glycoproteins
found on the surface of leucocytes, which can be used for paternity testing
because of their high degree of polymorphism.
Salient features:
(1) Dominant period - HLA typing started in 1970, and was predominantly used
until 1985, when it was superseded by DNA profiling
(2) Exclusion of paternity – can be done up to 80% just by HLA alone [Table
3].
4. Serum protein polymorphism
Human serum contains many proteins, many of which show polymorphism. In
1950s, it was discovered that these polymorphisms could be used for
individualization.

a. Serum haptoglobins
(1) Serum Haptoglobin (Hp) was the most widely used polymorphic serum
protein [before the advent of DNA].
(2) Function - To bind and transport Hb from the blood stream to the liver for
the recycling of the iron contained in the Hb.
(3) Genetics - Two alleles are known – Hp1 and Hp2. They combine to form
three genotypes Hp1-1, Hp2-2 and Hp1-2 (or Hp2-1, which is identical). The
resulting phenotypes are Hp1, Hp2 and Hp1-2 respectively.
(4) MLI - Hp is a relatively stable protein in dried blood stains. This makes it
very valuable for forensic work.

b. Group specific component (Gc)

(1) Gc is a vitamin D binding glycoprotein in the α-2 globulin fraction of
serum proteins.
(2) With electrophoresis, 3 different forms can be identified (Gc 1-1, Gc 2-2 and
Gc 2-1), but with isoelectric focusing (a more refined technique), 9 Gc
subtypes can be distinguished.

c. Ag Groups
(1) The Ag groups were discovered in 1961 in the serum of a multitransfused
patient.
(2) Family studies showed that the antigen was inherited in an autosomal
dominant fashion.
(3) Later, the serum protein was identified as LDL (low-density lipoprotein).
(4) Genetics - Two alleles are present"Ag(x) and Ag(y). The possible
phenotypes are Ag(x+y+), Ag(x+y-), Ag(x-y+) and Ag(x-y-).

d. Gm and Km systems
(1) Immunoglobulins are highly polymorphic and account for approximately
15% of the serum proteins.
(2) Two immunoglobulins which were widely used in forensic work were Gm
 and Km.
Location -
(i) Gm resides on the heavy chain (Gamma) of immunoglobulin G (IgG)
(ii) Km resides on the light chain (Kappa) of all immunoglobulins [IgG, IgA,
IgM, IgE, IgD]
(3) Inheritance - Both Gm and Km allotypes are inherited independently of
each other as autosomal, co-dominant alleles.
(4) Advantages -
(i) Stability - The antigens are stable at moderate heat, and may be stored at
room temperature for extended periods and frozen for years
(ii) Variety of types - Especially with Gm, which has more than 20 allotypes;
Km allotypes are only 3
(iii) They exhibit a high concentration in dried blood.

5. Red cell enzyme polymorphism

Several red cell enzymes show polymorphism. (1) Phosphoglucomutase (PGM)
has been most commonly used in forensic work. Others that have been used for
paternity are (2) Acid Phosphatase [AP] (3) Adenosine deaminase [ADA] (4)
Adenylate kinase [AK] (5) Carbonic Anhydrase [CA II] (6) Erythrocyte Acid
Phosphatase [EAP] (7) Esterase D [ESD] (8) Glucose-6-Phosphate
Dehydrogenase [G6PD] (9) Glyoxalase [GLO 1] and (10) Peptidase A.

6. Hemoglobin (Hb) variants

(1) More than 200 Hb variants have been identified.
(2) Commonest is Hb A.
(3) Some people have both Hb A and another variant Hb S or Hb C.
(4) Hb F -
(i) It is fetal Hb which appears in fetal blood after 3 months of gestation.
(ii) It disappears after birth within 6 months.
(5) The different alleles are expressed co-dominantly, and it is possible to
observe the heterozygous Hb AS, Hb AC, Hb AF types.
(6) Hb S is associated with sickle cell trait.
(7) Hb variants can easily be determined by electrophoresis or Isoelectric
focusing (IEF).
B. MLI of Blood Groups

1. Cause of death
Incompatible blood transfusions.

2. Crime investigation
(1) Blood stains found at scene of crime, clothing and person of suspect can
reveal identity of victim. Accused cannot allege it is his own blood because of
different blood groups.
(2) Blood does not adhere readily to swiftly moving metallic objects. It is
sometimes difficult to detect on a bullet which has passed through the body.
(3) Bloodstains on clothing may be due to crushing of bugs, fleas, louse and
mosquitoes. Differentiating features - Small in size, sharply angular in outline,
usually on the inside of garment, microscopy would reveal insect parts [eggs,
hair, scales etc].

3. Disputed maternity
Disputed maternity arises
(1) when there has been an exchange of child at hospital [either intentionally or
by accident]
(2) when two women claim the same child
(3) in case of kidnapped childzz
(4) suppositious child (please see ch 24 - Virginity, pregnancy and delivery).

4. Disputed paternity
(1) Question of disputed paternity can be solved by blood groups [Table 3]
(2) Bernstein’s laws [please see above] are used
(3) Such questions arise under following circumstances
(i) When the child is born in lawful marriage, but the husband denies that he is
the father
(ii) When a child is born out of lawful marriage, and the mother accuses a certain
man of being the father of child and the man denies the accusation
[Affiliation case, ch 24]
(iii) Suppositious child [ch 24]
(iv) Suits for nullity of marriage
(4) Procedure -
(i) Parents - 5 ml of venous blood is taken from mother and alleged [putative]
father and placed in plain tube. Neither party should have had a blood
transfusion within 3 months.
(ii) Infant – For taking blood, should not be <2 m; preferably >6 m. 1 ml blood is
taken in a plain tube by venepuncture, or prick [ear or heel]
(iii) Testing – to avoid artifacts, testing of all subjects [mother, child, alleged
father] should be done (a) by the same person, (b) in the same laboratory,
(c) on the same day, (d) using the same batch of antisera and reagents.

5. Doping in sports
Packed cell transfusions are common doping methods in endurance sports. May
be detected by different minor antigens eg Kidd (Jk).

6. Identification
Identification of a criminal from the blood stain found at scene of crime. Rarer a
blood group is, higher are the chances of inclusion or exclusion of an alleged
criminal.

7. Other biological stains

If the person is a “secretor”, blood group agglutinogens can be demonstrated in
other biological stains too.

C. ML Aspects of Blood Stains

(1) Infected blood spills – in hospitals etc blood [and other body fluids] must be
cleaned with sodium hypochlorite [NaOCl, 10,000 ppm chlorine]. Spread of
infection through inability to control infection across patients makes the
hospital liable for damages. In economically advanced countries sodium
dichloroisocyanurate (NaDCC) may be used; however hypochlorite is more
economical and easily available compared with NaDCC; hence it is used in
India and other economically less developed countries. Please also see
discussions under
(2) MLI of blood groups
(3) Examination of suspected blood stains
(4) Applications of DNA profiling.
D. DNA Fingerprinting (DNA Profiling)
DNA profiling [syn. DNA fingerprinting, DNA testing, DNA typing, genetic
fingerprinting) is an identification technique based on the fact that each
individual (except identical twins and clones) has a unique DNA. It was
developed by British geneticist Sir Alec Jeffreys (1950-) in 1984 and published
in 1985. The technique was made commercially available in 1987, when a
chemical company, Imperial Chemical Industries (ICI), started a blood-testing
centre in England. The FBI implemented this technique to forensic casework in
1988 after extensive validation studies.

a. Restriction fragment length polymorphism (RFLP) analysis

Restriction Fragment Length Polymorphism, or RFLP (commonly pronounced
“rif-lip”), refers to multiple variations within different individuals
[polymorphism] of DNA fragments [Restriction fragments] cleaved from their
genome by restriction endonucleases. Because of DNA polymorphism, the
length of DNA fragments obtained from different individuals is different. These
DNA fragments are typically 500-30,000 bp in size [Table 4]. In practice only
bands between 4,000 [4kbp] and 20,000 bp have been used for analyses. Below
the 4kbp level, the density of bands is such that reliable comparisons could not
be made. Thus they belong to the minisatellite [VNTR] region of DNA [Table
4].
Salient features:
(1) This was the first technique used for forensic DNA analysis [by Alec
Jeffreys]
(2) Terminology – VNTR and RFLP are sometimes used interchangeably and as
synonyms. There is a minor difference though. VNTR refers to Variable
Number of Tandem Repeats at a given loci [Table 4]. RFLP refers to
different lengths of DNA fragments that are produced as a result of these
repeats. These fragments are cut on either side by a restriction endonuclease
[giving rise to first two words “Restriction Fragment”]. Their lengths are
different in different individuals [giving rise to last two words “Length
Polymorphism”]
(3) Hypervariability - VNTR loci are hypervariable, each showing 100 or more
alleles [as determined by length polymorphism]. Polymorphism is so high that
 typing of 5 to 8 loci [or markers] is sufficient to differentiate most individuals
(4) Steps - (i) extraction of DNA (ii) Digestion of DNA into fragments using a
specific Restriction Endonuclease – Extracted DNA is incubated with an
appropriate RE, which cleaves it into different sized fragments in different
persons [Fig 29.1]. (iii) Electrophoretic separation of fragments based on size
by agarose gel electrophoresis - (a) Fragments are placed into one end of a bed
of agarose gel [1%] with electrodes in it. Agarose gel is a polysaccharide
made from sea weeds. (b) An electric current is passed overnight through the
gel, which separates fragments according to their sizes. (c) The negatively
charged DNA fragments [-ve charge is due to the presence of phosphate
groups] move through the gel, toward the positive electrode (anode). Smallest
DNA move fastest and furthest down the gel and the largest DNAs move the
least [Fig 29.2]. Fragments from 500 to 25,000 bp in length can be separated
by this method. (iv) Denaturing the double-stranded DNA fragments in a high
pH environment - Agarose gel is soaked in a weak alkaline solution. This
denatures the DNA strands [Two strands of DNA separate out. It becomes
single stranded]. (v) Transferring the single strands of DNA out of the gel onto
a membrane support [either nitrocellulose or nylon] - This technique is known
as “Southern blot”. Developed by the English molecular biologist Edwin
Southern [1938 -] in 1975. Somewhat akin to blotting up of ink by a blotting
paper. Plays on the name Southern blot were later made to denote other
techniques [they have nothing to do with directions]; northern blot is used for
detection of RNA [developed in 1977 at Stanford University], western blot
[syn protein immunoblot] to detect proteins and eastern blot to analyze
protein post translational modifications (PTM) [chemical modification of a
protein after its translation]. (vi) Hybridizing the immobilized DNA fragments
with specifically labeled DNA probes - The bands are still invisible to the
naked eye. A DNA probe is allowed to probe these bands. Excess probe is
washed off. (vii) Detection of the hybrid products by autoradiography or
chemiluminescence - The Nylon membrane is pressed against an X-ray plate
for about 24 hours. The bands appear on the X-ray plate as dark lines
depending on where the probe had attached. The result is known as an autorad
[short for autoradiograph]. These dark lines or bands are specific for each
individual and called his DNA fingerprints.
(5) Drawbacks [of RFLP technology]: (i) Degraded samples not useful - As
VNTR sequences are long, nondegraded DNA samples are needed to make a
profile. In degraded samples, VNTR sequences are broken. A typical allele
used in RFLP is 500-30,000 bp in size [Table 4]. Thus fragments of DNA as
large as 30,000 bp should be intact for successful RFLP. This is not possible in
degraded DNA. This can best be conceptualized as imagining a large thread
being broken into smaller pieces. The more pieces it is broken into, the lesser
will be the average length of each piece. More degradation of DNA breaks it
up into more number of pieces, and thus lesser length (bp) of each piece. (ii)
Large amount of DNA needed (typically 50–100 ng). (iii) Work with
radioactive substances is hazardous (iv) The procedure takes a minimum one
week.
b. Short Tandem Repeat (STR) profiling [Using PCR]
Short Tandem Repeat profiling refers to preparing a profile of multiple
variations within different individuals [polymorphism] of small DNA fragments
less than 500 bp in size, belonging to microsatellite region [Short Tandem
Repeats] of DNA [Table 4]. This technology came in 1990s, mainly to
overcome the drawbacks of RFLP technology [please see above].
Salient features:
Advantages of STR analysis over RFLP – (i) The main advantage is the
smaller size of STR alleles [10-500 bp; Table 4].

c. Y-chromosome profiling
Y-chromosome profiling [YCP] refers to the study and analysis of forensically
important loci on the Y-chromosome. Since Y-chromosomes are passed down
from fathers to sons, it is essentially a study of the history of Y-chromosomes
over time as they are passed from father to son to grandson to great-grandson,
along an unbroken line of biological fathers and sons. The study of Y-
chromosomes in many ways is similar to the study of male surnames, since
both are passed from fathers to sons.

d. Mitochondrial DNA analysis

Mitochondrial DNA (mtDNA) is a 16,569 base pair (bp) circular strand of DNA
located in mitochondria.
Salient features:
Inherited solely from the mother. Forensic value of mtDNA - arises from (a)
sequence variability of the D-loop between individuals, (b) its efficient PCR
amplification with limited biological material (c) In addition to the skin, blood,
semen and saliva, from which nuclear DNA can be extracted, mtDNA can also
be extracted from materials which fail to yield nuclear DNA, eg teeth, hair
shafts, bone fragments and even human feces. (d) It is more robust than nuclear
DNA for typing materials [due to its higher copy number per cell and its
resistance to extreme environmental conditions. It is more resistant to
putrefaction than nuclear DNA; thus useful in old materials. Also useful when
the material is derived from dead cellular material such as hair or nail. Its
circular nature confers protection from the action of exonucleases]. Ancient
historical material can also by typed. Can be performed on fewer cells due to
higher copy number. mtDNA can now be done from just 1 sperm cell. In contrast
about 67 sperm cells required for STR analysis using conventional nuclear DNA
[please see above] (e) the haploid nature of mtDNA makes it easier to sequence
than diploid nuclear DNA.

1. Biological samples for DNA profiling

Samples for DNA profiling must be collected using sterile uncontaminated
clothes. Usual samples to be collected are:
(1) Blood - Bloodstains on carpets, cloth, floor tiles, food, furniture, metal,
newspaper, plastic, vehicle, wallpaper, wood etc.
(2) Fetus – chorionic villus samples, muscle biopsy
(3) Hair – from head, moustache, beard, axilla, public regions.
(4) Nasal mucus
(5) Saliva - Cigarette butts, envelops, mouth swabs etc.
(6) Semen – suspected stains on cloth, floor tiles, fur, furniture, matted hair
[generally pubic], paper, vaginal aspirate and swabs from anus, mouth, penis
and vagina.
(7) Tissue - bone marrow, fingernail scrapings, muscle, spleen.

2. Applications of DNA profiling

a. Disputed paternity
Please see under MLI of Blood groups.

b. Extortion
(1) DNA profiling done from saliva samples [from envelops sent as extortion
letters] can be matched with that of accused.
(2) Similar profilings done from the material on face masks, gloves, nasal
secretions and saliva from cigarette butts.

c. Homicide
(1) Blood – DNA profiling done from blood [found on weapon or on clothes of
accused] can be matched with that of victim.
(2) Tissue – found on bullet recovered from scene of crime [ch 13]
(3) Hair roots – Similar matching from hair on a weapon with that of victim.

d. Identification
(1) Crime scenes - Crucial DNA evidence may by left at crime scenes which
may be matched to those to potential suspects. Besides usual biological
materials eg semen, blood, urine and feces, unusual trace evidences that can
lead to positive identification are a single human hair, lip cells left on a beer
can and saliva on envelope flaps and cigarette butts etc.
(2) Mutilated remains as in accidents, bomb blasts, burnt bodies, mass
 disasters, other catastrophes and putrefied bodies.
(i) DNA profiles from such remains may be compared with previous profiles.
(ii) DNA profiles of the deceased [during his life] may be prepared by taking
cells of the deceased from toothbrush, combs etc which the deceased had
been using.
(iii) If DNA profiles cannot be prepared from such material, profiles of close
relatives such as parents, children, siblings etc might be taken, which will
also be useful.

e. Sexual crimes
identification of accused from DNA profile of accused.

f. Other
(1) Authenticate consumables such as caviar and wine
(2) Environmental forensics - Detect bacteria and other organisms that may
pollute air, water, soil, and food
(3) Justice - Exonerate persons wrongly accused of crimes
(4) Wildlife forensics - Identify endangered and protected species as an aid to
wildlife officials (could be used for prosecuting poachers)
(5) Immigration - some visa applications may depend on proof of relatedness.
(6) Organ donation - Match organ donors with recipients in transplant programs
(7) Pedigree tracing.

3. Limitations
(1) Twins - DNA profiling of identical twins is same [fingerprints even in
identical twins are different]
(2) Expensive; elaborate equipment. Thus facility available at limited places
(3) Contamination of samples can give wrong results
(4) Older DNA profiling technologies are more time consuming [RFLP].
(5) Ethical –
(i) Invasion of privacy - Holding a person’s DNA profile on record is violation of
that person’s DNA ‘ownership’.
(ii) Deletion of records - If a person has been proved innocent after DNA
profiling, he has a right to demand removal of his DNA information from
police data bases, but this is rarely done.
(iii) Illegal sharing of information - DNA information can be shared by police
with others [eg medical researches, drug companies] without the
individual’s consent.
(6) Sabotage - DNA evidence is easily planted at a crime scene. [much more
difficult or even impossible with fingerprints]
(7) In blood and bone marrow transfusion – DNA profile of donor will be
generated and he may be indicted for a crime he did not commit.

4. DNA databases
A DNA database or DNA databank is a database of DNA.
Salient features:
(1) A DNA database is used much like a fingerprint database in identifying
criminals, but can also be used in the analysis of genetic diseases, or
genealogy.
(2) held electronically in the DNA database
(3) DNA Databases around the world -
(i) US – Has the largest DNA database in the world [CODIS]
(ii) UK - The United Kingdom National DNA Database [2nd largest].
(iii) Australia - The National Criminal Investigation DNA Database [NCIDD]
(iv) Canada - The National DNA Data Bank (NDDB)
(v) India – No similar DNA database till date.
(4) Genomic sequences in DNA databases - Full genomic sequence is not
recorded - Only patterns of STRs. Different databases record different STRs.
There is no unanimity.
(5) Privacy issues – Such databases pose ethical issues, eg threats to an
individual’s civil liberties. DNA databases may contain person’s health-related
data, including markers that identify various genetic diseases etc. This is
regarded as an invasion to privacy.
II. FECAL STAINS

Identification - is by Edelman test. Based on the fact that urobilinogen is

present in fecal stains. Suspect stain+ alcoholic mercuric chloride+ alcoholic
zinc chloride"green fluorescence if fecal stain. [urobilinogen in the stain is
oxidized to urobilin by alcoholic mercuric chloride. In the next stage, urobilin
forms a zinc-urobilin complex, which gives the green fluorescence.]

III. LEUCORRHOEAL STAINS

(1) Contain epithelial cells

(2) Have the feel and appearance of seminal stains
(3) Ova of Enterobius vermicularis have been found in them. The worm is
known to occur in female bladder and genitals.

IV. MILK

The detection of milk stains or colostrum on undergarments (eg blouse or

brassiere) may be important in crimes involving pregnancy, abortion or
concealment of birth.
V. NASAL SECRETIONS

(1) Nasal secretion is one of the most difficult body fluids to identify
(2) Especially difficult to discriminate from vaginal secretions and saliva.
(3) People usually blow the nose with paper tissues when the amount of nasal
secretion is increased under conditions such as acute nasopharyngitis and
allergic rhinitis, or rarely, vasomotor rhinitis or sinusitis.
(4) Composition of nasal secretions -
(i) fluid excreted from mucosal glands and cells,
(ii) plasma leaking from blood vessels,
(iii) tears excreted through the nasolacrimal duct from the lacrimal gland.

VI. SALIVA

Identification of saliva is important in alleged cases of fellatio, cunnilingus,

kissing, sucking, spitting, or biting.

A. Sources from where saliva may be recovered

(1) Face mask worn by a suspect
(2) Gag or smothering device
(3) Cup or bottle used for drinking
(4) An envelop related to a crime (saliva used for sealing or affixing stamp)
(5) Cigarette butt.

B. Tests
(1) Detection of amylase [Phadebas test]
(2) Buccal epithelial cells [DNA profiling can be done]
(3) RNA based assays.

VII. SEMINAL STAINS

For seminal stains, please see chapter on sexual offences.

VIII. SWEAT

Sweat stains may become important in cases of violent struggle.

(1) Dermcidin is an antibiotic peptide secreted by sweat glands. A monoclonal
antibody (G-81) has been developed which can react with dermcidin, helping
in the identification of sweat stains
(2) DNA typing can be done from sweat stains taken from inside of
undergarments.

IX. URINE

Examination of urine and its stains may be necessary in cases of murder and
sexual assault.

A. General
(1) May appear yellow.
(2) Characteristic “urine” smell from the stain (due to ammonia evolved by
bacterial degradation of urea).
(3) Fluorescent under UV light.

B. Chemical tests
Detection of urine stains is based in detection of amines, phosphate, sulphate,
urea or creatinine, each of which exists in urine in higher concentration than in
other body fluids. Urinary glycoproteins are also specific to urine.
(1) Urea in suspected stain is detected with urease-bromothymol blue paper. If
the stain is urine, urea would be enzymatically decomposed to ammonia and
carbon dioxide by urease. Liberated ammonia shifts the pH, changing the
color of the indicator (bromothymol) from yellow to blue.
(2) 0.005% cent soln of para-dimethylamino cinnamaldehyde can be used as a
colour test for urea.
(3) Uric acid (UA) and urea nitrogen (UN) ratio multiplied by 20 (UA/UN #
20) in human urinary stains is between 1 and 4; in all other stains and in
animal urinary stains this ratio is either < 1 or >
(4) This fact is exploited to identify urine stains.
(5) Urine contains a high molecular weight glycoprotein Tamm-Horsfall
protein (THP), named after its discoverers Tamm and Horsfall (also known
as uromodulin or uromucoid). This has been detected by
radioimmunoassay to identify unknown stains as urine stains.
(6) Jaffe reaction - In the presence of picric acid and a weak base, creatinine
would give a bright-red coloration.

C. Species origin
Precipitin test by the agar diffusion method, against the antiglobulins of various
relevant species, including humans.

D. Blood group
Blood group of the person can be determined if the person was a secretor
(individuals who secret blood group substances into body fluids such as urine).

E. DNA typing
DNA typing can also be done from urine stains.

X. VAGINAL FLUID

In cases of suspected sexual assault, traces of vaginal fluid may be detectable

on the penis of the accused.
(1) Vaginal fluid contain vaginal cells which are rich in glycogen (starch)
(2) If sticking on penis in cases of sexual assault, the vaginal cells would be
transferred to a moist blotting paper, if it is rubbed lightly against glans.
(3) Presence of Döderlein’s bacillus.
(4) The blotting paper is then exposed to iodine vapors
(5) Starch inside the vaginal cells turns into starch iodide, which is brown in
color.
(6) RNA based assays.

XI. VOMITUS
Vomitus can be detected by (i) Low pH resulting from stomach acids. (ii)
Microscopic and macroscopic identification of foodstuffs.

30. Forensic Science Laboratory

I. LOCARD’S EXCHANGE PRINCIPLE

Locard’s exchange principle states that when any two objects come into contact,
there is always a transfer of material from each object on to the other. This
principle is often used as a sure proof of crime. The principle was first
enunciated by Edmond Locard (1877–1966), often referred to as the Sherlock
Holmes of France.
II. INSTITUTE OF FORENSIC SCIENCE - ORGANIZATION

A comprehensive Institute of Forensic Science should comprise of 3 categories

of service (i) Clinical (ii) Pathological and (iii) Laboratory services. In
addition it should have several other facilities such as (iv) exhibit room (where
exhibits brought by police, e.g. blood stained weapons, viscera etc) are stored (v)
stores (for equipment, chemicals etc) (vi) workshop (for training) and (vii)
library.

A. Central and State FSLs

(1) Central FSLs are funded by central government.
(2) Central CFSLs (Central Forensic Science Laboratories) – 7 in India
[Bhopal, Chandigarh, Guwahati, Hyderabad (Telangana), Kolkata, New
Delhi, Pune]. Of these, 6 CFSLs [except the one at ND] are under the
Directorate of Forensic Science Services (DFSS). The one at New Delhi is
under CBI [Address: Block No.4, CGO Complex, Lodhi Road, New Delhi-
110003]. In addition there is one institute of serology, located at Kolkata. It
was established in 1912 starting with Forensic Serology as its core activity,
but now has branched out into different field of Serology. CFSLs meet the
demand of police from all over India.

B. Interpol
Interpol (International Criminal Police Organization), with headquarters in
Lyon, France, was established in 1923. It facilitates international police
cooperation. 190 countries, including India are its members. It has a
comprehensive forensic science laboratory.

III. FORENSIC SCIENCE LABORATORY – INDIVIDUAL

SECTIONS

The main functions of forensic science laboratory are: (i) to reconstruct a crime
and (ii) to analyze trace evidence (blood, hair, fiber etc from victim, accused and
the scene of crime and to link the three together. This work is carried on by
different sections. The student is advised to co-relate each section with
appropriate chapters in the book.

A. Lie Detection
Following techniques are mostly being used for lie detection.

Tests for lie detection

a. Brain mapping (Brain fingerprinting)
Brain mapping for brain fingerprinting is a forensic science technique that
determines whether specific information (regarding a crime) is stored in a
subject’s brain. Scientific name of the technique is Memory and Encoding
Related Multifaceted Electroencephalographic Response (MERMER).
Invented and developed by Lawrence Farwell of US in 1990s.

i. Principle
(1) Storage of information in brain - If the subject has committed a crime, the
information would be stored in his brain.
(2) EEG responses to crime related information:
(i) If crime related information (eg picture of the crime scene, photograph of
victim, motive of crime etc) are presented to the subject on a computer
screen, he may consciously deny the information, but his brain would
recognize the information.
(ii) This would elicit relevant EEG waves which could be detected.
(iii) EEG response to an image, sound etc is known as event related potential
(ERP)
(iv) Memory is an integral part of ERP. (a) If a subject is shown a familiar image
(e.g. inside of an aircraft engine to an aircraft mechanic), his EEG would
show memory related waves in ERP. Similarly if the suspect has killed
with a weapon, his brain would be familiar with the weapon. If the weapon
is shown to him, his brain would recognize it and would immediately
respond with a memory related ERP. These memory related ERPs are
called P300 (because delay between stimulus and response is 300 ms).
(b) If the subject is shown an unfamiliar image, memory related waves are
absent.

ii. Procedure
(1) The subject to be tested wears a special headband with electronic sensors
(electro-cap) that measure the EEG from several locations on the scalp.
(2) He is then shown (on a computer screen) several stimuli consisting of words,
phrases, or pictures. Stimuli are of three types:
(i) “irrelevant” stimuli that are irrelevant to the investigated situation and to the
test subject [an unknown person, house etc]
(ii) “target” stimuli that are relevant to the investigated situation and are known
to the subject (face of the victim), and
(iii) “probe” stimuli that are relevant to the investigated situation and that the
subject denies knowing (weapon of offence, scene of crime etc). Probe
stimuli contain information that is known only to the perpetrator and
investigators, and not to the general public or to an innocent suspect who
was not at the scene of the crime.

iii. Results and interpretation

If the subject has killed the victim, his brain would recognize scene of crime and
weapon. Even if he consciously denies information, his EEG would show
memory related P300 waves. He is thus the criminal.

b. Hypnosis
Use of hypnosis for legal purposes is known as Forensic Hypnosis. Hypnosis
may be used for retrieval of information from witnesses when it cannot be
acquired through any other means. Memories long forgotten or intentionally
suppressed may be recovered during sessions of hypnosis.

c. Lie detector (polygraph)

i. Principle
If a person is speaking a lie"Fear"-sympathetic activity"-heart rate, -blood
pressure, -respiratory rate. In addition -sweating"-skin conductivity. If a
person is asked a question and simultaneously these parameters are being
monitored, the investigator would know when he is speaking a lie. Also known
as psychophysiological detection of deception (PDD).

ii. Procedure
Two types of polygraphs (analog and computerized) are in use. Analog
instruments make actual ink tracings of above parameters; computerized
instruments make an inkless tracing on the computer. Stoelting polygraphs,
both analog and computerized versions, are used commonly. (i) Pre-test
interview - Polygraph test starts with a pre-test interview to gain some
preliminary information which will later be used for “control questions”, or CQ.
(ii) Explanation of the test - The tester explains how the polygraph is supposed
to work, emphasizing that it can detect lies and that it is important to answer
truthfully. (iii) Actual test – Questions asked are three types (1) “irrelevant” or
IR (Is your name Ram?) (2) “probable-lie” control questions (CQ) that most
people will lie about (“Have you ever stolen money?”) (3) “relevant questions”
(RQ), that the tester is really interested in. The different types of questions
alternate. The test is passed (i.e. the subject is not guilty) if the physiological
responses during the probable-lie control questions (CQ) are larger than those
during the relevant questions (RQ). (iv) Post-test interview - If responses to
RQ are smaller than responses to CQ, the tester attempts to elicit admissions
during a post-test interview. An example, “Your situation will only get worse if
we don’t clear this up”.

iii. Results and interpretation

If responses to RQ are greater than those to CQ, the person is experiencing fear,
and hence lying. Use of beta blockers e.g. propranolol, may vitiate the test.

d. Narcoanalysis (truth serum)

i. Principle
Narcoanalysis is based on the principle that a person lies using his imagination
[inventing lies], which requires full consciousness. By inducing a semiconscious
state [narcosis], his capacity of inventing lying is diminished.

ii. Procedure
Sedatives or hypnotics are administered to induce narcosis. Agents commonly
used are
(1) Anticholinergics:
(i) 3-quinuclidinyl benzilate [an odorless incapacitating agent used in military
also. Also known as BZ. It is an anticholinergic compound related to
atropine, scopolamine, hyoscyamine, and other deliriants]
(ii) Scopolamine [syn, hyoscine].
(2) Hypnotics:
(i) Barbiturates [eg sodium amytal (intermediate acting), sodium pentothal
(ultrashort acting)- ch 40]. Thus often known as Amytal interview. Long
 acting barbiturates are not suitable
(ii) Ethanol
(iii) Temazepam. The drugs are used either singly or in various combinations.

iii. Results and interpretation

Person loses inhibitions, is relaxed and becomes talkative. May speak truth
under loss of inhibitions. The effect is same as when a person speaks truth under
the effect of alcohol [Latin In vino veritas, “in wine there is the truth”]. Large
number of false negatives are common [i.e. when the person does not confess
despite being guilty].

iv. Medicolegal aspects

(1) Scientific validity - The scientific validity of the narcoanalysis test has been
questioned by medical professionals
(2) Legal validity:
(i) Forced use of truth drugs is considered a form of torture according to
international law, and according to Declaration of Tokyo [ch 2], a doctor
cannot participate in torture.
(ii) Article 20(3) of Constitution of India states that no person accused of any
offence shall be compelled to be a witness against himself. S.161(2), CrPC
states that a person cannot be bound to answer questions which expose him
to a criminal charge. Narcoanalysis contravenes both laws by forcing a
person to answer questions incriminating himself.
(iii) In 2010, Supreme Court of India has opined that this test cannot be forced
upon any suspect.
(3) Medical use – Its use is scientifically and legally valid in the evaluation of
certain psychiatric patients.
(4) May cause sudden death due to dose miscalculations or unpredictable
reaction to barbiturates.

B. Photography
Forensic photography (forensic imaging) is the use of photography for the
purposes of law and administration of justice. Forensic Photography is done for
(1) Recording evidence [e.g. scene of crime, injuries at body etc]. For
photography in vehicular accident cases, please see ch 18
(2) To reveal what normally cannot be seen. This can be done by (a) UV light (b)
IR light.

1. UV light
Memory Aid 1: Forensic applications of UV light
B4ritish academy of F4orensic S3ciences G2oT3 a P3 A L
B4"Bite, Blood, Bruises, Burns
F4"Fibers, Fingerprint, Fake currency, Forgery
S3"Scorpion, Semen, Skeleton
G2"Glass, GSR
T3"Tattoos, Teeth, Tetracycline
P3"Poisoning : Ethylene glycol, Lead, Phosphorus
A"Adipocere
L"Lead [repetition. Already mentioned]

2. IR light

Memory Aid 2: Forensic applications of IR light

GeT A B3 aD F an " GSR, Tattoos, Artwork, Bite, bloodstains, bruise, Document, Forgery

31. Introduction, Classification of

Poisons, Law Relating to Poisons and
General Considerations

I. INTRODUCTION

(1) Fatal dose – Amount of drug that would kill 50% of a test population.
(i) Same as LD50.
(ii) Minimum fatal dose [syn minimum lethal dose] is the smallest dose that has
been recorded as fatal to a healthy person. [Please also see “Toxicity
scales”].
(2) Fatal period – Time in which a person dies if given fatal dose.
(3) Toxicology is the study of the adverse effects of chemicals on living
organisms. It includes the study of symptoms, signs mechanisms, treatments,
postmortem appearances, detection of poisoning etc.
(4) Toxins are poisons produced by living cells or organisms. Ex - algae
[phycotoxins], animals [zootoxins], bacteria [bacterial toxins], fungi
[mycotoxins] and plants [phytotoxins]. They are generally small molecules
(peptides or proteins), and less complex than an poison or a venom. The
toxicity varies greatly in severity, ranging from minor (bee sting) to major
and severe (botulinum toxin). Toxinology is the study of toxins.
(5) Venom - is a special category of poisons, that must be injected by one
organism into another to produce harmful effect [e.g. snake venom]. Venoms
are generally high-molecular wt proteinaceous substances [cf poison]. Please
also see ch 38 and 39.
(6) Xenobiotics - are drugs and chemical compounds foreign to the body [e.g.
antibiotics, metals such as lead].

A. The Poisons Act, 1919

This Act regulates the import, possession and sale of poisons. Was amended in
1958.

B. The Drugs and Cosmetics Act, 1940

This Act was passed in 1940, in order to regulate the import, manufacture,
distribution and sale of drugs.

C. The Drugs and Cosmetic Rules, 1945

(1) Framed - Under The Drugs and Cosmetics Act, 1940
(2) Schedules – Contains several imp schedules at the end. (i) Schedule C –
Biological and Special Products. (ii) Schedule E – Omitted since 1982. Instead
there is schedule E1. which gives a list of poisonous substances under the
Ayurvedic, Siddha and Unani Systems of Medicine. (iii) Schedule F – (a) Part
I to XII-A - Omitted since 1999. (b) F1. prescribes specifications of following
products. Part 1– Vaccines. Part II –Antisera. Part III- Diagnostic antigens
[Bacterial Origin]. (iv) Schedule G – Contains about 65 drugs [eg
 Aminopterin, antihistamines, L-Asparaginase, Bleomycin, Insulin etc], which
must be labeled with the words “Caution: it is dangerous to take this
preparation except under medical supervision”. (v) Schedule H – contains
several prescription drugs, which must be labeled with the symbol Rx and
following warning: ‘Schedule H drug- Warning: To be sold by retail on the
prescription of a Registered Medical Practitioner only’. The label of innermost
container of drugs in schedules ‘G’ and ‘H’ should additionally bear a
conspicuous red vertical line on the left side running throughout the body of
the label which should not be <1mm in width. (vi) Schedule J – contains a list
of 51 diseases for the cure of which no drug can be advertises [eg AIDS].
Memory Aid 1: 6 important Schedules under The Drugs and Cosmetic Rules, 1945
C a B E P idemic. F i V e G e G s H elP J uD ges
Schedule C – Biological and special products
Schedule E (1) – Poisonous substances
Schedule F – Vaccines, antisera and diagnostic antigens
Schedule G – Medical supervision, drugs to be taken under
Schedule H – Prescription drugs
Schedule J – Disease for the cure of which no drug can be advertised

D. The Drugs Control Act, 1950

It provides for the control of the sale, supply and distribution of drugs.

E. The Drugs and Magic Remedies (Objectionable Advertisement)

Act, 1954
The objective of this Act is to ban advertisements which offend decency or
morality, and to prevent self medication and treatment, which cause harmful
effects.

F. The Medicinal and Toilet Preparations (Excise Duties) Act,

1956
This Act provides for the levy and collection of duties of excise on medicinal
and toilet preparations containing alcohol and narcotic drugs.
G. The Narcotic Drugs and Psychotropic Substances (NDPS) Act,
1985
The Narcotic Drugs and Psychotropic Substances (NDPS) Act was enacted in
1985, by the Indian Govt (i) to consolidate and amend the law relating to
narcotic drugs (ii) to make stringent provisions for regulation of Narcotic drugs
and psychotropic substances (iii) to provide for forfeiture of property derived
from narcotic drug trafficking, and (iv) to implement the provisions of the
International Convention on Narcotic Drugs and Psychotropic substances.

II. MEDICOLEGAL ASPECTS OF POISONS

(1) S.85, IPC - Criminal act done under involuntary intoxication - Person is
intoxicated without his knowledge or against his will"becomes incapable of
judgment"commits a criminal act"Did not know what he was doing"He is not
responsible for the crime. Example – X administers datura to Y without his
knowledge"Y murders Z under the effect of Datura"Y is not responsible.
(2) S.86, IPC - Criminal act done under voluntary intoxication - Person takes
intoxicating drug voluntarily"looses self control"Commits a crime"taken for
medical examination"Found disoriented in time, place and person [i.e. from a
medical standpoint, he did not know what he was doing]"Legally speaking it
would still be presumed that he knew what he was doing, but his intention to
do so cannot be presumed.
(3) S.274, IPC - Adulteration of drugs — 6 m or `1000 fine or both.
(4) S.275, IPC - Sale of adulterated drugs — 6 m or `1000 fine or both.
(5) S.276, IPC - Sale of drug as a different drug or preparation — 6 m or `1000
fine or both.
(6) S.277, IPC - Fouling water of public spring or reservoir — 3 m or `500 fine
or both.
(7) S.278, IPC - Making atmosphere noxious to health — `500 fine.
(8) S.284, IPC - deals with negligent conduct with respect to poisonous
substance. Punishment 6m or `1000 fine or both. Ex –Housemaid leaves toilet
cleaner (acid) negligently on a table"A young child drinks it believing it to be
water"Housemaid can be sued u/s 284, IPC.
(9) S.324, IPC*"ch 11
(10) S.326, IPC*"ch 11.
(11) S.328, IPC:
(i) Person gives or otherwise administers a stupefying, intoxicating or
unwholesome agent, (a) with an intention of causing hurt or (b) with intent
to commit or to facilitate the commission of an offence or (c) knowing it to
be likely that he will thereby cause hurt"10 y+fine
(ii) Drug facilitated sexual assault [ch 25] attracts provisions of this section.
(12) Secondary poisoning - Poisoning that results when one organism ingests
[or comes into contact with] another organism that has been poisoned.
(i) Occurs typically when a predator eats an animal, [eg mouse, rat, insect] that
has previously been poisoned by a commercial pesticide. It can affect
humans. Minamata Bay disaster [please see ch 36] was an example of
secondary poisoning. [cf Secondary drug fatalities. Please see below].
(ii) Sucking venom out of a snake bite wound [ch 38"MLI of snake venom].
(iii) Medical and paramedical staff can get secondary exposure to poisons during
treatment of certain poisons [OP, organochlorine, Nicotine]. They should
wear protective gear during entire management period [impervious gloves
and gowns].

III. NATURE OF POISONING

A. Homicide
Characteristics of an ideal homicidal poison are
(1) should be colorless, odorless and tasteless [most important]
(2) should be easily available
(3) should be cheap
(4) its symptoms should resemble a natural disease [Table 8]
(5) symptoms should appear late after administration, to avoid suspicion
(6) Should not produce vomiting [expulsion]
(7) should be highly toxic
(8) Fatal period – should be less once symptoms have appeared
(9) There should be no antidote available against it
(10) There should be no post-mortem changes
(11) should disappear from the body after death
(12) there should be no test available to detect it.
B. Suicide
Characteristics of an ideal suicidal poison are
(1) Should produce an easy death [most important criteria. Opium and
barbiturates fulfill this criteria]
(2) Easily available [organophosphorus, aluminum phosphide]
(3) Capable of being easily taken in food or drink. Cheapness is not a criteria,
as a dying man would not worry about the cost. Color, odor or taste are not
important on the same grounds. Table 1 gives some importance differences
between an ideal homicidal and ideal suicidal poison.

C. Parasuicide
Parasuicide (Gk para, “near” or “resembling”) or pseudocide refers to suicide
attempts or gestures and self-harm where there is no actual intention to die.
Salient features:
(1) Mostly done to threaten relatives by taking sublethal dose of a poison, e.g. a
few sleeping pills. Youngsters resort to it when their parents disallow marriage
with their loved ones.
(2) Also seen in psychologically disturbed.

D. Accidental
Accidental poisoning can occur in a number of ways
(1) Ingestion in mistake for harmless substance [acid may be ingested as it
appears like water]
(2) Inhalation of vapors through accident [MIC vapors inhaled in Bhopal gas
tragedy]
(3) incorrect preparation of medicines that contain a poison
(4) Excessive self medication
(5) drug addiction
(6) infected food
(7) Animals (snake and spider bite, scorpion sting).

E. Abortion
Most irritant poisons would cause abortion (by causing irritation of uterus,
causing it to contract). Ex. Aconite, Arsenic, Calotropis, Cantharides, Croton,
Ergot, Lead, Mercury, Oleander, Potassium permanganate, Semecarpus.

F. Aphrodisiacs
An aphrodisiac (from Aphrodite, the Greek goddess of sensuality and love) is a
substance that increases sexual desire. Usual substances considered aphrodisiacs
are arsenic, Cannabis, Cantharides, Cocaine, Opium and Strychnine.

G. Arrow Poisons
Arrow poisons are used at the tip of arrows for hunting and to kill enemies.
Salient features:
(1) Ideal arrow poison - must be
(i) Poisonous parenterally, but
(ii) Safe orally so prey killed by an ideal arrow poison would be safe for
consumption.
(2) Typical arrow poisons are
(i) Plant based - (a) Abrus precatorius, (b) aconite, (c) calotropis, (d) croton oil,
(e) curare, (f) Strophanthus (g) strychnine.
(ii) Animal based - (a) Batrachotoxin [BTX].

H. Cattle Poisoning
Used to kill cattle of enemies, or to obtain hides. Usual poisons are Abrus
precatorius, Aconite, Arsenic, Calotropis, nitrates, Oleander, Organophosphorus,
Strychnine, Zinc phosphide.

I. Stupefying
Used to stupefy travelers for robbery, or women for sexual assault. Ex.
Cannabis, Chloral hydrate, Datura.

IV. CLASSIFICATION OF POISONS

Classification of poisons can be (A) according to symptoms produced (B)

according to use (C) according to affected target organ.

A. According to Symptoms

1. Corrosives

a. Strong acids

i. Inorganic acids
Sulphuric, nitric, hydrochloric acids.
ii. Organic acids
Carbolic, oxalic, acetic, salicylic acids.

b. Strong alkalis
NaOH, KOH, NH4OH.

c. Metallic salts
Bichromates, Chromates, Copper sulphate, Ferric chloride, Potassium cyanide,
Silver nitrate, Zinc chloride.

2. Irritants

a. Inorganic

i. Non-metallic
Phosphorus, Chlorine, Bromine, Iodine.
ii. Metallic
Arsenic, Copper, Lead, Mercury, Thallium, Zinc.

b. Organic

i. Plant
(a) All parts poisonous
Calotropis, Cerbera thevetia, Nerium odorum.
(b) Leaves poisonous
Aloe vera, Conium maculatum (hemlock), curare, digitalis, tobacco.
(c) Fruits poisonous
Capsicum annum, Colocynth, Strychnos nux vomica.
(d) Seeds poisonous
Abrus precatorius (Ratti), Castor, Croton, Datura, Semecarpus anacardium.
(e) Bark / stem poisonous
Cinchona, Plumbago rosea.
(f) Root poisonous
Aconite, Colocynth, Plumbago.

ii. Animal
Snake and insect venom, cantharides, fireants, scorpion.

c. Mechanical
Diamond dust, hair, Powdered glass.

3. Systemic
a. CNS poisons

i. Cerebral
(a) CNS stimulants
Amphetamine, caffeine, cyclic antidepressants, methamphetamine,
methylphenidate, modafinil.
(b) CNS depressants
Alcohols, anesthetics, hypnotics, opioids, sedatives.
(c) Deliriants
Belladonna, Cannabis, cocaine, Datura, Hyoscyamus.

ii. Spinal
Gelsemium, Nux vomica.

iii. Peripheral nerve poisons

Conium, curare, several agricultural poisons such as OP compounds and
carbamates.

b. CVS poisons
Aconite, Oleander, Quinine, Tobacco, antiarrhythmic agents, aminoglycosides,
macrolides, General anesthetics.

c. Asphyxiants
CO, CO2, H2S, Cl2.

4. Miscellaneous
Botulism, Food poisoning.

B. According to Use
(1) Poisons causing abortion (2) Poisons used to stupefy (3) Cattle poisons (4)
Arrow poisons (5) Aphrodisiacs (6) Others. For details, please see above
under the heading “Nature of poisoning”.

C. According to Affected Target Organ

1. Poisons affecting the hematologic system
Anticoagulants (warfarin).

2. Poisons affecting the immune system (immunotoxic agents)

Immunosuppressive drugs.

3. Hepatotoxic agents
There are 2 good mnemonics for remembering hepatotoxic drugs – one short,
another longer.
Memory Aid 2: Hepatotoxic drugs
HEPATIC - Hemolytic poisons, Ethanol, Paracetamol, Aflatoxin, Toxaphene, Iron, Chlorpromazine
Memory Aid 3: Hepatotoxic drugs
A SOAP IN A CAPP - Alcohol, Sulphonamides, Oral contraceptives, Arsenic, Paracetamol, Iron,
Naphthalene, Aminoglycosides, Carbon tetrachloride, Anabolic steroids, Paraquat, Phosphorus

4. Nephrotoxic agents
(A) Poisons causing glomerular injury: cocaine, quinine, conjugated estrogens,
gold compounds, NSAIDs, penicillamine. (B) Poisons causing proximal
convoluted tubule (PCT) necrosis.
Memory Aid 4: Poisons causing PCT necrosis
[Mnemonic 1]
APPROACH MAG MOM
Aminoglycosides, Phenol, Pigments, Radiocontrast agents, Organohalides [eg Chloroform, CCl4],
Anesthetics (Fluorinated), Cantharides, Carbon tetrachloride, Cephalosporins (and other beta-lactam
antibiotics), Cresol, Halogenated alkenes [derivatives of CnH2n], Metals (Ar, Cd, Cr, Hg, Pb, Fe, U, Zn),
Antineoplastics, Glycols (e.g. ethylene glycol), Myoglobin (including hemoglobin), Cycotoxins
(Ochratoxin A, Fumonisin B).

[Mnemonic 2]
PCT [shorter mnemonic, but useful]
Phenol, Pigments
Cantharides, Cephalosporins (and other beta-lactam antibiotics), Corrosive sublimate [HgCl2]
[included in metals in 1st mnemonic], Cresol
Tetrachloride [carbon] [included as CCl4 in 1st mnemonic]

(C) Poisons causing distal convoluted tubule (DCT) necrosis.

Memory Aid 5: Poisons causing DCT necrosis
CAG
Cisplatin, Amphotericin, Glycols

(D) Poisons causing crystalluria: acyclovir, ethylene glycol, sulfonamides,

(E) General Nephrotoxic agents
Memory Aid 6: General Nephrotoxic agents
NEP2HRO
NSAIDS, Ergot alkaloids, Potassium chlorate, Pre renal failure, Heavy metals, ARhabdomyolysis
causing drugs, Oxalic acid, Chlorates

5. Pulmonary toxic agents

chlorine (bronchitis), titanium (hard metal disease), silica (silicosis), phosgene
(pulmonary edema), cholinergic drugs (bronchoconstriction), paraquat (acute
pulmonary fibrosis).

6. CNS toxic agents

See classification “According to symptoms” above.

7. CVS toxic agents

See classification “According to symptoms” above.

8. Dermatotoxic agents
Arsenic (carcinogenic), camphor (photoallergy), corrosives (chemical burns),
Furocoumarins (phototoxicity), industrial solvents (allergic contact dermatitis).

9. Agents affecting the reproductive system

alkylating agents (affect gonadogenesis), Chlorophenoxy herbicides (affect
spermatogenesis), Plasticizers (testicular toxicity).

10. Agents affecting the endocrine system

acrylonitrile (adrenal cortex), atenolol (adrenal medulla), Aluminum
(parathyroid), calcitonin (pituitary), Thiouracil (thyroid gland).

V. TYPES OF POISONING
The following types of poisonings depend on (i) the amount of poison taken and
(ii) the time period over which poison taken.

A. Hyperacute [Fulminant] Poisoning

Produced by a single massive dose. Death occurs very rapidly. There may be no
time for symptoms to occur.

B. Acute Poisoning
Acute poisoning is caused by excessive single dose (usually equal to fatal dose),
but less than that used in fulminant poisoning.

Types of acute drug fatalities

a. Primary drug fatalities

Victim dies primarily because of the toxic or adverse effect of drug/poison.
There may be contributing influence of pre-existing, unrelated disease.

b. Secondary drug fatalities

Victim dies from secondary complications of drugs (viral hepatitis, bacterial
endocarditis, air embolism, foreign body embolism). Most commonly occur due
to use of contaminated needles during drug abuse. [cf. Secondary poisoning.
Please see above].

c. Drug associated fatalities

Violence [accidental, homicidal, suicidal] arising directly or indirectly from
activities related to obtaining and use of illicit drugs.

C. Subacute Poisoning
Subacute poisoning occurs gradually over some time; occurs more slowly than
acute poisoning, but quicker than chronic poisoning. Doses taken are small and
over a short period of time. A typical example is drug automatism [ch 28].

D. Chronic Poisoning
Chronic poisoning is caused by very minute doses taken over a long period of
time. Typically seen in occupational poisoning, such as Plumbism. A murderer
who has access to victim’s food (e.g. spouse of the victim) is in a position to
administer minute doses of poison over a long period of time. Typical poison
used is arsenic. After months, the person may die of gastroenteritis.

E. Acute on Chronic Poisoning

Primarily the victim is suffering from chronic poisoning. Acute poisoning
occurs on top of it. Mostly happens in cases of chronic drug abuse, when one
day victim inadvertently takes more than the usual dose.

VI. DIAGNOSIS OF POISONING

A. In the Living
Diagnosis of poisoning in the living is done mainly by three points (Table 2).

1. Clinical history
Clinical history is of great importance [Memory Aid 7]. There is no single
symptom which is characteristic of poisoning. A constellation of symptoms
however (please see toxidromes below) may often point to poisoning.
Memory Aid 7: Major questions to ask in poisoning cases
In poisoning cases history really “MATtERS”
M"Medications or Materials ingested or exposed to
A"Amount ingested
Tt"Time of exposure
E"Emesis [did it occur? What came out?]
R"Reason for the ingestion or exposure. [Accidental, suicidal or homicidal]
S"Signs and symptoms
Suspicion should be aroused when
(1) There is sudden appearance of symptoms. Major symptoms associated
with poisoning are
(i) GIT - (a) abdominal colic and pain [Table 3] (b) vomiting, diarrhea [Table 4]
(c) Hematemesis - (I) Aminophylline, (II) corrosives, (III) iron, (IV)
salicylates (d) Constipation [Table 5]
(ii) Hepatic - (a) jaundice [please see list of hepatotoxic agents above]
(iii) CNS - (a) paralysis (b) tremors [Table 6] (c) convulsions and seizures
[Table 7] – cause rhabdomyolysis (d) coma (iv) Renal - (a) oliguria with
proteinuria and hematuria] (v) Natural diseases - A number of poisons
mimic them [Table 8]
(2) there is association with food – symptoms occur after taking food
(3) there are multiple victims - several persons fall ill simultaneously.
Confirmation is by detection of poison in food, vomit and feces.
2. Clinical signs
Important clinical signs which point to poisoning are:

a. BP
b. Heart rate
Poisons may cause bradycardia [Table 11], tachycardia [Table 12] or cardiac
arrhythmias [dysrhythmias] [Table 18]. Intoxication is the single commonest
cause of cardiac arrhythmias.
c. Ocular signs
(1) Normal pupil size in adults: 2-4 mm in dia (in bright light); 4-8 mm in the
dark. The iris allows the diameter of the pupil to change from 1 to 12 mm,
depending on illumination and accommodation; such changes are influenced
by a perfect balance between the sympathetic and parasympathetic nervous
systems.
(2) Miosis - Constriction of the pupil to <2mm diameter (i) Mechanisms – (a)
Central [eg Opium"ch 40] (b) Peripheral [eg OP"ch 35]
(3) Table 14, Table 15, Table 16, indicate common ocular signs and their
causes.
d. Ears
Buzzing in ears: (i) camphor (ii) ergot (iii) methyl alcohol (iv) quinine (v)
Salicylates (vi) streptomycin.

e. Oral signs
(1) Burns: (i) Corrosives (ii) oxalate-containing plants
(2) Dry mouth: (i) Amphetamines (ii) anticholinergics (iii) antihistamine
(3) Dysphagia: (i) botulism (ii) Corrosives
(4) Gum lines: (i) arsenic (ii) bismuth (iii) Lead (iv) mercury
(5) Salivation: (i) corrosives (ii) OP (iii) salicylates (iv) strychnine.

f. Pulmonary

Respiratory rate
Table 17, Table 18.
g. CNS signs
(1) Ataxia: (i) Alcohol (ii) antidepressants (iii) barbiturates (iv) anticholinergics
(v) phenytoin (vi) narcotics
(2) Coma: (i) barbiturates (ii) CO (iii) cyanide (iv) cyclic antidepressants (v)
lead [encephalopathy] (vi) narcotics (vii) OP (viii) PCP (ix) salicylates (x)
Sedatives
(3) Muscle fasciculation: (i) OP (ii) theophylline
(4) Muscle rigidity: (i) Cyclic antidepressants (ii) haloperidol (iii) PCP (iv)
phenothiazines
(5) Paresthesia: (i) Cocaine (ii) camphor (iii) PCP (iv) Monosodium glutamate
[MSG]
(6) Peripheral neuropathy: (i) Lead (ii) arsenic (iii) mercury (iv)
organophosphates.

h. Skin [cutaneous signs]

(1) Alopecia – ch poisoning with (i) arsenic (ii) lead (iii) mercury (iv) Thallium
(2) Blisters and bullae: (i) barbiturates (ii) CO [for a complete list please see ch
40]
(3) Diaphoresis: (i) alcohol [acute] (ii) arecoline (iii) arsenic (iv) aspirin (v)
cocaine (vi) Dinitrophenol (vii) fluoride (viii) insulin (ix) LSD (x) mercuric
chloride (xi) muscarinic mushrooms (xii) nitrates (xiii) OP (xiv) pilocarpine
(xv) salicylates
(4) Dry hot skin: (i) Anticholinergic agents (ii) botulism
(5) Erythema: (i) Anticholinergics (ii) Boric acid (iii) cyanide (iv) mercury.
(6) Formication – As [ch 36], Cocaine [ch 41]
(7) Hyperkeratosis and pigmentation: (i) ch arsenic
(8) Injection marks and Needle tracks: (i) Drug abuse (a) Amphetamines (b)
Heroin (c) PCP (d) Any other drug taken IV or S/c (ii) snakebite [two fang
marks]
(9) Jaundice - Hepatotoxic poisons (please see list of hepatotoxic agents above)]
(10) Petechiae and purpuric spots – Warfarin
(11) Sweating – please see diaphoresis.

i. Temperature
(1) Hypothermic patients [Table 19] may have a barely perceptible pulse and BP.
(2) Hypothermia may cause or aggravate hypotension, which will not reverse
 until the temperature is normalized.

*Ethanol adversely affects thermal regulation and, depending upon the ambient
temperature, may cause either hypothermia or hyperthermia.
Table 20 lists poisons causing hyperthermia.

j. Urine
May be colored in certain poisonings [Table 21].
k. Blood

i. Collection
[Collection of blood for toxicology in the dead"ch 5] Following precautions are
observed
(1) Equipment: (i) Use clean syringe, needles and containers. None should have
any trace of alcohol. (ii) Nowadays Vacutainers are used, which are sterile
glass or plastic tubes with a closure that is evacuated to create a vacuum inside
the tube facilitating automatic drawing of a predetermined volume of blood.
They already contain an anticoagulant and a preservative. (iii) Container –
screw-capped glass bottle of “universal” size. Not needed if Vacutainers are
used.
(2) Cleaning skin - (i) Do not use spirit (ii) use 1:1000 HgCl2 or plain soap and
water
(3) Use adequate preservative - ch 5.
(4) After collection: (i) sealing - (a) The container should be tightly clamped
and sealed to prevent loss of alcohol by evaporation. (b) Rubber stoppers
should be avoided because they may contaminate the sample with oxidizable
 substances. (c) In medicolegal cases, number of seals must be mentioned and a
sample of seal must be sent along with [chain of custody]. (ii) Labeling – label
with CR no, name, age, sex, date and time of collection of specimens
(5) Send for analysis immediately. If cannot be sent immediately for some
reason, refrigerate, but must not be frozen. Freezing causes cells to lyze
causing spurious concentrations.
(6) Analysis – should best be done within a week.

ii. Inspection
(1) Brown serum – Poisons causing rhabdomyolysis [myoglobin release]
(2) Chocolate color - methemoglo-binemia.
(3) Pink serum – hemolysis [eg sodium chlorate poisoning].

l. ECG
Useful in cardiotoxic ingestions, e.g. AlP, thallium.

m. EEG
Useful in neurotoxic ingestions.

n. Hair
Hair analysis can be done in chronic poisoning both in the living and in the dead.
First toxic substances to the analyzed in hair were heavy metals by means of
atomic absorption spectroscopy to document the exposure in the past. French
Emperor Napoleon Bonaparte [1769 – 1821] is now thought to have been
poisoned by arsenic, because it has been detected in his hair. In 1979, opiates
were detected in hair of heroin users. In the living it is done for
(1) intentional or unintentional chronic poisoning in criminal cases
(2) as preemployment and employment screening
(3) doping control of banned substances
(4) investigation of chronic drug consumption
(5) gestational drug exposure
(6) environmental exposure to toxins and
(7) to demonstrate even a previous single dose administration in a very low
amount.
(8) Segmental [syn, sectional, sequential] hair analysis can provide information
 about the time course of the substance use or exposure [presuming hair growth
of 0.4mm/day – ch 3]. Segments of hair closest to the scalp reflect the most
recent exposure, while those farthest from the scalp reflect earlier blood
concentrations. As one moves away from scalp, every 0.4mm represents one
earlier day, thus enabling an exact dating of toxic exposure.

o. Saliva [oral fluid]

(1) Advantages:
(i) Easy collection
(ii) Less invasive than taking other samples [eg urine, blood]
(iii) Carries a smaller risk of spreading infection
(iv) Collection can be directly supervised without the intrusion of privacy".es the
chance of adulterating or substituting the sample. Very useful in driving
under the influence of alcohol and drugs cases, when evidence of
intoxication is generally needed.
(v) Finding drugs in saliva is a better indication of recent use and possible
impairment than detecting them in a urine sample.
(2) Collection devices – A number of commercial collection devices are
available. However saliva can be collected in a small test tube simply by
asking the patient to chew on chewing gums, parafilm, rubber etc. They do not
affect testing of common drugs and poisons.

p. Sweat
Collected by wiping the skin surface with cotton, gauze or towel.

q. Urine
(1) Urine is often the sample of choice because
(i) Drugs present in higher concentration [it has 25% more water than an equal
volume of blood]
(ii) Large volumes easy to collect
(iii) No pain or discomfort
(iv) Non-invasive. Because of these advantages, it has been called
“toxicologists’ gold”.
(2) Drawbacks:
(i) If bladder contained urine before drug ingestion began, urine secreted during
 drug consumptions will be diluted with plain urine present already. Can
result in faulty estimates of blood concentrations.
(ii) Time lag – of about 30 minutes exists before equilibrium between blood and
urine is reached. Collection of urine before this period causes faulty values.
(iii) Passive diffusion – Most drugs would pass through the lining of bladder in
either direction both in life and after death, depending on the relative
concentration of alcohol in blood and urine.
(3) Method of collection:
(i) Analysis of 2 urine samples is preferable.
(ii) 1st sample should be taken immediately after the victim arrives, the bladder
being completely emptied.
(iii) The 2nd sample should be taken 30 min later.
(iv) The conc of poison [eg alcohol] in the 2nd specimen reflects the blood
poison level during the “interspecimen interval”.
(v) The difference in poison concentrations in the two samples indicates whether
the subject was in absorptive phase, at its peak or in the elimination phase.
[Ch 5"method of collection in the dead].

r. X-Ray
Useful in radio-opaque ingestions [Table 22].

B. In the Dead
Diagnosis of poisoning in the dead is done mainly by five points (Table 23).
1. Clinical history
Full clinical history should be taken from relatives, people present with the
victim at the time of incidence, investigating officer etc. A record should be
made of the drugs, medications to which the deceased had access. Visit to the
scene may give important clues in the form of empty bottles, foils of drugs etc.

2. PM appearances

a. External

i. Stains
(1) Clothes, corners of mouth, or other surface of the body may show poison
stains, marks of vomit or feces.
(2) Color changes in the gastric mucosa can provide a hint regarding poison.

ii. PM staining
For various colors of pm staining and associated poisons, please see ch 9.

iii. Smell

iv. Natural orifices

Mouth, nostrils, rectum and vagina may show the presence of poisonous material
or the signs of it having been used.

v. Skin
Should be examined for
(1) Alopecia
(2) Bullae
(3) Injection marks
(4) Jaundice
(5) hyperkeratosis and pigmentation. [For interpretation of findings, please see
above – Diag of poisoning in the living].

vi. Marks of violence

Abrasions, bruises, wounds may suggest violence in addition of poisoning.

b. Internal
All organs must be examined and all contents preserved.

i. Smell
(1) Usually the smell is obvious even before opening the body.
(2) If smell not obvious, skull should be opened first to note smell. If other
cavities are opened first, smell may be masked. In some cases, opening the
body merely makes the smell more obvious [as in alcohol]
(3) Table 24 gives some common smells associated with poisons.
ii. Mouth, throat and associated structures
(1) Mouth, throat and tongue – Examine for any evidence of inflammation,
 erosion, ulceration or staining. Causes of oral ulceration are same as those
causing esophageal ulcerations [please see below]
(2) Pharynx:
(i) Corrosion and ulceration – causes same as esophageal ulceration below
(ii) Areas of necrosis – seen in drugs causing agranulocytosis [Amidopyrine,
barbiturates, dinitrophenol, sulphonamides and thiouracil].

iii. Esophagus
(1) Softening and desquamation of mucosa – produced by alkalis [acids
produce more destruction in the stomach]
(2) Ulceration: (i) Cantharidin (ii) corrosives (iii) Iodine (iv) Mercuric chloride
(v) Paraquat and diquat
(3) Perforation – in (i) several corrosive ingestions (ii) swallowed foreign
bodies [e.g. button batteries and coins].

iv. The duodenum

(1) Strong acid reaction – in duodenum indicates acid ingestion [has more
value than a similar reaction in stomach]
(2) Normal duodenum – Rules out ingestion of strong corrosives
(3) Perforation – of duodenum usually caused by alkalis [e.g. NaOH].

v. Respiratory tract
(1) Edema of glottis, congestion and desquamation of the mucus membrane of
trachea and bronchi – in corrosive poisoning, especially if corrosive has
entered respiratory tract
(2) Non specific congestion and edema of lungs – in several poisonings,
especially gaseous poisons.

vi. Stomach
Poisons tend to collect in the rugae and crypts of the mucosa. These may have to
be scraped with the blunt end of knife and sent for chemical analysis. Following
points are of importance.

(a) Drugs secreted in the stomach

Please see above under the heading “Fate of poisons in the body”.
(b) Hyperemia
(1) Cardiac end and greater curvature involved - Hyperemia of the mucus
membrane caused by irritants is marked at cardiac end and greater curvature.
Very rarely at pyloric end.
(2) Color and extent – Usually patchy and of a deep crimson color
(3) Mucus membrane – (a) covered with sticky secretion (b) shows small
hemorrhagic foci
(4) Ridges – involved more
(5) Other conditions in which hyperemia is seen - (a) asphyxia (b) during
digestion (c) disease. In these conditions, hyperemia would be uniformly
spread over whole surface and not in patches
(6) Putrefaction – masks hyperemia. Histology and toxicology would be
helpful. Table 25 shows colors other than hyperemic red seen in poisoning.
(c) Softening
(1) Softening seen in – corrosives, especially alkaline corrosives. Areas
involved are (a) mouth (b) throat (c) esophagus (d) cardiac end and (e) greater
curvature of stomach
(2) Disease – If softening is due to disease, it would be limited to the organ
affected, e.g. stomach only
(3) Putrefaction – Softening due to putrefaction (a) begins in most dependent
parts (b) affects all coats of the stomach (c) softened patch is not surrounded
by inflammation.
(d) Ulcers
(1) Liquids generally pass from esophagus to the intestine, via a small ribbon
like passage along the lesser curvature of the stomach (Fig 31.2). This passage
has been called “Magenstrasse“ [German for “stomach street”], and it
constitutes longitudinal mucosal folds along with liquids travel so easily that
they may pass into the intestines within 10 minutes.
(2) Because liquids (including corrosives) preferentially take this path, ulceration
is usually found along the lesser curvature, and the stomach must be opened
along the greater curvature, so these ulcerations can be examined without
cutting through them.
(3) Ulceration beyond the pylorus – usually due to natural disease and not due
to corrosives
(4) Table 26 shows important differences between ulcerations due to corrosives
and disease.
(e) Perforation
(1) Perforation is seen in corrosives [both acids and alkalis]
(2) Commonest with sulphuric acid [Please also see ch 33 “Corrosives”]
(3) Rare with irritant poisons
(4) Table 27 shows differences in perforation due to corrosives and due to pm
autolysis.
(f) Stomach wall
Examine - for fragments of poison adherent to it, e.g. (i) cantharides (ii) capsule
fragments (iii) leaves or fruit fragments (iv) powdered poisons and (v) starch
from tablets.

(g) Contents of the stomach

Note: (i) Color (ii) Volume (iii) Nature of contents [including food]. Contents of
significance may include (a) Capsules (b) Foreign bodies [e.g. glass particles,
nails and pins etc] (c) Leaves (d) other plant matter and (e) Seeds etc. Cells from
plant material may be examined by a botanist [forensic botanist] to identity the
plant. Plant cells retain their characteristic shape, dimensions, surface
ornamentation and other characteristics in the stomach. They can also be
identified from the vomit.
vii. Intestines
(1) Colitis – Colitis of ascending and transverse colon, similar to diphtheric
colitis or enteritis of acute bacillary dysentery is seen in mercury poisoning.
(2) Normal GIT – Rules out poisoning by corrosives, arsenic, mercury and
phenol.

viii. Liver
Hepatotoxic poisons – Please see above – “Classification of Poisons according
to affected target organ”.

ix. Kidneys
Nephrotoxic poisons – Please see above – “Classifi-cation of Poisons according
to affected target organ”.

x. Heart
Subendocardial hemorrhages – in left ventricle seen in poisoning with arsenic,
antimony, phosphorus and viper bite.

xi. Genitourinary system

Criminal abortion – vagina and uterus of females must be examined for
inflammation, corrosion etc. These organs must be sent for chemical analysis.

3. Laboratory analysis

a. Collection of specimens at autopsy

Please see ch 5 – Collection of specimens.

b. Concentration of poison
(1) In the living - Concentration of poison is highest in the portal blood
[because this is the vein carrying ingested substances]
(2) In the dead – Concentration will vary. Causes (i) Uneven destruction of
poison by enzymatic and microbiological activity at different sites (ii)
Postmortem diffusion [please see ch 5] from sites of higher concentration.
c. Precautions in the Dead
(1) Postmortem Diffusion - [ch 5]
(2) Poisons which appear in the body due to putrefaction - [ch 9]

d. Separation of poison from tissue

The first stage of the analytical process involves separation of the drug or
compound of interest from the biological matrix in which it is contained.

4. Experiments on animals
(1) Experiments are performed on animals with the poison recovered from body
as well as from the possession of the accused.
(2) Not an ideal test - Because animals may behave differently to poisons than
humans.
(i) Alcohol - Atrial fibrillation occurs in humans [Holiday heart syndrome] and
rabbits, but not in dogs.
(ii) Atropine - Pigs, goats, sheep, and rabbits are insusceptible to atropine
[belladonna, Hyoscyamus and stramonium]. Horses and oxen are somewhat
more susceptible, while cats, dogs, and birds are sensitive to belladonna.
(iii) Carbon monoxide - Canaries and mice are excessively sensitive to CO and
methane [please see ch 44 for details]
(iv) Opium -Pigeons are not affected by opium
(v) Cats and dogs are affected by poisons much in the same way as man. These
are the best animals to conduct experiments on.

5. Moral and circumstantial evidence

This evidence consists of
1. Motive
2. Possible gain to accused from poisoning his victim
3. Evidence of witnesses [shopkeepers etc] about recent purchase of poison
[purchase of rat poison etc]
4. Behavior of the accused before and after commission of offence
5. Recovery of poison from possession of accused
6. Relationship between accused and victim.

VII. DUTIES OF A MEDICAL PRACTITIONER IN A CASE OF

SUSPECTED POISONING

Duties of a medical practitioner in suspected cases of poisoning are: (1) Medical

(2) Legal.

A. Medical
Includes treatment of the patient (see next chapter for details). If patient is
serious, medical duties will take precedence over legal duties.

B. Legal

1. Information to the police

Information to the police must be given in ALL cases of poisoning whether
suicidal, homicidal or accidental. This applies to both government and private
doctors

2. At the hospital
(1) Routine body fluids – e.g. gastric lavage, blood, saliva, sweat, urine, vomit,
feces, milk etc must be preserved and handed over to the police [please see
above - Diagnosis of poisoning " in the living " lab investigations. Also ch 5 –
“Medicolegal autopsy”, for an exclusive table enumerating all possible body
fluids to be sampled].
(2) Clothes:
(i) Soiled [with vomit, feces etc] etc should be preserved, sealed and handed
over to the police to be sent for chemical examination.
(ii) Unsoiled clothes – especially underwear and other undergarments should
also be sealed and handed over to police. They absorb sweat from which
poison may be detected, especially drugs of abuse.

3. Arrangement for dying declaration

If the doctor feels that the patient may not live, he must arrange for dying
declaration.

4. Information
If the case is of food poisoning, public health authorities must be notified.
 32. General Principles of
Management

I. INTRODUCTION

Treatment of poisoning follows following broad principles (Table 1).

II. IMMEDIATE RESUSCITATIVE MEASURES

1. Remove patient from poisonous environment (removal from scene of fire in

acute CO poisoning).
Memory Aid 1: ABCDE of resuscitation
Airway, Breathing, Circulation, Depression of CNS, Evaluation of patient. All are best done in an ICU.
ABCDE method was first used by Scandinavian physicians in mid-1940s in barbiturate poisoning, with
dramatic success. Looking after the ABCD is now also known as the Scandinavian method of treatment
(especially in barbiturates).
Additional measures:
D also stands for decontamination [Ocular—copious saline lavage; Skin—copious
water, then soap and water; GIT—emesis, lavage], dextrose, dialysis, disability
evaluation and drugs. An additional mnemonic is DEFG "Don’t Ever Forget the
Glucose.

A. Airway
(1) Assessment by (i) Assess protective reflexes (ii) Monitor oxygen saturation
continuously.
(2) If inadequate (i) open up and clean airway [of secretions, vomit etc] (ii)
Endotracheal intubation (iii) Tracheostomy if necessary.

B. Breathing
(1) Assessment by (i) noting if there is adequate tidal volume. (ii) Perform
arterial blood gases (ABG) (iii) Perform capnography [monitoring of the
partial pressure of CO2 or End-Tidal CO2 conc (ETCO2)]
(2) If inadequate: Supplemental O2 therapy [by a mask or by endotracheal
intubation]. Maintain tidal vol at 10-15mL/kg.

C. Circulation
(1) Assessment by (i) Check for presence or absence of radial, femoral, and
carotid pulses. (ii) Start continuous cardiac monitoring [12-lead ECG]
(2) If inadequate (i) Secure IV access (ii) IV fluid administration (iii)
Antidysrrhythmic therapy (iv) Vasoactive agents (v) Consider atropine,
NaHCO3, Mg (vi) CPR – Chest compressions.

D. Depression of CNS
(i) Turn unconscious patient to one side [prevents tongue blocking the throat,
allows fluids to gravitate out]. (ii) Depression of CNS is best evaluated
according to Glasgow Coma Scale (GCS) [Table 2] or Matthew-Lawson Scale
(MLS) [Table 3]. (iii) See pupillary size, reactivity.
E. Evaluation of Patient
Not an immediate resuscitative measure, yet should be done as soon as the
patient is stabilized
(1) Breath sounds - Auscultate (and re-auscultate), particularly after IV fluids
have been given. Helps to diagnose pulmonary edema, acute lung injury
and aspiration pneumonia. If crackles and rhonchi are present, especially if
coupled with an abnormal breath odor (such as seen in hydrocarbons), it may
point to pulmonary etiology rather than cardiac etiology. This is important
because administration of cardiac medications may be dangerous in case of
pulmonary etiology
(2) Heart sounds: (a) Murmurs - in an injection drug user, especially when
accompanied by fever indicate bacterial endocarditis (b) Dysrhythmias –
suggest overdose of cardiac poisons (e.g. digoxin, β-adrenergic antagonists)
(3) Abdominal examination: (a) Enlarged liver – Hepatoxic poisons, chronic
alcoholism (b) Bowel sounds – to diagnose or exclude
cholinergic/anticholinergic toxicity. Helps to decide if purgatives will be
useful, e.g. Lack of bowel sounds " anticholinergic poisoning " purgatives may
not be very useful.
(4) Examination of extremities. E also stands for Elimination of poison, ECG
and Expose [e.g. in cases of toxic gases].
F. Other Measures
(1) Additional – Pl see memory aid below.
Memory Aid 5: Other resuscitative measures in poisoning [besides the ones given in Memory Aid 1]
Other measures are " FGHIJKLMNOP. All of them are not necessarily immediate
resuscitative measures, but are important measures nevertheless.
F-Fluid management, also Fahrenheit (note temperature);
G-Get vital signs, Gastric lavage;
H-Head of toe examination;
I-Imaging [radiopaque poisons "ch 31], Interventions, Inspect back;
J-Jaundice, attend to (for hepatotoxic poisons);
K-Kidney failure, attend to;
L-Laboratory tests;
M-Magnesium hydroxide (cathartic);
N-Narcosis, attend to;
O – Observe, Oxygen
P- Pulse.
Most patients – whether conscious or unconscious- would recover by these measures alone.

(2) Shift patient to a proper environment: Dark and quiet room – (a) because
of photophobia – Datura, Methyl alcohol (b) because of hyperexcitability to
light and sound – strychnine.

III. REMOVAL OF UNABSORBED POISON FROM THE

BODY

A. Inhaled Poisons
In case of inhaled poisons [eg CO, H2S, Cl2 etc]
(1) Fresh air - Remove patient into fresh air.
(2) Air passages - Clear air passages of mucus by postural drainage or
aspiration.
(3) Endotracheal intubation if necessary.
(4) Artificial respiration and O2 [6-8 L/min]
(5) If bronchospasm present [as in irritant gases]:
(i) Aminophylline 250-500 mg, slow IV
(ii) Inhaled b2 agonist
(iii) Oral or parenteral corticosteroids
(6) Diuretics – if pulmonary edema is threatening.
(7) Monitor for respiratory distress.
(8) If cough or difficulty breathing develops, evaluate for respiratory tract
irritation, bronchitis, or pneumonitis.

B. Injected Poisons
In case of injected poisons (insect and snake bite, scorpion stings, drug abuse,
iatrogenic injection):
(1) Reassurance - Calm the patient. Reassure. Sedatives may be required.
(2) ABCDE - Monitoring patient’s ABCs (please see above)
(3) Shock - Treat shock
(4) Allergies - Observe patient for allergic reaction. Treat anaphylactic reactions
on standard lines.
(5) Remove sting – In case of bee, wasp, scorpion or centipede stings.
(6) Local vasoconstriction – adrenaline injection around injected area. Apply
ice locally or immerse injected part (finger etc) in cold water [10°C]
(7) Tight ligature above injection site, wound excision, sucking out poison with
mouth, local neutralization of poison with suitable chemicals are no more
recommended now.

C. Contact Poisons

1. Eye
(1) Irrigate exposed eyes with copious amounts of room temperature water for at
least 15 min
(2) Remove contact lenses if present.

2. Skin
(1) Remove contaminated clothing and wash exposed area thoroughly with soap
and water [for about 30 minutes]. Same procedure if poison applied to wound,
or is inserted into urinary bladder, rectum or vagina
(2) Remove jewellery if present.
D. Ingested Poisons

1. Emesis
An emetic is a substance that induces vomiting when administered orally or by
injection. Emesis is virtually obsolete now. May come in handy when nothing
else is available.
Salient features:
(1) When used:
(i) if there is difficulty in obtaining or using stomach tube
(ii) if vomiting center is still functional and responsive to emetics
(2) Position - During induction, the person must either be sitting or lying on his
side, which the head dependent; otherwise there is danger of inhaling gastric
contents
(3) Mechanically induced – by tickling throat [patient’s own fingers, doctor’s
fingers, feather, spoon handle, wooden tongue depressor]. Usually ineffective.
(4) Pharmacologically induced – All emetics considered obsolete now by many
authorities. Last to fall out of favor was ipecac in late 1990s. Many others
however continue to use it; for this reason emetics find mention in subsequent
chapters. (i) Ipecac – (a) Source – Root of a small shrub Cephaelis
ipecacuanha [syn Cephaelis acuminata]. Native to Brazil; In India grows in W.
Bengal. (b) Preparations – (I) ipecacuanha powder 1-2 g (II) Syrup of ipecac –
30 ml [adults]; 15 ml [children 1-12 y]; 10 ml [9-12 m]; 5 ml [6-9 m].
Administer several glasses of water afterwards. Induces vomiting in 90-95%
cases within 30 min. Dose is repeated if vomiting does not occur by this time.
(c) Active principles – Cephaeline, Emetine, Psychotrine [traces] (d)
Mechanism - (I) Central – stimulation of vomiting center (II) Peripheral –
stimulation of sensory receptors in GIT. (e) Current status – Although very
popular up to the final years of 20th c, no more recommended now. Reasons
(I) No evidence of clinical benefit (II) Poison removed is highly variable and
diminishes with time. (III) Reduces effectiveness of established and useful
therapies [activated charcoal, oral antidotes, Whole Bowel Irrigation]. (IV)
Adverse effects [cardiotoxicity, complications of emesis] (V) May be harmful
if administered to a patient who has a .ed level or impending loss of
consciousness. (VI) abuse by bulimics (VII) use as an agent for Munchausen’s
syndrome by proxy. (ii) Obsolete since long (a) Apomorphine - Not effective
 orally; must be given parenterally [s/c] (b) Copper sulfate (c) Hand
dishwashing liquid detergent. Its use was recommended only when time was
critical, and nothing else was available. (d) mustard water (e) Saturated soln of
common salt – causes fatal hypernatremia (f) Tartar emetic (g) Zinc sulphate.

a. Contraindications
(1) Same as those for gastric lavage [eg hydrocarbons having a high aspiration
potential, corrosives]
(2) Active or prior vomiting [eg nicotine]
(3) Ingestions that can alter mental status [coma]
(4) Exposure to a toxin with more pulmonary toxicity from inhalation than
toxicity from GI absorption [e.g., hydrocarbons]
(5) Poisons inducing seizures.
(6) Tricyclic antidepressants, emesis in contraindicated [although gastric lavage
may be done]
(7) If need for advanced life support within 60 min is anticipated.
(8) Debilitated, elderly patients
(9) Medical conditions that may be further compromised by induction of emesis
[heart disease, pregnancy].

b. Adverse effects
(1) Aspiration
(2) Boerhaave syndrome [Esophageal rupture]
(3) Coma
(4) intractable vomiting
(5) Mallory-Weiss syndrome [bleeding from tears in the mucosa at the junction
of the stomach and esophagus]
(6) Seizures.

2. Gastric lavage

a. Disadvantages
(1) May delay administration of activated charcoal, which is a more useful
procedure
(2) May push tablets further into the GI tract. In general, gastric lavage is better
 than emesis because of more discomfort caused to the patient in vomiting.

b. Procedure
Tubes used - are: (a) Ewald’s tube [devised by Carl Ewald (1845 - 1915) a
German gastroenterologist] [Fig 32.1], (b) Boas tube [devised by Ismar Boas
(1858 –1938) a German gastroenterologist, and quite similar to Ewald’s tube],
(c) Edlich tube [Fig 32.2] [devised by Richard Edlich (1939)]or (d) a Lavacuator
[Fig 32.3].
Ewald’s tube
(i) Diameter and length - A standard Ewald’s tube is 1 cm in diameter and 150
cm in length, with a funnel (1) attached at one end. (ii) The other end is rounded
(2) with lateral openings (3) (iii) Mark - There is a mark (4) 100 cm from the
funnel end and 50 cm from distal end (2) indicating the level up to which the
tube should be introduced. (iv) Suction bulb - At about the midpart of the tube,
there is a suction bulb (5) which is used to pump out the stomach contents. (v) A
wooden mouth gag (6) comes along with it. It has a hole (7) in the middle to
allow for the passage of the tube through it. One end of the gag is pointed (8) so
that it can forcefully be inserted by the side of the mouth in uncooperative
patients (vi) Size – Comes in different sizes, which are measured by F scale. “F”
stands for French scale, each unit on the French scale being equal to 0.3 mm.
The largest orogastric lavage tube that can reasonably be passed should be used
(1) Position of the patient - The patient should be on his left side or prone, with
head hanging over the edge of the bed, and face down. Patient is kept in
 Trendelenburg position [mouth is at a lower than feet to prevent
regurgitation of fluid leaking out through the sides of tube]. Face is supported
by an assistant. Trendelenburg position was first advocated by the German
surgeon Friedrich Trendelenburg [1844 –1924] in the 1860s. In the classic
Trendelenburg position the feet are higher than the head by 15-30°.
(2) Introduction of the tube - (a) If dentures are present they must be removed
(b) wooden mouth gag is placed in between teeth, so teeth do not bite tube (c)
end of tube is lubricated with glycerine, olive or sweet oil or paraffin (d)
Tongue is depressed with tongue depressor [or two fingers] (e) Lubricated
tube slowly passed downwards through the pharynx and esophagus into the
stomach, till the 50 cm mark is reached. (f) If there are no marks on the tube –
Measure distance between bridge of nose and tip of xiphoid process. The tube
should be passed for the same distance (g) Precautions – Do not use force.
(3) Confirmation of the tube in stomach – (a) Absence of coughing and of
breath sounds in the funnel will confirm that the tube has not entered trachea
(b) In case of doubt – insert free end of the tube, just below water surface. Air
from stomach is usually expelled completely in 2-3 expirations. Air from
lungs causes bubbling at each expiration.
(4) Lavaging the stomach – (a) Preserve first sample for chemical analysis:
(i) Pass about 250 cc of plain warm water through the funnel, held high above
the head
(ii) When funnel is empty, pinch tube just below the funnel between finger and
thumb
(iii) Lower it below the level of stomach
(iv) Release finger and thumb to relieve blockade
(v) contents will be emptied by siphon action
(vi) Preserve this sample for chemical analysis. This solution must be handed
over to police in all cases of poisoning [suicidal, homicidal or accidental,
and whether the doctor is govt or private] [Please also see ch 31, under the
heading “Information to police”]. (b) Precautions – Stop the procedure, if
there is any bleeding (c) Subsequent washings with lavage fluid - Normal
saline (50 to 100 mL in young children and 150 to 200 mL in adolescents)
is then introduced [or any other suitable lavage fluid - Table 4] and lavaged
repeatedly.
(5) Indication to stop lavage – (a) Stop when the returning fluid is clear,
 odorless, and is of the same nature as the fluid introduced. This indicates that
there is no further interaction between the poison and antidote (b) In case of
KMnO4, the returning fluid is initially colorless, because KMnO4 oxidizes
poisons and in the process itself gets reduced to colorless compounds. Lavage
should be stopped when the returning fluid has pink color (the color of normal
KMnO4).
(6) Late lavage useful in:
(i) Poisons causing .ed gastric motility or pyloric spasm – (a) Antihistamines (b)
Barbiturates (c) morphine (d) Phenothiazines (e) Tricyclic antidepressants
(ii) Poisons which cake together forming a doughy mass [it sticks to stomach
walls] (a) salicylates.
c. Contraindications
Contraindications of gastric lavage are [A] Absolute (i.e. must not be done
under any circumstances) and [B] Relative (i.e. Should not be done normally,
but may be done after taking precautions). [A] Absolute: (1) Corrosives -
because of risk of perforation. Exceptions are organic acids like (i) Carbolic acid
[stomach wall becomes thick and leathery] (ii) Oxalic acid and (iii) Acetic acid
etc [if patient is seen early and corrosion of stomach wall is not great]. (2)
Nontoxic ingestions (3) Sharp and pointed material ingestions – pins, needles,
glass – risk of perforation[B] Relative: (1) Cardiac arrhythmias (2) Children
(below toddler age group) " relative contraindication, because stomach wash
tube is too thick. Can be done with Ryle’s tube, or a number 10 to 12 French
catheter (3) Coma " because airway protective reflexes are suppressed; may
cause aspiration. Can be done with a cuffed endotracheal tube in place (4)
Convulsant poisonings (e.g. strychnine) " because it can exacerbate
convulsions. Convulsions need be controlled first (5) Esophageal varices –
Look for accidental rupture (6) Hemorrhagic diathesis – may cause bleeding
(7) Hypothermia " body temperature would need careful attention (8) Kerosene
poisoning " aspiration of kerosene in the respiratory tract setting up fulminant
chemical pneumonitis. Can be done with a cuffed endotracheal tube (9) Late
arrival of patient – Generally after 3 hours, the recovery of poison is none or
very little. Poisons in which late gastric lavage is useful (a) Poisons which cause
pyloric spasm or reduce GIT motility: (i) Anticholinergics (ii) Morphine, (iii)
Tricyclic antidepressants (b) Poisons which cake together forming a thick mass -
(i) salicylates (10) Poison having an effective antidote (11) Pregnancy
[advanced] "- intraabdominal pressure may be harmful for child (12) Surgery
[recent] " Risk of opening up of sutures (internal or external) (13) Volatile
poisons " eg gasoline, lighter fluid. Can cause aspiration pneuomonitis. Use
cuffed endotracheal tube to prevent aspiration (14) Vomiting [severe] " Poison
already expelled.

d. Complications
(1) Aspiration pneumonia [most dangerous. If it occurs, administer (a)
hydrocortisone 3-4 mg/kg IV (b) O2 (c) Broad spectrum antibiotics] (2)
Bradycardia (3) Cardiac arrhythmias and cardiac asystole - Due to vagal
stimulation and hypoxia during gastric lavage. (4) ECG changes – ST elevation
(5) Epistaxis (6) Hypochloremia (7) Hyponatremia (8) Hypoxia and hypercapnia
(9) Laryngospasm (10) Mallory-Weiss syndrome [esophageal tear] (11)
Mechanical injury to the throat, esophagus, and stomach (12) Metabolic
alkalosis [ch 31] (13) Perforation (14) Water intoxication [ch 45]. Combative
patients may be at greater risk of complications.

3. Cathartics
According to current thought, cathartics should never be considered part of
routine management of poisoning. Following principles must be kept in mind
(1) Poison adsorbable by AC - If poison is adsorbable by activated charcoal
(AC), a cathartic given with AC is as efficacious as AC alone
(2) Poison not adsorbable by AC - If poison is not adsorbable by AC, whole
bowel irrigation (WBI) [please see below] is better than cathartics
(3) When cathartics may be given – When facilities and expertise for WBI are
not available. In such cases, use if
(i) Sustained release preparations have been ingested
(ii) Poison not adsorbable to AC
(iii) large amounts of poison has been ingested
(iv) desorption from AC is a possibility (as with aspirin).
(4) Cathartics used:
(i) Magnesium citrate 6% soln 150-300 mL orally
(ii) Sorbitol. Given with the first dose of AC.
(5) Cathartics not to be used: (i) MgSO4. May produce CNS depression in
cases of renal failure.

4. Whole bowel irrigation (WBI)

Whole bowel irrigation (WBI) flushes out the entire GIT in 4-6 hours. It was
originally developed to cleanse the large bowel before surgery or colonoscopy.
Initially a solution of NaCl, KCl, and NaHCO3 was used but it was absorbed by
the body, leading to complications. This gave rise to specialized irrigation fluid
(polyethylene glycol) that is not absorbed. Induces a liquid stool.

a. Procedure
WBI involves rapid administration of large volumes of PolyEthylene Glycol-
Electrolyte Lavage Solution (PEG-ELS) [GoLYTELY, CoLyte, MoviPrep]
via a nasogastric tube, while the patients sits on a toilet seat. The solution is
administered at a rate of 500 mL/h in children and 2000 mL/h in adolescents and
adults. The procedure continues until the rectal effluent is clear. If patient
vomits, infusion must be slowed down or an antiemetic given.

b. Indications
Should not be used routinely in poisoning situations. Usually reserved for
patients
(1) who have ingested toxic doses of medications not adsorbed by activated
charcoal (such as lithium, heavy metals)
(2) toxic ingestions of sustained-release or enteric-coated drugs or
(3) body packing/stuffing (cocaine body packer syndrome).

c. Contraindications
(1) Bowel perforation (2) Bowel obstruction (3) Clinically significant
gastrointestinal hemorrhage (4) Ileus (5) Unprotected compromised airway (6)
Hemodynamic instability (7) Uncontrollable intractable vomiting.

IV. REMOVAL OF ABSORBED POISON FROM THE BODY

A. Diaphoretics
(1) Diaphoretics are drugs that - sweating.
(2) It is controversial if they - poison elimination through sweat.
(3) Common diaphoretic agents are: (i) Alcohol (ii) antipyretics (iii) Blankets
(iv) Hot beverages (tea, coffee, milk, lemonade) (v) Hot water bottles (vi)
Pilocarpine nitrate (5 mg s/c) (vii) Salicylates.

B. Enhanced Renal Excretion

Large amounts of fluid are given (forced diuresis). Method is much like flowing
buckets of water from top of stairs to clean them.

Dangers and pitfalls

Can cause pulmonary and cerebral edema.

C. Urine Alkalinization
[A] Urine alkalinization is a treatment regimen that - es poison elimination by
the administration of IV sodium bicarbonate to produce urine with a pH ≥ 7.5.
[B] Principle: (1) Uncharged ions can freely pass through biological
membranes, while charged ions cannot (Fig 32.5). (2) If a poison molecule is in
uncharged form, whatever molecules are filtered by glomeruli, would diffuse
back in the system. Poison molecules in charged form would be retained within
the tubules. (3) Normally a drug in the urine is both in ionized and unionized
forms. As pH of urine changes, the ratio between the two species changes. At its
pKa, the drug is 50% ionized (Fig 32.6).
(4) An acidic drug would be ionized more in an alkaline urine and vice-versa. (5)
If we want an acidic drug not to cross the tubule (in order to - elimination), we
must alkalinize the urine; reverse (acidification) should be done in case of
alkaline drugs. [C] Drugs/poisons in which urine alkalinization is useful: (1)
Barbiturates, eg. Phenobarbitone [ch 40] (2) Salicylates [ch 45] (3) 2-4
Dichlorophenoxyacetic acid [2-4D]- A herbicide [widely used by national Govts
to destroy illegal poppy plants] (4) Mecoprop (MCPP) – A selective hormone
type phenoxyherbicide [Please see more on this in chapter on agricultural
poisons] (5) Chlorpropamide (6) Diflunisal (7) Fluoride (8) Methotrexate (9)
Formate. (10) During BAL therapy – because BAL-metal complex dissociates
in acidic urine (11) In poisons causing rhabdomyolysis [eg nicotine]-helps
minimize risk of myoglobin-induced kidney damage.
Memory Aid 6: Urine alkalinization is useful in
(A) Most imp
Bed Side Dialysis in an M C D hospital
(1) Barbiturates (2) Salicylates (3) 2-4D (4) Mecoprop (5) Chlorpropamide (6) Diflunisal
Even among these 6, top 3 are most imp for student.
(B) Others
Forensic Medicine For Best Resident
(7) Fluoride (8) Methotrexate (9) Formate (10) BAL therapy (11) Rhabdomyolysis

[D] Goal – Normal pH of urine = 6.0. Goal in urine alkalinization is to achieve

urine pH of ≥ 7.5. Goal in urine acidification is to achieve urine pH of = 5.0.
[E] How to achieve alkalinization : (i) By giving NaHCO3 1-2 mEq/kg every 3-
4 h. [F] Urine output – Normal urine output in a 60 kg man is 1 ml/kg/hr. In
urine alkalinization it - s to 3-6 ml/kg/hr. [G] Contraindications to urine
alkalinization: (1) Congestive heart failure (2) renal failure (3) cerebral edema.

D. Urine Acidification
Also known as forced acidic diuresis. Principle same as above.
Memory Aid 7: Urine acidification is useful in
(A) Most imp - MAP
(1) Methadone
(2) Amphetamine
(3) Phencyclidine (PCP)
(B) Others – Comfortable questions are simply never asked
(4) Cocaine
(5) qu inine
(6) quinidine
(7) sympathomimetics
(8) Nicotine [theoretically beneficial, but almost never carried out because of risks – ch 43]
(9) Strychnine

How to achieve acidification

By giving IV ascorbic acid or ammonium chloride 1-2 g every 4-6 h.

E. Hemodialysis (HD)
Hemodialysis is a method for removing metabolic wastes as well as free water
from the blood when the kidneys are in renal failure. Hemodialysis was first
used in 1913 for the removal of salicylic acid in experimental poisoning, but was
not tried clinically until 1950 when it was used for the treatment of aspirin
poisoning. Since then it has been used on a considerable scale.
Salient features:
(1) Hemodialysis is one of three major renal replacement therapies, the other two
being renal transplant and peritoneal dialysis.
(2) Hemodialysis is useful in:
Memory Aid 8: Hemodialysis is useful in
(1) Mnemonic 1 – BLAST [B:Barbiturates, Boric acid, Bromides; L:Lithium; A:Alcohols (methyl, ethyl,
isopropyl etc); S:Salicylates, strychnine; T:Theophylline, thiocyanates]
(2) Mnemonic 2 - I STUMBLE [Isopropyl alcohol; Salicylates; Theophylline; Uremia; Methanol;
Barbiturates; Lithium; Ethylene glycol/Ethanol].
Memory Aid 9: Hemodialysis is not useful in
ABCD GOMP
A: Anticholinergics, antidepressants, antihistaminics
B: Belladona alkaloids, benzodiazepines
C: Chloroquine
D: Digitalis
G: Glutethimide
O: Opiates (morphine, heroin etc)
M: Methaqualone
P: Paracetamol, phenothiazines (antipsychotics)

F. Peritoneal Dialysis (PD)

Peritoneal dialysis (PD) is a procedure in which patient’s peritoneum is used as
a membrane across which toxins in the blood are exchanged.
Salient features:
(1) Procedure – The patient’s peritoneal membrane (A) serves as the
semipermeable barrier between the blood (in the peritoneal capillaries) and a
balanced dialysate solution (B). The dialysate is introduced into the patient’s
peritoneal cavity from a solution bag (C) through a catheter (D) and allowed
to dwell for a period of hours. A 3-way valve (E) allows the dialysate to go
into the peritoneum and then drain out into the drainage bag (F). The osmotic
gradient pulls toxins from the intravascular space into the dialysate.
(2) Dialysate used – For adults – 2L. For children <5 y – 200 ml
(3) Effectiveness – about 25% of that of hemodialysis
(4) Poisons effectively removed by PD: (i) Alcohols (ii) Barbiturates [long
acting] (iii) Bromides (iv) Chloral hydrate (v) Lithium (vi) Mercury
[inorganic] (vii) Quinidine (viii) Salicylates (ix) Sodium chlorate (x)
Theophylline.
G. Hemoperfusion (HP)
Hemoperfusion is a procedure in which large volumes of patient’s blood are
passed over an adsorbent substance in order to remove toxic substances.
Salient features:
(1) It is an extracorporeal form of treatment because the blood is pumped
through a device outside the patient’s body.
(2) Sorbents most commonly used - resins and activated charcoal [charcoal
hemoperfusion].
(3) Hemoperfusion is useful, even with highly protein bound substances, that
 have a high volume of distribution (Vd) and are lipid soluble (acetaminophen,
barbiturates, carbamazepine, digitalis, ethchlorvynol, glutethimide,
meprobamate, methaqualone, methotrexate, paraquat and theophylline).

V. ADMINISTRATION OF ANTIDOTES

According to the International Programme on Chemical Safety definition, an

antidote (Gk antididonai, “given against”) is a therapeutic substance used to
counteract the toxic actions of a specified xenobiotic.

A. Classification of Antidotes

1. Classification based on site of action

Antidotes may counter poisons
(1) when they are within the GIT
(2) when they are in the blood
(3) when they are acting on the target cells (Table 5, Fig 32.8).
a. Mechanical or physical antidotes
Mechanical or physical antidotes work mechanically on poisons within the
GIT. They are classified as
(1) Adsorbents – which adsorb poisons on to their surface [eg activated
charcoal]
(2) Demulcents - prevent their absorption by making a protective coating on
stomach wall [milk, ghee, oil, butter]
(3) Diluents – Dilute the poison rendering them ineffective [eg plain water,
bulky food]. Some antidotes may work in more than one way, eg. milk may
act as a demulcent as well as a diluent.

i. Adsorbents
Adsorbents are antidotes which adsorb poisons onto their surfaces [ex –
Activated charcoal, Bentonite [particularly calcium bentonite, which is also a
major constituent of fuller’s earth (Multani Mitti)]. Fuller’s earth [Fuller’s earth
was once used by fullers (workers who cleanse clothes -particularly wool- to
eliminate oils, dirt, and other impurities. The process is known as “fulling”. In
clinical toxicology it is mainly used for paraquat poisoning (ch 35)]. Most
important adsorbent is activated charcoal [syn Activated carbon, Activated coal,
AC, Medicinal Carbon, Medicinal Charcoal]. It is a form of carbon that has been
processed to make it extremely porous and thus to have a very large surface area
available for adsorption of poisons.
Salient features:
(1) AC is typically given after gastric lavage.
(2) It is considered to be the single most effective antidote available today.
(3) Dosage - The usual adult dose 50-100 g mixed in about 250 ml of water. The
pediatric dose is 1 g/kg.
(4) Drugs not well adsorbed (as well as some contraindications to AC) are given
in Table 6 and Table 7.

(5) Mechanism of action: (i) Adsorbs toxic substances, thus inhibiting GI

absorption (ii) For selected drugs - es clearance by interfering with
enterohepatic recycling (iii) By lowering intraluminal concentration of poison
in the GIT, AC creates a concentration gradient between the blood and bowel
fluid. This - es the flow of poison from the blood into GIT, a process known as
gastrointestinal dialysis or gut dialysis. (iv) the addition of sorbitol results in
hyperosmotic laxative action causing catharsis
(6) Palatability – Black and gritty nature of AC makes it unacceptable to
patients, especially children. This problem is overcome by giving it with
flavoring agents e.g. chocolate and cherry syrups, ice creams and sherbets.
(7) Adverse effects: (i) Gastrointestinal: (a) Black tongue and stools (b)
Constipation (c) intestinal obstruction (d) Vomiting (e) diarrhea (ii) Ocular: (a)
Corneal abrasions (iii) Respiratory: (a) Aspiration pneumonitis
(8) Contraindications: (i) Intestinal obstruction (ii) Perforation (iii) Patients at
risk of hemorrhage or GI perforation [please also see Table 7]
(9) Multiple Dose Activated Charcoal (MDAC) – MDAC is administration of
50 g of AC every 6 hours for 3 days.

ii. Demulcents
Demulcents (Latin demulcere, “caress”) are substances that form a protective
film over gastric mucosa, preventing entry of poison to the systemic circulation.
Salient features:
(1) Ex. aluminum hydroxide gel, egg white, fats, milk, milk of magnesia, oils,
starch.
(2) Precautions – Fats and oils dissolve fat soluble poisons and may - their
absorption. They should thus not be used in fat soluble poisons such as
acetone, aniline, CCl4, DDT, kerosene, OP, phenol, phosphorus and turpentine.

iii. Diluents
Dilute the poison and reduce its effectiveness. Ex. Boiled mashed potato, boiled
rice, boiled vegetables, halwa. Bulky food is particularly useful in ingestion of
powdered glass.

b. Chemical antidotes
Chemical antidotes neutralize the poisons chemically within the GIT. Ex
(1) Acids - neutralize alkalis. Weak solutions should be given eg Canned fruit
juice, Lemon juice, Vinegar. Neutralization of acids with strong alkalis and
vice-versa must be avoided, because the antidote may itself be injurious and
strong exothermic reactions cause further injury. Sodium carbonate and
bicarbonate to neutralize acids are avoided because of excessive release of
CO2, which may cause perforation of the weakened stomach walls.
(2) Albumen - Found in egg white. Can be given in mercuric chloride poisoning
[forms insoluble mercury albuminate] and Cu poisoning [forms insoluble
copper albuminate]
(3) Alkalis – Neutralize acids. Weak solutions should be given. Ex: Alkaline
hydroxides, e.g. (i) magnesium hydroxide (ii) calcium hydroxide [Ca(OH)2;
slaked lime] is a white powder obtained when calcium oxide [CaO; lime or
quicklime] is mixed, or “slaked” with water. Also called hydrated lime,
builders lime, slack lime, cal, or pickling lime. For medicinal use slaked lime
is sweetened [saccharated lime] for ease of ingestion. It may be given against
many acids.
(4) Common salt - May be given for silver nitrate poisoning. Forms insoluble
silver chloride.
(5) Copper sulfate - Was once given for phosphorus poisoning. Forms insoluble
cupric phosphide. Not used now.
(6) Dialysed iron – was once given for arsenic poisoning because it forms
insoluble ferric arsenite with arsenic salts. Not used now.
(7) Dicobalt edetate – chemically combines with cyanides
(8) Freshly prepared hydrated ferric oxide [Fe2O3]- was once given in arsenic
poisoning because it forms insoluble ferric arsenite with arsenic salts.
(9) Iodine - A soln of tincture iodine or Lugol’s iodine 15 drops added to half a
glass of warm water precipitates most alkaloids [eg quinine, strychnine etc],
lead, mercury and silver
(10) KMnO4 :
(i) Potassium permanganate in 1:5000 conc [Condy’s lotion] is a strong
oxidizing solution.
(ii) Useful in (a) Atropine (b) Barbiturates (c) Cyanides (d) Hydrocyanic acid (e)
Opium and its derivatives (f) Phosphorus and (g) Strychnine.
(iii) It oxidizes poisons [rendering them inactive], and in the process gets
reduced itself [loses its pink color]
(iv) Thus the stomach wash must be continued till the solution coming out is of
the same pink color as that of the solution introduced
(11) Tannic acid - 4% soln or tannin [strong tea] precipitates aconite,
apomorphine, cinchona, cocaine, metals [aluminum, cobalt, copper, lead,
mercury, nickel, silver, zinc], nicotine, pilocarpine and strychnine.

c. Chelating agents
Chelating agents (chelants) [Latin chela, claw; because they grip poison as if in
a claw] are chemicals that form soluble, complex molecules (chelates) with
metal ions, inactivating them so that they cannot react with other elements (may
act within GIT too).
Salient features:
Characteristics of an ideal chelating agent: (i) Ability to compete with natural
chelators, eg strong intracellular binding of cadmium to metallothionein
prevents most chelating agents from removing it from this natural chelate. (ii)
Complexes formed should be non-toxic (iii) Distribution - Same as that of metal
(iv) High affinity for toxic metals but low for essential metals (v) High water
solubility (vi) lipid solubility. (vii) minimal toxicity (viii) good absorbability
from the GIT (ix) Rapid elimination of the toxic metal.

i. BAL
BAL [British anti-Lewisite, Dimercaprol], is a compound developed by the
British at Oxford University during World War II.
Salient features:
(1) BAL has 2 unsaturated –SH groups, which combine with arsenic, rendering it
ineffective.
(2) Dose – BAL comes as a yellow, viscous, oily liquid with a disagreeable
sulphurous odor. Available as 3-mL ampules containing 100 mg/mL of BAL,
200 mg/mL of benzyl benzoate and 700 mg/mL of peanut (arachis) oil. Since
 it is oily it must be injected deep IM (gluteal region). IV infusion causes fat
embolism. Aqueous solutions are easily oxidized and therefore unstable.
Peanut oil stabilizes BAL. Benzyl benzoate makes BAL miscible with oil. The
dose is 3mg/kg every 4 hours for 48 hours and then twice daily for 10 days.
(3) Indications – Pl see below.
Memory Aid 12: Indications of BAL
Mnemonic 1 - BAL is primarily used in MAL - Mercury, Arsenic, Lead

Mnemonic 2 - A B C Gets Thumping Majority

BAL is also in several other heavy metals eg Antimony, Bismuth, Copper, Gold and Th alliuM

(4) Contraindications: (i) Cadmium - Cadmium is primarily a nephrotoxic

poison and BAL - es the uptake of cadmium in kidneys, thus - ing its
nephrotoxicity. (ii) Iron poisoning – must be avoided because BAL-iron
complex causes severe vomiting and - s metal chelation by other chelators. In
other metal poisonings, iron supplements must not be given for the same
reason. (iii) Organic Hg [eg Methylmercury] because causes redistribution
of organic Hg to brain, - ing its toxicity (iv) Hepatic dysfunction (v) peanut
allergy (because BAL is formulated in peanut oil)
(5) Precautions: (i) Alkalinize the urine – Must be done because BAL-metal
chelate dissociates in acidic urine (ii) Use with caution in G6PD deficiency –
causes hemolysis (iii) May cause deficiency of essential metals like zinc.

ii. BAL analogues

(a) DMSA
DMSA (2,3-DiMercaptoSuccinic Acid, Succimer, Chemet) was synthesized in
1949 in England.
Salient features:
(1) Both DMSA and DMPS are water soluble analogs of BAL.
(2) Used primarily for MAL (Mercury, Arsenic, Lead).
(3) In combination with EDTA, it is very effective.
(4) Its advantages over BAL and CaNa2EDTA are: (i) Can be orally
administered (ii) does not . levels of essential trace metals such as Zn (iii)
toxicity is less (iv) Fe can be co-administered (v) can be used in G6PD
deficiency (vi) Superior to CaNa2EDTA in Pb poisoning as it does not
redistribute Pb to the brain (vii) can be used in methylmercury.
(5) Dose – Succimer is available as 100-mg bead filled capsules. If capsule can
not be swallowed, it is separated and beads sprinkled over juice or ice-cream
and ingested. Dose is 10mg/kg tds # 5 days, followed by same dose bd # 14
days.
(b) DMPS
(1) DMPS (2,3-DiMercapto-1-Propane Sulfonic Acid, Dimaval, Unithiol) has
same indications as DMSA.
(2) Dosing regimen is same as DMSA, except that 12.5mg/kg is used.

iii. Calcium Disodium Edetate [CaNa2EDTA]

Calcium Disodium Edetate [syn. Edetic acid, EDTA,
Ethylenediaminetetraacetic acid, Versene] is capable of chelating many metals
[cadmium, cobalt, copper, iron, lead, mercury, and nickel], but is currently used
almost exclusively for lead poisoning.
Salient features:
(1) Mechanism - CaNa2EDTA combines with lead, to form a stable, soluble,
non-ionized compound which is subsequently excreted in the urine.
CaNa2EDTA - s urinary lead excretion 20-50 fold.
(2) Availability – Available in 5-mL ampules containing 200 mg of CaNa2EDTA
per mL (1 g per ampule).
(3) Administration - (a) Route - IM administration causes pain. So given by IV
infusion in a conc of 0.5% over 24 hours [in 5% dextrose or 0.9% NaCl]. (b)
Dose - 1500 mg/m2/d in adults; 1000 mg/m2/d in children. (c) Concentrations
> 0.5% may lead to thrombophlebitis and should be avoided. (d) CaNa2EDTA
is incompatible with other solutions.
(4) Contraindications - Anuria, hepatitis, renal disease.
(5) Precautions: (i) Lead encephalopathy and cerebral edema – patients may
experience a lethal - in intracranial pressure following IV infusion; the IM
route is preferred for these patients. Co-administration of BAL is useful. In
cases where the IV route is necessary, avoid rapid infusion. The dosage
schedule should be followed and at no time should the recommended daily
dose be exceeded.

iv. D-Penicillamine (DPA)

D-Penicillamine (Cuprimine, Depen) is a metabolite of penicillin, having no
antibiotic properties.
Salient features
(1) L-isomer - L-penicillamine is toxic (it inhibits the action of pyridoxine; may
produce optic neuritis), and is thus never used.
Memory Aid 13: Indications of D-Penicillamine
D-Peni ci l lam ine is useful against
1. copper, 2. lead and 3. mercury.
2 more indications are remembered by
Pencil is used as Zip GuN in India
It can be decoded as:
Pencil lamine is used in
4. Zinc
5. Gold
6. in chronic exogenous Cu poisoning, such as Indian childhood cirrhosis.
7. Some Non toxic conditions, eg cystinuria, rheumatoid arthritis, scleroderma, Wilson’s
disease (due to disorder of copper metabolism). Mnemonic – Wilson's disease is a C
UR SE.
(i) in chronic exogenous copper poisoning, such as Indian childhood cirrhosis.
(ii) some non toxic conditions [Wilson’s disease (due to disorder of copper
metabolism) cystinuria, rheumatoid arthritis and scleroderma].
(2) Dose – 30mg/kg body wt up to a total of 2 g/day in 4 divided does orally for
7 days.
(3) N-Acetyl-D-Penicillamine (NAPA): (i) It is another penicillin metabolite –
Useful in Hg. (ii) Dose – 1-2 g/day orally.

v. Deferoxamine
Deferoxamine [syn, desferrioxamine B or DFO] is a bacterial siderophore
produced by the actinobacter Streptomyces pilosus.
Salient features:
(1) The mesylate salt is commercially available.
(2) Useful – in acute iron poisoning.
(3) Availability – Deferoxamine mesylate (Desferal) is available in two vial
sizes containing either 500 mg or 2 g sterile, lyophilized powder. Adding 5 or
20 mL of sterile water for injection to either the 500-mg or the 2-g vial,
 respectively, results in a 100 mg/mL solution.
(4) Dose - (a) Oral – 5-10 g/day (b) IM - 1 g initially, followed by 0.5 g 4 and 8
hours later and then every 4-12 hours as necessary. Total up to 6 g in 24 hours.
(c) IV – Given only for patients in shock. 1 g at a rate of 15 mg/kg/h, followed
by two 0.5 g doses every 4 hours. Total up to 6 g in 24 hours. These
recommendations for total dosages are not scientifically developed and are
based on arbitrary assumptions.
(5) Effectiveness – 1 mole of DFO binds 1 mole of Fe3+; therefore 100mg DFO
binds 8.5mg Fe3+.

d. Serological antidotes [immunotherapy]

(1) Antisnake venom,
(2) Antispider venom
(3) Fab therapy for digitalis [ch 43] and PCP [ch 46]
(4) Immunotherapy for As [ch 36].

e. Physiological or pharmacological antidotes

Physiological or pharmacological antidotes work at the target cell by producing
pharmacological effects exactly opposite to those produced by poison. Also
known as dynamical antidotes.
Salient features:
(1) Act on principle of antagonism
(2) Action is mostly partial
(3) Their use is limited and somewhat dangerous
(4) Used after poison has been absorbed in circulation
(5) Ex - (i) Analeptics against barbiturates - Analeptics (Gk analeptikos,
restorative, strengthening) are arousal agents which include proconvulsants
(picrotoxin, strychnine, pentylenetetrazol, camphor), sympathomimetics
(amphetamines, methylphenidate), Xanthines (caffeine, ethamivan), and
nonspecific stimulants (nikethamide, bemegride, prethcamide, amiphenazole).
They were once recommended against barbiturates, but are no more
recommended. (ii) Amyl nitrite against cyanide (iii) Barbiturates against
amphetamine, picrotoxin and strychnine (iv) Physostigmine against atropine
Table 8 gives some common antidotes and poisons against which they are
used.
VI. ADJUNCTIVE THERAPIES AND SYMPTOMATIC
TREATMENT

Done on general well-accepted lines. Treat (1) Anxiety and Agitation (2)
Allergic Reactions (3) Cardiac arrhythmias (4) Cerebral edema and -ICP (5)
CNS Depression [Coma] – Give coma cocktail.
Memory Aid 14: Composition of coma cocktail
DNB
1. Dextrose – 100 mL of 50% soln
2. Naloxone – 2mg
3. Thiamine [Vitamin B1] – 100 mg
All given IV

(6) Convulsions (7) Delirium (8) ECG anomalies (9) Electrolyte disturbances
(10) Heart Block (11) Hypertension (12) Hypocalcemia (13) Hypoglycemia (14)
Hyperpyrexia [hyperthermia] (15) Hypoprothrombinemia (16) Hypotension (17)
Hypothermia (18) Parenteral nutrition (19) Respiratory insufficiency (20)
Rhabdomyolysis (21) Seizures (22) Sinus tachycardia and (23) Vomiting.

VII. ADEQUATE FOLLOW-UP

(1) Necessary to treat complications

(2) Psychiatric consultation – in suicidal cases.

33. Corrosives

I. INTRODUCTION

Corrosives [syn caustics] fix, erode and destroy living tissues with which they
come in contact with.
Salient features:
(1) Corrosives include both acids and bases and convert hemoglobin into
hematin.
(2) Dangerousness - (i) A l kalis are more dangerous. They produce l
iquefaction necrosis [Memory Aid 1], resulting in deeper penetration [details
below]. (ii) Acids are less dangerous, as they produce coagulative necrosis
[Memory Aid 2]. It results in hard eschar, which prevents deeper
 penetration. Hydrofluoric acid is the only acid that produces liquefactive
necrosis. It is thus more dangerous than other acids.

II. MINERAL ACIDS

An acid (L acidus; sour) is a substance that tastes sour, reacts with metals and
carbonates, turns blue litmus paper red [litmus test for acids], and has a pH <7.0.
A mineral acid (or inorganic acid) is an acid derived from one or more
inorganic compounds. It does not contain a carbon atom [unlike its organic
counterpart, which does].
Salient features:
(1) All mineral acids release hydrogen ions when dissolved in water.
(2) Mechanism of action: (i) Acids cause protein coagulation (coagulative
necrosis)"Form a hard eschar"Limits further penetration of acids"Penetration
by acids is thus self-limiting. (ii) Concentrated forms – React with tissue
water to generate significant heat"superimposed thermal injury.

A. Hydrochloric Acid
Hydrochloric acid [acidum salis (salt acid), muriatic acid (L. muria, brine) spirit
of salts] is a colorless, fuming, pungent liquid. Iranian chemist Geber [721-815]
first made HCl in 800 AD by mixing with common salt and sulfuric acid.
Salient features:
(1) It is often yellow in color due to impurities [traces of iron].
(2) It is a natural constituent of stomach secretions.
(3) Uses - (i) Bleaching agent [<10% HCl] (ii) Descaler in boilers (iii) Drain and
metal cleaner (iv) Dyeing industry (v) Flux for soldering (vi) Laboratory
reagent (vii) Metal refinery.

1. Signs and symptoms

a. Acute poisoning

i. Dermal contact and ingestion

(1) Corrosive action – Less than that of H2SO4.
(2) Skin – is not usually corroded or damaged
(3) Mucus membranes [MM]– readily corroded and destroyed. They are first
grey or grey-white"Later becomes brown and then black due to the production
of acid hematin.

ii. Inhalation
Same as in inhalation of nitric acid.

iii. Contact with eyes

Same as in nitric acid.

b. Chronic poisoning
Occurs due to chronic exposure to fumes.
(1) Eyes – (i) Conjunctivitis (ii) Corneal ulcers
(2) Nose - Coryza [inflammation of nasal mucous membranes]
(3) Oral cavity - (i) Inflammation of gums (ii) Loosening of teeth
(4) GIT – Pharyngitis
(5) Resp system - Bronchitis.

2. Diagnosis
Please see below under sulphuric acid.

3. Fatal dose
15-20 mL.

4. Fatal period
12-24 hours.

5. Management
Same as that for H2SO4.

6. PM appearances
(1) Same as that in H2SO4, but corrosion is less severe.
(2) Stomach – (i) Mucosal folds - discolored brownish (ii) contains brownish
fluid (iii) Perforation – rare
(3) Respiratory passages and lungs – (i) acute inflammation (ii) edema.
7. Tests
(1) Ammonia test – place an open bottle of ammonia near stomach contents,
vomitus or suspected poison"Thick white fumes of NH4Cl would result.
Normal HCl of stomach is too dilute [0.2-0.5%] to produce similar fumes [cf
diagnosis of ammonia].
(2) Litmus test – Same as for H2SO4.
(3) Silver nitrate test – suspected soln + AgNO3"AgCl [thick white ppt].

8. ML importance
(1) Suicide -
(i) Ingested as such
(ii) Used in detergent suicides by producing H2S [ch 44].
(2) Accident -
(i) Iatrogenic - May be confused with antiseptics by negligent medical staff. In
Nov 2011, in a hospital in West Bengal, a negligent paramedical staff
applied HCl on the private parts of Sikha Bibi, 32 after she had delivered a
male baby. As soon as it was applied, the victim felt a burning sensation
and lost consciousness. Her private parts and lower abdomen turned black.
The baby died later due to unrelated causes.
(ii) Accidental exposures in chemistry class [eg dropping a bottle, constant
inhalation by chemistry staff].
(3) Homicidal – Very rare due to its corrosive nature
(4) Abortifacient – rarely introduced in the vagina to produce abortion.

B. Nitric Acid
Nitric acid [syn. azotic acid; aqua fortis; Engraver’s acid; red spirit of nitre] is a
clear, colorless, fuming, heavy liquid having a peculiar choking odor.
Salient features:
Xanthoproteic reaction [Gk xanthos, yellow]- Conc HNO3 combines with
tyrosine or tyrosine-containing proteins [as in human skin, and mucosa] to form
a yellow color which is intensified to orange-yellow by the addition of alkali.
The yellow color is due to formation of xanthoproteic or picric acid.
1 Signs and symptoms

a. Dermal contact and ingestion

(1) Same as that of H2SO4.
(2) More eructation, greater abdominal distention owing to gas formation
(3) Yellow discoloration - of tissues with which it comes in contact [crowns of
teeth, gums, lips, tongue, esophagus, stomach wall]. Even clothing on which
acid falls turns yellow.

b. Inhalation
(1) Resp system -
(i) Coughing and dyspnea
(ii) Sneezing
(iii) Intense irritation of throat and lungs
(iv) Suffocation [a feeling of asphyxiation]
(2) General - cyanosis.

c. Contact with eyes

Eyes - (i) Lachrymation (ii) Photophobia.

2. Diagnosis
Please see above under sulphuric acid.

3. Fatal Dose
10-15 mL.

4. Fatal Period
12-24 h.

5. Management
Same as for H2SO4.

6. PM appearances
(1) Orange-yellow to brown stains on
(i) Skin of mouth and where contact with the acid has occurred
(ii) Hands and neck if any of the acid has been dropped on those parts [due to
xanthoproteic reaction]
(2) Esophagus - Mucous membrane softened, and is yellow [Xanthoproteic
reaction] or brown in color [due to acid hematin]
(3) Stomach and duodenum-
(i) Mucous membrane - (a) yellow-brown, or occasionally green [through the
action of HNO3 on the coloring matter of the bile] (b) Soft, friable,
ulcerated and easily detached.
(ii) Walls - may rarely be perforated
(4) Other changes - similar that in H2SO4.
(5) Inhalation of fumes –
(i) Larynx, trachea and bronchi - congested
(ii) Lungs - congested and edematous.

7. Tests
(1) Litmus test – Same as for H2SO4.
(2) Take stomach contents [or vomit] in a test tube"Add strong ferrous sulphate
soln and H2SO4 gently from the sides"Brown ring forms at the junction of
fluids if HNO3 is present
(3) Take stomach contents [or vomit] in a test tube"Drop a small piece of
copper"heat"pungent dark brown fumes of nitrogen dioxide emanate if HNO3
is present.

8. ML importance
(1) Suicide – most cases of poisoning are suicidal
(2) Accident – rare
(3) Homicide – extremely rare.

C. Sulphuric Acid

1. Signs and symptoms

a. Ingestion
(1) Immediate – (a) Burning pain in the mouth, (b) dysphagia, (c) epigastric
 pain [which soon spreads all over thorax and abdomen] (d) odynophagia
[painful swallowing](e) pharyngeal pain [most common presenting
symptom] (f) salivation, (g) stridor
(2) Intense thirst, eructations, nausea, vomiting – (a) Vomit is (i) brownish
black [due to acid hematin; coffee grounds vomit] (ii) mucoid (iii) strongly
acidic and (iv) contains shreds of charred wall of the stomach. (b) intense
thirst [attempts to drink water cause more vomiting]
(3) Findings in face - (a) Eyes – sunken (b) Pupils – dilated (c) Lips – Swollen,
excoriated (d) Angles of mouth – Brown or black streaks found extending
from angles of mouth to the sides of the chin, and sometimes to the front of
neck. (e) Mucus membranes of mouth, throat and esophagus – corroded (f)
Teeth – chalky white (g) Tongue – black, sodden, swollen
(4) Voice – hoarse and husky [dysphonia]. Due to coincidental damage to larynx
during swallowing or during vomiting
(5) Abdomen – (a) distended and tender, (b) tenesmus
(6) Constipation – severe
(7) Features of generalized shock
(8) Metabolic acidosis – due to (a) absorption of acid (b) severe tissue burns (c)
shock
(9) Leucocytosis
(10) Chemical peritonitis – if perforation occurs [of all acids, perforation is
commonest in sulfuric acid. Please also see ch 31 “General Principles” under
the heading “Perforation”]
(11) Mind - remains clear till death
(12) If victim recovers, late symptoms, signs and sequelae are – (a)
Permanent scars on skin (b) Strictures of esophagus and stomach [hour glass
deformity] (c) pyloric stenosis (d) -propensity for carcinomas.

b. Contact with eyes

Can occur accidentally or with an intention to injure [vitriolage – please see MLI
below]. (1) Conjunctivitis (2) Corneal edema and ulceration (3) iridocyclitis (4)
Necrotizing keratitis (5) Periorbital edema.

c. Contact with skin

Can occur accidentally or with an intention to injure [vitriolage – please see MLI
below]. (1) Intense burning pain, (2) Immediate corrosion, (3) destruction of
skin.

2. Diagnosis

a. For all corrosives

(1) Saliva – pH tested by litmus paper
(2) Stains on clothing, scene etc – Add few drops of Na2CO3 or
NaHCO3"Bubbles indicate acid.
(3) - prothrombin time (PT) and -partial thromboplastin time [PTT]
(4) Arterial pH < 7.22, indicate acid ingestion.
(5) Chest and abdominal radiographs – may show signs of esophageal or
gastric perforation [pneumomediastinum, pneumoperitoneum]. Pleural
effusion may also be seen. CT is much more sensitive than X-rays for
detecting viscus perforation.
(6) Contrast esophagram - For assessing the extent of esophageal injury. In late
ingestions, can detect strictures.
(7) Endoscopy - should be performed within 12 h [safest during this period].
Not later than 24 h, because risk of perforation -es after this period. Early
endoscopy permits early grading of injuries and helps to determine treatment
plan and nutritional support.

b. Specific for H2SO4

Vomitus"Add 10% BaCl2. Heavy white ppt [BaSO4].

3. Fatal dose
10-15 mL.

4. Fatal period
12-24 hours.

5. Cause of death

a. Immediate
(1) Circulatory collapse [due to trauma from corrosive injury] (2) Spasm or
edema of glottis (3) Perforation of stomach.
b. Delayed
(1) Hypostatic pneumonia (2) Renal failure (3) Secondary infection (4)
Starvation [due to esophageal strictures]

6. Complications

a. Immediate
(1) Atelectasis (2) GI hemorrhage (3) Obstructive lung injury (4) Perforation
[esophageal and gastric] (5) Sepsis (6) Tracheobronchial necrosis (7) Upper
airway injury.
b. Late
(1) Esophageal strictures (2) Pyloric stenosis (3) Upper airway obstruction (4)
Vocal cord paralysis (5) carcinoma.

7. Management

a. Systemic ingestion
Management depends on the extent of injury.

i. Grade 1 esophageal injury

(1) Diet as tolerated
(2) No further therapy needed, supportive care.

ii. Grade 2A esophageal injury

(1) If unable to tolerate PO, provide nutritional support via nasogastric,
orogastric, or percutaneous feeding tube; or total parenteral nutrition
(2) Admission recommended, supportive care.

iii. Grade 2B and 3 esophageal injuries

(1) Admission into intensive care unit
(2) Initiate early percutaneous feeding tube; or total parenteral nutrition.
(3) Prevention of stricture formation –
(i) Antacids
(ii) Antibiotics
(iii) Corticosteroids. Optimal management remains controversial. Some
authorities do not recommend steroids and antibiotics.
(4) If strictures have developed -
(i) Nasogastric tubes
(ii) Total parenteral nutrition [TPN]. Gastrostomy may be required.
(iii) Traditional treatment for focal esophageal stricture - Esophageal dilatation
with esophagoscopy.
(5) Requires additional imaging or surgical exploration for gastric injuries.

b. Contact with skin and eyes

(1) Wash - the affected part with
(i) Plenty of water and soap or
(ii) Sodium or potassium carbonate. In case of eyes, wash with very dilute soln
of sodium bicarbonate [since much weaker than sodium carbonate, it does
not injure eyes]; then instill a few drops of castor oil or olive oil.
(2) Neutralize – After washing apply a thick paste of magnesium oxide or
carbonate.

8. Progress of injury
Perforation occurs immediately. If perforation does not occur corrosive injury
proceeds as follows:
(1) immediate to 4th day – inflammation
(2) 4th day – 3 wks – Neovascularization and fibroblast proliferation take place,
laying down new collagen and replacing the damaged tissue with granulation
tissue.
(3) 8 wks onwards – Remodeling occurs. Progressive narrowing of the
esophageal lumen. The dense scar formation presents clinically as a stricture,
leading to dysphagia and significant nutritional deficits.

9. PM appearances
Depend on (1) strength of acid (2) quantity of acid and (3) survival time of
patient.

a. External
(1) Clothings – acid burns, stains
(2) Linear burns – coursing down the angles of the mouth.
(3) Burns – (a) of lip, chin, front of chest, hands (b) if acid is taken with a spoon
these areas will escape injury
(4) Swelling – of lips and mouth [due to inflammation]
(5) Color of burnt areas – initially grayish white, but soon becomes brown or
black and leathery. May simulate abrasions.

b. Internal
(1) Esophagus – perforation is rare [Please see above under “acids and bases –
differences in action”]
(2) Stomach – (a) Corrosion and perforation common (b) If corrosion is absent,
there will be (i) inflammation, (ii) swelling due to edema and (iii) severe
interstitial hemorrhages (c) Consistency – Stomach turns into a soft, spongy,
black mass, which readily disintegrates when touched (d) Lesser curvature –
 May be affected more because acid may travel along magenstrasse [please see
ch 31 for details] (e) Pyloric region – Because of pyloric spasm, acid cannot
pass through and collects here. Antral pooling occurs. Causes more injury to
pyloric region (f) Mucosal ridges – being raised, may show more injury than
intervening furrows, which lie deeper (g) Color of mucosa – Black. Charred
appearance.

10. Preservation of samples

(1) Organs - Vitreous humor and lungs have to be preserved [please see ch 5 for
more details].
(2) Clothings – may reveal acid, if accidentally spilled over them [ch 5].

11. Tests
(1) Litmus test - Suspected soln would turn blue litmus red.
(2) Suspect material + BaCl or BaNO3"white ppt of BaSO4.
(3) Pour suspect material over organic matter (eg cotton)"Charring.

12. ML importance
(1) Vitriolage - Vitriolage or vitriol throwing is throwing of a corrosive
substance over the face of an adversary due to jealousy or revenge.
Salient features:
(1) Corrosive used - Usually conc. H2SO4 is used, but sometimes an alkali, a
corrosive salt [e.g. corrosive sublimate or HgCl2] or irritant juice of a plant
[e.g. marking nut, calotropis] may be used. (ii) Aim - is not to kill but
disfigure. (iii) Used by – mainly by jilted lovers on their girl friends; but
anyone can use. Some common motivations are enmity, hatred, jealousy,
revenge, rioting and rivalry. (iv) Method - (a) corrosive is filled inside an
empty light bulb [or some other easily breakable container] and thrown over
the victim (b) Filled inside a pichkari [spray gun used in Holi] and sprayed
over victim. (v) Management – please see above [contact with skin and eyes]
(vi) Outcome - (a) Destruction of garments (b) Disfiguration of face, if not
treated promptly. (c) Sometimes blindness. (d) Contractures – around joints
may cause restriction of movements (e) Death may also occur. (vii)
Medicolegal investigation - (a) Clothes - must be collected and sent for
chemical examination (b) plain water swabs - from affected areas – sent for
chemical examination (c) Scene of crime - Spilt traces of corrosives may be
found – on ground, walls, nearby vehicles etc. If acid was contained in glass
bulb, pieces of broken glass may be found. Chemical examination of fluid on
glass pieces would reveal same corrosive as that found on the body of victim
(d) Identification of perpetrator – is rarely possible, if during the act of
throwing acid, few drops sprinkle on his own body. (viii) MLI [of vitriolage] –
(a) It is a grievous hurt, punishable u/s 326 IPC [ch 11]. (b) All hospitals,
whether Govt or private must provide immediate first-aid or medical
treatment free of cost to any victim of vitriolage [S.357C, CrPC]. If such
treatment is not provided, punishment is 1 y or fine or both [S.166B, IPC] (ch
11) (c) If a police officer fails to record FIR u/s154(1) CrPC of a victim of
vitriolage, he shall be fined and given rigorous imprisonment for a minimum
of 6 months and up to 2 years [S.166A, IPC (ch 25)].
(2) Accidental poisoning – results due to H2SO4 being mistaken for glycerine,
 castor oil or linseed oil
(3) Suicide – May be taken for suicide. Generally taken orally, but rectal
administration has been described.
(4) Homicide – Can not be used for homicide, because of its corrosive nature.
Food gets charred when mixed with it
(5) Disposal of dead bodies – May be used for criminal disposal of dead bodies
after murder.
(6) For blinding an enemy or to extort confessions – Acids have been used for
blinding an enemy. The police use acids in order to extort a confession.
(7) Occupational hazard - Inhalation of vapor may occur inadvertently in
chemical factories. May require compensation from factory owner
(8) Abortifacient – injected in vagina for criminal abortion
(9) Battery acid – is 30-35% )H2SO4. Used in the illicit manufacture of
several narcotic drug derivatives [e.g. cocaine sulfate] - (please also see
chapter on deliriant poisons – ML imp of Cocaine).
(10) Self defense - Acids have been used by women for defending themselves
against sexual assault.

III. ORGANIC ACIDS

A. Carbolic Acid (Phenol, C6H5OH)

1. Properties
(1) Appearance -
(i) Pure acid consists of short, colorless, prismatic, needle like crystals
(ii) Commercial phenol is a brownish liquid containing impurities like cresol.
(2) On exposure to air – crystals turn pink and liquefy
(3) Smell – Characteristic “carbolic” or phenolic [one that emanates from
hospitals, OTs]
(4) Taste - burning sweetish.
(5) Solubility –
(i) Sparingly soluble in water [6.6% at 17°C]
(ii) Freely soluble in alcohol, benzene, ether and glycerine.
(iii) Miscible with camphor
(6) Not a true acid – Does not turn litmus paper red
(7) Use – antiseptic, disinfectant.

2. Toxicokinetics

a. Absorption
Readily absorbed from all routes including GIT, Rectum, Respiratory tract,
Serous cavities, skin, Vagina and wounds.

b. Excretion
(1) Phenol is converted to pyrocatechol and hydroquinone in the liver before
being excreted in the urine partly free and partly in unstable combination with
sulphuric and glucuronic acid. Their further oxidation in the urine gives rise to
green colored urine. Initially the urine is colorless or slightly green, but later it
becomes dark green, which darkens further to almost black on standing. This
symptom is known as carboluria.
(2) Traces – excreted in lungs, salivary glands, stomach and skin.
(3) Time required for complete excretion – 36 hours.

3. Acute poisoning

a. Signs and symptoms

Poisoning by CA is known as carbolism.

i. Local
(1) Skin -
(i) Numbness [due to damage to nv endings]
(ii) Burns – (a) CA precipitates proteins and coagulates cell contents (b) When
comes in contact with skin"produces a painless white opaque eschar"falls
off in a few days"Leaves a brown stain. (c) Longer contact produces deep
burns"black (d) If necrosis and gangrene of tissue sets in"corroded area
becomes greenish-white or brownish-white. Dead tissue sloughs readily (e)
Lysol burns produce a brownish purple color
(2) Digestive tract –
(i) Nausea, vomiting – in about 20% cases.
(ii) Hot burning pain – Extends from mouth to stomach"followed by
tingling"anesthesia
(iii) Lips, mouth, tongue – corroded. Soon harden and become white
(iv) Deglutition and speech – become difficult.

ii. Systemic
(1) General -
(i) Odor - Strong odor of phenol in breath
(ii) Temp.
(iii) Pupils – variable. Usually contracted. But may sometimes be dilated.
(iv) Breathing – stertorous
(v) Pulse – Feeble, irregular, Rapid
(vi) Face – covered with cold sweat, Dusky cyanosis
(2) CNS -
(i) Phenol initially causes stimulation of CNS, but later acts as a depressant to
CNS, especially respiratory center
(ii) Stimulatory symptoms - (a) agitation (b) Convulsions, seizures, lockjaw
(iii) Depressant symptoms - (a) Headache, giddiness, confusion (b)
unconsciousness, coma towards the end
(3) CVS - Hypotension, arrhythmias.
(4) Resp system -
(i) Breathing – slow, labored, short and infrequent gasps"progresses to resp
failure and arrest.
(ii) Laryngeal and Pulmonary edema [due to irritation]
(iii) Bronchitis, bronchopneumonia [due to aspiration of vomit]
(5) Liver – damaged. Signs of hepatotoxicity.
(6) Blood -
(i) Hemolysis
(ii) Methemoglobinemia [in severe cases]
(7) Acid-base balance - (i) Metabolic acidosis (ii) Respiratory alkalosis
(8) Urine -
(i) Scanty, may be completely suppressed
(ii) Contains albumin and free Hb
(iii) Color – green [please see above under “excretion” for details].
(9) Rare symptoms – Fine, rapid, rhythmic contractions of the perioral
musculature [rate about 5 Hz] resembling the chewing movements of a rabbit
[rabbit syndrome]. Usually an extrapyramidal side effect of neuroleptic drugs.
Phenol causes tremors directly by inducing -ed Ach release both in the
peripheral nervous system at motor nerve endings and within the CNS.

b. Fatal dose
10-15 g.

c. Fatal period
3-4 h.

d. Management

i. Contact
(1) If phenol falls on clothing – remove clothing immediately. Clean skin as
below
(2) Mechanism of injury and treatment of phenol differs from that of standard
corrosive exposures. In contrast to other corrosives, phenols cause injury by
their ability to accept an electron pair to form a covalent bond. This difference
alters management of dermal burns in that irrigation should be done with
polyethylene glycol solution because water can actually worsen the injury. If
water is all that is available for irrigation, it should be mixed with soap.
(3) Washing - with (i) Ethyl alcohol [10%] (ii) Methylated spirit and (iii) Olive
oil is also helpful.

ii. Ingestion
(1) Emetics – would generally fail due to anesthetic effect
(2) Gastric lavage:
(i) Wash carefully with lukewarm water mixed with any of the following - (a)
castor oil (b) olive oil (c) glycerine [10%] (d) magnesium or sodium
sulphate (e) saccharated lime or (f) soap soln. Phenol combines with them
to form harmless products
(ii) Continue washing - till washings are clear, colorless and odorless
(iii) After completion of lavage – leave (a) medicinal liquid paraffin [about 250
 cc] or (b) MgSO4 [30 g] in the stomach
(3) Demulcents
(4) Normal saline with NaHCO3 [7g/L] IV – helps in 3 ways
(i) Combats circulatory collapse
(ii) Dilutes carbolic acid [CA] content of blood
(iii) Promotes diuresis "-ed excretion of CA
(5) Hemodialysis – if there is renal failure
(6) To correct methemoglobinemia -
(i) Methylene blue IV
(ii) Exchange transfusion – if methemoglobinemia is >70%.

e. Cause of death
(1) Asphyxia -
(i) Failure of respiration
(ii) Edema of glottis
(iii) Complications [eg bronchopneumonia]
(2) Syncope.

f. PM appearances

i. External
(1) Smell – of phenol from body, especially from mouth
(2) Corrosion of skin – around mouth; Especially as trickling marks from
angles of mouth. Color brownish or grayish
(3) Tongue – White, swollen, hardened.
(4) Lips, mouth, throat – mucus membrane is (i) coagulated (ii) corrugated (iii)
detached [partially] (iv) opaque (v) sodden and (vi) swollen (vii) color -
whitened, brown or ash-gray. (viii) Shows numerous small submucous
hemorrhages.

ii. Internal
(1) Esophagus –
(i) Mucosa same as that of mouth and throat.
(ii) In addition arranged in longitudinal folds
(2) Stomach –
(i) Contents – reddish fluid mixed with mucus and shreds of epithelium
(ii) Smell – of phenol
(iii) Mucosa - same as that of mouth and throat.
(iv) In addition, it is thick and leathery – because of longer duration of contact
(v) Necrotic mucosa – may show partial separation, with severe congestion of
underlying tissue
(vi) Furrows - show more damage. Intervening areas show less damage, are dark
red and are not opaque
(3) Duodenum, jejunum, upper part of ileum – show similar changes, but to a
lesser degree
(4) Resp tract – Changes are seen especially if inhalation of acid or vomitus has
occurred
(i) Coagulation necrosis of mucosa
(ii) Severe congestion of submucous layers
(iii) Laryngeal and pulmonary edema
(5) Liver, spleen – show a whitish, hardened patch where the stomach is in
contact with them, because of transudation of phenol
(6) Kidney – hemorrhagic nephritis, if death is delayed
(7) Brain – congested, edematous
(8) Blood – dark, semifluid, partially coagulated.

g. Tests
1 ml of solution to be tested (urine)+few drops of 10% ferric chloride
solution"Bluish color will develop if phenol is present. Salicylates also give +ve
results.

4. Chronic poisoning (phenol marasmus)

Occurs due to chronic exposure to phenol.

Signs and symptoms

(1) General - (i) Anorexia (ii) Headache (iii) Vertigo (iv) Wt loss
(2) Urine – dark
(3) Pigmentation –
(i) Yellowish (ocher-like) discoloration of cartilage, sclera and skin [ochronosis]
seen on microscopic examination.
(ii) However, macroscopically the affected tissues appear bluish grey because of
a light scattering phenomenon.
(iii) D/d – (a) Alkaptonuria – an inborn error of metabolism because of
deficiency of homogentisic acid oxidase. Homogentisic acid gets deposited
in cartilages, fibrous tissues and ligaments.
Memory Aid 3: Ochronosis
O chronosis occurs in chronic phenol poisoning

5. ML importance
(1) Used for suicide
(2) Accidental poisoning -
(i) due to carelessness in storage
(ii) misguided lay medical treatment, like application on raw wounds etc
(3) Criminal abortion – introduced into vagina and uterus. May cause
accidental poisoning
(4) Homicidal poisoning – rare because of odor and taste.

B. Oxalic Acid

1. Description
(1) Two forms - Oxalic acid (acid of sugar; salt of sorrel; IUPAC name-
Ethanedioic acid) occurs in two forms – anhydrous (without associated water
molecules) and dihydrate (with two water molecules). Typically it occurs as
the dihydrate.
(2) Colorless, transparent prismatic crystals
(3) Resembles in appearance to the crystals of magnesium sulfate (Epsom salt)
and zinc sulfate, but can be easily differentiated [Table 1]. Failure to
differentiate may result in accidental poisoning, especially as both are used as
medicines. Epsom salt is used as a laxative – a common household remedy,
and zinc sulphate is used in acne, ivy poisoning, lupus erythematosus, and
impetigo. Two patients at a mental hospital in Scotland died in 1956 after
receiving doses of oxalic acid administered in mistake for Epsom salts.
(4) Efflorescent. Solubility – 1 in 12 in H2O.
(5) Produced as a result of ethylene glycol metabolism, and is a major reason of
its toxicity.
2. Occurrence in nature
Oxalic acid (along with oxalates) are present in many plants and occur naturally
in animals.
(1) Plants containing oxalic acid (i) Cabbage (ii) Carambola fruit [unripe] (iii)
Jack-in-the-Pulpit [Arisaema triphyllum] (iv) monstera fruit [unripe] (v)
Rhubarb. (vi) spinach (vii) wood-sorrel. Daily excretion in urine is 20 mg.
(2) Kidney stones – most common component - Calcium oxalate.
(3) Bacteria - produce oxalates from oxidation of carbohydrates.

3. Uses
(1) Commercial - (i) Book binding [for cleaning leather used as jackets] (ii)
Calico printing (iii) Cleaning copper and brass articles, wooden and leather
surfaces (iv) Photography and (v) Straw hats [manufacture]
(2) Domestic - (i) bleach (ii) ink remover (iii) paint, rust, stain and varnish
remover
(3) Illegal - (i) removing writing and signature from papers [eg wills, contracts,
 bonds] (ii) removing election stain marks on fingers [to enable voting again].

4. Mechanism of action
(1) Locally – acts as a corrosive
(2) Systemically – Reacts with Calcium in plasma "Forms calcium oxalates"(i)
Hypocalcemia (ii) Precipitation of calcium oxalate crystals in liver, kidneys,
heart and lungs (iii) Excretion of envelop shaped crystals [calcium oxalate] in
urine.

5. Signs and symptoms

a. Contact
(1) Skin - is rarely damaged. May just be discolored
(2) Mucosa – of eye, mouth etc may be greatly damaged and may give rise to a
 “scalded” appearance. Sometimes production of acid hematin may give rise to
black color.

b. Ingestion

i. Immediate
(1) Burning, sour or bitter taste in the mouth which goes up to the stomach
(2) Sense of constriction around the throat
(3) Intense thirst
(4) Mouth – may appear “scalded” or sometimes black
(5) Severe pain – Begins in the epigastrium, but soon radiates all over the
abdomen
(6) Abdomen is tender
(7) Persistent vomiting, eructations and diarrhea. Vomitus contains altered blood
[“coffee-ground” appearance] and mucus.
(8) Signs and symptoms due to hypocalcemia -
(i) Tetany
(ii) Numbness and tingling of fingertips and legs
(iii) Chvostek sign +ve.

ii. Delayed
If patient survives initial poisoning episode, delayed symptoms may be due to
renal failure [calcium oxalate crystals in kidneys] Urine – Scanty or
suppressed. Contains traces of blood, albumin and calcium oxalate crystals.

6. Management
(1) Gastric lavage – If patient seen early, perform gastric lavage carefully with
calcium salts [chloride, gluconate, lactate, chalk powder (1.5g of chalk
neutralizes 1g of acid), lime water, milk]. Converts acid into insoluble calcium
oxalate.
(2) Antidote – Calcium preparations orally [same as those used for gastric
lavage].
(3) Calcium gluconate IV – 10 ml of 10% at frequent intervals
(4) Parathyroid extract – 100 units IM in severe cases. Mobilizes Ca+ from
bones.
(5) Dialysis or exchange transfusion – for renal failure
(6) Miscellaneous - (i) Demulcents (ii) Evacuation of bowels – by castor oil or
enema (iii) Symptomatic.

7. Fatal dose
600 mg/kg. For a 60 kg human 36 g.

8. Fatal period
1-2 hours.

9. PM appearances
(1) Mucus membrane of tongue, mouth, pharynx, esophagus -
(i) In case of concentrated solution - (a) Whitened as if “bleached”. Similar to a
“scalded” appearance (b) sometimes brown or black due to formation of
acid hematin
(ii) In case of weaker solution - Reddened because of irritation
(2) Esophagus – Mucosa corrugated. Shows longitudinal erosions
(3) Stomach – (a) Mucosa - (i) soft and reddened (ii) Shows punctate erosions
(iii) May be black [acid hematin] (iv) numerous dark brown or black streaks
are seen running longitudinally along the length of the stomach, often with
intercommunicating branches (v) Often entire mucosa is corroded (b)
Contents – Gelatinous and brownish [acid hematin] (c) Perforation is rare
(4) Intestines – Upper part of duodenum shows corrosion. Rest of the intestines
usually escape
(5) Liver - hepatic centrilobular necrosis
(6) Kidneys - (a) Congested and swollen by edema (b) Histologically - (i)
Glomeruli - Swelling and retraction (ii) Renal tubules – full of oxalate
crystals. Necrosed, especially PCT
(7) Urinary bladder – shows urine with calcium oxalate crystals. Under the
microscope look like envelops.
(8) All internal organs – show congestion
(9) Crystals of calcium oxalate – in renal cortex and vessels and capillaries of
liver, lung, and heart.

10. Test
Suspected soln + BaNO3"White ppt of barium oxalate, which is soluble in HCl
or HNO3.

11. ML importance
(1) Accidental poisoning – Due to mistaken identity with Epsom salt or ZnSO4.
May lead to charges of negligence against doctors and nursing staff.
(2) Homicide – rare due to acrid sour taste
(3) Suicide – rare because of severe pain and burning
(4) Abortifacient – by vaginal injection.

IV. CAUSTIC ALKALIS - GENERAL

A. Ammonia

1. General
(1) At room temperature, ammonia (NH3) is a highly water-soluble, colorless,
irritant gas with a unique pungent choking odor.
(2) Ammonia has a boiling point of -33°C and an ignition temperature of 650°C.
(3) Ammonium hydroxide – also known as ammonia liquor, ammonia solution,
ammonia water, ammoniacal liquor, aqua ammonia or aqueous ammonia is a
solution of ammonia in water. It contains about 30% ammonia.

2. Signs and symptoms

Inhalation - (a) Head, ears, eyes, nose, throat (HEENT) - Facial and oral burns
and ulcerations (b) Respiratory system – cough, decreased air entry, oxygen
desaturation, rhonchi, salivation, stridor, Tachypnea, wheezing (c) CNS - Loss of
consciousness [if exposure is massive].

3. Diagnosis
HCl test - place an open bottle of Conc HCl near stomach contents, vomitus or
suspected poison"Thick white fumes of NH4Cl would result [cf diagnosis of
HCl].

4. Management
(1) Largely supportive. Directed at treating hypoxia, bronchospasm, acute lung
injury (ALI), hypovolemia, and burns of the skin and eyes.
(2) Antibiotics and corticosteroids are controversial.

5. Fatal dose
15-20 mL.

B. Button Battery Ingestion (Disc Battery, Miniature Battery)

(1) Signs and symptoms - Irritability, pain, dysphagia, vomiting, refusal to eat.
May cause Hg poisoning [ch 36]
(2) Diagnosis - X-ray
(3) Management - Endoscopic or surgical removal is necessary because of the
risk of (i) burns (ii) perforation and (iii) metal poisoning.

C. Cement Burns

1. Mechanism of action
(1) Cement contains lime [calcium oxide], which penetrates clothing and reacts
with sweat causing an exothermic reaction.
(2) Even when not exposed to moisture, the dry powder is very
hygroscopic"causes a desiccation injury.
(3) Hydrated calcium oxide becomes calcium hydroxide that causes skin damage
primarily due to hydroxyl ion.
(4) If cement is not removed from the skin, it continues to corrode and painlessly
causes necrosis under clothing.

2. Signs and symptoms

Cement burns have an insidious onset. Most patients comment that they notice
only mild irritation initially. Rarely burns may be serious

3. Management
(1) remove soaked clothing
(2) abundant washing of the wounds
(3) Neutralization with buffered phosphate solution. However the practice is
debatable, as the heat produced by the exothermic chemical reaction of
 neutralization could worsen the burns.

D. Liquid Lye (NaOH, Caustic soda)

[A] Sodium hydroxide is found in many industrial solvents and cleaners,
[flooring stripping products, brick cleaners, cements], and many household
products (Aquarium products, Clinitest tablets, Drain cleaners, Hair
straighteners, Metal polishes and Oven cleaners) [B] Signs and symptoms –
Burns, Irritation, Necrosis of the skin and underlying tissues [C] Management –
As for general alkalis [D] MLI – May be seen in vehicular accidents as air bag
ruptures [ch 18].

V. OTHER CORROSIVES

A. Potassium Permanganate [KMnO4]

1. General
KMnO4 [syn, Condy’s crystals, permanganate of potash] occurs as dark purple
slender crystals, having a sweet astringent taste. it is a strong oxidizing agent and
is used as a disinfectant due to its strong oxidizing action on microbes. It
dissolves in water to give intensely purple solutions, the evaporation of which
leaves prismatic purplish-black glistening crystals. Its name Condy’s crystals
comes from UK chemist Henry Bollmann Condy [1826-1907], who first made
Condy’s Crystals and Condy’s Fluid from KMnO4 in 1857.

2. Mechanism of action
(1) Before absorption, in solid state or strong solution - acts as a corrosive or
strong irritant. Causes coagulation necrosis.
(2) After absorption - Cardiac stoppage.

3. Signs and symptoms

a. Ingestion
(1) Intense thirst, nausea, vomiting and diarrhea. Vomitus is purple brown in
color. Stools are black due to manganese sulfide. Excessive loss of fluids may
lead to shock and collapse.
(2) Burning pain - from mouth to stomach
(3) Dysarthria, dysphagia
(4) RS- Produces severe inflammatory edema resulting in dyspnea, stridor,
persistent spasmodic cough
(5) Purple brown discoloration - of skin and mucus membranes, with which it
comes in contact. Lips, gums, teeth, tongue, tonsils and pharynx. In a few
minutes the color changes to brown, dark brown and finally coal black due to
conversion to manganese dioxide.
(6) Systemic - Methemoglobinemia, because of oxidizing nature of KMnO4.

b. Local application
Locally applied as an abortifacient.
(1) Vaginal and cervical burns, erosions and ulcerations, resulting in severe
scarring.
(2) Extensive bleeding and shock.

4. Diagnosis
(1) Place either a drop of H2O2 or a soln of oxalic acid and traces of H2SO4 over
stains. They should disappear
(2) -Serum and Urine Manganese levels.

5. Fatal dose
5-10 g.

6. Fatal period
Few hours.

7. Management
(1) Immediate dilution - with water or milk
(2) Activated charcoal
(3) Demulcents
(4) Gastric lavage -
(i) May have to be done carefully, since KMnO4 is a corrosive.
(ii) Fluids used - (a) dilute H2O2 (b) 20% sodium thiosulphate.
(iii) End point - when returning fluid is colorless
(5) Methemoglobinemia - Treated with methylene blue 1-2 mg/kg IV over 5
min every 4 h.
(6) Chelation - Done if manganese toxicity is suspected. Administer EDTA and
sodium para-aminosalicylic acid.
(7) Supportive and symptomatic.

8. PM appearances
(1) Mucus membranes of GIT extending from lips up to intestines - Corrosion,
necrosis, hemorrhage.
(2) Liver and kidneys - show degenerative changes.

9. MLI
(1) Manner of poisoning - (i) Suicidal - mostly. (ii)Accidental - (a) may occur
in children, who may eat crystals mistaking them for candies. (b) When
ingested or injected as an abortifacient (iii) Homicidal - very rare due to its
color and peculiar taste
(2) Production of fictitious injuries - By applying a tablet to the skin for 10-20
min, lesions similar to those of tertiary syphilis may be produced.

VI. CHEMICAL BURNS

(1) In chemical burns, amount of tissue damaged depends upon the agent, its
duration of contact, extent of penetration, quantity, strength and concentration.
(2) Chemicals continue to act on tissue until - (i) Inactivated by tissue reaction
(ii) Neutralized by another agent.
(3) Hydrocarbon [eg gasoline] – Prolonged contact can cause burns due to their
irritant effect and high lipid solubility.
(4) Phosphorus – also causes burns.

34. Non-Metallic Irritants and

Mechanical Irritants
I. NON-METALLIC IRRITANTS

A. Phosphorus

1. Allotropes
Four allotropes of phosphorus are known:
(1) White [with impurities, it becomes yellow],
(2) Red [formed by heating white phosphorus to 250°C in vacuum],
(3) Violet [formed by dissolving white phosphorus in molten lead at 500°C, and
then cooling it slowly] and
(4) Black [formed by heating white phosphorus at 12,000 atm]. White
phosphorus is a tetramer (P4). Gaseous phosphorus is also known, which
exists as diphosphorus (P2).
Memory Aid 1: Allotropes of Phosphorus
Violet is formed by dissolving in lead.

Differences between the two most common allotropes - white and red are shown
in Table 1.
2. Mechanism of action
(1) Uncoupling of oxidative phosphorylation in the hepatocyte.
(2) Decreases ATP levels in the hepatocyte.
(3) Decreases transformation of triglycerides into b-lipoproteins. Rapid rise
in hepatic triglycerides. Massive hepatic steatosis is a hallmark of white
 phosphorus toxicity.
(4) Hepatic necrosis in zone 1 is prominent (located around the portal tracts
where oxygenation is good). Significantly, other hepatotoxins, such as
acetaminophen and CCl4 produce zone 3 necrosis (located around central
veins, where oxygenation is poor).

3. Symptoms and signs

a. Local application
P is an oxidizing agent, highly toxic to skin. Causes both thermal and chemical
burns. 2nd and 3rd degree (Dupuytren) burns are causes most often. Since P
continues to oxidize and injure tissue, it is extremely important to neutralize P
immediately.

b. Ingestion

i. Acute fulminant poisoning

Occurs when the victim takes more than 1 g (more than 15 times the average
fatal dose). Vomiting, diarrhea, peripheral vascular collapse. Death occurs
within 12 hours.

ii. Subacute poisoning

Occurs when the victim takes fatal or near fatal dose. Three stages are seen.

(a) First stage [2 days]

(1) Severe burning pain in the mouth. Abdominal pain, vomiting, diarrhea
[symptoms of GIT irritation]
(2) Garlicky odor (Ch 31).
(3) Luminous vomit and stools because of presence of phosphorus. Feces
expelled on the bed can burn a hole through the bed sheet.
(4) Fumes emanate from the stools, as phosphorus in stools combines with
atmospheric oxygen to form phosphorus pentoxide (Smoking or smoky stool
syndrome).
(b) Second stage [4 days]
Patient is symptom free. Wants to go home. Should not be discharged.
Something like “lucid interval” seen in head injury [cf ch 36"iron toxicity].

(c) Third stage [2 days]

(1) Hepatic toxicity develops. Major signs are
(i) Mousy odor of the breath [foetor hepaticus]
(ii) Flapping tremor of hands [asterixis]
(iii) Hepatomegaly, jaundice, bleeding tendencies [prothrombin deficiency],
pruritis.
(iv) Finally hepatic encephalopathy and death.
(2) Mortality - ranges from 20%-50%. Prolongation of QTC interval, ST-T
wave abnormalities, more than ten times increase in alanine
aminotransferase (ALT) and severe coagulopathy indicate poor prognosis.
(3) If death does not occur in eight days, patient goes on to recover.

iii. Chronic poisoning

(1) Signs and symptoms - Workers working with white phosphorus develop an
unusual mandibular osteonecrosis (phossy jaw, Lucifer’s jaw or glass jaw).
First described by Bristowe in 1862. Cachexia, anemia and fatigue also
occurs.
(2) Preventive measures - Since mandibular necrosis starts with toothache,
preventive measures include regular dental checkup of workers employed in
phosphorus factories.

4. Fatal dose
1 mg/kg [60 mg for a 60 kg person].

5. Fatal period
½ day to 8 days. No fatalities have been reported after 8 days.

6. Management

a. Protection of healthcare personnel

Doctors, nurses and other healthcare personnel should wear gloves and other
protective equipment to avoid direct contact with the patient. Phosphorus can
get absorbed through skin. Also it may be present in patient’s clothings and may
ignite spontaneously.
b. Supportive care
(1) Continuous cardiac monitoring.
(2) Fluid resuscitation.
(3) Vitamin K by IV drip [to treat hypoprothrombinemia]
(4) Prothrombin time (PT), Partial thromboplastin time (PTT), hepatic
enzymes, serum electrolytes, serum phosphate and serum calcium should be
measured.
(5) Whole blood/fresh frozen plasma [to correct coagulation defects]
(6) Evaluation of renal function and renal output.
(7) Ophthalmic irrigation if phosphorus has entered eye.

c. Skin decontamination
Continuous irrigation with water or saline.
(1) Application of silver nitrate on skin (prevents ignition by depositing a thin
film of silver over phosphorus particles).
(2) Application of CuSO4.
(i) Helps in identifying occult phosphorus particles by causing a characteristic
black color change
(ii) Neutralizes P at the same time [formation of cupric phosphide]
(3) Identification of phosphorus particles by Wood’s lamp [phosphorus particles
are seen to fluoresce blue], and their removal. If removal not possible,
thorough debridement of skin.

d. GIT decontamination
(1) Gastric lavage – with 1:5000 KMnO4. Converts white phosphorus to less
harmful oxide. Rarely as phosphorus comes out of the gastric lavage tube, it
can catch fire, leading to explosions. It is therefore recommended that
external end of gastric lavage tube be connected to a syringe filled with
water.
(2) Activated charcoal
(3) Whole bowel irrigation with polyethylene glycol (decreases the absorption
of phosphorus).

e. Other measures
(1) N-Acetylcysteine – Though primarily an antidote for paracetamol, has been
tried in phosphorus poisoning with some benefit.
(2) Ubiquinone, cysteine and sulfate decrease liver damage.
(3) Corticosteroids are of no use in preventing hepatotoxicity.
(4) Exchange transfusion.
(5) Liver transplantation.

7. PM appearances

Macroscopic
(1) Bleeding points in the skin [bleeding diathesis produced by phosphorus]
(2) Stomach contents - garlicky in odor.
(3) Luminous material in stomach and intestine can be demonstrated (using
Wood’s lamp, as phosphorus fluoresces easily).
(4) Erosions and hemorrhages in esophagus and stomach. Rarely perforation of
the stomach.
(5) Heart - subendocardial petechial hemorrhages
(6) Liver - fatty, enlarged, yellow.
(7) Petechial hemorrhages - in all internal organs.
(8) Individuals who have survived for a week or so would show acute yellow
atrophy.

8. Viscera analysis
(1) Stomach and intestines - should be tied at both ends before submitting for
toxicologic study. These viscera must be opened under nitrogen just before
analysis.
(2) Other viscera - preserve in saturated saline. Preservation in rectified spirit
may cause loss of phosphorus luminosity.
(3) Collect feces from rectum and submit for toxicology

9. Medicolegal importance
(1) Long retention in organs after death - Phosphorus continues to remain
unchanged in the organs in fatal cases. It has been found in bodies up to one
month after death. Can be detected even in exhumed bodies.
(2) Homicide - Because of its luminescence and strong garlicky odor, it is very
 rarely used for homicide. In some cases it was mixed with coffee, soup, jam
or rum, and given to the unsuspecting victim. In earlier days when match
heads contained yellow phosphorus, match heads were mixed in chewing
tobacco and given to the victim. Match heads were also inserted into rectum
for homicide.
(3) Suicide – Deliberate ingestion of rat paste.
(4) Accident – Inadvertent ingestion of rat paste.

II. MECHANICAL IRRITANTS

Mechanical irritants are sharp or blunt ingested foreign bodies, which cause
mechanical irritation upon ingestion.
Salient features:
(1) These should not be considered poisons in the true sense, as they do not
cause death on a biochemical basis.
(2) However since they do cause death on ingestion, they have been described as
poisons since long.
(3) These poisons act as local irritants and may cause perforation.
(4) Many of these substances are accidentally ingested by children.
(5) Important examples are: (i) bones [fish, chicken] (ii) button-type batteries [ch
33] (iii) chopped animal and vegetable hair (iv) coins (v) diamond powder (vi)
jewellery (vii) magnets (viii) nails (ix) pins and needles (x) powdered glass
and (xi) toys. (xii) Harmful substances that have been reported in food
(especially packaged food) from time to time are bone pieces, metal, cleats
(staple like wires used to hold together sections of conveyor belt in food
industry), fruit pits, herbaceous stems, rocks, insects and small animals.

35. Agricultural Poisons

Agricultural chemicals or agrochemicals are chemicals used in agriculture.

When ingested in toxic doses they may cause serious poisoning or death.
Agricultural poisons include fertilizers, pesticides, grain preservatives etc.
I. CLASSIFICATION

A. Classification of Agricultural Poisons

1. Classification [According to toxicity]

Pesticides (Chemicals used to kill pests, a subgroup of agricultural poisons) may
further be classified according to their toxicity.
(1) Least toxic [generally not fatal]
(i) Phenoxyacetic acid hormones [MCPA or 2-Methyl-4-ChloroPhenoxyacetic
Acid (Agritox); DCPA or 2,6-DiChloroPhenoxyacetic Acid; TCPA or
TriChloroPhenoxyacetic Acid. They are inhibitors of growth induced by
auxin. Used for weed control]
(ii) Cuprous oxide (Cu2O, fungicide)
(iii) Lime sulphur washes (orchard fungicides)
(iv) Tar oil emulsion (orchard ovicides)
(v) Petroleum washes (orchard insecticides)
(vi) Weak solutions of sulfuric acid, nitric acid, pelargonic acid or acetic acid
[Acids work by lowering pH level on target weeds just enough to kill them.
The residues left behind by these natural weed killers are either harmless or
useful to plants as fertilizer. Sulfuric acid, for example, oxidizes to form
sulfates]
(vii) Natural fungicides (a) Tea tree oil (b) Cinnamaldehyde (c) Cinnamon
essential oil (d) Jojoba oil (e) Neem oil (f) Rosemary oil.
(2) Mildly toxic [fatal dose >10 g]
(i) Chlorinated hydrocarbon insecticides [used as agricultural insecticides] (a)
DDT (b) Gammexane (c) Methoxychlor (d) Chlordane, aldrin, dieldrin
(ii) Sodium chlorate [used as a mass herbicide].
(3) Highly toxic [fatal dose <10 g]
(i) Arsenical compounds [used as weed-killers and orchard insecticides] (a)
Sodium arsenite (b) Lead and calcium arsenate (c) Copper Acetoarsenite
(Paris Green)
(ii) Nicotine, sulphates, tannates [used as horticultural insecticides]
(iii) HCN, KCN, NaCN [as disinfectants and raticides]
(iv) Dinitro compounds [dinitrophenol (DNP), DNOC (dinitro-orthocresol).
Selective weedkillers, ovicides and insecticides]
(v) Organophosphorus compounds [agricultural insecticides] (a)
Tetraethylpyrophosphate (TEPP) (b) Hexaethyltetraphosphate (HETP) (c)
Octamethylpyrophosphoramide (OMPA) (d) Parathion.

B. Classification of Insecticides
Insecticides (Chemicals used to kill insects, a subgroup of pesticides) may
further be classified according to their origin.
(1) Insecticides of vegetable origin
(i) Nicotine (ii) Pyrethrins (iii) Rotenone
(2) Chemical insecticides
(i) Inorganic (a) Compounds of arsenic, barium, mercury etc. (ii) Organic (a)
Organophosphorus compounds [OP] (b) Carbamates (c) Organochlorines
[OC] (i) Indane derivatives (chlordane, aldrin, dieldrin)
(ii) Chlorobenzene derivatives (DDT)
(iii) Benzene hexachloride (lindane, gammexane)
(iv) Chlorinated camphenes (Toxaphene, camphechlor, polychlorcamphene,
alltox, toxyphen, strobane-T).

C. Classification of OP
OP insecticides are divided into two main groups
(1) Alkyl phosphates
(2) Aryl phosphates depending on whether they have a liner side chain [alkyl]
or ringed side chain [aryl]. [1] Alkyl phosphates – Examples are (i) Demeton
(ii) Dimefox (iii) HexaEthyl TetraPhosphate [HETP] (iv) Isopestox (v)
Malathion (Killbug, Bugsoline) (vi) OctaMethyl PyroPhosphoramide
[OMPA] (vii) Sulfotepp (viii) TetraEthyl PyroPhosphate [TEPP] (Tetron) (ix)
Trichlorfon. [2] Aryl phosphates – Examples are (i) Chlorthion (ii) Diazinon
(Tik 20) (iii) Methyl parathion (Metacide) (iv) Paraoxon (v) Parathion
[nitrostigmine] (Follidol, Killphos, Ekato).

D. Absorption
OPs are well absorbed from the (1) skin, (2) lung, (3) GIT (4) Mucus membranes
[eg conjunctiva] and (5) direct injection. Plants absorb OP compounds through
leaves and stems.

E. Distribution
(1) widely distributed in the body
(2) Readily cross placenta
(3) Lipophilic"Thus cross BBB. Form deposits in fat and skin depending upon
lipophilicity of individual OP.

F. Metabolism
(1) Main sites – of metabolism are liver and blood. Minor sites are CNS, GIT,
Kidney, Lung and Skin.
(2) Enzymes responsible are
(i) A-esterases
(ii) Carboxylesterases [including B-esterases]
(iii) Fluorohydrolases and
(iv) Microsomal oxygenases [of these, cytochrome P450 (CYP enzymes) are
most imp.]
(3) Metabolism can both activate and deactivate OP. Aryl OP require liver
metabolism to become toxic.

G. Elimination
Prolonged over a week.

H. Mechanism of Action
OP are powerful inhibitors of carboxylic esterase enzymes, including
acetylcholinesterase (true cholinesterase) and pseudocholinesterase. Mechanism
may be understood in following steps:
(1) Normal transmission of impulse by Ach - With nerve impulse Ach is
released in neuromuscular cleft where it attaches to Ach receptors and
transmits impulse. It is then immediately deactivated by acetylcholinesterase
situated much deeper in the cleft.
(2) Normal deactivation of Ach - Normally Ach binds to cholinesterase at 2
sites -
(i) The quaternary nitrogen of choline attaches at the anionic site [
n
egatively charged] [Memory aid 1]
(ii) Carbonyl group attaches to a serine residue at esteratic site.
Memory Aid 2: Esteratic site
Serine residue is at e s t eratic site. Phosphate group attaches here to deactivate ChEase.
(3) Reaction catalyzed by AChE is: Ach + H2O"choline + acetate.
(4) OP deactivate cholinesterase [ChE]:
(i) by attaching a phosphate group to the hydroxyl group of a serine residue at
the enzyme’s active [esteratic] site.
(ii) The bond formed is strong and cannot be displaced even by high
concentrations of acetylcholine.
(iii) Recovery from such inhibition generally takes 10–14 days.
(iv) Deactivation of ChE results in accumulation of Ach molecules at (a)
ganglionic, (b) parasympathetic and (c) neuromuscular synapses, causing
overstimulation.
(v) OP inhibit all carboxylic esterase enzymes of which ChE is just one. Another
enzyme inhibited is Neuropathy target esterase [NTE], which is an integral
membrane protein present in all neurons. This results in OPIDP [please see
below].
(5) Aging:
(i) If cholinesterase reactivators [oximes] are not given in time, ChE undergoes a
process known as “aging”. It involves breaking away of one organic group
[R1] from the OP-ChE conjugate (dealkylation). This makes the OP-ChE
conjugate extremely stable and even oximes are unable to reactivate ChE
after “aging”.
(ii) Early administration - Thus oximes must be given within first few hours of
poisoning.
(iii) The rate of aging - varies with the particular OP compound [10 min with
soman; 48 hours with VX.].

I. Acute Poisoning

1. Clinical features
a. General considerations
(1) Ocular exposure causes persistent miosis
(2) Onset of symptoms most rapid following inhalation; least rapid following
dermal absorption
(3) First affected are secretory glands and involuntary muscles; then voluntary
muscles; and finally vital brain centers.

b. Signs and symptoms

i. Muscarinic manifestations
(1) General - Cyanosis
(2) Eyes -
(i) Pupils – (a) Constricted [mostly]. (b) Mechanism – peripheral. Local
cholinergic action [cf, morphine"ch40]. (c) Occasionally unequal. (d) May
be dilated rarely, if nicotinic effects prevail
(ii) Ciliary body – Blurred vision
(3) Glands – All secretions are -ed
(i) Sweat glands - -sweating
(ii) Lacrimal glands - (a) -lacrimation. (b) Chromodacryorrhea [shedding of
bloody tears] due to disturbance of porphyrin metabolism [porphyrinemia].
Porphyrin accumulates in the lacrimal glands.
(iii) Salivary glands - -Salivation
(4) Bronchial tree -
(i) Bronchoconstriction
(ii) -ed bronchial secretions [bronchorrhea]. These two are referred to as the
“killer B’s” of OP, as they are the leading cause of death.
(iii) Dyspnea
(5) Lungs – Pulmonary edema
(6) CVS -
(i) Bradycardia
(ii) Hypotension [rarely - opposite effects. It happens if nicotinic effects prevail]
(iii) ECG changes - (a) small voltage complexes (b) ST–T changes (c)
idioventricular rhythms, (d) ventricular extrasystoles, (e) prolonged PR
interval (f) polymorphic ventricular complexes.
(7) GIT - (i) Anorexia (ii) Nausea, vomiting (iii) Cramps (iv) Diarrhea (v) Fecal
incontinence (vi) Pancreatitis. Pseudopancreatic cyst forms rarely. (vii)
Tenesmus
(8) Poisoning during pregnancy -
(i) may mimic acute complications in pregnancy, eg eclampsia, seizures.
(ii) Spontaneous abortion.
(9) Bladder – Urinary incontinence.

ii. Nicotinic manifestations

(1) Striated muscle -
(i) Initially contraction [cramps]; later paralysis due to persistent depolarization
[muscular weakness, areflexia]
(ii) fasciculations
(2) Sympathetic ganglia -
(i) Hypertension
(ii) Tachycardia
(iii) Pallor
(iv) Mydriasis [These effects are exactly opposite to muscarinic effects.
Generally muscarinic effects are prevalent. Thus patient generally exhibits
bradycardia, hypotension and miosis].

iii. CNS manifestations

(1) Initially - (i) Ataxia (ii) Confusion (iii) Emotional lability (iv) Generalized
weakness (v) Headache (vi) Restlessness (vii) Slurred speech (viii) Tremor
(2) Later - (i) Depression of centers [resp and CVS] (ii) Drowsiness (iii)
hypothermia (iv) Convulsions (v) Coma.
Memory Aid 3: Symptoms of OP Poisoning
There are 2 mnemonics to remember muscarinic symptoms of OP Poisoning – 2 for muscarinic; 1 for
nicotinic and 1 for CNS manifestations.
[A] For muscarinic symptoms

1. SLUDGEM
Salivation
Lacrimation
Urination
Defecation
Gastrointestinal upset
Emesis
Miosis

2. DUMBBELS
Diarrhea
Urination
Miosis
Bronchorrhea
Bradycardia
Emesis
Lacrimation
Salivation, sweating

2. Lab diagnosis

a. Depression of cholinesterase activity

[A] Two types of cholinesterases - are found in the human body. (1) True
cholinesterase [Acetylcholinesterase, AChE, type I ChE].
Salient features:
(i) Found in (a) motor endplates (b) RBC and (c) gray matter (ii) At motor
endplates its function is to terminate nerve impulse transmission. It has a very
high catalytic activity — each molecule of AChE degrades about 25,000
molecules of Ach/s. (iii) RBC cholinesterase – a very similar enzyme - is found
in RBC membrane. Its function is unknown. Its levels are used to reflect
neuronal cholinesterase levels because (a) it is biochemically and structurally
quite similar to the neuronal AChE. (b) There is less inter- and intra-individual
variability.
(2) Pseudocholinesterase – [Butyrylcholinesterase, BChE, type II ChE].
Salient features:
(i) Synthesized in liver (ii) Found in (a) plasma, (b) white matter and (c) visceral
organs such as liver, heart and pancreas (d) GIT smooth muscle (e) Skin. (iii)
Activity - True cholinesterase hydrolyses acetylcholine more quickly;
Pseudocholinesterase hydrolyses butyrylcholine more quickly. (iv) Physiological
function - unknown. Postulated functions (a) role in the transmission of slow
nerve impulses, (b) in lipid metabolism (c) a regulatory role in choline
homeostasis (d) role in permeability of membranes (e) in the protection of fetus
from toxic compounds (f) a role in the degradation of acetylcholine and (g) in
tumorigenesis. (v) It hydrolyzes other esters on which AChE has no effect [eg
suxamethonium (succinylcholine), mivacurium, ester local anaesthetics,
diamorphine and aspirin]. Since it inactivates suxamethonium, it is of interest to
anesthesiologists. People with congenital deficiency of butyrylcholinesterase can
have hours of prolonged apnea after a normal dose of succinylcholine or
mivacurium. [B] Normal levels – (1) Normal values of cholinesterase activity as
measured by Michael’s method [in ΔpH/hour/0.02 ml red cells or plasma at
25°C] are given in Table 1.

[C] Levels of both RBC and plasma cholinesterase - .ed in OP poisoning.

Salient features:
(1) RBC cholinesterase is a better indicator of OP poisoning.
(2) Interpretation of levels - (i) 25% or greater depression"indicator of poisoning
(ii) 50% or greater depression"Clinical manifestations occur (iii) 90% or
greater depression"Death occurs.
(3) Regeneration:
(i) Rate of RBC cholinesterase regeneration"1%/day
(ii) Rate of pseudocholinesterase regeneration"3%/day. Thus RBC
cholinesterase falls slowly and regenerates slowly; pseudocholinesterase
falls early and regenerates early. In severe poisoning [>90% depression],
RBC cholinesterase would regenerate to normal levels in 90 days;
pseudocholinesterase would regenerate to normal levels in 30 days [Fig
35.1].
b. Blood
(1) RBC cholinesterase activity as above
(2) Hyperglycemia [hyperactivity of sympathetic ganglia"release of
catecholamines
(3) Hyperamylasemia.

c. Urine
(1) P-Nitrophenol test – P-Nitrophenol is a metabolite of several OP
compounds and is excreted in urine. Steam distillate of urine +
NaOH"Yellow color indicates presence of P-Nitrophenol.
(2) Glucosuria.

d. Thin layer chromatography

Ch 31.

e. Miscellaneous
Serum levels of OP – Not a prefereable method because (i) OP are difficult to
measure, because they are active at very low levels (ii) the levels are different in
different OP compounds (iii) Because of genetic differences, some people are
poisoned by lower levels of OP than others.

3. Management
(1) Prevention of further absorption –
(i) Remove patient from site of exposure
(ii) Remove contaminated clothing
(iii) Wash exposed areas with soap and water, followed by ethanol in water
(iv) Topical creams and lotions.
(v) In case of eye contamination irrigate eyes thoroughly in running water for
15 minutes
(2) Maintain airway – Most important step as copious secretions may be
blocking airways [cause of death in OP is respiratory failure]. (i) Clean airway
of secretions. (ii) Endotracheal intubation, (iii) Administration of Oxygen. (iv)
Positive pressure ventilation (v) Tracheostomy if necessary.
(3) Removal of unabsorbed poison - Stomach wash - with 1:5000 KMnO4
(4) Antidotes -
(i) Mechanical – Activated charcoal 1g/kg
(ii) Physiological – (a) Atropine sulphate – (I) Dose - 2-5 mg IV every 5-10
min until complete atropinization (dry flushed skin, Pulse 140/min,
pupillary dilatation) [pediatric dose 0.05 mg/kg]. A mild degree of
atropinization should be maintained for at least 48 hours. (II) Must be given
after cyanosis has been overcome. It is contraindicated in a cyanotic patient
because of the possibility of inducing ventricular fibrillation. (III) Reverses
the muscarinic and CNS actions of OP. No effect on nicotinic actions.
(5) Oximes – [A] Mechanism of action – (1) Main - Reactivate
acetylcholinesterase by attaching to the phosphorus atom and forming an
oxime-phosphonate which then splits away from the acetylcholinesterase
molecule. (2) Prevent formation of phosphorylated enzyme (3) Potentiate
actions of atropine; thus .the amount of atropine required (4) Directly detoxify
OP. [B] General points - (1) Should be started as early as possible, otherwise
aging occurs [please see above]. (2) Given until the patient is clinically well
and not requiring atropine. [C] Main oximes - (I) Pralidoxime – (i) Most
commonly used oxime (ii) Availability – Most commonly as (a) pralidoxime
chloride [2-PAM, Protopam. Used worldwide]. Other forms (b) mesylate
[P2S, used in the UK]. (c) Pralidoxime Iodide [2-Pyridine Aldoxime
MethIodide, 2-PAMI] (d) methylsulfate [2-PAM methylsulfate] (iii) Dose - (a)
1-2 g in 100 mL of 0.9% NaCl soln given IV over 15-30 minutes. (b) Repeated
in 1 h if muscle weakness and fasciculations are not relieved. Thereafter,
additional doses may be needed every 3-8 h as long as signs of poisoning
recur. (c) Maximum dose should not exceed 12 g in a 24 h period. (iv) Its
action is marked at nicotinic sites, often improving muscle strength within 10-
40 m. (v) Adverse effects – Rapid IV inj produces (a) temporary worsening of
cholinergic manifestations [because oximes are themselves mildly
anticholinergic. They bind to cholinesterase prior to regenerating its activity].
(II) Diacetylmonoxime [DAM] (III) Hagedorn oximes – [or H-Oximes].
These are newer oximes synthesized by Hagedorn and coworkers, because
traditional oximes [eg pralidoxime, obidoxime] are ineffective against OP
nerve gases [eg soman]. These are effective against all known OPs. Ex (i)
LüH-6 [syn by Lüttringhaus and Hagedorn] (ii) HI-6 – or Asoxime chloride
(iii) HLö-7 [syn by Hagedorn and Löffler]. (V) Methoxime [MMB-4] –
 Particularly useful against nerve agents, eg sarin. Also used is 4-Pyridine
aldoxime (4-PA), metabolite of MMB-4. (VI) Monoisonitrosoacetone
[MINA] (VII)Obidoxime Chloride – more potent, but more toxic also. Dose
250 mg IV or IM. (VIII) Sugar oximes - Traditional oximes [eg Pralidoxime
and even HI-6] do not effectively cross BBB [penetration of 2-PAM is <10%].
Therefore, they do not provide protection against the neurological effects of
OP-exposure [seizures, convulsions, behavioral and psychological changes].
Now new novel sugar–oximes have been developed, which cross the BBB
because they contain a sugar moiety. (IX) Trimedoxime bromide [syn
dipyroxime, TMB-4]
(6) Control of convulsions - (A) Benzodiazepines –
(i) Actions - (a) Anticonvulsant (b) .es synaptic release of ACh. Most useful
agent is diazepam.
(ii) Dose [WHO recommendation]- (a) Adults - 5–10mg IV in absence of
convulsions and 10–20mg IV in cases with convulsions. (b) Children - 0.2–
0.3 mg/kg IV [maximum 5mg in children <5 y, and 10mg in children >5 y].
Given slowly over 3min. Repeated as required. May be repeated in adults
every 10–15 min [max 30 mg]
(iii) Combination of atropine and diazepam is more effective in .ing mortality
than atropine or oxime alone.
(iv) Beneficial effects - (a) .es anxiety, apprehension, agitation and restlessness
(b) .es muscle fasciculation (c) arrests seizures, convulsions (d) Counteracts
some effects of CNS toxicity which are not affected by atropine (e) .es
morbidity and mortality when used in conjunction with atropine and an
oxime. If convulsions persist, use (B) Phenobarbital – 10-20 mg/kg IV or
(C) Phenytoin – 20 mg/kg IV. If status epilepticus develops give (D)
General anesthesia
(7) Plasma alkalinization - with NaHCO3 has been tried, but results are not
encouraging.
(8) Adjunct and alternative therapies -
(i) Bioscavenger therapy - involves the use of enzymes such as cholinesterases
(ChEs) in order to sequester OP compounds before they reach their
physiological targets. Just as OPs are anticholinesterases, cholinesterases
may be viewed as “anti-OP agents”. Main agents used are (a)
cholinesterases and related enzymes [Purified human BChE, beta-
 esterases]- They bind and neutralize OP. (b) OP hydrolases and anhydrases
– These are bacterial enzymes, which have recently shown promising
results in animal models. They catalytically hydrolyse and inactivate OP
compounds;
(ii) Antibiotics – to prevent pulmonary infections.

4. Fatal dose
(1) TEPP [TetraEthyl PyroPhosphate] (most toxic) – 100 mg orally [50 mg IM]
(2) OMPA [OctaMethyl-PyrophosphorAmide], Parathion – 175 mg orally [80
mg IM]
(3) HETP[HexaEthyl TetraPhosphate] –350 mg orally [60 mg IM]
(4) Malathion and Diazinon – 1 g orally.

5. Fatal period
(1) Untreated cases – 24 hours
(2) Treatment given, but turned out unsuccessful – 10 days.

6. Cause of death
Respiratory failure – Due to
(1) Weakness of the muscles of respiration and
(2) Accumulation of excessive secretions in the respiratory tract.

7. PM appearances

a. External
(1) Signs of asphyxia - (i) congestion of face (ii) cyanosis of lips, nose, fingers
and extremities. (iii) Blood stained froth at nose and mouth
(2) Pupils - constricted
(3) Kerosene like odor - from mouth, gastric contents and body [because OP are
dissolved in Aromax, a petroleum derivative]
(4) Insects and flies - die immediately after they alight on an opened cadaver at
autopsy.

b. Internal
(1) Gastric mucosa – (i) Congested (ii) Sometimes hemorrhagic (iii) Sometimes
 found to contain an oily greenish scum [due to indigocarmine. Please see
above].
(2) Respiratory passages - (i) Congested (ii) Contain frothy hemorrhagic
exudate.
(3) Heart – soft and flabby. May show epicardial hgs especially in survival of
more than a day.
(4) Lungs - (i) Gross congestion (ii) Sub pleural petechiae (iii) Hemorrhagic
pulmonary edema.
(5) Brain - (i) Congested and edematous (ii) Meninges congested
(6) Viscera - (i) Congested (ii) Show petechial hgs [asphyxia]

J. Intermediate Syndrome
(1) Sometimes delayed muscle weakness without fascicu-lations or cholinergic
features occurs 1-4 days after acute OP exposure.
(2) Signs and symptoms - (i) Upper body weakness. The most commonly
affected muscles are the facial, extraocular, palatal, respiratory, and proximal
limb muscles. The muscle weakness can progress to respiratory distress and
paralysis (ii) Cranial nerve palsies, (iii) Areflexia (iv) Fasciculations occur
rarely (v) Level of consciousness is rarely affected.
(3) Treatment -
(i) Mainly supportive with airway protection and ventilatory assistance.
(ii) Pralidoxime or atropine are ineffective
(4) Resolution - Syndrome may automatically resolve within 5–18 days when
the body burden of OP metabolites diminish and cholinesterase levels
normalize.

K. OPIDP [Delayed Sequelae]

OrganoPhosphorus Induced Delayed Polyneuropathy [OPIDP] [sometimes also
called OrganoPhosphorus Induced Delayed Neuropathy (OPIDN)] is a delayed
sequelae of acute exposure. It is due to inhibition of NTE [please see above
under “mech of action”]. Most typically acute poisoning occurs within 1-4
hours; intermediate syndrome within 1-4 days; and OPIDP within 1-4 weeks
after exposure. Signs and symptoms – Distal limb muscles are involved [in
contrast to proximal limb muscles in intermediate syndrome].
Memory Aid 4: Signs and symptoms of OPIDP
In Delayed polyneuropathy, Distal muscles are involved

L. Chronic Poisoning
Chronic poisoning with OP is different than OPIDP. Chronic poisoning develops
months or years after continued exposure. OPIDP on the other hand is merely a
delayed sequelae of acute exposure.
(1) Persons at risk:
(i) Usually occurs as an occupational hazard in agricultural workers [eg those
engaged in pesticide spraying of crops]
(ii) Persons engaged in manufacture and packaging of OP compounds
(iii) Research workers
(iv) Cholinergic ophthalmic preparations
(v) Family members of all workers exposed to OP
(2) Absorption - occurs through inhalation or skin contamination. Symptoms
may appear after several months or years of low grade exposure.

1. Signs and symptoms [of chronic OP poisoning]

(1) Neuropsychiatric symptoms – Most characteristic and typical. (i)
Personality change (ii) Mood destabilization (iii) Suicidal thinking (iv)
Cognitive impairment (v) Language disorder - Word-finding and expressive
disorders (vi) Handwriting deterioration - Significant decrease in legibility
worsening with length of text (vii) anxiety (viii) confusion (ix) drowsiness (x)
gait disorders [Parkinson disease like symptoms] (xi) irritability (xii) muscle
cramps (xiii) paresthesias (xiv) weakness
(2) Alcohol intolerance - Marked increase in the inebriating effect of alcohol;
may also involve severe hangover and quasi-allergic effects
(3) Heightened sense of smell - Typically to perfumes and scents; may be so
severe as to make patients feel ill
(4) Decreased exercise tolerance - Normal initial muscle power, but inability to
maintain it. This is not the same as generalized weakness.
(5) Dipper’s flu - One or more episodes of severe flu-like symptoms lasting
more than three days following exposure. May be accompanied by
hypersalivation, abdominal cramps and diarrhoea. Symptoms may be triggered
by extremely low concentrations of organophosphates.
2. Prevention
Workers in contact with OP compounds should have baseline cholinesterase
testing for comparison and monitoring, especially RBC cholinesterase.

M. Medicolegal Importance [of OP]

(1) Suicide - very common. Alone or mixed with other poisons.
(2) Homicide – rare because of strong smell and bad taste
(3) Organophosphates resist putrefaction - Can be detected in the viscera for
quite sometime after death.
(4) Accident – Quite common
(5) Restricted Use Pesticide (RUP) - A Restricted Use Pesticide is one that is
available for purchase and use only by certified pesticide applicators or
persons under their direct supervision. This designation is assigned to a
pesticide product because of its relatively high degree of potential human and
environmental hazard even when used according to label directions. Restricted
use OP compounds in India are (i) Diazinon (ii) Fenitrothion, (iii) Fenthion,
(iv) Methyl Parathion and (v) Monocrotophos.

II. CARBAMATES

Carbamates are organic compounds derived from carbamic acid (NH2COOH).

Salient features:
(1) Marketed in the form of dusts or solutions eg Aldicarb [Temik], Aminocarb
[Matacil], Carbaryl [Sevin], Carbofuran [Furadan], Fenobucarb [Merlino],
Propoxur [Aprocarb, Baygon]
(2) Table 3 shows some carbamates according to toxicity.
A. Toxicokinetics
(1) Absorption - Carbamates are rapidly absorbed from the small intestine or on
inhalation. Peak concentrations occur rapidly.
(2) Distribution - Usually large Vd.
(3) Elimination - Metabolized in the liver. Excreted in the urine within several
days. Aldicarb undergoes extensive enterohepatic recirculation.

B. Signs and Symptoms

Same as those of OP - It is helpful to visualize carbamates as “younger brothers
of OP”, in the sense that they produce similar symptoms, but much less
pronounced. This is because (i) unlike OP, they hydrolyze spontaneously by
cholinesterase within 24-48 h, whereas, OP does not (ii) They do not penetrate
BBB; thus CNS toxicity is minimal.

C. Management
(1) Atropine – Drug of 1st choice
(2) Oximes – contraindicated [because it produces a carbamylated oxime, which
is a more potent cholinesterase inhibitor than carbamate itself]. The only
situations when oximes my be given in carbamates are
(i) Unknown pesticide ingestion – signs and symptoms similar to OP
(ii) Mixed [OP+carbamate] ingestion
(iii) Continued excessive requirements of atropine
(iv) Symptoms are life threatening [severe muscle weakness, paralysis, .ed
respiration]
(3) Adjunct therapies – Same as in OP.

III. ORGANOCHLORINES

Organochlorines [OC] are organic compounds containing at least one chlorine

atom, which are used as insecticides.
Salient features:
(1) OC are nonselective insecticides
(2) They are cyclic in nature, have molecular weights between 300 and 550 D
(3) They are CNS stimulants
(4) Poorly soluble in water but readily soluble in organic solvents, lipids and
fats, which is why they accumulate in the human body [this is also why fat
must be preserved in cases of organochlorine poisoning; please see ch 5 –
preservation of viscera].
(5) Very stable, both in the environment and in the body tissues, and can be
demonstrated in the bodies of most people born since 1940.

A. Toxicokinetics

1. Absorption
(1) General - Absorption by any route depends on (i) vehicle and (ii) the physical
state (solid or liquid) of the compound.
(2) Ingestion and inhalation - All OCs are well-absorbed by these routes.
(3) Transdermal absorption -
(i) Variable. Factors which enhance dermal absorption are (a) Nature of the
compound (b) anatomic site
(ii) DDT, its analogues and toxaphene are very poorly absorbed.

2. Metabolism
OC are metabolized by the hepatic microsomal enzyme systems by
dechlorination, oxidation, with subsequent conjugation.
(1) OCs rapidly metabolized (i) Endrin (ii) Lindane. Have less persistence in
 body tissues
(2) OCs slowly metabolized - (i) DDT (ii) Dieldrin. Have significant adipose
tissue storage especially in chronically exposed populations.

3. Excretion
(1) Primary route of OC excretion is bile.
(2) Most OCs have significant enterohepatic or enteroenteric recirculation [eg
chlordecone, mirex]
(3) Excreted in maternal milk [because lipophilic]
(4) Half-lives - (i) lindane - 21 hours. (ii) Chlordecone, DDT – several months
[because of fat solubility and poor metabolism].

B. Mechanism of Action
(1) Selectively bind to open (activated) Na+ channels and slow their closing
(inactivation), thus allowing the influx of sodium ions.
(2) The mechanism is quite similar to that of pyrethrins [please see below],
despite their different chemical structures.
(3) The continuous inward ion current causes depolarization and repetitive firing
of the nerve membrane.
(4) This is clinically seen as prominent tremors.
(5) DDT-induced tremors can be prevented by pretreatment with phenytoin, a
Na+ channel blocker.

C. Acute Poisoning

1. Signs and symptoms

(1) Prodromal signs or symptoms – (i) agitation (ii) confusion (iii) dizziness
(iv) headache (v) hyperesthesia and paresthesias of the mouth, tongue face and
extremities (vi) leg weakness (vii) Nausea and vomiting. With lindane, the
cyclodienes, and toxaphene, there are no prodromal signs or symptoms. Often
the first manifestation of toxicity is a generalized seizure.
(2) CNS stimulation – (i) Myoclonus (ii) Tremors - May be the only initial
manifestation after DDT exposure (iii) Seizures - (a) occur only after very
high exposures (b) Occur within 1-2 hours of ingestion on an empty stomach;
in 5-6 hours on a full stomach. (c) Dermal application – of 1% lindane for
 treatment of ectoparasitic diseases may cause seizures. The time from
application to seizure onset can vary from hours to days. (d) Status epilepticus
- Seizures are mostly self-limited, but may recur or result in status epilepticus.
(e) EEG abnormalities – occur before, during, and following seizures. (f)
Recovery - If the seizures are brief and hypoxia has not occurred, recovery is
usually complete.
(3) Hyperthermia – Occurs due to (a) -ed muscle activity (b) aspiration
pneumonitis.
(4) Pupils - dilated
(5) Synergy - Ingestion of combinations results in significantly -ed toxicity [eg
DDT and lindane]
(6) Respiratory failure, and death.

2. Fatal dose
(1) Aldrin, Dieldrin, Endrin – 2-6 g
(2) DDT, Lindane [also known as Benzene hexachloride (BHC), Gamma-
hexachlorocyclohexane, (γ-HCH), Gammallin and Gammaxene] – 15-30 g.
When lindane is ingested therapeutically as an anthelmintic at 40 mg/d for up
to 2 wks, no symptoms are produced.

3. Fatal period
One to several hours.

D. Management
(1) Measures for rescue personnel and bystanders – should wear protective
gear (apron, gloves etc), because OC may be absorbed through skin [being oil
soluble].
(2) Immediate resuscitative measures – ABCDE of resuscitation [ch 32] (i)
Move patient from toxic environment to fresh air. Monitor for respiratory
distress etc. If present"start measures for respiratory insufficiency.
(3) Clothing, jewellery etc – remove immediately. Leather absorbs pesticides;
discard all contaminated leather items.
(4) Decontamination -
(i) Contact – wash [skin, hair, nails, eyes, other exposed areas] copiously with
water
(ii) Ingestion - (a) Emetics (b) Gastric lavage (c) Cathartics. Oil based cathartics
are contraindicated [please see below].
(5) Activated charcoal
(6) Fats, oils etc not to be given by mouth.
(7) Specific antidote - None
(8) Cholestyramine -
(i) It is a non-absorbable steroid binding ion exchange resin. Binds bile acids,
digitalis [ch 43]
(ii) -es fecal excretion of OC [especially chlordecone]
(iii) Dose – 4 g qid [16g/day] orally [mixed in fruit juice] for 2 weeks
(iv) Precautions – Interferes with absorption of other drugs, which must be
administered either 1 h before or 4 h after administration of cholestyramine.
(9) Symptomatic treatment – Manage (i) Hyperthermia (ii) seizures – [ch 32]
(10) Calcium gluconate
(11) Contraindicated drugs -
(i) Adrenergic amines [eg adrenaline]. -myocardial irritability, produce refractory
ventricular arrhythmias
(ii) Atropine
(iii) Oil based drugs [including cathartics].
(12) Hemodialysis, hemoperfusion – not effective.

E. PM Appearances
(1) Mouth and stomach contents – smell of kerosene
(2) Signs of asphyxia
(3) Liver - Centrilobular hepatic necrosis.

F. Chronic Poisoning
Many OCs, especially Chlordecone (Kepone) persist in the body and produce
chronic toxicity. Symptoms are (1) ataxia (2) exaggerated startle response (3)
intracranial hypertension (4) mental status changes (5) oligospermia (6)
opsoclonus [rapid, irregular, dysrhythmic ocular movements] (7) rash (8) Tremor
of head, hands and even entire body [Kepone Shakes] (9) weakness, (10) weight
loss, (11) -ed liver enzymes (12) .ed sperm motility.
G. Specific Organochlorines

1. DDT
DDT is an organochlorine insecticide. It is a colorless, crystalline solid with a
weak, chemical odor.
Salient features:
(1) It is nearly insoluble in water but has a good solubility in most organic
solvents, fats, and oils.
(2) It is a restricted use OC in India.

2. Endrin
Endrin, a cyclodiene, was once used chiefly against insect pests of cotton (about
80% of total use), paddy, sugarcane, tobacco and in a limited way on grain crops.
Salient features:
(1) It is a colorless odorless solid, although commercial samples are often off-
white.
(2) Active against a wide variety of insect pests (as well as rodents); hence is
commonly known as plant penicillin.
(3) It has been banned in India and several other countries.

H. Medicolegal Importance [of Organochlorines]

(1) Suicide - common
(2) Homicide – rare because of strong smell and bad taste
(3) Accident – Quite common
(4) Occupational exposure – leads to suits for compensation
(5) Endrin resists putrefaction. Can be detected in the viscera for quite some
time after death.
(6) Banned OCs in India - Following OCs are banned in India for manufacture,
import and use (i) Aldrin (ii) Chlordane (iii) Dieldrin (iv) Endrin (v)
Heptachlor (vi) Lindane (vii) Toxaphene
(7) Restricted use OCs in India are - (i) DDT (ii) Endosulfan (iii) Lindane [for
def of restricted use insecticides, please see under MLI of OP].

IV. ALUMINUM PHOSPHIDE

Aluminum phosphide (AlP) is a lethal solid fumigant pesticide, insecticide and
rodenticide.
Salient features:
(1) Common outdoor and indoor pesticide - in developing countries like India
as it is (i) cheap (ii) effective (iii) free from toxic residue and (iv) does not
affect seed viability. Considered an ideal grain and tobacco preservative in
India.
(2) Availability -
(i) Available as dark brown or grayish green tablets of 3 g each. Also available
as 0.6 g pellets.
(ii) Size – diameter - 20 mm; thickness - 5 mm
(iii) Container - sealed in tens and twenties in airtight aluminum containers
(iv) Composition - Tablets are composed of pure AlP [the active ingredient,
which releases phosphine gas; 56%] and ammonium
carbamate/carbonate/urea [the inert ingredient, which release CO2 and NH3
which prevents self ignition of phosphine gas; 44%].
(v) Tablets of AlP are sometimes referred to as “Rice Tablets”.
(3) Phosphine – On contact with moisture each 3 g tablet liberates 1 g of
phosphine [kills insects and rodents in all stages of development] along with
CO2 and NH3 [from inert ingredients].
(4) Trade names – Available in India under following trade names - Alphos,
Bidphos, Celphos, Chemfume, Degesch, Delicia, Fumigram, Phosphotek,
Phosphume, Phostoxin, Quickphos, Synfume and Talunex.
(5) Other pesticides similar to AlP in action are zinc phosphide [Zn3P2, please
see below] and calcium phosphide [Ca3P2].

A. Toxicokinetics [Absorption and Excretion]

(1) Absorption –
(i) GIT - Rapidly absorbed from GIT by simple diffusion
(ii) Lungs – Phosphine liberated from AlP can be readily absorbed through lungs
(2) Metabolism –
(i) AlP – Some AlP is transported to liver, where it is slowly metabolized to
phosphine, accounting for prolongation of symptoms.
(ii) PH3 - Oxidized to oxyacids. Excreted in the urine as hypophosphite and also
through the lung in the unchanged form.

B. Mechanism of Action
(1) Formation of phosphine - On coming to contact with moisture present in
the air [or with HCl and water in the stomach], AlP liberates phosphine
leaving behind aluminum hydroxide [or chloride], which is a harmless and
non toxic grayish white residue:
(i) AlP+3H2O"Al(OH)3+PH3- [in air or stomach].
(ii) AlP+3HCl"AlCl3+PH3- [in stomach].
(2) Mechanisms of toxicity of liberated phosphine:
(i) Esophagus - Causes esophageal strictures by more than one mechanism (a)
AlP – is thought to be corrosive. However it is controversial, since both
unexposed and exposed tablets produce strictures. (b) Tablets of AlP are
usually large"Get stuck in the oesophageal lumen causing local ulcerations
due to some preservative or adulterant present within the tablet.
(ii) Lungs - Direct injury to alveolar capillary membrane.
(iii) Liver - Disturbance of hepatic fat metabolism.
(iv) Heart - Exact underlying mechanism of cardiotoxicity and acute circulatory
failure not well understood.
(v) Cellular level - (a) Action on cytochromes - Phosphine reacts with
cytochrome c and cytochrome c oxidase, inhibiting mitochondrial oxygen
uptake [action similar to that of CN and H2S (ch 44)]. (b) Blockage of
oxidative phosphorylation (c) .catalase; -superoxide dismutase. (d)
Formation of highly reactive hydroxyl radicals. Leads to (I) Lipid
peroxidation [oxidative degradation of lipids; a process in which free
radicals “steal” electrons from the lipids in cell membranes, resulting in cell
damage]. (II) Oxidative stress"acute lung injury. .glutathione,
.malonyldialdehyde indicate oxidative stress.
(vi) Heme - Phosphine reacts with the heme moiety of hemoglobin in the
presence of oxygen.

C. Signs and Symptoms

Human toxicity occurs either due to the ingestion of AlP (commonest mode),
inhalation (uncommon) or even after absorption through the skin (rare).

1. Ingestion
Symptoms begin within half an hour. They are more pronounced if an unexposed
tablet is consumed [liberates more PH3]
(1) GIT – These are the initial and presenting symptoms
(i) Metallic taste
(ii) Excessive thirst
(iii) odor - Garlicky or of decaying fish [PH3 is colorless and odorless in the pure
form but due to the presence of substituted phosphines and diphosphines,
the patient has this characteristic odor].
(iv) Burning epigastric pain
(v) Vomiting and Diarrhoea
(vi) Esophageal strictures – AlP produces esophageal strictures much like
caustic-induced strictures [because of its corrosive action], in about 1/3rd of
patients. Onset of dysphagia is within 2 to 8 weeks of ingestion.
(vii) Tracheoesophageal fistula – for the same reason.
(2) Hepatic: (i) Hepatitis (ii) Hepatomegaly (iii) Jaundice
(3) Pancreas – pancreatitis
(4) CNS -(i) Restlessness (ii) Headache (iii) Dizziness (iv) Altered mental state
(v) acute hypoxic encephalopathy (vi) convulsions (vii) coma. Patients may
remain conscious till the late stage.
(5) Hematological – (i) intravascular hemolysis (ii) methemoglobinemia (iii)
microangiopathic hemolytic anemia
(6) CVS -
(i) ECG abnormalities – May be attributed to .Mg levels [this is the basis of
MgSO4 therapy](a) rhythm disturbances, (b) ST-T changes and (c)
conduction defects.
(ii) Arrhythmias
(iii) Myocarditis
(iv) Profound and refractory hypotension [in 75%-100% cases] - due to
myocardial damage, peripheral vasodilatation and fluid loss.
(v) Subendocardial infarction
(vi) Shock
(7) Respiratory - (i) Cough (ii) Tachypnea and dyspnea (iii) Cyanosis (iv)
Pulmonary edema (v) Respiratory failure.
(8) Renal - Renal failure
(9) Metabolic - Metabolic acidosis [due to the accumulation of lactic acid
caused by blockage of oxidative phosphorylation and poor tissue perfusion]
(10) Miscellaneous – (i) Acute adrenocortical insufficiency (ii) Bleeding
diathesis [due to widespread capillary damage] (iii) DIC (iv) hypo- or
hyperglycemia (v) Muscle wasting (vi) Spontaneous ignition at nose or mouth
– Due to liberated PH3. (vii) Tenderness. All these are rarely seen.

2. Inhalation [of phosphine]

a. Acute toxicity
Circumstances of poisoning:
(1) Opening a long closed fumigated godown - Inhalation [of PH3] may occur
if a person opens a long closed godown of grains preserved with AlP.
(2) During play - Children have died playing on fumigated wheat for just 1 h.
(3) During travel - Deaths have been reported when people were travelling in
fumigated boxcars containing grains fumigated with aluminum phosphide. In
one report, the victims had been in the car for approx 16 h and had even
periodically opened the hatch for fresh air as needed.
(4) House near a storage facility - Death can occur even if victim’s house is a
little away from a storage facility where grains are preserved with AlP.

i. Mild toxicity
(1) Nausea, vomiting, diarrhea, headache (2) Acute respiratory distress (3)
Dizziness (4) Fatigue (5) Irritation of mucus membranes (6) Tightness in the
chest.

ii. Moderate toxicity

(1) Ataxia (2) Diplopia (3) Incoordination (4) Jaundice (5) Muscular (6)
weakness (7) Numbness (8) Paresthesias (9) Tremor (10) Paralysis.

iii. Severe toxicity

(1) Arrhythmias (2) Congestive heart failure (3) Pulmonary edema (4)
Convulsions (5) Coma.

b. Chronic toxicity
Chronic toxicity may occur due to repeated occupational exposure with AlP
tablets [slow inhalation of PH3]. Symptoms are (1) Anemia (2) Bronchitis (3)
GIT, visual, speech and motor disturbances.

3. Complications
(1) Pericarditis (2) Acute CCF (3) Acute massive GIT bleeding (4) ARDS.

D. Management
Doctors, nurses, and all paramedical staff must take personal protection
measures, including full face mask and rubber gloves during management. One
should be beware of “spontaneous ignition” also.
(1) Immediate:
(i) If there is occupational or accidental exposure to phosphine gas - the patient
should immediately be removed to fresh air. As PH3 is absorbed through the
cutaneous route, decontamination of skin and eyes must be carried out
thoroughly with plain water as early as possible.
(ii) Confirm airway patency –At the hospital, protect airways with endotracheal
tube to prevent aspiration pneumonitis
(iii) Start supplementary oxygen
(iv) Check for pulse
(v) Establish IV access, preferably central venous, to start normal saline and
vasopressor therapy as appropriate
(vi) Monitoring of vitals
(vii) Investigations - ECG, chest X-ray, blood glucose, arterial blood gas,
electrolytes including magnesium, routine hemogram, LFT and KFT.
Repeated or continuous ECG and echocardiography can reveal cardiac
dysfunction early.
(2) Gastric lavage – In cases of ingestion. But only after endotracheal
intubation. KMnO4 [1:10,000] is used as it oxidizes PH3 to nontoxic
phosphate. Repeated 2-3 times.
(3) AC - 100 g of activated charcoal
(4) Antacids – (i) Reduce stomach related symptoms. (ii) Reduce absorption of
phosphine
(5) Fats and oils - (i) Mainly vegetable oils [coconut oil] and liquid paraffin. (ii)
Inhibit PH3 release from the ingested AlP.
(6) Maintain adequate renal perfusion and urine output - Phosphine
excretion is -ed.
(7) Magnesium sulphate –
(i) May cause up to 50% .in mortality.
(ii) Mechanism of action - (a) cell membrane stabilization ".es incidence of fatal
arrhythmias (b) combats free radical stress due to phosphine. (c) Corrects
hypomagnesemia and arrhythmias.
(iii) Dose –1g stat, then 1 g every hour for the next 2 h and then 1–1.5 g every 6
h for 5–7 days.
(8) Cathartics - Sorbitol [1–2 ml/kg]
(9) Hemodynamic Support:
(i) Rationale - Necessary because myocardial injury and hemodynamic
instability are major features.
(ii) Objectives - to attain adequate tissue perfusion and oxygenation and
physiologic metabolic milieu compatible with life
(iii) Measures undertaken - (a) continuous invasive hemodynamic monitoring (b)
IV fluids - 4-6 L of fluids during first 3-6 h, of which 50% must be normal
saline. Fluid therapy should be guided by central venous pressure (CVP) or
pulmonary artery wedge pressure (PAWP) monitoring. (c) vasoactive agents
- For refractory hypotension [Norepinephrine, phenylephrine]. Vasoactive
agents with more β-receptor agonist action [dobutamine, dopamine (4-
6μg/kg/min)] should be used cautiously as they are prone to inducing
arrhythmias. (d) following should be readily available at bedside for
emergency use - (I) Anti-arrhythmic agents, (II) DC cardioversion (III)
temporary pacemaker. (e) Repeated echocardiography – to assess the
reversibility of myocardial injury. (f) Advanced measures - (I) intra-aortic
balloon pump (IABP) to mechanically support the heart (II) extracorporeal
life support (ECLS) for intractable circulatory collapse.
(10) Early Identification and Managing Other Organ Failures:
(i) O2 therapy – for hypoxia (a) If no response, then rule out methemoglobinemia
by (I) multiple wave length co oximetry or (II) plasma level of
 methemoglobin. (b) If methemoglobinemia present – IV methylene blue
[1% soln] 2 mg/kg over 5 mins. Repeated if cyanosis is not resolved.
(ii) Endotracheal intubation and mechanical ventilation - for acute lung injury.
(iii) IV sodium bicarbonate - for metabolic acidosis
(iv) Hemodialysis - Not very effective in removing phosphine but is helpful
when renal failure, severe metabolic acidosis or fluid overload is present.
(v) Peritoneal dialysis – if hemodialysis not available or possible
(11) For survivors – Mortality is very high [35-100%] despite institution of
treatment. Following measures for survivors:
(i) If swallowing difficulty - conduct barium swallow study and upper GIT
endoscopy for detection of esophageal strictures [late complication]. If
present - (a) Endoscopic dilation of esophagus. About 5 dilations are
required. (b) Intralesional steroids to augment the effect of dilation. (c)
surgical intervention, if all other measures fail.
(ii) Psychosocial counselling – (a) to cope with possible reduction of quality of
life due to late complications (b) to prevent repeat suicidal administration.

E. Diagnostic Tests
(1) Tests for phosphine – AlP liberates Phosphine [please see above]
(i) Live patients - (a) Gastric aspirate – (I) Procedure - 5ml gastric aspirate +
15ml H2O"Put in a flask"Cover mouth with filter paper impregnated with
0.1N AgNO3"Heat at 50°C for 15 min"If AlP is present in gastric aspirate,
phosphine will form and blacken the filter paper due to formation of silver
phosphide. PH3+3AgNO3"Ag3P+3HNO3. (b) Face mask – A filter paper is
impregnated with 0.1 N AgNO3 and used as a face mask. Patient is asked to
breathe in and out of this filter paper for 15 min. If phosphine is present,
filter paper will turn black. The test is +ve only if the patient has ingested
>6g AlP. Thus it is less reliable
(ii) PM Samples – (a) Use gastric contents as gastric aspirate above. (b) Gas
chromatography with a nitrogen–phosphorous detector - is the most specific
and sensitive test. It can be used for analysis of airtight samples [viscera
and gastric content] collected during autopsy.
(2) -in SGOT and SGPT, leucine aminopeptidase, aldolase, alkaline phosphatase,
and albumin. [-ed liver enzymes are due to cell death and loss of cell
 membrane integrity].
(3) Magnesium levels - Both hypo- and hypermagnesemia may occur. Their
pathogenesis is not clear. There is a direct relationship between ECG changes
and .Mg levels. The mortality is also related directly to hypomagnesemia.

F. Fatal Dose
(1) AlP -
(i) Ingestion of 1-3 tablets [3-9 g].
(ii) Since active ingredient [AlP] is only 56% in the tablet, the adjusted fatal
dose of pure AlP is 1.5-5g. Survival is unlikely if more than 1.5 g is
ingested.
(iii) Survival has been reported after ingestion of 9.0 g or more. Possible
explanations - vomiting, exposure of tablets before ingestion, early
availability of supportive care.
(2) Phosphine -
(i) The permissible exposure limit of phosphine is <0.3 ppm in the working
environment.
(ii) Inhalation of 0.25 ppm (0.35 mg/m3) of PH3 for 8 hours can cause serious
illness
(iii) Inhalation of 7.2 ppm (10 mg/m3) of PH3 for 10 min is fatal.
(iv) >50 ppm - dangerous to life.
(v) 400–600 ppm - Lethal within 30 min.

G. Fatal Period
24 hours. Range 1 h-4d

H. Cause of Death
(1) Within 24 h - (i) Cardiogenic shock [CVS failure] (ii) hemodynamic
instability (iii) Myocardial injury (iv) arrhythmias
(2) After 24 h - (i) acidosis (ii) ARDS (iii) refractory shock.

I. PM Appearances

1. Gross
(1) Garlic like odor – at mouth, nostrils, stomach contents. Very specific
(2) Blood stained froth – at mouth and nostrils
(3) Congestion – lower part of esophagus, stomach, duodenum, intestines, all
internal organs.

2. Histopathological
Suggestive of cellular hypoxia.
(1) Stomach – (i) Congestion (ii) Edema (iii) Leukocytic infiltration (iv)
Sloughing of gastric mucosa
(2) Heart – (i) Congestion (ii) edema (iii) Fragmentation of fibres (iv) Focal
necrosis (v) Leukocytic infiltration (vi) Hemorrhagic myocardial lesions (vii)
Myocardial muscles show (a) myocyte vacuolation, (b) areas of myocytolysis
and (c) degeneration.
(3) Lungs – (i) Congestion (ii) Desquamation of respiratory epithelium (iii)
Edema (iv) Lymphocytic infiltration (v) Thickened alveoli (vi) Diffuse vessel
injury with edema and atelectasis
(4) Brain – (i) Congestion (ii) edema (iii) Disorganization of different layers,
(iv) paucity of glial cells, (v) degeneration of neurons and (vi) appearance of
necrotic patches.
(5) Liver – Centrizonal hemorrhagic necrosis
(6) Renal – (i) Congestion (ii) Cloudy swelling of renal tubular epithelia (iii)
Acute tubular necrosis.
(7) Suprarenal – (i) Congestion (ii) Hemorrhage (iii) Necrosis (iv) Lipid
depletion in cortex.

J. ML Importance
(1) AlP is a restricted use pesticide [RUP] in India. [for def of restricted use
insecticides, please see under MLI of OP]
(2) Suicidal poison - Most common cause of suicidal poisoning in northern
India. Cases of poisoning were first reported in India in 1980. Before that
poisoning in India was unknown.
(3) Accidental – occasionally
(4) Homicidal – rare. Difficult because of smell.

V. ZINC PHOSPHIDE
Zinc phosphide [Zn3P2] is a popular rodenticide available in India as dark grey
tetragonal crystals or crystalline powder.
Salient features:
Zinc phosphide used as rodenticide comes as a black powder containing 75% of
zinc phosphide and 25% of antimony potassium tartrate, an emetic to cause
vomiting if the material is accidentally ingested by humans. However, it is still
effective against rats and mice because they do not have a vomiting reflex.

A. Mechanism of Action
On coming to contact with moisture present in the air, zinc phosphide liberates
phosphine [just like AlP]: Zn3P2+6H2O"3Zn(OH)2+2PH3-. Toxicity is due to
phosphine. Please see above under Aluminum phosphide.

B. Uses
Grain preservation, rat poison.

C. Symptoms
Same as those by Aluminum Phosphide, but are slower to start, because of
slower release of phosphine.

D. Fatal Dose
5 g.

E. Fatal Period
24 h.

F. Management
Same as that of AlP.

G. PM Appearances
Same as those of AlP.
 36. Metallic Irritants

I. ARSENIC
Metallic arsenic is not poisonous, as it is insoluble in water and is not absorbed
from the alimentary canal. When heated, it volatilizes, combines with oxygen
and forms arsenic trioxide (As2O3), which is poisonous.

A. Toxic Salts of Arsenic

(1) Arsenious oxide [Arsenic trioxide, As2O3].
(i) Vernacular names - Also known as sankhya, somalkhar, white arsenic [or
simply arsenic]
(ii) Occurrence - Occurs in two forms – (a) powder and (b) porcelain type solid
mass.
(iii) Physical properties - (a) White in color, tasteless and odorless; thus could
be easily mixed with foodstuffs for homicide. (b) Sparingly soluble in
water. (c) Sublimates on heating. (d) Although heavier than water (sp gr
3.669), floats on it as a thin film.
(iv) Legitimate uses - Non-medicinal: Used in artificial flowers, calico
printing, fly papers, fruit sprays, as mordant in dyeing, preservation of
timber against white ants, rat poisons, Sheep dips [liquid insecticide used
by farmers to protect their sheep against ticks and lice], taxidermy, wall
papers and weed-killers.
(2) Arsenic acid [H3AsO4]
(3) Arsenic trichloride (AsCl3)- Butter of arsenic. Colorless poisonous oil
(4) Arsenic trisulfide (As2S3) comes as the mineral orpiment [hartal in India]
(5) Copper acetoarsenite [Paris Green, Emerald Green, Schweinfurt Green]
– Once used as a pigment and insecticide
(6) Copper arsenite [Scheele’s Green, CuHAsO3]. Made by Swedish chemist
Carl Wilhelm Scheele in 1775. Initially used as a green pigment. Not used
now due to its toxicity
(7) Tetraarsenic tetrasulfide (As4S4) comes as the mineral realgar (manseel in
India).

B. Mechanism of Action
Arsenic is absorbed through all portals of entry (oral, nasal, cutaneous).
(1) Trivalent arsenic (As3+) has a great affinity for sulfhydryl groups [SH
groups]. Binds to mitochondrial membrane SH groups"damages
them"Cytochrome c is released from the damaged mitochondria"activation of
caspases"Apoptosis [arsenic induced apoptosis]. Because of -er affinity for
SH groups [and also RBCs], the trivalent form is more toxic than pentavalent
form [same is true of antimony also].
(2) Downregulates gene expression of BCL2, a prosurvival protein, that
protects against apoptosis
(3) Inhibits pyruvate dehydrogenase (PDH) complex leading to disruption of
oxidative phosphorylation.

C. Toxicokinetics [Absorption, Distribution and Elimination]

1. Absorption
(1) Average daily intake - is ½ -1 mg [contained in food and water].
(2) Well absorbed from the GIT (pentavalent As), respiratory tract (arsine), or
skin (arsenite).
(3) Upon absorption, it is bound to the protein portion of Hb and a-globulins.

2. Distribution
(1) Once absorbed, arsenic is quickly distributed to all organs and tissues.
(2) In early stages, arsenic is found maximally in liver [in fatal cases >1mg%]
followed by kidneys and spleen.
(3) Does not cross blood-brain barrier. Brain has lowest levels
(4) Inorganic arsenic can cross placenta
(5) In ch poisoning:
(i) Found in muscles for several days, and in keratin containing tissues [skin,
hair, nails] for years. Can appear in hair and nails within hours of ingestion.
Attaches itself to –SH groups which are abundant in keratin. In intermittent
 ch poisoning, there are successive deposits of As in hair and nails, and their
sequential analysis can determine even the dates on which As was
administered [normal growth of hair 0.4mm/day – ch 3].
(ii) Gets incorporated in the bone by replacing P.
(6) Normal conc in hair – 2ppm
(7) Normal levels in urine <0.03mg/L.

3. Elimination
(1) Mainly by kidneys:
(i) As methylated As.
(ii) Found in urine within ½ h of ingestion. Then onwards, elimination is
continuous for about 10-12 days.
(iii) In acute poisoning 24 h excretion > 100 mg
(2) Breast milk – eliminated only in traces
(3) Bile, feces, sweat, other secretions – Other routes of elimination
(4) Has an enterohepatic circulation – Because of this, As is seen in stomach
and intestines, even if given by parenteral routes.

D. Acute Poisoning
Occurs within 24 h of ingestion.

1. Signs and symptoms

a. Ingestion
(1) GIT: (i) Odor – Garlicky (ii) Taste – sweetish metallic (iii) Intense thirst,
Ptyalism (iv) Nausea, Vomiting [projectile in nature] (v) Throat – feeling of
constriction, dysphagia (vi) Burning and colicky pain – in esophagus, stomach
and bowels (vii) Abdominal pain (viii) Diarrhea - (a) Accompanied by pain,
tenesmus and irritation around the anus. (b) Stools – (I) expelled frequently
and involuntarily (II) Color and odor - dark colored, stinking, bloody; later
become colorless, odorless and watery resembling rice-water stools of cholera.
(c) May mimic bacterial food poisoning or cholera [Table 1].
(2) Ocular: (i) Conjunctivitis (ii) Lacrimation
(3) Respiratory - Irritation of upper airways
(4) Liver - Fatty degeneration
(5) Renal: (i) Pain - during micturition (ii) Oliguria (iii) Uremia (iv) Urine –
contains albumen, casts and RBCs
(6) Muscular – Tenderness of muscles
(7) CNS: (i) Convulsions and tremors (ii) Formication (iii) Giddiness (iv)
Headache (v) Vertigo (vi) General paralysis (vii) Delirium (viii) Coma
(8) CVS: (i) Cardiac arrhythmias [ST-T wave changes, prolonged QT interval],
ventricular fibrillation (ii) Hypotension (iii) Ventricular tachycardia (iv) .ed
vascular permeability, vasodilation and acute circulatory collapse
(9) Skin – loss of hair [in case of survival], skin eruptions
(10) General – hyperthermia [Hyperpyrexia].
Presentation
Depending on dose ingested, and retention of arsenic within the system, the
patient may present in 3 major forms
(1) Fulminant type:
(i) Dose ingested is >10 times the fatal dose [3-5 g].
(ii) CVS symptoms are prominent, with almost complete absence of GIT
symptoms.
(iii) Death occurs within 1-3 h from shock and peripheral vascular failure.
(2) Gastroenteric type: (i) dose ingested – around normal fatal dose. (ii) Classic
type (iii) GIT symptoms are prominent
(3) Narcotic type - CNS and muscular symptoms are prominent; GIT symptoms
insignificant.

b. Inhalation [Arsine gas]

(1) Hemolysis [Fig 36.1] (2) hemoglobinuria (3) renal failure (4) death is almost
instantaneous.

2. Fatal dose
(1) As2O3 - 200-300 mg
(2) Arsine gas – 25-30 ppm is lethal in 30 min.

3. Fatal period
1-2 days.

4. Management [Ac arsenic]

(1) Emetics – Ipecac
(2) Gastric lavage – Repeated washings [to remove As adherent to walls] with
warm water and milk [acts as a demulcent]
(3) Demulcents – Butter, greasy substances [to reduce absorption]
(4) Whole bowel irrigation – If radiopaque material is visualized in the GIT.
Continue till the material is not visualized on repeat x-ray
(5) Continued nasogastric suction – Must be done because arsenic is resecreted
in gastric tract. It has been detected in the GIT 7 days after ingestion
(6) Activated charcoal – Arsenic poorly adsorbs to activated charcoal. Thus it
should only be administered in heavy ingestions.
(7) Cathartics – Castor oil, MgSO4.
(8) Supportive care in ICU
(9) Chelation therapies:
(i) BAL and BAL analogues [ch 32].
(ii) D-Penicillamine (Cuprimine, Depen) – May be used with BAL [ch 32]
(10) Immunotherapy - Arsanilic acid is conjugated to a carrier protein
[ovalbumin] and injected in small multiple dosages [100μg] in mice to
produce active immunization against arsenic. Serum from such mice is then
transferred to other mice [passive immunization]. Both actively and passively
immunized mice did not succumb to ordinary lethal dose of arsenic. Shows
promise in humans also.
(11) Symptomatic: Shock – Glucose saline.
(12) Older remedies:
(i) Freshly prepared hydrated ferric oxide.
(ii) Dialyzed iron – For details of both, please see ch 32 under the heading
“chemical antidotes”. None is used now.
Memory Aid 1: Arsenic poisoning [main points]
ARSENIC - used in Abortion stick, Aphrodisiac, found in charred bones and Ashes, Aldrich-Mees lines,
Raindrop pigmentation, Red velvety appearance of stomach mucosa, Subendocardial hgs of heart, ECG
changes, Neuropathy (motor & sensory), optic Neuritis, Iron preparations [older remedy], Cholera like
symptoms

5. PM appearances [Ac arsenic]

a. External
(1) Signs of dehydration – Eyeballs, sunken; body, shrunken
(2) Skin – Cyanosed.

b. Internal
(1) Mouth, pharynx, esophagus – Generally unaffected, but rarely may be
inflamed or ulcerated
(2) Stomach – displays major findings.
(i) Mucosa - (a) swollen, edematous and bright red, either diffusely or in patches.
(b) Shows erosions and ulcerations (c) Mass of sticky mucus covers mucosa
in which particles of arsenic may be seen
(ii) Congestion – Most marked along greater curvature, posterior part and
cardiac end of stomach. More prominent at the crests of rugae. Lines of
redness run along the walls. Rarely there may be no congestion
(iii) Submucous hemorrhages – in curved lines
(iv) Red velvety appearance – stomach wall is soft and red like a valvet [Fig
36.2].
Groups of petechiae scattered over mucosa. Sometimes large submucosal and
subperitoneal hemorrhages.
(v) Pyloric region - is especially affected.
(vi) If putrefaction has occurred – yellow streaks are found in the subperitoneal
layer of the stomach and to a lesser extent in intestines [As converts to
yellow sulphide due to H2S gas]
(3) Small intestine:
(i) Appears flaccid
(ii) Mucosa – Inflamed, pale violet. Shows submucous hemorrhages along the
entire length
(iii) Contains large flakes of mucus with very little fecal matter
(4) Cecum and rectum – slightly inflamed
(5) Liver, spleen, kidneys:
(i) Congested, enlarged, show cloudy swelling and if survival is for few days,
fatty change.
(ii) Glomerular nephritis
(6) Hemorrhages – in all abdominal organs, mesentery and occasionally in
larynx, trachea and lungs
(7) Lungs – congested with subpleural ecchymoses
(8) Heart:
(i) Subendocardial petechial hemorrhages [SEPH] of the ventricles. May be seen
even in absence of gastric inflammation.
(ii) Conditions in which SEPH are found - (a) Acute infectious diseases [eg
influenza], (b) Heat stroke, (c) Poisonings [Arsenic, Barium, Mercury,
Phosphorus] (d) Traumatic asphyxia
(iii) If survival is in days – fatty change
(9) Brain: (i) Edema - with patchy necrosis or hemorrhagic encephalitis (ii)
Meninges – congested.

E. Chronic Poisoning
WHO defines chronic arsenic poisoning [syn, arsenicosis] as a chronic health
condition arising from prolonged ingestion [not less than six months] of arsenic
above a safe dose, usually manifested by characteristics skin lesions, with or
without involvement of internal organs. Some authorities consider the period of
onset as within 4 wks of continuous ingestion.
Salient features:
Occurs in following circumstances:
(1) Occupational - due to repeated accidental ingestion of small doses of arsenic
 by those working with the metal
(2) Through contaminated water - People ingesting arsenic through water
contaminated with arsenic (as in several parts of West Bengal and
Bangladesh)
(3) Arsenophagists [please see below]
(4) Homicidal – when someone gives repeated doses to his enemy
(5) Recovery from single heavy dose.

1. Signs and symptoms

Occur in 4 stages.

a. 1st stage [Gastrointestinal]

(1) General:
(i) Circumscribed edema of lower eyelids and ankles [due to localized
transudation of intravascular fluid]
(ii) Loss of weight
(iii) Malaise
(iv) Pulse rate-
(v) Temp-
(2) GIT:
(i) Loss of appetite
(ii) Gums – (a) red and soft (b) Black line on gums due to arsenic sulphide
(iii) Tongue – coated with a thin, white, silver fur
(iv) Nausea, vomiting [vomitus contains mucus tinged with bile]
(v) Salivation
(vi) Abdominal cramps
(vii) Colicky pain
(viii) Constipation. Sometimes diarrhea.

b. 2nd stage [Dermatological]

(1) Dermatological:
(i) Hyperkeratosis – (a) Discrete, multiple, hard wart like growths appear on (I)
palms and soles (II) head and trunk [Less commonly]. (b) Due to epithelial
hyperplasia (c) Time taken – few months to 30 years (d) Complications –
may undergo a malignant change"(I) basal cell carcinoma (II) Carcinoma in
 situ [Bowen’s disease]. Arsenic is teratogenic. Can result in lung and skin
cancers, leukemias [please see hematologic changes below].
(ii) Pigmentation [melanosis]– (a) Color - finely mottled brown (b) site – skin
flexures of eyelids, temples, neck and other areas [raindrop type
pigmentation]. Covered parts are also affected (c) Persistence – for months
(iii) Rash – resembling fading measles rash [d/d]
(iv) Flexural eczema
(v) Hair – become dry and fall off
(vi) Nails - (a) irregular thickening (b) brittle (c) Mees’ lines. [As in subacute
poisoning]
(2) Eyes: (i) Congestion (ii) Lacrimation (iii) photophobia (iv) dimness of vision
(3) Nose:
(i) Intense coryza [inflammation of mucous membranes lining the nasal cavity]
(ii) Running of mucus
(iii) Nasal septum – painless perforation
(4) Throat: Feeling of dryness and itching
(5) Voice – hoarse and dusky
(6) Larynx and bronchi: inflammation"Spasmodic cough with bloody
expectoration, dyspnea
(7) Hepatic: (i) Cirrhosis (ii) Hepatomegaly (iii) Jaundice
(8) Cardiorenal: (i) Myocarditis (ii) Cardiac failure (iii) Chronic nephritis (iv)
Dependent edema.

c. 3rd stage [Neurological]

(1) General - edema of lower eyelids and ankles worsens
(2) CNS:
(i) Anesthesia, hyperesthesia, Paresthesia
(ii) Encephalopathy
(iii) Polyneuritis [glove & stocking type]– headache, numbness, tingling
(iv) Knee jerks - lost
(3) Muscles – Marked tenderness, cramps
(4) Joints – arthralgia
(5) Hematologic: (i) Anemia – (a) due to bone marrow suppression [aplastic]
and hemolysis. (b) type - Normocytic, normochromic. interference with the
absorption of folic acid also occurs, which complicates the picture with
 megaloblastic anemia. (c) Bone marrow examination shows bizarre nuclear
forms and karyorrhexis (ii) Leukemia (iii) Thrombocytopenia
(6) Impotence.

d. 4th stage [Neuromuscular]

(1) Peripheral neuritis and muscular atrophy predominate
(2) General: (i) Anemia (ii) General emaciation
(3) Muscular: (i) Ataxia (ii) Atrophy of extensor muscles [wrist drop, foot drop]
(iii) Interossei and intercostal muscles are affected (iv) Muscular weakness (v)
Tremors
(4) Kidneys - Dysuria
(5) CNS - Delusions

2. Cause of death
Cardiac failure.

3. Diagnosis
(1) 24-h urinary As >67 µmol/d [>50 µg/d]; no seafood should have been taken
in last 24 h;
(2) High As in hair or nails [Normal <1 µg/g; >2 µg/g indicates exposure.

4. Differential diagnosis
(1) 2nd stage: (i) Addison’s disease [due to pigmentation] (ii) Syphilis (iii)
chronic cocaine poisoning [due to perforation of nasal septum]
(2) 3rd stage - Alcoholic polyneuritis [APN]- APN shows following distinctive
features (i) history of heavy alcohol intake (ii) symptoms take more time to
appear (iii) Glycosuria
(3) 4th stage: Lead poisoning [due to wrist and foot drop].

5. Management [Ch arsenic]

(1) Removal from source (2) BAL (3) Vit B1 for peripheral neuritis (4) Good diet
helps quick general recovery.

6. PM appearances [Ch arsenic]

(1) General - jaundice
(2) Stomach: (i) ch gastritis (ii) rugae may show patchy inflammatory reddening
(iii) Patchy hemorrhagic gastritis (iv) acute and ch erosions
(3) Small intestines – dilated, reddened, mucosa thickened
(4) Cloudy swelling and fatty degeneration of heart, liver and kidneys
(5) Liver – additionally shows severe necrosis,
(6) Kidneys – additionally show tubular necrosis
(7) Brain – congested, hemorrhagic spots in white matter
(8) Peripheral nerves – fragmentation and resorption of myelin, disintegration
of axis cylinders.

F. Tests for Arsenic

(1) Marsh test – Hydrogen is passed through suspected material (e.g. vomit).
Arsenic if present combines with H2 to form AsH3, which is passed through a
jet and burnt. A thin film of arsenic over porcelain is formed. Developed by
the British chemist James Marsh (1794-1846) in 1836.
(2) Gutzeit test
(3) Reinsch test. Marsh, Gutzeit and Reinsch tests are now obsolete.
(4) Neutron Activation Analysis [NAA] and Atomic Absorption spectroscopy
[AAS]. Performed currently.

G. ML Importance
(1) Postmortem imbibition of arsenic – If high arsenic content is found in the
exhumed body, the defense may take the plea that the arsenic had leached into
the body from surrounding soil. There are two objections to this argument (a)
Solubility - Arsenic is found in an insoluble form in the soil. For it to be able
to leach inside the body, it must be in a soluble form (b) Concentration –
Concentration of arsenic found in the body cannot be higher than that in the
soil, if arsenic has leached. This is frequently the case. (i) There is a counter
objection to the first (a) Bacterial activity - Some anaerobic bacteria have
been demonstrated in grave soil, which can convert insoluble arsenic into
soluble arsenic. Furthermore their metabolic activity causes an exchange of
soil arsenic with that of sulphur in the hair.
(2) Homicidal poison – Most favorite homicidal poison before 1836, when
Marsh test was developed.
(3) Arsenophagists:
(i) These are people who take arsenic daily in the mistaken belief that it is an
aphrodisiac
(ii) Develop tolerance [ch 31]. Can take up to 300 mg or more in one dose,
without apparent harm
(iii) Develop sings of chronic toxicity
(iv) D/d of chronic arsenic toxicity
(4) Safe levels in drinking water:
(i) 10 parts per billion [ppb] or 10µg/L
(ii) Hydroarsenicism from contaminated groundwater - has resulted in large
scale environmental poisonings [esp in W. Bengal and Bangla Desh.] for
the past 5 decades.
(5) Blackfoot disease (BFD):
(i) It is an endemic peripheral vascular disease first seen in southwestern coast of
Taiwan.
(ii) Peak incidence was noted between 1956 and 1960.
(iii) Associated with the consumption of inorganic As from the artesian wells.
(iv) The incidence .ed dramatically after the implementation of tap water.
6. Arsenic in drugs of addiction:
(i) Cocaine [ch 41]
(ii) Opium - generally contaminated with arsenic. Opium is adulterated with
arsenic in varying quantities because it is believed to be a general tonic and
an aphrodisiac. When combined with opium, it is thought to enhance the
aphrodisiac quality of opium. Quite often opium eaters present with
neuropathy and hepatomegaly due to ch arsenic poisoning. Arsenic levels
are -ed in serum, urine, nails and hair of opium eaters with and without
neuropathy.
(iii) Homemade brew – shows - As levels.
(7) -As levels found in – Alcoholic cirrhosis, alcohol-related liver disease,
fulminant hepatitis, Indian childhood cirrhosis, non-cirrhotic portal fibrosis
and Wilson’s disease.
(8) Arsenic is a minor component of cigarette smoke. It is thought that it plays a
part in development of cancer.
(9) Seafood – is exceptionally rich in As. May contain from 2mg/kg for
freshwater fish up to 22mg/kg for lobsters. Mussels, oysters, prawns, shellfish
 all contain As in varying amounts. Urine of persons who consume large
amounts of seafood may contain -As [up to 0.7mg/L; normal levels
<0.03mg/L], which may mimic ch As poisoning.

II. BARIUM

A. Mechanism of Action
(1) Barium induces hypokalemia by two mechanisms (a) It competitively blocks
potassium channels, which are responsible for the efflux of intracellular K+
out of the cell. (b) Directly -s cell membrane permeability to Na+. This leads
to a shift of extracellular potassium into the cell. Intracellular trapping of K+
leads to
(i) Depolarization and paralysis
(ii) -ed vascular resistance and reduced blood flow " hypertension and lactic
acidosis
(2) Direct toxicity to skeletal muscle and neuromuscular transmission.
Hypokalemia occurs within 2 hours of exposure. Normal serum K+ is 3.5-5.5
mEq/L; in barium induced hypokalemia it may be reduced to half or even
lower.

B. Signs and Symptoms

(1) Severe GIT irritation – (a) Nausea, Abdominal pain, vomiting, diarrhea
occur within 1 hour of ingestion. (b) Esophagitis (c) hemorrhagic gastritis
(2) Signs and symptoms associated with hypokalemia - (a) ventricular
dysrhythmia (b) hypertension (c) profound flaccid muscle weakness (d)
respiratory failure (e) lactic acidosis, (f) hypophosphatemia (g)
rhabdomyolysis
(3) Secondary to tissue ischemia - (a) Altered level of consciousness (b) seizures
(c) basal ganglia manifestations.

C. Fatal Dose
1g.

D. Fatal Period
12 hours.

E. Management
(1) Gastric lavage – with Na2SO4 or MgSO4 (if seen early). Precipitates barium
as insoluble BaSO4.
(2) IV Na2SO4 or MgSO4 – Once advised but no more advisable, because it
may lead to renal failure as a result of precipitation of barium in the renal
tubules.
(3) Assisted ventilation – If patient is in respiratory failure
(4) Correction of hypokalemia – Administer large doses of K+.

F. PM Findings
(1) Stomach, intestines – congested.
(2) Heart - subendo-cardial petechial hemorrhages.

III. COPPER

A. Toxic Salts of Copper

(1) Copper acetoarsenite - please see under arsenic
(2) Copper arsenite - please see under arsenic
(3) Copper subacetate – Also known as Verdigris [Old French vert-de-Grèce,
“green of Greece”. Called so because used by Greek artists as a green pigment
in their paintings].
(4) Copper sulphate [blue vitriol].

B. Mechanism of Action
(1) Effect on SH groups:
(i) Copper inhibits the sulfhydryl groups on enzymes in important antioxidant
systems including G-6-PD and glutathione reductase, reducing their free
radical scavenging activities
(ii) Intravascular hemolysis is caused by the inhibition of G-6-PD.
(2) Copper -s the permeability of cell membranes by inhibiting the NA+/K+
ATPase pump.
(3) Copper intoxication can cause rhabdomyolysis, as it damages human
skeletal muscle cells.

C. Toxicokinetics [Absorption, Distribution and Elimination]

(1) Absorption - Copper is absorbed by an active process involving a Cu-
ATPase in the small intestinal mucosal cell membrane [also known as the
Menkes ATPase]
(2) If mucosa is damaged – as in acute overdose, the absorption is significantly
higher.
(3) Carriers of copper - After absorption, copper is rapidly bound to carriers
[albumin, ceruloplasmin, and amino acids eg histidine], for transport to the
liver and other tissues.
(4) Local release of copper - Copper is released locally [in liver and other
tissues] in the reduced form from its carrier
(5) Fate of copper - (a) In the hepatocyte, copper may either be incorporated
into enzymes or eliminated depending on body’s needs. (b) Cu-ATPase
located on trans-Golgi network assists in its incorporation into enzymes. (c)
Same Cu-ATPase on pericanalicular lysosomes assists elimination as a
metallothionein-copper complex, into the biliary system [final excretion in
feces]. Biliary excretion of copper is 2000 µg/24 h. Renal excretion is
negligible; about 5-25 µg/24 h
(6) Release of copper in plasma - (a) Excess copper is released into the plasma
from the liver, bound primarily to ceruloplasmin. (b) 1 Molecule of
ceruloplasmin binds 6 atoms of copper. (c) 90-95% of serum copper is bound
to ceruloplasmin, and 5-10% to albumin; unbound copper and copper bound to
other carriers [amino acids] is <1%. (d) Half life - (i) Ceruloplasmin bound
copper has a plasma half-life of 24 hours. (ii) Half-life of erythrocyte copper is
26 days. (e) The albumin-copper complex represents the “free” or
toxicologically active copper. (f) Following acute poisoning, the excess
copper binds only to albumin.

D. Acute Poisoning

1. Signs and symptoms

Symptoms appear within 15-30 minutes. In mild cases there is (i) a metallic
taste in mouth (ii) -salivation (ptyalism) (iii) thirst (iv) nausea, vomiting,
eructations and diarrhoea (v) burning pain in the stomach with colicky
abdominal pain (vi) Vomited matter is bluish-green.
In severe cases there may be (i) Hepatotoxicity – Acute hepatic necrosis and
jaundice (ii) Hemolysis – More common than hepatotoxicity. Seen invariably in
those who have undergone liver damage. Manifested by myoglobinuria,
hemoglobinuria and hemoglobinuric renal failure (uncommon in patients who
receive adequate volume replacement therapy) (iii) hematemesis, melena – Due
to ulceration in the GIT (iv) methemoglobinemia, methemoglobinuria (v)
Renal and pulmonary toxicity – Due to oxidative effects of copper ions. Renal
toxicity is manifested by oliguria (vi) Hypotension and cardiovascular
collapse – due to (a) intravascular volume depletion from vomiting and diarrhea
and (b) direct effect of copper on vascular and cardiac cells (vii) Neurological –
lethargy, seizures, coma. Result from hepatic encephalopathy. In Wilson’s
disease, neurological manifestations are prominent.

2. Fatal dose
0.15-0.3 g/kg (CuSO4), i.e. about 20 g or a 70 kg man.

3. Fatal period
1-3 days.

4. Management
(1) Gastric lavage – is of limited value, because copper salts themselves are
emetics. Emesis generally occurs within minutes of ingestion and is
protracted. In the past stomach wash with 1% potassium ferrocyanide
[formation of insoluble cupric ferrocyanide], and egg white [formation of
copper albuminate] was recommended. No more recommended now.
(2) Antiemetic therapy – because of protracted vomiting
(3) Activated charcoal - Contraindicated. It may hinder the ability to perform
gastrointestinal endoscopy to evaluate corrosive effects.
(4) Most critical steps before chelation therapy is started are (a) Supportive
care, (b) fluid and electrolyte correction and (c) normalization of vital signs
(5) Chelation therapy:
(i) BAL – Administered first. Less effective than d-Penicillamine, yet its initial
 use is appropriate. Reasons - vomiting or GIT injury prevents oral d-
Penicillamine administration. Furthermore, because the BAL-copper
complex primarily undergoes biliary elimination, whereas D-peni-cillamine
undergoes renal elimination, BAL proves useful in patients with renal
failure. When tolerated, D-penicillamine therapy should be started
simultaneously or shortly after the initiation of therapy with BAL.
(ii) Calcium disodium ethylenediaminetetraacetate (CaNa2EDTA) – ch 32.
(iii) d-Penicillamine - ch 32.
(6) Hemodialysis – is ineffective. Copper is nondialysable. May be considered
in patients with renal failure.
(7) Liver transplantation - in life-threatening hepatic failure.

5. PM appearances
(1) Mouth and nostrils – Greenish blue froth
(2) Gastric mucosa – Congested, eroded, swollen, inflamed. Color - greenish
blue. Contents – greenish blue [Fig 36.4].
(3) Liver – Soft, fatty
(4) Kidneys – Degenerative changes in proximal tubules
(5) Skin – Yellow [due to jaundice]
(6) Blood - hemolysis.

E. Chronic Poisoning
1. Causes
(1) Occurs in workers engaged in copper factories (inhalation of copper dust)
(2) Copper cooking vessels – If copper cooking vessels are not properly tinned
on the inside, food cooked in such vessels will cause formation of copper salts
[Acids used in cooking (citric acid, tartaric acid, acetic acid) react with copper
and form salts]. Their ingestion over a period of time will cause chronic
poisoning.
(3) Wilson’s disease: Wilson’s disease or hepatolenticular degeneration is an
autosomal recessive genetic disorder affecting approx 1 in 40,000 people.
Cause is the presence of abnormal allele of ATP7B gene at both loci (located
on chromosome 13). A single abnormal copy of the gene is present in 1 in 100
people. They are carriers and do not develop any symptoms. If an abnormal
allele is inherited from both parents, Wilson’s disease develops. The normal
gene codes for ATPase that transports copper into bile and incorporates it
into ceruloplasmin. In the absence of normal gene, copper accumulates in
tissues. This manifests as neurological or psychiatric symptoms and liver
disease. Symptoms usually appear between the ages of 6 and 20 years, but
cases in much older patients have been described.

2. Signs and symptoms

(1) Anemia
(2) Green line on gums
(3) Colic
(4) Peripheral neuritis
(5) Degeneration and atrophy of muscles
(6) Vineyard’s sprayer’s lung - Bordeaux mixture is copper sulfate (1-2%)
mixed with lime [Ca(OH)2]. It is sprayed in vineyards to control fungus on
grapes, melons, and berries. It is chronically inhaled by vineyard sprayers,
who develop interstitial pulmonary fibrosis and histiocytic granulomas
containing copper. Many workers also develop malignancies indicating the
carcinogenic effects of copper.
(7) Chalcosis lentis - (Gk chalkos, copper) Chronic poisoning may cause
deposition of copper in the cornea or lens turning them greenish-brown.
(8) Greenish discoloration of hair:
(i) Caused due to deposition of Cu over the hair.
(ii) Swimming pools - Copper salts [eg CuSO4] are used in swimming pools as
algaecides. Long time swimmers may get green discoloration of hair.
(iii) Tap water – Copper leeches from copper fittings by the acidic pH of the
water [caused by fluoridation of drinking water]"may turn hair green.
(iv) Exhaust gases containing copper and dusts from the copper processing
industry cause green discoloration of the hair [Chalcosis] - [please co-relate
with ch 3].

F. ML Importance
(1) Abortifacient
(2) Cattle poison
(3) Cheshunt compound - a mixture of copper sulfate and ammonium
carbonate used in horticulture to prevent fungal diseases in seeds. May cause
poisoning
(4) Manner of poisoning:
(i) Accident - (a) Children – may often put the crystals in their mouth attracted
by their shining green color (b) Coin ingestion – Indian `2 and `5 coins are
made of cupro-nickel. Their accidental ingestion may cause poisoning. (c)
Cookware - Copper tea kettles and other copper cookware can be a source
of copper toxicity if used frequently over a period of time. (d) Vegetables -
Copper salts are used to enhance the green color of vegetables"if vegetables
not washed properly before eating, can cause poisoning. Food vendors are
liable for punishment under The Prevention of Food Adulteration Act,
1954.
(ii) Homicide – Because of their color and taste, salts of copper can not normally
be used for homicide. However they can be mixed in blue colored liquids
eg sherbets or dark liquids eg Cola drinks
(iii) Suicide – Relatively common, as copper salts are used in many cottage
industries
(5) Medicine - Copper has been used in medicine for a variety of ailments,
which can cause iatrogenic poisoning
(i) Treatment of burns and other wounds
(ii) Contraceptive Pills - -es Cu levels in the body, because of close association
between estrogen and Cu levels.
(iii) Copper is a component of dental casting gold alloys, dental amalgams, and
IUDs. It corrodes"releases Cu ions into the surrounding tissue"toxicity.
(iv) As an emetic – In the 1960s, copper sulphate (250 mg) was used as an
emetic. No more used now because of its toxicity.
(v) Hemodialysis - Copper in dialysis heating coils can be released, especially if
acidic water is used in hemodialysis.
(vi) Phosphorus poisoning – in ingestions as well as topical exposures to
phosphorous.
(6) Metal fume fever [MFF] - Occupational disease recognized for centuries,
but first characterized by Potissier in 1822. Caused by freshly oxidized
metallic fumes (Most commonly with zinc, followed by copper and iron.
Cadmium and tin however produce a more severe illness) having a particle
size smaller than 0.5 to 1.0µ. Usually caused by welding or melting of metals,
soldering, forging and casting (all involve oxidation of metals. ZnO forms at
relatively lower temperatures, accounting for its frequency as a causative
factor). Quite common; more than 1000 cases are reported annually. Signs
and symptoms [of MFF] - Influenza like syndrome, with sudden onset of
chills, fever (104°C), thirst, myalgias and headache within 4-8 hours of
inhalation of freshly oxidized metallic fumes. Course is generally benign with
symptoms resolving completely within 24-48 hours without any sequelae.
Theories of causation (a) release of endogenous pyrogens (b) production of
antigenic metal proteinates (c) Delayed hypersensitivity pneumonitis (d)
Direct toxic effect on alveolar cells.

IV. LEAD

Lead is a silvery-gray soft metal, used in construction of buildings, bullets,

ceramics, electric cable insulations, fusible alloys, hair dyes, lead-acid batteries,
pewter, potteries, radiation shieldings, shots, solders, and weights. Lead and its
salts are potent poisons.

A. Toxic Salts of Lead

(1) Lead carbonate (PbCO3, safeda)
(2) Lead chromate (PbCrO4)- has a bright yellow color and is insoluble in
 water. As a result used in paints as “chrome yellow”
(3) Lead diacetate [Pb(C2H3O2)2 - Commonly known simply as lead acetate] –
Called sugar of lead because of its sweet taste. Other names are salt of Saturn,
and Goulard’s powder (after Thomas Goulard). It was used medicinally in the
early 19th century for control of bleeding and diarrhea.
(4) Lead monoxide (PbO)- Occurs in two polymorphs, red (litharge) and
yellow (massicot). Used in the manufacture of lead glasses, ceramic glazes
and fine dinnerware
(5) Lead sulfide (PbS, Galena) – Insoluble and stable at blood pH. Thus least
toxic forms of lead
(6) Lead tetraacetate [Pb(C2H3O2)4]
(7) Lead tetroxide (Pb3O4 or 2PbO·PbO2)-Also known as red lead, sindoor,
vermilion. HgS has the same color and has same names. Once both Pb3O4 and
Hgs were applied by married Indian ladies on their heads. Largely abandoned
now because of toxicity
(8) Tetraethyl lead [CH3CH2)4Pb; TEL] - Once a common antiknock additive
in petrol. Now largely discontinued because of toxicity. Still used as an
additive in aviation fuel for piston engine-powered aircraft.

B. Toxicokinetics

1. Absorption
Absorption by (i) oral route is less efficient (10%-15% of total absorbed Pb
comes via this route) than by (ii) inhalation (40-50%). Essential trace elements
(Fe, Ca, Zn) reduce absorption by competitive absorption. Children have a 3
fold higher lung deposition rates than adults. (iii) Cutaneous absorption is poor
(iv) Placenta – Readily crossed. Causes fetal toxicity when mother is poisoned
(v) Other routes – Lead bullets or pellets lodged in bones, muscles and joints
(souvenir bullets) may get slowly absorbed causing poisoning.

2. Distribution
(1) Mostly stored in bone:
(i) Distribution of Pb is beautifully illustrated by the classic 3-compartment
model [ch 31]. In adults, app 95% of the body Pb is stored in bone (70% in
 children). (a) In bones Pb is stored mainly as insoluble phosphate and
carbonate. (b) -Ca++ levels favor storage; Ca++ deficiency causes Pb to be
released into blood stream. CaCl2 is thus advocated in treatment.
(ii) Most of the remainder is distributed to the soft tissue pool.
(iii) Very little is present in blood; 99% of that is bound to RBCs
(2) Toxicity is associated with soft tissue lead uptake - Most of the toxicity
associated with lead is a result of soft-tissue uptake.
(3) Toxic Lead levels:
(i) Normal asymptomatic tissue lead levels are 200-500 parts per billion
(ii) Brain lead content in encephalopathy is 1000-2000 ppb.
(iii) Blood lead levels (BLLs) of 100 ppb (>10 µg/dL) are considered toxic.
[Normal BLL <10µg/100mL]. Symptoms in adults may begin with BLL 40
µg/dL, but usually begin with levels >50-60 µg/dL.

3. Excretion
(1) Retention rate - Adults retain 1-4% and children 33% of ingested lead
[because Pb mimics Ca, which is used by growing children]. Rest is excreted.
(2) Excreted through urine and bile - Lead is primarily excreted in urine
(approx 65%; normal urinary excretion of Pb =80µg/L) and bile (approx
35%). Negligible amount is lost via sweat, hair, and nails.
(3) Biologic half-lives in various body tissues for lead are: (a) blood (adults),
25 days; (b) blood (children), 10 months; (c) soft tissues (adults), 40 days; (d)
bone (labile, trabecular pool), 90 days; and (e) bone (cortical, stable pool), 10-
20 years.

C. Mechanism of Action
(1) Inhibition of heme synthesis [Fig 36.5]. Heme is synthesized in 9 steps.
Enzymes at step 2-3 [porphobilinogen synthase or ALA dehydratase], 6-7
[coproporphyrinogen oxidase] and 8-9 [ferrochelatase] are inhibited by Pb.
This causes an overall . in heme synthesis resulting in anemia. Also the
substrate catalyzed by the inhibited enzyme shows - [Fig 36.5].
(2) Inhibition of –SH groups - Pb interferes with the action of –SH groups,
which are components of several enzymes, receptors and structural proteins.
D. Acute Poisoning
1. Signs and symptoms
Acute poisoning is characterized by (1) an astringent and metallic taste, (2)
headache, (3) dry throat, (4) nausea and vomiting [occasionally diarrhea], (5)
thirst, (6) peripheral circulatory collapse [due to loss of water from GIT], (7)
neurological signs [(i) paresthesias (ii) rarely encephalitis (iii) cerebellar ataxia
is common in children]. (8) Hemolysis causes anemia and presence of
hemoglobin in the urine, (9) decreased urine output (damage to kidneys). (10)
Death in severe cases.

2. Fatal dose
(1) Lead acetate – 20 g;
(2) Lead carbonate – 40 g;
(3) Tetraethyl lead – 100 mg/kg.

3. Fatal period
1-2 days.

4. Diagnosis
(1) Lab findings:
(i) - δ-Aminolevulinic acid
(ii) - Coproporphyrin
(iii) - Protoporphyrin IX [Fig 36.5].
Memory Aid 2: Lab findings in Pb Poisoning
ACP – Assistance Commissioner of Police

(iv) Blood Lead Levels [BLL] >20µg/100mL. May not be so useful in ch

poisoning because Pb migrates to bony compartment]
(v) Urinary excretion of Pb >150µg/L. But if there is renal damage, Pb may not
be secreted at all.
(2) Radiology – Abdominal X-ray may reveal lead paint chips or other ingested
lead foreign material.

5. Management
(1) Gastric lavage – with 1% soln of Na2SO4 or MgSO4.
(2) Demulcents
(3) CaCl2 - 5 mg of 10% soln causes Pb to move from blood to bony
 compartment, where it lies inert
(4) Magnesium or sodium sulphate – 8-12 g. Covert unabsorbed Pb salts to the
highly insoluble lead sulphate "hastens fecal excretion
(5) For convulsions - (a) Diazepam – 0.1 mg/kg IV [max 10 mg] if patient is
convulsing (b) Phenytoin and/or phenobarbital.
(6) For -Intracranial tension – Mannitol, steroids
(7) Chelation therapy:
(i) If blood lead level (BLL) is >70 µg %, chelation is done with both BAL and
EDTA. On the first day of EDTA therapy symptoms may paradoxically
worsen [please see above under the heading “distribution”]. To prevent this,
administer BAL first. It is a small molecule that crosses into cells, and
protects them against the initial - in Pb levels caused by EDTA. Also see ch
32
(ii) Penicillamine
(8) Peritoneal and hemodialysis
(9) symptomatic treatment.

6. Cause of death
Gastroenteritis"shock.

7. PM appearances
(1) Signs of acute gastroenteritis – thickened red mucosa with eroded patches
(2) Grayish white deposit on stomach mucosa.

8. Tests
To the suspected material, add hydrochloric acid. White ppt of lead chloride
will form. It is soluble in boiling water; crystallizes on cooling.

E. Chronic Poisoning

1. Causes
Chronic poisoning [syn. colica pictonium, Devon colic, miner’s disease,
painter’s colic, Plumbism (from Latin plumbum, lead), or saturnism] is caused
by
(1) Food and drinking water:
(i) Drinking water stored in lead cisterns.
(ii) Ghee stored in brass or copper vessels lined inside with lead. Fat in ghee
reacts with lead to form lead oleate which is absorbed
(iii) Food cooked in similar vessels
(iv) Tinned food – contaminated with lead from solder
(v) If water supply to homes is through lead pipes or copper pipes with lead-
soldered joints.
(2) Use of hair dyes and cosmetics containing lead
(3) House dust from deteriorated lead paint
(4) Occupational exposure - Common in people who work with lead, e.g.
painters, pewters, plumbers, potters and printers. Other professions who may
be affected are enamel workers, glass polishers, glassblowers, glass polishers,
makers of white lead and smelters. Poisoning caused by continuous inhalation.
(5) Retained lead ammunition– In old gunshot wounds, if some bullet or
pellets remain lodged in body [souvenir bullet or pellets]
(6) Sindoor - Use of sindoor (red lead) applied to scalp. Lead can combine with
oils used on scalp to form lead oleate, which can be absorbed.
(7) Smoking:
(i) Particularly among workers in Pb based industries.
(ii) Mechanisms - (a) Tobacco plants absorb Pb from soil (b) lead arsenate is
used as a pesticide on tobacco crops"gets deposited on leaves (c) General
poor personal hygiene habits among smokers [inadvertent contact and
ingestion] (d) Inadvertent touching of lips with contaminated hands during
smoking.
(iii) Thus lead-handling workers are advised to improve their hygiene by
refraining from smoking in the workplace, regularly washing their hands
and face, and bathing immediately after their day’s work.
(8) Consumption of wildlife killed with lead ammunition - may cause lead
intoxication.
(9) Children can get poisoned if they continuously chew or lick on leaded
objects, eg furniture and walls painted with lead based paints and toys.

2. Signs and symptoms

a. Facial pallor
(1) Facial pallor, particularly circumoral pallor is one of the earliest and most
consistent signs
(2) Causes: (i) anemia (ii) vasospasm [Mechanism – please see above].

b. Anemia
(1) Initially – there is polycythemia with polychromatophilia [syn
polychromasia – RBCs are of multiple colors, particularly gray-blue. This is
due to differing amounts of Hb in each cell, which in turn is due to their
premature release from the bone marrow.]
(2) Other RBC abnormalities:
(i) Anisocytosis [unequal sized RBCs]
(ii) Nucleated RBCs [sideroblasts]
(iii) Poikilocytosis [abnormally shaped RBCs]
(iv) Punctate basophilia [presence of many dark blue colored pinhead sized spots
in the cytoplasm of RBC.]
(v) Reticulocytosis
(3) Other blood cells: (i) -Mononuclear cells (ii) .platelets (iii)
.polymorphonuclears
(4) Significant anemia:
(i) Usually a sign of more chronic poisoning.
(ii) Initially it is microcytic, hypochromic [as seen in Fe deficiency anemia], but
later changes to normocytic normochromic.
(iii) Anemia is not a significant feature in organic lead poisoning.
(iv) Causes - (a) .ed Heme synthesis [Fig 36.5] (b) .ed survival time of RBCs.

c. Lead line
(1) Morphology - A stippled blue line [Burtonian line - first described by
Henry Burton (1799-1849), a British physician] is seen on gums in 50-70%
cases.
(2) Characteristics:
(i) More common in upper jaw
(ii) Appears within a week of exposure
(iii) Not seen in edentulous persons
(iv) Removal from exposure obliterates line gradually (v) More common in
persons with bad orodental hygiene, carious teeth
(3) Mechanism:
(i) Subepithelial deposition of black Pb granules
(ii) Bad oral hygiene"food sticking in gums" decomposition " H2S formed "
Reacts with Pb in tissues " forms PbS [black]
(4) D/d – similar lines seen in poisoning by bismuth, copper, iron, mercury and
silver.

d. Colic and constipation

(1) Also known as colica Pictonum, Devon colic, or painter’s colic
(2) Mechanism – please see above
(3) Usually appears late
(4) Colic of smooth muscles – occurs in about 85% cases. Blood vessels,
intestines, ureters and uterus are involved
(5) Colic occurs at night
(6) Pain is very severe
(7) Individual attacks last a few minutes; keep recurring
(8) Constipation is usual. Diarrhea may also occur.

e. Lead palsy
Weakness of muscles due to lead.
Salient features:
(1) Sex – more in men than in women
(2) age – more in adults than in children
(3) Onset - late
(4) Frequency <10% of cases
(5) Symptoms preceding – Before actual muscle weakness following symptoms
may be seen (i) cramps (ii) Hyperesthesia (iii) Numbness (iv) Tremors
(6) Muscles affected: (i) Those which are most prone to fatigue (a) extensor
muscles of wrist. [wrist drop] (b) Anterior tibial [foot drop]. Occurs in ch
arsenic poisoning also (ii) biceps (iii) deltoid (iv) rarely (a) eye muscles (b)
intrinsic muscles of hand and foot. Associated neuropathy also occurs making
the condition worse.
(7) Recovery – complete but slow. Occurs when the person is removed from
source.
f. Encephalopathy
(1) More common in children
(2) usually irreversible; 85% have permanent brain damage
(3) commonly associated with tetraethyl lead
(4) Symptoms: (i) Delirium (ii) Hallucinations (iii) Headache (iv) Insomnia (v)
Irritability (vi) Restlessness (vii) Visual disturbances (viii) Vomiting (ix)
Convulsions, coma (x) death occurs in about 25% cases.

g. Cardiorenal manifestations
(1) Hypertension:
(i) Mechanism – (a) arteriolar contraction [please see above] (b) nephritis
(ii) HT ultimately causes permanent arteriolar degeneration.
(2) Nephritis:
(i) Chronic arteriosclerotic nephritis
(ii) Interstitial nephritis
(3) Saturnine gout [syn, lead gout]- Pb .es renal excretion of uric acid "-Uric
acid in blood [hyperuricemia]"Gout.

h. Reproductive system
(1) Sterility and impotence [in both sexes].
(2) Menstrual disorders [Amenorrhea, Dysmenorrhea, Menorrhagia]
(3) In pregnant females:
(i) Abortion – generally between 3-6 months [Mechanism – please see above]
(ii) Premature labor
(iii) Intrauterine growth retardation.
(4) Occupational exposure of a father just before conception -es the risk of
cancer in his offspring through toxic inheritance. [Mech: Pb exposure" genetic
change in sperm"cancer in offspring].

i. Eye
Ophthalmoscopic examination reveals retinal stippling. Glistening grayish lead
particles are seen.

j. Other systems
(1) Anorexia (2) Drowsiness (3) Dyspepsia (4) Emaciation (5) Exhaustion (6)
Foul breath (7) General weakness (8) Headache (9) Irritability (10) Loss of hair
(11) Peripheral neuritis [rare] (12) Vertigo.

3. Diagnosis
(1) History
(2) Clinical features
(3) Laboratory tests – As in acute poisoning. Additional tests useful in ch
poisoning (a) Normal Pb levels in human seminal plasma are 31 µg/dL. In
chronic poisoning, the levels may be more than double.
(4) Blood picture - (a) Anemia [as above] (b) Leukocytosis
(5) Erythrocyte protoporphyrin [EP]:
(i) Lead impairs heme-based enzymes
(ii) EP reflects lead inhibition of the heme synthesis pathway.
(iii) It was used as a screening tool in the past, but is no longer considered
 sufficiently sensitive.
(iv) Still useful as secondary diagnostic tools for (a) tracking response to therapy
(b) distinguishing acute from chronic Pb poisoning [EP levels normal in
acute Pb].
(v) EP>35µg/100mL "Chronic Pb Poisoning.
(6) Free erythrocyte porphyrin (FEP): >70 μmol/mol heme.
(7) Radiology – Dense transverse bands or lead lines just underneath the
metaphyseal plates. They indicate -Pb deposition. Usually develop in 4-8
weeks of heavy exposure.
(8) X-ray fluorescence (XRF)- Estimates bone lead, and is thus indirectly a
measure of body lead exposure.

4. Prophylaxis
(1) Factory management should ensure:
(i) Maintenance of proper ventilation in factories
(ii) Maintenance of personal hygiene of workers
(iii) Periodic medical examination
(iv) Shifting of poisoned worker to administrative side
(2) Diet - rich in calcium
(3) Other measures:
(i) Small amount of sulphuric acid in water
(ii) Weekly saline purgative.

5. Management
(1) Removal for source – Most important. If poisoning is a result of
occupational exposure, person should be shifted to another job.
(2) Chelation:
(i) Both BAL and CaNa2EDTA – If there is lead encephalopathy, BAL is
administered first. 4 hours later CaNa2EDTA is started [1500 mg/m2/d by
continuous IV infusion]. In patients with renal dysfunction limit daily dose
to 50 mg/kg.
(ii) Duration - Continued for 5 days, followed by a rest period of at least 2-4
days, which permits lead redistribution [please see 3-compartment model
above].
(iii) Adjuncts - (a) Folic acid, (b) pyridoxine, and (c) thiamine [10-50 mg/kg] -
 the antidotal properties of CaNa2EDTA. Thiamine also improves
neurological manifestations
(iv) Penicillamine – ch 32.
(v) Only BAL – is the chelator of choice in presence of renal impairment as its
main route of excretion is bile. Two molecules of BAL combine with 1
atom of Pb to form an insoluble complex" excreted in bile
(vi) BAL Analogues – DMSA [Succimer], DMPS [ch 32]. Succimer is
increasingly replacing CaNa2EDTA as the chelator of choice in lead-
poisoned children without encephalopathy.
(3) Calcium gluconate IV – for colic.
(4) Magnesium or sodium sulphate – as in acute poisoning.
(5) To mobilize Pb from bones:
(i) Diet – Poor in calcium.
(ii) Ammonium chloride – 1 g ten times daily
(iii) Parathormone
(6) Surgery – Rarely surgery may have to be performed.
(7) Symptomatic.

6. Cause of death
(1) Encephalopathy
(2) Failure of vital functions (i) Liver failure (ii) Renal failure (iii) Respiratory
failure
(3) Intercurrent infection
(4) Malnutrition.

7. PM appearances
(1) Gums – Burtonian line
(2) CNS:
(i) Brain – (a) pale (b) greatly swollen (c) PAS +ve, pink staining, homogenous
material seen in the perivascular spaces
(ii) Peripheral nerves – segmental demyelination
(3) CVS:
(i) Heart – hypertrophied
(ii) Aorta, aortic valves - atheromatous
(4) Stomach and intestines:
(i) Hemorrhagic and ulcerative changes
(ii) Contracted, thickened
(5) Liver:
(i) Contracted
(ii) Hepatocytes – Show eosinophilic intranuclear inclusions [EII]
(6) Kidneys:
(i) Contracted
(ii) Proximal tubules - Show EII.
(7) Muscles – fatty degeneration [paralyzed during life]
(8) Bone marrow:
(i) Hyperplasic of erythroblasts and leukoblasts
(ii) . in fat cells.

8. ML importance
(1) Abortion – Lead salts used for abortion, eg Diachylon [lead oleate] (pl also
see ch 26)
(2) Artificial insemination - Donors with Pb poisoning [↑ seminal plasma Pb
levels] have lower fertility rates than donors with no Pb poisoning or low
seminal plasma Pb levels.
(3) Cattle poison – Red lead alone or mixed with arsenic
(4) Drug abusers - Chronic Pb poisoning may sometimes be seen in drug
abusers [because of intentional or unintentional adulteration with lead]
(i) Cocaine – Lead is a contaminant of manufacture in cocaine paste [ch 40, 41]
(ii) Marijuana - Lead in marijuana samples is a diluent [ch 40,41].
(5) Employer’s liability to pay compensation in cases of occupational disease
due to Pb – Same as MLI of Arsenic above.
(6) Lead pellets or bullets -
(i) Ingestion – Suicide has been attempted by ingesting lead pellets [pl see
management above]
(ii) Souvenir bullets - These are pellets or bullets which remain in the body after
a shooting incident [ch 13]. May cause ch lead poisoning.
(7) Manner - Suicidal, and homicidal poisoning rare
(8) Rapidity of poisoning -
(i) Acute poisoning – rare
(ii) Chronic poisoning is an occupational disease.
V. MERCURY (QUICKSILVER)

A. General
Mercury is a liquid metal, having bright silvery appearance. It is volatile at room
temperature.

B. Toxic Salts of Mercury

Mercury occurs in three forms – Metallic mercury, inorganic salt and organic
salts. Metallic mercury if swallowed as such is not poisonous, as it is not
absorbed from GIT. It is however absorbed in vapor form, and is very toxic,
because inhaled Hg vapors readily cross biological membranes.

1. Organic salts
Organic salts are most poisonous, especially (1) methyl mercury and (2)
dimethyl mercury.

2. Inorganic salts
Among inorganic salts, mercuric salts (Hg++) are more poisonous than
mercurous salts(Hg+). Mercurous salts are less soluble in water than mercuric
salts, accounting for their lesser toxicity.
(1) Mercuric Chloride [HgCl2, Corrosive sublimate] – White crystalline
powder, soluble in water, but much more so in alcohol. Before the advent of
antibiotics, used to treat syphilis. Once available as a blue coffin-shaped tablet
with the inscription “POISON”. This 0.5 g tablet dissolved in water was
intended to be used as an antiseptic solution.
(2) Mercurous Chloride [Hg2Cl2, Calomel (Gk. kalos, fair; melas, black; its
original preparation involved converting a black powder into white), sweet
mercury] - A white, tasteless powder, used chiefly as a fungicide and
abortifacient [ch 26]. Less toxic than HgCl2 due to its lower solubility in
water.
(3) Mercuric ammonium chloride - ointment containing 10% HgNH2Cl is used
for eczema. May cause toxicity.
(4) Mercuric cyanide – [Hg(CN)2]- Odorless, toxic white powder with a bitter
 metallic taste. Once used as an antiseptic. As an antisyphilitic, its solution was
applied with a brush on syphilitic sores. Still used in homeopathy as
Hydrargyrum bicyanatum
(5) Mercuric iodide - (HgI2, Protiodide) Red-orange crystals. Once used as a
treatment for syphilis
(6) Mercuric nitrite
(7) Mercuric oxide (HgO)- Brick red powder. Used as cathode for mercury
batteries
(8) Mercuric sulfate (HgSO4)- odorless white crystalline powder
(9) Mercury sulphide [cinnabar, red sulphide of mercury, sindoor, vermilion,
HgS. Vermilion is primarily HgS, but broadly it refers to any of various red
pigments.]
(10) Mercury thiocyanate [Hg(SCN)2] - Best known for its former use in
Deewali, as it produces a large, winding “snake” when set on fire. This is
known as the Pharaoh’s Serpent [After a Biblical story when Pharaoh of Egypt
calls his magicians, who turned their staffs into snakes].

C. Mechanism of Action
(1) Mercury binding to (i) sulfhydryl (ii) phosphoryl (iii) carboxyl and (iv)
amide groups - results in widespread dysfunction of enzymes, transport
mechanisms, membranes and structural proteins
(2) Direct oxidative effect of mercuric ions - results in PCT necrosis. Mercury
ion accumulates predominantly in the renal cortex
(3) Immune mechanism – results in membranous glomerulonephritis and
acrodynia associated with Hg
(4) Methylmercury inhibits astrocyte uptake of cysteine"Results in
.production of glutathione (a major antioxidant).

D. Toxicokinetics [Absorption, Distribution and Elimination]

(1) Absorption:
(i) Elemental Hg – (a) GIT [Not absorbed]" nonpoisonous orally. (b) inhalation
[80% absorption]. (c) Cellular membranes - diffuses rapidly including the
blood-brain barrier and placenta. (d) Half life - 60 days.
(ii) Inorganic Hg – GIT [10%], skin and mucus membranes.
(iii) Organic Hg – Long chain alkyl compounds"GIT [>50%]; short chain
alkyl compounds"GIT [90%]
(2) Distribution – Mercury distributes widely to all tissues. Major deposition in
CNS, kidneys, liver and spleen. Methylmercury concentrates in hair (due to
presence of sulfhydryl groups). Its concentration in hair is 250 times more
than in whole blood. Within blood, methylmercury concentrates more in
RBC than in plasma. RBC:Plasma ratio of methylmercury is 10:1, while the
same ratio for inorganic Hg is 1:1.
(3) Elimination – The total body half life of elemental and inorganic Hg is 30-
60 days. In contrast half life of organic Hg is 70 days (due to its
enterohepatic recirculation). Inorganic mercury is excreted both through urine
and feces. Excretion of organic Hg is predominantly fecal.

E. Acute Poisoning
Signs and symptoms differ according to the type of Hg ingested [elemental,
inorganic or organic].

1. Signs and symptoms

a. Elemental mercury

i. Inhalation
Usually occurs following gold refining in a closed room.
(1) General – Headache, blurring of vision, Fever, chills [metal fume fever],
Erythematous pruritic papular rash, conjunctivitis, salivation
(2) Pulmonary – chest pain, cough, dyspnea, interstitial pneumonitis,,
necrotizing bronchiolitis, pulmonary edema, pulmonary failure,
(3) GIT – Metallic taste, deep red oral mucosa, gingivitis, stomatitis, strawberry
tongue, swelling of salivary glands, teeth [loosened]
(4) Miscellaneous – Reddened palms and soles, manifestations similar to
Kawasaki disease (mucocutaneous lymph node syndrome) especially in
children. May be mistaken for scarlet fever.

ii. Ingestion
Absorption is minimal [<0.01% is absorbed]. Large quantities can be ingested
without obvious toxic manifestations. In 1515, an English nobleman on his
honeymoon drank a large amount of elemental Hg by mistake, but did not suffer
any harm.

iii. Injection
(1) S/c or IM - Abscess formation, ulceration [exuding tiny droplets of Hg].
(2) IV – [generally suicidal, or taken with a false belief that it acts as an
aphrodisiac] bloody sputum, dry cough, granuloma, pulmonary embolism,
tachypnea, thrombophlebitis.
(3) Intra-arterial – Can occur inadvertently from arterial blood gas sampling
with syringes containing Hg as anaerobic seal. Peripheral embolization with
ischemia and gangrene. X-ray in all cases reveals Hg globules.

b. Inorganic mercury
Manifestations occur in 2 phases.

i. First phase
(1) Immediately after ingestion of corrosive mercury salts – Hot burning
pain, sense of constriction, ashen discoloration of the mucous membrane in
mouth and throat. Burning pain extends down to stomach and abdomen.
(2) Within a few minutes - Intense epigastric pain, followed by diffuse
abdominal pain. Nausea, retching and almost continuous vomiting of mucoid
material, which frequently contains blood and shreds of mucous membrane.
Hoarse voice.
(3) Mouth, tongue and fauces – are corroded, swollen and show a grayish
white coating.
(4) Acrid metallic taste, excessive salivation and thirst.
(5) Severe purging, with liquid, bloody feces and considerable tenesmus.
(6) Rapid, weak pulse; breathing shallow and difficult; Pallor; Prostration,
circulatory collapse, and death.
(7) Above Signs and symptoms are not seen with mercury compounds of low
irritancy or with portals of entry other than the mouth.

ii. Second phase

If death does not intervene, phase 2 begins in 1-3 days in untreated cases (unless
vomiting effectively removed most or all poison).
(1) Oral - Marked salivation, mercurial stomatitis, glossitis and ulcerative
gingivitis within 24-36 hr. Loosening of teeth, necrosis of the jaw.
(2) Severe infections
(3) Renal - PCT Necrosis in 2-3 days, transient polyuria, albuminuria,
cylindruria, hematuria, anuria, azotemia and renal acidosis. Recovery may
occur within 10-14 days, but death may also occur in some cases.
(4) Late - After many days after the original exposure (especially in untreated
cases), a membranous colitis may appear; dysentery, tenesmus, ulceration of
the colonic mucosa, and hemorrhage. Liver necrosis sometimes develops.

2. Fatal dose
1-4 g of HgCl2

3. Fatal period
3-5 days.

4. Management (acute Hg)

a. For inorganic mercury

(1) Removal of patient – from further exposure
(2) Gastric lavage – Avoid. It is hazardous (due to corrosive nature of HgCl2, it
can lead to perforations) and unnecessary (excessive vomiting already)
(3) Activated charcoal [AC]
(4) Fluid resuscitation – Done on a priority basis. Otherwise there is danger of
cardiovascular collapse is caused by severe gastroenteritis and fluid loss.
(5) Hemodialysis and peritoneal dialysis – Not useful because of high degree
of protein binding
(6) Whole bowel irrigation – with polyethylene glycol is useful. Progress
should be followed with serial radiographs.
(7) Chelation therapy:
(i) BAL and DMSA- 5 mg/kg every 4 hours deep IM for 48 hours; then 2.5
mg/kg every 6 hours for 48 hours; then 2.5 mg/kg every 12 hours for 7
days. When the patient is able to take oral medication, replace BAL with
DMSA (Succimer) at 10 mg/kg orally tds x 5 days; then twice a day x 14
 days. This regimen is the treatment of choice for inorganic Hg poisoning
(ii) D-penicillamine (Cuprimine) – 1-1.5 g/day orally in 4 divided doses
(alternative chelator)
(iii) N-acetyl-DL-penicillamine (NAP)- An investi-gational analog of D-
penicillamine is a better chelator of Hg than D-penicillamine, because of its
greater stability
(iv) DMPS – 5 mg/kg IV, followed by 100 mg orally bd for 3 weeks.

b. For organic mercury

(1) BAL – should not be used. BAL comes as a lipid solution and may - Hg
mobilization into the brain, causing severe toxicity. Instead
(2) DMSA (Succimer) and
(3) DMPS are used. Both are water soluble analogs of BAL (ch 32).

c. For elemental mercury

(1) Postural drainage and endotracheal suction – useful if mercury vapors
have been inhaled.
(2) Surgical excision – if there has been IM Hg deposition
(3) Environmental decontamination – If there is spillage of elemental Hg on
solid surfaces, following measures are useful (a) Adsorb on sand - and
discard in tightly sealed containers (b) Mercury decontamination kit –
Should be used. Contains calcium polysulfide, which converts Hg to HgS
(Cinnabar) (c) Remove absorbent surfaces – eg. carpets (d) Do not vacuum
Hg – can volatilize it.

5. PM appearances
(1) Lips, mouth, tongue and esophagus - Mucous membrane more or less
whitened, swollen and soft.
(2) Stomach and esophagus: (i) congestion (ii) corrosion (iii) inflammation (iv)
severe hemorrhagic necrosis
(3) Large intestines – Mucus membrane inflamed, swollen, corroded and
hemorrhagic [lesions seen if person survived for a few days. Due to re-
excretion of Hg in the large intestines] – Necrotic areas. Small intestine is also
affected but to a lesser degree.
(4) Heart – subendocardial petechial hemorrhages
(5) Lungs – Thrombosis in capillaries.
(6) Liver – congested. Shows cloudy swelling and fatty change.
(7) Kidney – Interstitial nephritis
(8) H/P:
(i) Severe proximal convoluted tubule (PCT) necrosis, hemorrhagic glomerular
nephritis
(ii) Mercury deposition in renal cortex and renal macrophages
(iii) Neuronal necrosis and glial proliferation in cerebral cortex [seen in
Minamata disease].

F. Chronic Poisoning (Hydrargyrism)

Clinical pictures are different in inorganic and organic mercury toxicity.
Inorganic mercuric chloride mainly affects the renal and gastrointestinal systems.
The characteristic neurological feature is a fine tremor, particularly of the hands
and fingers.

1. Signs and symptoms

May result from (1) External application of Hg as ointment (2) occupational
exposure (3) recovery from a large dose (4) excessive therapeutic use of Hg.

a. General
(1) Anemia (2) anorexia (3) loss of weight (4) Inflammation of gums (5) blue
line at the junction of teeth and gums (6) Sore mouth and throat (7) loosening of
teeth (8) GIT disturbances (9) chronic nephritis with progressive uremia.

b. Ptyalism
Common causes of ptyalism.

c. Mercurial tremors
Mercurial tremors (syn. Danbury tremors or shakes, Glassblowers tremors or
shakes, Hatter’s shakes) are static and intentional tremors seen in chronic
mercury poisoning. The first description of mercurialism in hatters was
published by J. Addision Freeman, in Transactions of the Medical Society of
New Jersey in 1860.
Salient features:
(1) Tremors – Two types are seen (i) Static or resting tremor - occurs when the
muscle is at rest. It is a fine trembling motion, most evident in the upper
extremities (ii) Intentional or ataxic tremor – (a) occurs when there is
purposeful movement of an extremity, or (b) as an aggravation of an
established static tremor. Concussion mercurialis (Tetanus mercurialis)
refers to the last stage where tremors are so intense that they prevent daily
activities.
(2) Predisposing factors – Alcohol predisposes to tremors. Severe shakes are
never seen in teetotalers. Alternative names: (1) Hatter’s shakes
(3) Glassblower’s shakes - Glassblowers often blow colored mercury
compounds in ornamental glass. May get poisoned.

d. Mercurial erethism
Mercurial erethism (or erythism) is the name given to neuropsychiatric
manifestations seen in chronic mercury poisoning. The classical triad of chronic
mercury poisoning is (i) gingivostomatitis (ii) mercurial tremors and (iii)
mercurial erethism. Main symptoms seen in erethism are – Anorexia, emotional
instability, fatigue, insomnia, loss of memory, mood changes [anxiety, shyness,
withdrawal, depression, loss of confidence, nervousness, irritability, timidity],
resentment at being observed, rough temper, delusions, hallucinations, suicidal
melancholia, manic depressive psychosis (mad hatter). The Mad Hatter is a
character in Alice’s Adventures in Wonderland, a novel written in 1865 by Lewis
Carroll. He showed signs of mercurial erethism.

e. Mercuria lentis
Mercurial lentis is a peculiar eye change seen in chronic mercury poisoning due
to deposition of mercury through the cornea on to the anterior lens capsule.
Salient features:
(1) Slit lamp examination demonstrates a matt-brown reflex from anterior lens
capsule
(2) It is bilateral and has no effect on visual acuity. In contrast methyl mercury
toxicity results in visual blurring and tunnel vision.
(3) Mercury pigmentation of the anterior lens capsule may occur secondary to
topical medication containing mercury too [Mercuria Lentis
Medicamentosus]. These are mainly miotics containing phenyl-mercuric
 nitrate (PMN).
(4) Other eye changes:
(i) Lens opacities
(ii) Well marked vascularity at the corneoscleral junction.

f. Acrodynia (pink disease)

Acrodynia (also known as calomel disease, erythredema, erythredemic
polyneuropathy, Feer’s disease, pink disease, Selter’s disease and Swift’s
disease) is a peculiar manifestation of mercury poisoning seen in children.
Salient features:
(1) Hands and feet of the child became painful, paresthetic, peeling, [Fig 36.6]
perspiring, pink and puffy (Gk acro, extremity; dynia, pain).
(2) Other symptoms – Anorexia, hypertension, hypotonia, insomnia, irritability,
photophobia, rashes [due to excessive perspiration].
(3) Symptoms of catecholamine excess (perspiration, tachycardia, hypertension)
occur because mercury blocks the degradation pathway of catecholamines.
(4) D/d includes pheochromocytoma and Kawasaki disease.
(5) Acrodynia was relatively common amongst children in the first half of the
20th century, due to the use of calomel in teething powders (analgesic action)
and for washing nappies (bactericidal action).
(6) There is lack of correlation of symptoms with mercury levels, so it is thought
to be an idiosyncratic hypersensitivity reaction to mercury.
(7) Mortality is about 10%.
Memory Aid 4: Symptoms of ch Hg poisoning
Mnemonic for chronic Hg poisoning"TABLE – Tremor, Acrodynia, Blue-Black line on gums, Lentis,
Erethism

g. Hunter russell syndrome

Occurs due to ch exposure to methyl mercury. Most disastrous epidemic
occurred in 1953 [Minamata disease]. Symptoms:
(1) CNS – Peripheral neuropathy is a major feature. Major symptoms are
akinesia, ataxia, auditory impairment, blurred vision, cerebellar ataxia,
constricted vision, dementia, depression, diminished or absent deep tendon
reflexes, but up to 40% may have enhanced tendon reflexes, dysarthria,
impaired hearing, smell and taste, malaise, memory loss, numbness, olfactory
impairment, paresthesia with a peroral and glove and stocking distribution,
rigidity, sensory impairments, spasticity, taste impairment, tremors, visual
blurring and tunnel vision, and weakness.
(2) The immature brain is especially susceptible to the effects of
methylmercury and is often damaged in an irreversible and profound manner.
(3) Congenital poisoning - mental retardation, deafness, blindness, dysphasia,
 ataxia, microcephaly, and cerebral palsy. However, signs of peripheral
neuropathy are not found.
(4) Pathology - The symptoms are due to loss of myelinated nerve fibers,
autonomic dysfunction, sensory nerve conduction delay, abnormal neuronal
migration, and abnormal central nervous system cell division.

2. Diagnosis
(1) Normal levels of Hg: (i) Blood - <10 µg/L (ii) Urine - <20 µg/L. (iii)
Normal urinary Hg excretion in 24 h is <50 µg.
(2) Ch exposure - (i) Blood >35 µg/L (ii) Hair. (iii) Urine >150 µg/L
(3) MRI [in patients with ingestions of organic Hg]- Atrophy of cerebellar
hemispheres, postcentral gyri and calcarine area. These findings co-relate
with clinical findings of ataxia, sensory neuropathy and visual field
constriction respectively.

3. Management (Chronic Hg)

(1) Removal of patient from further exposure
(2) Demulcents
(3) Saline purgatives
(4) Maintain oral hygiene
(5) Chelation therapy – same as in acute poisoning.

G. Tests for Mercury

Suspected solution + A piece of copper wire + Few drops of HCl"A silvery
colored coating of mercury on copper wire will form.

H. MLI
(1) Blood - Stains of red sulphide of mercury resemble blood stains. They need
to be differentiated [ch 29].
(2) Blood transfusions - Blood conc of Hg may be higher in persons taking a
diet rich in sea food. If blood from such individuals is transfused to premature
infants [especially multiple transfusions in a short period], there is a
possibility of Hg poisoning.
(3) Component of:
(i) HgCl2 is a component of cavity fluid for embalming [ch 9]
(ii) Hg2Cl2 is a component of Vibert’s fluid [ch 29]
(4) Criminal abortion – Mercury salts [eg HgCl2] introduced in vagina for
criminal abortion or as contraceptive measures. May cause death.
(5) Dentistry – Hg used in dental amalgams.
(i) Patients - Chronic absorption produces grayish blue mucosal discoloration.
(ii) Dentists – Many still knead the amalgam mass in their hands. While
squeezing the mass to express out excess Hg, droplets often fall on the
floor. Since they are difficult to scoop up, they are allowed to remain their
and vaporize causing the Hg conc in the environment to rise. This may
cause chronic Hg poisoning in dentists.
(6) Employer’s liability to pay compensation in cases of occupational disease
due to Mercury – Same as MLI of Arsenic above.
(7) Manner of poisoning:
(i) Accident– can occur as a result of (a) thermometers breaking in the mouth. It
is usually harmless. (b) as a complication of Hg-sealed syringes for arterial
blood drawing. It can give rise to radiopaque shadows in the head
(embolization in brain), chest (embolization in lungs) and other areas of the
body. D/d of such shadows are (I) embolization of bullet fragments or lead
shots, (II) heavy metal and metal salt deposits (bismuth) in gluteal areas and
(III) cysticercosis (c) Disk battery ingestions – Mercury oxide may release
if battery opens within GIT causing Hg poisoning.
(ii) Homicide and suicide – rare.
(8) Quacks – Mercury salts are quacks’ favorites. Acute Hg poisoning may
result from the external application of some mercurial preparation, or from the
injection into the uterus, or into large abscess cavities of a soln of corrosive
sublimate. Symptoms of acute Hg poisoning, followed in some cases by death,
have resulted from the external application of corrosive sublimate to tumors or
ulcers, a method sometimes resorted to by quacks for the destruction of so-
called cancer; similar toxic symptoms have resulted from injecting a solution
of corrosive sublimate into psoas abscess cavities, and into the uterus after
childbirth.
(9) Therapeutic use of Hg:
(i) Mercuric chloride – Strong soln used for washing abscess cavities or
irrigating vagina, uterus or rectum. May cause accidental poisoning.
(ii) Mercurous chloride – (a) Can cause acrodynia [please see above]. Even
today it is sometimes used as a laxative. (b) As an abortifacient, it caused
death of pregnant mothers [ch 26]
(iii) Metallic mercury is generally not poisonous. At one time oral Hg in doses
of 100 to 500 g was given for the treatment of adynamic ileus and bowel
obstruction. It usually passed off in the feces harmlessly, but sometimes
diarrhea and stomatitis resulted. Occasionally fatal poisoning also
occurred. Hg was also put as a weight at the end of a gastroduodenal tubes,
which were passed to relive GIT obstructions. Sometimes the Hg containing
balloons used to rupture, releasing Hg in the GIT. Generally such events
were harmless, but occasionally acute appendicitis used to occur.
Sometimes Hg used to escape from a perforated appendix and formed
intraperitoneal mercury granulomas.,
(10) Thiomersal controversy – Thiomersal, an organomercury compound, is a
well established antiseptic and antifungal agent, and has been used as a
preservative in vaccines, immunoglobulin preparations, skin test antigens,
antivenins, ophthalmic and nasal products, and tattoo inks. Its use in vaccines
allows the use of multidose vials instead of single-dose vials, which are more
expensive. There have been concerns that its use in vaccines leads to the
development of autism and other brain development disorders in children.

VI. THALLIUM

In the early 1900s, thallium [Tl] salts were used as a depilatory and to treat
syphilis, gonorrhea, TB and ringworm of the scalp. The dose given (7-8 mg/kg)
was very near fatal dose, and caused severe poisoning (thallotoxicosis). Because
thallium sulfate is odorless and tasteless, it was very useful as a rodenticide
(Thalgrain, Echol’s Roach powder, Martin’s Rat Stop liquid). Since it could
easily be purchased as a rodenticide, it became a popular homicidal poison too.
Thallium acetate was once used to check the “night sweats” in tuberculosis.
When it was noticed that it caused loss of hair, Sabouraud instituted its
therapeutic use for tinea in 1898. It was supplied as a cream (Koremlou cream),
containing 7.18% thallium acetate. This practice was abandoned half a century
later, when it was realized that it was a potential poison. Thallium is used in
electronics industry [App 60–70% of Tl production], pharmaceuticals, in glass
manufacturing and in infrared detectors.

A. Acute Poisoning
Can occur from
(1) Oral ingestion [most common]
(2) Inhalation from contaminated dust from pyrite burners, cadmium
manufacturing, lead and zinc smelting, and
(3) As a contaminant of heroin or cocaine. Symptoms occur after a latent period
of 12 hours to 12 days.

1. Signs and symptoms

(1) GIT:
(i) Abdominal pain [most common]. Accompanied by
(ii) Vomiting and either
(iii) Diarrhea [if irritant effect of Tl is predominant] or
(iv) Constipation [if involvement of vagus nerve is predominant ".d intestinal
motility, .d peristalsis]
(v) Severe symptoms, eg hematemesis and bloody diarrhea are more rare.
(2) Chest – Tightness and pain [vagus involvement]
(3) CVS:
(i) Tachycardia and
(ii) Hypertension [both develop after 1-2 wks. These are due to (a) vagus
involvement (b) Tl stimulates ATPase in the chromaffin
cells"catecholamines -"sinus tachycardia. Persistent and pronounced
tachycardia points to poor prognosis
(iii) ECG changes [due to direct myocardial damage] – (a) prolongation of the
QTc interval, (b) T-wave flattening or inversion, and (c) nonspecific ST-
segment abnormalities
(4) Skin – Maculo-papular skin eruption having butterfly distribution on face
[very characteristic]
(5) Coma – Occurs with large exposures. If recovery occurs, patient may suffer
from permanent Guillain-Barré like polyneuritis.

2. Fatal dose
6-40 mg/kg of Tl salts. Death is due to coma with loss of airway-protective
reflexes, respiratory paralysis, and cardiac arrest.

3. Fatal period
24-36 h.

B. Chronic Poisoning
Due to repeated administration [homicidally or taken as medicine]. Most
characteristic lesions are abdominal pain [seen also in acute poisoning],
alopecia and neurologic symptoms [Thallium triad].
(1) Alopecia: [Fig 36.7]
(i) Most common and classic manifestation of Tl toxicity.
(ii) Typically it is the presenting symptom.
(iii) Begins in 10 days. Total hair loss in 30 days.
(2) Neurologic symptoms: (i) painful ascending peripheral neuropathy [appears
after 2-5 days]
(3) Skin: (i) acne, (ii) palmar erythema, (iii) anhidrosis and (iv) dry scaly skin
[results from damage to the sebaceous glands].
(4) Nails - Mees lines appear within 2-4 weeks after exposure [also seen in
arsenic].
C. D/d
Must be differentiated from neuropathy seen in
(1) Poisoning by (i) arsenic, (ii) colchicine, and (iii) vinca alkaloids;
(2) Botulism;
(3) Thiamine deficiency; and
(4) Guillain-Barré syndrome.

D. Management
(1) Gastric lavage - with 1% KI or Prussian blue. After the lavage Prussian
blue is instilled through a duodenal tube directly into the duodenum [since Tl
diminishes gastric and intestinal motility]. The dose is 125 mg/kg bd, with 50
ml of 15% mannitol [laxative to counter constipation].
(2) Activated charcoal [AC]– Since Tl undergoes enterohepatic recirculation,
AC may be useful both in acute and chronic poisoning.
(3) Whole-bowel irrigation with polyethylene glycol
(5) Prussian Blue [potassium ferric hexacyanoferrate]- 125 mg/kg bd orally via
a nasogastric tube. Causes -ed fecal elimination, and .ed blood Tl+ conc.
Mechanism - Acts as an ion exchanger. Interferes with the enterohepatic
circulation by exchanging K+ ions for Tl+ ions in GIT"formation of a conc
gradient causing"-ed movement of Tl+ into GIT.
(6) Charcoal hemoperfusion and hemodialysis - especially if the patient has
renal insufficiency
(7) Forced diuresis.

E. PM Appearances
In fulminant cases, death occurs before any gross changes become apparent. In
cases which death occurs days or weeks later, following changes may be seen.
Of these GIT and lung changes are seen in acute poisoning too.
(1) Hair – Alopecia
(2) Mouth – Stomatitis
(3) CNS –
(i) Cerebral cortical changes, especially in autonomic nervous system.
Widespread degeneration of axons and nerve cells in the brain
(ii) Meninges – congested
(4) CVS - Fatty degeneration of the heart [seen as a “tabby cat” striation of both
ventricles
(5) Lungs – Edema
(6) Kidneys – Renal damage. Nephrosis
(7) GIT -
(i) Stomach and intestines – (a) Signs of gastroenteritis. (b) Mucosa inflamed,
ulcerated. (c) Submucosal petechial hemorrhages
(ii) Liver - fatty degeneration
(8) In cremated bodies – Thallium can be detected in the ashes.

37. Vegetable Poisons

I. RICINUS COMMUNIS (CASTOR, ARANDI)

The pathology of ricin and abrin poisoning was described by Flexner in 1897.
Salient features:
(1) Habitat - Ricinus communis [Latin for “common tick” because the seeds
resemble ticks (Fig 37.2)] grows all over India.
(2) Plant [arandi, wonder tree] -
(i) The plant [family Euphorbiaceae, (spurge family)], is native to tropical
Africa.
(ii) Grows like a bush [Fig 37.1].
(iii) Cultivated in many countries as an ornamental annual plant in gardens.
(iv) It is a shrub, 1–4 m high, branched with green or reddish leaves.
(v) Has clusters of seed pods covered with fleshly spines.
(3) Leaves – (i) Glossy, (ii) 15–45 cm long, (iii) long-stalked, (iv) alternate and
palmate with 5–12 deep lobes with coarsely toothed segments.
(4) Fruit - The fruit [pod] is a spiny, greenish to reddish purple capsule [Fig
37.1] containing large, oval, shiny, bean-like, highly poisonous seeds with
variable brownish mottling. Contain three seeds per capsule.
(5) Seeds – There are two varieties of seeds (i) Large red seed with brown
blotches [Fig 37.2] – yield 40% oil. Double the size of small seeds. Used
mainly for illumination (ii) Small grey seed with brown spots – (a) Size -
1.2x0.8 cm (b) resemble croton seeds [Table 1] (c) yield 37% oil. (d) Better
quality. Used for medicinal purposes. Oil does not contain ricin; it remains
behind in bean pulp during extraction. Extraction during heated conditions
inactivates ricin within the pulp too.
(6) Poisonous parts - All parts of the plant are poisonous but seeds are most
poisonous [ricin: 1-5%; ricinine: 0.3–0.8%].
(7) Uses - The seeds contain between 40% and 60% of a yellowish oil (castor
 oil or ricinus oil), which is used as an
(i) Additive - in candles, cosmetic creams, diffusion pump oils, linoleum,
lipsticks, lubricants, paints, plasticizers, printing-inks, soaps, transparent
paper and varnishes.
(ii) Lubricant - From World War I until the 1960s it was used as a lubricant for
jet engines, high-speed automotives, and industrial machinery. Castor plants
were cultivated in large quantities until synthetic oils became available for
use.
(iii) Food industry - Flavorings, candy (eg chocolate), as a mold inhibitor and in
packaging. Castor oil is used, which is not poisonous. In Nigeria, the whole
beans are eaten as food, after boiling [heat inactivates ricin]
(iv) Medicinal [purgative] and lighting purposes
(v) Manure – seed cake is used
(vi) Fuel, thatching material or for preparing paper pulp – Plant stalks are used
(vii) Silkworm feed - In the silk-producing areas, leaves are fed to the
silkworms.
(viii) Ornamental - In countries where synthetic oils have become common, the
plant is now grown only for its ornamental value.

A. Active Principles
(1) Ricin [toxalbumin]
(2) Ricinine –
(i) A piperidine alkaloid.
(ii) A toxalbumin or phytotoxin is a toxic protein found in certain plants and
bacteria, capable of stopping protein synthesis. Common toxalbumins are
 ricin, crotin and abrin.

B. Mechanism of Action
Biochemically toxalbumin is a Ribosome Inactivating Protein (RIP), capable
of inactivating ribosomes and hence protein synthesis. 3 types of RIP are known
– Type I, Type II and Type III. It is best to study type II RIP first.
(1) Type II RIP [syn: type 2 RIP] is composed of an A chain (or effectomer)
that is enzymatically Active (Memory Aid: A"Active) and a B chain
(haptomer) that Binds (Memory Aid. B"Binds) the toxin to the surface of
cells (Fig 37.3) [Type II RIP is thus sometimes referred to as A–B toxin].
Once the RIP binds to the cell surface by the B chain, it enters cell by
endocytosis. In the cytosol, the A chain inactivates ribosomes"Protein
synthesis ceases. One A chain molecule can inactivate approximately 1500
ribosomes per minute, leading to rapid inhibition of protein synthesis and cell
death. [Ex – Abrin, Crotin, Ebulin [from Sambucus ebulus], Modeccin [from
Adenia (Modecca) digitata], Ricin, Shiga toxin (from Shigella dysenteriae)
and the related Shiga-like toxin (from certain enterohemorrhagic strains of
E.coli), Viscumin (from Viscum album)]. Type II RIPs evolved from type I
RIPs.
(2) Type I RIP [syn: type 1 RIP] consists only of A chain, and is thus active
against ribosomes only in vitro; it can not enter the cell on its own. [Ex -
Agrostin (from Agrosternma githago), Asparin (from Asparagus officinalis).
(3) Type III RIP [syn: type 3 RIP] - are actually inactive precursors (proRIPs)
that require proteolysis before they become active. They are the least
prevalent of all 3 types. Till date, they have been isolated only from maize
and barley.
C. Ricin
After oil is extracted, the bean pulp (or fibrous residue) that is left behind
contains ricin (approx 1 to 5% of seed’s wt). Ricin is a water soluble toxalbumin.
It is not present in the oil; castor oil is thus non-toxic (unlike croton oil which is
toxic). If oil is extracted under heated conditions, ricin is inactivated. Ricin is a
type II ribosome-inactivating protein [RIP] (Fig 37.3). The seeds also contain
ricinolein, a triglyceride which is mainly responsible for their purgative action.

D. Signs and Symptoms

1. Ingestion
(1) Method of ingestion –
(i) Swallowed - Do not cause poisoning. They pass through the GIT with little or
no toxic effects, because the hard seed coat cannot be digested by gastric
juices.
(ii) Chewed - Toxic because ricin is released.
(2) Severity of poisoning –
(i) Mild - results in nausea, vomiting, diarrhea, and abdominal pain.
(ii) Moderate to severe - GIT symptoms progress to dehydration, hypotension,
 liver and renal dysfunction [-BUN, -creatinine], and death.

2. Inhalation
Dust of seeds causes conjunctivitis, cough, sneezing, acute nasal inflammation,
dyspnea, arthralgias, fever, respiratory distress and death.

3. Injection
Generalized weakness, myalgias, hypotension, multiorgan failure and death.
Anaphylactic reactions may occur.

E. Diagnosis
(1) H/o ingestion of Ricinus seeds
(2) Detection of seeds in vomitus or stool
(3) Occurrence of compatible clinical signs
(4) Detection of ricin or ricinine in antemortem or postmortem samples.

F. Fatal Dose
(1) Seeds - 5 well-chewed seeds. Intact seeds are typically not digested and
therefore do not release ricin.
(2) Ricin –
(i) By injection or inhalation - 20 μg/kg (1.4 mg for an average adult weighing
70 kg). This is less than 1/250th of a standard aspirin tablet
(ii) By ingestion - About 1000-fold less [20 mg/kg], due to relatively low
bioavailability of ricin (≤1%).
(3) Castor oil [unlike croton oil] is not poisonous.

G. Fatal Period
2 days.

H. Management
(1) Mainly supportive - IV fluids and vasopressors (eg, dopamine) for
hypotension. There is no antidote for ricin
(2) Activated charcoal - if vomiting has not begun and airway is secure
(3) Gastric lavage - if ingestion has occurred within an hour
(4) Whole bowel irrigation
(5) Demulcents.

I. Prophylaxis
Animal studies have shown that anti-ricin antibodies administered by inhalation,
1 h prior to an aerosolized ricin challenge, .es lung damage.

J. PM Appearances
(1) GIT mucosa – congested, softened and inflamed. Erosions and submucosal
hemorrhages are seen
(2) Hemorrhages – in internal organs
(3) Serous cavities – contain blood
(4) Fragments of seeds – Found in stomach or intestines.

K. ML Importance
(1) Manner of poisoning:
(i) Accidental - Necklaces made of castor oil seeds can cause
(ii) Suicide – Can be used. A case is reported of the death of a 49 y old man who
injected himself s/c and IV with approx 10 mL of a ‘self-made’ acetone
extract of castor beans, with an intent to commit suicide. He died within 9 h
despite being given the best medical care.
(iii) Homicide – Rarely used
(2) Destruction of unwanted children – by giving crushed castor seeds in their
foods
(3) Infanticide – In East Africa, unwanted children are murdered by adding
castor beans to their food
(4) Abortifacient – Castor oil used as abortifacient [ch 26]
(5) Malingering – Powder of seeds applied to eye produces conjunctivitis.
(6) Biological Weapon – Ricin is codenamed “Compound W”. During World
War II, the U.S. and Great Britain worked together to develop a “W bomb”,
but abandoned research midway. Remains a potential biological warfare agent.
(7) Medicinal use of ricin - treatment of cancer and AIDS.
(8) Terrorist weapon – Ricin is a potential terrorist weapon.
(i) 1978 - The Russian secret police KGB assassinated the Bulgarian defector
 Georgi Markov by ricin. A weapon disguised as an umbrella injected a
small metal pellet containing ricin into Markov’s thigh. More recently ricin
has been stockpiled by terrorist organizations.
(ii) 1989 - Iraq reportedly conducted tests to spread ricin as an aerosol.

II. CROTON TIGLIUM (JAMALGOTA, NAEPALA)

Croton tiglium (Purging Croton) [family Euphorbiaceae] grows all over India.
Name comes from Gk kroton, “tick”; seeds resemble ticks. Seeds are poisonous
and contain a toxalbumin crotin. They are odorless, dark brown and oval with
longitudinal lines (Fig 37.4). Croton oil [Crotonis Oleum] present in the seeds is
about 50-60% by weight of seeds. Like croton seeds, croton oil is also poisonous
(unlike castor oil, which is non-poisonous), as it contains crotin. Croton oil is
carcinogenic also. Physically, croton oil appears as a thick, brown, viscid oil
having an unpleasant odor and acrid, burning taste.
A. Active Principles
(1) Crotin [toxalbumin] (2) Crotonal [a non-purgative fraction] (3) crotonic acid
(4) crotonic resin (5) crotonoleic acid [A mixture of croton resin with inactive
fatty acids. A powerful vesicating resin] (6) Crotonoside [glycoside] (7)
Glyceryl crotonate (8) Tiglic acid [syn, methyl crotonic acid]. Also present are
(9) several volatile acids (10) fatty acids (11) tumor-promoting phorbol esters (i)
phorbol formate, (ii) phorbol butyrate, and (iii) phorbol crotonate.
B. Signs and Symptoms
1. Ingestion
(1) GIT - (i) Vomiting and diarrhea (ii) Salivation (iii) Hot burning pain from
mouth to stomach
(2) Systemic - (i) Vertigo (ii) Prostration (iii) Collapse (iv) Death.

2. Application on skin
Application of oil on skin produces (1) burning, (2) redness, (3) vesication.

C. Fatal Dose
(1) Seeds – 4 (2) Croton oil – 20 drops.

D. Fatal Period
6 hours -3 days.

E. Management
(1) Gastric lavage (2) Demulcents (3) symptomatic.

F. PM Appearances
(1) Mucosa of GIT- congested, inflamed, excoriated
(2) All internal organs - congested.

G. ML Importance
(1) Accidental poisoning – results from ingesting croton seeds or oil by
mistake, or when taken in large doses as medicine (purgative), or by inhalation
of dust
(2) Abortifacient – Root and oil [ch 26]
(3) Arrow poison – paste made by crushing the soft parts of plant [not the seeds]
(4) Ayurveda - In Ayurvedic system of medicine croton seed oil is used in
minute doses in cerebral affections [apoplexy, convulsions, insanity], dropsy,
high blood pressure, intestinal obstruction, lead poisoning and obstinate
constipation. May cause poisoning if incorrectly used. Formerly also used as a
counterirritant in all systems of medicine.
(5) Suicide and homicide – Rare. Fruit is boiled in water and added to food
(6) Poisoning animals – croton oil has been used to poison fish in tanks. Mixed
with beef it has been used mischievously to kill pet tiger belonging to a circus
party.
(7) ordeal poison [ch 31]
(8) As a counterirritant - Diluted with a suitable inactive vehicle, croton oil
was once used as a counterirritant.
(9) Chemical peels – Due to its caustic exfoliating effects, croton oil [in
combination with phenol] has been used in chemical peels. Leads to initial
skin sloughing and then eventual regeneration.
(10) As an additive to fuel to render it unsafe for drinking – Can be added to
fuel (comprising of alcohol) to render it unsafe for drinking (much as methyl
alcohol is added to ethyl alcohol to denature it). US did so in World War II to
prevent sailors from drinking fuel (comprising of grain spirits). Reportedly a
number of sailors distilled alcohol away from the mixture and still consumed
it!

III. ABRUS PRECATORIUS (RATTI)

Abrus precatorius (Ratti, Gunchi, Jequirity, Crab’s Eye, Rosary Pea) is a

slender, perennial climber found all over India that twines around trees, shrubs,
and hedges. In 1891, Hellin discovered the agglutinating properties of abrin.
Salient features:
(1) Leaves – compound, feather like; 1-2.5 cm long; 10-15 pairs of narrow
leaflets.
(2) Flowers – small and pale violet, arranged in clusters, with a short stalk.
(3) Seed pods – 2.5-5 cm long, borne in clusters. Green when immature; on
maturing, become dry and brown; split open while remaining on vine with 4-6
seeds exposed. All parts of the plant are poisonous.
(4) Seeds – (i) Size - Pea sized. (ii) Color - Bright scarlet color with a large black
spot at one end [Fig 37.5]. Rarely the color may be white, yellow, blue, or all
black. (iii) Odorless and tasteless. (iv) Weight - Supposed to be quite uniform
in weight. In India, it was traditionally used as a standard weight (0.12125
grams) by jewelers.
A. Active Principles
(1) Abrin [a toxalbumin similar to viperine snake venom] (2) Abrine (N-
methyl L-tryptophan) [an amino acid] (3) N,N-dimethyl-L-tryptophan [plant
growth inhibitor] (4) Hypaphorine (5) Precatorine (6) Choline (7) Trigonelline.

B. Mechanism of Action
(1) RIP - Abrin has a structure similar to ricin, and acts essentially in the same
manner.
(i) Abrin has 2 chains A and B [Fig 37.3]. A chain [molecular weight 30 kDa]
has 251 amino acid residues, and is divided into three folding domains.
(ii) B chain [molecular weight 35 kDa] is a galactose-specific lectin. Consists of
268 residues. Both are linked by a disulphide [S-S] bond between Cys247
of the A chain and Cys8 of the B chain. A single molecule of abrin is
sufficient to kill a cell.
(2) Abrin-induced endothelial cell damage -
(i) Many clinical features can be explained by it.
(ii) Endothelial damage "- in capillary permeability "fluid and protein
leakage"tissue edema [vascular leak syndrome]. This is also a recognized
feature of ricin poisoning.
(3) Direct toxic effect on CNS.
(4) Agglutination of RBCs.

C. Signs and Symptoms

1. Topical contact
(1) Ophthalmic exposure - (i) severe inflammation of the conjunctiva (ii)
localised necrosis. (iii) An infusion instilled in the eye may ran through the
tear duct into the throat.
(2) Dermal exposure - No reports of human or animal toxicity.

2. Inhalation
(1) Human toxicity - has not been reported.
(2) Rats exposed to abrin dust -
(i) Onset of symptoms - 18–24 h
(ii) Mild poisoning - general malaise, lethargy, anorexia, piloerection, respiratory
difficulties.
(iii) Severe poisoning - exudation of blood-stained fluid from nostrils.

3. Ingestion
(1) Immediate [onset few hours – 1 day] –
(i) GIT - (a) Severe irritation (b) Abdominal pain (c) Nausea and vomiting (d)
hemorrhagic gastritis (e) Bloody diarrhea, Rectal bleeding
(ii) Pupils – constricted
(iii) Pulse – rapid, weak
(iv) Dyspnea
(v) General - (a) Cold perspiration (b) Trembling of hands (c) Weakness, general
prostration, faintness, vertigo
(2) Delayed [onset 2-5 days] –
(i) Delayed cytotoxic effects in CNS, liver, kidneys and adrenal glands.
(ii) Convulsions.

4. Injection
Injected in the form of sui [Fig 37.6]
(1) Local - (i) Painful swelling and edema (ii) ecchymosis (iii) Inflammation (iv)
 Oozing of hemorrhagic fluid and necrosis around site of puncture
(2) General – (i) General weakness, faintness, vertigo (ii) inability to make
movements, (iii) no desire to take food (iv) tetanic convulsions (v) temp. (vi)
drowsiness, coma and death in 3-5 days. Symptoms resemble viperine snake
bite.

D. Fatal Dose
(1) Abrin [IV]- 0.1–1.0 μg/kg.
(2) Seeds [ingestion]- 1-2 crushed seeds [i.e. if they are chewed]. As many as 20
unchewed seeds may be harmless.

E. Fatal Period
3-5 days.

F. Management

1. Topical contact
Eyes -wash eyes with running water for ten minutes. Rest as in ingestion below.

2. Inhalation
(1) Remove from exposure.
(2) Maintain clear airway; ensure adequate ventilation ensured
(3) Treat pulmonary edema conventionally. Rest as in ingestion below.
3. Ingestion
(1) Remove all seed particles from the mouth
(2) Collect remaining seeds or plant material for identification
(3) Induce vomiting and send it for chemical examination
(4) gastric lavage
(5) Activated charcoal
(6) Sodium bicarbonate – 10 g orally/d"maintains alkalinity of urine; prevents
agglutination of RBCs, and thus blockage of renal tubules
(7) Antiabrin antibodies – no role in management [in all routes of exposure];
very limited role in prophylaxis [please see below]
(8) Hospitalization - Patient should be hospitalized for several days because
severe symptoms can develop several days after ingestion.

4. Injection [Sui]
Sui (needle) should be dissected out. Rest as above.

G. Cause of Death
Cardiac failure.

H. Prophylaxis
(1) Hyposensitization - Mice injected with increasing sub-lethal doses of seed
extract develop tolerance. Not similarly tested in humans.
(2) Abrin Toxoid - Rats administered with abrin toxoid were protected against
aerosolized abrin
(3) Ascorbic Acid – Repeated bolus doses of ascorbic acid, sodium ascorbate
and calcium ascorbate over a 48-hour period "-es survival time.
(4) Anti-Abrin Antibodies – Very limited role.

I. PM Appearances
(1) Puncture marks - as in snakebite
(2) edema and petechial hemorrhage [in quick deaths] and purulent sepsis and
necrosis [in late deaths] in the area where sui was introduced
(3) Fragments of sui in the skin
(4) Internal organs – congested; show hemorrhages
(5) Stomach – In ingestions, gastric lining shows congestion with submucous
hemorrhagic spots
(6) Other Mucus membranes – pleura, pericardium, peritoneum may show
petechial hemorrhages
(7) In inhalation – Lungs strongly congested.

J. ML Importance
(1) Cattle poison –
(i) Seeds are used.
(ii) Leather workers use this method to obtain leather from cattle
(iii) Cattle of enemy may be killed for revenge
(2) Homicidal poison:
(i) In the form of Sui or sutari [needle]
(ii) Method of preparation of Sui - (a) Seeds are decorticated (b) Mixed with
datura, opium, glass powder and onion"powdered. Sometimes used alone
(c) A paste is made by mixing this powder with spirit and water (d) Sharp
pointed spikes [suis, needles] about 15 mm long and weighing 90-120 mg
are made from this paste (e) Dried in the sun
(iii) Method of killing - (a) Two such suis are mounted on a wooden handle [Fig
37.6] (b) The handle is struck on the back of a cattle or human. Sometimes
needles are kept between fingers and the person is slapped. (c) Needles
lodge inside the flesh; the person thinks he has been struck only with a
blunt instrument [or slapped] and after picking up a little fight allows the
assailant to go away (d) the injection site suppurates and person dies within
3-5 d.
(iv) Advantage to killer – Since symptoms resemble viper snake bite, killer is not
under suspicion.
(3) Malingering –
(i) Powdered abrus introduced in eye produces strong conjunctivitis. Used by
persons [especially army jawans, where getting leaves is difficult] to obtain
medical leave.
(ii) Unilateral conjunctivitis should arouse suspicion.
(4) As contraceptive and abortifacient – Because of irritant action. Used by
vaids and hakims and sometimes by patient herself. Action not reliable.
(5) Arrow poison.
IV. CAPSICUM ANNUUM (CHILI)

(1) The Capsicum genus is a member of the Solanaceae family which includes
tomatoes, potatoes, and the deadly nightshades. This genus includes chili
peppers, red peppers, and paprika, but not black pepper.
(2) Capsicum annuum (chilies, red pepper, lal mirch) has a pungent odor and
taste and is widely used in India and around the world as a condiment. In
India, it is widely used in preparing curries and chutneys. Though it causes
intense irritation, it is not fatal. The active principles are (i) capsaicin and (ii)
capsicin.

A. Signs and Symptoms

(1) On oral ingestion – Burning pain in mouth, difficulty in swallowing, pain in
abdomen
(2) On eye contact – intense blepharospasm, inflammation, lachrymation
(3) On dermal contact –Hunan hand - Intense burning pain, hyperalgesia,
erythema and dermatitis, after handling chili powder with bare hands.
Common in cooks, who prepare food with chilies without using gloves.
Hunan hand is so named because it was common in Hunan province of
China. Capsaicin releases Substance P, an undecapeptide (peptide composed
of 11 amino acids) from afferent sensory neurons, causing pain (Substance P is
the neurotransmitter for communication of pain and itch sensation from the
periphery to the CNS). The symptoms are due to nerve receptor stimulation
and not local injury to the skin.

B. Management
(1) Wash local skin with ice-cold water for 15 minutes
(2) emollient creams
(3) irrigation of eyes
(4) give demulcents and ice cubes to suck if symptoms due to ingestion.

C. ML Importance
(1) Robbery - Chili powder is thrown in eyes to facilitate robbery
(2) Burning of chili powder - by superstitious people to scare away ghosts and
spirits
(3) Introduced in vagina - for infidelity
(4) For obtaining confession of crime – chili powder introduced in vagina,
urethra etc
(5) Pepper spray - used by ladies in the west to drive away potential rapists
(6) Homicidal asphyxia in children - by forcibly introducing pepper in the
nostrils and mouth of unwanted young children
(7) Hyderabadi goli - Police torture. A lathi is liberally plastered with chili
powder and is thrust up the victim’s anus to extort confession.
(8) Datura seeds - must be differentiated from chili seeds (see chapter on
deliriant poisons).

V. SEMECARPUS ANACARDIUM (DHOBI’S MARKING NUT)

Semecarpus anacardium (Hindi: Bhilwa, Sanskrit: Agnimukh) [family

Anacardiaceae] is a native of India.
Salient features:
(1) Tree – Moderate sized deciduous tree with large stiff leaves.
(2) Fruit (nut) – (i) ripens from Dec-Mar (ii) 1 inch long, ovoid, oblong or heart
shaped [Fig 37.7], smooth and shining, black when ripe, seated on a fleshy
orange-colored cup [Fig 37.7]. Has a rough projection at the base. (iii) has a
thick cellular pericarp which contains a bitter, irritant juice which is acrid,
brownish and oily. It turns black on exposure to air. It is used in India as a
substitute for marking ink for clothes by washermen [Dhobi Nut, Dhobi’s
marking nut]. The tree sometimes is called “Ink tree”.
A. Active Principles
(1) Bhilawanol [15-17%] – A mixture of cis- and trans isomers of urushiol
(2) Semecarpol [0.1%].

B. Signs and Symptoms

(1) External application –
(i) Produces a dark colored lesion which resembles a bruise [artificial bruise].
(ii) Eczematous eruptions of the neighboring skin with which it comes in contact
(iii) Irritation, itching
(iv) Painful blister which contains acrid serum.
(v) Later an ulcer is produced.
(vi) Skin may slough off.
(2) Ingestion -
(i) GIT - Blisters on throat, severe GIT irritation with vomiting and diarrhea
(ii) RS – Dyspnea
(iii) CVS – Cyanosis, Hypotension, Tachycardia
(iv) CNS - Reflexes absent, Delirium, coma and death.
C. Fatal Dose
5-10g.

D. Fatal Period
12-24 h.

E. Management
(1) If applied externally –
(i) Wash with lukewarm water and water. If patient has presented with suspected
fabricated bruises, preserve for chemical analysis.
(ii) Apply antiseptics.
(2) If ingested -
(i) Gastric lavage, (ii) demulcents. (iii) Preserve gastric lavage for chemical
analysis in all cases.

F. PM Appearances
(1) Mouth, palate, throat, other oral structures – inflamed, show blisters
(2) Stomach – congested. May show fragments of seed.

G. MLI
(1) Artificial bruises – are made on arms, thighs, breasts etc to bring about a
false charge of assault.
(2) Criminal abortion – juice is applied to the cervical os.
(3) Infidelity – juice is introduced in the vagina as a punishment.
(4) Injury - Juice is sometimes thrown on the body of other to cause injury
(5) Malingerers – put the juice inside their eye to produce ophthalmitis
(6) Manner of poisoning -
(i) Accidental poisoning – Common. Poisoning may occur because the nut is
used in Indian medicine for a variety of disorders eg allergic dermatitis,
ascites, asthma, colitis, cough, diarrhea, dyspepsia, leprosy, leukoderma,
piles, poisonous bites, scaly skin, tumors and worms. The oil is topically
applied on swollen joints and traumatic wounds. May result in false bruises.
(ii) Suicidal and homicidal poisoning – Rare
(7) Occupational poisoning - Dhobie mark itch (Dhobie mark dermatitis) is
 urushiol dermatitis seen in Indian washermen who use marking nut in their
work. Has been reported even in persons, who wear clothes laundered and
marked in this way. The latter mode was the cause of dermatitis affecting
several English soldiers stationed in pre-independent India.

VI. CALOTROPIS GIGANTEA (AKDO, MADAR)

A. Active Principles
Calactin, calatoxin, calotropin, trypsin, uscharidin and uscharin. They have CNS
depressant and anticonvulsant activity.

B. Signs and Symptoms

1. Dermal application
(1) Redness (2) vesication and bullous eruptions.

2. Instillation in eye
Instillation of juice in the eye is often done for local eye ailments. Produces
1.keratitis, 2.conjunctivitis, 3.corneal edema, 4.dimness of vision.

3. Ingestion
(1) Acrid bitter taste
(2) Burning pain in mouth, throat and stomach
(3) Salivation
(4) Stomatitis
(5) Vomiting and diarrhea
(6) Pupils – dilated
(7) In animal models – cardiotoxic and hepatotoxic. In rats and sheep produces
tracheal exudates, pulmonary edema, tachycardia, transitory cardiac
arrhythmias, ascites, liver hemorrhages, hydropericardium, flaccid heart, and
pale juxtamedullary renal cortex.
(8) Tetanic convulsions
(9) Collapse and death.

C. Fatal Dose
Uncertain.

D. Fatal Period
6-12 hours.

E. Management
(1) Gastric lavage (2) demulcents (3) symptomatic.

F. PM Appearances
(1) Pupils – dilated
(2) Mouth – stomatitis, froth
(3) nostrils – froth
(4) GIT – mucosa congested
(5) Brain, meninges, abdominal viscera - Congested.

G. ML Importance
(1) Artificial or false bruises - are produced by its juice [ch 12].
(2) Cattle poison –
(i) Smeared on a cloth, and pushed into the rectum of animal [cf ch 38"snake
venom]
(ii) Given with fodder
(3) Criminal abortion – ingested or applied locally by abortion stick
(4) Folk medicine -
(i) Indian medicine - Flowers, leaves, root and juice are used. Leaves are used in
body pain, burns, jaundice, mumps, rheumatism, sinus fistula and snake
bite. Juice is used as a depilatory, in skin diseases and as a vesicant. May
cause poisoning if injudiciously used.
(ii) In several countries, juice is instilled in eyes for ailments like chalazion. Can
produce corneal edema and disturbances of vision.
(5) Infanticide
(6) Manner of poisoning -
(i) Suicidal poison
(ii) Accidental– White flowers used in India for worshipping Lord Shiva. May
cause accidental poisoning, and ocular toxicity [conjunctivitis].
(iii) Homicide – rare because of bitter taste
(7) Arrow poison
(8) Snakes - Root of calotropis procera is thought to be highly poisonous to
snakes, which cannot stand even its smell. It is thus kept by snake charmers in
their baggage.

38. Animal Poisons

I. SNAKES

Snakes are elongate, legless, carnivorous reptiles of the suborder Ophidia [Class
- Reptilia; Subclass: Lepidosauria; Order – Squamata (Scaled reptiles); Suborder
– Ophidia (syn, Serpentes)] that are distinguished from legless lizards by their
lack of eyelids and external ears. Living snakes are found on every continent
except Antarctica and on most islands.

A. Classification
(1) There are about 3,500 species of snakes in the world, but only about 350
species are venomous and only the minority of these are likely to cause
significant envenoming in humans.
(2) In India 330 snake species exist. Of these 70 are venomous [40 land snakes,
30 sea snakes].
(3) All snakes dangerous to humans may be divided into venomous and non-
venomous.
Venomous snakes
All venomous species of the world are grouped in just five families:

a. Colubridae
(1) Fixed and rear-fanged (Opisthoglyphous).
(2) Only few are dangerous to humans [ex. Boomslang, mountain racer, tree
snake].
(3) The family includes about 2/3rd of all snake species on earth. Includes some
non-poisonous also, eg rat snake.
b. Elapidae
(1) Fixed and front-fanged (Proteroglyphous).
(2) Cobras, kraits, mambas, coral snakes.
(3) They are a major global cause of snakebite.

c. Atractaspididae
(1) Side-fanged. (2) Include burrowing asps (3) Not a major cause of snakebites.

d. Viperidae
(1) Folding and front-fanged; fangs are like hollow syringe needles,
[Solenoglyphous].
(2) Most important cause of snakebite globally.
(3) Classification -
(i) Divided into 4 subfamilies of which 2 are major – (a) Viperinae [true, typical
or “Old World” vipers, eg African puff adders, European adders, Gaboon
vipers, Russell’s vipers and saw-scaled or carpet vipers] (b) Crotalinae [pit
vipers eg, bushmasters, copperheads, cottonmouths, green pit vipers, habus,
jararacusus, Malayan pit vipers, mamushi, rattlesnakes, water moccasins].
In addition, there are 2 monotypic [containing only one biological type]
subfamilies (c) Azemiopinae [Fea’s viper] and (d) Causinae [night adders].
(ii) Most US venomous snakes belong to Crotalinae. Both major Indian vipers
[saw scaled viper and Russell’s viper] belong to Viperinae.

e. Hydrophidae
[Gk. hydros, water; ophis, serpent]
(1) Fixed and front-fanged [like elapids], but habitat is water.
(2) Sea snakes. evolved from terrestrial ancestors [elapidae]; now adapted to a
fully aquatic life; unable to move on land, except for the genus Laticauda [sea
kraits], which retain ancestral characteristics, allowing limited land
movement.

2. Non venomous snakes dangerous to humans

Pythons [family Pythonidae] and Boas [family Boidae] kill by constricting
around chest causing traumatic asphyxia.
B. Venomous Snakes of India

1. Commonly encountered
Saw scaled viper, Russell’s viper, Common cobra [Indian cobra] and
common krait are traditionally referred to as the “Big four”, because they are
responsible for virtually all snakebites in India.
a. Saw scaled viper
Zoological name - Echis carinatus [Gk Echis, viper; Latin carinatus, like a keel,
referring to keeled scales]. 8 species of Echis are currently recognized.

b. Russell’s viper
Zoological name - Vipera russelli, or Daboia russelli. Genus is named after the
Hindi Daboia meaning “that lies hidden”; species in honor of Patrick Russell
(1726–1805), a Scottish herpetologist who first described many of India’s snakes

c. Common cobra
Common Names – (i) Bengali – Gokhra (ii) Hindi, Sanskrit, Oriya, Marathi –
Naag, Kala saanp.

d. King cobra
The king cobra (Ophiophagus Hannah, Humadryad, Nagraj, Rajnag) is not a
“true cobra” despite its name. True cobras belong to genus naja; it belongs to its
own genus. It is the sole member of genus Ophiophagus.

e. Common krait
Common Names - (i) Bengali - Kalach (ii) Gujarati - Kala taro. (iii) Hindi -
Karait.

f. Banded krait
Zoological name - Bungarus fasciatus. [from Telugu bungarum, gold, an
allusion to the yellow rings around its body; Latin fasciatus, banded]

g. Sea snakes
Habitat - They are found in warm coastal waters from the Indian Ocean to the
Pacific. Also in rivers, estuaries and even fresh water lakes.

C. Snake Venom
(1) Venoms of different snakes differ in antigenic structure, composition and
toxicity
(2) Cobra venom – faint transparent yellow, slightly viscous, when exposed to
 sun, it becomes slightly turbid
(3) Russell’s viper venom – white or yellow
(4) Composition -
(i) Venom is the saliva of snake.
(ii) Composed of 90% proteins, polypeptides and many other organic and
inorganic substances. Together they are classified as enzymatic and non-
enzymatic components. Enzymes produce local and systemic effects and
non-enzymatic components produce lethality. Proteome [from proteins and
genome] is the entire set of proteins expressed by a genome, cell, tissue or
organism. Venom proteome is the entire set of proteins present in snake
venom. The study of snake venom proteomes is snake venomics.
(iii) No venomous snake has all components. Most snakes have 6-12 of these
enzymes in their venom.
(iv) Each of these enzymes has its own special function. Some aid in the
digestive process, while others specialize in paralyzing the prey.

Absorption and excretion

(1) Transport - Snake venom travels through lymphatics and superficial veins
[that is why a light tourniquet may be useful – please see below].
(2) Routes of absorption - Poisonous only when injected; harmless when taken
by mouth, as it is not absorbed through stomach. Oral sucking of venom may
not harm the rescuer, if he accidentally swallows poison, but if he has ulcers in
the mouth, venom can get absorbed from there and cause harm.
(3) Excretion - by kidneys, milk, salivary glands and mucus membranes.

II. SNAKEBITES

A. General
(1) When a snake bites, it normally leaves two faint impressions, the distance
between them being 8 mm to 4 cm.
(2) A side swipe may produce a single puncture, and also small marks of other
teeth
(3) The exact number of fang marks vary because of (i) Glancing bites (ii)
Multiple fangs (iii) Multiple strikes (iv) Protection from clothing and shoes
(4) Non venomous snakebites leave a number of small impressions in a row.
(5) Season - During summer months, venom output is more and the venom is
more toxic than during winter.
(6) Dry bite - When a snake bites, but venom fails to get injected, it is known as
a “dry bite”. Approx 20% of all snakebites are dry bites, except in sea snake
bites, where the incidence is 80%. Causes - (i) Layers of clothing or shoes-
over the bitten part (ii) When a snake bites but does not inject venom (iii)
Superficial bite - Discharge orifice of a viper is usually well above its tip.
Thus if the fang has not penetrated deep enough, most or part of the venom
may be ejected superficially or externally without entering the wound. (iv)
sideswipes - rather than head-on bites. Dry bites occur from other venomous
animals also eg spiders such as tarantulas.

B. Signs and Symptoms

Most snakebites are from non-venomous snakes, simply because they outnumber
venomous snakes almost ten times [please see above under classification].

Venomous snakebites
Ophitoxemia (Gk. ophis, serpent; toxon, poisoning) is poisoning by snake
venom. In more than 50% of cases, inadequate venom is injected, producing
mild symptoms. Signs and symptoms depend upon
(1) Snake dependent factors:
(i) Species and size of snake
(ii) Condition of its fangs and venom glands
(iii) Pathogens present in the snake venom
(iv) Nature of bite – Location, number and depth of bite. 98% of bites occur
over the extremities
(v) Length of time the snake holds on
(vi) Amount of venom injected
(vii) Extent of anger or fear of snake [motivation of snake]
(2) Victim dependent factors - (i) Age and size of victim (ii) Victim’s
sensitivity to the venom
(3) Community dependent factors - First aid and medical care immediately
given.

a. General [seen with all venomous snakes]

(1) Fright – Most common, especially the fear of rapid and unpleasant death.
Following features are seen [within a few minutes of bite] due to fright (i)
Hypotension (ii) Pulse feeble (iii) RR- (iv) Semiconsciousness with cold
clammy skin.
(2) Gas gangrene
(3) Tetanus
(4) Psychological shock and death [due to fright]
(5) Fang marks:
(i) Two in number – (a) most common. (b) Distance between the two puncture
wounds varies from 8 mm to 4 cm depending on species (c) Occasionally
other teeth marks are also visible (d) Lower jaw does not leave any fang
marks [Fig 38.5]
(ii) One – (a) Less common. (b) Seen in sideswipes
(iii) More than two – (a) less common. (b) Seen in (I) multiple bites (II) Single
bites by snakes having more than 1 set of fangs
(iv) Depth - 1-8 mm, depending of species and strength of bite. Vipers generally
cause deeper bites than Elapids, because they have longer teeth.
b. Specific

i. Cobra
(1) Local – manifestations start within 6-8 min. Local manifestations in elapidae
[cobra, krait] are minimal in sharp contrast to viperidae [Russell’s viper, saw
scaled viper] in which they are quite marked.
(i) A small reddish wheal or bullae - develops at the site of bite
(ii) Tenderness – of bitten area with slight radiating burning pain and oozing of
bloodstained fluid
(iii) Swelling – minimal or even absent
(2) Systemic – Symptoms appear after 30 min
(i) Nausea, vomiting – early symptoms
(ii) After ½ -1 h"Excessive salivation, headache, vertigo, paresthesia around the
mouth, myalgia, irritability
(iii) CNS depression- (a) Patient feels sleepy (b) slightly intoxicated, (c)
weakness of legs, (d) reluctant to stand or move.
(iv) Paralyzing effects – (a) Paralysis is first detectable as ptosis and external
ophthalmoplegia, in that ocular muscles are most sensitive to
neuromuscular blockade. Other ocular symptoms [due to involvement of
oculomotor nv] are - blurring of vision, diplopia, dysconjugate gaze,
strabismus (b) later, paralysis of lower limbs, trunk, neck and head [head
falls forward, inability to raise head], palate, vocal cords [inability to speak
(dysphonia)], jaws, tongue, muscles of deglutition [dysphagia], absent gag
reflex. (c) After 2h"complete paralysis
(v) Respiratory arrest – Causes (a) paralysis of intercostal muscles and
diaphragm (b) obstruction of upper airway by the paralyzed tongue (c)
inhaled vomitus
(vi) Stoppage of heart
(vii) Convulsions, coma.
(viii) Cause of death - respiratory failure [causing hypoxia and acidosis]
(ix) If recovery occurs – skin and cellular tissues surrounding the bite mark
undergo necrosis.
Memory Aid 1: Signs and symptoms of cobra bite
COBRA causes PARALYSIS
Convulsions, Coma [towards the end]
Ophthalmoplegia, Ocular symptoms [blurring, diplopia, dysconjugate gaze, strabismus]
Bulla at the Bite site
Respiratory arrest
Airways obstructed by paralyzed tongue
Paralysis, Ptosis, Paresthesia around the mouth,
Area tender [bitten area]
veRtigo
Absence of swelling at bitten site [in contrast to viper]
Lameness [inability to walk due to weakness of legs]
mYalgia,
Salivation
Irritability
Stoppage of heart [towards the end]

ii. Krait
(1) Time of bite - Most patients are bitten while asleep on the floor of their huts.
(2) Site - Because people are bitten while lying down, the target may be any part
of the body, including the head, neck, and shoulders.
(3) Local –
(i) local signs are minimal or insignificant.
(ii) invisible or scarcely perceptible puncture marks
(iii) mild tenderness, itching, numbness, paresthesia
(iv) negligible or no local swelling.
(v) Painful enlargement of local lymph nodes [rare].
(4) General –
(i) Abdominal pain [very common]
(ii) Fasciculations
(iii) Feeling of drowsiness and intoxication
(iv) Paralysis - develops within 2 hours or be delayed for 12 hours.
(v) Sometimes severe generalized muscle pains with moderately elevated plasma
myoglobin concentrations [due to generalized rhabdomyolysis].
(vi) Urine – shows albumin.
(5) Fatality - in the absence of antivenom treatment and assisted ventilation >
 75%.

iii. Viper
(1) Local:
(i) Swelling - around bite. Quickly spreads around to involve entire limb and
even adjacent trunk. Followed by malignant edema of the entire limb
(ii) Pain, paresthesias, reddening, tenderness
(iii) Peristent bleeding - from bite site
(iv) Regional lymphadenopathy
(v) Bruising – over (a) path of superficial lymphatics (b) lymph nodes
(vi) Blisters – (a) in and around bite site start appearing within 12 hours. (b)
Spread around to involve entire limb. (c) Contain either clear or blood
stained fluid. If patient survives, they heal in about 4 weeks.
(vii) Extensive necrosis - of skin, s/c tissues, muscles in 10-15% cases. Followed
by extensive suppuration, sloughing
(viii) -ed intracompartmental pressure – due to edema. In tight fascial
compartments [eg anterior tibial compartment] causes (a) -ed pain on
stretching intracompartmental muscles (b) s/c anesthesia (c) Severe pain
and (d) tense swelling
(2) Systemic:
(i) Hematologic abnormalities – most characteristic of viper bites.
(ii) Pathology - (a) DIC"fibrin is used up" defibrination"Blood becomes
incoagulable. (b) Primary pathological fibrinolysis [PPF] (c) widespread
microvascular fibrin deposition [microthrombi] (d) Blood – shows (I) early
hemoconcentration followed by (II) .RBC and (III) .platelets (IV) -bleeding
time (V) -clotting time (e) Urine – contains blood, protein, sugar
(iii) Main hemorrhagic manifestations - (a) Bleeding in (I) Anterior pituitary (II)
floor of the mouth (III) Genitourinary tract (IV) GIT and (V) tympanic
membrane (b) Ecchymosis and petechial hemorrhages over entire body (c)
Epistaxis (d) Gingival bleeding (e) Hematuria (f) Hemoptysis (g)
Intracranial hemorrhages [SAH presenting as severe headache, intracerebral
hemorrhage presenting as hemiplegia, unconsciousness and convulsions]
(h) Intravascular hemolysis [resulting in hemoglobinuria, acute renal
failure] (i) rectal bleeding (j) Retroperitoneal and intraperitoneal
hemorrhages [presenting as abdominal distension, peritonism, tenderness]
 (k) Subconjunctival hemorrhages
(iv) General – headache, dizziness, weakness
(v) CVS - (a) Hypotension (b) tachycardia (c) Hemorrhagic shock
(vi) Temp-
(vii) Pupils - dilated, insensitive to light, blurring of vision
(viii) Respiratory depression
(ix) Scalp, mouth, tongue – tingling and numbness
(x) Paralysis is not seen – this differentiates viper bite from elapid bites [Table
3]
(xi) Abortions - in pregnant females
(xii) Cause of death – hemorrhagic shock.
iv. Sea snake
(1) Local reaction -
(i) Little or none.
(ii) The bite is usually painless and may not be noticed by the swimmer.
(iii) Teeth may be left in the wound.
(iv) Minimal or no local swelling, and involvement of local lymph nodes is
unusual.
(2) After ½ - 1 h –
(i) Headache, generalized pain
(ii) Generalized aching, stiffness and tenderness of the muscles,
(iii) Trismus is common
(iv) A thick feeling of the tongue, thirst, sweating and vomiting.
(v) Generalized rhabdomyolysis - Myoglobin and K+ are released from damaged
skeletal muscles. Hyperkalemia develops within 6–12 hours
(vi) Weakness of muscles [persists for several months]. Passive stretching of the
muscles is painful.
(vii) Marked polymyositis with a “limb-girdle” distribution [muscles of
shoulders and hips]
(3) Later – progressive flaccid paralysis, beginning with ptosis [as in elapids].
Patient remains conscious until the respiratory muscles are sufficiently
affected to cause respiratory failure.
(4) Renal failure [due to -myoglobin and -K+]
(5) Serum and plasma - appear brownish
(6) Lab tests -
(i) Muscle enzymes-
(ii) Plasma K+-
(iii) Myoglobinaemia and myoglobinuria [develop 3–8 h after the bite]
(iv) Urine - dark reddish brown [Coca-Cola colored]. Tests for Hb in urine are
+ve [due to presence of myoglobin]
(7) Death – due to respiratory paralysis or cardiac arrest [due to -K+].

C. Diagnosis
(1) If snake has been killed and brought, it is easy to identify [Table 1, Table 2].
(2) Snake venom components – as mentioned above may be detectable
(i) Can be detected in aspirates, biopsies, CSF, serum, body fluids, urine and
wound swabs
(ii) Collect and send for analysis (a) Skin and underlying tissues surrounding
 fang marks [in PM only] (b) Wound and blister aspirates (c) Serum (d)
Urine
(3) Radioimmunoassay (RIA) – Most sensitive and specific test [detection level
0.4μg/L]. Snake venom components like cholinesterase and thromboplastin
can be detected
(4) Enzyme immunoassay (EIA) - Detection level 5μg/L. Simpler. More widely
used.
(5) Immunological detection - by ELISA
(6) Urine – Venom is detectable, even when the patient is treated with antivenin
(7) Animal testing – swab from fang marks or an extract from skin injected into
a small animal [eg a frog] and see for toxicity.

D. Management

1. Field management [first aid]

(1) Reassure the victim.
(2) Do not tamper with the bite wound in any way.
(3) Immobilize the bitten limb using a splint or sling.
(4) Avoid elevation of an extremity – as it may hasten absorption.
(5) During transport to hospital, whole patient should be immobilized, especially
the bitten limb, because any muscular contractions will promote spread of
venom.
(6) Avoid harmful and time-wasting treatments.
(7) Because species diagnosis is critically important, the snake should be taken
along to the hospital if it has already been killed. However, if the snake is still
at large, do not risk further bites and waste time by searching for it.
(8) Sutherland wrap [syn - Pressure Immobilization, The splinting and crepe
bandaging method ]:
(i) Developed and advocated by Struan Sutherland in Australia.
(ii) Procedure [Fig 38.6] - An elasticated, stretchy, crepe bandage, app 10 cm
wide and 4.5 meters long is used. If that is not available, any long strips of
material can be used. The bandage is bound firmly around the entire bitten
limb, starting distally around the fingers or toes and moving proximally, to
include a rigid splint. The bandage is bound as tightly as for a sprained
ankle, but not so tightly that the peripheral pulse (radial, posterior tibial,
 dorsalis pedis) is occluded or that a finger cannot easily be slipped between
its layers. When applied in this manner, it exerts a pressure of about
55mmHg [ideal in snakebite; for reasons please see below]. The bandages
should not be released until the patient is under medical care in hospital,
and antivenom treatment has been started.
(iii) Recommended - in bites by cobras, king cobras, kraits or sea snakes
[localizes venom, slows down absorption].
(iv) Not recommended - in viper bite, because its venom has locally-necrotic
effects. Pressure-immobilization localizes the venom, -ing the locally-
necrotic effects.

2. Management in the hospital

a. Admit in ICU
(1) Monitor closely – cardiac rhythm, oxygen saturation, urine output, vital
signs.
(2) Obtain history
(3) Evaluate progression of envenomation objectively
(i) Mark level of swelling in the bitten extremity
(ii) Measure limb circumferences every 15 min until swelling has stabilized.
(iii) During this period of observation and monitoring, the extremity should be
positioned at approximately heart level.
(4) Establish large-bore IV access - in one or two unaffected extremities.
(5) Remove measures applied in the field [eg constriction bands or tourniquets
etc] as soon as IV access has been obtained. Keep in mind that release of such
ligatures may result in hypotension or dysrhythmias when stagnant acidotic
blood is released to the central circulation.
(6) Fluid resuscitation -
(i) Isotonic saline (20–40 mL/kg IV) should be initiated if there is any evidence
of hemodynamic instability
(ii) 5% albumin (10–20 mL/kg) - if patient fails to respond to saline.
(7) Blood - should be drawn for typing and cross-matching and for laboratory
evaluation as soon as possible.

b. Polyvalent antisnake venom [PAV] therapy

(1) The key to management of venomous snakebite is the administration of
specific antivenom or PAV. However it should never be started as a matter of
routine, because of it being potentially hazardous.
(2) PAV - Prepared in India by (a) Bharat Serums & Vaccines Ltd, Mumbai (b)
Central Research Institute, Kasauli (c) Haffkine Biopharmaceutical Co,
Mumbai (d) Kings Institute of Preventive Medicine, Chennai (e) Serum
Institute of India Ltd, Pune (f) VINS Bioproducts Ltd, AP.
(3) Method of preparation of PAV:
(i) By hyperimmunizing horses [or sheep] against the venom of 4 common
poisonous snakes (a) Cobra (b) Common Krait (c) Russell’s Viper (d) Saw
Scaled Viper
(ii) Plasma obtained from them is concentrated and purified
(iii) Serum is lyophilized and sealed in vials
(iv) Lyophilization - (a) It is a dehydration process used to preserve sera. (b)
Process – Sera frozen"High vacuum applied"Frozen water sublimates"Sera
reduced to powder with no water content"microorganisms and enzymes
 cannot degrade sera"Can be stored for 5 y.
(4) When sera is needed - it is rehydrated (reconstituted) by adding 10 ml of
water per vial]. Half life of reconstituted serum is 90 h. If the reconstituted
serum is opaque or turbid, it should not be administered [indicates
precipitation of proteins"loss of activity, -ed risk of adverse reactions.
(5) Cost of one vial - `350-500
(6) Production - 5 lakh vials/y].
(7) Useful when given within 4 h of bite; lesser value after 8 h and of doubtful
value after 24 h.
(8) Efficacy [Table 4].
(9) Indications for antivenom administration:
(i) Viperid bites - (a) any evidence of systemic envenomation [systemic
symptoms or signs, lab abnormalities] (b) significant progressive local
findings [e.g., soft tissue swelling crossing a joint or involving more than
half the bitten limb].
(ii) Elapid bites - first sign of any evidence of neurotoxicity [cranial nerve
dysfunction (e.g., ptosis) or peripheral neuropathy].
(10) Best time of administration – within 4 h. Less value after 8 h, and of
doubtful value >24 h.
(11) Hypersensitivity testing -
(i) By s/c or intradermal inj or intraconjunctival instillation of diluted antivenom
was once tried.
(ii) Not recommended now because (a) delay the start of antivenom treatment (b)
risky, because may presensitize patient to PAV (c) are poor predictors of
early anaphylactoid reactions (d) In serious Envenomations, PAV therapy
has to be administered anyway
(12) Complications:
(i) Allergic reactions
(ii) Blindness
(iii) Serum sickness [fever, chills, urticaria, myalgias, arthralgias, and possibly
renal or neurologic dysfunction] may develop 1–2 weeks after antivenom
administration. Treat with systemic glucocorticoids [eg, oral prednisone, 1–
2 mg/kg daily] until all findings resolve; the dose is then tapered over 1–2
weeks. Also oral antihistamines and analgesics.
c. Other treatments
(1) Vasopressors (eg. dopamine) – Given only after aggressive volume
resuscitation and antivenom administration. Invasive hemodynamic
monitoring [central venous and/or pulmonary arterial pressures] may be
helpful, although obtaining access is risky if coagulopathy has developed.
(2) Acetylcholinesterase Inhibitors – useful in Neurotoxic Snake
Envenomation.
(i) Patients with clear, objective evidence of neurotoxicity after snakebite (e.g.,
ptosis or inability to maintain upward gaze) should receive a trial of
edrophonium or neostigmine. (a) Pretreat with atropine: 0.6 mg IV
[children, 0.02 mg/kg; minimum of 0.1 mg] (b) Follow with Edrophonium:
10 mg IV (children, 0.25 mg/kg) or Neostigmine: 1.5–2.0 mg IM (children,
0.025–0.08 mg/kg)
(ii) If objective improvement is evident at 5 min, continue neostigmine at a dose
 of 0.5 mg (children, 0.01 mg/kg) IV or SC every 30 min as needed, with
continued administration of atropine by continuous infusion of 0.6 mg over
8 h (children, 0.02 mg/kg over 8 h).
(iii) Maintain vigilance regarding aspiration risk and secure the airway with
endotracheal intubation as needed.

d. Wound care
Application of a dry, sterile dressing and splinting of the extremity with padding
between the digits.

e. General measures
(1) Tetanus immunization
(2) Prophylactic antibiotics (e.g. cephalosporins) – especially if misguided first
aid efforts have included incisions or mouth suction.
(3) Pain control - with acetaminophen or narcotic analgesics. Salicylates and
nonsteroidal anti-inflammatory agents should be avoided because of their
effects on blood clotting.
(4) Muscle-compartment syndrome:
(i) Most snake envenomations involve s/c deposition of venom.
(ii) Sometimes however, venom can be injected more deeply into muscle
compartments, particularly if the offending snake was large and the bite
occurred to the lower leg, forearm or hand.
(iii) If swelling in the bitten extremity raises concern that subfascial muscle
edema may be impeding tissue perfusion (muscle-compartment syndrome),
intracompartmental pressures (ICPs) should be checked by any minimally
invasive technique [eg wick catheter or ICP monitor].
(iv) If any ICP is high (>30–40 mmHg), the extremity should be kept elevated
above heart level while further antivenom is given.
(v) IV mannitol (1 g/kg) - to . muscle edema if the patient's hemodynamic status
is stable. (vi) Fasciotomy - If after 1 h of IV mannitol, the ICP remains
elevated.

3. Treatments on which opinion is divided

Application of tourniquet
(1) Conflicting evidence - There is conflicting evidence regarding the use of
tourniquets. Some workers believe that there is no convincing evidence of its
efficacy. But proponents think it could be because in most cases, tourniquet is
not properly applied. They assert that positive results have been seen with
properly applied tourniquets.
(2) Technique:
(i) Correct technique - Application of 55mm Hg pressure and no more, since it
would only block lymphatics [and some superficial veins], but not arteries
and deep veins [BP is 120/80 mm Hg]. Venom spreads mainly through
lymphatics and superficial veins. The best way to do this is to use a
sphygmomanometer cuff and inflate it to 55mm Hg.
(ii) Earlier recommendations to ensure the right pressure were (a) tighten until
the pulse can just be felt (b) it should be possible to force a finger between
the tourniquet and the limb (c) if the part becomes bluish or cold, the
tourniquet is too tight
(iii) Multiple tourniquets were sometimes recommended
(iv) The use of a crepe bandage is generally effective if sphygmomanometer is
not available.

E. Fatal Dose
Please see [Table 5].
Memory Aid 2: Fatal doses of venoms from lowest to highest
Kill Snakes by Cutting Rapidly [or Ruthlessly]

F. Fatal Period
(1) Common Cobra – 8 hrs
(2) Common Krait– 18 hrs
(3) Russell’s Viper – 3 days
(4) Saw scaled Viper – 5 days.

G. Cause of Death
(1) Cobra - Respiratory paralysis.
(2) Viper – Hemolysis, Hemorrhage.

H. PM Appearances

1. Common to all poisonous snakes

(1) Fang marks – 1, 2 or several depending on the type of bite
(2) Washings from the site of the bite and tissues underneath – show venom
 components [please see “Diagnosis” above for details].
(3) Internal organs – congested.

2. Elapids
(1) Local changes – minimal (2) Brain - congested.

3. Vipers
(1) Local changes - extensive local cellulitis, discoloration and swelling.
(2) Hemorrhages – Prominent. Occur from puncture, mucus membranes, into
bowel, lungs, and almost all other tissues; Purpuric spots on pericardium
(3) Kidneys – inflamed, hemorrhagic.

4. Sea snakes
(1) Signs of rhabdomyolysis
(2) Kidneys – congested, tubules blocked with myoglobin.

I. ML Importance
(1) Manner of death –
(i) Accidental - most common
(ii) Homicidal - (a) throwing snake on the bed of a sleeping person (b)
Infanticide – may be committed in this way
(iii) Suicidal - very rare. Queen Cleopatra committed suicide by snake bite.
(2) Cattle poison – Procedure - A cobra is shut up in an earthen vessel
containing a banana"Heat is applied to the vessel"Snake is irritated"Bites
fruit"Venom is injected into banana pulp"Pulp taken out"Smeared on a
rag"Rag thrust into the animal’s rectum using a split bamboo [cf ch
37"calotropis; ch 43"Nerium oleander for similar uses].
(3) Excretion - occurs through milk, saliva, urine and mucus surfaces. There are
cases on record where a young child died after suckling mother’s breast who
was bitten by a poisonous snake.
(4) Ingested venom - Snake venom if ingested is not poisonous, as the venom
proteins are digested.
(i) Animals killed by snake venom may be eaten without ill effects
(ii) A rescuer who sucks snake venom from wound may not be poisoned if he
swallows poison. However if he has minor abrasions in mouth, the poison
 may be absorbed from there and secondary poisoning may occur in the
rescuer.

III. SCORPION

Scorpions are predatory arthropods of class Arachnida.

A. Mode of Action
Scorpion venom opens neuronal sodium channels [Memory Aid 3]. This
causes (i) repetitive and spontaneous depolarization of both sympathetic and
parasympathetic nervous system, causing an autonomic storm [pl co-relate with
signs and symptoms].
Memory Aid 4: MOA of scorpion venom
Sco r pion venom causes – repetitive and spontaneous sympathetic and parasympathetic depolarization

Typically the parasympathetic effects are transient, but sympathetic are more
prolonged. (ii) "catecholamine release from adrenal gland (iii) catecholamine
induced cardiac hypoxia (iv)" renin secretion at the juxtaglomerular
apparatus. (iv) Hyperkalemia, hyperglycemia, "insulin secretion,
"aldosterone.

B. Signs and Symptoms

Most stings occur on extremities. There are significant differences in signs and
symptoms produced by different species. Stings from M. tamulus [Indian red
scorpion] produce following symptoms.
(1) Local - (i) edema (ii) erythema (iii) pain [severe, excruciating] (iv) regional
lymphadenopathy. Last 1-2 h.
(2) Systemic - (i) Nausea, vomiting (ii) extreme restlessness (iii) Allergic
reactions, including anaphylaxis (iv) Cyanosis (v) Pupils - dilated (vi) Fever
(vii) Paralysis (viii) Respiratory depression
(3) Sympathetic - (i) cardiogenic shock (ii) BP- [BP. if parasympathetic
predominates] (iii) MI (iv) myocarditis (v) pulmonary edema (vi) arrhythmias,
tachycardia
(4) Parasympathetic - (i) priapism (ii) sweating (iii) vomiting
(5) Other - (i) coagulopathy (ii) pancreatitis (iii) stroke
(6) Rare - (i) Intracerebral hemorrhage [Mechanism - venom induced autonomic
storm"hypertension, vasculitis].
(7) Death – if occurs is preceded by convulsions and coma. Mortality except in
children is negligible.
Memory Aid 5: Signs and symptoms of scorpion stings
All S C O R P I O N S cause MI, but fe w dilate pupils
Allergy
Salivation, sweating
Cyanosis, cardiogenic shock, coagulopathy,
Oedema
Regional lymphadenopathy, restlessness, respiratory depression
Pain, paralysis, pulmonary edema, priapism, pancreatitis
Inspirations slow [respiratory depression]
St O rm [autonomic]
Nausea & Vomiting
Stroke
Convulsions and coma precede death
MI , Myocarditis
fever
dilated pupils
C. Fatal Period
Few hours.

D. Diagnosis
ECG – (i) Peaked T waves in leads V2-V6. (ii) Q wave, ST segment elevation in
leads I and aVL (iii) Left anterior hemiblock.

E. Differential Diagnosis
Snake bite – Snake bite shows two punctures; scorpion stings shows one.
Confirmation by ELISA.

F. Management
(1) First aid - (i) Immobilize limb (ii) Tourniquet – Technique and pressure as in
snakebite (iii) Local washing – with weak soln of ammonia, borax or KMnO4
has doubtful value (iv) Tetanus toxoid (v) local wound care (vi) topical
antibiotic to the wound.
(2) Supportive care – Pain control - (a) ice packs (b) local anesthetic injection
 (c) oral analgesics - (I) Paracetamol (II) Barbiturates control both pain and
convulsions.
Memory Aid 6: Main drugs in scorpion stings
SCOR P ION DIES AT FOOT - Prazosin, Nifedipine, Dehydroemetine, Dopamine, Aprotinin,
Furosemide

G. Cause of Death
(1) Cardiac failure (2) pulmonary edema.

H. PM Appearances
(1) Local - (i) Stung area is usually a limb. (ii) reddened and edematous. (iii)
Shows one hole in the center. (iv) Skin, s/c and muscle around the hole should
be excised and sent for chemical analysis
(2) Viscera – congested.

IV. SPANISH FLY (CANTHARIDES)

Spanish fly (Lytta vesicatoria, Cantharis vesicatoria) is an emerald-green beetle

(Fig 38.9) in the family Meloidae.
Salient features:
(1) Size - 2x0.5 cm.
(2) Active principle - Cantharidin [5%], a strong irritant.
A. Mechanism of Action
Cantharidin, an anhydride of cantharidic acid, is almost insoluble in water but
readily soluble in acetone (1:40). Its chemical formula is C10H12O4. It is a potent
inhibitor of protein phosphatases types 1 and 2A.

B. Signs and Symptoms

1. Applied Externally to the skin

(1) Redness (2) burning pain (3) blisters

2. Ingested
Symptoms begin within 2–4 hours of ingestion.
(1) Burning in the mouth, severe thirst
(2) dysphagia, dysarthria (difficulty in speech)
(3) blistering of the lips and tongue
(4) Upper GIT symptoms – nausea, vomiting, hematemesis, retrosternal
burning [due to irritant effects on the esophageal and gastric mucosa]
(5) Lower GIT symptoms - intestinal colic, bloody diarrhea, tenesmus (if
 poison passes into the lower GIT in large amounts)
(6) Renal symptoms - severe costovertebral angle pain, dysuria, scanty urine
though there is an - desire to pass urine [strangury], hematuria
(7) Terminal events are priapism (painful erection of penis), abortion (in
pregnant women), convulsions, coma, peripheral vascular collapse and death.
Because it causes priapism, cantharides gained reputation as an aphrodisiac.
But the erection of penis is pathological, painful and devoid of any sexual
pleasure.

Priapism
Priapism is due to the engorgement of the dorsal corpora cavernosa, resulting in
dorsal penile erection and ventral penile flaccidity.
Salient features:
Etiology - (i) Drugs [Anticoagulants, antihypertensives, Cantharides, drugs of
abuse (e.g., alcohol, cocaine, marijuana), phenothiazines, sedative-hypnotics,
SSRI] (ii) Immunosuppressive disorders (iii) Intracavernosal injections
[papaverine, phentolamine, and prostaglandin-1] (iv) Leukemia (v) Sickle cell
disease (vi) Spinal trauma.

C. Fatal Dose
10 to 80 mg.

D. Fatal Period
24-36 hours.

E. Management
(1) Control of pain – pethidine
(2) control of emesis
(3) Stomach tube - A soft No. 14 Levine tube passed with caution. Stomach
wash done and tube retained. The dysphagia may be so marked that oral
feedings will have to be given through it for 7 to 10 days. Dilute milk (50%
water and 50% milk) given (demulcent as well as a nutritional)
(4) vasopressor agents – eg norepinephrine for peripheral vascular collapse
(5) Replacement of fluids.
F. Cause of Death
Renal failure.

G. PM Appearances
(1) Mouth – Shows inflammation and vesication
(2) Mucosa of esophagus, stomach and intestines – congested, swollen, show
ulcerations
(3) Shiny green particles – found sticking to the stomach mucosa
(4) trachea, bronchi – contain blood stained mucus
(5) Lungs – edematous
(6) Kidneys, ureters, bladder, urethra – Show inflammation
(7) Heart – surface of the heart and endocardium shows hemorrhages.

H. ML Importance
(1) Accidental poisoning -
(i) Cantharidin is a rubefacient (produces redness of the skin by causing dilation
of the capillaries) and vesicant.
(ii) As a counterirritant it was once employed in the treatment of pleurisy,
pneumonia, arthritis, neuralgias, rheumatism and various dermatological
conditions (warts and molluscum contagiosum) but has been abandoned
because of its excessively toxic effects.
(iii) May cause accidental poisoning, if used therapeutically
(2) Aphrodisiac – Frequently taken as aphrodisiac or given to partners for
causing sexual excitement. Case study - On Apr 27, 1954 Arthur Ford of
Britain, who was infatuated with two female colleagues gave Spanish fly to
them in coconut candies. Both died and autopsy revealed Spanish fly in their
stomach. Ford was convicted of manslaughter and sentenced to 5 y in prison.
(3) Criminal abortion
(4) homicide [rarely].

39. Food Poisoning and Poisonous

 Foods

I. POISONING DUE TO BIOLOGICAL CONTAMINANTS

A. Bacterial Contamination (Bacterial Food Poisoning)

1. Infection type
In infection type of food poisoning [syn, long incubation type, because
incubation period is long], the bacteria multiply within the body and cause
typical symptoms like diarrhoea and vomiting.

2. Toxic type
In the toxic type of food poisoning [syn, short incubation type, because
incubation period is short], bacteria have already produced toxins in the food,
and the patient ingests preformed toxins.

3. Botulism
The third type of food poisoning is botulism. Though it is caused by preformed
bacterial exotoxins produced by C. botulinum, it is not clubbed with toxic type
of food poisoning, because unlike it, its major feature is not diarrhoea and
vomiting but muscle paralysis.
Salient features:
(1) Most dangerous type of food poisoning.
(2) Clostridium botulinum is an anaerobic, gram-positive spore-forming rod.
(3) Seven immunologically distinct neurotoxins (A to G) are produced which
block the release of acetylcholine (ACh) from presynaptic fibres, causing
flaccid paralysis [Botulinum toxin is used as a therapeutic agent for cervical
torticollis, strabismus, and blepharospasm]. Foodborne botulism in humans is
caused by toxin of types A, B, and E. Type E is associated with consumption
of seafood products.
(4) Nature of the toxin– Botulinum toxin in solution is colorless, odorless, and
tasteless. Botulinum toxin is denatured by heat at 80°C for 30 min. and 100°C
for 10 min. Thus, foodborne botulism is always transmitted by foods that are
 not heated thoroughly, before eating.
(5) Symptoms and Signs:
(i) Almost every type of food has been associated with outbreaks of botulism,
but the most commonly implicated foods are vegetables, particularly “low
acid” (ie, higher pH) vegetables such as beans, peppers, carrots, and corn.
(ii) Symptoms appear within 12-48 hours of ingestion
(iii) Initially GI symptoms predominate – nausea, vomiting, diarrhea, abdominal
pain with distension
(iv) Later, neurological symptoms due to cholinergic blockade – Visual
disturbances, dry mouth, dysarthria and dysphagia are 4 most common
neurological symptoms
(v) Mortality has fallen from 60% to 5% now.
(6) D/D – Disease most commonly confused with botulism is Guillain-Barré
syndrome.
(7) Fatal dose of botulinum toxin - Most poisonous substance known. Fatal
dose - 1 ng/kg.
(8) Treatment–Symptomatic. Trivalent (A,B,E) antitoxin.

4. Prophylaxis (of bacterial food poisoning)

(1) Meat inspection at slaughter houses.
(2) Control of rodents.
(3) Regular check up and removal of food carriers from food industry.
(4) Food should be properly cooked.

5. Treatment (of bacterial food poisoning)

(1) Glucose saline infusion. Mainstay of therapy.
(2) Antibiotics - only in prolonged (>5 days), profuse (>6 stools/day) or bloody
diarrhea, in fever (> 38.50C), or severe abdominal pain. Of no use in toxic
type.
(3) Anti-diarrheals - loperamide, diphenoxylate, bismuth sub-salicylate,
probiotics, or prebiotics are of little value.

6. PM appearances in bacterial food poisoning

(1) Mucosa of stomach and intestines - intensely congested and swollen. May
be ulcerated.
(2) Microscopic examination – Liver shows fatty degeneration.
(3) Culture – Causative organism can be isolated from blood and viscera.

B. Fungal Contamination (Mycotoxicosis)

Mycotoxins are toxic secondary metabolites produced by fungi (molds, and
yeasts).
Salient features:
(1) The term ‘mycotoxin’ is usually reserved for toxins produced by fungi that
colonize crops.
(2) Mycotoxins are heat stable and survive cooking
(3) Major mycotoxins of interest are:

Ergot
Ergot is the dried sclerotium (a compact mass of hardened fungal mycelium
containing food reserves) of fungi belonging to genus Claviceps (most
prominent member C. purpurea) [Fig 39.1].
Salient features:
(1) The fungus grows on cereals like bajra, barley, oats, rye, wheat etc.
(2) It gradually replaces the grain, and forms a curved, black, compact mass
about 1 cm long and 0.5 cm thick (resembles droppings of a rat).
(3) Has a peculiar odor and a disagreeable taste.
(4) Contains about 30 alkaloids. Most important are (i) ergotoxine (ii)
ergotamine [a precursor of LSD] and (iii) ergometrine.
(5) If the sclerotia are not removed from contaminated grain by beating or
sieving, humans may accidentally ingest them causing poisoning.
a. Mechanism of action
(1) Ergot alkaloids stimulate adrenergic receptors, both peripherally and
centrally.
(2) Directly stimulate muscle fibres.

b. Acute poisoning

i. Signs and symptoms

(1) GIT - thirst, abdominal colic, vomiting, diarrhea.
(2) Resp - tightness in chest, difficulty in breathing.
(3) CVS - tachycardia; pulse - rapid, weak; BP-↑.
(4) CNS - confusion, giddiness, numbness and tingling in hands and feet,
paresthesias, pupils dilated, dimness of vision.
(5) Muscular system - exhaustion, marked muscular weakness, cramps,
convulsions, twitching in muscles.
(6) Hematologic - Bleeding from nose and other mucus surfaces, especially after
a large dose.
(7) Misc - cold skin.

ii. Management
(1) Gastric lavage
(2) Activated charcoal
(3) Emetics [ch 32]
(4) cathartics
(5) Nitroprusside - for hypertension and severe ischemic changes
(6) Benzodiazepines - for convulsions [ch 32]
(7) Vasodilators - eg nitrites

c. Chronic poisoning
Due to repeated consumption of ergot alkaloids [infected rye (Fig 39.1) ,
ergoline-based drugs, migraine preparations containing ergotamine tartrate
(Migril) ]. Known as ergotism or ergotoxicosis.

i. Signs and symptoms

(1) GIT - nausea, vomiting, diarrhea, cramping abdominal pain
(2) CNS - headache, vertigo, ataxia, numbness and tingling of skin, paresthesias,
sensation of insects creeping under the skin [formication - pl also see ch
41"cocaine bugs], psychosis [hallucinations, madness], convulsions [St. Vitus’
dance], coma
(3) Vascular - vasospasm, cold skin,3 Intermittent claudication, Intense burning
sensation and gangrenous extremities [Holy Fire, Ignis Sacer, St. Anthony’s
Fire], dry gangrene of the fingers, toes, ears, nose etc, thrombosis [rarely].

ii. Management
Same as for acute, except for stomach lavage, emetics, cathartics and activated
charcoal.

d. Fatal dose
2-10 g.

e. Fatal period
one to several days.

f. PM appearances
Not characteristic
(1) Internal organs - congested
(2) Blood vessels - Degeneration of intima of smaller arterioles, thrombus
formation.

g. MLI
(1) Ergot is used as an abortifacient
(2) Excessive and long use of anti-migraine drugs may produce ergotism
(3) Consumption of bread made of contaminated rye may cause ergotism.
Seller of such grains may be prosecuted U/s273, IPC [Sale of noxious food or
drink (ch 31)]
(4) Ergot administration during postpartum period (for reduction of blood loss)
may be associated with puerperal psychosis.

II. POISONS OF VEGETABLE ORIGIN

A. Lathyrus Sativus [Grass pea, Kesari dal]

Lathyrus sativus is an annual leguminous crop [pulse] cultivated in India and
several other geographical regions for animal and human consumption.
Salient features:
(1) Belongs to family Fabaceae [older name – Leguminosae], commonly known
as the legume family, pea family, bean family or pulse family. Vicia faba also
belongs to the same family.
(2) Popular in India, because (i) grows in conditions of extreme drought, famine
and in poor soil (ii) high protein content of seeds (iii) resistant to pests. Seen
as an ‘insurance crop’ as it produces reliable yields when all other crops fail.
(3) Staple food for low income groups in India
(4) Toxic principles: β-N-oxalyl-L-α, β-diamino-propionic acid [β–ODAP] also
known as β-N-oxalyl-amino-L-alanine, [BOAA]. It is a glutamate analog
present in seed cotyledons as free amino acid (1%).
(5) Removal of toxin: (i) Prolonged cooking .es the amount of β-ODAP to the
less toxic isomer, α-ODAP. (ii) β-ODAP is water soluble; boiling grass peas
for 1 hour followed by decanting the water removes about 70% of the ß-
ODAP from the pea.
(6) Toxic amounts – If more than 30% of total diet contains kesari dal, and is
taken for >6 m, spastic paralysis results.
1. Signs and symptoms
(1) Causes a form of spastic paralysis known as neurolathyrism.
(2) Incidence - in epidemic areas is 4%.
(3) Epidemiology:
(i) Men [especially young men between 10-20 y]are more susceptible than
women.
(ii) Neurolathyrism is rare in well-nourished adults and postmenopausal women.
(4) Onset - 3 types
(i) Acute (ii) subacute (iii) insidious
(5) Main signs and symptoms are:
(i) CNS – (a) Initially - pain in the back and weakness of legs; difficulty in
sitting down and getting up (b) Later – Gait is affected. -ed muscle tone in
the legs [thigh extensors, thigh adductors, gastrocnemius] + muscle
weakness"inversion of the feet"lurching, cross-legged gait [scissors gait].
Legs tremble and dragged along with difficulty. Patient may walk on
tiptoes, and must use a stick to walk. (c) Still later – Complete spastic
paraplegia (d) Evidence of peripheral neuropathy - does not usually occur
unless the patient has severe neurolathyrism. (e) Superficial sensation,
rectal sphincter tone, cranial nerve function, upper extremity muscle tone,
and mental activity are usually normal. (f) There is no atrophy or loss of
tone of muscles. There is no reaction of degeneration. (g) Knee jerks are -
ed, ankle clonus is marked and Babinski’s sign is +ve.
(ii) Miscellaneous - GIT distress, urinary frequency and urgency, sexual
dysfunction, neurasthenic symptoms [insomnia, thirst, short-term memory
loss].

2. Prevention and treatment

(1) Exclusion of pulse from diet.
(2) If used, it must be parboiled.
(3) Massage and application of electricity.

3. PM appearances
Death is rare.
(1) Macroscopic - Lateral columns of spinal cord show sclerosis.
(2) Histopathology - Degeneration of the corticospinal pathways (eg, lateral
 pyramidal tracts) distal to the mid-thoracic level with preservation of anterior
horn cells in the spinal cord.

B. Poisonous Mushrooms

1. Signs and symptoms

Symptoms are collectively known as phalloides syndrome.
(1) General:
(i) Cyanosis
(ii) Pulse – slow, bradycardia
(iii) Respiration - labored
(2) Irritant symptoms – Delayed for 6-12 h.
(i) Salivation, nausea, vomiting, diarrhea
(ii) Throat – sense of constriction
(iii) Stomach - Burning pain
(iv) There may be acute pseudoobstruction and dilation of the colon in the
absence of any mechanical obstruction [Ogilvie’s syndrome].
(3) Neurotic symptoms – (i) Cramps (ii) Delirium (iii) Diplopia (iv) Giddiness
(v) Headache (vi) Pupils – constricted (vii) sweating, (viii) Twitching of limbs
(ix) coma, convulsions, collapse, death
(4) Hepatic and renal toxicity – develops in 3-6 days, in cases of survival.
2. Fatal dose
One mushroom.

3. Fatal period
24 hours.

4. Test
Meixner test -
(1) Sample (stool, gastric lavage) + methanol" centrifuge"filter
(2) Add 2 drops of filtrate to a newspaper
(3) Encircle the spot with a pencil and dry it
(4) Add a drop of conc. HCl to the dry spot"blue color"Amatoxins present.
Phallotoxins do not give blue color.
Memory Aid 1: Meixner test
Meixner test is done in Mushroom poisoning

5. Management
(1) Stomach wash – with KMnO4.
(2) Activated charcoal
(3) Forced diuresis, Hemodialysis
(4) Benzyl penicillin 3-10 lakh units daily
(5) Atropine sulphate
(6) Antidotes:
(i) Anti-phalloidin antibodies
(ii) Cimetidine - Potent cytochrome P450 system inhibitor. Protects liver against
alpha-amanitin. Dose 4-6 g/day.
(iii) Iridoid glycosides - These are a class of secondary metabolites found in a
wide variety of plants and in some animals. Named after Iridomyrmex
genus which contains a defensive chemical iridomyrmecin. (a) Aucubin -
derived from the leaves of Aucuba japonica. Found to be protective against
Amanita phalloides. (b) Kutkin - Kutkin is a mixture of iridoid glycosides
picroside I and kutkoside isolated from the roots of Picrorhiza kurroa.
Found to be protective against Amanita phalloides. Efficacy is superior
even to silibinin.
(iv) N-acetylcysteine - Same dose as in paracetamol poisoning
(v) Silibinin - A semi-purified fraction of silymarin derived from milk thistle
[Silybum marianum].
(vi) Thioctic acid - Once thought to be useful in hepatic damage. But now
obsolete.
(7) Management of acute liver failure.
(8) Symptomatic

6. PM findings
(1) GIT - inflammation of mucosa.
(2) Heart, kidneys - Fatty degeneration. Kidneys may be pale and swollen.
(3) Liver - Shows most characteristic findings as mushrooms are hepatotoxic.
Central zonal necrosis, centrilobular hemorrhage, fatty degeneration and
steatosis. Findings of hepatic failure, eg anasarca, pulmonary edema, scleral
 icterus and serous effusions are seen.
(4) Brain - Congestion, petechial hemorrhages in serous membranes and in
substance of brain, especially if neurotic symptoms were present during life.

7. ML importance
Poisoning is usually accidental. Rarely homicidal.

C. Argemone Mexicana
Argemone mexicana (Kutila, Mexican poppy, Phirangi Datura, Pila-Dhatura,
prickly poppy, Satyanasi, Sial Kanta, Ujar kanta) grows wild all over India in the
cold season.
Salient features:
(1) It is an annual herb, belonging to the family Papaveraceae [Another
poisonous plant of this family is P. somniferum. Please see ch 40], which
grows wild all over India during winters [Fig 39.3]
(2) Plant:
(i) It grows 1-4 ft high, with spreading branches.
(ii) Leaves – sessile, spiny, thistle like
(iii) Flowers - 1-3 inch across and are colored yellow.
(iv) Capsules – Prickly oblong or elliptic 2-4 cm long. Contain seeds
(v) Seeds - (a) blackish brown, round and netted and resemble those of mustard
[Brassica nigra] (b) Differences - (I) Argemone seeds have spiny edges.
Mustard seeds do not have such spiny edges. (II) When seeds of A.
mexicana are pressed on a slide, they burst with a report; mustard seeds
collapse quietly.
(3) Alkaloids - All parts of plant are poisonous. The extract of the whole plant
(latex) contains two alkaloids Berberine and Protopine.
(4) Katkar oil:
(i) A. mexicana seeds yield 22-36% of a pale yellow, nauseous, bitter, non-edible
oil [Katkar oil or Argemone oil].
(ii) The oil is rich in two alkaloids sanguinarine and dihydrosanguinarine, the
former being more toxic than the latter. They are mainly responsible for the
poisonous symptoms (a) Mechanism of toxicity - sanguinarine inhibits Na+-
K+-ATPase activity of heart"degenerative changes in cardiac muscle
(iii) Other alkaloids of lesser importance are cheletrythrine and coptisine.
(iv) If katkar oil is heated to 240°C for 15 minutes, it loses its toxic properties.
(v) Uses - (a) used medicinally in several countries in the treatment of dropsy,
jaundice and skin diseases. (b) given as an aperient [laxative] (c) used for
lighting lamps, as it is very cheap.
(vi) Abuses – used as an adulterant of mustard oil. Causes abnormal
permeability of blood vessels resulting in epidemic dropsy.
1. Signs and symptoms

(a) Local application

Application on scalp causes burning and fall of hair.
(b) Systemic
Consumption of adulterated oil causes epidemic dropsy. Symptoms appear
gradually
(1) General:
(i) Marked edema of the legs
(ii) General anasarca [due to -ed BV permeability. Not attributable to CCF in
most cases].
(iii) Pyrexia
(iv) Anemia
(2) GIT - (i) Loss of appetite, (ii) nausea, vomiting, dyspepsia, diarrhea
(3) CVS - (i) BP. (ii) pulse – feeble and rapid (iii) CCF
(4) Liver – enlarged, tender. Not attributable to CCF in most cases
(5) Resp system – Dyspnea
(6) Skin and mucosa:
(i) Bluish mottling (Erythrocyanosis) [due to dilatation of peripheral vessels].
Blanches on pressure"May develop into s/c telangiectasis or hemangiomata.
As erythrocyanosis resolves, it leaves post inflammatory
hyperpigmentation.
(ii) Small fleshy dark red warty growths may be noticeable on various body
parts, and also on cheek, gums, nose and tongue
(iii) Tingling
(iv) Hyperesthesia
(7) Neuromuscular - (i) Calf muscles – tender; (ii) Tendon reflexes feeble or
absent
(8) Eyes - Dimness of vision [in 10% cases]. Due to -IOP
(9) Death – CCF due to myocardial damage.

2. Lab
(1) -ESR
(2) X-ray – moderate to severe pulmonary congestion.

3. Treatment
(1) Good diet
(2) Supportive treatment especially of heart
4. PM findings
(1) Body shows generalized anasarca, or local edema of legs
(2) Heart - Myocardial damage, dilatation
(3) Liver - enlarged
(4) Skin – may show mottling
(5) Gastric contents show +ve tests for argemone oil.

III. POISONS OF ANIMAL ORIGIN

Poisonous animals and venomous animals are different. Former cause

poisoning when eaten; the latter attack and inject venom in human victims.
Please also see ch 31 “introduction to poisons”. In this chapter, only poisonous
animals would be discussed. They are poisonous fish and mussel.

A. Poisonous Fish
(1) Ichthyotoxicosis [Gk. ichthyo, fish] is poisoning produced by poisonous
fishes.
(2) Ichthyotoxin is a natural toxin produced by fish.
(3) Ichthyosarcotoxic fishes are those fishes that produce ichthyotoxicosis.
They contain a poison in the flesh [Gk. sarx, flesh] including musculature,
viscera, skin, or slime.
(4) Ichthyotoxicology is the study of natural toxins produced by fish, their
cause, detection, and effects, and the treatment of conditions produced by
them.
(5) Ichthyotoxicity is poisoning caused to fishes, eg by sessile animals such as
sponges, coelenterates or tunicates which produce toxins to deter potential
predator fish.

IV. MEDICOLEGAL ASPECTS OF FOOD POISONING

A. Information to Public Health Authorities

Doctor must inform all cases of food poisoning to public health authorities, as
well as to police, because such cases are liable to be registered u/s 269, IPC
(negligent act likely to spread infection dangerous to life), 272, IPC
(Adulteration of food or drink intended for sale) and 284, IPC (negligent conduct
with respect to poisonous substance).

40. CNS Depressants

I. INTRODUCTION

[A] CNS depressants are psychoactive drugs which temporarily diminish the
function or activity of brain. Since they lower or “down” the functional activity
of brain, they are sometimes referred to as “downers”. In contrast, stimulants
are referred to as “uppers” (increase the function or activity of brain).
Depressants are widely used as prescription medicines and as drugs of abuse.
[B] Hypnotic (soporific) drugs are psychoactive drugs whose primary function is
to induce sleep. [C] Narcotic – (1) Medical definition – Same as hypnotic
[from Gk. narke, numbness, stupor]. (2) Legal definition - Drug that is totally
prohibited, or one that is used in violation of strict governmental regulation.
Narcotic drug is defined in S.2(xiv) of The Narcotic Drugs and Psychotropic
Substances Act, 1985 [NDPSA 1985] as follows - “Narcotic drug” means coca
leaf, cannabis (hemp), opium, poppy straw and includes all manufactured drugs.
[D] Sedatives are psychoactive drugs that induce sedation by reducing irritability
or excitement. A sedative drug in a high dose would act as a hypnotic.

II. CLASSIFICATION

CNS depressants may be classified as follows:

(1) General Anesthetics – Chloroform, Ether
(2) Alcohols (a) Ethyl alcohol (b) Methyl alcohol (c) Other alcohols (e.g.
Isopropyl alcohol)
(3) Opium and its derivatives
(4) Sedative-hypnotics (a) Barbiturates
(i) Long acting
(ii) Short acting
(iii) Ultra-short acting (b) Hydrocarbons (e.g. Kerosene, Naphthalene,
Turpentine) (c) Paraldehyde (d) Chloral Hydrate (e) Bromides - potassium
bromide (f) Quinazolines – Methaqualone (g) Phenytoin sodium (h)
Benzodiazepines – Diazepam, Fletazepam, Flurazepam, Lorazepam,
Oxazepam, Prazepam, Chlordiazepoxide (i) Propanediol carbamates –
Meprobamate (j) Piperdinediones – Glutethimide.

III. ALCOHOLS

A. Ethyl Alcohol(C2H5OH)
Ethyl alcohol [EA, ethanol, ETOH, grain alcohol, aqua vitae, water of life], is a
transparent, volatile, flammable, colorless liquid, having a characteristic
alcoholic odor and a burning taste.
Salient features:
(1) Sp gr - 0.79.
(2) Caloric content - 7 Kcals/g [29 kJ/g]
(3) It is a powerful psychoactive drug used in alcoholic beverages.
(4) Frequency of use – Alcohol is a socially acceptable drug. Among socially
acceptable drugs, it is the 3nd most common drug of abuse after caffeine and
nicotine [Please also see chapter on deliriant poisons].

1. Common forms of alcohol

(1) Absolute alcohol [syn, anhydrous alcohol, dehydrated alcohol] is 99.5%
ethyl alcohol.
(2) Rectified spirit [syn, neutral spirit, rectified alcohol] is 95% ethyl alcohol.
(3) Methylated spirit or denatured alcohol is 90% ethanol + 9.5 parts
methanol+ 0.5% crude pyridine.
Memory Aid 1: Concentrations of various forms of alcohol
ARM: Absolute [99.5%] "Rectified spirit [95%]"Methylated Spirit [90%]

(4) Standard drink – Definition of standard drink differs from country to

country. But 10 g of absolute alcohol is usually taken as one standard drink or
1 unit.
2. Proof spirit
Proof spirit (100 proof) is defined in three ways
(1) Most common definition – That conc. of ethanol, which weighs exactly
12/13 of the weight of an equal volume of distilled water at 11°C. It is 57.06%
ethanol by volume
(2) In the US, it is twice the conc. of alcohol by volume. Thus 50% ethanol is
100 proof
(3) that minimum conc. of ethanol which when mixed with gunpowder would
ignite (57.06%). Spirits weaker than 57.06% are underproof; stronger are
overproof.
3. Concentration of ethyl alcohol in beverages
Table 1 gives the alcoholic content of some common alcoholic beverages.
4. Absorption
(1) Digestion prior to absorption - Ethanol is not digested prior to absorption
and is absorbed as such.
(2) Molecular size - Its small molecular size allows it to pass readily through
membranes by simple diffusion.
(3) From mouth and esophagus – Only traces are absorbed.
(4) From stomach and intestines - About 20% is absorbed from the stomach
and 80% through small intestine. Absorption is rapid; about 60% of alcohol
taken on an empty stomach is absorbed in 30 minutes and 90% in one hour.
(5) Appearance in blood - It can be detected in the blood within 2-3 minutes of
ingestion. Maximum blood levels are achieved within 45-90 minutes of
ingestion [30 min if stomach is empty]. Table 2 gives various conditions,
where absorption of alcohol is - or .. Most conditions where absorption is - can
be explained by the fact that it passes immediately to small intestines, where
absorption is maximum (and vice versa). Blood alcohol concentration is often
abbreviated as BAC or BAL [level].
(6) Vd - 0.5-0.7 L/kg)
(7) Because of first-pass metabolism by gastric and liver alcohol dehydrogenase
(ADH), oral ingestion of ethanol leads to lower blood levels than would be
obtained if the same quantity were administered IV.
(8) Absorption phase is followed by elimination phase, when rate of
elimination is higher than that of absorption.
5. Distribution
(1) Alcohol is distributed to the tissues in proportion to their water content
[Table 3].
(2) Blood brain barrier – crossed by ethanol easily.
(3) Solubility in fat -
(i) Alcohol is not distributed to adipose tissue as it is insoluble in fat.
(ii) Thus same amount of alcohol given to an obese person [or a woman]
produces -er blood levels, as their aqueous compartments are smaller.
(iii) In general females acquire 25% higher blood levels from same amount of
drinks.
(4) As arterial blood passes through the lungs - some alcohol is lost by
diffusion into the alveolar air.
(5) Venous blood alcohol – is about 10% lower than arterial blood in
absorption phase. Since alveolar air is in equilibrium with arterial blood, this
accounts for a -er conc of alcohol in alveolar breath compared to venous
blood. After one hour or more of drinking, both arterial and venous blood
show same concentration.
(6) Equilibrium of arterial blood level with muscle – occurs in about 2 hours.
(7) RBCs - contain . alcohol than plasma; thus whole blood conc is slightly .
than in plasma or serum.
6. Metabolism and excretion
(1) About 90% of alcohol absorbed is oxidized in liver; 10% is excreted -
(i) Breath – 5%
(ii) Urine – 5%
(iii) Feces, milk, saliva, sweat, tears – negligible amounts. Peculiar odor of
alcoholic is due to alcohol in breath and sweat.
(2) Metabolism -
(i) First to acetaldehyde by ADH and then
(ii) To acetic acid by aldehyde dehydrogenase [AlDH]
7. Mechanism of action
(1) At organ level -
(i) Brain - CNS depressant (a) Causes an irregularly descending type of
depression; higher centers within cerebrum are depressed first, followed by
"midbrain " reticular activating system "thalamus"spinal cord "medulla
[respiratory center is inhibited last of all resulting in death]. (b) Within the
cerebrum, frontal lobes are depressed first [they are sensitive even to low
conc, resulting in mood changes]; followed by "occipital lobes [visual
disturbances]"cerebellum [loss of co-ordination].
(ii) Other organs – EA has direct effects on cardiac muscle, thyroid and hepatic
tissue.
(2) At molecular level -
(i) GABA receptors - EA binds directly to GABA receptors in the CNS " causes
sedative effects similar to those of benzodiazepines, which bind to the same
GABA receptor.
(ii) N-Methyl-D-aspartate (NMDA) receptors - (a) EA potently and selectively
inhibits N-methyl-D-aspartate (NMDA) type of inotropic glutamate
receptors [NMDARs] (b) prolonged ethanol exposure produces a
compensatory ‘upregulation’ of NMDAR functions. (c) These changes
underlie the development of ethanol tolerance, dependence as well as acute
and delayed signs of withdrawal.

8. Acute poisoning
(1) Cause - Serious acute alcohol poisoning occurs usually as a result of
deliberate heavy drinking.
(2) Constancy - Signs and symptoms are not constant in all people; at the same
blood concentration, they would vary according to whether the person is a
beginner, moderate drinker or heavy drinker.
(3) Phases - Seven phases of intoxication are known. Table 4 must be referred
for most common signs and symptoms. Main text includes additional features
and explanations.

a. Signs and symptoms

(1) Stage of sobriety [BAC=0-50 mg%; Table 4] –
(i) No significant effect or (ii) mild euphoria (iii) easy socialization. (iv) Roughly
midway is the legal limit of driving in India [30 mg%].
(2) Stage of euphoria [BAC = 50-100 mg%]–
(i) Higher centers of brain are inhibited " (a) .ed attention span (b) .ed cognitive
function (c) .ed inhibitions [feeling of well-being] (d) .ed sensory
perceptions (e) -ed self confidence (f) -ed sociability (g) -ed talkativeness
(h) Alteration of judgment
(ii) Alcohol flush reaction [AFR]- (a) Flushing of the face, neck, and shoulders
after the ingestion of alcohol, often accompanied by nausea, dizziness, and
palpitations. (b) Very common in Asians with almost 50% involvement of
some Mongoloid groups [for this reason, also known as Asian flush
syndrome, Asian flush, Asian glow and Oriental flushing syndrome] (c)
caused by a defective allele of AlDH, which encodes for aldehyde
dehydrogenase [please see “metabolism and excretion” above]. Its
deficiency causes accumulation of acetaldehyde, which is responsible for
AFR. The defective allele originated among Han Chinese in central China,
and was positively selected in the past, because - concentrations of
acetaldehyde conferred protection against parasitic infections especially
Entamoeba histolytica. (d) The reaction also occurs when alcohol is taken
by people receiving treatment with alcohol sensitizing drugs such as
disulfiram (Antabuse), which inhibit aldehyde dehydrogenase. (e)
associated with - risk of esophageal cancer in those who drink (f) Also with
auto-brewery syndrome [please see below].
(iii) Pulse – rapid, full and bounding.
(iv) BP – slight - especially at systolic level.
(v) Temp – usually - at this stage. During later stages it may be subnormal.
(vi) Muscular system - (a) Fine movements affected (b) muscular incoordination
[mild]. (c) If driving - Incidence of vehicular accidents is -ed [Roughly
midway is the legal limit of driving in UK (80 mg%)].
(vii) Slurring of speech begins [-es in all subsequent stages].
(viii) Nystagmus – due to effects of alcohol on vestibulocochlear system. Two
types are described – AGN and PGN. (a) Alcohol Gaze Nystagmus (AGN)
- Seen in a vertical position, with subject sitting or standing. (I) Two types –
Horizontal gaze nystagmus [HGN] and Vertical Gaze Nystagmus [VGN].
HGN is an involuntary jerking of the eye that occurs naturally as the eyes
 gaze to the side. Under normal circumstances, nystagmus occurs when the
eyes are rotated at high peripheral angles. However, when a person is
impaired by alcohol, nystagmus is exaggerated and may occur at lesser
angles. In the HGN test, the examiner observes the eyes of a suspect as he
follows a slowly moving object such as a pen [thus also known as pen test]
or small flashlight, horizontally with his or her eyes. The examiner looks
for three indicators of impairment in each eye: if the eye cannot follow a
moving object smoothly, if jerking is distinct when the eye is at maximum
deviation, and if the angle of onset of jerking is within 45 degrees of center.
If, between the two eyes, four or more clues appear, the suspect likely has a
BAC ≥80mg%. VGN is demonstrable at higher levels. (b) Positional
Alcohol Nystagmus [PAN]- Seen in a lying down position (I) Nystagmus
is seen when the head is placed in a sideways position. (II) Two types –
PAN I [nystagmus to the right when the right side of the head is down, and
to the left when the left side is down] and PAN II [opposite directions as in
PAN I]. (III) Time of appearance - (A) PAN I occurs first [within ½ h; lasts
for 3-4 h]. Occurs during rising and peak BACs; begins at 40 mg%; but
most often observed at ≥80mg%. (B) PAN II appears later [1-2 h after
disappearance of PAN I; lasts for 4-5 h, i.e. up to 10 h after drinking
episode] during the ‘morning after’ stage [hangover] as the BAC is .ing as
alcohol is being eliminated from the bloodstream, and the vestibular canals
are beginning to regain balance. It is claimed to be a true, objective after-
effect of alcohol and form a part of the so-called hangover syndrome. (IV)
How to elicit – person made to lie down; head turned to either side. PAN is
best elicited with eyes closed [seen through eyelids as mild flutter].
Opening the eyes will block PAN if its intensity is low, but not if intensity is
high.
(3) Stage of excitement [BAC = 100-150 mg%]–
(i) Higher centers of brain – Inhibited further (a) Lack of self control and loss of
critical judgment - may cause the person to disclose secrets (b) .ed
concentration (c) Emotional instability (d) Excitement (e) Lack of self
control (f) Loss of critical judgment (g) Comprehension, memory and
reasoning impaired (h) dizziness (i) Mental confusion (j) Sleepiness
(ii) Eyes – (a) Visual acuity .ed – (I) In dim light objects may not be
distinguished at all; strong light is needed. (II) After being dazzled by
 strong light, it takes longer to see clearly again (b) eyelids – swollen and
red (c) Conjunctivae - congested (d) Pupils – dilated. [contracted in later
stages, and then dilate once again just before death. Similar situation is seen
in chloroform. Mechanism is the same.
Memory Aid 2: Pupils in alcohol poisoning at the stage of excitement
D"C"D. Same as for chloroform [pl see above]. MacEwen sign [pl see below] is elicited at the stage of
contraction.

(iii) Time and space perception – Altered [person may underestimate speed of
objects and distances travelled]
(iv) Muscular system - (a) Ataxia [mild] (b) Slowed reaction time.
(4) Stage of disorderly behavior [BAC = 150-200 mg%]–
(i) Higher centers of brain – Inhibited further (a) Normal good manners -
forgotten
(ii) Eyes – (a) Visual acuity, eyelids, conjunctivae - same as in earlier stages (b)
Diplopia (c) Pupils - may now be unequal. Reaction to light has lost its
briskness. Contract slowly when light is shown, and equalize. Then dilate
slowly even if light is continually shown.
(iii) Muscular system - (a) Ataxia [worsened], Staggering, unsteady gait (b)
Disorientation (c) emotions exaggerated (d) Mental confusion exacerbates
(e) Vertigo
(5) Stage of stupor [BAC = 200-300 mg%]–
(i) .ed response to painful stimuli
(ii) Drowsiness
(iii) Inability to stand or walk
(iv) Inertia
(v) Loss of muscular co-ordination
(vi) Vomiting
(6) Coma [BAC = 300-500 mg%]–
(i) Anesthesia
(ii) Eyes: Pupils – now contracted. MacEwen sign +ve. An irritating stimuli eg
pinching, slapping or pulling beard or hair causes them to dilate with slow
return back to contraction even though the patient does not regain
consciousness to any degree. It may take up to 20 min to reach their
previous contracted state. Such mild stimulus would not cause dilatation if
 coma was caused by a structural disease. Also known as MacEwen’s sign
or MacEwen’s pupil.
Memory Aid 3: McEwen sign
Memory aid C"D"C.

Discovered by Scottish surgeon Sir William MacEwen (1848–1924), whose

main problem as a casualty surgeon was to distinguish coma due to alcohol
from that produced by conditions such as concussion, skull fracture,
apoplexy, and opium use.
(iii) Incontinence of urine and feces
(iv) Reflexes abolished
(v) Respiratory depression
(vi) Temp [subnormal]
(vii) Unconsciousness
(7) Death [BAC = >500 mg%] - due to respiratory failure. Pupils dilate just
before death just as in chloroform.
(8) Rare and unusual symptoms - allergic reactions [urticaria]. May result in
death.

b. D/d

(1) Trauma
(2) Various illnesses causing confusion and delirium.
Memory Aid 5: Confirmation of ethyl alcohol poisoning
CONFIRMED
C - Confusion or confabulation or memory loss for recent events.
O - Odour of breath, stale alcohol / ingredients / metabolites.
N - Nystagmus.
F - Funny expressions, slurred speech and fuddled thinking.
I - Inco-ordination and postural instability.
R - Rapid, full and bounding pulse.
M - Maudlin. Half-drunk, tearfully affectionate or “familiar”
E - Eyes bloodshot. Pupils dilated and sluggish in reaction.
D - Demeanour. Deviations of behaviour, bearing and deportment.

c. Management
(1) ABCDE of Immediate resuscitative measures – ch 31.
(2) Gastric lavage – preferably with an alkaline soln.
(3) Activated charcoal – not useful
(4) IV fluids – 1 L normal saline + 10% glucose + 100 mg thiamine + 15 units
insulin
(5) Hemodialysis – very useful.
(i) Eliminates ethanol 4 times faster than that metabolized by liver.
(ii) Not employed normally, but may have to be used if (a) Blood levels are
excessive (b) Liver function is compromised [as in ch alcoholics] (c)
Condition is deteriorating continuously
(6) Peritoneal dialysis – useful. Indications same as hemodialysis.
(7) Drugs – Not much useful. Following have been tried
(i) Caffeine
(ii) Flumazenil - May be considered for patients with hepatic encephalopathy.
Reverses respiratory depression associated with ethanol.
(iii) Naloxone
(iv) Physostigmine.

d. Tests
(1) Woodbury’s test [syn - Dichromate test] - 5 mL urine + 5 mL of 10%
sodium dichromate in 50% H2SO4"Green color if ethanol is present.
(2) Bedside test - 5 mL urine + 1 mL acetic acid + 1 drop H2SO4 [heat gently in
a test tube for 1 min]"A characteristic strong fruity odor [due to ethyl acetate]
if ethanol is present.

e. Fatal dose
(1) Ingestion –
(i) Adults - 5-8 g/kg absolute ethanol [6-10 mL/kg].
(ii) Children - 3 g/kg (4 mL/kg). Paradoxically larger doses, especially taken
quickly may not kill, because of violet emesis set up due to GIT irritation
[ch 31"Causes modifying action of poisons. CuSO4 behaves the same way
(ch 36)].
(2) Blood conc – >500 mg% is fatal
(3) Inhalation -
(i) Does not cause problems unless concentrations are high.
(ii) Irritating to eyes and skin.
(iii) MAC in air – 1000 ppm.

f. Fatal period
12-24 h.

g. Cause of death
(1) Depression of brain stem"Depression of Respiratory Center"respiratory
paralysis.
(2) Aspiration of vomit.

h. Postmortem appearances [acute poisoning]

(1) Conjunctiva - Congested
(2) On opening the body – Alcoholic odor from body cavities, stomach
contents and from viscera
(3) Stomach – congested with a coating of mucus [due to irritation]
(4) Internal organs – Brain and meninges, liver, spleen, kidneys etc congested
(5) Blood – Fluid and dark
(6) Microscopically – Cloudy swelling of parenchymatous organs
(7) changes seen in chronic alcoholism, if subject is a ch. alcoholic. Please see
below.

i. Collection of specimens [at PM]

(1) For collection of specimens in the living, please see “Clinical examination of
a case of drunkenness” below.
(2) For general guidelines regarding collection of specimens in the dead,
please see ch 5.
(3) Specimens helpful specifically in alcohol are (i) Blood (ii) Brain (iii) CSF
(iv) Lung (v) SDH [in cases of long survival] (vi) synovial fluid (vii) Vitreous
(4) Specimens in embalmed bodies – ch 9.

9. Chronic poisoning
Syn - Alcohol addiction, chronic alcoholism, ethanolism.

a. Definitions
DSM-IV-TR, classifies “Alcohol Use Disorders” into 2 broad groups - Alcohol
Dependence (Diagnostic Code - 303.90) and Alcohol Abuse (Diagnostic Code -
305.00). Definitions are same as for substance dependence and substance abuse
[please see ch 46 – Drug dependence and drug abuse]. Alcohol addicts or
chronic alcoholics are people who cannot stop drinking for long periods or who
experience withdrawal symptoms if they do so. Most of them have reached a
state of irreversible somatic or brain changes induced by alcohol.
b. Tolerance to alcohol
Tolerance to alcohol means that after continued drinking, consumption of a
constant amount of alcohol produces a lesser effect or increasing amounts of
alcohol are necessary to produce the same effect.
Salient features:
(1) Tolerance may - with alcohol use, till liver gets damaged with . capacity to
metabolize. Thus tolerance is restricted by liver damage
(2) Relationship with barbiturates – The signs and symptoms of alcohol and
barbiturate intoxication are similar, as are the signs and symptoms of
abstinence from these drugs and their routes of metabolism. Barbiturates will
suppress alcohol abstinence phenomena, and alcohol will suppress, at least
partially, the symptoms of barbiturate withdrawal. The two drugs are
essentially additive and interchangeable in chronic intoxications. Consumption
of alcohol along with barbiturates -es their duration of action. Because of
these similarities one of the 7 types of drug dependence has been termed
"barbiturate-alcohol type" [ch 46].

c. Signs and symptoms

(1) GIT - Nausea, vomiting, anorexia, diarrhea
(2) Hepatic – Jaundice
(3) CNS – tremors of tongue and hands, insomnia, loss of memory, impaired
power of judgment. Peripheral neuritis and dementia occur in advanced stages
(4) nutritional – Hypoproteinemia, general anasarca.

d. Subtypes of chronic alcoholism

American physiologist Elvin Jellinek (1890-1963) identified five subtypes of
alcoholism.

i. Alpha alcoholism
(1) Psychological dependence only
[Memory Aid 6: AlPha - Psychological].
(2) Syn - Problem drinking, escaPe drinking.

ii. Beta alcoholism

(1) Results in physical disease states (ulcers, cirrhosis, damage to the nerves,
kidney problems).
(2) No physical dependence.

iii. Gamma alcoholism

(1) Mild physical dependence occurs.
(2) Tolerance to alcohol, withdrawal symptoms, craving, loss of control of
drinking.
(3) Despite craving, addict can live without alcohol for a short period of time.
(4) Syn - “Anglo-Saxon” alcoholism, malignant alcoholism] [Memory Aid 7-
Gamma alcoholism - mild physical dependence].

iv. Delta alcoholism

(1) Strong physical dependence.
(2) Addict cannot stay away from liquor even for 1-2 days without suffering
from withdrawal symptoms.
(3) high blood alcohol level is maintained.
(4) Syn – alcoholization.

v. Epsilon alcoholism
(1) Individuals engage in [Memory Aid 8 - Epsilon - periodic] periodic
binges, with long periods of abstaining in between.
(2) Syn – dipsomania, Paroxysmal or periodic alcoholism.

e. Specific conditions seen in chronic poisoning

i. Acute alcoholic hallucinosis

(1) Persistent hallucinations [auditory, visual] develop within 48 h of alcohol
intake.
(2) Content is unusually disturbing and unpleasant
(3) May last for several weeks or months.

ii. Alcoholic Brain Syndrome

A general term for a range of disorders due to the effects of alcohol on the brain -
amnesic syndrome, delirium tremens [DT], dementia, hallucinosis, psychotic
disorder. Specific terms are preferred.

iii. Alcoholic epilepsy

(1) 45% of alcoholics have seizures at some stage.
(2) Seizures [syn, rum fits, withdrawal seizures] are grand mal in type and
classically occur as part of the withdrawal syndrome. Seen after about a day of
termination of drinking session. But may occur rarely even while the patient is
drinking.
(3) Pathogenesis
(i) Cerebral atrophy
(ii) Alcohol promotes Mg2+ excretion " resultant electrolyte disturbances lower
convulsive threshold
(iii) Faulty carbohydrate handling mechanisms, as evidenced by peculiar oral
GTT curves
(iv) Alcohol has a biphasic stimulant depressant action on CNS.

iv. Alcoholic paranoia

(1) Alcoholic paranoia - alcohol-induced psychotic disorder in which delusions
of reference and persecution occur.
(2) Alcoholic jealousy [syn, amorous paranoia, conjugal paranoia, morbid
jealousy] is a form of alcoholic paranoia characterized by delusions of
infidelity.
(i) There is intense searching for evidence of infidelity.
(ii) Direct accusations lead to violent quarrels.

v. Alcoholic polyneuritis
Alcoholic polyneuritis [syn, alcoholic peripheral neuropathy] is a painful
condition produced by ch alcoholic consumption.
(1) Signs & symptoms -
(i) Allodynia [Gk allos, other; dynia, pain], i.e. pain from stimuli which are not
normally painful [bedsheets, air movement], or pain which occurs other
than in the area stimulated [cf thermal allodynia, which occurs in ciguatera
- ch 39]
(ii) Hyperalgesia
(iii) Loss of deep reflexes
(iv) Spontaneous burning pain
(v) Tenderness of muscles of arms and legs
(vi) Unsteady gait
(vii) Weakness
(viii) Wrist and foot drop
(2) D/d – ch arsenic poisoning [ch 36].

vi. Battered alcoholic syndrome

Defined as the presence of three or more fractures in different chronological
stages of healing in an alcoholic. Etiology - (i) direct toxic effects of alcohol (ii)
greater exposure to trauma [- incidence of falls, being involved in fights etc]. In
some of these deaths, there may be a genuine concern of alcoholic having been
strangulated because of finding of fractures of thyrohyoid complex. Death of
chronic alcoholics generally occurs from liver failure, and not from fractures.

vii. Cardiac Conditions

[A] Beriberi heart - Due to deficiency of thiamine. Characterized by cardiac
failure and edema. No CNS involvement. [B] Dysrhythmias – Alcohol
withdrawal " -Adrenergic activity " tachyarrhythmias " Sudden death. [C]
Munich beer Heart - First reported by the German pathologist Bollinger in
1884. Dilated hearts were found in heavy beer drinkers on autopsy. He called it
Münchener Bierherz (Munich beer heart. Now known as alcoholic
cardiomyopathy. Mechanisms - (1) .ed myocardial protein synthesis, (2)
calcium channel dysfunction (3) Disturbance of ion homeostasis (4) oxidative
stress. [D] Myocarditis - (1) It is part of a bigger syndrome [alcoholic
cardiomyopathy]. Not to be confused with beer drinker’s cardiomyopathy. (2)
Etiology - Direct toxic effect of alcohol and its metabolite acetaldehyde.
Consumption - 80 g/d for > 5 years for cardiomyopathy to develop.

viii. Cirrhosis
(1) Alcoholic cirrhosis develops in 10-20% of individuals who drink heavily for
a decade or more.
(2) Mechanism - Alcohol injures the liver by blocking the normal metabolism of
protein, fats, and carbohydrates. There may be concurrent alcoholic hepatitis
with fever, hepatomegaly, jaundice, and anorexia. Aspartate transaminase
 [AST] and Alanine transaminase [ALT] are both -ed but < 300 IU/L with a
AST:ALT ratio > 2.0, a value rarely seen in other liver diseases.
(3) Liver biopsy - hepatocyte necrosis, Mallory bodies, neutrophilic infiltration,
perivenular inflammation.

ix. Delirium tremens

Delirium tremens [Latin, shaking frenzy] [syn, DTs, “the horrors”, “the shakes”]
is an acute episode of delirium precipitated by alcohol withdrawal.
Salient features:
(1) First described in 1813 by Pearson. Sutton in same year called it delirium
tremens.
(2) Incidence – occurs in 5% of patients with alcohol withdrawal.
(3) Pathology -
(i) Loss of the inhibitory influences of GABA receptor system
(ii) - in catecholamine release [hyperadrenergic state]
(iii) Hypocalcemia and hypomagnesemia - occur during alcohol withdrawal.
Contribute to CNS hyperexcitability by altering neuronal-evoked potentials.
(iv) .ed oxygen use and ATP turnover and release" contributes on the cellular
level, to the physiologic changes of alcohol withdrawal.
(4) Precipitating factors -
(i) Sudden withdrawal of alcohol [most common] – typically occurs 72-96 h
after last drink
(ii) Acute infections [erysipelas, influenza, pneumonia]
(iii) Shock – as occurs after an injury [eg fractures]
(iv) Temporary excess
(5) Signs and symptoms –
(i) CNS and psychiatric – Most significant (a) Agitation (b) Coarse muscular
tremors of face, tongue and hands (c) Confusion (d) Delirium (e)
Disorientation [in time and place] (f) Hallucinations [auditory, visual and
tactile with a predominantly horrific content, eg patient may believe insects
are crawling under the skin or snakes are crawling in his bed; syn, delirium
of horrors] (g) Insomnia (h) Memory loss (i) Restlessness (j) Seizures (k)
Tendency to commit suicide, homicide, violent assault, damage to property
(l) Uncontrollable fear
(ii) General - (a) Pupils - Dilated (b) -Temp – due to seizures
(iii) GIT - Diarrhea (iv) Resp – Tachypnea (v) CVS - (a) Tachycardia (b) BP –
Variable. May be - or .
(6) Management -
(i) Drugs - (a) Drug of choice: Benzodiazepines - Diazepam IV 5 mg every 5 m
(b) Other drugs: Rectal paraldehyde, 10 ml every 30 m.,
(ii) Supportive - (a) large amounts of parenteral saline and (b) dextrose to control
hypotension.
(7) Death – occurs in 5-15% cases.
(8) Cause of death –
(i) Cardiac arrhythmias associated with hypokalemia
(ii) Fat emboli
(iii) Hyperpyrexia, poor hydration and hypotension
(iv) Infections
(v) Respiratory failure
(vi) Heat stroke [rarely].
(9) PM appearances – Same as in ch alcoholic poisoning.

x. Gastric and peptic ulceration

Due to irritant effects of alcohol.

xi. Korsakoff’s psychosis

Korsakoff’s psychosis (Korsakoff’s dementia, Korsakoff’s psychosis,
Korsakoff’s syndrome, amnesic-confabulatory syndrome), is a neurological
disorder caused by the lack of vitamin B1 (thiamine).
Salient features:
(1) First described by Russian neuropsychiatrist Sergei Korsakoff [1854-1900]
(2) Late neuropsychiatric manifestation of Wernicke’s encephalopathy. Also
known as Wernicke-Korsakoff syndrome [WKS]
(3) Clinical features – 3 salient features
(i) Amnesia [anterograde (inability to form new memories) and retrograde (loss
of existing memories)]
(ii) Confabulation [falsification of memory in an alert, responsive individual].
The memory problems associated with Korsakoff ‘s syndrome are
irreversible.
(iii) Polyneuropathy [psychosis polyneuritica]
Memory Aid 9: Korsakoff’s psychosis
Korsakoff’s psychosis is a more Kronic condition than Wernicke’s encephalopathy. Konfabulation is
seen. All features are remembered by PAK – Polyneuropathy, Amnesia, Konfabulation

xii. Mallory-Weiss syndrome

Ruptured esophagus with mediastinitis

xiii. Malnutrition
Due to lack of food intake, calorie requirement being satisfied by alcohol.

xiv. Mania a potu

Mania a potu [“madness from drinking”] is a state of pathological intoxication,
consisting of extreme excitement, sometimes with homicidal attacks and
resulting from the ingestion of comparatively small amounts of alcohol by a
susceptible individual.

xv. Marchiafava syndrome

(1) Also known as Marchiafava-Bignami syndrome [MBS] or disease [MBD].
(2) Signs and symptoms - Marked impairment in brain functioning. Severe
global dementia.
(3) Cause - Necrosis and atrophy of corpus callosum.

xvi. Mental illness

Depression, suicidal tendencies.

xvii. Pancreatitis
Alcoholic pancreatitis is a major complication of alcohol abuse.
Salient features:
(1) Alcohol exerts dose-related toxic effects on the pancreas.
(2) Risk of developing pancreatitis -es with -ing doses of alcohol.

xviii. Tryptophan metabolism disturbance

In ch alcoholics, conversion of tryptophan to 5-hydroxyindoleacetic acid is
depressed.
xix. Wernicke’s encephalopathy
Wernicke encephalopathy is a syndrome, caused by lesions in the medial
thalamic nuclei, mammillary bodies, periaqueductal and periventricular
brainstem nuclei, and superior cerebellar vermis, caused by inadequate intake or
absorption of vitamin B1 (thiamine), especially in conjunction with carbohydrate
ingestion.
Salient features:
(1) First described by German physician Carl Wernicke [1848 –1905]
(2) Etiology –
(i) Ch alcoholism - Alcoholic fulfils his caloric demands from alcohol [empty
calories]; thus avoiding food
(ii) Thiamine deficiency arising from gastric disorders - (a) carcinoma (b)
chronic gastritis, (c) Crohn’s disease, (d) repetitive vomiting, particularly
after bariatric surgery and
(iii) Starvation.
(3) Signs and symptoms – [A] Classical triad - (i) Ataxic gait (ii)
Encephalopathy [agitation, amnesia (short term memory loss), indifference
and inattentiveness, confusion, disorientation, disturbance of consciousness,
delirium, drowsiness and stupor] (iii) Oculomotor disturbance [nystagmus,
external ocular palsies (commonly lateral rectus palsy), ophthalmoplegia,
sluggish pupillary reflexes, anisocoria (unequal size of pupils)].
Memory Aid 10: Wernicke’s encephalopathy
Classical triad of Wernicke’s encephalopathy includes 3 vowels - A; E; O

[B] Other imp signs - (i) Peripheral neuropathy. [C] Atypical symptoms -
Dysphagia. (1) If left untreated – 80% cases progress to Korsakoff’s psychosis
[a more chronic condition]. (2) Management - (i) IV thiamine (ii) IV glucose
[both of these are part of coma cocktail]. (3) Mortality – high. Can cause death
within 48 h of onset.

f. Management

i. Drug treatment
(1) Baclofen (Kemstro, Lioresal, Liofen, and Gablofen) - Derivative of GABA,
primarily used to treat spasticity but now found useful in alcoholism also.
(2) Benzodiazepines
(3) Clomethiazole [syn, chlormethiazole] – Sedative and hypnotic. Used in
treating and preventing symptoms of acute alcohol withdrawal.
(4) Chlorpromazine – 25-50 mg every 4-6 h.
(5) Citrated Calcium carbimide [CCC, Temposil] -
(i) Works in the same way as disulfiram [please see below].
(ii) Dose – 50 mg od
(iii) Advantages - Adverse effects of disulfiram, hepatotoxicity and drowsiness,
do not occur.
(6) Clonidine – 60-180 mg IV/hr. MOA same as that in opioid withdrawal.
(7) Disulfiram – [Antabuse, Antadict, Esperal] –
(i) Mechanism - It inhibits the metabolism of alcohol beyond acetaldehyde stage.
When patient on disulfiram takes alcohol, he gets unpleasant effects of
acetaldehyde [Alcohol flush reaction], forcing him to abstain from alcohol.
(ii) Dose - start with single daily dose of 250 mg. Dose is .ed till a daily dose of
0.125-0.25 mg is reached.
(8) Ibogaine [ch 46].
(9) LSD [ch 46].
(10) Naltrexone (Trexan) – Mechanism - (a) Alcohol causes the body to release
endorphins, which in turn release dopamine " reward pathways are activated.
This is one of the mechanisms of addiction. (b) Naltrexone is a competitive
antagonist for opioid receptors; blocks effects of endorphins ".es craving for
alcohol and encourage abstinence.
(11) N-Methyl-D-aspartate (NMDA) receptor blockers –
(i) Mechanism - (a) Prolonged use of alcohol upregulates NMDARs [please see
above under “Mechanism of Action”] (b) NMDAR blockers are thus useful
for pharmacotherapy of alcoholism. They attenuate not only the physical
symptoms but also some affective and motivational components of alcohol
withdrawal.
(ii) NMDAR blockers useful in alcohol dependence - (a) Acamprosate
[Campral] (b) Memantine (c) Neramexane
(12) Ondansetron [Zofran] –
(i) 5HT3 antagonist.
(ii) .s cravings for alcohol, especially in early-onset alcoholics.
(iii) Combination of ondansetron and naltrexone is superior than either treatment
alone.
(13) Topiramate (Topamax)
(14) Vitamin supplements - esp thiamine.

ii. Conditioned reflex treatment

(1) Mechanism – Conditioned reflex treatment [CDR] works on the principle of
classical conditioning [syn, Pavlovian or respondent conditioning]. He
observed that the dogs began to salivate in the presence of the lab technician
who normally fed them. Pavlov called these psychic secretions. He then used
a bell to call the dogs to their food and, after a few repetitions, the dogs started
to salivate in response to the bell. Terminologies used in such experiments are
(i) Unconditioned stimulus (US) – food
(ii) Unconditioned response (UR) – Salivation
(iii) CS – Light
(iv) Conditioned response (CR) – Salivation in response to light
(2) Procedure -
(i) With a backdrop of bottles of various alcoholic beverages [CS] the patient is
given various types of liquor [US] together with drugs that will cause
immediate nausea and vomiting [UR].
(ii) After 5-8 daily treatments, unpleasant symptoms are brought on simply by
the sight of a bottle [CR].

g. Cause of death
(1) Hepatotoxicity [most common]
(2) most of above mentioned complications.

h. Postmortem appearances [ch alcoholism]

(1) Esophagus - shows varices
(2) Stomach mucosa -
(i) Hypertrophied
(ii) Color – Deep reddish brown with patches of congestion and effusion.
(iii) Gastritis and peptic ulcer disease
(3) Brain -
(i) Central pontine myelinosis [CPM] - may be associated with a low-salt
vitreous electrolyte pattern.
(ii) Cerebellar vermis atrophy
(iii) Mamillary body atrophy or necrosis [indicative of Wernicke–Korsakoff
syndrome in association with thiamine deficiency]
(iv) Remote (old) brain contusions [consistent with falls, being involved in
fights].
(4) Lungs - Pulmonary infections including pneumonia, aspiration pneumonia,
and abscesses
(5) Heart -
(i) Alcoholic cardiomyopathy
(ii) Dilated
(iii) Shows fatty degeneration.
(6) Peritoneum - Bacterial peritonitis is commonly seen.
(7) Liver –
(i) Congested
(ii) Alcoholic hepatitis
(iii) May be greasy to touch, steatosis.
(iv) May show fatty changes or cirrhosis [contracted, nodular].
(8) Kidneys – Granular degeneration
(9) Bones – Chronic alcoholics show -ed incidence of incidental old healed
fractures. Please see “Battered alcoholic syndrome” above.

10. Alcohol withdrawal syndrome

The alcohol withdrawal syndrome (AWS) is a syndrome seen in alcohol-
dependent individuals, typically within 24–48 hours of consumption of their last
drink.

11. Clinical Examination of a case of drunkenness

Drunkenness is a condition produced in a person, who has taken alcohol in a
quantity sufficient to cause him to lose control of his faculties to such an extent,
that he is unable to execute safely the occupation in which he was engaged at the
particular time.
Salient features:
(1) Clinical diagnosis – Depends on a combination of symptoms and signs. No
single sign or symptom is reliable, except odor of alcohol from breath.
(2) Variability – Different individuals would show different signs and symptoms
with same amount of alcohol intake. Even same individual may show different
 signs and symptoms at different times, depending upon his state of
metabolism.
(3) Individuals showing excessive reaction –
(i) Epileptics (ii) Liver and kidney disease (iii) Mentally unstable subjects (iv)
Past cerebral trauma
(4) Situations needing examination - Police officer would bring a case of
alcoholic for examination most often when the person was driving or causing
disturbance in public after taking alcohol. The following scheme of
examination has been suggested by the Special Committee of the British
Medical Association.

a. Consent
(1) Consent is tricky for examination of an alcoholic.
(2) If consent not taken "Legally it is application of criminal force [S.350, IPC;
ch 2]
(3) If consent taken, and person is later proved to be under the influence - he
may claim that his consent had no value
(4) Examination u/s 53 CrPC - Virtually in all cases police will bring an
alcoholic for examination, after arrest [S.202 Motor Vehicle Act, 1988; S.510,
IPC etc]. Doctor can examine all such cases without consent u/s 53, CrPC.

b. Preliminaries
Record name, age, sex, date of examination etc as in any MLC [ch 11]. Note
specifically the time at the beginning and end of examination.

c. Exclusion of injuries and pathological states

Conditions which simulate intoxication should be excluded. These are
(1) CO poisoning
(2) Drugs [antihistamines, hyoscine, insulin, morphine, sedative hypnotics (eg
barbiturates), tranquillizers]
(3) Head injury
(4) High fever
(5) Impending cerebrovascular accidents
(6) Metabolic disorders [Diabetic precoma, Hyperthyroidism, Hypoglycemia,
Uremia]
(7) Neurological conditions associated with ataxia, drowsiness, dysarthria and
tremors [acute aural vertigo, disseminated sclerosis, epilepsy, intracranial
tumor, Parkinson’s disease] and
(8) Psychiatric disorders [Hypomania, General paresis].

d. History
(1) Take history directly from the accused [even if he is accompanied by a
relative] and observe him keenly as he speaks [note dysarthria, shifting gaze
etc]
(2) ask the time of intake, amount of alcohol, brand [whisky, rum, wine, as it
would indicate conc], mode of intake [Table 2]
(3) Ask history of above illnesses and whether he is under treatment for any
disorder.

e. General physical examination

Please co-relate with signs and symptoms given earlier
(1) Pulse – at the beginning and end of examination.
(2) BP
(3) Temp
(4) skin – dry, moist, pale or flushed
(5) Mouth
(6) Ears –
(i) Examine for gross impairment of hearing
(ii) If there is impairment, is there any gross pathology accounting for it, eg
rupture of TM
(7) Pulmonary – lung disorders, asthma, bronchitis, emphysema
(8) CVS – Pulse, BP etc. Alcoholic heart disease
(9) GIT – enlargement of liver, indicating ch alcoholism
(10) CNS – Whether alert and oriented to time, place and person [ch 11]. In
presence of CNS diseases, tests like gait, stance, muscular co-ordination,
reflexes etc become meaningless. Systemic examination is done to rule out
any pathology or disease.

f. General behavior
(1) General manners and behavior –
(i) Whether excessively aggressive, resists examination, abusive, or overly
submissive. Both situations indicate drunkenness
(ii) Drooling, driveling, dribbling, slobbering etc [saliva flowing outside the
mouth].
(2) State of dress -
(i) Presence of nasal secretions, saliva, vomit etc on clothing. If yes, note their
character, color, smell etc. Whether dried, drying or wet. Is there a wet layer
over dried ones [indicates repeated vomiting etc over a long period of time]
(ii) Soiling of underwear or pants etc by urine, feces. Preserve clothing for
examination
(3) Speech – Note type of speech [over-precise, slurred, thick etc]. Slight
blurring of certain consonants is one of the earliest signs of incoordination of
the muscles of tongue and lips. Certain test phrases or mild tongue twisters
may be used to bring out this difficulty in speech. English speaking nations
mostly use “British Constitution”, “Truly rural” or “West Register Street”, but
local language tongue twisters should preferably be used. In Hindi, two most
common phrases, the author has used with success are “Nandu ke Nana Ne
Nandu ki Nani ko Nand Nagari me Nagin dikhaie” and “Pital ke patile mein
papita pila pila”. A sober person might utter out the sentences or honestly
admit that he is not good at such phrases. Intoxicated person would always
insist on getting them correctly, and make repeated mistakes.
(4) Self-control – Whether able to control himself in response to demands made
on him by the medical staff.

g. Memory and mental alertness

(1) Ask few questions about his movements during preceding few hours.
(2) Details of accidents if any
(3) If he drank at a party, details about who were with him; for what purpose was
the party organized.
(4) If he drank at a pub, what was the cost of each drink, and how much did he
pay in all
(5) few simple sums of addition and subtraction.

h. Handwriting
(1) Ask to copy a few lines from a book or newspaper. Give him a paper without
 lines. Note (i) time taken (ii) repetition and omission of letters or words (iii)
ability to read his own handwriting
(2) Retain both original and the copy for production in court.
(3) Ask subject to sign. Compare signature with those on I-card, or driving
license etc.

i. Eyes

i. General appearance
(1) Eyelids (2) Conjunctivae.

ii. Visual acuity

Note any gross defect. Co-relate with any existing defect before the drinking
episode.

iii. Intrinsic muscles

(1) Pupils – equal or unequal; contracted or dilated; any other abnormality
(2) Reaction to light – Show light in one pupil. Watch both pupils closely. Note
(i) If reaction is brisk, slow or absent [pupillary reflex time].
(ii) What is the reaction in unexposed pupil
(iii) If pupil contracts, how much time does it take to come back to normal
(iv) Does it dilate even if light is continued to be shown.
(v) Whether the pupils become unequal on exposure to light
(vi) Do they equalize immediately or after some time. All observations may need
light to be shown 4-5 times.

iv. Extrinsic muscles

(1) Convergence –
(i) Show a finger to subject and ask him to follow its movement. Then take the
finger in all directions, and see if subject can follow finger. Alcohol
impaired subjects have difficulty smoothly tracking a moving object.
(ii) Next bring finger gradually nearer to the subject. Observe if he is able to
converge his gaze.
(2) Nystagmus – HGN, VGN and PAN. please see above.
(3) Strabismus – note its presence or absence.
j. Gait
(1) Integrity of neuromuscular system is determined by balance and gait.
(2) Ask subject to walk across room – Observe (i) Whether he can walk at all
or not (ii) Manner of walking – If walks, whether feet wide apart or close
together and whether gait is irregular, overprecise, straight or unsteady. (iii)
Reaction time to a direction to turn – does the subject turn at once, or takes a
step or two before turning? (iv) Manner of turning – Does the subject keep his
balance, lurch forward or reel to one side? Does he correct his mistakes in a
normal or exaggerated way?
(3) Walk-and-Turn (WAT) test – One of the 3 tests which form part of the
Standardized Field Sobriety Test (SFST). Usually conducted by police
officers on the spot [in the US], but can be employed by the doctor also. The
subject is directed to take nine steps, heel-to-toe, along a straight line. After
taking the steps, the suspect must turn on one foot and return in the same
manner in the opposite direction. The examiner looks for eight indicators of
impairment:
(i) if the suspect cannot keep balance while listening to the instructions,
(ii) begins before the instructions are finished,
(iii) stops while walking to regain balance,
(iv) does not touch heel-to-toe,
(v) steps off the line,
(vi) uses arms to balance,
(vii) makes an improper turn, or
(viii) takes an incorrect number of steps. 80% of individuals who exhibit ≥2
indicators in the performance of the test will have a BAC ≥ 80 mg%.

k. Stance
(1) Romberg’s test [syn, Romberg maneuver] – Ask the subject to stand erect
with feet together and eyes closed and observe if he sways. Note presence of
any tremors during standing. Stand close by as a precaution in order to stop
the person from falling over. Romberg’s test is +ve if the patient sways or falls
[Romberg’s positive, Rombergism, Romberg’s sign].
(2) One-Leg Stand test [OLS]- One of the 3 tests which form part of the
Standardized Field Sobriety Test (SFST). The suspect is instructed to stand
 with one foot approx 6” off the ground and count aloud by thousands [One
thousand-one, one thousand-two, etc] until told to put the foot down. The
examiner times the subject for 30 seconds. Four indicators of impairment are
observed
(i) swaying while balancing,
(ii) using arms to balance,
(iii) hopping to maintain balance, and
(iv) putting the foot down. Like the WAT test, 80% of individuals who exhibit ≥2
indicators in the performance of the test will have a BAC ≥ 80 mg%.

l. Muscular co-ordination
(1) Following tests are performed -
(i) Lifting 2 objects, eg water filled tumblers from the table and replacing them
side by side in a different position.
(ii) Lighting a cigarette with match
(iii) Picking up medium sized objects from floor
(iv) Placing finger to finger
(v) Placing finger to nose
(vi) Unbuttoning or rebuttoning a coat
(2) Precautions and interpretations -
(i) Non-performance or inadequate performance may indicate alcohol
consumption
(ii) In general no task should be asked to perform which a normal person cannot
perform
(iii) Some persons may have difficulty performing above tasks even under
normal conditions
(iv) A chronic alcoholic may not be able to perform above tasks even when he
has not consumed alcohol.
(v) CNS diseases should have been ruled out.

m. Reflexes
(1) Knee and ankle reflexes – delayed or sluggish
(2) Plantar reflex – May be extensor or flexor.

n. Miscellaneous tests
(1) Color difference threshold
(2) Complex reaction time
(3) Delayed auditory feedback
(4) Flicker fusion test
(5) Glare recovery test
(6) Nerve conduction speed.

o. Field sobriety tests [FST]

(1) Administered by police officers on the spot during drunken driving rather
than by doctors. May be usefully employed by doctors also
(2) The Standardized Field Sobriety Test (SFST) is a battery of 3 tests
developed by the National Highway Traffic Safety Administration
(NHTSA), USA.
(3) The tests are
(i) Horizontal Gaze Nystagmus (HGN)
(ii) Walk-and-Turn (WAT)
(iii) One-Leg Stand (OLS) [please see above for all].

p. Breath alcohol analyser

Also used by police officers on field rather than by doctors
(1) Commonly known as breathalyzer, one can detect alcohol in breath both
qualitatively and quantitatively.
(2) Principle - Ratio of alcohol between blood and breath is 1:2100.
(3) Advantages – can be administered at the spot without requiring complicated
apparatus
(4) Disadvantages - Not reliable, because for venous blood, this ratio keeps
changes as ethanol metabolizes.

q. Bedside tests
Please see above under “acute poisoning”.

r. Collection of specimens
For collection of specimens in the dead, please see “Acute poisoning” above.

i. Blood
(1) Collection procedure "ch 31.
(2) To establish whether the blood alcohol level is rising or declining – two
specimens must be taken at spaced intervals and their alcohol content
compared
(3) Preservatives - [ch 5]. (i) Loss of alcohol etc is prevented through bacterial
action, glycolysis etc. (ii) Samples with adequate preservatives can be kept at
room temperature even for several weeks.
(4) Serum or plasma alcohol concentration is 12-20% higher than that of whole
blood.

ii. Saliva
For collection, please see ch 31.

iii. Urine
(1) Collection procedure "ch 31.
(2) urine conc must be multiplied by 0.75 to get blood concentration, based on
blood-urine alcohol ratio of 1:1.3 [Table 3]
(3) Extrapolation from this blood level back to the time of incident would
indicate blood levels of subject at the critical moment when the accident
occurred [please see rate of fall under “Metabolism and excretion”].

s. Lab tests for alcohol

i. Chemical oxidation methods

Utilize chemical oxidation of ethanol by potassium dichromate.

(a) Cavett’s test

(1) Described by Cavett in 1938.
(2) Micro method - works well with smaller volumes of sample (eg blood,
urine) eg 0.1 mL.
(3) Principle - alcohol is oxidized to acetic acid by oxidizing agents such as
potassium dichromate and sulphuric acid. 1 ml of N/20 dichromate solution
oxidizes 0.575 mg of alcohol.
(b) Kozelka and Hine Test
(1) Described by Kozelka and Hine in 1941.
(2) Macro method - Requires larger volumes of sample, eg 1 mL.
(3) It is a color or spot test. Reagents used are same as above.
(4) Like all color tests the rate of false +ve and false –ve is high.
(c) Weaknesses of above methods
(1) Both are not specific for ethanol. Problems may arise if a dead body is
decomposed or a living subject suffers from diabetes and ketoacidosis
(2) Neither method can be automated. Multiples samples difficult to analyze
(3) one needs to work with corrosive reagents - sulphuric acid and potassium
dichromate in both methods.

ii. Gas liquid chromatography

Most reliable method.

t. Other lab tests

Osmolal gap - -ed. Ethanol is the most common cause of -osmolal gap [ch 31].

u. Opinion
(1) Opinion is given in 4 standard formats
(2) Opinion - After examination of the accused I am of the opinion that the
person examined (i) did not consume alcohol (ii) has consumed alcohol, but is
not under the influence (iii) has consumed alcohol and is under the influence
[intoxicated] (iv) is under the influence of alcohol, and is/but is not a public
nuisance if kept at large.
(3) Samples - The samples collected [blood, urine, saliva etc] must be
mentioned in a separate box in the MLC and following line must be added
after the opinion – Blood [urine, saliva etc] has been sent for chemical
analysis to determine the conc of alcohol. These must be sealed and handed
over to the police along with sample of seal and report.

12. ML importance (of ethyl alcohol)

(1) Alcohol and traffic accidents – (i) Progressive loss of driving ability as
BAC -es. Reasons (a) Concentration impaired (b) Confidence levels -ed, so
more risks are taken by -ing speed etc (c) Judgment dulled – they believe they
are driving better than they are (d) Muscular co-ordination .ed (e) Reaction
time -ed (f) Visual and auditory acuity .ed. Because of this drunken driving is
 prohibited in most countries. [Driving under influence of drugs"ch 46].
(2) BAC and driving ability -
(i) <50 mg% - majority of drivers are not affected
(ii) 50 mg% - (a) tasks which are affected are those which require control of
speed, [eg braking] and those which are required in keeping a vehicle on
course [eg sensorimotor coordination] (b) Boldness -ed (c) Impulsiveness -
ed (d) Tendency to drive faster and more erratically
(iii) 60 mg% - Driver is twice as likely to be involved in an accident as
compared to a sober driver
(iv) 80 mg% - Risk of accident begins to - markedly
(v) 100 mg% - (a) Risk of accident is 12 fold (b) All drivers are affected and
accidents are common
(vi) 150 mg% - (a) Risk of accident is 20 fold (b) driving is distinctly impaired
(3) Drunken driving in India– is prohibited by Motor Vehicles Act, 1988
[MVA, 1988]. (i) S.185(a) – (a) sets legal limit of blood alcohol levels for
driving in India as 30 mg%. (b) Punishment for 1st offence – 6 months or
`2000 fine or both. (c) 2nd or subsequent offence [if committed within 3 y]- 2 y
or `3000 fine or both.
(4) Alcohol and trauma, delayed deaths – Drunk person "suffers trauma
"Intracranial hemorrhages [EDH, SDH] are produced " dies after several days
or weeks "alcohol may have disappeared from blood, but would be present in
EDH and SDH [because it is sequestered from metabolic actions of liver].
Thus in delayed deaths due to alcohol, intracranial hemorrhages may be sent
for chemical analysis [please also see ch 5]. In fact any sequestered
hemorrhage anywhere in the body, eg retroperitoneal hematoma, perinephric
hematoma, hematoma around fractured bones and joints etc may be used for
chemical analysis.
(5) Auto-brewery syndrome –
(i) It is the natural production of alcohol from carbohydrates in the GIT by
persons suffering from intestinal candidiasis [hence the term ‘auto-brewery’
syndrome].
(ii) Candida albicans readily produce ethanol both in-vitro. In-vivo levels may
go up to 80 mg% in Asians who show a -er incidence of a defective allele
of ALDH2 [please see above under “metabolism and excretion”] involved
in metabolism of alcohol.
(iii) Some drunken drivers caught driving under influence of alcohol have taken
the defense that they never consumed any alcohol, but were suffering from
intestinal candidiasis, which produced alcohol in the body. In rare cases this
defense has been accepted.
(6) Brompton’s cocktail– one of its constituents is ethyl alcohol [ch 41].
(7) Drug facilitated sexual assault – Alcohol is one of the drugs used in DFSA
[ch 25].
(8) Embalming fluids – contain both ethanol and methanol. In an embalmed
body determination of these compounds carries no legal value [ch 9].
(9) Endogenous production of alcohol - Endogenous alcohol [syn, endogenous
ethanol, EnEth] is alcohol, which is not ingested but is produced within the
body through metabolic processes [normal metabolism, bacterial activity in
the GIT]. It can be produced both during life and after death
(i) During life - Traces of alcohol are found in all persons, because of
endogenous production.
(ii) After death – due to putrefaction [may vitiate the interpretation of PM
alcohol concentration – ch 9].
(10) Fetal alcohol syndrome [FAS]-
(i) Caused by alcohol consumption by pregnant women.
(ii) The children have a pattern of retarded growth and development, both mental
and physical, with cranial, facial, 1imb, and CVS defects.
(iii) The commonest abnormalities are - (a) abnormal palmar creases (b) cardiac
[especially septal] defects (c) developmental delay (d) mental retardation
(e) microcephaly (f) prenatal and postnatal growth deficiency (g) short
palpebral fissures (h) short upturned nose with sunken nasal bridge (i) thin
upper lip
(11) Forced and voluntary ingestions - S.85, S.86, IPC - please see ch 31.
(12) Loss of alcohol after death -
(i) by evaporation – insignificant
(13) Manner of poisoning -
(i) Accidental– Deaths far rarer than those due to methyl alcohol.
(ii) Suicidal– possible, but virtually unknown
(iii) Homicidal– virtually impossible, because of peculiar smell, taste and large
fatal dose.
(14) Misconduct in public by a drunken person – Punishable u/s 510, IPC -
 Punishment is simple imprisonment for up to 24 hours, or `10 fine, or both.
(15) Mixed ingestions -
(i) Meptazinol - Meptazinol [Meptid] is an analgesic drug used for pain
[postoperative, obstetrical, renal colic]. Death may occur with sublethal
conc of alcohol if ingested concomitantly. A case has been reported where
the victim died with BAC of just 232 mg%.
(16) Mortality rates – Among alcoholics are 2 fold -er. Reasons are same as
those of -er mortality rates among drug abusers [ch 46].
(17) Postmortem diffusion - please see ch 5.
(18) Sudden death -
(i) Alcohol has a toxic effect on myocardium. Produces cardiac arrhythmias
causing sudden death. Other poisons which cause arrhythmias "ch 31.
(19) Widmark’s formula -
(i) Used for - calculating amount of alcohol ingested by a suspect if his blood
alcohol level is known and vice-versa.
(ii) The formula for blood conc : a=cpr, where ‘a’ is the alcohol ingested in gm,
‘c’ the concentration of alcohol in the blood in decigrams%, ‘p’ weight of
the body in kg, and ‘r’ the Widmark constant.
(iii) The formula for urine conc : a=3/4 x cpr, since conc in urine is 4/3 of that
of blood
(iv) Widmark constant - (a) represents Vd for alcohol, which is less for women,
who have more fat compared to men. (b) Value: Males - 0.68; Females -
0.55.
(20) Workplace drug testing [WDT] – is done by many employers to check
alcohol intake among employees during work [ch 46].

B. Methyl Alcohol (CH3OH)

Methyl alcohol (Gk. methy “wine” + hyle “wood) is a colorless, volatile liquid
with an odor similar to ethyl alcohol, and having a burning taste.
Salient features:
(1) Methyl alcohol (methanol, wood alcohol, wood naphtha, wood spirit) is
produced by destructive distillation (heating under vacuum) of wood. What
remains behind is activated charcoal.
(2) Common household products containing it are – antifreeze, paint removers,
 varnish. Used as a solvent in these products
(3) Slang names - In India, it is known as bewada, dalda, French polish, hooch,
khopadi and ladda.

1. Toxicokinetics
(1) Methanol is rapidly absorbed through stomach, intestines, lungs and skin.
(2) Metabolized - to formaldehyde [33 times more toxic than methanol] and
formic acid [6 times more toxic than methanol] [Fig 40.3].
(3) Rate of oxidation – 1/5th of that of ethanol
Memory Aid 11: Toxicity of methanol metabolites
Formaldehyde is a larger word – thus it has a larger toxicity.
3+3=6 " Thus formaldehyde is 33 times more toxic, and formic acid is 6 times

(4) Takes about 3-4 days to completely disappear from body

(5) With repeated doses, tends to accumulate in the blood
(6) Distribution in the body – According to water content of the tissues
[Vd=0.6-0.7 l/kg]. High concentration is found in vitreous [vitreous should be
collected in all cases of alcohol related deaths] and optic nerve.
(7) Elimination –
(i) 80% is excreted unchanged from lungs
(ii) 3-5% is excreted unchanged in the urine.

2. Mechanism of action
(1) - formaldehyde and formic acid conc - formed through metabolism [Fig
40.3]. Both are highly toxic. Slow degradation of formic acid causes its
accumulation in human body.
(2) The selective neurotoxicity of methanol is due to histotoxic hypoxia as a
result of
(i) Inhibition of the cytochrome oxidase complex of the mitochondrial
 respiratory chain
(ii) Inhibition of oxidative phosphorylation by .ing both the intracellular
synthesis of ATP and the ratio of NAD/NADH+.
(iii) -ed oxidative stress [ch 31], caused by formic acid.
(3) Formic acid [metabolite of methanol] causes -
(i) Retinal toxicity and (ii) metabolic acidosis [Formic acid"inhibits
mitochondrial cytochrome oxidase"lactic acid accumulation]. Formic acid
causes most of the characteristic signs and symptoms of methanol toxicity.

3. Signs and symptoms

(1) Toxicity may result by absorption through (i) GIT (ii) respiratory tract (iii)
skin
(2) Onset - Symptoms appear after a latent period of 24 h [range 1-72 h]. The
latent period may be longer if ethyl alcohol is a co-ingestant or shorter if the
volume of methanol is large.
(3) GIT - (i) Nausea, vomiting (ii) Abdominal pain in the form of severe cramps
(iii) Pancreatitis
(4) Vision – Most characteristic symptoms relate to vision
(i) Blurred, misty or dimmed vision [“flashes” or “snowstorm” vision,
“snowfield” vision – as if seeing through a snowstorm]
(ii) Constricted visual fields
(iii) Photophobia
(iv) Nystagmus
(v) .ed light perception
(vi) Seeing spots
(vii) Central and peripheral scotomata [Partial degeneration of field of vision
surrounded by normal vision]
(viii) Complete blindness [Causes - (a) formic acid inhibits cytochrome oxidase
in the optic nerve (b) causes optic neuritis and optic atrophy]
(ix) Ocular examination - (a) pupillary dilatation, (b) loss of pupillary reflexes.
(x) Fundoscopy - (a) Hyperemia of optic disc (b) retinal edema
(5) CNS - (i) Confusion (ii) Dizziness, vertigo (iii) Headache with stiff neck
[meningismus] (iv) Neck stiffness (v) Drunkenness – is not as prominent as
that in ethyl alcohol. Effects are however more prolonged (vi) Delirium and
coma may last 2-3 days [effect on CNS more intense and persistent than with
 ethyl alcohol] (vii) Pupils - dilated and fixed in later stages
(6) Muscular system - Marked muscular weakness
(7) Respiratory system – Dyspnea, cyanosis, odor of alcohol from breath
(8) CVS - Depressed cardiac action leading to (a) Tachycardia (b) severe
hypotension [Alcohol-induced vasodilation, combined with vomiting]
(9) Urinary system - (i) Acute tubular necrosis (ii) Urine – strongly acidic.
Contains albumin traces and acetone
(10) Temperature – Hypothermia
(11) Metabolic acidosis - (i) is of high anion gap type. Causes (a) formation of
formic acid (b) respiratory depression (ii) Blood pH <7.0 indicates poor
prognosis
(12) Elevated osmolal gap
(13) Permanent sequelae in survivors –
(i) Blindness [most common]
(ii) Extrapyramidal movement disorders –
Parkinsonism like syndrome [due to putamen damage]
(iii) Toxic encephalopathy
(iv) Neuropathy

4. Fatal dose
(1) 60-200 ml. Paradoxically larger doses, especially taken quickly may not kill,
because of violet emesis [same as ethyl alcohol above]
(2) Blood levels of 200 mg% are fatal
(3) Hemodialysis must begin when blood levels are 20 mg% or above.

5. Fatal period
(1) 24-36 hours
(2) in some cases may be delayed up to 4 days.

6. Management
(1) Gastric lavage – with 5% bicarbonate solution. 500 mL may be left in the
stomach
(2) Emesis – not recommended, because of potential for CNS depression
(3) Activated charcoal – Not of much use because of limited adsorption of
methyl alcohol. Yet it may be given because it adsorbs other co-ingested
 poisons
(4) Specific antidote is ethanol
(i) Mechanism of action - It competes with methyl alcohol for ADH [step 1 in
Fig 40.3], and prevents conversion of methanol to more toxic
formaldehyde. Methanol is excreted unchanged in the urine.
(ii) Mode of administration - (a) IV route – (I) Dose - 10% ethanol [available as
vials of pyrogen free absolute alcohol] in a dose of 10mL/kg. Serum
concentration to be maintained is 100 mg%. (I) Dose – 1ml/kg of 95%
ethanol in fruit juice [200 mL], over 30 min. For maintenance 0.2mL/kg/hr
as 50% ethanol in fruit juice.
(5) 4-methyl pyrazole [4MP, Fomepizole] -
(i) Competitive antagonist of ADH.
(ii) Advantages over ethanol - (a) reliably inhibits ADH (b) conc do not need to
be monitored as with an ethanol (c) does not cause inebriation (d)
associated with fewer side effects (e) does not require ICU monitoring. For
these reasons, it has become the preferred method of ADH blockade,
despite being significantly more expensive than ethanol.
(iii) Dose - (a) 15 mg/kg IV as an initial loading dose (b) followed by 10 mg/kg
every 12 h. (c) After 48 h of therapy, fomepizole induces its own
metabolism, so the dose must be -ed to 15 mg/kg every 12 h.
(6) Abacavir.

7. Cause of death
(1) Mainly due to acidosis from production of organic acids [mainly formic
acid]
(2) Respiratory failure
(3) CNS depression [minor factor].

8. Postmortem appearances
(1) Cyanosis – marked. Blue color of skin may also be due to methyl violet, a
blue dye often present in methylated spirits
(2) PM clotting of blood – absent
(3) Lungs – congested, edematous
(4) GIT –
(i) Mucus membranes - of stomach and duodenum is congested, inflamed and
 shows hemorrhages
(ii) Small and large intestines - both contracted. Resemble a thick pipe of very
narrow lumen.
(5) Liver – early necrosis, fatty change.
(6) Kidneys – Acute tubular degeneration.
(7) Urinary bladder – mucosa congested.
(8) Brain – congested, edematous, shows hemorrhages.
(9) H/P – Retinal ganglion cells and optic disc show degenerative changes.

9. ML importance (of methyl alcohol)

(1) Manner of poisoning -
(i) Accidental - Mostly. (a) Consumption of spurious liquor [hooch tragedy] (b)
due to its similar smell to white wine. (c) Villagers consume it when ethyl
alcohol is not available, as by ingesting methylated spirit, which is available
as fuel.
(ii) Suicidal – rare.
(iii) Homicidal – rare because of taste and odor, but can be mixed in ethyl
alcohol and offered. Homicidal poisoning in children is known.
(2) Consumption of solox – Solox is the trade name for a shellac and paint
solvent consisting primarily of ethyl alcohol and methanol. Victim may
consume solox as a cheap alternative to alcohol.
(3) Illicit liquor – Illicit liquor, which is made without license and with poor
infrastructure is called hooch, moonshine [because it was produced in night or
during moon light], mountain dew, Tennessee white whiskey or white
lightning. It is mostly methyl alcohol, which can cause accidental poisoning.
Other unintentional adulterants which have been recorded are: Heavy metals,
eg arsenic and lead – Arsenic is a contaminant of lead or solder used in the
stills [apparatus used to distill illegal alcohol]. Thus persons who regularly
consume illicit liquor may slowly develop arsenic or lead poisoning. Secondly
since alcohol is produced by grain and grain is stacked near sills, rodents are
attracted to the area of stills. To kill them rat poison containing arsenic is
frequently used in close proximity to the grain and mash stores. Careless use
of arsenic results in contamination of alcohol.

IV. OPIUM AND ITS DERIVATIVES

A. Opium
Opium (Afim, Poppy tears, Lachryma papaveris) is the coagulated juice of the
opium poppy (Papaver somniferum) or any mixture containing it [S2(xv)
NDPSA 1985]. Powdered Opium is opium dried at a temperature not exceeding
70°C, and reduced to a very fine powder. Powdered Opium yields between 10.0-
10.5% of anhydrous morphine. Endogenous opioid peptides [dynorphins,
Enkephalins, endorphins, endomorphins and nociceptin] are the naturally
occurring ligands for opioid receptors. The term endorphin is used
synonymously with endogenous opioid peptides but also refers to a specific
endogenous opioid, β-endorphin.

1. Plant

a. Cultivation
Because the lab synthesis of morphine is difficult, morphine is still obtained
from opium. It is cultivated in India and other Eastern countries. In India, it is
mainly grown in MP, UP, and Rajasthan.

b. Licensing
In most countries including India, it can be grown only by license from the govt.
In India, legal cultivation is carried out only in MP, Rajasthan and UP. Licenses
are issued by the Central Bureau of Narcotics [CBN].

c. Extraction of raw opium

(1) Opium - comes from the unripe capsules of Papaver somniferum (Gk
papaver, poppy; Somniferum, sleep), which is an annual herb belonging to
family Papaveraceae
(2) Flowers - are white, red or purplish, depending on variety
(3) Capsules - One plant bears 5-8 capsules. Capsules ripen to about 4 cm in
diameter; on ripening, their color changes from bluish-green to yellow.
(4) Extraction of opium – The color change from bluish-green to yellow signals
the optimum time for latex collection. while the capsules are still attached to
the plant, very shallow incisions are made into their wall (lancing) with a
special nushtar having three or four small blades, separated by spaces of about
 3 mm.
(5) Poppy tears - The latex which collects on the capsule walls is known as
‘poppy tears’ (Fig 40.4). On drying up, it becomes raw opium [Gk opos,
juice].
(6) Poppy seeds -
(i) The capsule has several chambers (loculi) which contain thousands of white,
tiny, kidney-shaped seeds known as khus khus. They are less than 1mm in
length, and very light. One capsule contains more than 1000 seeds. 3500
poppy seeds weigh about 1 gram.
(ii) Poppy seeds are non poisonous, demulcent and nutritive and used for
flavoring food. Poppy seed bagels are common in the West.
(iii) They yield 45–50% oil (poppyseed oil), which is used for cooking purposes.
Also contain traces of morphine [7-60μg/g] and codeine.
(iv) Poppy straw – Empty poppy capsule without the seeds (also opium straw,
poppy chaff, poppy head, poppy pod or post ka doda).

d. Raw opium
(1) Physical characteristics -
(i) Appearance - Opium appears as a more or less rounded, oval, brick-shaped or
elongated, somewhat flattened mass, usually about 8-15 cm in diameter and
weighing about 0.3-2 kg each.
(ii) Odor - Strong characteristic
(iii) Taste - bitter [due to alkaloids present]
(iv) Consistency - It tends to be plastic when fresh, but becomes more dense and
tough on storage.
(2) Alkaloids – contains about 25 alkaloids, combined with meconic, lactic and
sulfuric acids. Chemically they form two groups (a) Phenanthrenes
[morphine [Indian Opium yields approx 9.5-14%. The morphine content is
standardized in the Govt opium factory at Ghazipur, to contain 10% morphine.
This is known as Standard or Standardized Opium. The total alkaloids of
this opium are 40%], codeine (0.5%) and thebaine (0.2%)] and (b)
Benzylisoquinolines [noscapine (formerly called narcotine) (6%), papaverine
(1%), narceine(0.2%)].
(3) Terminology – Differences between opiates and opioids - Opiates are
drugs derived from opium, and include natural products morphine, codeine,
thebaine and semisynthetic congeners derived from them eg heroin. Opioid
(Gk eidos, similar to) on the other hand – is a much broader term which refers
to any agent that binds to opioid receptors. It is a more inclusive term applying
to all agonists and antagonists with morphine-like activity. The term opioid
would thus include completely synthetic products such as diphenoxylate,
fentanyl, loperamide, methadone, pethidine (meperidine), propoxyphene,
which are not included under opiates.
Memory Aid 12: How to differentiate opioids from opiates
Opioi d is a much broader term.

2. Classification of opioids
(1) Natural – morphine, codeine
(2) Semi-synthetic – Heroin, Pholcodeine. Many others like -Hydrocodone,
Hydromorphone, Oxycodone and Oxymorphone are not used in India.
(3) Synthetic – Dextropropoxyphene, Diphenoxylate, Fentanyl, Methadone,
Paregoric, pethidine [Meperidine], propoxyphene, Tramadol.

3. Absorption, distribution, fate and excretion

(1) Opioids -
(i) Absorbed from the GI tract and through rectal mucosa.
(ii) Placental barrier - Most opiates cross placenta, and appear in fetal circulation
within 5 min following maternal IV injection.
(2) Morphine -
(i) There is significant first-pass metabolism in the liver, because of which oral
 routes are less effective than parenteral.
(ii) Half life of morphine - in plasma is 2 hours.
(iii) Elimination of morphine - (a) is by glomerular filtration. (b) Enterohepatic
circulation of morphine and its glucuronides occurs, which accounts for the
presence of small amounts of morphine in feces and urine for several days
after the last dose.
(3) Codeine - and its analogs [levorphanol, oxycodone, methadone] have a
lower first-pass metabolism in the liver.
(4) Heroin (diacetylmorphine) - is rapidly hydrolyzed to 6-monoacetylmorphine
(6-MAM), which in turn is hydrolyzed to morphine.

4. Mechanism of action
Opium acts through opioid receptors, which are a group of G protein-coupled
receptors (GPCRs). These are mainly located in the CNS.

5. Acute poisoning

a. Signs and symptoms

i. On contact
(1) If a person is sensitive to opium, he may experience
(2) Erythema
(3) Itching dermatitis
(4) Urticaria.

ii. Ingestion
Symptoms begin within half an hour upon oral ingestion. It is customary to study
the symptoms as occurring in 3 stages.

(a) Stage of excitement [1st stage]

(1) Duration – Very short. This stage may even be absent, if a large does is
taken
(2) Euphoric Symptoms - -ed mental activity, -ed sense of well-being, Euphoria,
Freedom from anxiety, Talkativeness
(3) Dysphoric Symptoms – Seen sometimes. Excitement, Flushing of face,
Hallucinations, Maniacal condition and Restlessness
(4) Seizures – Seen especially in neonates.
(i) May cause rhabdomyolysis, hyperkalemia and ARF.
(ii) Mechanism - Hypoxia.
(5) Signs –
(i) Odor of opium + [in all stages]
(ii) Pulse rate -ed
(6) In children – Convulsions may be seen.
(b) Stage of stupor [2nd stage]
(1) Symptoms –
(i) Initially - Drowsiness, feeling of heaviness in the limbs, giddiness, headache,
incapacity for exertion, itching sensation all over the body [through release
of histamine], nausea and vomiting [through stimulation of CTZ].
(ii) Later – Uncontrollable desire to sleep. The patient lies motionless with eyes
closed. Initially he can be roused, but later goes into stupor.
(2) Signs -
(i) Pupils - contracted
(ii) Conjunctiva - congested
(iii) Face and lips - cyanosed
(iv) Pulse and respiration normal.
(c) Stage of narcosis or coma [3rd stage]
(1) CNS depression -
(i) Patient passes into coma from which he cannot be roused.
(ii) All reflexes lost
(2) Signs -
(i) BP., RR. [3-4/min], stertorous breathing [bronchospasm via histamine
release], Gurgling [accumulation of pulmonary edema fluid], Temp.
(ii) Conjunctiva congested
(iii) Face - pale
(iv) Pupils - (a) Pin point [most characteristic]. (b) Do not react to light (c)
During last agonal phase, they dilate. (d) The classic triad of opioid toxicity
is miosis, respiratory depression, and CNS depression (coma)
(v) Pulse – slow
(vi) Secretions - abolished, except sweat
(vii) Skin - cold and clammy [covered with perspiration]
(viii) Muscles - flaccid and relaxed
(ix) Gastric emptying – delayed due to coma
(3) In cases of fatality –
(i) Lividity of the body -s.
(ii) Pulse becomes slow, irregular and imperceptible,
(iii) Respiration becomes Cheyne-Stokes in type.
(iv) Finally death occurs from asphyxia.

b. D/d
Look for following 7 characteristic signs in opium poisoning: (i) Pupils –
pinpoint, not reacting to light (ii) R/R., (iii) pulse., (iv) temp. (v) Odor –
characteristic (vi) Skin – moist, perspiring (vii) Coma. None of the other
conditions will show all seven. D/d is as follows.
(1) Alcoholic poisoning [acute] – (i) breathing – slow, stertorous (ii) eyes -
congested (iii) face - hyperemic (iv) pupils – dilated; reacting to light (v) odor
- of alcohol (vi) Temp – subnormal
(2) Barbiturate – (i) BP - . (ii) Coma – deep (iii) Deep reflexes – depressed (iv)
Pulse – thready (v) Pupils – dilated (vi) Respiration – shallow (vii) Response
to painful stimuli – diminished or none (viii) Temp – subnormal
(3) Carbolic acid – (i) Lips and mouth – show white patches (ii) Odor –
phenolic (iii) Urine – greenish black [carboluria]
(4) Cerebral hemorrhage - (i) Onset - sudden (ii) History - of hypertension (iii)
Muscular – Paralysis, usually hemiplegia (iv) Old age (v) Plantars – bilateral
extensor (vi) Pulse – slow, full (vii) Pupils – dilated (viii) Respiration –
Cheyne-Stokes (ix) Temp -
(5) Cerebral malaria – (i) Fever with chills and rigors (ii) Hepatosplenomegaly
(iii) MP+
(6) Cerebral trauma – (i) History – of head injury (ii) Bleeding – from nose,
mouth, ears (iii) Cranial nerves – dysfunction (iv) Pulse – initially rapid; later
slow (v) Pupils – contracted, unreactive to light, sometimes unequal (vi)
Respiration – Cheyne-Stokes, irregular, rapid, (vii) Subconjunctival
hemorrhages
(7) CO poisoning - (i) History – of exposure to gas [eg sleeping in a closed
room with fire] (ii) Skin color – cherry red (iii) Convulsions (iv) Blood
examination – shows COHb
(8) Coma [Diabetic] - (i) Onset – Gradual (ii) Breath – acetone odor (iii) Face-
flushed (iv) Intraocular pressure - . (v) Respirations – slow and deep (vi) Temp
– subnormal (vii) Urine – contains sugar and acetone
(9) Coma [Epileptic] - (i) Characteristic epileptiform seizures (ii) Face and lips
– cyanosis (iii) Mouth and nostrils – show froth (iv) Tongue – bitten (v) Pupils
– fixed and dilated (vi) Respiration – slow (vii) Skin – flushed (viii) Recovery
from coma – rapid
(10) Coma [Hysterical] - (i) More common in – females (ii) Previous history –
of convulsions (iii) Attitude – unusual (iv) Reflexes – normal (v) Usually
occurs – in presence of audience
(11) Coma [Uremic] - (i) Onset – gradual (ii) General anasarca (iii) Face – pale
(iv) Breathing – Cheyne-Stokes (v) Odor – ammoniacal (vi) Urine – shows
albumin, blood casts
(12) Encephalitis - (i) Onset – acute (ii) Involuntary movements + (iii) Ocular
palsies + (iv) Temp - - (v) CSF – specific changes
(13) Heatstroke - (i) History of – prolonged exposure to high temperature or sun
(ii) Conjunctivae – congested (iii) Skin – dry (iv) Sweating – absent (v) Temp
- - (vi) Circulatory collapse, convulsions
(14) Meningitis - (i) Onset – gradual (ii) Signs of – meningeal irritation (iii)
Temp - - (iv) CSF – specific changes.

c. Tests
Marquis’ test - Suspect residue + 3 cc of Marquis Reagent [prepared by
dissolving 5 ml of 40% formaldehyde in 100 ml of conc H2SO4]"(i) If morphine
present, it gives a fine purple-red color, changing to violet and then to blue. (ii)
Amphetamine - gives a yellow–orange color.

d. Fatal dose
e. Fatal period
6-12 hours.

f. Management
(1) ABCDE of resuscitation - Ventilation support, oxygenation[ch 32].
(2) Decontamination –
(i) Emesis - induced by ipecac is not recommended, because of potential for
CNS depression and seizures
(ii) Gastric lavage – with KMnO4. Useful even if opioids are taken parenterally
because of enterohepatic circulation. For the same reason, leave about 250-
300 cc of KMnO4 after lavage is over [ch 32 for details].
(3) Evacuation of intestines – to prevent reabsorption (i) sodium sulphate orally
30 g (ii) enema twice daily for 2 days
(4) Activated charcoal [ch 32]
(5) Antidotes –
(i) Naloxone - (a) Routes - (I) IV [most preferred]. May also be given (II)
sublingually, (III) intramuscularly, (IV) intranasally or (V) instilled down an
endotracheal tube. Since repeated doses are required, naloxone infusion is
better. (b) Dose - 1.2 mg [adult]; 0.4 mg [child]. Repeated till a total of 75
mg in 24 hours is given. (c) Dangers - (I) Reversal of a narcotic coma can
 precipitate sudden narcotic withdrawal and may cause the patient to behave
dangerously towards himself and staff. (II) Neonates of addicted mothers
may have severe withdrawal effects. (III) Anticholinergic crisis - if ingested
narcotic was contaminated with scopolamine [please see below – “additives
of Heroin”].
(ii) Naltrexone - Orally. Dose 50 mg/day. Also used to treat opiate addiction.
(iii) Nalmefene - Naltrexone derivative. Pure opiate antagonistic effects. (a)
Route - IV most common. Also IM or S/c. (b) Dose - Begin with 0.1 mg. If
withdrawal reaction does not occur, administer 0.5 mg, followed by 1 mg in
2-5 minutes if necessary.
(iv) Physostigmine – 0.04mg/kg IV for reversing respiratory depression, if
regular opiate antidotes [naloxone] are not available. Mechanism – it -es
Ach content of reticular formation of brainstem which is suppressed by
opiates.
(v) Antidotes and other therapies no more recommended - (a) Amiphenazole (b)
Analeptics – eg amphetamine, caffeine, ephedrine (c) Atropine – Once a
favorite antidote because most pharmacological actions of the two drugs are
antagonistic. Atropine stimulates respiration; morphine depresses it.
Atropine dilates pupil; morphine contracts it. Atropine -es body temp, and
reddens skin; morphine .es body temp and produces pallor. Atropine .es
body secretions; morphine -es them. Thus it intuitively appeared to be a
good antidote. However it is no more recommended because it can cause
death by paralyzing the motor and sensory nerves just like morphine. (d)
Levallorphan [Levorphanol] (e) Nalorphine (f) Once it was common to ask
patients to walk about in the open air to help excretion. No more
recommended.
(6) Rhabdomyolysis induced ARF –
(i) Aggressive fluid replacement
(ii) Diuretics – furosemide, mannitol to maintain urine output.
(7) Coma cocktail – only when identity of poison not known [ch 32].
(8) Immunotherapy - Vaccines that would generate antibodies to sequester the
drug and prevent its access to the brain. Currently under development for 4
major drugs of abuse – cocaine, methamphetamine, morphine/heroin and
nicotine.
(9) Symptomatic treatment -
(i) Convulsions – Benzodiazepines 5-10 mg stat; repeat every 5-10 min if
needed. Generally not needed if naloxone is available.
(ii) Hypotension – ch 32.

g. Cause of death
Respiratory failure.

h. PM appearances
(1) PM Staining – well marked, cyanotic
(2) Smell – of opium from corpse. More noticeable as abdomen is opened. Not
felt if body is putrefied
(3) Signs of asphyxia (i) Face and nails-cyanosed
(4) Mouth – Froth
(5) Trachea, bronchi – congested, full of froth, inhalation of vomit
(6) Lungs – edematous, congested
(7) Stomach – lumps of opium
(8) Brain, meninges - congested
(9) All viscera – congested
(10) Blood – dark and fluid.

6. Chronic poisoning
Chronic poisoning [morphinism, morphinomania] is seen in addicts after a long
period of usage.
Salient features:
(1) Habit is acquired by young people as morphine is considered an aphrodisiac
(2) Addicts can tolerate 3-6 g/d.
(3) This section deals with chronic poisoning due to oral [classical] use [opium
eaters]. More modern use is to take injections of heroin [please see below].

a. Signs and symptoms

(1) General – (i) Emaciated (ii) disturbed sleep, insomnia (iii) Restlessness and
irritability [with periods of disinterest and depression in between] (iv) weak
(2) Pupils - contracted
(3) Tongue – dry, furred
(4) GIT – Anorexia, nausea, marked constipation
(5) Immune system – is compromised.
(i) Innate immunity and adaptive immunity - both depressed. (a) .es proliferative
capacity of macrophage progenitor cells and lymphocytes. (b) functioning
of immune cells is compromised
(ii) Mechanism - (a) direct action of opioids on immune cells. immune cells
differentially express classical opioid receptors. These binding sites mediate
the antiproliferative effects of morphine. (b) indirect centrally mediated
pathways.
(6) CNS – (i) Dementia or mania (ii) hallucinations (iii) intellectual and moral
deterioration (iv) Loss of memory (v) mental fatigue (vi) neurasthenia
(7) Sexual- impotence.
(8) Skin –(i) pigmentation around mouth and eyelids (ii) generalized pruritus.

b. Management
Please see under Heroin.

c. PM appearances
Same as that of heroin [please see below]. Only appearances related to IV
injection would be missing.

7. ML importance (of opium)

(1) Ideal suicidal poison – because death is painless. In order to commit suicide,
opium is usually mixed with mustard oil or asafetida [Hing in Hindi] under the
mistaken notion that these substances - the absorptive power of opium.
However their presence does make it more difficult to remove opium by
gastric lavage.
(2) Homicidal poison – Used only rarely, because of bitter taste, characteristic
smell and dark brown color.
(3) Euthanasia – Morphine is one of the favored drugs for euthanasia [ch 2]
[also barbiturates; please see below]. Many believe that the British general
practitioner John Bodkin Adams [1899 –1983] euthanized his patients with
morphine [see case studies below].
(4) Accidental poisoning –
(i) Occurs in addicts
(ii) Children – can be accidentally poisoned (a) when they accidentally swallow
 crude opium or opium pills meant for their addict parents (b) Parents –
generally of the labor class – usually drug their children intentionally so
they can sleep while they go to work (c) In olden times, Ayahs [ladies hired
for baby-sitting] were known to smear their nipples with opium mixed with
honey, and allow child to suckle their breasts, so the child could go to sleep.
(5) Persons extraordinarily prone to opium poisoning – children, adults
suffering from
(i) Addison’s disease
(ii) Asthma [morphine causes histamine release]
(iii) Ch liver disease
(iv) Myxedema.
(6) Cattle poison – rarely
(7) For doping race horses
(8) -ed Arsenic levels are found in opium eaters [please see ch 36 – MLI of
arsenic].
(9) Consumed before undertaking acts of courage
(10) Opium frequently smuggled in condoms which are swallowed [please see
ch 46 – Body packer syndrome]. May cause death if condoms rupture in GIT.
(11) Opium habit – Opium is usually taken by mouth but may be taken in some
unconventional ways
(i) Kasoomba [poppy tea] – A decoction made by boiling opium poppies in
water, and consumed on festive occasions. Has mild euphoriant properties.
Used for psychoactive effects, but also as a herbal remedy for minor
ailments. [please see ch 41 for “cannabis tea”]
(ii) Bhujri - A preparation made by frying green ripe capsules in butter or ghee
(clarified butter) is eaten by addicts
(iii) Halwa - A sweet prepared from the juice of green poppy capsules is also
consumed by addicts.
(iv) Chandu, Madak or Opium dross – Smokable form of opium

B. Heroin (Diacetylmorphine)
Heroin (3,6-diacetylmorphine, diamorphine, morphine diacetate), is a semi-
synthetic opioid drug synthesized from morphine.
Salient features:
(1) Chemistry - It is the 3,6-diacetyl ester of morphine [di-acetyl-morphine] and
a morphine prodrug. Can be prepared by mixing morphine with acetic
anhydride [(CH3CO)2O].
(2) Potency - Administered orally, heroin is 1.5 times more potent than
morphine. Parenterally it is 2-4 times more potent. The enhanced euphorigenic
effect is called “rush”.
(3) Metabolism – Metabolized rapidly to 6-monoacetylmorphine, and then to
morphine. Chemical analysis will reveal morphine and 6-monoacetylmorphine
but not heroin. Half life of heroin is 38 min.
(4) Reason for higher potency - Heroin has a lower affinity for the µ receptor
than does morphine, yet is more potent, because
(i) Its metabolite 6-monoacetylmorphine, is a more potent µ agonist than
morphine.
(ii) Enhanced blood-brain barrier penetration.

1. Forms of heroin
Heroin is available in 2 distinct chemical forms: salt [hydrochloride] or base
[pure alkaloid].
(1) The hydrochloride salt – is typically a white powder. It was the common
form of heroin available prior to the 1980s. Its high water solubility allows IV
and IM administration.
(i) IV administration - is called mainlining, and users are known as mainliners.
Because the needles used are contaminated, the user gets needle track
ulcers.
(ii) IM or SC administration - If the user cannot locate a vein, he would lift the
skin and inject subcutaneously or IM [Skin popping]. Such users get map
shaped ulcers [geographical ulcers]
(2) Alkaloidal base – is currently the more prevalent form of heroin. Its color is
brown [brown sugar] or black [black tar heroin].
(i) Brown sugar - acquires a brown color because heroin may be mixed with
coffee powder, coco, jaggery [gur] or even brick powder by some dealers.
(ii) Black tar - refers to an impure South American variety. It is black, heat
stable, insoluble in water, rubber-like. Usually produced in provisional
factories in the vicinity of poppy fields and is thus often contaminated by
spores. Drug abusers avoid to inject it IV because it causes sclerosis. S/c
 injection causes spores to gain access to the s/c tissues"They multiply there
due to the anaerobic environment and produce neurotoxins which inhibit the
release of Ach at the NMJ"respiratory paralysis.

2. Additives [of street drugs]

Additives of heroin
Heroin mixed with additives is known as dope, junk or smack. Common
additives are
(1) Quinine -
(i) Mimics the bitter taste of heroin [misleads clients].
(ii) Supposed to prevent malarial transmission due to shared needle use. First
used in 1930s in New York City when an epidemic of malaria among IV
heroin users was common.
(iii) Quinine adulteration currently is much less important than it was in the past.
(2) Scopolamine – Was commonly used in the northeastern US in 1995.
Normally symptoms of scopolamine remain unmasked due to heroin.
Administration of naloxone causes reversal of the opioid effects " unmasking
of the effects of scopolamine " anticholinergic crisis.
(3) Strychnine -
(i) Mimics the bitter taste [as quinine]
(ii) May cause sudden death if quantity of strychnine is too much. The needle
may still be in the vein [accidental hot shot]. Also seen when the addict
gets a purer sample than the one he has been using. Another situation is
when an addict is given a deliberate overdose, and then either smothered,
strangled or drowned in the bath [homicidal hot shot].
(4) Others - Acetaminophen, amphetamines, caffeine, cocaine, lactose, lead,
mannitol, methaqualone, phenobarbital and thallium. Thallium is a common
component of traditional depilatory powders which are used to - the wt of
heroin.

3. Combinations
Speedball - Refers to the hazardous IV use of heroin and cocaine [or
amphetamine] together. The combination when smoked is known as
moonrocks.
4. Administration

a. Hydrochloride salt
This is usually injected.
(1) The works – refers to the IV apparatus used by narcotic addicts [please see
ch 46 for diagram].
(2) Typical heroin bag – contains 100 mg of white or brownish powder [1-15
mg heroin + 0-40 mg quinine + various other additives mentioned above]. If
the addict has been using a bag containing, say, 1 mg of heroin, and on one
occasion he gets a purer brand, say containing 15 mg, he may die suddenly
[hot shot; please see above also].
(3) Cooker – Bottle top or spoon.
(i) Contents of envelop are emptied in it, water is added and heated by a match
till the powder dissolves.
(ii) Solution is drawn through a piece of cotton [sometimes obtained from the
tongue of a shoe].
(iii) The belief is that cotton absorbs impurities and germs, making the solution
sterile. [it actually causes “cotton fever”. Please see below]
(iv) Scene of crime examination [ch 46] often reveals cooker with recent soot
underneath its surface [due to heating].
(4) Syringe – The homemade eyedropper syringe is preferred to traditional
medicinal syringe, because it is more easily manipulated with one hand.
(5) Tourniquet – belts, elastic bands or shoe laces are used as tourniquets. The
needle is inserted into the vein [mainlining]. Skin poppers do not use
tourniquet.
(6) Booting – Once the needle is in the vein, the addict pushes the drug and then
draws the blood up. The process is repeated several times in order to fully
inject the drug. This is known as booting.

b. Alkaloidal base
(1) Chasing the dragon - Because of its heat stability it can be smoked. Addicts
inhale a thick, white pyrolysate that is generated by heating heroin base on an
aluminum foil using a hand-held flame. Although there is some wastage [some
of the heroin effluvium is dissipated into the surroundings], it is still preferred
 because it does away with injections, which can cause infections and leave
tell-tale signs on arms. Sometimes it is mixed with caffeine or barbiturates;
this improves the sublimation of heroin and enhances the yield.
(2) IV usage – is difficult, because of alkaloid’s insolubility in water. Possible in
2 ways - heating the heroin until it liquefies or mixing it with acid.

5. Metabolism
Please see above under the heading “Opium”.

6. Signs and symptoms

Heroin is rarely – if ever – taken by mouth. Signs and symptoms are same as in
opium, but due to IV administration, all stages seem to merge in one.

a. Acute
(1) Intense euphoria, which lasts for several minutes
(2) followed by sedation for about 1 hour
(3) Effects completely lost in 3-6 hours.
(4) There may be systemic reaction with fever and chills after injection (‘dirty
hits’).
(5) spongiform leukoencephalopathy - caused by inhalation of heroin
pyrolysate.
(6) Allergic skin reactions – due to allergens in the drug sample. Angioedema,
bullous drug reaction, Eczemas, maculopapular exanthema, urticaria,
vasculitides.

b. Chronic
(1) General – Emaciation [lack of nutrition]
(2) GIT - (i) Anorexia (ii) Constipation
(3) Sexual - Impotency
(4) Signs associated with use of infected needles -
(i) Systemic infections - hepatitis, HIV, malaria.
(ii) Muscles – (a) myopathy. (b) Partly due to chronic infection, but is
exacerbated by an auto-immune response to damaged muscle. (c) H/p –
affected areas show fibre necrosis, replacement fibrosis and infiltration by
lymphocytes and polymorphs, which extends far beyond the area of
 injection.
(iii) Region lymph nodes - enlarged
(iv) Cutaneous infections - (a) abscesses, erysipelas, phlegmons [walled off
inflammatory mass with or without pus that is palpable on physical
examination]. Pathogens involved belong to body’s own flora [S. aureus,
streptococci species]; often multibacterial infections; rarely gram-negative
bacteria, anaerobes. (b) Anthrax - Rare after i.v. injections; caused by
Bacillus anthracis. (c) Necrotizing fasciitis - Rare after “skin popping” (d)
Nodes, pustules caused by Candida albicans (e) Wound botulism - after
“skin popping”, -ed risk with black tar heroin. Caused by Clostridium
botulinum.
(5) Skin –
(i) Injection marks – Most common injection site is the antecubital fossa
followed by forearms and back of hands. As these sites get scleroses other
sites are chosen eg neck, groin, ankles and penis
(ii) Some fingers and toes may have been lost due to vascular damage
(iii) Dermal abscesses
(iv) Dry, postinflammatory hyperpigmentation along sclerosed vessels.
(v) Ulceration - (a) geographical ulcers, needle track ulcers, skin tracks, track
marks. (b) Site - on scalp, neck, sublingual areas, shoulder, inguinal region,
penis, vagina, popliteal area, ankle and foot. May be on unusual sites eg
inner surface of lip, beneath the tongue or beneath penile foreskin. (c)
Healing by fibrosis – may produce hyperpigmented macules or
circumscribed, retracted scars which resemble those from smallpox
vaccinations. May be atrophic, sunken, translucent [tissue paper scars].
Microscopic examination of scar tissue shows – foreign material eg
fragments of cloth, cotton, talc or unidentifiable matter with surrounding
foreign body giant cell reactions.
(vi) Signs due to addict’s attempts to hide needle puncture marks from law
enforcement authorities - (a) Elaborate tattoos (b) cigarette burns (c)
damage to skin caused by abrading it with pumice stone or sandpaper or by
using escharotic chemicals
(vii) Prurigo nodules, excoriations.
(viii) Hematoma, necroses - due to wound healing disturbances
(ix) Punctures, petechiae - Below the tourniquet.
(x) Shooting tattoo – Punctate areas of black discoloration [soot tattooing]. Due
to foreign material introduced through injection.
(xi) Scabies, pediculosis capitis/corporis, tinea, impetigo contagiosa - Due to
secondary neglect, homelessness.
(6) Hands - Chronic edema, secondary to occlusive thrombophlebitis in the
forearms, lymphatic insufficiency and direct toxicity of injected drugs [Puffy
hand syndrome]. Arm and forearm edema are voluminous and may cause
functional disturbances.
(7) Pulmonary hypertension – due to excessive microcrystalline pulmonary
emboli.

7. Tolerance
Occurs very rapidly (within days). Dose may have to be increased more than 100
times the original.

8. Complications
These are general complications of drug dependence, where drug is injected
through unsterile equipment
(1) Abscess formation
(2) endocarditis
(3) Infections transmitted through needles [AIDS, hepatitis, malaria]
(4) Pigmented scars at sites of injection
(5) Veins – in arms, hands, legs etc are damaged and thrombosed. Show
phlebitis. Become dark in color, hard and cord like due to thrombosis and
fibrosis, and may ulcerate. Upon healing, show white or silvery linear scars
(6) septicemia
(7) Due to general apathy and self neglect - (i) Dental decay (ii) Malnutrition
(iii) Infections – pneumonia, tuberculosis
(8) Renal –
(i) Amyloidosis - associated with s/c drug injection, and chronic soft tissue
infection [‘skin poppers’ amyloidosis]. It particularly affects African-
Americans
(ii) Heroin associated nephropathy - characterized by nephrotic syndrome and
rapid progression to renal failure, proteinuria. H/P - focal segmental
glomerulosclerosis.
(iii) Renal disease related to HIV, HBV and HCV
(iv) hepatitis-C-related membranoproliferative glomerulonephritis (MPGN).
(9) Cotton fever -
(i) It is a febrile condition due to inadvertent injection of cotton fibers in their
veins by drug addicts.
(ii) Etiology - (a) It is due to the practice of addicts putting cotton in their drug
solutions to remove germs [please see above under the heading “method of
injection”]. (b) Also because many addicts use heroin reclaimed from
previously used cotton filters. Enterobacter agglomerans [a bacterium]
thrives in cotton fibers; enters bloodstream " fever.
(iii) Symptoms - (a) fever, (b) chills [violent shaking or shivering – thus cotton
fever also known as “the shakes”], and (c) shortness of breath. Occur
immediately after injection or within an hour.
(iv) Prognosis - good.
(10) Drug abuser’s elbow - Myositis ossificans develops in drug abusers,
caused by repeated, inept needle punctures. The muscle around the elbow is
replaced with scar tissue or with a calcific mass (extraosseous metaplasia).
(11) Foreign-body embolism - Talcum powder embolism.
(12) Psychiatric complications
(13) Involvement in accidents – is common due to .ed alertness
(14) Need for money – leads to crime, theft, prostitution, living in squalor
(15) Personal violence and murder
(16) Clostridial Infections – Uncommon. Present as wound botulism or tetanus.
(17) Death – due to hot shot [please see above], hypersensitivity to heroin or any
of its adulterants.

9. Management

a. Acute intoxication
(1) Decontamination – Gastric lavage [as in opium above] even if drug was
administered IV, because of enterohepatic circulation of all opioids coupled
with duodenogastric reflux. In fact in IV administration, stomach
concentration of drug is often higher than that in blood.
(2) Coenzyme Q – 300 mg qds, for spongiform leukoencephalopathy
(3) Rest same as in opium.
b. Chronic intoxication
Detoxification is the primary aim. This is a mode of treatment in which the
dependent person is “taken off” heroin. Detoxification should only the done
under expert guidance of a specialist. Paradoxically two contrasting
approaches are followed – one in which agonists are given [substitution drugs,
eg methadone], and the other in which antagonists are used [eg naltrexone]. Both
are so-called conventional detoxification methods and both require between 3-
21 days for completion of treatment. In contrast anesthesia-assisted opiate
detoxification is completed within 4-6-hours.

i. Conventional detoxification methods

(a) Use of substitution drugs [Opioid replacement therapy (ORT)]
(1) Principle -
(i) Replaces an illegal opioid drug [eg heroin] with a longer acting but less
euphoric opioid taken under medical supervision. As the treatment
completes, the addict does not experience withdrawal symptoms and drug
cravings.
(ii) Results - (a) while receiving opioid maintenance therapy - 40-65% of
patients are able to maintain complete abstinence from opioids. 70% to 95%
are able to reduce their use significantly. (b) After discontinuing
maintenance therapy - About 7% patients remain abstinent from opioids for
90 days after discontinuing maintenance therapy. <2.5% patients remain
abstinent from opioids for 1 year.
(2) Drugs –
(i) Methadone – Synthetic μ receptor agonist (a) Dose - 40 mg daily. Prevents
withdrawal symptoms. 80 mg in chronic addict (b) dose must be .ed
gradually by 20% daily. If signs of withdrawal reappear, dose reduction is
slowed down [Methadone Maintenance Treatment Program (MMTP)].
There are concerns that by this therapy heroin addict will ultimately
become methadone addict, but this is not entirely true. Reasons are
(1st)Methadone is less addicting (2nd)Has a longer half-life (3rd).s possible
criminal behavior [which is generally associated with procurement of drug]
(4th) Has a much milder withdrawal syndrome. (c) Although often
successful, some methadone users continue to use heroin or other illicit
 substances. (d) It was not available in India for a long time, but since 2012,
it has become available.
(ii) Buprenorphine (Subutex) - Partial µ agonist. Produces a “generalized feeling
of contentment” rather than a heroin-like rush and euphoria. Withdrawal
syndrome from buprenorphine is milder. It is a gentle agent for use in rapid
opioid detoxification. (a) Dose – 8-16 mg sublingually [because of its poor
oral bioavailability]. (b) Initial dose - Because it competes with the extant
opioid for the µ receptor, it may produce acute opioid withdrawal. For this
reason the initial dose must be administered in the presence of a physician.
(c) Subsequent doses - Following the initial doses of buprenorphine,
tablets containing both buprenorphine and naloxone (Suboxone) are
prescribed.
(iii) LAAM [Levo-α-acetylmethadol] [syn levomethadyl acetate] [trade name,
Orlaam] - It is a synthetic opioid similar in structure to methadone.
Approved in 1993 by the U.S. Food and Drug Administration for use in the
treatment of opioid dependence. It is indicated as a second-line treatment
for the management of opioid dependence if patient fails to respond to
drugs like methadone or buprenorphine. Not available in India.
(b) Opioid antagonists
Most preferred is
(1) Naltrexone – Orally effective, potent. Dose – 100 mg on Mondays and
Wednesdays. 150 mg on Fridays. Combined with clonidine, it is a very
effective method of treatment. Less preferred are
(2) Nalorphine – partial antagonist
(3) Naloxone – has to be administered parenterally.
ii. Other methods
Clonidine [Catapres]- (i) Dose - 0.3-1.2 mg/d orally. Tapered off in 10-14 days.
Can be started after the stoppage of opioid itself or the substitution drugs
(methadone etc).

10. Fatal dose

50 mg.

11. PM appearances
Autopsy must be performed with full precautions as the body may be having
hepatitis B and AIDS.

a. External
(1) General appearances: signs of wasting and self-neglect - May be dirty,
emaciated, unkempt, unwashed for days
(2) Needle, syringe and tourniquet may be found on the body if death occurred
due to hot shot.
(3) Hidden drugs - They may be stuffed in rectum or vagina, or may be taped to
be body under the breasts, between buttocks and toes, or attached to a string
tied around a tooth and then swallowed.
(4) Findings associated with use of infected needles – please see above under
Heroin"signs and symptoms of ch poisoning.
(5) Findings related to attempts at revival – If an addict has “passed out”
during or after drug injection, his colleagues try to revive him by peculiar and
specialized methods popular only within the drug community.
(i) Pouring milk in mouth – milk may be found in oral cavity, esophagus etc
(ii) Injection of milk, saline or water into the arm, back of hands or buttocks –
needle marks may be found at these places with traces of milk etc in s/c
tissues
(iii) Immersion - in cold shower or tub of water
(iv) Putting ice - on genitalia
(6) Mouth and nostrils: Froth [due to pulm edema]
(7) Skin, Hands – Same findings as seen in ch poisoning with heroin [please see
above]
(8) Needle puncture mark – on the skin must be searched for. May be seen as a
 tiny hemorrhagic focus. Incision through the skin may show a perivenous
hemorrhagic track.

b. Internal
(1) Upper respiratory tract – contains froth
(2) Examination of upper limb veins - for phlebitis, phlebosclerosis,
thrombosis and recent and resolving perivenous hemorrhage [ch 5]. Preserve
vein and surrounding tissues for chemical analysis.
(3) Lungs –
(i) Heavy, congested, edematous with focal hemorrhages
(ii) Texture – gritty, multinodular
(iii) Pleurae – may show petechial hemorrhages
(iv) Non specific pulmonary triad of (a) Severe pulmonary edema [due to sudden
ventricular dysrhythmia] (b) bronchopneumonia and (c) aspiration of
gastric contents
(v) Microscopically – Foreign body [eg talcum powder, other adulterants]
granulomas. They may erode capillary walls and unite forming larger
granulomas. Under polarized light large quantities of cellulose, starch and
talc can be seen.
(4) Heart -
(i) Myocardial damage
(ii) Valvular diseases
(iii) Right ventricular hypertrophy – due to pulmonary hypertension, in turn
caused by extensive pulmonary emboli.
(iv) Microscopically – Due to prolonged hypoxic coma following heroin
intoxication (a) Degenerated, necrotic myocardial fibres (b) small
mononuclear inflammatory cells
(5) Effusions – in all major body cavities – pericardial, pleural, peritoneal
(6) Liver –
(i) Congested, enlarged, may show evidence of cirrhosis
(ii) Enlargement of hepatic lymph nodes – may measure up to 3-4 cm each
(iii) Chemical analysis of LN reveals its metabolites 6-MAM and morphine
(iv) H/P – Portal LN show nonspecific hyperplasia. chronic Triaditis, Dense
lymphocytic and mononuclear infiltrates involve all portal triads with or
without parenchymal pathologic stigmas of viral hepatitis
(7) Reticuloendothelial system – hyperplastic changes, lymph nodes show large
germinal centers [most common finding]
(8) Spleen –
(i) Enlarged due to malaria [transmitted through infected needles],
(ii) large germinal centers [most common finding],
(iii) presence of birefringent material
(iv) Shows lysozyme containing cells [indicate bacterial contamination]
(v) Shows IgE and IgM containing cells [indicates antigen stimulation]
(9) Brain -
(i) Cerebral edema
(ii) Focal areas of necrosis, involving globus pallidus and hippocampus due to
hypoxia
(iii) Spongiform degeneration of white matter
(iv) Fluid accumulation in myelin sheaths
(10) Associated findings – infections transmitted through contaminated needles,
eg hepatitis B, AIDS.

12. Samples to be preserved

(1) Tissue from inj site. Can demonstrate morphine as well as additives eg talc or
starch
(2) Blood -
(i) Bilirubin level may be - [Hepatitis].
(ii) Tests for Australia antigen, HIV may be +ve
(iii) Blood film may show malarial parasites.
(3) Samples of urine, bile, liver, kidneys, lungs and brain
(4) Hair, bone and bone marrow can show opioids in completely putrefied bodies
or exhumation after several months.
(5) Empty syringes and other paraphernalia. Drug packets full as well as empty.
(6) Common methods of detection are – GLC, TLC and
spectrofluorophotometry.

13. ML aspects [of heroin]

(1) Same as ML aspects of drug abuse [ch 46].
(2) Determination of route of administration – may have to be determined in
many cases.
V. SEDATIVE-HYPNOTICS

A. Barbiturates
Barbiturates are white, crystalline, odorless powders, with a faintly bitter taste.
Salient features:
(1) Barbiturates are derivatives of barbituric acid, which itself has no CNS
depressant properties.
(2) Barbital became the first commercially available barbiturate in 1903.
(3) They were popular sedatives and hypnotics up to 1960s, which led to their
widespread abuse.

1. Classification
Please see [Table 6].

2. Mechanism of action
(1) Barbiturates are CNS depressants. They depress neuronal activity in the
midbrain reticular formation
(2) They facilitate and prolong the inhibitory effects of GABA and glycine.
(3) Their actions are not antagonized by flumazenil [Flumazenil reverses the
CNS effects of benzodiazepines and is classified as an antagonist at BZ
receptors].

3. Toxicokinetics
(1) Barbiturates are rapidly absorbed from GIT including the rectum
(2) After ingestion, barbiturates are preferentially absorbed from the small
 intestine
(3) They are concentrated in the liver for a short time, and then evenly
distributed in the body fluids
(4) Longer-acting barbiturates tend to be more lipid soluble and more protein
bound, a more rapid onset and shorter duration of action, and are metabolized
almost completely in the liver.
(5) Barbiturates are eliminated by hepatic and renal systems
(6) Urinary excretion of unchanged drug is significant for phenobarbital.

4. Acute poisoning
May result from a single large dose or with repeated small doses.

a. Signs and symptoms

(1) CNS – CNS depressant effect mimics that of ethanol. [A] Symptoms (i)
drowsiness [usually the earliest symptom] (ii) Ataxia (iii) Confusion (iv)
Delirium (v) Excitement (vi) Hallucinations (vii) Headache (viii) nystagmus
[lateral and vertical] (ix) Paresthesias (x) Slurred speech (xi) Vertigo (xii)
Visual disturbances (xiii) Finally stupor progressing to deep coma. (a) Coma
may persist for a few hrs to a few days, and then the patient makes a gradual
recovery. (b) Temporary failure of accommodation, leading to diplopia may
occur during recovery. (xiv) Rapid anesthesia – seen in lipophilic barbiturates
[eg thiopental] because penetrate brain tissue quickly. (xv) Psychological – (a)
.ed anxiety (b) euphoria (c) loss of inhibitions (d) relaxed contentment. These
symptoms make them a popular drug of addiction [B] Signs -(i) Babinski toe
sign +ve (ii) Loss of response to painful stimuli (iii) Pupils – (a) slightly
contracted (b) react to light (c) Dilate [may be unequal] during terminal stages
[due to hypoxia] (iv) Superficial and deep reflexes - inhibited or completely
lost.
(2) Respiratory –
(i) Barbiturates cause a depression of the medullary respiratory center " induce
respiratory depression " leads to (a) bronchopneumonia (b) respiratory
acidosis [contributes to CVS depression]
(ii) COPD patients more susceptible [even at therapeutic doses].
(iii) Respiration (a) either rapid and shallow or (b) slow and labored
(iv) Minute volume .ed in all cases
(v) In terminal stages "irregular "Cheyne Stokes "stops completely ["death].
(3) CVS -
(i) Depression of medullary vasomotor centers " Cardiovascular depression
(ii) Cardiac output.. Patients with CHF more susceptible to these effects
(iii) -capillary permeability [because of compromised vascular tone]"-ECF
(iv) Signs of cardiovascular collapse [hypotensive shock] – (a) Cold, clammy
skin (b) Cyanosis (c) Hypotension (d) Pulse – weak and rapid. Shock and
respiratory failure are more common and more serious with medium and
short acting barbiturates than with long acting barbiturates.
(4) GIT -
(i) Bowel sounds absent [due to .peristalsis; bad prognostic sign]. Occurs in
deeply comatosed patients
(ii) As condition improves " peristalsis returns to normal " -drug absorption "
worsening of condition again " fluctuating levels of consciousness
(iii) Incontinence of feces
(5) Renal -
(i) Urine (a) Scanty and suppressed (b) contains albumen, hematoporphyrin,
sugar (c) Incontinence
(6) Dermatological -
(i) Cutaneous bullae [barb burns, barbiturate blisters, coma blisters, friction
blisters] - (a) Seen most commonly in (I) barbiturates, but in almost any
other condition which produces coma. They have been reported in
poisoning by (II) benzodiazepines, (III) CO, (IV) glutethimide, (V)
hydrocodone, (VI) imipramine, (VII) meprobamate, (VIII) methadone, (IX)
methaqualone [Mandrax], (X) tricyclics, valproic acid and in (XI)
prolonged contact with cantharidin, paraffin and petrol. Seen also in
pemphigus [but they are non tense and larger]. Thermal blisters will show
associated signs of burns eg singeing of hair. (b) Frequency - seen in 6-10%
cases (c) site – where friction or pressure naturally occurs, eg interdigital
clefts, buttocks, back of thighs, calves and forearms, inner aspects of knees
and ankles. Occasionally entire side of a forearm or thigh is blistered. Have
been reported in non pressure points, eg around IV site. (d) Characteristics -
(I) Tense subepidermal blisters which develop within 48–72 h of the onset
of unconsciousness (II) Self-limiting lesions; heal spontaneously in 1-2
wks. (III) Inflammation usually absent or minimal. (IV) contain clear serous
 fluid. May be hemorrhagic. Rupture of blister leaves a red raw surface,
which dries to a brown parchment like area. May be mistaken for burns. (e)
Mechanism - (I) External uninterrupted pressure + arterial hypotension due
to shock"hypoxia, local ischemia " metabolically most active cells are
affected earliest [eccrine sweat glands]"sweat gland necrosis"necrotic
bullae. (II) direct toxic action on epidermis (III) Immune mechanisms. (IV)
Barbiturate poisoning"muscle flaccidity"cessation of venous
return"cutaneous edema.
(7) Body temperature -
(i) .ed
(ii) May be -ed in late stages"indicates bron chopneumonia [please co-relate with
respiratory symp].
(8) Uncommon symptoms [adverse effects] –
(i) Paradoxical excitement [especially in the elderly]
(ii) Hypersensitivity reactions [erythematous or exfoliative dermatitis, localized
swelling of eyelids, cheeks, lips].
(9) Death -
(i) In early stages due to – (a) respiratory failure [commonly], (b) ventricular
fibrillation. Death is rapid if alcohol or antihistamines are ingested
simultaneously [synergistic action]. [please also see above –
Alcohol"Relationship with barbiturates]
(ii) In late stages due to –(a) bronchopneumonia (b) pulmonary edema (c) acute
renal failure (d) cerebral edema.
Memory Aid 13: Major symptoms of barbiturate poisoning
BARBITURATES
Babinski +ve, BP .
Ataxia
Rresponse to painful stimuli lost, Reflexes ., R/r .
Bowel sounds absent
Incontinence of urine and feces
Temperature .ed
verTigo
Urine .; contains albumen, hematoporphyrin, sugar
paResthesias
Reflexes lost
Abnormal senses [hallucinations]
nysTagmus
Eye can not see properly [visual disturbance]
Small pupils [contracted], Skin cold and clammy and shows bullae, Sleepiness, Slurred speech, Stupor
progressing to deep coma [final stage]

b. Fatal dose
(1) Fatal dose - (i) Short acting:1-2 g (ii) Medium acting:2-3 g (iii) Long
acting:3-5 g
(2) Fatal blood levels - (i) Short acting:3 mg% (ii) Medium acting:7 mg% (iii)
Long acting:10 mg%.

c. Fatal period
1-2 days.

d. Management
(1) Gastric lavage –
(i) With warm water mixed with KMnO4 and suspension of activated charcoal or
tannic acid
(ii) Leave a concentrated soln of MgSO4 in the stomach "(a) produces purgation
(b) minimizes intestinal absorption
(iii) Effective up to 24 h post ingestion
(2) Emesis – contraindicated, because (i) possibility of impending coma (ii)
Ipecac can - potential for CNS depression.
(3) Activated charcoal – usual dose. MDAC [ch 32].
(4) Enema – to evacuate bowels
(5) Specific antidote – (i) None. (ii) Analeptics – Once recommended.
Contraindicated now [ch 32].
(6) Urine alkalinization – ch 32.
(7) Scandinavian method – ch 32.
(8) Hemodynamic support– for hypotension [ch 32].
(9) Hemodialysis or hemoperfusion – ch 32.
(10) Exchange transfusion – ch 32.
(11) Hemoperfusion – ch 32.
(12) Management of prolonged coma – deep vein thrombosis, orthostatic
 pneumonia etc [ch 32].
(13) Immunotherapy - Barbiturates are conjugated to Bovine Gamma
Globulins [BGG] and injected in rabbits to produce active immunization.
Serum from these rabbits is then injected in other rabbits to produce passive
immunization. Both actively and passively immunized rabbits show a .ed
pharmacological response to barbiturates indicating the presence of an
antibarbiturate gamma globulin. [please see ch 36"Arsenic also].
(14) Intravenous Lipid Emulsion (ILE) – [Ch 32"“General principles of
treatment”].
(15) THAM [trometamol; tris-hydroxymethyl aminomethane] – Useful as an
alternative to NaHCO3 in the treatment of acidosis.
(16) Symptomatic treatment.

e. PM appearances
(1) Signs of asphyxia – congestion of all internal organs, cyanosis, petechial hgs
in lungs and on pleura and pericardium
(2) Nose and mouth - Froth
(3) Skin - Barbiturate blisters
(4) Lungs –
(i) Intensely congested. May even be turned completely black [full of dark
deoxygenated blood]
(ii) Show edema and bronchopneumonia in late deaths
(5) Esophagus – lower end may show erosion from regurgitation
(6) Stomach – (i) congested. (ii) erosions. (iii) White particles on ingested
barbiturates seen (iv) Fundus – thickened, granular, hemorrhagic
(7) Kidneys – degeneration of convoluted tubules
(8) Brain – edematous, especially in late deaths. In delayed deaths there is
symmetrical necrosis of globus pallidus and corpus callosum, focal areas of
necrosis in cerebrum and cerebellum and a variety of vascular lesions.

f. Laboratory detection
(1) Dille-Koppanyi Test - Two solutions are used.
(i) Soln 1 - 1% cobalt acetate in methanol [Co(C2H3O2)2].
(ii) Soln 2 - 5% isopropylamine in methanol [CH3CH(CH3)NH2].
(iii) Add two drops of Soln 1 to the drug, followed by one drop of Soln 2"If
barbiturates are present a lavender-blue color will develop.
(2) Calorimetric methods
(3) GC-HPLC.

5. Chronic poisoning
(1) Etiology -
(i) Prolonged therapeutic use [as in epilepsy and psychoneurotic patients].
Unintended addiction may occur. Dependence is both psychic and physical
(ii) Prolonged recreational use.
(2) Signs and symptoms - Similar to those of chronic alcoholism [please also
see above – Alcohol" Relationship with barbiturates].
(i) Physical deterioration - (a) Ataxia (b) cerebral function impaired (c)
depression (d) Dysarthria (e) hypertonia and tremors of Parkinsonian type
(f) Tendon reflexes depressed
(ii) Social deterioration – Impairment of mood, behavior and intellectual
functions.
(3) Barbiturate abstinence syndrome [syn, Barbiturate withdrawal syndrome] -
(i) Barbiturates can produce psychological and physical dependence and produce
a withdrawal syndrome on the 2nd to 4th day after the drug is suspended.
(ii) Symptoms (a) anxiety (b) Disturbances of vision (c) dizziness (d)
Hypotension (e) insomnia (f) Nausea and vomiting (g) psychosis (h)
restlessness (i) rhythmic intention tremor (j) Tremors, convulsions, seizures
and (k) Weakness. May persist for 2 wks. If the syndrome is not recognized
and correctly treated, hyperthermia, circulatory failure, and death may ensue.
Treatment - Administration of barbiturates.

6. ML importance
(1) Popular drug as an agent of suicide – Famous people who committed
suicide with an overdose of barbiturates include
(i) Cesare Pavese [1908 –1950] Italian author
(ii) Dalida [1933 –1987] Italian singer
(iii) Margaux Hemingway [1954 –1996] American fashion model and actress
(iv) Marilyn Monroe [1926 –1962] American actress and
(v) Robert Hayward Barlow [1918 –1951] American author.
(2) Euthanasia - Barbiturates are a popular drug for euthanasia. In Switzerland,
Exit Association [an organization providing assistance to individuals wishing
to end their lives] utilizes oral pentobarbitone for the purpose.
(3) Barbiturate automatism – ch 28.
(4) Drug of abuse, recreational use –
(i) Popular drug of abuse because of psychological symptoms it produces. Short-
acting and intermediate-acting barbiturates are preferred [amobarbital
(Amytal), pentobarbital (Nembutal), secobarbital (Seconal), combination of
amobarbital and secobarbital (Tuinal)]. Known in drug world as barbs,
bluebirds, blues, dolls, downers, goofballs and tooties.
(ii) Physical and psychological dependence develops with repeated use.
(iii) Sometimes used to alleviate adverse or withdrawal effects of other illicit
drugs.
(5) Used in narcoanalysis – As truth serum [ch 30].
(6) Judicial Execution - Used in judicial execution by injection. A sequential
drug combination of sodium thiopental [CNS depression], pancuronium
bromide [paralysis of respiratory muscles], and potassium chloride [cardiac
arrest] is used. The first lethal inj execution however took place 5 y later in
1982 in Texas, with the execution of Charles Brooks, Jr. [1942 – Dec 7,
1982]. (i) Currently major methods of State execution (capital punishment)
around the world are (a) electrocution [ch 16] (b) firing squad (c) gassing [ch
44] (d) hanging [ch 19] (e) lethal injection and (f) strangulation [garroting, ch
19]. Oklahoma and Texas became the first US states to introduce lethal
injections in the spring of 1977.
(7) Secondary poisoning [please see ch 31]– has been described in dogs, who
have eaten carcass of a horse euthanized with pentobarbital, up to 2 y
previously. Barbiturates resist putrefaction. There is a necessity of proper
disposal of animals euthanized with barbiturates. Can occur in humans also.

B. Chloral Hydrate
Chloral hydrate (CH) was first synthesized in 1832 by Justus von Liebig. First
used as a sedative and hypnotic in 1869; before this time the only sleep inducing
drugs [soporifics] were alcohol and opium. It is often used as a recreational
drug. Its structure is quite similar to that of ethyl alcohol.
1. General
Chloral hydrate is a colorless, crystalline substance with a pungent pear like
odor and bitter taste. Several formulations containing CH are still marketed.
Some are gargles, lotions, or solutions used as mouth bath owing to CH
analgesic and disinfectant properties. Also used in syrup forms prescribed as
sedatives in the elderly population; for short term sedation in children (during
non painful procedures eg CT scan, MRI of brain, and detailed
echocardiography); in the treatment of alcoholism and strychnine poisoning.
CH exhibits a significant risk of mutagenesis and carcinogenicity. Therapeutic
oral dose in adults -> 0.5 to 2.0 g.

2. Mechanism of action
Chloral hydrate is metabolized by hepatic alcohol dehydrogenase.
Trichloroethanol (TCE) –its first active metabolite- is lipid soluble (high
affinity for neurons) and is responsible for chloral hydrate’s hypnotic effects.

3. Absorption, metabolism and excretion

(1) Absorption - Well absorbed from entire GIT including rectum [may be
administered rectally]
(2) Metabolism – Metabolized rapidly in liver mainly to TCE
(3) Excretion – TCE has a plasma half life of 4-12 hours; it is metabolized to
inactive trichloroacetic acid by aldehyde dehydrogenase. Part of it is
conjugated with glucuronide and excreted in urine as urochloralic acid.

4. Acute poisoning
The clinical picture of acute CH poisoning resembles acute barbiturate poisoning
in many respects
(1) Nausea, vomiting, retrosternal burning sensation, hemorrhagic gastritis.
Rarely gastric and intestinal perforation or esophagitis with stricture
formation.
(2) Odor - The peculiar pear-like odor of CH may help distinguish it from other
sedative-hypnotics.
(3) Pupils - may be miotic initially and then dilate as the stage of coma deepens.
(4) Skin – Scarlatinal or urticarial rash [due to idiosyncrasy]
(5) CNS - Ataxia and lethargy. Deep coma within 1 to 2 hours.
(6) CVS - atrial fibrillation, supraventricular tachycardia, ventricular
tachycardia, multi focal premature ventricular contractions, torsade de pointes,
ventricular fibrillation, asystole and hypotension. The combination of deep
coma and dysrhythmias in a patient who is not hypoxic is typical of CH
poisoning.
(7) Hepatorenal - Dysfunction of liver [jaundice] and kidney [albuminuria]
(8) Death – Occurs from CVS disorders.

5. Chronic poisoning
Occurs after prolonged therapeutic use.
(1) Skin - Erythematous and urticarial eruptions
(2) GIT irritation
(3) CNS – convulsions, tremors
(4) Respiratory system – Dyspnea
(5) Hepatic – Liver damage
(6) Dependency syndrome with withdrawal symptoms when drug is withdrawn.
Delirium tremens, seizures and psychosis may result.

6. Fatal dose
5-10 g.

7. Fatal period
8-12 hours.

8. Management
(1) Stomach wash - with alkaline solution, if patient is seen early. Chloral
hydrate is rapidly absorbed, particularly after ingestion of liquid forms
(2) Treatment of cardiac arrhythmias – This should be the main concern.
(i) Propranolol
(ii) Esmolol – Short acting ß-blocker. Preferable to propranolol because of its
rapid action.
(iii) Bretylium – Adrenergic neuron blocking drug
(3) Treatment of hypotension – Infuse 10-20 mL/kg of isotonic fluid.
Catecholamines are contraindicated because they precipitate ventricular
arrhythmias in chloral hydrate overdose.
(4) Flumazenil - 200µg by infusion followed by 100µg at 1 min intervals, up to
3 times. Total 500µg.
(5) Hemodialysis and hemoperfusion.

9. Tests
Fujiwara test - 1 mL Urine + 1 mL NaOH + 1 ml pyridine. Heat in a boiling
water-bath for 2 minutes. An intense red/purple colour indicates the presence of
trichloro compounds [chloral hydrate, chloroform, trichloroethylene].

10. Postmortem appearances

(1) Stomach mucosa congested, eroded and softened. Smells of chloral hydrate
(2) Congestion of all internal organs
(3) Necrosis of liver and kidney.

11. ML importance
(1) Used for rape and robbery - Chloral hydrate is soluble in both water and
alcohol. A solution of chloral hydrate in alcohol called “knockout drops” or
“Mickey Finn”. It renders a person helpless immediately. Used for robbery
[by giving it to watchmen] or date rape [date rape drug]. Chloral hydrate is
sometimes referred to as dry wine
(2) Used to knock out private detectives in movies. However it takes a lot
longer to put people to sleep with this drug, than the movies would show.

C. Hydrocarbons
Hydrocarbons are organic compounds consisting entirely of hydrogen and
carbon. Signs, symptoms and treatment etc of all hydrocarbons are the same as
that in kerosene poisoning.

1. Kerosene poisoning
Kerosene is a thin, clear liquid consisting of a mixture of hydrocarbons that
boils between 150°C and 275°C.
Salient features:
(1) Kerosene is derived from refined petroleum, and is commonly used as a fuel
or solvent.
(2) It is primarily used in oil lamps, as a heating oil, as fuel in jet engines, and
 as a solvent for insecticide sprays.

a. Signs and symptoms

(1) Kerosene has a strong smell and taste. Thus it can not be used as a homicidal
poisoning.
(2) Suicidal poisoning is rare.
(3) Most poisoning cases are accidental in nature, when a child ingests kerosene.

Acute poisoning
(a) Ingestion
(1) Kerosene taste, Burning sensation in the throat, nausea, vomiting, colicky
pain, diarrhea.
(2) Breath, vomit and urine smell of kerosene.
(3) Fever
(4) Lungs – Main organ system affected. (i) Bronchospasm, (ii) chemical
pneumonitis, (iii) pulmonary edema, (iv) atelectasis. (v) dyspnea,
tachypnea, gasping, coughing and choking indicate aspiration (vi) cyanosis
(vii) intercostal retraction(viii) Nasal flaring
(5) Heart –Dysrhythmias. Kerosene sensitizes the myocardium to
endogenous catecholamines producing dysrhythmias. Myocardial function
may also be depressed resulting in a poor left ventricular ejection fraction.
(6) CNS - Neural tissue is rich in myelin (lipid). Myelin is dissolved by
kerosene. This causes depression of CNS and of ventilatory drive.
(i) Depression of CNS leads to " Giddiness, weakness, drowsiness.
(ii) Depression of ventilatory drive leads to " cyanosis.
(7) Skin lesions (bullae, blisters and burns) – Kerosene (like allo
hydrocarbons) is lipophilic in nature. Hence it dissolves the lipids in the
stratum corneum making the skin more vulnerable to drying. This in turn leads
to skin lesions varying from (i) bullae, (ii) blisters, (iii) maculopapular rash
and (iv) first degree burns (v) chronic eczematoid dermatitis with redness,
itching and inflammation
(8) Kidneys - Renal damage results in type 2 renal tubular acidosis.
(9) Autonomic dysfunction - Hypotension, excessive sweating.
(b) Inhalation
Kerosene is sometimes “sniffed” by addicts [inhalant abuse - please see also ch
46]. Inhalation of fumes causes (1) nausea, (2) vomiting, (3) headache (4)
vertigo (5) Lung complications and (6) convulsions. Sometimes (7) elation
may occur.

b. Diagnosis
(1) X-ray -
(i) Changes may be evident as early as 30 min after exposure, and sometimes
may precede clinical symptoms.
(ii) Chest – (a) perihilar densities (b) Bronchovascular markings (c) Pneumonic
consolidation
(iii) X-ray of abdomen gives the classical double bubble sign [two liquid
densities in the stomach – air:kerosene and kerosene:fluid. Air is lightest,
then kerosene and finally fluids]
(2) Arterial blood gases – Hypoxemia
(3) Blood – Leucocytosis during first 48 hours.

c. Treatment
(1) Decontamination -
(i) Contact poisoning – Remove all clothings; copious washing of skin with
soap and water.
(ii) Gastric lavage and emetics – avoided because of high risk of aspiration
(2) Antidote - No specific antidote
(3) Supportive treatment -
(i) Oxygen administration (a) High Frequency Jet Ventilation (HFJV) – ch
32 (b) Extracorporeal Membrane Oxygenation (ECMO) – ch 32
(ii) Antibiotics - to prevent secondary pulmonary infection
(iii) Corticosteroid therapy – Was given once for severe bronchospasm. May
increase bacterial superinfection though, and thus no more recommended
now.

d. Fatal dose
30-100 ml. Fatality rate is low. Children younger than four years old are more
often affected.
e. Fatal period
One day.

f. ML significance
If a parent has stored kerosene oil negligently resulting in accidental intake by a
child, he is liable to be prosecuted u/s 284 of IPC (negligent conduct with
respect to poisonous substance; 6 months and/or $ 1000).

Chronic poisoning
Chronic exposure to kerosene causes (1) acne (2) bone marrow depression (3)
liver damage (4) polyneuritis and (5) skin eruptions.

41. Deliriant Poisons

I. DATURA

Datura [from Sanskrit Dhurta, cheat] is a genus of vespertine [flowering in the

evening] flowering plants belonging to the family Solanaceae.
Salient features:
(1) Hyoscyamus and Atropa are related genera.
(2) Habitat – Grows on waste places all over India
(3) Species -
(i) D. ceratocaula
(ii) D. discolor – Desert Thorn-apple
(iii) D. ferox – Long Spined Thorn-apple D. Metel and D. Stramonium are
important. D. Metel has two varieties (a) White flowered plant [sometimes
loosely referred to as D. alba] (b) Deep purple flowered plant [called D.
niger]. Table 1 gives botanical and common names of some common
deliriant plants.
(4) Plant – Characteristics of D. fastuosa
(i) Plant -Leafy herb with a woody stalk that grows up to five feet tall.
(ii) Flowers – bell shaped. Have five petals, which open after dusk and close by
mid-morning the next day [Datura is a nocturnal plant]. They exude a
pleasant, narcotic scent, especially at night.
(iii) Fruits – spherical, have sharp spines [Fig 41.1]. Give rise to the plant’s
English name ‘Thornapple’. Contain up to 500 yellowish brown seeds [Fig
41.1]. They look very much like chili seeds and must be differentiated from
them [Table 2].
(iv) Poisonous parts – All parts are poisonous [seeds, fruit, nectar (honey)].
A. Active Principles and MOA
(1) Datura plant contains about 0.2%-1.4% of alkaloids (i) scopolamine [l-
hyoscine], (ii) atropine [d,l-hyoscyamine, older name Daturine] and (iii)
hyoscyamine [older name Duboisine]. Atropine and hyoscyamine are
isomers, the latter being levo-isomer of atropine. During extraction
hyoscyamine may be converted to atropine. These alkaloids competitively
inhibit the muscarinic effects of Ach.
(2) There are also traces of glycoside scopolin.

B. Signs and Symptoms

1. Contact
Contact with leaves or flowers "Dermatitis in sensitive persons.
2. Ingestion
(1) Appearance of symptoms -
(i) Ingestion of seeds - appear within 30 min
(ii) Decoction of seeds – within 5 min
(iii) Ingestion of alkaloids – within few seconds. It results in the appearance of
anticholinergic toxidrome [ch 31], with all its typical signs and symptoms
[remember “blind as a bat” mnemonic].
(2) Symptoms - (i) Initially - Bitter taste, vomiting, burning pain in the stomach.
Later "(ii) Face – flushed (iii) Conjunctiva – congested (iv) Loss of
accommodation for near vision – results in (a) temporary blindness (b)
photophobia (c) diplopia (d) Pupillary reflex – at first sluggish; later absent (v)
Voice – hoarse (vi) Skin – Scarlatinal rash, or exfoliation of skin over most of
the body (vii) CNS and psychiatric– (a) agitation (b) confusion (c) giddiness
(d) restlessness (e) failure to recognize relatives and friends (f) Delusions (g)
Hallucinations of sight and hearing (h) tonic convulsive seizures (viii) 15 D’s
[Memory Aid 1]. Additional points – (a) dysuria may progress to complete
urinary retention. (b) skin is dry [due to loss of sweating (hypohidrosis)] and
also hot. (c) Drunken gait is ataxia (d) Delirium – patient is restless, makes
purposeless movements [eg pulling imaginary threads, threading imaginary
needles, picking at bed clothes - Carphologia or floccilation] [also ch
28"delirium]. Pt is initially excited, incoherent, noisy, talkative and tries to run
away from bed (ix) Excitement remains for 1-2 h after which patient goes in
deep sleep [coma] (x) Lastly – resp depression, resp paralysis and death [also
see ch 31"anticholinergic toxidrome].
Memory Aid 1: Datura’s signs and symptoms
Remember 15 D’s (1) Decreased muscle coordination (2) Delirium (3) Delusions (4) Dermatitis (5) Dilated
pupils (6) Dreadful hallucinations (7) Drowsiness (8) Drunken gait (9) Dry hot skin (10) Dry membranes
(11) Dryness of mouth and throat (12) Dysarthria (13) Dysphagia (14) Dysuria (15) Death due to respiratory
failure

(3) Signs –
(i) Pulse – (a) - [120-150/min]. (b) Volume – Initially- full and bounding; later –
weak and irregular [arrhythmia].
(ii) BP- [systolic BP may be up to 180]
(iii) R/R- [later resp failure]
(iv) Temp -ed by 3-4°C [other poisons causing hyperpyrexia"ch 31].
(v) Muscle tone and reflexes "-ed [hyperreflexia] with positive Babinski’s sign.

C. Fatal Dose
(1) Atropine or hyoscyamine – 120 mg
(2) Scopolamine – 30 mg
(3) Datura seeds – 50-100.

D. Fatal Period
24 hours.

E. Diagnosis
(1) Mydriatic test [animal testing]– Instill patient’s urine [or a soln of suspect
seeds in water or alcohol] in cat’s or rabbit’s eye"immediate mydriasis.
(2) Pilocarpine test – instill 2-3 drops of 1% pilocarpine [or physostigmine] in
patient’s eye"no constriction within half an hour"Datura [or other
anticholinergic] poisoning
(3) Blood - Neutrophil leucocytosis.
(4) Hair analysis by MS – Atropine and scopolamine can be identified in hair
up to 3 weeks after exposure. Timing of exposure can be determined by
segmental hair analysis [ch 31].

F. Management
(1) Shift patient to a quiet and dark environment [ch 32"gives all poisons in
which pt is shifted to dark].
(2) Monitor and correct
(i) Vitals – ECG, Pulse, R/r, temp.
(ii) For sinus tachycardia – Requires treatment only if hemodynamic
compromise develops. If required, give short acting cardioselective agent
eg esmolol.
(3) Respiratory assistance – If seen late, patient may be in respiratory failure.
Endotracheal intubation, assisted ventilation.
(4) Decontamination -
(i) Emetics
(ii) Gastric lavage – with a weak soln of tannic acid. Even late gastric lavage is
 useful, because gut motility is .ed. Datura seeds may be recovered from
stomach even 36 h after ingestion.
(iii) WBI
(iv) Purgatives – to continue for 3-4 days to remove seeds. Light diet during this
period.
(5) Activated charcoal
(6) IV fluids. Monitor input, output, renal function
(7) Catheterize bladder
(8) Dialysis and hemoperfusion – not effective
(9) Antidotes -
(i) Physostigmine – Antidote of choice. It is a tertiary amine that easily passes
BBB [reverses central effects too]. Dose – (I) Adult - 2 mg IV slowly;
repeated if required in 20-60 min [Duration of action – 20-60 min]. (II)
Pediatric – 0.5 mg IV slowly; repeated if required in 5 min, up to a
maximum of 2 mg.
(ii) Neostigmine, pilocarpine and pyridostigmine – do not pass BBB because
they are quaternary amines. Central effects are not countered.
(iii) Contraindicated drugs - Antihistamines, Disopyramide, morphine [depresses
respiratory center], Phenothiazines, Procainamide, Quinidine and
Tricyclics.
(10) Symptomatic -
(i) Agitation – diazepam IV. Generally antihistamines and phenothiazines are to
be avoided because they -anticholinergic effects. Cyamemazine
[antipsychotic] is however recommended.
(ii) Delirium – bromides, chloroform, ether, short acting barbiturates
(iii) Hyperthermia – cooling measures, hydration.

G. PM Appearances
(1) No characteristic findings
(2) Findings of asphyxia
(3) Stomach and intestines –
(i) Walls - inflamed
(ii) Fragments of seeds and plant may be found. Seeds resist putrefaction for a
long time
(4) Lungs – edematous.

H. ML Importance
(1) Abortifacient
(2) Aphrodisiac - Believed to be an aphrodisiac. Used as a love philter.
(3) Autumnal High – If youth are seen with hallucinogenic symptoms during
autumn months, it could be a case of Datura poisoning. Seeds of Datura
appear around autumn, and youth may consume its seeds for their mild
hallucinogenic effects.
(4) Beer - Solanaceous plants have been used to fortify beer since time
immemorial in order to potentiate the effect of the alcohol. Mandrake was
used in Egypt and thornapples in Russia for the same purpose.
(5) Cornpicker’s pupil - (a) Corn fields are usually infested with Datura plants.
Harvesting of corn invariably exposes the cornpickers to Datura dust. This
results in persistent mydriasis (cornpicker’s pupil). (b) A similar condition is
gardener’s mydriasis, where gardeners dealing with Datura plants [grown as
a hobby in gardens] get persistent mydriasis. (c) Laboratory technicians, who
weigh out atropine powder for experiments may show same sign. This has led
doctors to wrongly diagnose cranial lesions, and has even led to lumbar
punctures and MRIs. In all cases of persistent dilatation of pupil, the
occupation of person must be asked.
(6) Criminal responsibility – If Datura is administered to a victim without his
knowledge [as for stupefying him before robbery], he is not responsible for
any criminal act done under its influence [S.85, IPC (ch. 31)]. If the person
took Datura himself [eg as a drug of abuse], he is responsible for his criminal
actions.
(7) Drug of abuse
(i) Seeds and leaves are mixed with tobacco or ganja and smoked in a pipe.
(ii) Decoction of seeds is added to liquor or toddy to -their intoxicating property.
(iii) Use of Datura is more lucrative to addicts because of absence of legislation
regarding it.
(8) Manner of poisoning -
(i) Suicide and homicide - rare.
(ii) Accidental poisoning - may occur (a) in children who eat its fruits by mistake
(b) When used as a medicine - (I) after instillation as eye drops. (II) When
 used as antiinflammatory - In some regions it is believed that it acts as an
antiinflammatory for conditions such as local trauma, erysipelas and
gingivitis. (c) When used topically as a magic charm - Medieval Europe
witches supposedly obtained hallucinatory effects by rubbing their bodies
and genitals with ointments containing Datura, and Yaqui Indians in
Mexico used crushed Datura leaves on their genitals, legs and feet for
similar purposes. Still used as a magic charm in many places.
(9) Poisoning to poultry – D. stramonium is toxic to livestock, including
poultry. Its seeds can contaminate grains and is the most common cause of
poisoning in chickens.
(10) Relief of Asthma - During the 19th century, Datura was marketed as
“Spanish Herbal Cigarettes.” Advantage was taken of its antihistaminic and
bronchiodilating properties; used as a smoke, it relieved the symptoms of
asthma.
(11) Stupefying poison –
(i) Ingestion - Criminals mix crushed or powdered seeds in food and drink
[chapattis, curry, sweets, tea, liquor] to stupefy a victim [usually travelers in
railways] before robbery, rape or kidnapping [Road poison]
(ii) Inhalation – Seeds may be mixed with incense wood and victim exposed to
fumes.
(12) Toxic honey – If during their nectar collecting activity, bees collect nectar
from Datura plants, the honey may become contaminated with Datura
alkaloids. This may give rise to unintentional poisoning [toxic honey. Please
see more in ch 39 – “Food poisoning”]. Some hummingbirds, eg sword-billed
hummingbird (Ensifera ensifera), can feed on the nectar from Datura flowers
without ill-effects.

II. ATROPA BELLADONNA

Atropa belladonna [syn. Belladonna, Devil’s Berries, Death Cherries, Deadly

Nightshade], is a perennial herbaceous plant of the family Solanaceae.
Salient features:
(1) Active principles are hyoscyamine [82-97%], atropine [3-15%] and
scopolamine [2.5%].
(2) Signs, symptoms, treatment and pm appearances are same as that of Datura.
(3) Because it produced senselessness, it was used in the Middle Ages as an
anesthetic for surgery.
(4) The plant has reddish-purple flowers.

ML Importance
(1) Arrow poison.
(2) Manner of poisoning - Homicide - The ancient Arabs used it as a poison.
The wife of Emperor Augustus and the wife of Claudius both used it to
murder their enemies.

III. CANNABIS

Cannabis (Indian hemp, pot, dope, grass) is a genus of flowering plants that
includes three species, Cannabis sativa, Cannabis indica, and Cannabis
ruderalis. All three are found in India, Central Asia, and South Asia (Fig 41.3).
Salient features:
(1) Plant - (i) Cannabis is an annual, dioecious (male and female plants
occurring separately), flowering herb. (ii) The leaves are digitate with serrate
leaflets
(2) Frequency of use - Currently it is the most commonly used illicit drug of
abuse. If socially acceptable drugs are also taken into account, then it is 4th
most common drug of abuse - (i) Caffeine (ii) Nicotine (iii) Alcohol (iv)
Cannabis.
A. Active Principles
(1) Active principles are cannabinoids [syn, phyto-cannabinoids], secreted by
trichomes. At least 90 plant Cannabinoids have been isolated from cannabis.
(2) Cannabinoids of importance are
(i) Tetrahydro-cannabinols or THC. Most important THCs are Δ8-
tetrahydrocannabinol and Δ9- tetrahydro-cannabinol(pronounced as
delta-8 and delta-9 tetrahydrocannabinol)
(ii) Cannabinol [CBN]
(iii) Cannabidiol [CBD].

B. Mechanism of Action
(1) Endogenous cannabinoid receptors -
(i) Cannabinoids exert their effects by interaction with specific endogenous
cannabinoid receptors [CB1, CB2, GPR18, GPR55 and GPR119].
(ii) Discovered in 1990s.
(iii) All are G protein-coupled cannabinoid receptors [GPRs].
(iv) Location - CB1 is located in the brain, and CB2 in peripheral tissues of the
immune system.
(2) Endogenous cannabinoids - Anandamide [from Sanskrit word “Anand”,
happiness], an endogenous cannabinoid, attaches to these receptors. Produces
natural pain relief and controls immunity.
(3) THC – Additionally acts on CB1 and enteric nervous system to suppress
emetogenic stimuli communicating between them. Acts as an effective
antiemetic.

C. Forms of Cannabis

1. Bhang
Bhang [Patti, Siddhi, Sabji] consists of dried mature leaves and stems of
cannabis.
Salient features:
(1) Potency - It is the mildest form of Cannabis and contains 15% of active
principle. Fresh Bhang is more potent; it loses its potency on storage. Bhang
stored for 2-3 years has very mild euphoriant properties.
(2) Forms in which consumed - (i) As an infusion – Seeped in water, strained
through a muslin cloth and used as a beverage (ii) Cannabis tea – leaves boiled
in water just like tea leaves [please see ch 40 for “poppy tea”]. The resulting
infusion is supposed to have more Δ9-THC [main bioactive component of
cannabis], because heat converts tetrahydrocannabinolic acid (THCA) to Δ9-
THC. (iii) As a pill or bolus – Leaved rubbed with black pepper on a stone.
Sugar is added to make a pill or bolus [Bhang golis or balls] (iv) Mixed with
milk – Almonds and spices (mainly black pepper) are also added and served
on festive occassions such as Holi in March and Vaisakhi in April, especially
in places like Mathura and Varanasi [Bhang Ki Thandai, Shardai] (v) Mixed
with fruit juice
(3) Commonly used - (i) to produce a cheerful mood before singing and dancing
(ii) as an appetizer (iii) for enhancing sexual pleasure (iv) part of many
Ayurvedic medicinal preparation.
(4) Duration of action - Intoxication lasts for about 3 hours, ending with sleep.

2. Majoon
Majoon is a sweet prepared with Bhang.
Salient features:
(1) Made by mixing Bhang with honey, and ghee. Sometimes henbane, datura
seeds and poppy seeds [for flavoring] are also added
(2) Sold in the market as lozenge shaped pieces [barfi]
(3) Used as an appetizer and aphrodisiac.

3. Ganja (Marijuana)
Ganja is is a rusty-green powder with a characteristic odor, which is prepared
from the flowers of female plants.
Salient features:
(1) Potency - It is a stronger form of Cannabis and contains 15-25% of active
principle.
(2) Method of use – (i) Smoked in a pipe [Chillum or hukka] – About 4-5 g of
ganja is taken with little water on palm and rubbed till it becomes sticky. It is
then mixed with tobacco and smoked. Sadhus, faqirs and poor laborers in
India use this method. (ii) in the form of cigarettes [reefers or joints] – This
method more common in the West, and among the affluent in India. A good
 quality reefer may contain up to 500 mg of ganja.
(3) Other names - (i) Known as Marijuana in the West.

4. Charas (Hashish)
Charas (syn hashish) refers to the dried resin of cannabis.
Salient features:
(1) Contains 25-40% of the active principle.
(2) Slang names – dope, shit
(3) Dark green or brown in color
(4) Mixed with tobacco and smoked just like ganja.
(5) The best charas grown in India comes from the mountains [6-8000 ft above
sea-level].

D. Acute Poisoning

1. Signs and symptoms

(1) Signs and symptoms may differ in different persons. They depend upon
(i) life experiences,
(ii) Personality styles and
(iii) Environmental [eg in familiar or unfamiliar environment] and
(iv) social setting [eg in a group of friends or strangers] in which drug is
consumed.
(2) Time of appearance –
(i) Smoking – Appear soon after smoking and last for 1-2 h. Characteristic odor
[of burnt rope] is apparent on smoking, but not on ingestion
(ii) Ingestion - Appear within ½ h and last for 2-3 h.

a. Psychiatric
(1) When small doses are taken –
(i) General euphoria - -ed well-being, -ed self confidence, feelings of clarity,
cleverness, detachment, disinhibition, dreaminess, elation, jocularity,
laughing, relaxation, sometimes silliness
(ii) Emotions – labile. change rapidly [laughing followed by weeping and back
to laughing]
(2) When Moderate doses are taken –
(i) Sensory – (a) -ed awareness of stimuli (b) Illusions and hallucinations (c)
Sensory novelty (d) Vivid images
(ii) Memory, judgment and thought processes – are affected with moderate
dosages. (a) .ed attention span [lapses of attention] (b) .ed concentration (c)
Altered reality testing (d) Disorders of perception [person may feel
superhuman, and may feel he can stop buses with one hand, or could fly out
from high windows. Can actually jump leading to death] (e) Altered sense
of identity (f) Disorientation [Altered concepts of time and space] (g)
Impaired judgment (h) Irresponsible behaviour, Failure to meet
responsibilities [eg of home, children etc] (i) Maladaptive behavioral effects
(j) Disturbed and irrelevant thoughts (k) Impaired memory (l) Subjective
feeling of unfamiliarity. Symptoms mentioned below are seen with -ing
dosages.
(iii) Speech changes [speech is rapid, impaired. Person becomes talkative]
Flight of ideas.
(iv) Sexual feelings – May be heightened. That is why, sometimes used as an
aphrodisiac
(v) Somnolence
(3) When high doses are taken -
(i) Changes in body image,
(ii) Depersonalization,
(iii) Marked sensory distortion,
(iv) Sensitive individuals,
(v) Particularly persons recovering from mental illness may become paranoid
even after a relatively low dose.

b. Physical
(1) -ed appetite and thirst (2) ataxia (3) congestion of conjunctiva (4) dizziness
(5) dry mouth (6) dysesthesias and paresthesias (7) Skin - Acute generalized
exanthematous pustulosis (AGEP). (8) precordial distress (9) restlessness (10)
Slight nausea (11) heaviness and pressure in the head (12) tachycardia (13)
tightness in chest (14) tremors and (15) urinary frequency. (16) Victim becomes
drowsy and passes into deep sleep. Wakes with exhaustion and impaired mental
function (17) Recovery occurs in 6 h.
c. Intravenous marijuana syndrome
First described in 1968 by Henderson and Pugsley. Seen with IV injections.
Usual practice is to boil marijuana, strain it through cotton and inject into a vein.
(1) Symptoms – appear within 1 h. (i) nausea, vomiting and diarrhea (ii)
myalgia (iii) abdominal pain (iv) weakness and (v) hypotension.
(2) Signs – (i) fever, (ii) hepatomegaly, (iii) hypotension [due to hypovolemia
resulting from emesis and diarrhea; vasodilation due to circulating endotoxins,
due to unsterile equipment etc] (iv) muscle tenderness, (v) Renal insufficiency
(vi) tachycardia, (vii) tachypnea.
(3) Lab findings -
(i) Pronounced leukocytosis [>20,000/μl]
(ii) Platelets <100,000/μl [thrombocytopenia]
(iii) -Partial thromboplastin time
(iv) Azotemia [BUN >75 mg/dl; creatinine >5.8 mg/dl]
(v) -bilirubin in serum [> 4.1 mg/dl]
(vi) -creatine kinase [CK] in serum
(vii) -myoglobin in both serum and urine
(4) Pathophysiology – Vasodilation is the major mechanism.
(5) Management - IV administration of fluids, mannitol, vasopressors.

2. Fatal dose
(1) THC – 30mg/kg; (2) Charas - 2g/kg; (3) Ganja - 8g/kg; (4) Bhang - 10g/kg
(5) Some pointers - (i) Due to high FD [eg 700 g of bhang for a 70 kg person],
death occurs very rarely. If occurs, it is due to respiratory failure. (ii) In few
recorded deaths due to cannabis, there were either multiple drug ingestions, or
his health was already compromised [eg heart surgeries, pulmonary diseases
etc].

3. Fatal period
Several days.

4. Management
(1) Assurance
(2) Decontamination – Stomach wash or emesis following by activated
charcoal. Cathartics
(3) If patient is aggressive or violent – 5-10 diazepam IV
(4) If flashbacks occur – antianxiety agents
(5) antipsychotics, eg haloperidol
(3) psychotherapy.

5. PM appearances
(1) Not characteristic (2) Findings of asphyxia.

E. Chronic Poisoning

1. Signs and symptoms

(1) General - (i) Facial expressions – sleepy, vacant (ii) Loss of appetite (iii)
Suffused eyes (iv) Tremors (v) Wasting (vi) Weakness.
(2) Amotivational syndrome - A constellation of effects associated with
substance use [especially cannabis], including apathy, loss of effectiveness,
diminished capacity to carry out complex or long-term plans, low tolerance for
frustration, impaired concentration, and difficulty in following routines.
(3) Medical conditions –
(i) Cancers - of mouth and lung [cannabis is a potential carcinogen]
(ii) Cannabis [or cannabinoid] Hyperemesis Syndrome [CHS] – First described
in 2004. Had been described earlier as psychogenic vomiting, but known to
be associated with cannabis. Occurs after several years of moderate to
heavy use of cannabis in susceptible individuals. (a) Characterized by (I)
recurrent episodes of vomiting (II) symptomatic relief with a hot bath and
showers (b) Treatment - The only effective treatment is cannabis cessation.
(c) Mechanism – It is paradoxical that despite THC being antiemetic, CHS
is produced on prolonged use. Appears to be through dysregulation of endo-
cannabinoid receptors and episodic gastroparesis [THC delays gastric
emptying]. Relief from hot baths and showers appears to be due to
temporary improvements in autonomic dysfunction. (d) A history of
cannabis use should be enquired in all patients presenting with unexplained
recurrent or cyclical vomiting.
(iii) Chronic lung disease - airway narrowing
(iv) Dermatology - Striae on body. Etiology not clear.
(v) Digital clubbing
(vi) Heart - Bradycardia, CCF, Non-specific ST wave changes
(vii) CNS – Degeneration of neurons, poor cognition
(viii) Hormonal and sexual – in males [.fertility, .serum testosterone, .sperm
count, Gynecomastia, Impotence]
(ix) Infarctions – (a) May cause infarctions [eg cerebral infarction, MI] (b)
Mechanisms -(I) cardio embolism [because of -ed risk of arrhythmia] (II)
coagulopathy (III) disruption of atherosclerotic plaque in response to stress
(IV) hypotension or hypertension (V) reversible cerebral vasoconstriction
syndrome (VI) vasculitis (VII) vasospasm.
(x) URI - Chronic sore throat, Rhinitis, Bronchitis.
(4) Psychiatric conditions - Hashish insanity [syn, Charas insanity] may
develop
(i) Existing schizophrenia – (a) exacerbation of condition (b) behavioral
problems (c) criminal behavior (d) Delusions [of persecution] (e)
Hallucinations [auditory, visual] (f) Moral and mental deterioration (g)
Culture bound syndromes [CBS]–Conditions occurring in certain cultures
only. Two main CBS are seen in cannabis (I) Amok - Running amok
[Malay mengamuk, to make a furious and desperate charge] is a psychiatric
condition in which a person runs about deliriously killing anyone who
comes in way [killing spree]. Salient features: [1] Etiology - Consumption
of cannabis. [2] Sequence - Period of depression"followed by sudden
running around and killing people with whatever comes in his hand [knife,
gun] " depression once again, during which he either commits suicide or
surrenders himself to police. (II) Koro [Malay koro, turtle’s head] – Male
person has a belief that his penis is shrinking and may disappear in to his
abdominal wall and then he may die. Females are affected similarly with a
corresponding belief that their breasts [and/or vulva] are shrinking.
(ii) Normal people – (a) may become psychotic, and show same symptoms as
above. However it is possible that latent schizophrenia already exists in
people who abuse cannabis chronically. (b) Manic or paranoid psychosis
may develop.
(iii) Normal people with no latent schizophrenia – no authentic proof of
development of psychosis.
(5) Diseases due to contamination of street marijuana. Long term use of such
contaminated drug use may cause diseases. Some common contaminants are
 (i) Animal feces (ii) Aspergillus spores [Aspergillosis] (iii) Formaldehyde (iv)
Fungi [Histoplasmosis] (v) Heavy metals [lead, mercury] (vi) Herbicides
[paraquat] (vii) Insects (viii) Microorganisms [Salmonella] (ix) Other drugs
[PCP etc].

2. Withdrawal
Known as “Marijuana Withdrawal Syndrome“. (1) Insomnia (2) Irritability
(3) Mild agitation (4) Nausea, cramping (5) Restlessness (6) Sleep EEG
disturbance.

F. Tests
(1) Colour tests -
(i) Duquenois-Levine test - Suspected material + Duquenois-Levine reagent
[2% vanillin + 1% ethanol] + Conc HCl + chloroform " Purple colour in
the chloroform layer indicates a +ve result. This is a presumptive test for
THC and other cannabinoids. Lacks specificity, and is thus good only as a
screening test.
(ii) Fast blue B salt test - Wine red colour indicates presence of cannabis. Also
known as KN test.
(iii) p-dimethylaminobenzaldehyde (p-DMAB) test - Red colour changing to
violet indicates presence of cannabis.
(2) Thin Layer chromatography.

G. ML Importance
(1) Aphrodisiac – cannabis is consumed because it is falsely thought to - sexual
desire and duration of coitus.
(2) Driving under influence of cannabis – Cannabis is the 2nd most common
drug of abuse found in drivers [after alcohol]. It does not affect driving
performance significantly when used alone, but when taken with alcohol, the
effects are pronounced. It is possible for a driver to be driving within safe
legal alcohol limit [BAC <30 mg%], but driving may still be impaired if
cannabis is ingested concomitantly. Police officer can arrest u/s185(b) of
Motor Vehicles Act 1988,and produce the accused for medical examination
u/s202 MVA. Laboratory tests can be ordered u/s204 of MVA [ch 40].
(3) Heavy metal poisoning – Lead and mercury poisoning have been described
 in marijuana abusers.
(4) Manner of poisoning-
(i) Abuse - Most cases of poisoning are due to abuse,
(ii) Accidental ingestion or inhalation - occurs also.
(iii) Suicidal – extremely rare. Virtually not known
(iv) Homicidal – Not possible, because of large fatal dose and peculiar odor
(5) Physiological dependence or addiction – is not seen with cannabis
(6) Run amok - Please see above
(7) Reasons for which cannabis is taken – (i) To produce euphoria [most
common] (ii) to overcome feeling of tiredness (iii) to overcome feelings of
hunger and thirst (iv) to achieve union with God [most often by ascetics, fakirs
and religious mendicants] (v) to improve concentration
(8) Second Hand Marijuana Smoke – A person may passively inhale
marijuana smoke from the environment if an addict is smoking nearby. In
random workplace testing [ch 46] such an innocent person may be falsely
implicated. To avoid such complications, most labs set a higher threshold
before reporting THC in the system.
(9) Stupefying poison – Unsuspecting strangers are given majoon and charas to
commit (i) rape (ii) robbery (iii) Other criminal acts, which are committed as
soon as stupefying effects begin to take over. Majoon and charas are offered
by road poisoners to unsuspecting travelers often in trains and buses. After
stupefaction sets in, they are robbed of valuables.
(10) Sometimes taken by criminals themselves to gather courage before
committing a criminal act.

IV. COCAINE

Cocaine [Blow, “C”, Charlie, Coke, Devil’s Dandruff, lady or “she” (as opposed
to “he”-heroin), Snow] is a colorless, odorless, crystalline substance with a bitter
taste.
Salient features:
(1) The alkaloid cocaine comes from the leaves of Erythroxylon coca, which
grows in South America, India and Java (Fig 41.4).
(2) A coca leaf typically contains less than 2% cocaine.
(3) By treating the leaves with sulfuric acid, cocaine sulfate is produced, which
 in turn is converted to cocaine hydrochloride by treating it with HCl. Cocaine
HCl contains 90% cocaine and is either snorted or injected. It cannot be
smoked, as its vaporization point is high at which cocaine disintegrates.
Smokeable form of cocaine (free cocaine, free base or crack – makes a
“crackling” sound when heated) is produced by treating cocaine HCl with
baking soda. Act of snorting free base is referred to as freebasing.
(4) Second most commonly used illicit drug of abuse after cannabis. [please see
ch 46 for full list].

A. Mechanism of Action
(1) Blocks reuptake of biogenic amines [dopamine, norepinephrine,
epinephrine, serotonin]. -epinephrine" tachycardia; -norepinephrine"
hypertension; -dopamine, -serotonin" reward" cocaine addiction. -serotonin
 also causes seizures.
(2) -es excitatory amino acid concentrations in the brain (psychomotor
agitation, hyperthermia, seizures). Excitatory amino acid antagonists
prevent seizures and death in experimental animals.
Memory Aid 2: Reuptake of biogenic amines blocked by cocaine
SEND – Serotonin; Eepinephrine; Norepinephrine; Dopamine
Memory Aid 3: Main side-effect of cocaine
-Serotonin at Synapses causes Seizures

B. Toxicokinetics
(1) Absorption - Rapidly absorbed following all routes of exposure. Marginally
slower when applied to mucus membranes (nasal, urethra, vagina, rectum) or
when ingested because of its vasoconstrictive action [limits absorption].
Smoking cocaine produces immediate effects; intranasal administration takes
5-10 min. 90% bound to plasma proteins. Vd is 2.7L/kg.
(2) Metabolism - occurs through three routes (i) 50% is hydrolyzed to
benzoylecgonine (BE) (ii) 45% metabolized by plasma cholinesterase
(PChE) to ecgonine methyl ester (EME). Persons with low PChE activity
demonstrate increased sensitivity to cocaine (iii) 5% undergoes N-
demethylation in the liver to form norcocaine.

C. Acute Cocaine Poisoning

1. Symptoms and signs

[A] Modes of administration - (1) On smoking and IV administration onset
of action is within 1 minute, peak action in 3-5 minutes; (2) nasal insufflation
" onset of action in 1-5 min, peak action in 20-30 min; (3) Oral ingestion "
onset of action in 30-60 min, peak action in 60-90 min. Duration of action varies
from half hour to 2 hours. Since the duration of action is short, cocaine has to be
repeated frequently to maintain a high. [B] Cocaine produces organ toxicity in
every organ due to (a) its vasospastic action (b) -hemorrhagic tendencies
secondary to vasospasm and (c) enhanced coagulation. [C] Symptoms and signs
- (1) Initially - there is bitter taste, dryness in the mouth, dysphagia, euphoria.
Headache may occur due to vasospasm. (2) Sympathomimetic toxidrome - (i)
Arrhythmias, (ii) diaphoresis, (iii) hypertension, (iv) hyperthermia [cocaine
fever], (v) mydriasis, (vi) tachycardia, (vii) tachypnea – [Please also see ch 31
under the heading “toxidromes”]. (viii) -ed inotropic and chronotropic activity of
heart + - in peripheral vascular resistance"(a) acute MI (b) CAD (c) coronary
vasoconstriction (d) SAH (e) stroke (f) thoracic aortic dissection. (3)
Neuropsychiatric manifestations – Hypomanic picture with -d psychomotor
activity, -d speech output, agitated delirium, grandiosity, elation of mood,
hypervigilance [being constantly tense and “on guard”], seizures. (4) Eyes –
acute angle closure glaucoma (due to mydriasis). Loss of vision (vasospasms of
retinal vessels). Madarosis (loss of eyebrow and eyelash hair) occurs from
thermal injury associated with smoking crack cocaine. (5) Chest pain – due to
ischemia to heart. (6) Asthma like symptoms – Smoked cocaine (not IV
cocaine) produces asthma like symptoms (cough, shortness of breath, wheezing).
This is because of (a) thermal insult to bronchi (b) AEME (AnhydroEcgonine
Methyl Ester) – the unique pyrolytic metabolite of cocaine produces
bronchospasm. (7) Abdomen – abdominal pain due to local ischemia of GIT, -
acid production associated with -sympathetic activity. Bloody stools. Intestinal
infarction. (8) Renal – Renal failure. Mechanism is agitated
delirium"Seizures"rhabdomyolysis"release of myoglobin. (9) Paralysis -
Vasospasm in the spinal cord can produce paralysis from an anterior spinal
artery syndrome. (10) Crack dancing - Choreoathetoid movements.

2. Fatal dose
1 g IV. Toxic symptoms occur after 200 mg. Regular users can take up to 10 g.

3. Fatal period
Few minutes to few hours.

4. Management

a. Decontamination
(1) Gastric lavage with warm water containing KMnO4, if taken orally
(2) If snuffed, nasal irrigation with NaCl
(3) in cocaine body packer, surgical removal of cocaine packets.

b. General supportive care

(1) Maintain airway, breathing and circulation. Tracheal intubation may be
required. Succinylcholine which is usually given prior to tracheal intubation
is contraindicated in cocaine toxicity. Reasons (a) cocaine
seizures"Rhabdomyolysis"hyperkalemia"exacerbation of hyperkalemia by
succinylcholine"dysrhythmia. (b) PChE metabolizes both cocaine and
succinylcholine. Their simultaneous use could cause either prolonged cocaine
toxicity, or paralysis or both.
(2) For hyperthermia – rapid cooling with ice water immersion. Avoid
antipyretics (acetaminophen or salicylates), drugs that prevent shivering
(chlorpromazine, meperidine) and dantrolene. Reason"potential for adverse
drug reactions.
(3) For agitation – sedation with benzodiazepines (midazolam, diazepam). If
benzodiazepines fail, give short acting barbiturate or propofol. Avoid
phenothiazines and butyrophenones (enhance cocaine toxicity, interfere with
heat dissipation, exacerbate tachycardia, prolong QTc interval).
(4) For hypoglycemia – Hypertonic dextrose.
(5) For hypertension – Use direct acting vasodilators (nitroglycerin or
nitroprusside), or α adrenergic antagonists (e.g. phentolamine). β
adrenergic antagonists are absolutely contraindicated (resultant unopposed α
adrenergic effect produces life threatening vasospasm and hypertension).

c. Specific management
(1) For acute coronary syndrome (cocaine induced coronary vasoconstriction,
and MI) – high-flow oxygen therapy, aspirin (reduces platelet aggregation),
morphine (reduces cocaine-induced vasoconstriction, preload reduction,
reduction of catecholamine release), nitroglycerin, diltiazem (for tachycardia,
atrial fibrillation). In patients with underlying atherosclerotic heart disease,
consider revascularization (cardiac catheterization). If cardiac
catheterization can not be done, consider thrombolytic therapy.
(2) For wide-complex dysrhythmias – hypertonic sodium bicarbonate,
lidocaine.

5. Additives of cocaine
(1) Levamisole - Used to adulterate cocaine because
(i) adds bulk and weight to powdered cocaine [similar appearance to cocaine]
(ii) makes it appear more pure
(iii) possible stimulant effects, and
(iv) an ability to pass street purity tests. It thus acts as a diluent and synergistic
adulterant both [ch 40].
(2) Others - (i) Amphetamine, (ii) local anesthetics, (iii) phencyclidine, (iv)
strychnine, (v) thallium. Cases of thallium poisoning after cocaine use have
been reported. (vi) Thiamine.

6. Tests for cocaine

(1) Gold Chloride test –
(i) Reagent - Gold Chloride in Acetic Acid.
(ii) Suspected material + one drop of reagent" characteristic crystals form
immediately.
(2) Scott test - Suspected material + 5 drops of Cobalt thiocyanate [shake]"Blue
colour develops at once.

7. PM appearances

a. External
(1) perforated nasal septum – only if the victim was a chronic cocaine addict
[For details – please see below under ch cocaine poisoning].
(2) Nasal swabs and injection sites would reveal cocaine.
(3) Oropharynx - burns from inhaling superheated fumes of crack cocaine
(4) Injection site - Toxic contaminants (particulate matter, strychnine) may be
demonstrated.

b. Internal
(1) Nasal passages and nasopharynx - congestion
(2) GIT – Mucosal edema, congestion
(3) Brain - Subarachnoid, intraventricular and intraparenchymal hemorrhages.
These hemorrhages are second to intense vasospasm produced by cocaine.
(4) Lungs -
(i) Crack lung – diffuse alveolar hemorrhage [due to pulmonary vasoconstriction
" damage to epithelial and endothelial cells], hemorrhagic alveolitis
(ii) Pulmonary infarction – due to vasospasm and thrombosis of pulmonary
 artery
(iii) Pneumothorax and pneumomediastinum are sometimes seen. These are not
due to cocaine per se, but due to Valsalva maneuver that the addict
performs after inhalation of smoke (bearing down against a closed
epiglottis). This -es intrathoracic pressure. An alveolar bleb may rupture
against the pleural or mediastinal surface
(iv) Toxic contaminants (particulate matter, strychnine) may be demonstrated in
the lungs.

c. Viscera
Cocaine may be recovered from liver and brain.

D. Chronic Cocaine Poisoning

[syn. Cocainism, cocainophagia, cocainomania] Sniffers generally use 0.5 g
daily.

1. Signs and symptoms

(1) Magnan’s symptom (cocaine bugs, formication) - illusory sensation of ants
crawling under the skin. The patient scratches his skin as a result, causing
irregular scratches, excoriation and ulcers.
(2) Nasal septum -
(i) Perforation – due to necrosis which in turn occurs due to vasospasm and
enhanced coagulation. (a) size – varies from a pinhead to several mm (b)
Shape – may be round, oval or irregular (c) Seen in 5% of cocaine snorters.
(d) Seen also in ch arsenic poisoning [ch 36]. (e) Perforation of the nasal
septum reduces the nasal support and results in a broad, flat nose (saddle
nose).
(ii) Granulomas of the nasal septum.
(3) Perforation of the palate - Seen more in females. Addicts with a palatal
perforation suffer from serious speech impairment. Their speech becomes
hypernasal and articulation may be so poor that they can not communicate
effectively. In addition, eating and drinking is difficult due to oronasal reflux
of both solids and liquids. Some addicts resort to obturating the defect by
inserting chewing gum, a piece of white bread or a plug of tissue paper into
the palatal defect.
(4) Tongue – black.
(5) Bruxism (grinding of the teeth accompanied by clenching of the jaw)- occurs
frequently in cocaine addicts. Gives rise to pain in the temporomandibular
joint and masticatory muscles. Attrition of teeth is seen.
(6) Crack eye - Corneal defects are seen.

2. Cocaine withdrawal
(1) Bradycardia
(2) Cocaine craving
(3) Dysphoria, depression
(4) Sleepiness, fatigue. Cocaine is probably the best example of a substance to
which neither tolerance nor physical dependence develops and with which
simply psychic dependence can lead to profound and dangerous levels. Out of
7 types of drug dependence, one is cocaine type [ch 46].

3. Management [of chronic cocaine poisoning]

Management for cocaine abuse is quite ineffective, especially in comparison
with those for other abused substances.
(1) Drugs for reducing craving - (a) Amantadine [antiparkinsonian] (b)
Bromocriptine [dopaminergic agonist] (c) Aripiprazole – It is a second
generation antipsychotic. Blocks cocaine-seeking behaviour, due to its action
on dopamine receptors.
(2) Drugs for both reducing craving and for antidepressant effect - (a)
Desipramine (b) Imipramine (c) Trazodone
(3) Recent drugs -
(i) Agonist replacement therapy [sustained-release methylphenidate, d-
amphetamine]
(ii) Dopamine agents (disulfiram).
(iii) GABAergic agents [vigabatrin]
(iv) Glutamatergic agents [N-Acetylcysteine, modafinil, topiramate]
(v) Ibogaine [ch 46].
(4) Psychosocial management techniques – (a) Contingent behavior therapy
and (b) Supportive psychotherapy are useful in the post-withdrawal treatment
and in prevention of relapse.
(5) Vaccination - TA-CD is a vaccine against cocaine. It is a cocaine derivative
 coupled to the recombinant cholera toxin B (rCTB) carrier protein. It
inactivates the cocaine molecule and also inhibits its passage to the brain.

4. PM appearances
As above in acute poisoning.

E. Medicolegal Importance [of Cocaine]

(1) Brompton’s cocktail is a mixture of cocaine, morphine (or heroin),
chlorpromazine and alcohol. It is sometimes provided to patients suffering
from pain associated with terminal illness such as cancers. Named after the
Royal Brompton Hospital in London, England, where it was invented in the
late 1920s for patients with tuberculosis.
(2) Contaminated currency - ch 46.
(3) Prostitutes sometimes inject cocaine into vagina to produce local
constriction.
(4) Rubbed on glans penis sometimes by addicts, as it is wrongly considered to
be an aphrodisiac.
(5) Control of illegal coca plants with herbicides – In several countries [eg
Colombia], large tracts of lands where illegal coca plants are grown are spray
aerially with herbicides [eg glyphosate]. This may cause off-target spraying
[about 1% of the total area sprayed]. Exposures to humans and wildlife is also
a concern.

42. Spinal and Peripheral Nerve

Poisons

I. SPINAL POISONS

A. Strychnos Nux Vomica

(1) Active principles: The whole tree, including the seeds, is poisonous. The
active principles are alkaloids strychnine and brucine. Strychnine is about
 10-20 times more poisonous than brucine. The alkaloidal content of the seeds
ranges from 1.8 to 5.3%. They also contain a glucoside loganin.
(2) Use - (i) used as rodenticides, and for killing stray dogs. The commercial
baits available contain < 0.5% strychnine and are dyed red or green to make
them distinctive. (ii) Once used as a tonic and a reflex stimulant of gastric
secretion (because of its bitter taste) (iii) Analeptic and Respiratory
stimulant – But only in toxic doses.
Strychnine – It occurs as colorless, odorless rhombic prisms, and has an
intensely bitter taste. Strychnine is one of the most bitter substance known;
its taste is detectable in a dilution of 1:70,000.

1. Absorption and excretion

(1) Strychnine is rapidly absorbed from the GIT, nasal mucosa, and all parenteral
sites.
(2) It is rapidly metabolized in the liver (up to 80%) by microsomal enzymes.
(3) The highest concentrations of strychnine are found in the liver, kidneys and
blood.
(4) Strychnine taken up by liver and muscles may be released into the blood
stream, as its concentration falls. This may produce convulsions on 2nd or 3rd
day of poisoning after sedation is discontinued.
(5) About 15% appears unchanged in the urine within 24 hours.
(6) Traces appear in bile, milk and saliva.
(7) Elimination half life of strychnine is 10h.
(8) Strychnine may be found in the cadaver up to 4 y.

2. Mechanism of action
Strychnine mainly acts at the anterior (ventral) horn cells of the spinal cord,
where glycine is a major post-synaptic inhibitory neurotransmitter, and prevents
its effects. By inhibiting the inhibitory transmitter, it brings about excitation
(convulsions).

3. Signs and symptoms

[A] Uncrushed seeds - swallowed as such do not cause poisoning, as the hard
coat is not dissolved by GIT juices. They are passed as such in the feces. [B]
When crushed seeds are taken, the symptoms start after one hour. [C] When
pure alkaloid is swallowed, symptoms appear within 5 minutes. [D] Dermal
exposure - Tingling sensation locally. Other symptoms as in ingestion. [E]
Ingestion - Symptoms are (1) Bitter taste in mouth, a sense of restlessness and
uneasiness, anxiety, fear and a feeling of suffocation (2) difficulty in
swallowing (3) Prodromal symptoms – appear before onset of convulsions: (i)
-acuity of perception (ii) -rigidity of muscles and (iii) muscular twitchings (4)
Convulsions - First clonic, eventually become tonic. During convulsions (i)
patient has an anxious look (ii) Eyes - are prominent and staring (iii) Pupils -
are dilated (iv) Mouth – is covered with froth, which is frequently bloodstained
(v) Face - is cyanosed (vi) Duration of convulsions – ½ to 2 minutes.
Breathing stops (spasm of diaphragm, and other accessory muscles of
respiration) (vii) Period between convulsions – Muscles are completely
relaxed. Patient looks relatively better, although severely exhausted. Breathing
resumes. Cyanosis .s. Cold perspiration covers the skin. Dilated pupils may
contract (viii) Resumption of convulsions – Occurs after 5-15 minutes, or
earlier if there is slightest sensory stimulus (eg touching the patient, a current of
air, lights, noise etc) (ix) Opisthotonus - (a) Most common convulsive symptom
(b) Spasms are most marked in antigravity muscles. Results in hyperextension of
the body. In supine position, the body may be supported only by the heels and
head. The body assumes a bow like form. The arms are flexed over the chest or
rigidly extended; hands are tightly clenched and the legs are abducted and
extended. (x) Emprosthotonus - Sometimes spasms of abdominal muscles are
more prominent. This is the “mirror image” of opisthotonus, in which the body
is bent forwards (xi) Pleurosthotonus - bending of the body sideways, if lateral
muscles are in greatest spasm (xii) Risus sardonicus - (L. risus, laughter; Gk.
sardonius, mocking) Highly characteristic, abnormal, sustained spasm of the
facial muscles (appears as if patient is grinning). Results from contraction of jaw
muscles. Corners of mouth are drawn back. Spasms may have to be
differentiated from tetanus [Table 1]. (xiii) In non fatal cases – Interval
between convulsions -s. Spasms .. Recovery occurs in 1-2 days (xiv) In fatal
cases - Convulsions rapidly succeed one another. Severity and duration -s. Death
occurs usually after 4-5 cycles of convulsions and relaxations (5) Effects of
Convulsions: (i) Temp - -ed; up to 43°C (ii) Lactic acidosis – Blood pH may fall
to 6.6 "leads to death (iii) Rhabdomyolysis - Myoglobin released in blood "Renal
tubular blockage "Renal failure. (6) Consciousness – is not lost. Mind remains
clear till death (strychnine does not act at cerebral level). Patient is conscious of
his impending death, and suffers greatly. (7) Cause of death: (i) Medullary
hypoxia (ii) spasm of diaphragm leading to respiratory arrest (iii) fall of blood
pH (iv) Renal failure due to myoglobinuria.
4. Fatal dose
(1) One crushed seed (2) Strychnine - 30mg/kg.
5. Fatal period
1-2 hours.

6. Management
(1) Control of convulsions - (i) Room – Patient should be kept in a dark, noise
free room, free of all disturbances [any sensory stimulus can start convulsions]
(ii) Drugs – (a) Diazepam 0.1-0.5 mg/kg slow IV, followed by (b)
Barbiturates - Phenobarbital IV. Short acting barbiturates [pentobarbital
sodium, sodium Amytal in doses of 0.3-0.6 g IV] (c) Muscle relaxants (eg.
Curare, Gallamine, Mephenesin, Pancuronium bromide, Succinylcholine) (d)
General anesthesia – if all measures fail to control convulsions. Inhalation
anesthetics would fail during convulsions (because respiration stops). During
relaxation phase administer any inhalation anesthetic (eg ether)
(2) Gastric lavage and emesis – Not recommended because of -risk of
convulsions.
(3) Activated charcoal – to minimize absorption
(4) After control of convulsions – Correct fluid, electrolyte and acid-base
abnormalities. These would have been caused by repeated convulsions.
(5) Diuresis - Opinion is divided regarding forced acidic or alkaline diuresis.
Forced acidic diuresis is advantageous in strychnine [ch 32]. However urine
alkalinization is useful as prophylaxis against renal failure secondary to
rhabdomyolysis, which in turn is secondary to convulsions. Physician’s
judgment is important.

7. PM appearances
(1) Signs of asphyxia
(2) Rigor mortis – starts early. Prolonged.
(3) Stomach, duodenum – congested. Show patches of ecchymoses
(4) All internal organs including spinal cord - Congested
(5) Peritoneum – may show hemorrhages
(6) Muscles – show microscopic tears [due to violent convulsions], extravasated
blood.

8. Tests
(1) Sonnenschein’s test - Suspected material + 1 drop of H2SO4 + cerosoceric
oxide"stir with a glass rod"a deep blue color is formed, changing to violet, and
finally to cherry red.
(2) Wenzell’s test - Suspected material + [KMnO4 – 1 part + H2SO4 – 2000
parts]"Color reaction [after William Wenzell (1829–1913), an American
physician].
(3) Physiological test – Aqueous soln of Suspected material"Inject into the
dorsal lymph sac of a frog"produce tetanic convulsions in a few min.

9. ML importance
(1) Used for homicide – in the form of (i) alkaloid (ii) Powdered Nux vomica
seeds. It has a very strong bitter taste; thus usually given in alcohol [a pungent
drug] to mask its taste.
(2) Suicide – Rare, because of painful death
(3) Accident – More common (i) Administration by mistake (ii) Eating seeds
[children] (iii) Medicinal preparation overdose
(4) Cattle poison - Seeds
(5) Arrow poison
(6) Used as an aphrodisiac.
(7) Used as an adulterant in street drugs [eg amphetamines, cocaine and
heroin].
(8) Secondary poisoning [please see ch 31] – Strychnine is used as a
rodenticide. Secondary poisoning have been recorded in many non target
domestic and wildlife species, who eat rodents killed with strychnine.
(9) Used as a stimulant and performance enhancing drug - In low dosages
has been used by athletes to enhance their performance.
(i) 1904 St. Louis Olympics - British marathon winner Thomas Hicks took it.
There were no restrictions on performance enhancing drugs then.
(ii) 1992 Barcelona Olympics - Wu Dan, female Chinese volleyball player took
it.
(10) Strychnine both delays and resists putrefaction [please also see ch 9].
(11) Used for extortion – Paracetamol laced with strychnine.

II. PERIPHERAL NERVE POISONS

A. Curare
Curare is a common name for various arrow poisons originating from South
America.
Salient features:
(1) Curare is not a single chemical, but a mixture of several chemicals
(2) Source: (i) Chondodendron sp [C. platyphyllum; C. tomentosum] (ii)
Strychnos sp [S. curare, S. toxifera]
(3) Types: (i) Tubocurare [syn, tube or bamboo curare, because it is packed in
hollow bamboo tubes]. (a)Active principle: D-tubocurarine [a mono-
quaternary alkaloid; isoquinoline derivative]. It is the best known of all active
principles of curare (ii) Calabash curare [syn, gourd curare, because it is
packed into hollow gourds]. (a) Active principles: Alloferine and toxiferine
(iii) Pot curare [because packed in terra cotta pots]. (a) Active principles:
protocurarine, protocurine, and protocuridine. Calabash curare is most toxic.
(4) Mechanism of Action: (i) Curare is a non-depolarizing muscle relaxant.
Occupies nicotinic acetylcholine receptors (nAChR) with greater affinity than
Ach, eliciting no response [competitive antagonist]"flaccid paralysis of
skeletal muscles. (ii) Action is entirely peripheral, at myoneural junction.
(5) Toxicokinetics: (i) Not absorbed through oral or GIT mucosa [molecules are
too large and highly charged to pass through GIT lining]. Thus harmless when
swallowed. Animals killed by curare tipped arrows are thus safe to eat (ii)
Absorbed through wounds or abrasions.

1. Signs and symptoms

The drug has little or no effect if taken by mouth, unless swallowed in very large
doses. Symptoms after arrow poisoning are
(1) Muscular:
(i) The muscles of the jaw, neck, and head are the first to become weak and
relaxed.
(ii) Then the arms and legs begin to feel heavy and difficult to move. Soon it is
impossible to move at all.
(2) Eyes: (i) Pupils – dilated (ii) Vision – Blurred
(3) Hearing - Low tones are heard better because small muscles in the middle
ear relax.
(4) Respiration:
(i) Becomes harder.
(ii) Victim experiences “shortness of breath,” even with artificial respiration.
(iii) Paralysis of respiratory muscles
(iv) Feels like he is choking because saliva accumulates in the throat.
(5) Swallowing – becomes difficult
(6) CNS – Headache, dizziness, vertigo. No loss of consciousness and mental
faculties are clear till the end. In large doses, short phase of excitation with
muscular movements, convulsions and loss of consciousness
(7) Hypotension [due to liberated histamine]
(8) Death - from respiratory failure and asphyxia.

2. Fatal dose
60 mg.

3. Fatal period
1-2 h.

4. Management
(1) Artificial respiration – Effects of curare do not last long, and if artificial
respiration is provided, effects begin to wear off after about 20 minutes.
(2) Antidotes:
(i) AChE inhibitors - (a) Physostigmine [3 ml of 1:200 soln IV] (b)Neostigmine
[5-10 mg IV].
(ii) Aminopyridine - Acts by blocking K+ channels, prolonging action potentials
and thereby -ing neurotransmitter release at the NMJ [please see ch 39
also].

5. PM appearances
Similar to those of asphyxia.

6. MLI
(1) Curare was introduced for general anesthesia by Harold Griffith in 1942.
(2) Used as an arrow poison
(3) Homicide – Possible, but has to be administered parenterally. Case study -
In 1917 Alice Wheeldon [1866-1919] of UK and her family were convicted
 for planning to murder British Prime Minister David Lloyd George by
administering curare to him through a spiked nail in his boots [Other imp
forensic case involving British Prime Minister - ch 28].

B. Conium Maculatum (Poison Hemlock)

(1) Conium maculatum (Poison hemlock, spotted hemlock, poison parsley,
spotted cowbane) is a member of the parsley family [Umbelliferae] and is
often mistaken for it’s edible relatives - fennel, anise and chervil.
(2) It grows to 8 to 10 feet.
(3) It has white, umbrella-shaped flower clusters, which appear in spring and
strongly resemble those of Queen Anne’s lace [wild carrot].
(4) Stems are hollow, ribbed and purple-spotted.
(5) The leaves emit a strong musty odor when crushed
(6) All parts of the plant are highly toxic.
(7) Active principles – Alkaloids present in Hemlock are coniine and some
congeners.
(8) Coniine content is highest in the (i) leaves [especially at flowering time] (ii)
roots [especially during summer] (iii) seeds and (iv) unripe fruit.

1. Signs and symptoms

(1) Burning in the mouth and throat
(2) Nauseating taste and unpleasant mousy odor
(3) Vomiting, diarrhea
(4) R/R.
(5) Pulse-. Later.
(6) CNS: (i) Ataxia (ii) Blindness [sometimes] (iii) Mental confusion (iv)
Progressive motor paralysis extending upwards from the extremities (v)
Tremors
(7) Death from respiratory failure.

2. Fatal dose
60 mg of coniine.

3. ML importance
Socrates, the Greek philosopher was executed in 399 B.C. by forcing him to
drink a cup of poison hemlock. The plants stems show purple mottling, which
are sometimes called the “blood of Socrates”.

43. Cardiac Poisons

I. ACONITE

Aconitum [aconite, blue rocket. Devil’s helmet, helmet flower, leopard’s bane,
Meetha Bikh, Meetha Bish, Meetha zeher, monkshood, wolfsbane, women’s
bane] is a genus of flowering plant belonging to the buttercup family
(Ranunculaceae).

A. Active Principles
(1) Main - C19-diterpenoid-ester alkaloids - (i) aconitine, (ii) mesaconitine, (iii)
hypaconitine, (iv) jesaconitine, (v) Yunaconitine.
(2) Other alkaloids - (i) aconine, (ii) bikhaconitine, (iii) indaconitine (iv)
lappaconitine (v) picraconitine (vi) pseudoaconitine.

B. Mechanism of Action
Na+ channel activation - Aconite alkaloids opens up Na+ channels [by binding
at site 2] "- Na+ influx through them "- inotropy while delaying the final
repolarization phase of action potential " promotes premature excitation of
myocardial muscle. [Tetrodotoxin (ch 39) has an exactly opposite action. That is
why mixing up the two can delay death]. As a consequence of repeated
depolarization, the Na+ channels become refractory to excitation. In older books
this was often described as initial stimulation followed by depression of CNS.

C. Toxicokinetics
Absorbed through all routes. Eliminated mainly through urine, but through other
routes as well.

D. Signs and Symptoms

1. Routes other than ingestion

(1) Eyes exposed to Pollen " pain and swelling
(2) Touching – Leaves or roots handled for a long time or rubbed on the skin
"numbness, tingling
(3) Inhalation – Root inhaled for a long time has a narcotic effect.

2. Ingestion
Symptoms appear immediately or within a few minutes.
(1) GIT -
(i) Burning sensation from the mouth to stomach
(ii) Numbness, tingling in the mouth tongue and pharynx
(iii) Salivation, nausea, vomiting, diarrhea
(iv) Later – Mouth is dry, thirst, dysphagia.
(2) CVS –
(i) ECG and heart rhythm changes - (a) Atrial and ventricular arrhythmias,
resistant to electric defibrillator. (b) AV block (c) Bundle branch block (d)
 Ectopic beats (e) Tachycardia followed by bradycardia (f) Torsades de
pointes [Fr “twisting of the points] (g) Ventricular ectopics
(ii) BP.
(iii) Pulse – slow, feeble, irregular.
(3) Respiratory –
(i) Feeling of constriction in the chest
(ii) Respirations slow, labored and shallow.
(4) CNS –
(i) Consciousness clear. Sometimes there may be hallucinations
(ii) Headache and giddiness
(iii) Numbness and tingling over entire body
(iv) Restlessness
(v) Vertigo.
(5) Muscular –
(i) Marked weakness of muscles with spasms and twitchings
(ii) Shooting pain in muscles
(iii) Limbs become weak
(iv) Patient unable to stand or walk
(v) Cramps and convulsions.
(6) Skin – (i) Pallor (ii) profuse sweating (iii) cold and clammy skin.
(7) Other – temp..
(8) Eyes - (i) Diplopia (ii) Impaired vision (iii) Hippus - Pupils contract and
dilate alternately. Fluctuations in pupillary diameter [about 1-2 mm] occur
with a marked periodicity [5s]. Remain dilated in later stages.

E. Cause of Death
Ventricular fibrillation mainly. May be by respiratory failure.

F. Fatal Dose
(1) Root – 1-2 g (2) ild plant – 1 g. (3) Aconitine – 2 mg. (4) Extract – 250 mg
(5) Tincture – 5 mL.

G. Fatal Period
2-6 hours.
H. Management
(1) Gastric lavage – with warm water and weak soln of tannic acid, or I2 in KI.
Precipitates alkaloids
(2) Activated charcoal
(3) Atropine – 1 mg
(4) Cardiac monitoring
(5) Symptomatic

I. PM Appearances
GIT mucosa – congested, ecchymosed. Stomach may contain root pieces
Viscera – congested Toxicological analysis clinches the diagnosis. Aconitine is
extremely unstable and is destroyed by putrefaction. Quick analysis is most
important.

J. ML Importance
(1) Arrow poison – The name aconite itself derives from Gk akon, dart or
javelin.
(2) Cattle poison
(3) Suicide – Used as a suicidal poison.
(4) Homicide –
(i) Used alone - Once very popular with killers, but not very commonly used
now. In India, traditionally it was given with betel leaves to conceal its
taste. Occasional cases still occur.
(ii) Mixed with other poisons – When mixed with tetrodotoxin, the death may
be greatly delayed.
(iii) Reasons why aconite was once a popular homicidal poison - (a) Cheap and
easily available (b) Lethal dose small (c) Fatal period short (d) Taste is
somewhat sweetish. Can be made more acceptable by mixing it in paan (e)
Destroyed by putrefaction, hence cannot be detected
(5) Accidental poisoning – Caused under following circumstances (a) Usually
mistaken for horseradish root, which is edible. (b) Mixed with liquor to -
intoxication (c) Used as abortifacient. (d) Used in traditional medicine - Roots
[“bushi”] are used in Chinese herbal medical practice to treat rheumatic pain,
 paralysis due to stroke, carbuncle and furuncle. May cause accidental
poisoning. (e) Used by quacks in India.

II. CINCHONA ALKALOIDS

Cinchona (after a Countess of Chinchon, the wife of a viceroy of Peru) genus

belongs to family Rubiaceae, and contains between 30-40 species.
Salient features:
(1) The plant is native to tropical South America. They were transported for
cultivation in India by the British in nineteenth century.
(2) The bark of the tree [Jesuit’s bark, Peruvian bark] contains quinine, a
levorotatory alkaloid. Its d-isomer is quinidine, which is used as
antiarrhythmic [and as an antimalarial in some countries].
(3) Active principles – The bark contains more than 20 alkaloids, most
importantly (i) quinine. Other important alkaloids are (ii) dihydroquinine, (iii)
quinidine, (iv) dihydroquinidine, (v) cinchonine and (vi) cinchonidine.
(5) Mechanism of action – Quinidine blocks myocardial Na+ channels.

A. Signs and Symptoms

Signs and symptoms after a single large dose or high therapeutic doses taken for
a few days are grouped under the term cinchonism. The symptoms are:
(1) Ophthalmologic - blurred vision, Visual field loss, color vision defects, optic
nerve edema, optic atrophy, blindness
(2) Vestibuloauditory symptoms – hearing loss, tinnitus, and vertigo
(3) CNS – Headache, giddiness, confusion, delirium, seizures, coma, and
encephalopathy
(4) GIT – abdominal pain, nausea, vomiting, and diarrhea.
(5) CVS - arrhythmias, conduction defects, and hypotension
(6) Hematologic – hemolysis, anemia
(7) Skin – diaphoresis, flushing, erythematous or urticarial rash.

B. Fatal Dose
(1) Quinine 2-8 grams; (2) quinidine 4-6 grams.
C. Fatal Period
6 hours.

D. Treatment
(1) Gastric lavage - of doubtful value because vomiting usually occurs before
admission and that quinine is rapidly absorbed
(2) Activated charcoal
(3) Forced acidic diuresis
(4) Stellate ganglion block – causes return of vision immediately
(5) IV hydrocortisone – if signs of hemolysis appear
(6) Hemodialysis and peritoneal dialysis – are useless as cinchona alkaloids are
largely protein bound.

E. PM Appearances
(1) Organs - congested
(2) red cell hemolysis
(3) Kidneys
(i) Renal tubules blocked by hemoglobin.
(ii) Papillae swollen
(iii) Engorgement of the peritubular capillaries
(4) Liver – fatty change.

F. ML Importance
(1) Accidental - Poisoning is usual accidental due to overdose
(2) suicide – rare
(3) Homicide – very difficult because of bitter taste. May be mixed with alcohol
and given
(4) Abortifacient. Please see ch 26 for its use as an ecbolic
(5) Urine - Quinine is often found in the urine of patients who drink gin and
tonic. Malaria was endemic in India in the 19th century. The British stationed
in India needed quinine to prevent malaria. Since quinine is soluble in very
small quantities of alcohol, they would dissolve it in the gin they drank and to
mask the bitter taste, they would use lemon or lime. This was the “gin and
tonic” (tonic because quinine preserved health by preventing malaria). By
 tradition, tonic water still contains small amounts of quinine, although the
intention now is never to prevent malaria – it is simply preservation of
tradition. Quinine fluoresces under ultraviolet light. Gin containing tonic
water glows blue in bars having UV lights.

III. DIGITALIS PURPUREA

(1) English physician William Withering (1741 –1799) first learned of the use
of Digitalis purpurea [Common Foxglove, Purple Foxglove, Lady’s Glove],
in congestive heart failure from an old woman who practiced as a folk
herbalist in Shropshire. He studied it scientifically in 1775 demonstrating its
value in dropsy [edema]
(2) In 1905 James Mackenzie showed its special value was in heart failure with
atrial fibrillation. Digitalis prepared from it is widely used in cardiology today.
(3) In 1930 Sydney Smith isolated a new glycoside, which he called digoxin,
from the Balkan or woolly foxglove Digitalis lanata. Digoxin is extracted
directly from the plant, and is not synthesized.
(4) It is thought that the Dutch painter Vincent Van Gogh may have been
poisoned by digitalis (used at that time as a treatment for epilepsy). His art
shows prevalent use of yellow color, which could be because he was suffering
from Xanthopsia (yellow vision) due to foxglove poisoning. He also painted
his physician, Dr Gachet twice showing him holding a foxglove.
(5) Etymology – The word digitalis comes from the finger shaped flowers [L,
digitus, a finger]. The word foxglove comes from an old tradition according to
which fairies gave the flowers to foxes to wear on their feet so that they could
move in magic silence up to hens or away from men.

A. Active Principles
(1) Leaves - (i) Digitoxin, (ii) Gitoxin
(2) Seeds - (i) Digitalin. It does not contain digoxin, which is present only in the
leaves of its cousin Digitalis lanata.

B. Signs and Symptoms

Cardiac – Almost every type of dysrhythmia is produced. Most frequent
dysrhythmia is ectopic ventricular rhythm. Bidirectional Ventricular
Tachycardia (activity arising alternately from the left anterior and posterior
fascicle, giving rise to “bidirectional” appearance) is virtually diagnostic of
poisoning. Extracardiac – GIT – Nausea, vomiting (due to gastric irritation and
CTZ stimulation) Abdominal pain (due to mesenteric vasoconstriction) CNS –
anxiety confusion delirium depression disorientation drowsiness Fatigue, no
desire to walk or lift an arm, mental confusion, restlessness hallucinations
headache muscle weakness trigeminal neuralgia Endocrine - Gynecomastia.
Skin – Urticaria Visual disturbances - transient amblyopia, blurring of vision,
chromatopsia (aberrations of color vision), decreased visual activity,
photophobia, photopsia (perceived flashes of light), scotoma and Xanthopsia
(yellow halos).

C. Fatal dose
Digitalin – 15-30 mg Digoxin [present in D. lanata] – 10 mg Digitoxin – 4mg;
Leaves 1-2 (2g) Therapeutic blood levels for digoxin are 0.5-1.0 ng/mL. Toxic
levels for digoxin are >2.0 ng/mL.

D. Fatal period
24 h.

E. Management
(1) Gastric decontamination – by emesis or lavage is rarely needed because
digitalis is emetic It is rapidly absorbed from GIT. If required, tannic acid is
used.
(2) Whole bowel irrigation.
(3) Activated charcoal – Even late administration is useful as both digoxin and
digitoxin have enterohepatic and enteroenteric circulation. Multiple Dose
Activated Charcoal (MDAC) is useful for the same reason [ch 32].
(4) Steroid-binding resins - eg cholestyramine and colestipol prevent
reabsorption from the GI tract. Also interrupt enteroenteric and enterohepatic
circulation.
(5) Digoxin-Specific Antibody Fragments or Fab [Digibind, DigiFab].
(i) Availability – Digibind [38 mg/vial] or DigiFab[40 mg/vial] in lyophilized
form.
(ii) Administration – (a) Vial is reconstituted with 4 mL of sterile water. (b)
 Dose – (I) Acute ingestions - 10-20 vials in both child and adult. (II)
Chronic toxicity – Adult – 3-6 vials; children - 1-2 vials. (c) Used in -
Toxicity with digoxin, digitoxin, and all natural cardioactive steroids, eg
nerium, oleander, squill, and toad venom.
(6) If Fab fragments are not available - Antiarrhythmics - (a) Lignocaine -
1mg/kg IV bolus. Followed by continuous infusion at 1-4mg/min in adult; 20-
50 μg/kg/min in child. (b) Phenytoin [dilantin]- 50 mg/min slow IV. Max 1g in
adult; 15-20 mg/kg in child. Maintenance oral dose - 300-400 mg/day in
adults; 6-10 mg/kg/day in child. (c) Propranolol and Reserpine - have been
found useful.
(7) Management of bradycardia -
(i) Mechanism of bradycardia and varying degrees of heart block - digitalis
induced effects of -ed vagal tone on SA node rhythmicity and on AV node
conduction
(ii) Atropine - 0.5 mg IV in adult; 0.02 mg/kg in child. Repeat every 5 min till
normalization of heart rate.
(iii) External or transvenous pacemaker - in severe bradycardia.
(8) Management of extrasystoles and arrhythmias -
(i) Magnesium - 20mL of 20% soln over 20 min by slow infusion. To be used
with caution in renal failure
(ii) Potassium salts.
(9) For hypercalcemia - Trisodium EDTA.
(10) Hemodialysis - Does not remove digitalis, but restores serum K+ levels to
normal.
(11) Hemoperfusion - using antidigoxin antibodies.
(12) Percutaneous cardiopulmonary bypass - for therapy resistant cardiac
arrest.
(13) Symptomatic - Electrolyte disturbances must be treated, eg magnesium and
potassium levels which may be abnormally low or high.

F. Postmortem Appearances
Fragments of leaves in GIT – if leaves were consumed GIT mucosa –
inflamed Pulmonary congestion Confirmatory - Detection and measurement of
Digoxin and other cardiac glycosides is confirmatory.
G. ML Importance
(1) Bitter taste - Although foxglove is widely grown as an ornamental plant,
few people ingest it because of its bitter taste
(2) Accidental ingestion - may occur from consumption of contaminated
water in or near which plants have been standing or from smoke from
burning plants
(3) Mistaken for comfrey [Symphytum officinale] - Comfrey leaves resemble
those of foxglove when the plant is not in bloom. Comfrey is used as a herbal
medicine for treating fractures, tendon injury, GIT ulceration, lung congestion,
joint inflammation, and promoting wound healing. Comfrey tea is usually
taken for these ailments, and leaves must be gathered from wild. Wild-food
gatherers mistake the plant for comfrey, and use it in their herbal concoctions.
This accounts for most cases of toxicity.
(4) Iatrogenic poisoning – Can occur during overambitious treatment with
digitalis.

IV. NERIUM OLEANDER

Both Nerium oleander (white or pink Oleander, Kaner) and Thevetia peruviana
(yellow oleander) belong to the Dogbane family, Apocynaceae. Description [Fig
43.1] -
(1) N. oleander grows wild in India. It is an evergreen shrub that grows to about
6-7 m in height.
(2) Leaves are lanceolate [spear-shaped], 10-25 cm long, leathery, dark green on
upper surface, lighter beneath; display distinct light yellowish veins.
(3) Flowers, usually fragrant, are present in clusters at the tip of twigs. They are
white to pink to deep red in color [rarely pale yellow], with 5 spreading petals.
Width is 2.5-5 cm.
(4) Fruit [seed pod] – Slim, cylindrical, narrow, ribbed pod, about 15 cm long.
Upon drying it turns brown and splits, releasing many small seeds with brown
silky hairs.
(5) Sap is thick, gummy and clear
(6) Nectar yields toxic honey [please see ch 39 – Food poisoning for more on
“toxic honey”].
Salient features:
(1) Poisonous parts - (i) All plants of the plant including (ii) nectar are
poisonous. (iii) Seeds and roots contain the highest percentage of cardiac
glycosides followed by (iv) fruits and leaves.
(2) The total cardiac glycoside content is higher in plants producing red flowers
than in plants producing white flowers. Highest concentration occurs during
the flowering stage.
(3) Active principles – (i) Adynerin, (ii) Digitoxigenin, (iii) Folineriin, (iv)
Nerioside [Nerin] (v) Oleandrin (OD). Also present are (vi) Oleandrigenin
(ODG), a potentially toxic deglycosylated congener of OD, and other
glycosides namely (vii) adynerin, (viii) desacetyloleandrin (ix) gitoxigenin, (x)
neriantin, (xi) neritaloside, (xii) odoroside H (xiii) Rosagenin (xiv) strospeside
and (xv) urechitoxin.
A. Mechanism of Action
All active principles mentioned above are cardiac glycosides resembling digitalis
in action, i.e. inhibition of Na+ K+ ATPase.

B. Signs and Symptoms

(1) Contact – Dermatitis
(2) Inhalation – of emanations from flower, especially when fading cause
nausea, headache, dizziness and respiratory difficulty.
(3) Ingestion – (A) Symptoms – (1) GIT - (i) Profuse frothy salivation (ii)
Vomiting and Diarrhea (iii) Difficulty in swallowing and articulation (iv)
Abdominal pain (2) Neuromuscular - (i) Muscular twitchings (ii) Tetanic
spasms (iii) Lock-jaw (iv) Drowsiness (v) Coma. (B) Signs - (1) Pupils -
dilated (2) Pulse – initially slow. Later rapid and weak. (3) RR - Initially -.
Later respiratory paralysis. (4) BP. (5) Heart - Atrial and ventricular
fibrillation, AV block. In severely poisoned patients, fatal cardioversion-
resistant ventricular fibrillation or refractory cardiogenic shock may occur. (6)
ECG abnormalities – [observed both in N. oleander and T. peruviana] (i)
lengthened PR segment, (ii) shortened and depressed S-T interval, (iii)
absence of P wave (iv) flattened or inverted T wave. (v) ventricular
arrhythmias, (vi) bradyarrhythmias, (vii) sinus and AV block. Death occurs
from cardiac failure.

C. Fatal Dose
(1) Root: 15-20 g
(2) Leaves: 5-15 in number
(3) Children have died after ingesting a handful of flowers.

D. Fatal Period
24-36 h.

E. Management
(1) Emergency measures - Resuscitate. Monitor pulse, BP, and oxygen
saturation. Place on a cardiac monitor and take a 12-lead ECG. Insert IV
cannula and give fluids IV.
(2) Gastric lavage or emesis followed by activated charcoal.
(3) Treat marked hypotension (systolic <70 mmHg) and bradycardia
 [<40/min] - Bolus doses of atropine (2–3mg) or an infusion (0.6mg/h). Aim is
to keep the heart rate around 70–80 bpm.
(4) Treat hypokalemia and hypomagnesaemia - until both concentrations are
back in the high normal range. Measure serum electrolytes and magnesium on
a continuous basis.
(5) Antidote –
(i) Specific antidote is Digoxin-Specific Antibody Fragments (Fab) [Please see
above under “Digitalis”].
(ii) Indications [of Fab]- (a) AV node and/or severe sinus node block (b)
ventricular tachycardias, (c) serum K+ > 5.5 mEq/L [Normal levels 3.5 - 5.0
mEq/L].
(iii) Dose - 400 mg over 20 min followed by 400–800 mg over 4–8h by infusion.
(6) In the absence of anti-digoxin Fab -
(i) Administer insulin/dextrose
(ii) Do not give calcium
(iii) Temporary pacing – for severe bradycardia due to AV block
(iv) Low energy DC cardioversion – to treat VF.

F. PM Appearances
Not characteristic
(1) Congestion of all organs
(2) Leaves may be found in stomach.

G. ML Importance
(1) Suicide – Root, leaves, fruit or seeds are used as a paste or decoction for
committing suicide. In one study in Sri Lanka, oleander and paraquat were
responsible for 74% of suicides in people under 25 years old.
(2) Homicide – Rare because of bitter taste.
(3) Abortifacient – Root applied locally or ingested.
(4) Folk treatment –
(i) Swellings – decoction of leaves is applied externally
(ii) Venereal diseases - Root is applied locally or ingested
(iii) Cancers and ulcers – Root is applied as paste
(iv) Miscellaneous – Various parts of the plant used in asthma, cancer, cardiac
 illnesses, corns, diabetes mellitus, epilepsy and scabies. However, in none
of these conditions is there good evidence for genuine cure.
(5) Cattle poison – Juice of root is applied on piece of cloth and inserted into the
anus of the animal to kill it [cf ch 37"calotropis; ch 38"snake venom for
similar uses].
(6) Smoke – from burning plant is toxic and can cause death.
(7) Heating food directly over burning twigs – Can cause death as poisonous sap
is transferred to the food.
(8) Arrow and dart poison.
(9) It can be detected long after death.
(10) During the Persian campaign, Alexander’s army lost horses that had fed on
N. oleander, and some soldiers died who had grilled their meat on skewers
made from the wood.

V. THEVETIA PERUVIANA

T.peruviana [syn, Cascabela thevetia, Cerbera thevetia, T.neriifolia][common

names; be still tree, lucky nut, pila kaner, yellow bells, yellow oleander] is an
evergreen tropical shrub or small tree that bears yellow or orange-yellow,
trumpet like flowers.
Salient features:
(1) Family - Dogbane family [Apocynaceae].
(2) Tree -
(i) Flowers [Fig 43.2]– large, yellow, bell-shaped, 5-7 cm long, 5 cm wide; 5
lobes spirally twisted and spreading.
(ii) Leaves –[Fig 43.2]– lanceolate [lance like].
(iii) Fruit [Fig 43.2]– Globular, light green, 4-5 cm in diameter, encases a single
large nut, which is triangular having a deep groove along the edge. Each nut
contains 5 pale yellow seeds. All parts of are poisonous. Highest
concentration of cardiac glycosides is in the kernel of seeds, followed by
leaves, fruit and sap.
(3) Active principles – Neriifolin, Peruvoside, Ruvoside, Thevetin A,
Thevetin B, Thevetoxin (all are cardiac glycosides resembling digitalis in
action, i.e. inhibition of Na+ K+ ATPase.
VI. NICOTIANA TABACUM (TOBACCO)

Nicotiana tabacum, [syn tobacco] is a perennial herbaceous plant belonging to

the Solanaceae family [Other poisonous plants of the Solanaceae family are
Datura, A. belladonna, H. niger, S. tuberosum].
Salient features:
(1) The plant - grows to heights between 1 to 2 meters.
(2) Leaves -
(i) Elliptical or oblanceolate
(ii) Dried leaves [tobacco, tambaku] contain 1-8% of nicotine. They are chewed,
snuffed or smoked.
(3) Flowers –
(i) are bell shaped [much like those of oleander]
(ii) clustered at the end of the branches
(iii) Reddish in color at their upper parts
(iv) Have a cylindrical calyx
(4) Fruit – has different forms with globular seeds
(5) Active principles - (i) Acrolein (ii) Anabasine [an alkaloid similar to the
nicotine but less active] (iii) Anatabine (iv) Anatalline (v) Anethole (vi)
Anthalin (vii) Cembrene (viii) Choline (ix) Glucosides [tabacinine, tabacine],
 (x) Nicotelline (xi) Nicotine (xii) Nicotianine (xiii) Nornicotine and (xiv)
Pyrene
(6) Nicotine –
(i) It is a bitter, colorless to pale yellow, hygroscopic, volatile, oily liquid
alkaloid, with an unpleasant pungent odor, and sharp, burning, persistent
taste. It gradually becomes brown on exposure to air or light
(ii) Uses – extensively used in agricultural and horticultural work, for fumigation
and spraying, as insecticides and worm powders etc.
(7) All parts of the plant are poisonous except ripe seeds. Leaves have the
highest concentration of nicotine.
(8) Frequency of use –
(i) Tobacco is a socially acceptable drug. Among socially acceptable drugs, it is
the 2nd most common drug of abuse after caffeine [please see ch 41 for
most common illicit drugs].
(ii) Smoked in cigarettes, bidis; chewed as betel leaf; inhaled as snuff.

A. Toxicokinetics
(1) Absorption -
(i) Nicotine is readily absorbed through all mucus membranes, lungs and skin
(ii) One standard cigarette contains – 15-20 mg of nicotine, of which only 1-2
mg is absorbed by smoking [More than half escapes during idling. A large
amount remains in the butt and filter].
(iii) An average cigar contains – 15-40 mg nicotine. About 2-4 mg is absorbed.
(2) Metabolism -
(i) Nicotine has a high degree of first-pass metabolism, with 70–80% being
metabolized in liver to cotinine.
(ii) Some is metabolized in kidneys and lungs.
(3) Distribution -
(i) Rapidly and widely distributed throughout most of the body.
(ii) Vd 1–3 L/kg.
(iii) There is also enterohepatic and enteroenteric circulation - Following IV
administration, it appears in GIT.
(iv) Freely distributed in breast milk
(v) Plasma protein binding – low [5 to 20%].
(vi) Crosses - blood brain barrier, placenta.
(4) Excretion -
(i) Nicotine is predominately excreted by kidneys
(ii) Negligible elimination in sweat or feces.
(iii) Half-life of nicotine - 2 h [range 1–4 h]. Half-life of Anabasine - 15.9 h.
(iv) Urinary excretion of both nicotine and anabasine are pH dependent, with
excretion -ed in an acid urine and by high urine output.

B. Mechanism of Action
(1) Nicotine acts agonistically at nicotinic-type acetylcholine (cholinergic)
receptors (nAChRs). It is a classic cholinergic agonist.
(2) These receptors exist widely throughout the body, particularly in
(i) Adrenal medulla
(ii) Autonomic ganglia
(iii) Chemoreceptors of aortic and carotid bodies
(iv) CNS [brain stem, limbic system, midbrain, reticular activating system
(RAS)]
(v) NM junctions and (vi) Spinal cord.
(3) Direct stimulation of nicotine receptors in endocrine glands + stimulation of
neurohumoral pathways in CNS"-ed release of hormones [ACTH, ADH
(vasopressin), catecholamines, cortisol, GH, prolactin, serotonin, β-
endorphins] and enzymes [amylase, chymotrypsin, trypsin].
(4) At moderate doses – Nicotine stimulates the RAS"- in alertness"favorable
effects of attention and memory.
(5) At high doses – CNS disinhibition"convulsions, tremors.

C. Signs and Symptoms

1. Acute poisoning
(1) GIT – (i) Nausea, salivation, vomiting [stimulation of CTZ, - in
gastroesophageal reflux due to lowering of sphincter pressure and - acid
secretion]
(ii) Abdominal pain
(iii) Burning acid sensation
(iv) diarrhea [both central and parasympathetic excitation].
(2) Cardiopulmonary –
(i) Initially - -HR, -RR, Hypertension, followed after about 1 hour by
bradycardia, hypotension, shock.
(ii) Later – .HR, .RR, hypotension, cardiac arrhythmias.
(3) RS – initially bronchorrhea, Tachypnea. Followed after about 1 hour by
hypoventilation and apnea.
(4) CNS -
(i) Initially - (a) agitation (b) anxiety (c) ataxia (d) blurred vision (e) confusion
(f) headache (g) hyperthermia (h) miosis (i) restlessness (j) sweating (k)
tremors (l) vertigo.
(ii) Later - (a) hyporeflexia (b) hypotonia (c) lethargy and weakness (d)
mydriasis (e) muscular fasciculations and convulsions and (f) coma.
(5) Eyes -
(i) Nystagmus
(ii) Pupils – Constricted at first, but may dilate later
(iii) Photophobia and disturbed vision.

2. Chronic poisoning
(1) General - anemia, faintness.
(2) RS - Asthma, bronchitis, cough, dyspnea, emphysema, pneumonia,
wheezing.
(3) GIT - anorexia, vomiting, diarrhea, peptic ulcer.
(4) CNS - Alzheimer’s disease, impaired memory, tremors.
(5) Eyes - amblyopia, blindness.
(6) CVS - angina pectoris, arrhythmias, arterial thrombosis, coronary heart
disease, extrasystoles, hypertension, stroke.
(7) In women -
(i) Osteoporosis - .estrogen levels due to enhanced hydroxylation of estradiol"-
ed risk of osteoporosis.
(ii) Obstetric conditions - abortion, abruptio placenta, placenta previa, pre-
eclampsia, preterm labor.
(iii) Neonatal effects - congenital malformations, fetal or neonatal death, growth
retardation, SIDS.
(8) Occupation dermal exposure – to wet uncured tobacco may produce “green
 tobacco sickness”, characterized by
(9) .appetite; -BMR"Wt loss [reverse symptoms during withdrawal].
(10) Long term effects - pulmonary cancer, non pulmonary cancers - brain,
mouth, larynx, esophagus, breast, stomach, liver, pancreas, bladder, cervix.

D. Withdrawal Symptoms
(1) Symptoms (i) -appetite and wt gain (ii) -RR (iii) -sweating (iv) -urge to
smoke (v) Anxiety and depression (vi) Concentration and memory – impaired
(vii) Headache (viii) Hostility (ix) Muscle cramps (x) Sleep disturbances.
(2) Treatment – Nicotine Replacement Therapy [NRT]. Use of nicotine
products [gum, lozenge, inhaler, nasal spray, transdermal patch].

E. Fatal Dose
(1) Nicotine - 50-100 mg
(2) Crude tobacco – 15-30 g.

F. Fatal Period
5-15 minutes. Rivals cyanide [ch 44] as a poison capable of producing quick
death.

G. Diagnosis
(1) plasma nicotine level > 50 ng/mL indicates serious toxicity. Most valuable
test [early withdrawal of blood required because of short half life].
(2) sample of suspected plant is taken to a botanist for identification.
(3) Corroborative - (i) glycosuria (ii) polymorphonuclear leucocytosis.
(4) Cotinine levels are -ed in tobacco workers and persons exposed to tobacco
smoke.

H. Management

1. Acute poisoning

a. Dermal exposure
(1) Dermal exposure to wet tobacco leaves – wash skin thoroughly with soap
 and cold running water to reduce absorption.
(2) The medical staff must wear impervious gloves and gowns during these
procedures to avoid secondary exposure.

b. Ingestion
(1) Protect airways – as vomitus may be aspirated. Also consider assisted
ventilation, intubation, oxygen, +ve pressure ventilation.
(2) Gastric lavage – with warm water containing charcoal, KMnO4, tannin.
(3) Whole bowel irrigation (WBI).
(4) Activated charcoal – MDAC [ch 32]. Because nicotine undergoes
enteroenteric and enterohepatic circulation.
(5) Emetics – contraindicated because of active prior vomiting [ch 32]. Further
vomiting may lead to fluid and electrolyte imbalances and hypovolemic
hypotension.
(6) -ing Elimination -
(i) Forced acidic diuresis – Since nicotine is a weak base [pKa = 8.0–8.5],
excretion can theoretically be enhanced by acidification of the urine. But
not recommended because of seizures and rhabdomyolysis. Furthermore
symptoms in nicotine poisoning are short-lived.
(ii) Simple fluid diuresis - safer but unnecessary because of limited urinary
elimination.
(7) Antidotes -
(i) Atropine sulphate – 1-2 mg IM – for bradycardia
(ii) Hexamethonium - ganglionic blocker. Prevents nicotine-induced seizures.
Dose – 25-50 mg s/c
(iii) Mecamylamine (Inversine) - competitive and noncompetitive antagonism to
the central effects of nicotine. Has been used in nicotine dependence also
[please see below]
(iv) Pempidine – action same as mecamylamine.
(8) General supportive measures -
(i) Seizure control [benzodiazepines]
(ii) IV fluids, hemodynamic support, vasodilators [dopamine, noradrenaline] for
hypotension [ch 32].

2. Chronic poisoning
Aim is to . dependence [. craving] and treat signs and symptoms.
(1) Clonidine – Also used in alcohol and opiate withdrawal. Mechanism same
[ch 40]. Dose 150-200 µg/day for 1 month.
(2) Nicotine partial agonists – Bind weakly and competitively to nicotine
receptor sites .ing craving.
(i) Cytisine - syn baptitoxine, sophorine.
(ii) Lobeline [CigArrest].
(iii) Varenicline (Chantix).
(3) Nicotine antagonists - Mecamylamine - start with 5-10 mg/day orally and -
progressively until the subject experiences nicotine blockage and/or toxic
effects. Only after 3 weeks subjects undergoing therapy either cease smoking
totally or . cigarette consumption. Side-effects of therapy are constipation,
urinary retention, abdominal cramps, and weakness. These are responsible for
drop-outs in some cases. Useful for recalcitrant nicotine dependence.
(4) Nicotine replacement therapy [NRT] - (i) Nicotine gum [Polacrilex] (ii)
Nicotine spray (iii) Nicotine transdermal patch.
(5) Immunotherapy - Vaccines that would generate antibodies to sequester the
drug and prevent its access to the brain. Currently under development for 4
major drugs of abuse – cocaine, methamphetamine, morphine/heroin and
nicotine.
(6) Miscellaneous – Antidepressants – (a) Doxepin, sertraline - combat
depression associated with withdrawal of smoking. (b) Bupropion [Wellbutrin,
Zyban] - Atypical antidepressant. Also .es severity of nicotine cravings and
withdrawal symptoms.

I. Cause of Death
Respiratory failure

J. Postmortem Appearances
(1) Same as those of asphyxia
(2) skin – brownish stains
(3) Mouth and nostrils – brownish froth
(4) Lungs – pulmonary edema
(5) GIT –
(i) Stomach - Smell of tobacco, contents show small fragments of leaves,
brownish discoloration of stomach wall
(ii) Hemorrhagic congestion.

K. ML Importance
(1) Application of wet tobacco compresses to cutaneous eruptions - can result
in poisoning.
(2) Malingering – Tobacco leaves are soaked in water for some hours"placed in
axillae at bedtime [held in place by a bandage]"poisonous symptoms are seen
next day
(3) Nicotine resists putrefaction.
(4) Manner of poisoning -
(i) Accidental poisoning –due to (a) ingestion (b) excessive smoking (c)
application of leaves or juice to wounds or skin
(ii) Suicidal - rare
(iii) Homicidal poisoning – rare, but occurs from time to time. Please see
Bocarmé case above
(iv) infanticide - (a) nicotine is applied over nipples of a nursing mother and
baby allowed to suck milk (b) mixed with milk which is given to infant.
(5) Smugglers - sometimes transport tobacco by hiding it under their clothes.
They suffer from severe nicotine poisoning, as it is absorbed from skin. In one
case a convict brought tobacco in his jail cell by smuggling it in his rectum,
and suffered severe nicotine poisoning.
(6) Insecticide – Nicotine functions as an antiherbivore with particular
specificity to insects; therefore nicotine was widely used as an insecticide in
the past [in conc up to 40%, in the 1920s and 1930s]. Currently nicotine
analogs such as imidacloprid are widely used. May cause accidental
poisoning.
(7) Has been used to control stray dog population [for euthanizing stray dogs].
(8) used in animal tranquillizer darts.
(9) Lead arsenate is used as a pesticide on tobacco crops"risk of Pb poisoning
among smokers [ch 36].
(10) Chop chop tobacco [syn, loose tobacco] – cheap, home grown, illegal,
untaxed tobacco, sold in Australia. The term was coined in the mid-1890s.
Originates from the fact that it is produced by chopping up the cured tobacco
 leaves. It is popular because it avoids heavy excise and taxation levies and is
much cheaper than the legal product. It contains several contaminants eg
cabbage leaves, chloride products, grass clippings, hay, twigs and pulp from
raw cotton. Mould and fungi are also present which cause toxic responses in
the lungs, liver, kidneys and skin eg allergic reactions, asthma, chronic
bronchitis, legionnaire’s disease and lung cancer.
(11) Miscellaneous - Nicotine has differential effects on the left- and right-hand
sides of developing neural system. Prenatal exposure to tobacco -es tooth
crown asymmetry between antimeric permanent teeth [ch 3].

44. Asphyxiants and Toxic Gases

Asphyxiants, toxic gases, noxious gases, or irrespirable gases refer to gaseous

poisons, which kill either by displacing oxygen from the environment (e.g.
Nitrogen) or by a variety of more complex mechanisms (e.g. Carbon Monoxide,
Chlorine). If oxygen is supplied along with the former, the organism would not
be affected. It would be immaterial, if oxygen is supplied with the latter; the
organism would still suffer ill health or death.

I. CLASSIFICATION

Asphyxiants may be classified as follows: I. Simple Asphyxiants – inert gases,

which will not have any action on their own, and would not kill if sufficient
oxygen were available along with. They kill by excluding oxygen from the
lungs. Ex. nitrogen, all inert gases (helium, argon, xenon etc), methane. II.
Respiratory Irritants – injure air passages or both and produce inflammatory
changes. Ex. Ammonia (NH3), tear gas, formaldehyde, chlorine, phosgene,
nitrogen dioxide, sulfur dioxide. III. Chemical Asphyxiants (systemic
asphyxiants) – produce ill health, disease or death, by specialized mechanisms,
such as by combining with Hb. Ex. Carbon monoxide, hydrogen sulfide, carbon
disulfide, hydrogen cyanide gas, CO2 [earlier CO2 was thought to be a simple
asphyxiant]. IV. Volatile drugs – essentially chemical asphyxiants, with the
exception that normally they are used therapeutically. Ex. Anaesthetic gases.

II. CARBON MONOXIDE (CO)

Salient features:
(1) Physical properties - Carbon monoxide (syn. Exhaust gas, flue gas, carbonic
oxide, carbon oxide) is a colorless, odorless, tasteless and nonirritant gas
which is lighter than air and insoluble in water. It burns with a blue flame,
producing carbon dioxide. It is highly toxic to humans and animals in higher
quantities.
(2) Normal atmospheric CO conc <0.001%.
(3) CO is formed normally in the body as a byproduct of heme degradation (via
heme oxidase); one molecule of CO is produced per molecule of heme
degraded. This produces sufficient CO to result in low levels of COHb even in
non-smoking persons (up to 1%). In hemolytic anemia this may rise up to
8%.
(4) CO, like NO, is a gaseous neurotransmitter in the CNS; it can diffuse and
signal adjacent cells much like nitric oxide (NO). Endogenously produced
CO serves as a signaling molecule in multiple cellular functions, such as
inflammation, proliferation, and apoptosis.

A. Mechanism of Action
CO is readily absorbed after inhalation. COHb levels can be predicted by the
Coburn-Forster-Kane (CFK) model. Assuming that the weight of individual is
70 kg, the model predicts the following:
COHb(%) =
100
1+
643
ppm CO

For example breathing 100 ppm CO would result in

COHb(%) =
 100
1+
643
100

or
COHb(%) =
100
7.43

or about 14%.
This is confirmed by actual volunteer experiments.
(1) Greater affinity to Hb - The affinity of CO to Hb is approximately 200-250
greater than that of oxygen. It also binds to other Fe-containing
hemoproteins, e.g. myoglobin (affinity 60 times greater than that of O2),
cytochrome P450, dopamine hydroxylase and cytochrome oxidase. 10-15% of
body stores of CO in poisoned patients are extravascular, primarily binding to
myoglobin. Binding to myoglobin explains myocardial impairment in CO
toxicity, especially in IHD patients.
(2) Leftward shift of the oxyhemoglobin dissociation curve - This .es the
release of O2 from oxyhemoglobin to tissue.
(3) Nitric Oxide (NO) induced endothelial damage - Neuronal cell death and
neuronal deficits produced by CO can not simply be explained by above
mechanisms. This is because comparable levels of anemia (as that produced
by CO) fail to produce similar neuronal lesions. The following mechanism is
now thought to be a major pathway of CO toxicity: CO displaces NO from
platelets"Displaced NO causes endothelial damage to brain
microvasculature"perivascular oxidative stress"activation of excitatory amino
acids"neuronal cell loss and neuronal deficits. (NO synthase inhibitors have
been shown to prevent CO toxicity via this mechanism).
(4) Apoptosis – Another mechanism suggested in CO toxicity. CO exposure has
been shown to activate caspase-1, a protease involved in cell death. (caspase-
1 inhibitors prevent CO toxicity).

B. Elimination
CO is not metabolized in the body. Nor is it excreted via skin, bile, perspiration,
urine or feces.
(1) Half life of CO in a healthy adult breathing 21% O2 is 4-5 hours (240-300
min).
(2) If breathing 100% O2 at NTP"40 min
(3) If breathing 100% O2 at 2.5 ATmospheres Absolute (ATA)"20 min.

C. Sources
CO would always be produced whenever there is fire in confined spaces
limiting the availability of O2. some common sources which produce CO in this
way are:
(1) Coal gas, smoke from fires and fumes from defective heating appliances (gas
and wood stoves, furnace, oil lamps, fire places, kerosene and gas water
heaters, angithi). Leaking chimneys
(2) Component of the fumes of coke kilns and lime kilns. Heating unit used only
occasionally and not well maintained. Barbecues.
(3) Produced after explosion in mines and detonation of explosives.
(4) Exhaust fumes of internal combustion engines.
(5) Tobacco smoke. Average levels of COHb in an average smoker is about
4%. In a heavy smoker it may be up to 20%. A smoker is estimated to be
exposed to 400 to 500 ppm of CO while actively smoking.
(6) Inhalation of fumes of methylene chloride (an ingredient of some
commercial paint removers) can cause severe intoxication. Fumes of
methylene chloride are metabolized within body to produce CO. People using
paint removers in poorly ventilated rooms have been poisoned with CO.

D. Acute Poisoning

1. Signs and symptoms

(1) Symptoms due to tissue hypoxia - headache, nausea, vomiting, dizziness,
lethargy and a feeling of weakness. D/d: (i) acute delirium tremens (ii) alcohol
poisoning (iii) cerebral vascular disease (iv) flu (v) food poisoning (vi)
hysteria (vii) migraine headache (viii) viral fever.
(2) Symptoms develop in severity as conc of COHb -es [Table 1].
(3) CO particularly affects organs that have high O2 utilization (CVS, CNS)
(4) Infants - may be irritable and feed poorly.
(5) Skin - There may be a cherry red discoloration of skin.
(6) CVS – Chest pain, palpitations, -Heart rate.
(7) CNS - Neurological signs include poor concentration, confusion,
disorientation, visual disturbance, syncope and seizures.
(8) Respiratory – Shortness of breath.
(9) Ophthalmoscopic examination - Retinal hemorrhages may be seen.
(10) Exposure during pregnancy may result in fetal loss. [More rapid metabolic
rate of fetus, high affinity of fetal Hb for CO].

2. Delayed sequelae
Neuropsychiatric syndrome [delayed CO encephalo pathy]: (i) Seen in about
30% cases. (ii) Occurs 2–40 days later [due to white matter demyelination]. (iii)
Main manifestations are (a) Akinetic mutism (b) cognitive deficits [impaired
attention, memory (due to damage to hippocampus, which is very vulnerable to
anoxia and ischemia) and visuospatial skills] (c) dementia (d) psychosis (e)
dystonias [and other motor impairments] (f) mood disorders (g) Parkinsonism
(h) personality changes (i) suicidal tendencies.
3. Diagnosis and investigation
(1) COHb levels – Most useful diagnostic test. COHb conc average 1% in
nonsmokers and 4% in smokers. >2% in a non-smoker and >10% in a
smoker confirm exposure to CO.
(2) Direct CO assays – with IR spectrophotometry. [CO conc 1 mmol/L = 11%
COHb].
(3) Cardiac monitoring and 12-lead ECG – essential for detecting ischemia
and dysrhythmias.
(4) Scintigraphy of heart with 99mTc - has been proposed as a method of
choice for evaluation of heart injury in patients after acute CO intoxication.
(5) Creatine phosphokinase (CPK) – slightly raised. Results from
rhabdomyolysis.
(6) Troponin - -(diffuse cardiac myonecrosis).
(7) Serum S100B levels - -. S100B is a structural protein in astroglia. Released
from brain after hypoxic stress.
(8) Plasma glutathione - -in rats exposed to CO. Oxidative stress"glutathione
release from RBCs (currently under investigation in humans).
(9) Serum pH and lactic acid levels – Monitor closely. Anaerobic metabolism
in the presence of tissue hypoxia generates lactic acid (metabolic acidosis). -
lactic acid is a highly reliable indicator of CO poisoning.
(10) Neuropsychological testing
(11) Neuroimaging:
(i) CT- Symmetric low-density areas in globus pallidus, putamen, caudate
nuclei (within 12 hours of exposure). Negative CT up to 1 wk"favorable
outcome.
(ii) Xenon enhanced CT – Shows .blood flow in cerebral cortex.
(iii) MRI – superior for detecting basal ganglia lesions. Periventricular white
matter changes.
(iv) PET scan - .blood flow in frontal and temporal cortex.
(v) EEG mapping (vi) SPECT – (Single photon Emission computer
tomography). Very promising. Shows .blood flow in cerebral cortex.

4. Management
(1) Removal - from source.
(2) Airway - Immediately secure airway and ensure adequate ventilation.
(3) Oxygen therapy:
(i) Normobaric oxygen [NBO] – Oxygen at NTP
(ii) Hyperbaric oxygen [HBO] – Oxygen at higher pressures, up to 3 ATA.
Administer HBO for 90-120 min. Benefits of HBO"(a) .es half life of CO
(b) -es amount of dissolved O2 by 10 times (c) prevents lipid peroxidation
in cerebral neurons, thereby minimizing incidence of neurologic damage (d)
prevents leukocyte adherence to brain microvascular endothelium (e)
accelerates regeneration of inactivated cytochrome oxidase. This is the
treatment of choice in patients who present with syncope, coma, or seizure,
focal neurological deficit, if COHb > 25% (or >15% in pregnancy).
(4) Sodium bicarbonate – If pH < 7.15. Exercise caution while administering
NaHCO3, because CO2, a by-product of its metabolism, could lead to
respiratory acidosis. Proper ventilation must be maintained.
(5) Close follow-up - Required for delayed sequelae.

5. Fatal dose
COHb conc.>60%

6. PM appearances
(1) Cherry red coloration – of skin, conjunctivae, mucus membranes, nail beds,
all internal organs.
Salient features:
(i) Seen when conc. of CO is > 40%. (ii) In dark colored individuals, seen more
easily in the inner aspects of lips, tongue, nail beds, palms and soles. (iii) D/d –
CN poisoning, exposure of dead body to cold (iv) With onset of putrefaction –
color changes to dark green and then brown.
(2) Blood – fluid
(3) Serous effusions in all body cavities
(4) Skin blisters [cutaneous bullae] – in wrists, interdigital surfaces of fingers,
buttocks, calves and knees. Friction areas are affected more. Complete list of
poisons causing blisters – [ch 40].
(5) Trachea – sometimes soot may be there
(6) Lungs:
(i) Congestion
(ii) Pulmonary edema
(iii) Pleural hemorrhages
(iv) Bronchopneumonic consolidation
(7) Heart:
(i) Pericardial hemorrhages
(ii) Frank MI [especially in the presence of pre-existing coronary disease]
(iii) Focal areas of necrosis [in delayed deaths].
(8) Brain:
(i) Consistency – firmer than normal. Brain retains its shape better after removal
from skull
(ii) Meninges – show hemorrhages
(iii) Basal ganglia – necrosis and cavitation, especially in globus pallidus and
putamen [in delayed deaths] - considered most characteristic lesions. Other
areas affected are cerebellum, cerebral cortex, hippocampus and substantia
nigra. This occurs because these areas have limited vascularity and a
watershed blood supply.
(iv) White matter – (a) punctiform and ring shaped hemorrhages with
widespread edema (b) Ganglion cells – selective cellular necrobiosis.
E. Chronic Poisoning
Chronic CO poisoning involves exposure to lower levels of the CO for longer
periods (>24 hours). Typically it results in lower blood CO (COHb)
concentrations. Exposure may continue for many days, months, even years, eg in
polluted industrial environments. (Diff: acute - one exposure lasting less than 24
hrs; chronic – exposure for more than 24 hrs).

1. Symptoms and signs

(1) Persistent headaches, lightheadedness, depression, confusion, memory loss.
(2) CVS patients – symptoms may worsen (chronic hypoxia to heart).
(3) Permanent neurological damage (chronic hypoxia to brain).
(4) Visual disturbances
(5) Elevated RBC count. Symptoms resolve, when removed from source.

2. Diagnosis and investigation

PET scan - metabolism .in the orbitofrontal and dorsolateral prefrontal

cortex and temporal lobes.

F. Different Air Concentration of CO and Its Effects

1% CO level (1000 ppm) causes death in 30 min without exertion and in 10 min
with exertion. 5% (5000 ppm) kills in 5 min. CO conc >50% (50,000) would kill
within seconds. Various %COHb and associated symptoms are given in (Table
1)

G. ML Importance
(1) Accidental CO poisoning - is usually found in poor people during winters,
 who sleep in small rooms with coal burning inside for warmth. Holiday
campers have been found dead, who slept in tents with propane gas stoves or
charcoal grills burning inside.
(2) Bruises - formed during [or after] CO poisoning are cherry red in color
[please also see ch 12 – Mechanical inj].
(3) COHb levels are -ed in burns. Presence of COHb is considered the surest
sign of antemortem burns [ch 14].
(4) Employer’s liability to pay compensation in cases of occupational disease
due to CO exposure – Same as MLI of Arsenic [ch 36].
(5) Hookah use - Hookah [also known in different cultures as goza, hubble
bubble, Narghile, qalyan, shisha, waterpipe] can lead to CO poisoning. A 25-
year-old man was brought to the emergency department (ED) after
experiencing two syncopal episodes in 1 week. An arterial blood gas analysis
was performed which revealed a high COHb level of 31.1%. Both syncopal
episodes had developed after hookah use.
(6) Postmortem production of CO – CO is produced due to decomposition of
Hb and myoglobin. This can cause a false interpretation of death due to CO
poisoning. In a case of true CO poisoning spuriously high concentrations [up
to 20%] may be recorded.

H. Tests

1. Hoppe-Seyler’s test
Blood to be examined (1 vol) + NaOH (2 vol)"if COHb present, solution
becomes red; otherwise dingy brown mass with a green shade. Spreading thin
on a white surface such as a porcelain tile brings out the colors better. Developed
first by the German Ernst Felix Immanuel Hoppe-Seyler (1825–1895).

2. Katayama test
Blood to be examined (10cc) + water (50cc) + orange-red ammonium sulphide
soln(4 drops) + 30% acetic acid (4 drops). Mixture is filtered. If COHb present,
filtrate remains red. If normal blood present, filtrate becomes green or grey.

3. Kunkel’s test (tannic acid test)

Blood to be examined (1cc) + water (10cc) + 3% tannic acid (4
drops)"Crimson red coagulum indicates presence of COHb.

4. Wetzel’s test
Blood to be examined (1 vol) + water (4 vol) + 1 % tannin soln (3 vol). If
COHb is present, the blood becomes carmine red; normal blood slowly assumes
a grayish hue.

5. Spectroscopic test
Characteristic absorption bands between Fraunhofer’s lines D and E.

6. Potassium ferrocyanide test

Blood to be examined (15 cc) + 20% Potassium ferrocyanide (15 cc) + dilute
acetic acid (2 cc)"Shake gently. If COHb is present, red coagulum will form;
normal blood"dark brown coagulum.

III. CHLORINE

A. General
(1) Properties - (i)Chlorine is a commonly used highly toxic industrial gas
having a greenish-yellow color and an unpleasant irritating odor. It was
discovered in 1772, by Carl Wilhelm Scheele. (ii)Oxidizing agent; causes
extensive destruction of organic tissue
(2) Uses - Berthollet recognized that it could be used to remove color from cloth.
Tennant in 1799 made bleaching powder (calcium hypochlorite) from it,
which was safer to transport, and remains in widespread industrial use.
Chlorine is currently used for (i) bleaching of wood pulp newsprint and for (ii)
chlorination of water, disinfection and bleaching. (iii) It has been used as a
war gas [please see below].

B. Signs and Symptoms

Exposure is likely in laboratories, bleaching powder factories and other chemical
works.

1. Acute
a. Symptoms
Has irritating effect on all mucosal surfaces, because of formation of
hydrochloric and hypochlorous acids. Cl2+H2O"HCl+ HOCl
(1) Eyes – intense irritation, redness, lacrimation
(2) GIT - Nausea, vomiting, mild gastritis
(3) Respiratory – Spasm of glottis, extreme dyspnea, tachypnea, oral mucositis,
violent cough, haemoptysis
(4) General – dehydration, stupor, and syncope.

b. Signs
-ed respiratory tract sounds and wheezes.

c. Lab
(1) Complete blood count - erythrocytosis and lymphopenia.
(2) Biochemistry - Serum hepatic enzymes and creatine kinase-
(3) Arterial blood gas conc - consistent with hypoxemia and hyperventilation.
(4) Chest X-ray:
(i) Widespread pulmonary alveolar infiltrates predominantly affecting the ventral
portions of both lungs, consistent with noncardiogenic pulmonary edema.
(ii) Taken in expiration shows an -in lung volume"Indicates pulmonary edema
will develop.

2. Chronic
In chemical works chronic poisoning may occur causing anaemia, cachexia,
emaciation, progressive wasting, gastritis, dental caries (because of acid
production), bronchitis, and emphysema.

C. Fatal Dose
Exposure to 1 part in 1000 causes death in 5 min.

D. Fatal Period
Few hours to 2 days.

E. Management
(1) Remove from toxic atmosphere, fresh air, steam inhalations
(2) supplemental O2
(3) Nebulized sodium bicarbonate.
(4) IV electrolytes
(5) General - treatment of shock, circulatory failure, pulmonary edema
[Atropine and rapidly acting diuretic (frusemide) can counter pulmonary
edema].

F. Cause of Death
Cardiac failure following pulmonary congestion and inflammatory edema of
lungs.

G. PM Appearances

1. Acute poisoning
(1) Signs of asphyxia
(2) Respiratory tract – Inflamed
(3) Lungs – congested, edematous, alveolar walls – ruptured, hemorrhages and
thrombosis in lung beds
(4) GIT – esophagitis, gastritis
(5) Blood - -ed viscosity.
(6) Chemical tests - HCl and HOCl may be recovered from tracheal walls
[diagnostic].

2. Chronic poisoning
As mentioned earlier under ch signs and symptoms.

H. ML Importance
(1) Leak from storage tanks – On July 14, 2010, chlorine leaked out from one
of the 140 canisters of chlorine lying unattended at the Mumbai Port Trust.
More than 120 people were admitted with respiratory symptoms, although
none died. May lead to negligence suits
(2) Leak during transportation - Chlorine can leak during transportation and
cause fatalities. Transportation is predominantly by rail car. Rail car accidents
 are rare, but potentially catastrophic, as the rupture of a normal 90-ton rail car
could release a potentially lethal, 20-mile-wide cloud of chlorine
(3) Exposure in factories and laboratories
(4) War gas – Used as a war gas. In 1st World War, several thousand soldiers
died due to chlorine.

IV. HYDROCYANIC ACID (HCN)

Hydrogen cyanide (HCN) was isolated in 1782 by Scheele (1742–1786), who

became its first victim in 1786 when he accidentally broke a vial of the chemical
in the laboratory and died from vapor poisoning. The name cyanide (Gk
Kyaneos, dark blue) is derived from the colorful Prussian blue from which HCN
[syn, prussic acid] was first synthesized.

A. Properties
Boiling point is 26°C.

B. Uses
Dyeing, electroplating, fumigants, manufacturing processes [several], metal
extraction, metal hardening, metal polishes, pesticides, photography, printing.

C. Mechanism of Action
(1) Inhibition of cytochrome oxidase - Cyanide has a high affinity for Fe3+
ions. In normal cells, cytochrome oxidase has a high concentration of Fe3+
ions. CN attaches to cytochrome-C oxidase and stops cellular respiration
[causes histotoxic anoxia - ch 8].
(2) Other enzymes, which have high concentration of Fe3+ ions are carbonic
anhydrase, decarboxylases, succinic dehydrogenase and superoxide
dismutase; these are inhibited as well. Their inhibition has no recognizable
relation to the toxic action.

D. Toxicokinetics
(1) Absorption:
(i) Rapidly absorbed from GIT, resp system and skin
(ii) Delayed - (a) when taken on full stomach (b) with alcohol
(2) Conversion - Cyanide salts are acted upon by stomach HCl to generate
HCN. Achlorhydric individuals may be difficult to be poisoned by cyanided
salts [please see Rasputin’s case below]. However water in stomach may still
produce HCN.
(3) Metabolism - Cyanide precursors are present in many natural foods
[cyanogenetic plant products]. Thus human body has evolved a natural route
of CN detoxification. It converts cyanide to thiocyanate with enzyme
rhodanese (thiosulfate cyanide sulfurtransferase), a mitochondrial enzyme
present in great amounts in liver and kidneys, acting as a catalyst.
Glutathione acts as a sulfur donor [Fig 44.1]. Humans can remove 1 mg of
cyanide/kg/h by converting it to thiocyanate.
(4) Excretion:
(i) Mainly in urine as thiocyanate
(ii) Small amounts unchanged in breath.

E. Acute Poisoning

1. Signs and symptoms

Most rapid of all poisons. Causes histotoxic anoxia [Gordon’s classification"ch
8]. Cyanide toxicity should be considered in patients with sudden CVS collapse,
especially in the appropriate context of occupational exposure [e.g. laboratory or
industrial work] or in a fire victim with hemodynamic instability, -ed lactic acid,
or coma.

a. Inhalation
When inhaled as a gas, action is instantaneous. (1) Sense of constriction about
the throat and chest (2) Dizziness, vertigo (3) Insensibility (4) Death from
respiratory failure.

b. Ingestion
Symptoms may not appear immediately.

i. Small [less than fatal] doses

(1) Nausea (2) Giddiness (3) Headache (4) Confusion (5) Loss of muscular
power.

ii. Intermediate [fatal] dose

(1) Symptoms occur immediately.
(2) In some cases appear after 1 min or so. During this time, may perform certain
voluntary acts eg corking or throwing away the bottle, or walking a little
distance. This may give impression of death being homicidal, eg when a
person takes CN and throws a bottle out of the window.
(a) CNS
Initially: (1) Anxiety (2) Confusion (3) Drowsiness (4) Excitement (5) Faintness
(6) Headache (7) Perspiration (8) Vertigo. Towards the end (9) Stupor (10) Coma
and (11) death.

(b) CVS
(1) Initially – hypertension, reflex bradycardia, sinus arrhythmia
(2) Later – Hypotension, reflex tachycardia, cardiovascular collapse.
(c) Resp system
(1) Breath:
(i) Odor of bitter almonds - (a) Detectable at an air concentration of 1 ppm by
some persons, but up to 50% of population is unable to recognize the odor.
(b) It is believed to be due to a genetic defect similar to color blindness. (c)
Believed to be common among medical men. (d) Certain firms, where
cyanide is used in a manufacturing process will not engage staff unable to
smell cyanide. (e) Alternative method for those who cannot smell cyanide –
HCN vapor taints cigarette smoke, and is thus detected by smoking. Also
the flavor of tobacco is rendered a distinctly unpleasant smell. Other
poisons making tobacco smell unpleasant are mercury and phosgene. Those
able to smell CN should not smoke, because CN odor is very delicate and
may be masked by cigarette smoke. (f) Nitrobenzene has similar smell and
may cause confusion
(ii) Ammoniacal smell sometimes - KCN"formamide "Formic acid+NH3.
(2) R/R:
(i) Initially - Tachypnea and dyspnea. Due to stimulation of chemoreceptors and
respiratory center by CN.
(ii) Later – severe respiratory depression"R/R." Cyanosis.
(d) Neuromuscular
(1) Convulsions [epileptiform or tonic; localized or generalized (more
commonly)] (2) Cramps (3) Opisthotonus and trismus (4) Prostration (5)
Twitchings (6) Paralysis towards the end.

(e) GIT
(1) Nausea, vomiting [rarely] (2) Salivation (3) Taste - Bitter, acid burning (4)
Throat - Constriction, numbness (5) KCN and NaCN cause corrosive burns on
mouth, throat and stomach. May cause epigastric pain due to this.

(f) Renal
Acidosis.
(g) Temperature
Hyperthermia.

(h) Skin
(1) Bullae (2) Perspiration.

(i) Eyes
(1) Glassy, prominent (2) Pupils – dilated, unreactive.

(j) In cases of survival

Delayed neurologic sequelae develop especially in the form of Parkinsonian
symptoms.

iii. Massive [larger than fatal] doses

(1) Sudden loss of consciousness.
(2) No voluntary act can be performed after ingestion.
(3) Prompt death from respiratory arrest.

2. Fatal dose

a. Ingestion
(1) HCN - 50 to 60 mg (2) NaCN, KCN – 200 to 300 mg.

b. Inhalation
Air concentration of HCN: (i) 1:50,000 is fatal in few hours (ii) 1:10,000
within few minutes (iii) 1:2,000 almost immediately.

3. Fatal period
(1) HCN - 2-10 minutes. Rivals nicotine [ch 43] as a poison capable of
producing quick death.
(2) KCN or NaCN - 30 min, because of delay of chemical conversion of salt to
HCN by gastric juices.

4. Tests

Lee-Jones Test
5 ml gastric aspirate + Few crystals of ferrous sulphate + 5 drops of 20%
NaOH"Boil and cool"Add 10 drops of 10% HCl"Greenish blue colour [or
precipitate] which intensifies on standing indicates cyanide, which is due to the
formation of Prussian blue. Purple color is seen in the presence of salicylate.

5. Management
(1) Treatment should be started immediately because fatal period is very short.
(2) Principles:
(i) To restore cellular respiration [by giving 100% O2 etc]
(ii) To remove unabsorbed CN [by decontamination]
(iii) To reverse cyanide-cytochrome combination [by antidotes].

a. Immediate
(1) Mouth-to-mouth resuscitation should not be attempted.
(2) Clear airways
(3) 100% O2 by tight fitting face mask or ventilate via endotracheal tube if
necessary. There is inconclusive evidence of further benefit from the use of
hyperbaric oxygen.
(4) Establish iv access.
(5) Check arterial blood gases. Lactic acidosis indicates severe poisoning
[Mechanism: Oxidative phosphorylation blocked"-ed glycolysis ".ed
utilization of lactic acid"lactic acid accumulation].
(6) If poisoning has occurred by inhalation, remove patient at once to fresh air
 and start artificial respiration as above.

b. Antidotes

i. Classes
CN Antidotes can be divided in 3 broad classes - Methemoglobin [MethHb]
generators, sulfur donors and direct binding agents. Of these, MethHb generators
are given in combination with sulfur donors. This combination is the drug of
choice in CN poisoning. Direct binding agents may be given alone.

(a) Methemoglobin generators

(1) Principle - to generate an alternate supply of Fe3+ ions, so CN ions release
cytochrome oxidase and attach to fresh supply of Fe3+ ions. Methemoglobin
is an Hb molecule in which Fe is in Fe3+ state. Process can be explained
biochemically in 3 stages
(i) Stage of cytochrome oxidase inactivation : CN + Cytochrome oxidase"CN-
cytochrome oxidase complex. This inactivates cytochrome oxidase,
stopping cellular respiration
(ii) Stage of MethHb generation: MethHb generators [eg nitrites] +
Hb"MethHb.
(iii) Stage of cytochrome oxidase recovery: CN-cytochrome oxidase complex +
MethHb"CN-MethHb [cyanmethemoglobin] + Free Cytochrome
oxidase. This happens because MethHb competes with cytochrome oxidase
for CN. Since it has greater affinity for CN, it leaves cytochrome oxidase
and attaches itself to MethHb.
(2) Methemoglobin [MethHb] generators are oxidizing agents that change the
ferrous (Fe2+) ion of Hb to the ferric (Fe3+) ion. The resultant methemoglobin
binds stronger with cyanide than cytochrome oxidase"Forms
cyanmethemoglobin.
(3) Levels of MethHb should not exceed 25%, otherwise death can occur due to
MethHb.
(4) The drugs used are
(i) Amyl nitrite [C5H11NO2]
(ii) Sodium nitrite [NaNO2]
(iii) Methylene blue - Methylene blue (methylthionine chloride) was once
 recommended, but is not found to be useful.
(iv) Phenones - (a) 4-DiMethyl AminoPhenol (4-DMAP) - (I) This German-
developed compound is used in the German military and by the civilian
population. (II) Dose - 3mg/kg i.v. produces a level of 15% methHb within
1 minute. (III) Disadvantages - (1) IM administration causes necrosis in the
area of injection, -in pain, fever, and muscle enzymes. (2) Extremely high
levels of methHb may occasionally result. (3) may be a mutagen. (b) p-
aminoheptanoylphenone [PAHP] (c) p-aminooctanoylphenone [PAOP]
(d) p-aminopropiophenone [PAPP]. PAHP is the safest phenone of the
series.
(b) Sulfur donors
Cyanmethemoglobin formed in the above step cannot be detoxified by the body
by itself. A sulfur donor is needed for its detoxification. It acts by taking away
CN ion from cyanmethemoglobin and forming thiocyanate. This is unlike
sulfmethemoglobin, which is formed during treatment of H2S. Since body can
detoxify it on its own, no sulphur donor is needed in H2S. During treatment of
CN poisoning sodium thiosulphate is administered which acts as a sulfur donor,
with rhodanese catalyzing the reaction [Fig 44.2].
Addition of sulfur to the cyanide molecule (formation of thiocyanate) is
irreversible. Thus cyanide can not diffuse back in the system. Thiocyanate
(though it contains cyanide) is harmless and is excreted in the urine.

(c) Direct binding agents

Bind directly to CN rendering it non-toxic. Ex
(1) Dicobalt edetate [Kelocyanor]. Cobalt binds to CN ion directly. Dose -
300mg IV over 1 minute. If there is no response in 1 minute, repeat up to a
max. of 900mg.
(2) Hydroxocobalamin (syn, Vit B12a) [Cyanokit].
(i) Mechanism - (a) Combines with CN to form cyanocobalamin [Vit B12]
which is renally excreted (b) One molecule of hydroxocobalamin binds one
molecule of CN. According to weight, 4 g of hydroxocobalamin combines
with 80 mg of CN.
(ii) Advantages - (a) relatively safe (b) does not compromise the blood’s
oxygen-carrying capacity (c) unlike the nitrites or sodium thiosulfate, does
not produce hypotension.
(iii) Dose - 5 g slow i.v. as infusion in 200 ml saline soln over 30-min. Infusion
repeated if necessary. The pediatric dose is 70 mg/kg, up to a maximum of
the adult dose, administered at the same infusion rate. Should not be
administered through the same line as other agents, as no data is available
on the compatibility of hydroxocobalamin with other substances.
(3) Cyanohydrin-Forming Drugs:
(i) Aldehydes and carbonyl-related compounds form cyanohydrins from
cyanide.
(ii) This action may be a mechanism for improving the protection provided by
nitrites.
(iii) Examples: (a) Dihydroxyacetone [DHA] (b) Glyoxal (c) Pyruvate (d)
Reducing sugars (e) α-ketoglutaric acid [α-KG]
(iv) Glyoxal may be the most effective compound of the group.
(v) Limitations - (a) relatively short half-lives of reversible reactions (b) high
dosage required. Dose of α-KG is 2g/kg.

ii. Method of administration

2 Methemoglobin generators and 1 sulfur donor are used in sequence in three
steps. Eli Lilly & Company, Indianapolis once manufactured the so-called Lilly
antidote kit or Lilly Cyanide kit, which contained all 3 major antidotes of
cyanide. This company no longer manufactures it. It is now available from
Taylor pharmaceuticals, a Division of Akorn, Inc. Each package contains 12
amyl nitrite pearls, two 10-mL vials of 3% sodium nitrite, and two 50mL vials of
25% sodium thiosulfate. This kit is the mainstay of cyanide antidotal therapy.
(1) 0.2 ml Amyl nitrite ampoule is broken, a handkerchief soaked in it and
patient asked to inhale over it for 15-30 s.
(2) Sodium nitrite - 10 ml of 3% given i.v. very slowly over a period of 5
minutes [otherwise there is a risk of developing hypotension, sodium nitrite
being a strong vasodilator]. Do not remove needle. All nitrites including amyl
nitrite are vasodilators. Vasodilatation is disadvantageous in conditions such as
hypotension, hypoxia, hypercapnia and acidosis which are commonly seen in
cyanide poisoning; however, their function to form methemoglobin is given
priority.
(3) Sodium thiosulphate - slow IV infusion of 50 ml of 25% sodium
thiosulphate in 1000 ml of 5% glucose solution [infusion rate 5 ml/min].
(4) Repeat – both sodium nitrite and sodium thiosulfate at half the initial dose at
the end of 1 h, if symptoms persist or reappear.

c. Decontamination
(1) GIT:
(i) Decontamination is typically performed after antidote administration.
(ii) Gastric lavage - Solutions used (a) activated charcoal (b) KMnO4 1:5000.
Leave 200 mL in stomach (c) mixture of citric acid [3%], ferrous sulfate
[15%] and sodium carbonate [6%] (d) mixture of sodium bicarbonate,
ferrous and ferric chloride; or a mixture of potassium carbonate with
ferrous and ferric sulfate. Both act as chemical antidotes. Iron combines
with CN to form inactive Prussian blue [syn, Ferric Ferrocyanide; Ferric
hexacyanoferrate; [Fe4[Fe(CN)6]3 or Fe7(CN)18]. Please co-relate with
Thallium poisoning [ch 36], where potassium salt of Prussian blue is given
as an antidote. (e) sodium thiosulfate [5-10%]
(2) Skin - Thorough washing of the affected area with soap and water.

d. Exchange transfusion
If methHb levels>50%.

e. Supportive therapy
(1) Observe for 24-48 h as CN toxicity may recur.
(2) For lactic acidosis resulting from anaerobic metabolism - NaHCO3 IV.
(3) Control of seizures - Anticonvulsants eg diazepam.
(4) Cardiopulmonary resuscitation.

6. Cause of death
Respiratory failure.

7. PM appearances
(1) Precautions - Pathologist and all paramedical staff should wear masks.
Exposure may also be reduced by carrying out autopsy in the open or putting
on the exhaust.
(2) Odor - Characteristic odor of “bitter almonds” from the body. Cranial cavity
is opened first as odor is well marked in brain
(3) PM staining – Pinkish, because of oxyhemoglobin, as oxygen could not be
utilized by cells. Oxygen remains in the cells as oxyhemoglobin. Color of
cheeks may be pinkish.
(4) Eyes - Bright, glistening, prominent. Pupils dilated.
(5) Jaws - firmly closed
(6) Blood stained froth – at mouth, in trachea and bronchi
(7) Oral and perioral erosions
(8) Stomach wall:
(i) Congested.
(ii) May be eroded [hemorrhagic] or blackened due to formation of alkaline
hematin.
(9) Lungs – edematous
(10) Serous cavities - ecchymosed
(11) Viscera – congested. May be discolored blue or dark green if methylene
blue had been given as a treatment.
(12) Blood vessels - All vessels of the body including veins contain oxygenated
blood
(13) CNS - Degenerative changes
(14) Chemical examination – In fatal cases, blood contains about 12mg/L of
cyanide [range 1-53 mg/L].

8. Laboratory identification
HCN is an extremely volatile chemical.
(1) Blood – should be covered with a layer of liquid paraffin to avoid
 evaporation
(2) Alkali - should be added to blood and viscera
(3) Viscera - should be stored in well stoppered bottles.
(4) Analysis - should be done immediately. Up to 70% may be lost after some
weeks of storage from reaction with tissue components and conversion to
thiocyanate.

F. Chronic Poisoning
(1) Etiology - Produced by continued inhalation of low conc of CN over long
periods. Usually occurs in smokers after a long period.
(2) Symptoms:
(i) Leber hereditary neuropathy.
(ii) Tobacco amblyopia [progressive loss of visual function]
(iii) Tropical ataxic neuropathy. Not all smokers are affected. Affected smokers
have lower plasma cyanocobalamin and thiocyanate concentrations than
unaffected smoking counterparts, suggesting a reduced ability to detoxify
cyanide. Cessation of smoking and administration of hydroxocobalamin
often reverses symptoms.
(iv) Thyroid disorders - Thiocyanate is a competitive inhibitor of iodide entry
into the thyroid, thereby causing the formation of goiters and the
development of hypothyroidism.

G. ML Importance
(1) Achlorhydria – Action of KCN and NaCN depend on the presence of HCl in
the stomach (converts them to HCN). Russian politician Grigori Rasputin
(1869 – 1916) was given pastries laced with KCN, but he survived, because he
had achlorhydria [due to chronic alcoholism]
(2) Blood stain solvent - KCN is an important solvent for blood stains [ch 29].
(3) Building fires:
(i) Cyanides are produced during the combustion of many nitrogen-containing
compounds [melamine, nylon, synthetic polymers, polyurethane etc]. These
are parts of clothes and common domestic furnishings. Their combustion
produces HCN.
(ii) Thus fire victims in a burning building [having polyurethane furniture] may
 show HCN in their blood; indeed, the greatest danger of CN toxicity is from
smoke in household or building fires.
(iii) Levels – usually up to 0.3mg%.
(4) Cherry laurel water - or aqua laurocerasi [distilled from leaves of cherry
laurel] contains HCN. Has been used for asthma, cough, indigestion and
dyspepsia. Can cause poisoning. The Arabic emperor Nero used cherry
laurel water to poison the wells of his enemies
(5) Embalming – If there is suspicion of CN poisoning, body should not be
embalmed [ch 9]. Formaldehyde rapidly destroys cyanide. Even containers
used to send specimens to lab must not have been used to hold formalin-fixed
material.
(6) Judicial Execution [Judicial gassing]: (i) In some US states, judicial
execution is done with cyanide. (ii) Other gases used - Rarely CO and CO2 are
also used. For all official methods of judicial execution, please see ch 40.
(7) Latent Fingerprint development by cyanoacrylate fuming may generate
HCN, especially if cyanoacrylate is heated >200°C.
(8) Manner of poisoning:
(i) Accidental poisoning – From (a) inhalation of HCN vapors used as a
fumigating agent (b) ingestion of HCN mistaking it for some drug (c)
injection of KCN into rectum (d) Topical application to a raw wound
(ii) Homicide – rarely.
(iii) Suicide – especially by terrorists [especially LTTE], who hide pellets in
hollow teeth.
(9) Putrefaction:
(i) Production during putrefaction – Fatal cyanide poisoning has occurred
because of handling spoiled fish. It is formed by the action of
Chromobacterium violaceum and Pseudomonas aeruginosa on fish proteins
[please see production of CN by living organisms above].
(ii) Resists putrefaction – has been detected in exhumed bodies upto 18 months
after death.
(iii) Retards putrefaction, and acts as a preservative to some extent
(10) Chemical terrorism and warfare – CN is an agent that can be used in
terroristic activities.
V. HYDROGEN SULFIDE (H2S)

Hydrogen sulfide is a colorless, flammable, gas with the characteristic foul odor
of rotten eggs.
Salient features:
(1) Production: (i) Natural - It is formed during decomposition of organic
substances containing sulfur. Thus foun d in cesspools [an underground
reservoir for liquid waste], privy vaults, sewers, swamps, and volcanic gases
(ii) Industrial - Produced as a byproduct during distillation of petroleum oil, in
manufacture of artificial silk, gas works, glue factories, tannery vats and in
other industries where sulphur compounds are used.
(2) Physical properties - Heavier than air; tends to collect at ground level.
(3) Sewer gas is a mixture of gases [H2S, NH3, CH4, CO2, SO2 and nitrogen
oxides] produced and collected in sewage systems by the decomposition of
organic wastes.
(4) Sour gas is natural gas (mined from earth as fossil fuel) containing
significant amounts of H2S. The human body produces small amounts of H2S
and uses it as a signaling molecule.

A. Mechanism of Action
(1) Inhibition of cytochrome oxidase: (i) Action similar to that of CN and PH3
[ch 35]. H2S adheres to cytochrome-c oxidase and inhibits its action. Cellular
respiration comes to a halt. For this reason, its toxicity and rapidity of action
are comparable with that of HCN and even treatment is essentially similar. (ii)
 Lack of oxygen to brain causes sudden loss of consciousness [H2S often
known as “knockdown gas”].
(2) Interaction with vital macromolecules - H2S interacts with a number of
other enzymes and other macromolecules, including hemoglobin [leading to
formation of sulfhemoglobin – responsible for greenish discoloration of
putrefaction (ch 9)], methemoglobin [formation of sulphmethemoglobin]
and myoglobin. Most macromolecules are held together by disulphide bonds,
which are easily disrupted by H2S.
(3) Olfactory paralysis - occurs very quickly at higher levels. Although not a
mechanism of death, it contributes to death, by removing warning signals.

B. Signs and Symptoms

1. Acute exposure
a. Exposure to low conc [<250 ppm]
(1) Cyanosis
(2) Irritation of all mucus membranes
(i) Eye - (a) Cornea opacity (b) Corneal ulceration (c) Keratoconjunctivitis [Gas
eye]. (d) blepharospasm, lacrimation and photophobia (e) blurred vision (f)
colored halos are seen (g) Corneal bullae (h) Ocular pain
(ii) Nose – (a) Olfactory fatigue – occurs 2-15 min after exposure at 100 ppm.
Recovery of smell may take several months (b) Rhinitis
(iii) Throat – sore throat
(iv) Bronchus – Bronchitis
(v) Lungs – Acute lung injury, pulmonary edema
(3) Dullness and sleepiness – death may result during sleep without the victim
regaining consciousness [same as in CO]
(4) Discoloration of coins - in the victim’s pocket due to oxidation may be a
clue to H2S exposure. [cf lightning where they are molten, fused together or
even magnetized – ch 16].

b. Exposure to moderate conc [250-500 ppm]

(1) General -Nausea, vomiting, diarrhea, feeling of oppression
(2) CNS - Amnesia, Disorientation, Dizziness, Headache, Vertigo, Coma
(3) Resp system – cough, labored breathing, apnea
(4) CVS - Hypotension, Palpitations, Tachycardia
(5) Skin – burning, erythema, itching, severe pain, especially in moist area [gas
dissolves]
(6) Muscular - Muscle cramps, prostration, weakness
(7) Metabolic acidosis – secondary to anaerobic metabolism, which in turn
results in CNS, respiratory and myocardial depression.

c. Exposure to high conc [750-1000 ppm]

(1) General - Weakness, malaise, sweating, abrupt physical collapse
[knockdown]
(2) CVS – cardiac arrhythmias, conduction defects
(3) CNS – amnesia, confusion, delirium, hallucinations, convulsions,
Nystagmus, Somnolence 4.Respiratory paralysis, asphyxial seizures, delirium,
death.

d. Recovery
Associated with
(1) Impairment of vision, hearing, smell
(2) Neurological sequelae:
(i) Memory failure [amnestic syndrome]
(ii) Ataxia, rigidity, tremor [due to damage to basal ganglia].

2. Chronic exposure
May occur in industrial workers.
(1) General – Headache, Weakness, Nausea, Weight loss
(2) Gas eye is common. Associated with reversible chromatic distortion and
visual changes.
(3) Basal ganglia abnormalities [ataxia, dystonia, choreoathetosis]
(4) Spontaneous abortions in female.

C. Diagnosis
(1) Rotten egg odor from patient
(2) Blackening of copper and silver coins in patient’s pockets; darkening of
jewellery
(3) -blood sulfide [normal <0.05 mg/L].

D. Scene of Poisoning
At the scene, filter paper moistened with lead acetate will turn black.

E. Fatal Dose
(1) 20ppm - Maximum allowable conc
(2) 400-700ppm - dangerous after an exposure of half to 1 h.
(3) >1000 ppm - instantly fatal.

F. Fatal Period
Few minutes to few hours.

G. Management
(1) Immediate removal to fresh air
(2) Artificial respiration
(3) Oxygen therapy:
(i) Hyperbaric oxygen [HBO, 100% O2 at 2.5 atm]
(ii) High-flow oxygen [ch 32]
(4) Antidote: Nitrites [dose same as that in CN]"induce
methemoglobinemia"H2S has greater affinity for methHb"releases its hold on
cytochrome oxidase and attaches to methHb"formation of
sulfmethemoglobin"spontaneously detoxified by body [cf CN in which
cyanmethemoglobin is formed, which cannot be detoxified by body on its
own. A sulphur donor is needed].

H. Spot Test
A filter paper moistened with lead acetate exposed at the scene will blacken if
gas is present.

I. PM Appearances
(1) Odor of rotten eggs – from the body. Most characteristic sign
(2) Signs of asphyxia – especially cyanosis
(3) Demonstration of sulfmethemoglobin - in blood
(4) Brain:
(i) Edematous
(ii) Greenish discoloration of grey matter [due to sulfhemoglobin]
(5) Lungs:
(i) Acute bilateral pulmonary edema
(ii) Chronic passive congestion.
(iii) Cut sections show extremely wet frothy congested surfaces. Color - diffuse
red, red-brown or purple
(6) Tracheobronchial tree: Lined with a tenacious pale grayish-yellow to
grayish-red material. Contains a great amount of mucus which extends deep
into the bronchiolar system
(7) Liver and spleen - chronic passive congestion
(8) Color – of blood and viscera is greenish [due to sulfhemoglobin].

J. ML Importance
(1) Accidental poisoning - Poisoning by H2S is almost always accidental [most
commonly in sewer workers].
(2) Suicidal – rare, but has been described.
Detergent Suicide - In Japan detergent suicide is especially common since 2007.
(a) Called so because carried out by mixing 2 common household chemicals –
usually detergents - to produce H2S, one an acid [generally toilet bowl
cleaner] and the other, a sulfur source [insecticides or bath salts]. (b) Common
availability of this information over the internet has contributed to a dramatic
increase in the number of such cases [internet assisted suicide, cybersuicide].
While in 2007, there were only 27 cases of H2S suicides in Japan; they
increased to 517 cases between Jan and July 2008. The number has been
continually rising. (c) Typically the suicide would sit in an enclosed
environment [eg cars, closets] and post notes warning the first responders
[paramedics, doctors etc] of the toxic gas within. Yet there have been reports
of injuries to first responders.
(3) Gas masks – Workers going down in sewer lines to clean them must wear
gas masks. Quick death may occur otherwise
(4) Stink bombs – Small phials containing an aqueous soln of the gas are
 sometimes used by schoolboys for pranks.
(5) Decomposition occurs faster
(6) Employer’s liability to pay compensation in cases of occupational disease
due to H2S exposure – Same as MLI of Arsenic [ch 36].

VI. WAR GASES AND RIOT CONTROL AGENTS

War gases are gases used to incapacitate or kill enemy (against soldiers and
citizens of an enemy country) in times of war. Riot control agents are gases used
by law enforcement agencies during riots (generally against own citizens).
Killing is not the aim; it is merely to disperse mob. Thus less toxic agents are
preferable. Although the term “war gases” is used, it includes both solids and
liquids, which rapidly convert into gas on being liberated. Inhalation causes
problems, but direct contact with the liquid or solid forms also causes symptoms.
The two are best studied together.

A. Classification
War gases and riot control agents may be classified in two ways.

1. According to persistence [environmental classification]

a. Non-persistent
They are gases, or solids which when liberated are rapidly converted into gas or
smoke, which is quickly dissipated, leaving the area free from pollution. Good as
riot control agents, but not very good as war gases.

b. Persistent
Persistent gases are solids or liquids which on being exposed to the air change to
gas only slowly [eg mustard gas, lewisite]. They thus persist in the environment
for long. They are not good as riot control agents, as they can affect citizens for
long periods after they have been liberated.

2. According to their physiological action [medical classification]

Given in Table 2.
Table 2 [with Memory Aid 1]: Classification of war gases and riot control agents
VALSHoN
Vesicants or blistering agents
Asphyxiants or lung irritants
Lachrymators or tear gases
Sternutators or nasal irritants
Hemolytics – act on RBCs
Gases with miscellaneous [other] effects
Nerve gases

a. Vesicants or blistering agents

Vesicants (blistering agents) are cytotoxic alkylating compounds, which are
rarely lethal but inflict painful burns and blisters, requiring medical attention
even at low doses.
Salient features:
(1) Main blistering agents are (i) Sulfur mustard [king of the battle gases. Also
known as mustard gas] (ii) Nitrogen mustard (iii) Lewisite and (iv) Phosgene
oxime (halogenated oxime).
(2) Of these mustard gas and lewisite are most dangerous. They are liquids,
which continue to give off vapor for days or even weeks.
(3) Sulfur mustard – Also known as yellow cross.
(4) Because vesicants can inflict many casualties and create confusion and panic,
they were used in battle throughout the twentieth century.

i. Symptoms
Sulfur mustard is a powerful vesicant, mutagenic and carcinogenic. Exposed
victims rarely suffer immediate symptoms; they may thus unknowingly receive
high dosages. The predominant organs affected are the skin, eyes, and lungs.
(1) Skin - However, within 24 hours of exposure to mustard agent, victims
experience intense itching and skin irritation which gradually turns into
large blisters filled with yellow fluid. These are highly debilitating chemical
burns.
(2) Eyes- Conjunctivitis, swelling of eyelids swell, temporary blindness.
(3) Lungs - Bleeding and blistering within the respiratory system; mucous
membrane damage; pulmonary edema.
ii. Prevention
Respirators protect the face and respiratory tract against vesicants, but they
would still damage any other part of the body they come in contact with.

iii. Treatment
(1) Decontamination:
(i) Remove clothing
(ii) Remove any visible agent on the skin [wiping off the agent with dry powders
(such as flour, powdered soap, or dirt), showering, washing with soap and
water, or using resin decontaminants].
(iii) Bleaching powder - rapidly neutralizes mustard gas and Lewisite, and is
used in the form of a jelly, or as a 0.5% hypochlorite solution. (iv) Move to
an area free of vapor hazards (v) irrigate eyes with water.
(2) Antidotes:
(i) N-acetyl-cysteine .es the inflammatory response in mustard exposure
(ii) Povidone-iodine ointment – applied within 20 minutes of exposure to
mustard liquid protects the skin from vesication
(iii) BAL [binds the arsenic group of lewisite].

b. Asphyxiants or Lung irritants

Asphyxiants [syn, respiratory irritants, suffocants], cause irritation of lungs.
Salient features:
(1) Examples: (i) Chlorine [please see above for details] (ii) Chloropicrin (iii)
Diphosgene (iv) Phosgene.
(2) Toxicity - Phosgene [COCl2] is most toxic; chlorine is least toxic. Phosgene
is 10 times and Chloropicrin, 4 times more toxic than Chlorine.
(3) The ease with which Chlorine and Chloropicrin are detected by their irritant
nature makes them as less suitable war gases.
(4) Mode of delivery - gas shells, tanks. Chloropicrin and diphosgene are
liquids. Can be used in gas shells.
(5) Site of action - lung alveoli
(6) Signs and symptoms: (i) General - headache, restlessness, vomiting (ii) RS -
coughing, cyanosis, dyspnea, stertorous breathing, tightness of chest (iii)
Mucus membranes - watering of eyes (iv) Collapse (v) Death occurs in 24-48
 h due to acute pulmonary edema.
(7) Management: (i) Eye wash with boric acid (ii) Oxygen (iii) Antitussives (iv)
Antibiotics (v) Adrenaline.

c. Lachrymators or tear gases

Lachrymator (L lacrima, “tear”), lachrymatory agent or tear gas is a non-lethal
chemical compound that stimulates the corneal nerves in the eyes to cause
tearing, pain, and even blindness.
Salient features:
(1) Symptoms: (i) Irritate all mucous membranes (oral, nasal, conjunctival and
tracheobronchial). (ii) Burning sensation (iii) immediate forceful and
uncontrollable shutting of the eyes (iv) tears streaming from the eyes (v)
coughing (vi) running nose full of mucus (vii) burning in the nose and throat
areas
(2) Examples – [A] Primarily used as war gases - Principal lachrymators or tear-
gases used in World Wars I and II were (i) Acrolein (ii) Benzyl bromide (iii)
Bromoacetone (iv) Bromobenzyl cyanide (B.B.C.) [liquid and persistent] (v)
Chloraceto phenole (C.P.A.) [solid and non-persistent] (vi) Ethyl iodoacetate
(K.S.K.) [liquid and persistent. Called so because used by Germany’s
‘Kommando Spezialkräfte’] (vii) Monobromomethyl ethyl ketone (viii) Xylyl
bromide [B]Primarily used as riot control agents - (i) CN [syn Phenacyl
chloride] – (a) Supplied to paramilitary and police forces in a small
pressurized aerosol can known as tear gas or “Mace” [brand-name]. (b)
Symptoms – In addition to general lachrymator symptoms mentioned earlier
(i) Rarely may cause syncope, disorientation, allergic dermatitis. (ii) At high
concentrations causes corneal epithelial damage and chemosis. Rarely death
due to pulmonary injury. (c) Because of its greater toxicity, it has largely been
supplanted by CS and pepper spray. (ii) CR [syn Dibenzoxazepine].
Developed by the British Ministry of Defense as a riot control agent in the late
1950s and early 1960s. (iii) CS [syn Orthochlorobenzylidene malononitrile, 2-
chlorobenzalmalononitrile, tear gas, C10H5ClN2] – (a) First synthesized in
1928 by two Americans, Corson and Stoughton. Their first letters gave the
name to this gas, but a new name was later derived from this acronym [Captor
Spray]. (b) Of about 15 different types of tear gases in use, CS is the most
popular due to its strong effect and lack of toxicity (c) Symptoms - general
 lachrymator symptoms mentioned earlier. Rarely miscarriages, chromosome
changes. Cyanide is formed upon its metabolism. (d) Treatment - Washing
with 5% sodium bisulfite. (iv) OC (from “Oleoresin Capsicum”) [syn Pepper
spray, capsicum spray] - (a) Active ingredient – Capsaicin (b) Generally non-
lethal, may be deadly in rare cases (v) nonivamide (vi) Bromoacetone (vii)
phenacyl bromide (viii) xylyl bromide and (ix) syn-propanethial-S-oxide
(found in onions).

d. Sternutators or nasal irritants

Sternutators [from Latin sternuo, sneeze] or nasopharyngeal irritants are
nonlethal agents capable of producing extreme irritation of the nose and throat.
Salient features:
(1) The symptoms are comparatively short in duration (i) Intense pain and
irritation of not only nose, sinuses and throat, but also of eyes (ii) sneezing
(iii) nausea and vomiting [thus sometimes known as “vomiting gases” also]
(iv) severe headache (v) salivation (vi) tightness in the chest and prostration
(2) Sternutators are not effective when a mask is worn. However their inhalation
before the application of mask makes mask wearing very uncomfortable.
Person feels compelled to remove it and thus subject himself to the effects of
more disabling gases which usually accompany or immediately follow the use
of the sternutators.
(3) Examples: (i) Pepper [black and red] (ii) Organoarsenicals eg (a)
Diphenylchloroarsine (DA) (b) Diphenylamine chlorarsine [also known as
Adamsite or DM] (c) Diphenylcyanoarsine (DC) (d) phenyldichloroarsine

e. Nerve gases (Paralysants)

Nerve gases [syn, nerve agents] are a class of OP compounds.
Salient features:
(1) These are classified as weapons of mass destruction [WMD] by the UN April
1991. Their production and stockpiling is outlawed by the Chemical Weapons
Convention of 1993; it officially took effect on April 29, 1997.
(2) Classes of nerve agents: (i) G-series - (a) Named so because developed by
German scientists. This naming system was created by the US when it
uncovered the German activities (b) First and oldest family of nerve agents.
(c) 2nd generation chemical weapons [1st generation - vesicants, asphyxiants
 etc] (d) Non-persistent in contrast to V series which are persistent. (e) All
members in this class were discovered and synthesized during or soon after
World War II, led by Dr. Gerhard Schrader. (f) Examples - w GA [tabun] -
first to be synthesized in 1936. Origin of tabun and other names except sarin
are not clear. Probably represent some kind of code names. w GB [sarin] in
1939. Discovered by Schrader and his team and named after their initials:
Schrader, Ambrose, Rüdiger and van der Linde. The term GC was not taken
because it was already in medical use. w GD [soman] in 1944 w GE - Ethyl
sarin w GF [cyclosarin] in 1949. ABDF were added after G in order of
discovery. There are no GC and GE.
Memory Aid 2: Major nerve gases (paralysants)
Take Sandwich to School on an English Cyele - Tabun, Sarin, Soman, Ethyl sarin, Cyelosarin

(ii) V-series - (a) V stands for Venomous or Viscous. (b) 3nd generation
chemical weapons - Prevalent during cold war years [1947–1991] (c)
Examples - VE, VG [Amiton], VM, VR, VX [best known] (d) All V-agents
are persistent; they do not degrade or wash away easily and can therefore
remain on clothes and other surfaces for long periods. This allows V-agents to
be used to blanket terrain to guide or curtail the movement of enemy ground
forces. (e) They are oily in consistency. Contact hazard is mainly dermal. (iii)
Novichok agents - The Novichok [Russian for “newcomer”] agents are a
series of OP compounds that were developed in the Soviet Union from the mid
1960s to the 1990s. (a) Belong to “4th generation chemical weapons”. (b)
More toxic than all other nerve agents. (c) Objectives - (I) To be undetectable
using standard NATO chemical detection equipment (II) To defeat NATO
chemical protective gear (III) To be safer to handle (d) Examples - Novichok-
5, novichok-fracture, novichok-7 (iv) Insecticides - phenothiazines, OP
[dichlorvos, malathion and parathion]
(3) Portals of entry: (i) Respiratory system [because they are easily vaporized
or aerosolized] (ii) skin
(4) Signs, symptoms, management - same as that of OP [ch 35]
(5) Protection - Full body suit must be worn in addition to a respirator for
protection.

f. Gases with miscellaneous effects

Affect other systems:
(1) Agents acting on blood: (i) Arsine [ch 36] (ii) Cyanogen (iii) cyanogen
bromide (iv) cyanogen chloride (v) HCN (vi) phosgene (vii) vinyl arsine.
(2) Psycho Agents: (i) BZ - 3-quinuclidinyl benzilate (ii) K - LSD (iii) SN -
Sernyl (PCP)

45. Pharmaceutical Toxicology

NON-STEROIDAL ANTI-INFLAMMATORY DRUGS AND

ANTIPYRETIC ANALGESICS

Nonsteroidal anti-inflammatory drugs [NSAIDs] are drugs with analgesic,

antipyretic and anti-inflammatory effects. They are non-narcotic. The term
“nonsteroidal” distinguishes them from steroids, which have a similar
eicosanoid-depressing, anti-inflammatory action. Main steroidal anti-
inflammatory drugs [SAIDs] are
(1) Dexamethasone [Decadron]
(2) Methylprednisolone [Medrol]
(3) Prednisone [Deltasone]
(4) Prednisone [Sterapred, Sterapred DS].

A. Classification
(1) Nonselective COX inhibitors [traditional NSAIDS]
(i) Salicylates - (a) Aspirin (acetylsalicylic acid) (b) Diflunisal (c) Salsalate
(ii) Propionic acid derivatives - (a) Fenoprofen (b) Flurbiprofen (c) Ibuprofen
(d) Ketoprofen (e) Loxoprofen (f) Naproxen (g) Oxaprozin
(iii) Anthranilic acid derivatives - Mefenamic acid [Ponstel, Ponstan]
(iv) Aryl-acetic acid derivatives - (a) Aceclofenac (b) Diclofenac (Safety alert
by FDA)
(v) Oxicam (Enolic acid) derivatives - (a) Droxicam (b) Isoxicam
(c)Lornoxicam (d) Meloxicam (e) Piroxicam (f)Tenoxicam
(vi) Pyrrolo-pyrrole derivatives - (a) Ketorolac
(vii) Indole derivatives - (a) I ndomethacin
(viii) Pyrazolone derivatives - (a) Phenylbutazone (b) Oxyphenbutazone
(2) Preferential COX-2 inhibitors:
(i) Meloxicam
(ii) Nabumetone
(iii) Nimesulide [systemic preparations are banned by several countries for the
potential risk of hepatotoxicity]
(3) Selective COX-2 inhibitors (Coxibs):
(i) Celecoxib [FDA alert]
(ii) Etoricoxib
(iii) Parecoxib
(iv) Rofecoxib [withdrawn from market]
(v) Valdecoxib [withdrawn from market]
(4) Analgesic-antipyretics with poor antiinflammatory action -
(i) Para aminophenol derivates - Paracetamol [acetaminophen]
(ii) Pyrazolone derivatives - Metamizol [Dipyrone], Propiphenazone
(iii) Benzoxazocine derivative - Nefopam
(5) Others - Licofelone [dual COX/LOX (Lipoxygenase) inhibitor].

B. Mechanism of Action
(1) NSAIDs are nonselective inhibitors of the enzyme cyclooxygenase (COX).
Inhibit both the cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2)
isoenzymes. Most NSAIDs inhibit COX reversibly, but salicylates inhibit it
irreversibly. Acetaminophen inhibits COX centrally.
(2) COX catalyzes the formation of prostaglandins and thromboxane from
arachidonic acid.
(3) Since COX-1 serves physiological “house-keeping” functions, selective
inhibition of COX-2 is preferable
(4) Prostaglandins act as messenger molecules in inflammation.
(5) Inhibition of prostaglandins reduces inflammation.

C. Nonselective COX Inhibitors [traditional NSAIDS]

1. Salicylic acid and derivatives

Preparations of salicylic acid include
(1) Acetylsalicylic acid - Please see below
(2) Methyl salicylate - colorless liquid, aromatic odor, sweetish taste
(3) Sodium salicylate - odorless, white scaly crystals. Unpleasant saline taste.

2. Acetylsalicylic acid [Aspirin]

a. General
(1) It is a white, odorless, crystalline powder, having a slight acidic taste.
(2) Popularly used as an analgesic and antipyretic.

b. Absorption, metabolism, excretion

(1) Absorption - is rapid from stomach, because of its low pKa (3.5; 50% is
unionized at pH=3.5; only unionized form can be absorbed). Theoretically at
higher pH in the intestine, absorption should be less (because of -ionization),
but this is offset by the large surface area of the small bowel. Thus absorption
is rapid from intestine also.
(2) Maximum plasma conc achieved in – 30-60 min.
(3) Metabolism - Salicylates are conjugated with glycine and glucuronides in
the liver
(4) Elimination - by kidneys. More than 30% of ingested salicylate is eliminated
as free salicylic acid in alkaline urine and as little as 2% in acidic urine (hence
the role of alkalinization of urine in its treatment).

c. Blood therapeutic levels

15-30 mg%. Toxicity appears at >30 mg%. Levels >100 mg% are fatal.

d. Acute poisoning

i. Signs and symptoms

Imp: Many of the signs and symptoms may be mistakenly attributed to the
illness for which the salicylates were administered (eg hyperthermia), with
disastrous consequences.

(a) GIT
These occur immediately.
(1) Mild burning pain in throat and stomach,
(2) Nausea, vomiting, thirst, diarrhea [occasionally]" Then there may be a latent
period of several hours. During latent period, only mild -in temp, sweating and
lassitude is seen"After this other symptoms follow [mentioned below].
(b) CNS
(1) Agitation (2) Cerebral edema (3) Coma [rare] (4) Convulsions (5) Delirium
(6) Hallucinations (7) Hyperactivity (8) Lethargy (9) Pupils - dilated (10) Stupor
(11) Syndrome of inappropriate antidiuretic hormone (12) Tinnitus [most
pathognomonic] following by diminished auditory acuity or even complete
hearing loss (13) Vertigo.

(c) CVS
(1) Pulse - rapid and irregular
(2) Hypovolemia, severe dehydration.
(d) Pulmonary
(1) Hyperpnea and tachypnea (2) Respiratory alkalosis (3) Acute lung injury.

(e) Renal
(1) Tubular damage (2) Proteinuria (3) NaCl and water retention (4)
Hypouricemia.

(f) Skin
flush and moist.

(g) Metabolic
(1) Diaphoresis (2) Hyperthermia [resulting from the uncoupling of oxidative
phosphorylation. An indication of severe toxicity and typically a preterminal
condition]. Temp may be up to 42°C (3) Hypoglycemia or hyperglycemia (4)
Hypoglycorrhachia [.concn of glucose in CSF] (5) Ketonemia (6) Ketonuria.

(h) Hemorrhagic diathesis

Because salicylates interfere with coagulation mechanisms.

(i) Acid-base and electrolyte disturbances

(1) Metabolic acidosis [due to -ed excretion of HCO3-, Na+, K+] and
(2) Respiratory alkalosis predominate early
(3) Metabolic alkalosis [sets in if there is -vomiting]
(4) Respiratory acidosis [late, grave prognosis]
(5) Hyponatremia or hypernatremia
(6) Hypokalemia
(7) -Anion gap.
(j) Diagnosis
virtually confirmed if there is – Tinnitus + -Anion gap metabolic acidosis +
Respiratory alkalosis + Ketonemia.

(k) Reye’s syndrome

First described by an Australian pediatrician Douglas Reye in 1963. Occurs if
aspirin is given to children <15 y with viral fevers usually influenza or varicella.
The classic features are (1) rash (2) vomiting and (3) liver damage. Other
associated findings (4) encephalopathy (5) fatty infiltration of the viscera (6)
hypoglycemia. Potentially fatal. Cause is damage to mitochondria in liver cells.

(l) Late complications

Esophageal strictures.

(m) Idiosyncratic reactions

Occur in 0.2% patients. Even therapeutic doses produce alarming symptoms (1)
Angioneurotic edema (2) Bronchial spasm (3) Cyanosis (4) Erythema of face
with edema of eyelids (5) GIT hemorrhages [due to capillary damage] (6)
Hypotension (7) Maculopapular exanthemata (8) Mucus membranes - edema
with hypersecretion [eg excessive salivation, laryngeal edema]. Erosion and
ulceration in severe cases (9) Rhinitis [vasomotor] (10) Urticaria (11) Vomiting.

ii. Laboratory investigations

(1) Blood: (i) Hypokalemia (ii) hypoprothrombinemia (iii) Prolonged clotting
time, prothrombin time [PT].
(2) Urine: (i) strongly acidic. (ii) Contains (a) acetone (b) albumin (c) bile
[traces] due to hepatitis.

iii. Management
(1) Emetics
(2) Gastric lavage:
(i) When a large number of tablets have been ingested, they may form a large
dirty gray lump [bezoar], which may not pass for a long time [lumps not
 easy to pass + pylorospasm].
(ii) Lavage with NaHCO3 is helpful in dissolving such bezoars.
(3) Activated Charcoal (AC):
(i) 1 gram of AC adsorbs 550 mg of salicylic acid.
(ii) A 10:1 ratio of AC:salicylate ingested results in maximal efficiency.
(iii) Multiple-dose activated charcoal (MDAC) is better than single-dose AC.
(4) Cathartics
(5) Urine alkalinization - [ch 32].
(6) Peritoneal dialysis
(7) Hemodialysis – Very effective.
(8) Exchange transfusion - in severe cases
(9) For idiosyncratic reactions - ACTH, antihistamines.
(10) Supportive measures:
(i) Cerebral edema and -ICP [correction of] - ch 32.
(ii) Convulsions - ch 32.
(iii) Fluid and electrolyte imbalance [correction of]
(iv) Hemorrhages [control of] - (a) blood or blood products - fresh frozen plasma
(b) Vitamin C (c) Vitamin K - 2.5-5mg IV daily to correct
hypoprothrombinemia
(v) Hyperpyrexia [treatment of] - ch 32.
(vi) Hypocalcemia [treatment of] - ch 32.
(vii) Hypoglycemia [correction of] - ch 32.
(viii) Metabolic acidosis [correction of] - with NaHCO3.

iv. Fatal dose

(1) Sodium salicylate and aspirin = 15-20 g
(2) Salicylic acid = 70-80 g
(3) Methyl salicylate=10-20 ml. For fatal blood levels, please see “therapeutic
levels” above.

v. Fatal period
Few minutes to several hours

vi. Tests
(1) Ferric chloride test - 1mL of urine + few drops of 10% ferric chloride"purple
color indicates salicylates
(2) Trinder spot test - 1mL of urine + 1mL of Trinder reagent"purple color
indicates salicylates.

vii. Cause of death

Mortality rate is 7-8%.
(1) Early stages: (i) Acidosis (ii) peripheral failure due to shock (iii) uremia
(2) Late stages: (i) Cardiac arrhythmias and sudden cardiac arrest can occur
anytime up to a day or so (ii) Respiratory failure.

viii. PM appearances
(1) Pupils – dilated
(2) Skin – Petechia, rashes
(3) CNS - cerebral edema
(4) Heart - Subepicardial hemorrhages
(5) Lungs: (i) Pulmonary edema and some collapse (ii) subpleural hemorrhages
(6) GIT: (i) congested, (ii) erosions, (iii) hemorrhagic gastritis, (iv) black altered
blood in stomach, (v) concretions of tablets [sometimes]
(7) Liver – Hepatitis
(8) Renal – Widespread shedding of renal tubular cells into the calyces of
kidneys and into the urine.
(9) If patient survives for a few days – the myocardium, liver and kidneys are
soft, dirty in appearance and greasy to touch.

e. Chronic poisoning [Salicylism]

Chronic salicylate poisoning most typically occurs in the elderly as a result of
unintentional overdosing on salicylates used to treat chronic conditions such as
rheumatoid arthritis and osteoarthritis.

Signs and symptoms

(1) Hearing loss and tinnitus, nausea, vomiting, dyspnea and hyperventilation,
tachycardia, hyperthermia, and neurologic manifestations such as confusion,
delirium, agitation, hyperactivity, slurred speech, hallucinations, seizures, and
coma.
(2) Delayed recognition - The slow onset and lesser severity of signs in the
elderly often causes delayed recognition of the true etiology of the patient’s
presentation.
(3) D/D - Typically, ill patients who suffer from chronic salicylate poisoning
may be misdiagnosed as having delirium, dementia, encephalopathy of
undetermined origin, diseases such as sepsis (fever of unknown origin),
alcoholic ketoacidosis, respiratory failure, or cardiopulmonary disease,
especially congestive heart failure, acute pulmonary edema, or unstable
angina.

f. ML Importance
(1) Almost always suicidal. Because of bitter taste, ingestion of large quantities
cannot occur accidentally
(2) Frequent monitoring – Elderly people who are chronically taking aspirin
for painful conditions must be frequently monitored. Failure of recognition of
symptoms may result in allegations of negligence against doctors.

D. Analgesic-Antipyretics with Poor Antiinflammatory Action

1. Paracetamol (Acetaminophen)

a. General
(1) Paracetamol is an aniline analgesic.
(2) It is the active metabolite of phenacetin, once itself popular as an analgesic
and antipyretic. But unlike phenacetin, paracetamol is not a carcinogenic at
therapeutic doses.
(3) The words paracetamol (used in India) and acetaminophen (used in the US,
Canada and some other countries) both come from chemical names for the
compound: para-acetylaminophenol and para-acetylaminophenol. The
chemical name can also be written as N-acetyl-para-aminophenol; it is then
known as APAP.

b. Metabolism
Absorbed rapidly from GIT, and metabolized quickly in the liver, via four
pathways (1) glucuronidation (60%) (2) sulfation (35%) (3) conjugation with
cysteine (3%) (4) Cytochrome P-450-mediated N-hydroxylation to form N-
acetyl-p-benzoquinoneimine (NAPQI) (1%).

c. Mechanism of toxicity
NAPQI is a strong oxidizing agent. It binds covalently to hepatocytes, causing
liver necrosis and occasionally to renal cells causing renal damage. It is normally
detoxified by conjugation with reduced glutathione and excreted in the urine as
mercapturic acid and cysteine conjugates.

d. Signs and symptoms

i. Acute poisoning
The usual clinical course can be divided into three phases.
(1) Phase I – (½-24 hr). Nausea, vomiting, diaphoresis, pallor, mild drowsiness.
(2) Phase II – (24-48 hr) symptom free. LFT abnormal
(3) Phase III – (3-5 days) Symptoms of severe hepatic necrosis [eg asterixis
(coarse flapping tremor of hands)] with jaundice, Right upper quadrant
tenderness, coagulation defects, hemorrhages, fetor hepaticus, hypoglycemia,
hepatic encephalopathy, and in rare cases, renal failure and cardiomyopathy.

ii. Chronic poisoning

(1) Circumstances - Occurs when an individual consumes large doses of
paracetamol over years for control of pain.
(2) More common in - alcoholics, AIDS patients [in whom there is depletion of
glutathione], patients receiving cytochrome P450 inducers [barbiturates,
carbamazepine, isoniazid, phenytoin, rifampicin], and in children where
dosages have been wrongly calculated.
(3) Clinical features: (i) .temp (ii) Anorexia (iii) Hepatomegaly (iv) Lethargy
(v) oliguria (vi) Vomiting

e. Fatal dose
(1) 20-25 g(40-50 tablets). 20 tablets in normal persons may produce severe
hepatotoxicity
(2) more dangerous in alcoholics, so they succumb at lower doses
(3) Children <10 y are more resistant.
f. Fatal period
2-4 days.

g. Management
(1) Gastric lavage
(2) Activated charcoal (should not be given if NAC or methionine are intended
to be administered, as it would bind them)
(3) Antidotes - (a) N-acetyl cysteine or NAC (Mucomist, Mucosil). (i) Oral
loading dose 140 mg/kg followed by 70 mg/kg every 4 hours for 17 doses
[total 18 doses] (ii) The golden time for administration is the first 8 h after
overdose. (I) Also effective (II) NAC has a foul smell and taste. Thus if given
orally it must be diluted with soft drinks to make a 5% soln. The soln must be
consumed within one hour of preparation. (III) Mech of Action - NAC
prevents paracetamol toxicity by following mechanisms (i)Prevents binding of
NAPQI to hepatocytes (ii) Directly binds to NAPQI (iii) Enhances synthesis
of additional glutathione (iv) Acts intracellularly as a glutathione substitute (v)
Reduces NAPQI back to paracetamol. (IV) NAC within paracetamol - It has
been suggested that for high risk populations such as psychiatric patients
[particularly those with depression and personality disorders who may attempt
suicide by AP], paracetamol tablets should incorporate a sustain release
preparation of NAC. (b) Methionine - (i) Oral antidote. (ii) Glutathione
precursor. (iii) Dose – 2.5 g at 4 hourly intervals up to 4 doses. (c)
Cysteamine - Once popular, but not now, because efficacy is less if
administered late (>10 h after ingestion).
(4) Liver transplantation – When fulminant liver failure develops.
(5) Treatments of no use in paracetamol - (a) Forced diuresis - as only 5% is
excreted in urine. (b) Hemodialysis - reduces the half-life of paracetamol, but
there is no evidence that it alters the clinical course. (c) hemoperfusion with
activated charcoal (d) peritoneal dialysis. These lines of treatments should be
avoided.

h. PM appearances
(1) Acute centrilobular hepatic necrosis
(2) Acute tubular necrosis
(3) Necrosis of myocardium
(4) Cerebral edema.

i. ML importance
(1) Mostly suicidal
(2) Rarely accidental
(3) Homicidal poisoning virtually unknown because of large dose required
(4) Organ donation after paracetamol poisoning – Can be done.

46. Drug Dependence and Abuse

I. INTRODUCTION

A. Definitions

1. Drug
Any substance, other than that required for the maintenance of normal health,
which when administered to a living organism modifies one or more of its
functions.

2. Drug habituation
Psychological and emotional dependency resulting from repeated consumption
of a drug (caffeine in tea and coffee, nicotine in cigarettes).

3. Drug addiction
Physical, psychological and emotional dependency resulting from repeated
consumption of a drug (opium, cocaine, cannabis). Compulsive use - There is
compulsive use of drugs (craving) resulting in physical, psychological and
social harm. Use is continued despite awareness of that harm. Relapse - Relapse
is the return to drug taking following extended periods of abstinence. Relapse is
characteristic of addiction and is a major problem for its treatment. Table 1 lists
major differences between drug habituation and drug addiction. Drugs known to
cause addiction - include illegal drugs as well as prescription or over-the-counter
[OTC] drugs [Prescription drug abuse, Kiddie dope].

4. Drug dependence
Drug dependence includes both drug habituation and drug addiction. The terms
drug habituation and drug addiction were first defined in 1957 by World Health
Organization (WHO) Expert Committee on Addiction-Producing Drugs. In
1964, a new WHO committee suggested the term drug dependence.

Types of Drug dependence

A proposal has been made to classify drug dependence into 7 types, but it has
not been widely accepted. The suggested types are (1) Morphine Type (2)
Barbiturate-Alcohol Type (3) Cocaine Type (4) Cannabis (Marihuana) Type (5)
Amphetamine Type (6) Khat Type (7) Hallucinogen (LSD) Type.

i. Morphine type
Characteristics:
(1) Psychic dependence - Strong; an overpowering drive or compulsion to
continue taking the drug and to obtain it by any means, for pleasure or to
avoid discomfort.
(2) Physical dependence - Develops early. -es in intensity, paralleling - in
dosage. This requires a continuation of administration of the same drug, or a
congener, to prevent the appearance of the symptoms and signs of withdrawal.
Withdrawal of the drug or administration of a specific antagonist precipitates a
definite, characteristic, self-limited abstinence syndrome.

ii. Barbiturate-alcohol type

(1) This type has been named thus, because the signs and symptoms of alcohol
and barbiturate intoxication are similar [ch 40].
(2) Within this type, loose subtypes of the two drugs have been described
[barbiturate type and alcohol type] because there are psychological and
sociological differences between the two.
(3) Characteristics of barbiturate type - Similar to morphine type dependence.
Differences -
(i) In contrast with morphine type, there is a dose limit up to which a person can
become tolerant in barbiturate type. This limit is characteristic of the
individual and varies widely.
(ii) Following withdrawal of barbiturates, tolerance is rapidly lost. Indeed some
patients may become more sensitive to barbiturates than they had been
earlier.
(4) Characteristics of alcohol type - Overt pathology in tissues; a similar
development with barbiturates [or morphine] has not been demonstrated.

iii. Cocaine type

Characteristics:
(1) Psychic dependence - Strong
(2) Physical dependence - None; therefore absence of a characteristic abstinence
syndrome when the drug is withdrawn.
(3) Tolerance - Absent; rather, there is sensitization to the drug’s effects in some
instances.
(4) A strong tendency to continuation of administration, as in coca-leaf chewing,
or rapid repetition of the dose, as in the current practice of IV administration.
 Quantitatively, the effects are strikingly different, according to the mode of
abuse. [please also see ch 41].

iv. Cannabis (Marihuana) type

Characteristics:
(1) Psychic dependence - Moderate to strong because of desired subjective
effects.
(2) Physical dependence - None; so that there is no characteristic abstinence
syndrome when the drug is discontinued.
(3) Tolerance - None. Little tendency to - the dose.

v. Amphetamine type
Characteristics:
(1) Psychic dependence - variable.
(2) Physical dependence - None; consequently, no characteristic abstinence
syndrome, though withdrawal will be followed by a state of mental and
physical depression as the individual escapes from the persistent stimulation.
(3) Tolerance - Slow development of a considerable degree of tolerance to many
effects, but not participated in equally by all components of the cerebral
system, so that nervousness and sleeplessness persist and psychotoxic effects
such as hallucinations and delusions may occur.

vi. Khat type

Characteristics:
(1) Psychic dependence - Moderate but often persistent as long as its
maintenance is practicable.
(2) Physical dependence - None.
(3) Tolerance - None

vii. Hallucinogen (LSD) type

Characteristics:
(1) Psychic dependence - varies greatly, but it usually is not intense. Users may
wish to repeat them, but if such agents are not readily available, they will
either do without them or substitute another substance. A minority of users
may develop very strong psychic dependence.
(2) Physical dependence - None.
(3) Withdrawal symptoms - None.
(4) Tolerance - A high degree of tolerance to (i) LSD and (ii) psilocybin
develops rapidly and disappears rapidly. Tolerance to (iii) mescaline develops
more slowly. Persons who are tolerant to any of these three drugs are cross-
tolerant to the other two.

5. Drug abuse
The term “drug abuse” is not mentioned in DSM-IV-TR at all. However it
loosely refers to the self administration of any drug in a manner that deviates
from the approved medical or social pattern within a given culture. It is a
tradition within some cultures to use psychoactive drugs [eg hallucinogenic
mushrooms, Catha edulis, Bhang on Holi and Kasoomba [ch 40] on cultural
festivities in India]. Such use would not be called drug abuse.
Salient features:
Drug abuse may not necessarily involve any dependency [physiological or
psychological]. For example occasional experimental use of LSD by a college
student perhaps on his colleague’s insistence is drug abuse, but not drug
dependence.

6. Physical dependence (physiological dependence)

Alteration in neural systems which is manifested by tolerance and appearance of
withdrawal phenomena, when a chronically administered drug is discontinued or
displaced from its receptor.

7. Substance abuse
Substance abuse refers to a maladaptive pattern of substance use that results in
recurrent and significant adverse consequences related to the repeated use of
substances [DSM-IV-TR]. While substance abuse is an official term used in
DSM-IV-TR, in day-to-day communication, the term drug abuse is used
synonymously.
Salient features:
(1) Characteristics - There are (i) repeated failure to fulfill major role
obligations [i.e. role of a good parent, son etc], (ii) repeated use in situations in
which it is physically hazardous [e.g. during car driving], (iii) multiple legal
 problems, and (iv) recurrent social and interpersonal problems.
(2) Difference from substance dependence - Unlike the criteria for substance
dependence, the criteria for substance abuse do not include tolerance,
withdrawal, or craving. Instead it includes only the harmful consequences of
repeated use.
(3) Stage - Substance abuse is the initial stage in an individual who has only
recently started taking the substance. Substance dependence is the later stage.
(4) Difference between drug abuse and substance abuse – These are
synonymous terms. Till 1960s and 70s WHO favored the former term.
Substance abuse is an official term mentioned in DSM-IV-TR. This term now
appears in several WHO publications also.
(5) Causes of substance (drug) abuse – (i) User starts taking drug for
legitimate medical use (e.g. morphine for pain), and then starts abusing drug.
This group is more easily cured than the second (ii) User takes drug for non-
legitimate use from the very beginning. Drug is taken for (a) relaxation and
recreation (b) better performance in sports (c) relieving tension, frustration
arising from loss and failures in life (d) spiritual purposes – for getting in
touch with God closely. Such drugs are called entheogens [Gk en, in; theo,
God; gen, generates] e.g. Iboga, Peyote (e) Aphrodisiac (f) Curiosity.

8. Substance dependence
Substance dependence refers to repeated self-administration that results in (1)
tolerance (2) withdrawal symptoms when use is reduced or stopped and (3)
compulsive use of drugs (craving) despite significant substance-related problems
[DSM-IV-TR]. Substance Dependence does not occur with caffeine. Both
Substance abuse and substance dependence are grouped under “Substance Use
Disorders” by DSM-IV-TR.

9. Substance intoxication
Clinically significant maladaptive behavioral or psychological changes
associated with excessive intake of substance (e.g. belligerence, mood lability,
cognitive impairment, impaired judgment, impaired social or occupational
functioning). Substance Intoxication is often associated with substance abuse or
dependence. Does not occur with nicotine. Evidence for recent intake of the
substance can be obtained from the history, physical examination (e.g., smell of
alcohol on the breath), or toxicological analysis of body fluids (e.g., urine or
blood).

10. Tolerance
Need for greatly -ed amounts of the substance to achieve intoxication (or the
desired effect) or a markedly diminished effect with continued use of the same
amount of the substance.
Salient features:
(1) Mechanisms - (i) Adaptation of the cells of the CNS and (ii) -ed peripheral
metabolism of the drug (iii) Immune-like mechanism.
(2) Loss of tolerance – (i) During hospitalization or imprisonment, when the
addict is weaned off from drug, there may be loss of tolerance (ii) When he is
released, he goes back to his old environment"takes same amount of drug as
before"Tolerance has been lost"death.

11. Cross-tolerance
Decrease in response to one drug due to exposure to another drug [e.g. exposure
to amphetamine results in tolerance to methamphetamine; cigarette smokers
show tolerance to caffeine; exposure to psilocybin results in tolerance to
Mescaline and DMT].

B. Epidemiology
(1) Worldwide 5 % of the population (about 200 million people) consume illicit
drugs annually.
(2) Most commonly abused substances -
(i) Legal - In order of frequency are (a) Caffeine (b) Nicotine (c) Alcohol.
Adverse effects with caffeine and nicotine are not significant enough to
generally include them in the category of substance abuse.
(ii) Illegal – (a) Cannabis. (b) cocaine.

C. Symptoms [of Drug Dependence]

(1) Symptoms of drug dependence would depend upon the drug being abused.
Some general symptoms while the person is using the drug are: Anxiety
Blurring of vision Clumsy movements Depersonalization and emotional
detachment Depression Impaired memory and concentration Lethargy and
 passivity Loss of appetite and weight Loss of interest in surroundings Mood
changes Preference for solitude Reddening and puffiness of eyes Sleeplessness
Slurred speech Sweating Temper tantrums Tremors and Unsteady gait. Drug
paraphernalia are discovered at home. The addict commits theft and other
crimes to procure money to buy drugs.
(2) If the drug is suddenly withdrawn, the person develops withdrawal
symptoms.
(3) Combination of drugs – each drug may potentiate each other. The total
effect of a combination may be more than the algebraic sum of effects of each
drug separately [eg alcohol+benzodiazepines].

D. Withdrawal Symptoms
Withdrawal symptoms (Abstinence syndrome) refer to symptoms with
physiological and cognitive components, that occur when blood or tissue
concentrations of a substance decline in an individual who had earlier
maintained high levels following prolonged heavy use of the substance.
Salient features:
(1) Repeated administration becomes necessary - After developing unpleasant
withdrawal symptoms, the person is likely to take the substance to relieve or
to avoid those symptoms, typically using the substance throughout the day
beginning soon after awakening.
(2) Variation - Withdrawal symptoms, which are generally the opposite of the
acute effects of the substance, vary greatly across the classes of substances.
(3) Substances showing marked withdrawal symptoms - (i) alcohol (ii)
anxiolytics (iii) hypnotics (iv) opioids and (v) sedatives
(4) Substances showing weak withdrawal symptoms - (i) amphetamines (ii)
cannabis (iii) cocaine (iv) nicotine.
(5) Substances showing no withdrawal symptoms - (i) Hallucinogens (ii)
phencyclidine (however withdrawal to phencyclidine has been demonstrated
in animals).
(6) Typical withdrawal symptoms [of opiates] – Time period - Begin within 6-
8 h of stoppage of drug. May last up to a week. Intensity of symptoms depend
upon dose and type of drug that was being used, duration of addiction and
suddenness of the withdrawal of drug. Stages - 1st Stage [early; up to 12 h] -
Intense fear Chilliness Cold sensation Craving -ed sensitivity to pain
 Lacrimation Muscle aches Rhinorrhea Sweating Tachycardia Uneasiness,
restlessness, irritability and Yawning 2nd Stage [intermediate; 12-24 h] - -ed
Bronchial secretions"predispose to chest infections Dilated pupils Piloerection
[“flesh creeping“ or “Goose skin“] Respirations labored and rapid
Spontaneous orgasms Tremors. Symptoms of 1st and 2nd stages together are
referred to as “cold turkey” Such skin is called “turkey skin” since it
resembles the plucked bird. 3rd Stage [late; 24 h – 10 days] – sleep [lasts 8-16
h] Upon awakening all previous symptoms become intense. In addition there
are Cramps and Pain in abdomen and legs Fever Hypertension Perspiration
Tachypnea and Vomiting and diarrhea. Sudden withdrawal in opioid
dependent pregnant females may be life threatening to the fetus. All
symptoms are maximal in 72 h. Anorexia is present in all stages. Symptoms
pass off in 7-10 d. Newborns of addicted mothers - Also show withdrawal
symptoms, which appear within 1 h of birth and require treatment Symptoms
are convulsions hyperactivity and twitchings.

E. Complications [of Drug Dependence]

Mainly due to IV use. Same as that of heroin. [Please see ch 40 – CNS
depressants].

F. Management [of Drug Dependence]

1. Treatment
(1) Admission to an institution
(2) Constant supervision – so that he can not secretly get drugs
(3) Detoxification – Gradual reduction of drug
(4) Administration of sedatives.
(5) Ibogaine – An indole alkaloid obtained from a West African plant
Tabernanthe iboga. Used in the management of addiction to alcohol, cocaine,
heroin, methadone and methamphetamine.
(6) Occupational therapy – Engaging in meaningful occupation
(7) Psychotherapy – family, group or individual therapy
(8) General health improvement
(9) Symptomatic.
2. Drug rehabilitation
Drug rehabilitation [syn - drug rehab, rehab) is the process of medical and
psychotherapeutic treatment for drug dependency enabling the patient to cease
substance abuse.
Salient features:
(1) Aims -Social rehabilitation and training for gainful employment.
(2) Uses psychosocial approaches to rehabilitate drug abusers.
(3) Requires strong family and social support
(4) Persons with history of childhood abuse are more likely to leave drug
rehabilitation program midway.

II. PSYCHOACTIVE DRUGS

[A] Psychoactive drugs, psychotropic drugs or psychopharmaceuticals are

drugs that act primarily upon the CNS, resulting in changes in perception, mood,
consciousness, cognition, and behavior.
Salient features:
(1) Legal status - Many of these drugs are used recreationally, and are outlawed.
(1) They are the common drugs of abuse or addiction.
(3) They are commonly referred to as street drugs
(4) Additives – These are substances added to psychoactive drugs. Three main
additives are present— contaminants, diluents, and adulterants. [ch
40"“Additives”]. Common adulterants for drugs of addiction (mainly heroin)
are (i) Baking soda (ii) Lactose(iii) Magnesium silicate (iv) Mannitol (v)
Quinine (vi) Sucrose (vii) Talcum powder. Since heroin is white in color, an
adulterant must be white. Charcoal cannot be used as an adulterant of heroin.
(5) Entheogen (Gk en, in; theo, God; gen generates"A drug which generates
God within) is a psychoactive substance used for religious or spiritual
purposes. Mostly derived from plant sources (ex. kykeon, ambrosia, iboga,
peyote, ayahuasca).

[B] Classification of psychoactive drugs [drugs of abuse, drugs of addiction]

(A) CNS Depressants (.CNS activity) – (1) Alcohol [Ethanol] (2) GHB
(gamma-hydroxybutyrate) (3) Hydrocarbons (4) Inhalants (Solvents, volatile
substances) – e.g. Gasoline, Glue (5) Ketamine (6) Opioids [morphine, codeine,
pentazocine (Talwin), oxycodone (Oxycontin), hydromorphone (Dilaudid),
heroin, fentanyl, methadone (7) Sedatives/Hypnotics/tranquillizers/Anti-anxiety
medications (i) Benzodiazepines [diazepam (Valium), Lorazepam (Ativan),
oxazepam (Serax), clonazepam (Rivotril), alprazolam (Xanax"), temazepam
(Restoril")] (ii) Barbiturates [phenobarbital, butalbital] (8) Snake [cobra] venom
[ch 38]. (B) CNS Stimulants (-CNS activity)– (1) Amphetamines
[methylphenidate (Ritalin), dextroamphetamine (Dexedrine), mixed
amphetamines (Adderall), methamphetamine (crystal meth) (2) Caffeine (3)
Cocaine (Crack) (4) Decongestants (ephedrine, pseudoephedrine, norephedrine
or phenylpropanolamine) (5) Ecstasy [syn. 3, 4 - Methylenedioxy
methamphetamine or MDMA] It is a designer drug [please see below]. It also
has hallucinogenic actions. (6) Ephedra (including Guarna, Ma huang) (7) Khat
(Catha edulis) (8) MDA – 3, 4- methylenedioxyamphetamine (9) Nicotine. (C)
Psychedelics or Hallucinogens (distort CNS activity) – (1) Alkyl nitrites (2)
Anabolic steroids (3) Cannabis (Marijuana, Pot, Hash)[also has CNS depressant
activity] (4) Datura (5) DOM [STP] (6) Hallucinogenic Mushrooms (Psilocybin)
(7) LSD [d-lysergic acid diethylamide] (8) Mescaline (9) Nutmeg [Myristica
fragrans] (10) Phencyclidine (PCP) (11) Salvia divinorum [Diviner’s Sage,
Seer’s sage]. (D) Other Psychotherapeutic Agents (Medications) - (1) Agents
for treating Alcohol Dependence [disulfiram (Antabuse), Naltrexone (Revia),
Acamprosate [Campral] (2) Antidepressants (3) Antipsychotics (4) Anxiolytics
[Buspirone (Buspar), Benzodiazepines (5) Bronchodilators (6) Mood Stabilizers
(7) Muscle relaxants [Carisoprodol (Carisoma, Sanoma, Soma)] (8) Opioid
Substitution Therapy [methadone, buprenorphine/naloxone]. Anticonvulsants
and antiparkinsonian drugs are not used as drugs of addiction, although they are
psychotherapeutic agents]. (E) Designer drugs - Drugs created to get around
existing drug laws, usually by modifying the molecular structures of existing
legal drugs to varying degrees or less commonly by synthesis of a new drug with
an entirely different chemical structure., Ex – MDMA, Cathinones. (F)
Combination drugs - Psychoactive drugs used in combination. Ex – speedball
[Please see ch 40 – CNS depressants, under the entry “Heroin”], Tuinal
[combination of amobarbital and secobarbital]. Both designer and combination
drugs are not additional classes of drugs, but combinations or new forms of first
four classes.
A. CNS Depressants

1. Inhalant abuse
Inhalant abuse [glue sniffing, solvent abuse, volatile substance abuse, volatile
substance misuse (VSM)] refers to inhalation of volatile substances (inhalants)
which produce euphoriant effects.
Salient features:
(1) Commonly abused inhalants– [A]Hydrocarbons usually available as
household products - (i) acetone (ii) alkyl nitrite and other nitrites (iii) benzene
[in glues, paints, and fuels] (iv) butane (v) butyl nitrite (vi) carbon
tetrachloride (vii) fluorocarbons (viii) gasoline or petrol (ix) isopropane (x)
kerosene [ch 40] (xi) methylene and ethylene chloride (xii) propane (xiii)
toluene [most studied and most commonly misused volatile solvent globally.
Present in paint thinners, varnishes, inks, fuels, and adhesives] (xiv) TCE or
1,1,1-trichloroethane [in fabric protectors and cleaners] (xv) trichloroethylene
and (xvi) xylene (in permanent markers and laboratory reagents)].
[B]Anesthetic gases – (i) Chloroform (ii) ether (iii) halothane (iv) nitrous
oxide
(2) Unique risk groups – (i) Air conditioning repairers (ii) anesthesiologists (iii)
dentists (iv) dry-cleaning workers (v) hair stylists (vi) nurses (vii) painters and
(viii) shoemakers because of access to these chemicals or anesthetics in the
workplace.
(3) Inhalation methods – Mainly 5 methods (i) Bagging – Volatiles are poured
in a plastic bag, which is then closely applied to nose and mouth and deep
inhalations taken [Both oral and nasal inhalation] (ii) Dusting - Spraying an
inhalant directly in mouth or nose (iii) Glading - Inhaling air freshener
aerosols by first spraying them in the room and then inspiring deeply (iv)
Huffing – Cloth is saturated with the volatile and kept over mouth (oral
inhalation) (v) Sniffing [syn, snorting]– inhalation directly from the neck of a
bottle or container (nasal inhalation). Jerry cans or petro-fillers may be used.
Occasionally, the chemical product is heated [eg glue] to - volatilization,
bubbled through water to remove irritants [eg aluminum chlorohydrate in
antiperspirants], or combined with ethanol prior to inhalation.
a. Epidemiology
Most abusers are male teenagers.

b. Signs and symptoms

i. Acute poisoning
Symptoms start within seconds, with the “intoxicating” effects lasting from 15 to
60 min. Effects are dose-dependent.
(1) Drunkenness – The effects vary from a state resembling alcoholic
intoxication, and distortion of perception to actual hallucinations. Symptoms
begin with disinhibition and progress to euphoria, excitement, a sensation of
“floating”, dizziness, slurred speech, ataxia and a feeling of heightened power.
(2) Detachment from reality – Heightened sensations, powerful dreams
(3) Behavior –
(i) Complete irrational behavior
(ii) Commission of antisocial acts
(iii) Complete amnesia for behaviors
(iv) Injuring self or even commission of suicide
(4) Physical withdrawal syndrome – not seen.

ii. Chronic poisoning

(1) Solvent syndrome –
(i) Depression, fatigue, headache, insomnia, intolerance to alcohol, irritability,
memory lapses, restlessness, vague and confused thoughts, violent temper.
(ii) When seen in painters (due to chronic exposure to paint thinners etc), also
known as painter’s syndrome.
(iii) Inhalant abuse during pregnancy may cause maldevelopment of fetal brain
[fetal solvent syndrome, inhalant embryopathy], which is characterized
by mild brain atrophy and behavioral, cognitive, and emotional
abnormalities.
(2) Degreaser’s flush - chronic exposure to trichloroethylene [for at least 3 wks]
followed by intake of alcohol can cause vivid red blotches on face. Called
degreaser’s flush, because industrial workers who work with trichloroethylene
as degreasers [they remove grease used as a protective coating on machinery
and steel cables] suffer from it when they drink beer after work. So unsightly
 has been this skin redness that the workmen shunned taverns to avoid derision.
Occurs due to alcohol apparently inhibiting the normal metabolism of TCE,
transiently producing an above normal blood TCE concentration, which in
turn causes vasodilation of superficial skin vessels.
(3) Solvent psychosis - Dementia like conditions. May form a part of solvent
syndrome.

c. Cause of death

i. Acute intoxication
(1) Sudden cardiac arrest –
(i) Major COD
(ii) Commonly follows arrhythmias [eg ventricular fibrillation], which in turn is
precipitated by any sudden “fight, flight or fright” stimulus
(iii) Such stimulus can precipitate arrhythmic attacks, even considerable time
after sniffing has ceased.
(2) Anoxia, hypoxia and hypercapnia –
(i) From persistent rebreathing solvents, to the exclusion of oxygen.
(ii) Accidental asphyxia - (a) plastic bag asphyxia] [a type of environmental
suffocation; ch 19] (b) accidental smothering.
(3) Aspiration – fluids, vomit etc
(4) Loss of tolerance [please see under “tolerance” above].
(5) Accidents –
(i) Drowning
(ii) Falls - from balcony, windows etc
(iii) Burns and explosions - lighting a cigarette after inhaling a volatile substance
in a closed space like a car.
(6) Violence - during street fights.
(7) Other - (i) allergic reactions (ii) CNS depression (iii) severe injury to the
lungs.

ii. Chronic intoxication

(1) Liver tumors and liver failure
(2) Renal failure.
d. PM appearances
(1) Nose and mouth – surrounding skin may be reddened or excoriated from the
irritant action of the solvent.
(2) Bone marrow, CNS, Kidneys, Liver – cellular damage.

e. Preservation of samples
(1) Organs, viscera – (i) Blood (ii) Brain (iii) Fat (iv) lungs (v) nasal swabs [ch
5"details of techniques, especially of blood and lungs].
(2) Clothings – may reveal inhalants, if accidentally spilled over them.

2. Sedatives/Hypnotics/Tranquillizers

a. Benzodiazepines
Benzodiazepines (BZD) are psychoactive drugs whose core chemical structure is
the fusion of a benzene ring and a diazepine ring.
Salient features:
(1) History - The first benzodiazepine, chlordiazepoxide (Librium), was
discovered accidentally by Leo Sternbach in 1955, and made available in 1960
by Hoffmann–La Roche. It also marketed diazepam (Valium) since 1963.
(2) Uses - (i) Antianxiety drugs, (ii) muscle relaxants. (iii) sedatives.
(3) Common preparations are (i) Alprazolam [Xanax] (ii) Chlordiazepoxide
[Librium] (iii) Diazepam [Valium] (iv) Flurazepam [Dalmadorm] (v)
Lorazepam [Ativan] (vi) Nitrazepam [Mogadon] (vii) Oxazepam [Seresta]
(viii) Quazepam [Doral] (ix) Triazolam [Halcion]
(4) Potentially addictive drugs if used for long time. Excretion in urine may
continue for several days.

i. Mechanism of action
Enhances the inhibitory actions of the neurotransmitter GABA located in the
brain.

ii. Signs and symptoms

(1) Acute poisoning – Symptoms appear within 1 h. (i) Ataxia (ii) Breathing is
shallow (iii) Diplopia (iv) Dysarthria (v) Nystagmus (vi) Sedation (vii) Slurred
speech (viii) Somnolence (ix) Staggering walk and (x) Vertigo. (xi) Coma
 occurs in final stages.
(2) Chronic poisoning – Long term administration with high doses [eg 30-40
mg diazepam daily] produces chronic poisoning. Withdrawal symptoms occur
on sudden withdrawal. Withdrawal symptoms are (i) CNS – (a) Anxiety (b)
Convulsions [rare] (c) Headache (d) Insomnia (e) Muscle spasms (f)
Psychiatric disturbances (g) Tremors (ii) GIT – (a) anorexia (b) vomiting (iii)
Resp Sys - respiratory depression [rarely].

iii. Management
(1) Decontamination -
(i) Gastric lavage. Use cuffed endotracheal tube if comatosed
(ii) Emesis – not recommended because of potential for CNS depression
(iii) Activated charcoal.
(2) Airway and breathing - (i) Establish clear airway (ii) Assisted ventilation
(iii) oxygen.
(3) IV Fluids.
(4) Antidote – Flumazenil
(i) Dose - (a) 0.2 mg/min, slow IV to a total dose 3 mg. 1.5 mg of Flumazenil
leads to 55% receptor occupancy; 10 times [15 mg] is required to 100%
blockade [as revealed by PET]. (b) Extravasation should be avoided
because of the risk of local irritation. (c) Resedation may occur at 20–120
minutes, and readministration of flumazenil may be necessary [repeated
doses are required because duration of action of flumazenil is shorter than
that of most benzodiazepines. Vigilance is also required].
(ii) Also useful in Zolpidem and in select cases of ethyl alcohol [ch 40]
(iii) Mechanism of action - Competitive benzodiazepine receptor antagonism on
the GABA-A receptor complex. Blocks CNS actions of BZDs. But does not
reliably reverse respiratory depression induced by IV BZDs.
(iv) Ideal for patients who are new to benzodiazepines and who overdose solely
on a benzodiazepine.
(v) Induces benzodiazepine withdrawal symptoms [eg seizures in
benzodiazepine dependent patients].
(5) Correction of hypotension [ch 32].
(6) Forced diuresis and hemodialysis are ineffective.
iv. Fatal dose
100-300 mg/kg [20g for a 70 kg man]. 4000 tablets of 5 mg. Thus death is
extremely rare if taken alone. May cause death if taken with alcohol or other
potentiating drugs.

v. MLI
Mortality rates – Among benzodiazepine users are 2 fold -er. Reasons are same
as those of -er mortality rates among drug abusers [please see below under MLI
of drug abuse].

B. CNS Stimulants

1. Amphetamine
Amphetamine is a psychostimulant drug that produces increased wakefulness in
association with decreased fatigue and appetite.

a. Derivatives
The title “amphetamines” includes amphetamine itself and its derivatives (1)
Dextroamphetamine, (2) Fenfluramine, (3) MDA. (4) MDEA - 3, 4-methylene-
dioxyethylamphetamine (5) MDMA (Ecstasy) (6) Mephentermine, (7)
Methamphetamine [methylamp-hetamine] (8) Methylphenidate, (9)
Phentermine, (10) Synthetic amphetamines.

b. Mechanism of action
Amphetamine -s the synaptic conc of dopamine, serotonin, and norepinephrine
in the brain. Dopamine is involved in various reward pathways of the brain
causing euphoria.

c. Signs and symptoms

i. Acute poisoning
(1) GIT - Nausea and vomiting
(2) CVS - (i) Aortic dissection (ii) Dysrhythmias (iii) Hypertension (iv)
Myocardial ischemia (v) Tachycardia (vi) Vasospasm
(3) CNS - (i) Agitation and restlessness (ii) Anorexia (iii) Bruxism (iv)
 Choreoathetoid movements (v) Confusion (vi) Euphoria (vii) Headache (viii)
Hyperactivity (ix) Hyperreflexia (x) Hyperthermia (xi) insomnia (xii)
Intracerebral hemorrhage (xiii) Paranoid psychosis (xiv) Seizures "
Rhabdomyolysis (xv) talkativeness
(4) Other sympathetic symptoms - (i) Diaphoresis (ii) Mydriasis (iii)
Tachypnea (iv) sweating (v) Tremor
(5) Other organ systems - (i) Acute lung injury (ii) Ischemic colitis (iii) Muscle
rigidity.

ii. Chronic poisoning

(1) Amphetamine psychosis - Characterized by (i) Delusions [usually of
persecution] (ii) Hallucinations [usually visual, sometimes tactile] (iii)
Paranoid personality (iv) Stereotyped compulsive behavior
(2) Aortic and mitral regurgitation
(3) Cardiomyopathy
(4) Permanent damage to dopaminergic and serotonergic neurons
(5) Pulmonary hypertension
(6) Vasculitis.
(7) Skin - Grey, dry [due to methamphetamines]. Pruritus, tactile hallucinations
similar to cocaine bugs [meth mites].
(8) Meth mouth–darkly stained and crumbling teeth, akin to baby bottle tooth
decay, extreme cavities, rampant caries, xerostomia and lockjaw.

d. Dangers of misuse
(1) -d risk of accidents - because of both the excitation produced by these
agents and the excessive fatigue which may break through and manifest itself
at an inopportune time.
(2) -d risk of suicide
(3) intraventricular hemorrhages [ch 17]
(4) Overactivity and aggressive behavior
(5) Paranoid psychosis
(6) Serious antisocial behaviour - especially in abuse by IV administration,
with its concomitant bizarre mental effects.
(7) Shock and collapse
(8) Toxic Epidermal Necrolysis.
e. Diagnosis
(1) History - rarely reliable as patients often do know the exact drug they have
used. However the prevalence of amphetamine abuse in the local geographic
region should heighten the suspicion of amphetamine toxicity in patients
presenting with typical signs and symptoms.
(2) Laboratory Findings – Non-specific (i) -CPK (ii) -liver enzymes (iii)
Hyperglycemia (iv) hyperkalemia (v) Hyponatremia (vi) Leukocytosis (vii)
Myoglobinuria
(3) Qualitative urine immunoassay testing [QUIT]- Available, but several
pitfalls exist
(4) ECG – Findings of ischemia, hyperkalemia.

f. Management
(1) Gastric lavage
(2) Activated charcoal
(3) Continuous cardiac monitoring
(4) Acidification of urine
(5) Chlorpromazine [for amphetamine psychosis]
(6) Immunotherapy - Vaccines that would generate antibodies to sequester the
drug and prevent its access to the brain. Currently under development for 4
major drugs of abuse – cocaine, methamphetamine, morphine/heroin and
nicotine.
(7) Symptomatic – mainly treatment of agitation, delirium, hypertension,
hyperthermia and seizures [ch 32].

g. Fatal dose
Oral Amphetamine - 150-2000 mg.

h. Tests
(1) Mandelin test - Mandelin reagent [1% soln of ammonium vanadate
(NH4VO3) in conc H2SO4] is added to sample. Amphetamine gives a blue-
green colour.
(2) Marquis’ test - please see ch 40.
(3) Simon’s test [modified sodium nitroprusside test] -
(i) Reagents (a) Reagent 1 - 1 g of sodium nitroprusside in 100 mL water + 2
mL of acetaldehyde. Mix thoroughly. (b) Reagent 2 - Freshly prepared 2%
sodium carbonate in distilled water.
(ii) Procedure - Suspect sample + 1 drop of reagent 1 + 2 drops of reagent (2)
(iii) Interpretation – (a) Primary amines [e.g. amphetamine,
methylenedioxyamphetamine (MDA)]"Pink to cherry–red colour. (b)
Secondary amines [e.g. methamphetamine, ephedrine, 3,4–
methylenedioxymetamfetamine (MDMA)]"A dark blue colour.

i. PM appearances
(1) Appearances similar to those of asphyxia.
(2) Meth mouth.
(3) Amphetamine can be detected in blood, body fluids and viscera.

j. ML importance
(1) Drug Facilitated Sexual Assault – MDMA is one of the drugs used in
DFSA [ch 25].
(2) Liquid gold - Kidney excretes 40% of amphetamine unchanged. Some users
ingest amphetamine up to 2000 mg per day. About 800 mg amphetamine
would be excreted unchanged in these users. They bottle this urine in vials and
sell this yellow fluid in the underworld market as liquid gold [reasons for
calling it “liquid gold” (i) liquid state (ii) golden yellow (iii) sold at very high
cost]. Liquid gold refers to urine containing any psychoactive drug.
Classically Eastern Siberians who ingested hallucinogenic mushrooms [fly
agaric] would collect their urine; this would be drunk by others while still
warm.

2. Ecstasy [MDMA]
Ecstasy [MDMA (3,4-MethyleneDioxyMethAmphetamine)] is an entactogen of
the phenethylamine and amphetamine families, having a tendency to induce
euphoria, a sense of intimacy with others, and diminished anxiety and
depression. An Empathogen or Entactogen [Gk en, within); Latin tactus, touch
and Gk gen, produce; literally “producing a touching within”] is a drug that
produces feelings of empathy, love, and emotional closeness to others.
a. Clinical uses
Post-traumatic stress disorder (PTSD) Anxiety associated with terminal cancer.

b. Signs and symptoms

100 mg orally produces effects within 30 minutes. General signs and symptoms
of stimulants are seen hyperactivity [e.g. an uncontrollable urge to dance]
Increased alertness, awareness, and wakefulness and Feelings of empathy,
compassion, and forgiveness towards others bruxism [grinding to teeth] trismus
[spasm of muscles of mastication].

c. Cause of death
Death may be due to Disseminated intravascular coagulation [DIC] – dural sinus
thrombosis [DST], particularly in the superior sagittal sinus is an imp PM
finding [ch 5]. hyperthermia, rhabdomyolysis and renal failure.

d. Tests
Simon’s test - Please see under amphetamines.

e. ML importance
(1) Candyflapping – Intentional combination of Ecstasy with LSD.
(2) Stacking - Combination of Ecstasy with another drug [most typically a
depressant, e.g. alcohol]. This - the danger of overdose, and both Ecstasy
[stimulant] and alcohol [depressant] mask each other’s effect
(3) Sexstacy - Combination of Ecstasy with sildenafil [Viagra] to - sexual
pleasure.

C. Psychedelics (Hallucinogens)
A psychedelic substance is a psychoactive drug whose primary action is to alter
the cognition and perception of the mind.

1. Agents

a. Alkyl nitrites (Poppers)

(1) Alkyl nitrites inhaled for recreational purposes are (i) amyl nitrite [also
used for treatment of CN poisoning] (ii) butyl nitrite (iii) isopropyl nitrite
 and (iv) isobutyl nitrite.
(2) Uses - used in common household products eg air freshener, finger nail
polish remover and video head cleaners.
(3) Abuse -
(i) As club drugs. To get a “high”. Cause a rush of warm sensations and
dizziness when inhaled (due to sudden vasodilation).
(ii) Heterosexual males - use them as aphrodisiacs, sexual enhancer, for
prolonging sexual orgasm
(iii) Homosexual males - to relax anal sphincter.
(4) Adverse effects -
(i) Methemoglobinemia
(ii) Neurological damage [heavy long-term use]
(iii) Swallowing or aspirating the liquid rather than inhaling can prove fatal.
They have a low risk of harm to society and the individual compared to
other recreational drugs.

b. Anabolic steroids
(1) Taken orally or by injection.
(2) Acneiform skin lesions.
(3) May produce sudden mood swings, paranoia, depression (-suicidal
tendencies) and aggressive behavior [“roid rage”].

c. DOM [STP]
2, 5-Dimethoxy-4-methylamphetamine [DOM; known on the street as STP,
standing for “Serenity, Tranquility, and Peace”]. Signs and symptoms -
perceptual changes eg blurred vision, multiple images, vibration of objects,
visual hallucinations, distorted shapes, enhancement of details, slowed passage
of time, -ed sexual drive and pleasure, -ed contrasts, pupillary dilation, -ed BP.

d. Hallucinogenic mushrooms
Also known as psychoactive mushrooms [please see ch 39].

e. Lysergic acid diethylamide (LSD)

LSD is a colorless, odorless and mildly bitter semisynthetic compound, the
lysergic acid portion of which is a natural product of the ergot fungus Claviceps
purpurea.

i. Mechanism of action
(1) Serotonin receptor agonist - LSD binds to most serotonin receptor subtypes
except for 5-HT3 and 5-HT4 [There are 7 subtypes in all – from 5-HT1 to 5-
HT7].
(2) Psychedelic effects of LSD - (i) Attributed to its strong partial agonist
effects at 5-HT2A receptors.

ii. Toxicokinetics
(1) Absorbed from GIT. Data about the binding of LSD to human plasma
proteins is not available.
(2) Distribution – Rapidly distributed to body tissues. Highest conc appears in
lungs, liver, bile, kidneys and brain.
(3) Half-life in humans - 175 min.

iii. Mode of administration

(1) Oral – Most common.
(i) Taken after placing on - (a) absorbent blotter paper [“blotter acid”, “postage
stamps”]. Most common mode (b) gelatin squares [“window panes”] (c)
sugar cube
(ii) in blue pills
(iii) in capsule (iv) as tiny tablets [“microdots”].
(2) IM and IV - In liquid form.
(3) Smoked – very rarely. Heating destroys LSD, so smoking is not much
effective.

iv. Dose
(1) Effects appear at: 25 µg.
(2) Average recreational dose: 100-500 µg [equal to one-tenth the mass of a
grain of sand].

v. Availability
LSD (usually as the tartrate salt) is distributed as tablets, liquid, powder, and in
gelatin squares. Recently it has been available as “blotter acid,” which are sheets
of paper soaked with LSD, dried, and perforated into small squares.

vi. Signs and symptoms

(1) Symptoms from LSD [“taking a trip”] are of rapid onset and relatively mild.
(2) Duration - A trip usually occurs within half an hour of ingestion, peaks in 2-
6 h and fades after 12 h. In the recovery stage there may be apprehension and
distraction that is not immediately obvious to onlookers.
(3) Effects - depend very much on the individual and the circumstances. Same
user may have a good or a bad trip on different occasions and even within the
same trip.
(4) Sequence - Somatic symptoms appear first, then mood and perceptual
changes and finally psychological changes, although effects overlap.
(5) Symptoms –
(i) Pupils – Dilated. There may be intense photophobia.
(ii) Muscular - -ed deep tendon motor reflexes and muscle tension, mild motor
incoordination, and ataxia.
(iii) -HR, -RR, and -BP General - Nausea, salivation (sometimes dry mouth),
sweating, intestinal cramping, .ed appetite.
(iv) Psychological – (a) illusions (b) hallucinations. (c) Perceptual changes
occurring in a clear consciousness. These are (I) intensification of
perceptions (II) depersonalization [Individuals feel separate from their own
personal physicality [A similar state occurs in Locked-in Syndrome (LiS) –
ch 8]. They sense
their body sensations, feelings, emotions and behaviors as not belonging to
themselves. Life “feels like a movie”. Things seem unreal or hazy] (III)
derealization [external world seems strange or unreal]. Victim may become
violent or panic stricken. May attack others or hurt himself from disregard
of reality (IV) synesthesias [stimulation of one sense leads to experiences in
another sense, eg colors are heard, sounds are felt] (V) Feeling of being
able to fly – may jump out of windows.
(v) Bad trip – LSD may trigger panic attacks or feelings of extreme anxiety
[good trip is when symptoms are pleasurable].
(vi) Return trip – Reappearance of symptoms long after the last dose of LSD was
taken.
(vii) The symptoms produced by LSD resemble those produced by mescaline,
 psilocybin, and some of the amphetamine analogs. The major difference
between LSD, psilocybin, and mescaline is potency. A 1.5 µg/kg dose of
LSD = 225 µg/kg of psilocybin = 5000 µg/kg of mescaline. With mescaline
onset is slower.

vii. Adverse effects

After effects may persist for days or weeks. These are (1) Chronic dread (2)
Depression (3) Mood swings (4) Panic attacks (5) Paranoid states (6) psychosis
(7) Schizophrenic episodes. Repeated intake of
LSD causes permanent psychosis. LSD does not cause chromosomal breakage
and is not teratogenic.

viii. Tolerance
(1) Tolerance is associated with frequent use of any of the hallucinogens.
(2) Tolerance to LSD – develops in 2-3 days with daily intake
(3) Loss of tolerance – occurs in 4-6 days if LSD is not taken.
(4) Cross-tolerance - between mescaline, psilocybin, and LSD occurs, but not
between amphetamine and LSD, despite the chemical similarity of
amphetamine and mescaline.

ix. Withdrawal syndrome

(1) Withdrawal syndrome - does not occur with LSD.
(2) Flashback phenomenon - (i) Spontaneous recurrence of the LSD use
experience in a drug free state (ii) Occurs weeks to months after the last
experience. (iii) Induced by – alcohol intake, fatigue, marijuana intoxication,
severe physical illness and stress. Can sometimes also be self-induced by will
for positive reexperiences [free trips]. (iv) Occurs with abuse of most
psychotomimetics eg (a) LSD (b) Mescaline (c) psilocybin (d) STP (e)
Tryptamines (e) May lead to eccentric behavior – Homicide, suicide.

x. Fatal dose
200 µg/kg. Thus 14,000 µg [or 14mg] for a 70 kg human.

xi. Tests
Van Urk’s Test – A Spot Test for LSD, psilocin and psilocybin. Ehrlich’s [or
Van Urk’s] Reagent [1% p-dimethylaminobenzaldehyde in 10% HCl] gives
following colors in the presence of following psychedelics. (i) LSD – purple (ii)
Psilocin - blue-grey (iii) Psilocybin - red-brown.

xii. Cause of death

Paralysis and respiratory failure.

xiii. Management
Treatment is required if a “bad trip” occurs.
(1) Anxiolytic agents - eg diazepam (Valium) 10-20 mg or other
benzodiazepines.
(2) Removal of stimuli – eg bright lights and loud noises are helpful [same as in
strychnine].
(3) Prolonged talking – known as “Talking the person down”. Continues for 12-
18 h.
(4) Psychotherapy.

xiv. MLI
Please see MLI of psychedelics below.

f. Phencyclidine (PCP)
Phencyclidine [PCP, angel dust], is a recreational hallucinogenic drug, formerly
used as an anesthetic agent.
Salient features:
(1) First synthesized in 1926, it was patented in 1952 by the Parke-Davis
pharmaceutical company and marketed under the brand name Sernyl.
(2) MOA - It acts as an NMDA receptor antagonist [blocks the activity of
NMDA receptor]. Other NMDA receptor antagonists are dextromethorphan,
ketamine, nitrous oxide and tiletamine. Primary psychoactive effects last for a
few hours, but total elimination takes more than a week.
(3) Signs and symptoms – see box.
Memory Aid 1: Signs and symptoms of PCP poisoning
RED DANES had BAD COLD: Rage, Erythema, Dilated pupils, Delusions, Amnesia, Nystagmus,
Excitation, Skin dryness. Bizarre behavior, BP-, Acute psychosis [delusions and hallucinations],
Agitation, Ataxia, Dysarthria, Catatonia, Coma, Lethargy, violent tenDencies +Tachycardia, tremors
(4) Fatal dose - (i) ingestion – 100 mg (ii) blood levels – 0.1mg%.
(5) Management - (i) Gastric lavage (ii) AC (iii) Immuno-therapy - PCP-
specific antigen binding fragments [Fab] therapy has been tried in animals.
Shows promise in humans also. [please also see ch 36"Arsenic].

2. MLI of psychedelics (Hallucinogens)

(1) The chief dangers to the individual arise from the psychological effects.
Impairment of judgment could lead to dangerous decisions or accidents.
Occasional persons may become depressed, so that suicide is a possibility in
users of these drugs.
(2) Hallucinogens are mainly used for self-exploration, to experience varied
hallucinations and to get out of day-to-day boredom.
(3) LSD Has been used in treatment of alcoholism [ch 40].

D. Other Psychotherapeutic Agents (Medications)

1. Antidepressants
Antidepressants are used to alleviate mood disorders, e.g. major depression and
dysthymia (chronic mood disorder). Major antidepressants are
(1) Monoamine oxidase inhibitors (MAOIs),
(2) Tricyclic antidepressants (TCAs),
(3) Selective serotonin reuptake inhibitors (SSRIs) and
(4) Serotonin-norepinephrine reuptake inhibitors (SNRIs). Amphetamine was
used earlier.

a. MAO inhibitors

i. Classification
Following MAOI are important.
(1) Nonselective MAO-A/MAO-B Inhibitors -
(i) Hydrazines - (a) Benmoxin [Nerusil] (b) Iproniazid [Iprozid] (c)
Isocarboxazid [Marplan] (d) Nialamide [Niamid] (e) Octamoxin [Nimaol]
(f) Phenelzine [Nardil] (g) Pheniprazine [Catron] (h) Safrazine [Safra]
(ii) Non-Hydrazines - (a) Caroxazone [Surodil] (b) Tranylcypromine [Parnate]
(2) Selective MAO-A Inhibitors-(i) Brofaromine (Consonar)
(3) Selective MAO-B Inhibitors-(i) Lazabemide [Pakio].

ii. Mechanism of action

Inhibiting the activity of monoamine oxidase" breakdown of monoamine
neurotransmitters prevented "-Monoamines [serotonin, noradrenaline and
dopamine].

iii. Signs and symptoms

Mortality occurs from acute ingestions of 200 mg tranylcypromine (typical daily
dose 20-30 mg) and 400 mg phenelzine (typical daily dose 60-90 mg). Effects
appear within 24 hours.
(1) Symptoms - Sympathetic hyperactivity, anxiety, agitation, delirium,
diaphoresis, flushing, hallucinations, headache, hyperthermia, hypertonia,
Irritability, seizures, trismus
(2) Clinical findings – Dysrhythmias, DIC, multiorgan failure, mydriasis,
neuromuscular irritability, nystagmus, opsoclonus [alternating “ping-pong”
gaze], tachycardia, tachypnea, Severe hypertension followed by hypotension
and cardiovascular collapse.

iv. Fatal dose

2-5mg/kg.

v. Treatment
Gastric lavage, symptomatic.

2. Antipsychotics [Neuroleptics]
Antipsychotics were earlier called neuroleptics.

a. Classification
(1) Phenothiazines -
(i) Aliphatic side chain – Chlorpromazine, Triflupromazine
(ii) Piperidine side chain – Mesoridazine, Thioridazine
(iii) Piperazine side chain – Fluphenazine, Perphenazine, Prochlorperazine,
Trifluoperazine.
(2) Butyrophenones -
(i) Haloperidol
(ii) Penfluridol [Exceptionally long acting]
(iii) Trifluperidol.
(3) Thioxanthenes -
(i) Chlorprothixene (Cloxan, Taractan, Truxal).
(ii) Clopenthixol (Sordinol).
(iii) Flupenthixol or Flupentixol (Depixol, Fluanxol) – “Cis” form is effective,
but not “trans” form, because that does not block DA
(iv) Thiothixene (Navane)
(v) Zuclopenthixol (Cisordinol, Clopixol, Acuphase).
(4) Other heterocyclics -
(i) Loxapine
(ii) Pimozide.
(5) Atypical neuroleptics (second generation antipsychotics)-
(i) Benzepines - (a) Clozapine [Clozaril] (b) Loxapine (c) Olanzapine [Zyprexa]
(d) Quetiapine [Seroquel]
(ii) Indoles - (a) Risperidone [Risperdal] (b) Sertindole (c) Ziprasidone (Geodon,
Zeldox).
(iii) Quinolinones - (a) Aripiprazole [Abilify]: Partial agonism at the D-2
receptor.

b. Mechanism of action
All antipsychotics (except atypical) have potent dopamine D-2 receptor blocking
action; antipsychotic potency has shown good correlation with their capacity to
bind to D2 receptor. Blockade of dopaminergic projections to the temporal and
prefrontal areas constituting the ‘limbic system’ and in mesocortical areas is
responsible for the antipsychotic action.

c. Signs and symptoms [of toxicity]

(1) General-.ed sweating, hypothermia or hyperthermia.
(2) Eyes - corneal opacities, miosis.
(3) CNS - sedation, seizures.
(4) CVS - Myocardial depression, orthostatic hypotension, ventricular
tachycardia.
(5) RS - laryngospasm.
(6) GIT - .ed intestinal motility and secretions, .ed salivation, cholestatic
jaundice.
(7) Blood - agranulocytosis, hemolytic anemia.
(8) Skin - dermatitis, gray-blue pigmentation, photosensitivity, urticaria.
(9) Male specific - gynecomastia, priapism.
(10) Female specific - amenorrhea.
(11) Movement disorders - Occur within 60 days of initiating therapy. (i) Acute
dystonia - oculogyric crisis, spasms of jaw, tongue, lip and throat, neck
twisting, facial grimacing, Rabbit syndrome – Peri-oral tremor, abdominal
wall spasms, opisthotonos. Symptoms rapidly resolve with parenteral
antihistamines, anticholinergics or benzodiazepines. (ii) Akathisia -
Restlessness and inability to sit, feeling of discomfort, apparent agitation
[compelling desire to move about, but without anxiety]. May be mistaken for
exacerbation of psychosis. Mechanism not known. No antidote. Central
anticholinergics only reduce intensity in some cases. (iii) Parkinsonism -
Bradykinesia [slowness of movement], fine movements, mask like expression,
muscle weakness, pill rolling, resting tremor, rigidity and shuffling gait.

d. Fatal dose
2-5 g.

e. Management
(1) Emesis and gastric lavage
(2) Multiple Dose Activated Charcoal (MDAC)
(3) Catharsis
(4) Symptomatic.

III. BODY PACKER AND BODY STUFFER SYNDROMES

The Body packer syndrome is accidental and unintentional poisoning with illicit
drugs in persons, who attempt to transport drugs illegally across national borders
by packing them in plastic packets, ingesting them or inserting them in body
orifices, and then subsequently retrieving them in a foreign country, thus safely
bypassing custom authorities.
Salient features:
(1) Smuggling procedure – (i) Methods of transportation - (a) Ingestion -
Typically the persons who smuggle drugs (variously known as couriers,
internal carriers, mules and swallowers) pack drugs in small plastic packets
and ingest them. Usually about 100 packets are ingested, each packet
containing about 10 g of drug. The total smuggled drug is 1 kg. Occasionally
persons carrying more than 200 packets have been described. (b) Body
cavities and orifices - Occasionally the drug is inserted in ears [ear packing],
anus, vagina, under the foreskin of uncircumcised males or strapped under the
breasts. (c) Unusual methods - Rarely A drug packet may be tied to a thread
and swallowed, the other end tied to a tooth for easy retrieval at destination.
(ii) Composition of packets - Instead of plastic packets the drug may be
packed in balloons, capsules, condoms, fingers of rubber gloves, heat sealed
plastic films or multiple layers of latex. (iii) Measures to reduce gut motility –
Antidiarrhoeals, antipropulsives [eg diphenoxylate, loperamide] and
antiemetics during drug transportation. (iv) Evacuation – When the body
packer reaches the country of destination, he takes a laxative, defecates,
retrieves the packets from feces and delivers them to the drug dealer
(“pusher”). Enema and suppositories may also be used.
(2) How the smuggler comes to notice – (i) Bursting or leaking of packets - If
one or more packets begin to leak or rupture while the smuggler is still at
airport or in the flight, he suffers poisoning symptoms and comes to the notice
of law. Sometimes death also occurs. (ii) Osmotic seepage – Even if packets
do not rupture, osmotic seepage occurs across latex wrappings, causing traces
of drug to appear in circulation and urine. Suspicious persons may be retained
for urine examination and X-ray.
(3) Terminology: (i) Body packers - are those, who smuggle illicit drugs across
nations by either ingesting them or inserting them in body cavities. (ii) Body
stuffers - do not smuggle illicit drugs. They peddle drugs locally. When police
comes to arrest them, they quickly ingest drugs available with them to
eliminate potential incriminating evidence. Practice is also used to hide drugs
by prisoners from prison officials during sudden checking and concealing drug
from other addicts.

A. Investigation
1. Physical examination
Gentle rectal and vaginal examination may disclose packets.

2. Stomach lavage
to recover packets [ch 32].

3. Radiography

a. X-ray
(1) Unusual number of rounded cigar-shaped or oblong masses with a complete
gas halo
(2) Radiodensities of different drugs of abuse -
(i) Hashish is denser than stool;
(ii) Cocaine appears similar to stool; and
(iii) Heroin has a gaseous transparency.
(3) Tic Tac sign – [Tic tac is a brand of small, hard oblong shaped mints].
Multiple oblong, uniformly shaped packages (of the shape of tic tac) are seen
in the abdomen.
(4) Double-condom sign - Well-defined, homogeneous oval or oblong densities
surrounded by a translucent rim (which represents air trapped between the
individual layers of packaging material – most often two condoms). If these
densities are multiple, and found in the proximal ascending colon or upper
GIT, the diagnosis is almost assured.
(5) Rosette sign - Densities associated with a translucent rosette at one end.
Indicates air trapped in the knot where the condom is tied.
(6) Parallelism - Relatively rigid packages align parallel to each other in the
bowel lumen.

b. CT scan

c. Barium contrast studies

d. Ultrasonography and MR imaging

Do not have an important role.
4. Lab tests
Blood and urine tests for illicit drugs.

B. Management
(1) Nil orally – till packets are within GIT.
(2) Removal of packets -
(i) Whole bowel irrigation – to remove packets [ch 32]. Some recommend
polyethylene glycol as an irrigation solution, but others do not approve of it
because it can dissolve packages causing their rupture. Following
alternatives must also be kept in mind
(ii) Metoclopramide – 10 mg, 8 hourly, to promote gastric emptying
(iii) Rule out bowel obstruction; wait and allow packets to pass in colon"high
volume saline enemas, or low volume phosphosoda enemas
(iv) Bisacodyl suppository – to empty rectum
(v) Endoscopy or surgery – If all measures fail, or if there is bowel obstruction.
(3) Symptomatic - Appropriate to the drug which has leaked and caused
poisoning.

C. PM Findings
(1) Presence of drug packets in stomach and intestines, some of which may be
ruptured
(2) Congestion of gastric and intestinal mucosa
(3) Congestion of lung, meninges and abdominal organs Edema of lung and
brain.

D. Medicolegal Aspects
Body packing increased after 9/11, because of the increased border security,
which made conventional smuggling more difficult.

IV. INVESTIGATION OF DRUG ABUSE DEATHS

A. History
Bizarre acts, irrational behavior or unexpected coma followed by death,
especially in younger people returning from night long parties, points to drug
related death.

B. Clothes
Drugs may be hidden in belt, eye glass case, jewellery, matchboxes, money
purse, pens, pockets, seams, shoes, socks etc. These must be thoroughly
searched.

C. Scene of Death
(1) Follow all protocols of a scene of death investigation [ch 1]. Following
specific points are important.
(2) Psychedelic posters – indicate drug addicts.
(3) Drug may be hidden anywhere in the room – either in obvious places eg
cupboards, or cleverly hidden eg between pages of a book, tourniquet etc. Any
sample of drug recovered should be preserved and sent for analysis.
(4) Equipment [syn, works]– may be found at the scene (i) intravenous
apparatus [Fig 46.1] used by drug addicts consists of paper for mixing drugs
(1), drug (2), needles (3), homemade eyedropper syringe (4), a teaspoon
cooker (5), cotton to remove impurities (6), shoelace tourniquet (7) and a
source of heat (8). Method of injection [ch 40"Heroin]. Half filled syringes or
even empty syringes should be preserved and sent for chemical analysis. (ii)
Aerosol cans, bags, balloons, plastic tubes etc – indicate death due to inhalant
abuse.
D. Autopsy
PM findings are same as in heroin [ch 40], cocaine [ch 41], amphetamines or
inhalants [please see above for both] if any of these drugs were used. Because
any other illicit drug may be involved, there may be additional, specific findings
related to that drug.

1. External
Body – Stains – on tips of fingers. Color and smell indicates possible type of
capsule or pill handled.

2. Internal
GIT – (i) may contain pills or capsules (ii) Stomach – (a) dye from capsules –
may color mucosa with various colors (b) microscopic examination under
polarized light may show particles of optically active filler material [cellulose,
starch, talc] adherent to the gastric mucosa.

E. Toxicology
Drugs of abuse may be detected by modern analytical methods from various
body fluids.

V. TOXICOLOGIC RADIOLOGY

Radiology in Drug Abuse

Body packers – drug packets are revealed by x-rays [please see above].

VI. GLOSSARY OF DRUG ABUSE

(1) Acid head – heavy user of LSD.
(2) Bad, bum or freak out trip – LSD experience in which the drug effects are
unpleasant and frightening. Lasts 8-12 h.
(3) Bang - To inject drugs.
(4) Bean - Capsules for drugs.
(5) Bombed out - Very much intoxicated by drugs.
(6) Burned out - poor psychological functioning in someone who has taken drugs
for too long.
(7) Busted – to be arrested.
(8) Buzz, flash, rush - euphoric reaction to a drug.
(9) Connect - To purchase drugs.
(10) Crash - the end of a drug experience.
(11) Cutting – adulterating a drug with additives.
(12) Flip – to go psychotic.
(13) Flying - Under the influence of drugs.
(14) Guide – A person who “babysits” for the drug user during a drug session.
(15) Hard drug, soft drug, gateway drug – These are arbitrary terms, with no
clear criteria or scientific basis. Hard drugs are drugs that lead to severe
physical addiction. They are generally injectable [heroin, methamphetamine].
Soft drugs do not cause physical addiction [cannabis, mescaline, psilocybin
and LSD]. Gateway drug is a “midway drug” that opens the door to the use
of other, harder drugs. Cannabis is sometimes considered a gateway drug.
(16) Hook up, connect, score - make a drug purchase.
(17) Jones; jonesing - experiencing drug withdrawal.
(18) Junkie - heroin addict.
(19) k-hole - under the influence of ketamine, unable to move.
(20) Line - a measured amount of cocaine.
(21) Needle freak - A person who prefers to take drugs with a needle.
(22) Pot – Marijuana.
(23) Roached - under the influence of Rohypnol (roofies).
(24) Rolling - under the influence of MDMA (Ecstasy).
(25) Shooting – IV injection.
(26) Speed freak - Person who repeatedly takes Amphetamines, usually
intravenously.
(27) Spaced out - Under the influence of drugs.
(28) Spunion - someone under the influence of MDMA or other club drugs.
(29) Stoned – intoxicated.
(30) Taste - A small sample of drugs.
(31) Tripping - hallucinating, usually associated with LSD or psilocybin.
(32) Tweeking - prolonged drug use, usually meth.
(33) Works, rig - equipment for injecting drugs.
(34) Zombi - Heavy user of drugs.
(35) Zonked - Extremely high on drugs.

VII. ML ASPECTS OF DRUG ABUSE [GENERAL]

For MLI of individual drugs, please see under relevant sections.

(1) Contaminated currency - Paper money in almost all parts of the world
shows drug contamination
(i) Causes - (a) handling during drug deals (b) use of rolled up notes for snorting
drugs (c) Cross-infection - After the initial contamination, the drug is
“infected to” other notes in close contact, often stacked together. Money-
counting machines are infected which further infect clean notes.
(ii) Smaller notes are more likely to be contaminated because of more frequent
use
(iii) May even serve as vectors of disease if associated infective agents are
 present.
(2) Death – is more often the result of combinations rather than the abuse and
overdose of a single agent.
(3) Driving under influence of drugs - Drowsiness and accidents may be
caused by amphetamine, antihistamines, benzodiazepines, cannabis products,
cocaine, hypotensive drugs, opiates and opioids [morphine and congeners],
sedating antidepressants and tranquillizers. Sedating antidepressants [eg
amitriptyline, imipramine, doxepin, and mianserin] impair driving equally as
blood alcohol conc of ≥80mg%. Driving under influence of drugs is prohibited
by S.185(b) of Motor Vehicles Act, 1988 [MVA, 1988]. Punishment same as
that for alcohol [ch 40].
(4) Children of mothers who used drugs of abuse during pregnancy have - risk of
SIDS [ch 27].
(5) Can cause several complications, eg needle embolism [please see ch 40 for
details].
(6) Mortality rates –
(i) Among drug abusers are substantially -er than in normal populations.
Unnatural causes far exceed those natural causes.
(ii) Reasons - (a) Diseases (I) cirrhosis (II) HIV (b) Homicide [Attempts to
procure drug, Disinhibition, Paranoia] (c) Overdose [particularly among
opioid users] (d) Suicide - - levels of suicide risk factors [childhood abuse,
effects of acute intoxication, psychopathology, social isolation,
unemployment] (e) Trauma [falls, vehicular accidents].
(7) EDH, SDH etc can be preserved for chemical analysis in late deaths, when
drug has disappeared from peripheral blood [ch 40"MLI of ethyl alcohol].

47. Miscellaneous Poisons

I. FORMALDEHYDE

Formaldehyde (HCHO) is a gas at room temperature. Aqueous solutions of

formaldehyde are referred to as formalin. Saturated solution of formaldehyde
(100% formalin) contains 40% by volume or 37% by mass of formaldehyde (i.e.
if 1000 g of commercial solution of formalin is taken, 370 g of it would be
formaldehyde. It is customary to add a small amount of stabilizer, usually 10%
to 12% methanol; it helps prevent oxidization and polymerization of the
formaldehyde, either of which could result in fire or explosion). (i) For
histopathology work 10% formalin is prepared by mixing 1 part formaldehyde
(100% formalin) with 9 parts water. Since it contains 4 parts by volume of
formaldehyde it is also known as 4% formaldehyde. Thus 4% formaldehyde =
10% formalin.

A. Signs and Symptoms

1. Acute exposure
(a) Dermal Contact: (1) skin hardening (2) cracking (3) bleeding (4) Contact
dermatitis (b) Inhalation: (1) Burning of eyes and lacrimation (2) violent
coughing (3) constriction in chest and palpitation4.asthma like symptoms (c)
Ingestion: (1) Similar to strong corrosive acid. (2) Since methanol is added to
formalin solution, concomitant methanol toxicity is also seen. (3) Extreme
tachycardia – is a prominent feature (4) .body temperature.

2. Chronic exposure
(1) Chronic obstructive pulmonary disease
(2) Reduction in ventilatory capacity
(3) Optic neuritis.

B. Fatal Dose
60-90 ml4

C. Fatal Period
1-2 days.

D. Management
(1) Stomach wash – with milk, water, 1% ammonium carbonate or 0.1%
solution of ammonia. The latter reacts with formalin to form harmless
Hexamine. (2) Activated charcoal (3) Mild saline catharsis (4) Keep the patient
warm (5) Watch for GIT hemorrhage.

E. PM Appearances
(1) Smell – of formaldehyde on opening the body
(2) Mucosa of stomach – Hard and tough like leather. Red, inflamed and eroded
(3) Internal organs – congested
(4) Liver – Fatty degeneration.

F. ML Importance
(1) Accidental poisoning - occurs mostly. But suicidal and homicidal poisoning
are also known
(2) Occupational hazards - Formaldehyde is used by embalmers and laboratory
workers. It is a potential occupational carcinogen. Embalmers and funeral
directors exhibit (i) a higher incidence of leukemia and cancers of brain and
colon. (ii) “Embalmer’s eczema”, a persistent skin condition. Embalmers
must use masks and wear gloves during embalming work.
(3) Toxicology - Formalin should never be used as a preservative [ch 5].
(4) Used illegally as a food preservative – Formaldehyde is not allowed as a
food preservative, but it continues to be used so. In 2005 in Indonesia and in
2007 in Vietnam, it was found to be used for preservation of noodles and
other food products. Causing a major scare.

II. NITRITES AND NITRATES

Nitrites (NO2–) and nitrates (NO3–) are naturally occurring inorganic ions that
can cause toxicity.
Salient features:
(1) Microbial action - in soil or water decomposes wastes containing organic
nitrogen into ammonia, which is then oxidized to nitrite and nitrate.
(2) Production - Nitrite is easily oxidized to nitrate"Nitrate is thus
predominantly found in groundwater and surface waters.
(3) Contamination - with nitrogen containing fertilizers (e.g. potassium nitrate
and ammonium nitrate), or animal or human organic wastes, can raise the
 concentration of nitrate in water.
(4) Migration - Nitrate-containing compounds in the soil are generally soluble
and readily migrate with groundwater
(5) Major salts:
(i) Inorganic nitrates - (a) Nitrates may be converted to nitrites in a number of
ways and can cause poisoning [eg by intestinal bacteria, by Bacillus subtilis
spores in dried milk powder] (b) Poisoning with nitrates is easy because it
tastes like and may be mistaken for common salt. (c) Ex - w Bismuth
subnitrate - present in contaminated well water w Potassium nitrate w
Silver nitrate w Sodium nitrate.
(ii) Organic nitrates - (a) ethyl nitrate (b) isosorbide dinitrate (c) mannitol
hexanitrate (d) nitroglycerin
(iii) Inorganic nitrites - Sodium nitrite
(iv) Organic nitrites - Alkyl nitrites
(6) Uses:
(i) Amyl nitrite - used as medicines.
(ii) Alkyl nitrites - drugs of abuse [ch 46]
(iii) Sodium nitrate - as a mordant by weavers.

A. Mechanism of Action
(1) Relaxation of smooth muscles, especially of small blood vessels.
(2) Converts Hb to methHb by oxidizing iron from Fe2+ to Fe3+.
Memory Aid 1: Understanding oxidation at atomic level
LEO - Loss of Electrons is Oxidation

B. Signs and Symptoms

(1) General - cyanosis, syncope, especially when attempting to stand upright
(2) GIT - nausea, vomiting, bloody, colicky diarrhea
(3) CNS: (i) disorientation, (ii) -Intracranial pressure, (iii) paralysis (iv)
throbbing headache (v) vertigo (vi) coma followed by clonic convulsions
(4) Blood - methemoglobinemia
(5) RS - dyspnea
(6) CVS - .BP, palpitations, .pulse
(7) Eye - -Intraocular pressure.
C. Cause of Death
Hypotension or methemoglobinemia. Earlier a non-specific term “circulatory
collapse” was used.

D. Fatal Dose
(1) Barium Nitrate – 15 g.
(2) Nitroglycerine – 200 mg
(3) Potassium Nitrate - 30 g.
(4) Silver Nitrate – 2-10 g
(5) Sodium nitrate – 1-2 g.

E. Fatal Period
Few hours to few days.

F. Management
(1) Emetics
(2) Activated charcoal
(3) Gastric lavage with intubation
(4) Cathartics [ch 32]
(5) For methemoglobinemia - Levels >25% may be dangerous.
(i) Supplemental oxygen
(ii) Methylene blue [MB] - converts MethHb back to Hb. (a) Routes - (I) IV -1%
soln [10 mg/ml] 1-2 mg/kg administered IV slowly over 5 min followed by
IV flush with normal saline. (II) 50mg/kg orally. (b) Mechanism of action -
Normal blood level of MethHb is <1%. Its half-life is 1-3 h. When blood
levels >1%, methemoglobinemia results. Methylene blue is an electron
acceptor. Thus it is an oxidizing agent.
Memory Aid 2: Methylene Blue
MBA - Methylene Blue is Acceptor

In low doses [1-2 mg/kg] it accepts electrons from NADPH and passes them to
MethHb3+, reducing it back to Hb. Interestingly it behaves in diametrically
opposite manners when in higher concentrations. At ≥ 5 mg/kg, it starts
accepting electrons from Hb itself producing methemoglobinemia.
(iii) Exchange transfusion - Indications (a) infants (b) patients who do not
respond within ½-1 h (c) MethHb ≥ 70%.

Appendix 1: Medicolegally Important

Sections and Acts
Note
1. Q indicates a potential question [theory, viva, MCQ]. They have also been
rendered in bold type. Other sections may be remembered for extra credit.
2. This appendix is meant to help the student quickly revise important
sections. For details, chapter number mentioned must be referred to.
3. Abbreviations
SI- Simple Imprisonment [no work allotted to prisoner]
RI - Rigorous Imprisonment [work allotted to prisoner]
4. Chapter numbers in blue refer to chapters of IPC, CrPC and IEA [Also
mentioned as a whole word “Chapter”]; chapter numbers in black refer to
chapters within this book [mentioned as an abbreviated word “ch”]. Exact
page within the chapter can be seen from the index.

I. IPC
Chapter II: General Explanations [S 6-52A]
1. S.31. – Definition of a will - ch 28
2. S.34. - Acts done by several persons in furtherance of common intention —
each person is liable equally - ch 28
3. S.40 - Definition of offence – ch 1.
4. S.44Q. Definition of Injury - ch 11.
5. S.46. Definition of Death – ch 8.
6. S.51. Oath - The word “oath” includes a solemn affirmation substituted by law
for an oath, and any declaration required or authorized by law to be made
before a public servant or to be used for the purpose of proof, whether in a
Court of Justice or not - ch 1.
7. S.52. Good faith — Nothing is said to be done or believed in “good faith”
 which is done or believed without due care and attention – ch 2.

Chapter IV: General Exceptions [S 76-106]

8. S.80. Accident in doing a lawful act — Nothing is an offence which is done
by accident or misfortune, and without any criminal intention or knowledge in
the doing of a lawful act in the lawful manner by a lawful means and with
proper care and caution – ch 1.
9. S.81. Act likely to cause harm, but done without criminal intent, and to
prevent other harm — Nothing is an offence merely by reason of its being
done with the knowledge that it is likely to cause harm, if it be done without
any criminal intention to cause harm, and good faith for the purpose of
preventing or avoiding other harm to person or property – ch 1.
10. S.82Q. Age of criminal responsibility in India is 7 y - ch 3.
11. S.83Q. Act of child between 7-12 y of immature understanding — not an
offence - ch 3.
12. S.84Q. Criminal responsibility of mentally ill. Indian equivalent of British
McNaugthen rule - ch 28.
13. S.85Q. Person intoxicated against his will - not responsible for his criminal
actions - ch 31.
14. S.86. Person intoxicated voluntarily - Knowledge of act is presumed;
intention to do the act is to be proven by prosecution - ch 31.
15. S.87. To participate in a risky activity, the consenting person must be >18 y.
Not meant for doctors - ch 2.
16. S.88Q. Act done is in good faith for the benefit of the person [as in case of
doctor treating patient] the consenting person must be >12 y. Meant for
doctors - ch 2.
17. S.89Q . Consent on behalf of minors - ch 2.
18. S.90Q. Conditions of a valid consent - ch 2.
19. S.92Q. Consent not required to save the life of person - ch 2.

Chapter X - Of Contempts Of The Lawful Authority Of Public Servants [s

172-190]
20. S.172. Absconding to avoid service of summons or other proceeding — ch 1.
21. S.174. Non-attendance in obedience to an order from public servant -
 Applies also to non-attendance in court after service of summons — ch 1.
Not to be confused with S.174 CrPC.
22. S.176. Omission to give notice or information to public servant by person
legally bound to give it — ch 31.
23. S.178. Refusing oath or affirmation when duly required by public servant to
make it — ch 1.

Chapter XI: Of False Evidence And Offences Against Public Justice [S.191-
229A]
24. S.191Q. Definition of perjury [Giving false evidence] — ch 1.
25. S.193Q. Punishment for perjury — ch 1.
26. S.197. Issuing false certificate — ch 1.
27. S.198. Using false certificate — ch 1.
28. S.201Q. Causing disappearance of evidence of offence — ch 31.
29. S.202. Intentional omission to give information of offence by person bound
to inform — ch 31.
30. S.228A. Identity of victim of rape cannot be disclosed - ch 25.

Chapter XIV: Of Offences Affecting The Public Health, Safety,

Convenience, Decency And Morals [S268-294A]
31. S.268. Public nuisance - Exhibitionism, transvestism, fetishism, masturbation
in public - ch 25.
32. S.269. Negligent act likely to spread infection of disease dangerous to life,
eg HIV - ch 2, 25. [Mnemonic - 69 is a sexual position]
33. S.270. Malignant act likely to spread infection of disease dangerous to life -
ch 2, 25.
[Both 269 and 270 are applicable in ML aspects of HIV and AIDS. Also sale
of adulterated food]
34. S.272. Adulteration of food or drink — ch 31.
35. S.273. Sale of noxious food or drink — ch 31.
36. S.274. Adulteration of drugs — ch 31.
37. S.275. Sale of adulterated drugs — ch 31.
38. S.276. Sale of drug as a different drug or preparation — ch 31.
39. S.279. Rash driving or riding on a public way so as to endanger human life
"6 months or 1000 Rs fine or both.
40. S.284Q. Negligent conduct with respect to poisonous substance — ch 31.
41. S.285. Negligent conduct with respect to fire or combustible matter — ch 14.
42. S.287. Negligent conduct with respect to machinery — ch 11.
43. S.290. Punishment for public nuisance in cases not otherwise provided for,
eg transvestism — ch 25.
44. S.294. Obscene acts and songs, eg Exhibitionism, masturbation in public —
ch 25.

Chapter XV: Of Offences Relating to Religion [S.295-298]

45. S.297. Trespassing on burial places, etc, eg necrophilia — ch 25.

Chapter XVI: Of Offences Affecting The Human Body [S.299-377]

46. S.299Q. Definition of culpable homicide - ch 11.
47. S.300Q. Definition of murder - ch 11.
48. S.301. Culpable homicide by causing death of person other than person
whose death was intended - ch 11.
49. S.302Q. Punishment for murder - ch 11.
50. S.303 - Punishment for murder by life-convict - ch 11.
51. S.304Q. Punishment for culpable homicide - ch 11.
52. S.304AQ. Causing death by rash and negligent act [including death by
medical negligence] - ch 11.
53. S.304BQ. Dowry death - ch 11.
54. S.305. Abetment of suicide of child or insane person - ch 11.
55. S.306. Abetment of suicide - ch 11.
56. S.307. Attempt to murder - ch 11.
57. S.308. Attempt to commit culpable homicide - ch 11.
58. S.309Q. Attempt to commit suicide - ch 11.
59. S.312. Causing miscarriage - ch 26.
60. S.313. Causing miscarriage without woman’s consent - ch 26.
61. S.314. Death caused by act done with intent to cause massacring - ch 26.
62. S.315. Act done with intent to prevent child being born alive or to cause it to
die after birth - ch 26.
63. S.316. Causing death of quick unborn child by act amounting to culpable
homicide - ch 26.
64. S.317. Exposure and abandonment of child <12 y, by parent or person having
care of it - ch 3.
65. S.318. Concealment of birth by secret disposal of dead body - ch 27.
66. S.319Q. Definition of Hurt - ch 11.
67. S.320Q. Definition of Grievous Hurt - ch 11.
68. S.321. Voluntarily causing hurt - ch 11.
69. S.322. Voluntarily causing grievous hurt - ch 11.
70. S.323Q. Punishment for voluntarily causing hurt - ch 11.
71. S.324Q. Punishment for voluntarily causing hurt by dangerous weapons
or means - ch 11.
72. S.325Q. Punishment for voluntarily causing grievous hurt - ch 11.
73. S.326Q. Punishment for voluntarily causing grievous hurt by dangerous
weapons or means - ch 11.
74. S.326AQ. Voluntarily causing grievous hurt by use of acid – Definition
and punishment - ch 11.
75. S.326BQ. Voluntarily throwing or attempting to throw acid – Definition
and punishment - ch 11.
76. S.328. Causing hurt by means of poison, with intent to commit an offence, eg
Drug Facilitated Sexual Assault - ch 31.
77. S.336. Punishment for negligent act when no injury to the patient occurs - ch
2.
78. S.337. Punishment for negligent act when hurt is caused to patient - ch 2.
79. S.338. Punishment for negligent act when grievous hurt is caused to patient -
ch 2.
80. S.339. Wrongful restraint - ch 11.
81. S.340. Wrongful confinement - ch 11.
82. S.341. Punishment for wrongful restraint - ch 11.
83. S.342. Punishment for wrongful confinement - ch 11.
84. S.350. Intentionally using force on any person - ch 2.
85. S.351Q. Assault - ch 2.
86. S.352. Punishment for Assault or Criminal force -
ch 11.
87. S.354Q. Assault or criminal force to woman with intent to outrage her
modesty - 1-5y +fine
88. S.354A. Sexual harassment - ch 25.
89. S.354B. Assault or criminal force to woman with intent to disrobe or
compelling her to be naked- ch 11.
90. S.354C. Voyeurism – ch 25
91. S.354D. Stalking – ch 25
92. S.361. Kidnapping from lawful guardianship - ch 3.
93. S.362. Abduction - ch 3.
94. S.363Q. Punishment for kidnapping - ch 3.
95. S.363A. Kidnapping or maiming a minor for purposes of begging - ch 3.
96. S.364. Kidnapping or abducting for murder - ch 3.
97. S.364A. Kidnapping or abducting for ransom - ch 3.
98. S.365. Kidnapping or abducting to secretly and wrongfully confine - ch 3
99. S.366. Kidnapping or abducting woman to compel marriage or illicit
intercourse - ch 3
100. S.366A. Procuring of girl <18 y for illicit intercourse - ch 3
101. S.366B. Importation of girl <21 y from J&K or from foreign country for
illicit intercourse - ch 3
102. S.367. Kidnapping or abducting for causing grievous hurt, slavery or
unnatural sexual act - ch 3
103. S.368. Wrongfully concealing or keeping in confinement, kidnapped or
abducted person - ch 3
104. S 369. Kidnapping or abducting child <10 y with intent to steal from its
person - ch 3
Memory Aid 1: S.363, 366 and 369: Most imp sections related to kidnapping
363, 366 and 369 are in arithmetic progression with a difference of 3. Furthermore 363 has 2 sub-laws, 366
has 3 and 369 has 1. [First write 1"2"3. Then transpose 1 to the end to get 2"3"1]

105. S.372. Selling minor for purposes of prostitution, etc. - ch 3

106. S.373. Buying minor for purposes of prostitution, etc. - ch 3
107. S.375Q. Definition of Rape - ch 25
108. S.376Q. Punishment for Rape - ch 25
109. S.377Q. Unnatural offences - ch 25

Chapter XX: Of Offences Relating To Marriage [S493-8]

110. S. 494. Marrying again during lifetime of husband or wife - ch 23
111. S. 495. Same offence with concealment of former marriage from person
with whom subsequent marriage is contracted - ch 23
Memory Aid 2: S.497, IPC
Sum of all digits in 497 is 20 [a round figure]. Also comes immediately before 498A, another vital section
in relation to women]

Chapter XXA: Of Cruelty By Husband Or Relatives Of Husband [S.498A –

only one section]
112. S. 498AQ. Punishment to husband or relative of husband of a woman
subjecting her to cruelty - ch 23.

Chapter XXI - Of Defamation [S.499-502]

113. S. 499Q. Defamation. Breaking of professional secrecy - ch 2.
114. S. 500Q. Punishment for defamation - ch 2.

Chapter XXII: Of Criminal Intimidation, Insult And Annoyance [S.503-510] -

CIIA
115. S. 509. Word, gesture or act intended to insult the modesty of a woman -
Similar to s354 - ch 25.
116. S. 510. Misconduct in public by a drunken person - ch 40.

Chapter XXIII: Of Attempts To Commit Offences [S.511 – only one section]

117. S. 511. Punishment for attempting to commit offences punishable with
imprisonment for life or other imprisonment - ch 26.

II. CRPC

Chapter I: Preliminary [S.1-5]

1. S.2(c) – Definition of cognizable offence – ch 1.
2. S.2(l) – Definition of non-cognizable offence – ch 1.
3. S.2(u) Public prosecutor [PP]– ch 1.

Chapter II: Constitution of criminal courts and offences [S.6-25A]

4. S.8. Definition of metropolitan areas – ch 1.
5. S.9. Court of Session – ch 1.
Chapter III: Powers of courts [S.26-35]
6. S.26a. Rape cases to be tried by a Court presided over by a woman – ch 25.
7. S.28. Sentences which High Courts and Sessions Judges may pass – ch 1.
8. S.29. Sentences which Magistrates may pass – ch 1.

Chapter IV-B: Aids to the Magistrates and the Police [S.37-40]

9. S.39Q. Public to give information of certain offences – ch 31.

Chapter V: Arrest of Persons [S.41-60]

10. S.53Q. Examination of accused by medical practitioner at the request of
police officer – ch 11.
11. S.53AQ. Examination of person accused of rape by medical practitioner –
ch 25.
12. S.54Q. Examination of arrested person by medical officer – ch 2.

Chapter VI: Process to compel appearance [S.61-90]

Chapter VII: Process to compel the production of things [S.91-105]

13. S.91. Summons to produce document or other thing (Subpoena duces tecum)
– ch 1.

Chapter IX: Order For Maintenance Of Wives, Children And Parents [S125-
128]
14. S.125. Order for maintenance of wives, children and parents. This section is
important for paternity disputes, illegitimacy, affiliation cases etc – ch 24.

Chapter XII: Information To The Police And Their Powers To Investigate

[S.154-176]
15. S.154. Information in Cognizable cases – ch 1.
16. S.155. Information in non-cognizable cases – ch 1.
17. S.157(1)(b) - Investigation in relation to an offence of rape – ch 25.
18. S.164(5A) - Judicial magistrate to record the statement of victim of rape and
some other sexual offences – ch 25.
19. S.164AQ. Medical Examination of the victim of rape ch 25.
Memory Aid 3: S.164A, CrPC
Corresponding section for accused is (S.53) Add 111 164A
20. S.173(1A). Investigation in relation to rape of a child – ch 25.
21. S.174Q. Police inquest - ch 1.
22. S.175. Power of police to summon persons - ch 1.
23. S.176Q. Magistrate inquest- ch 1.

Chapter XIV: Conditions requisite for initiation of proceedings [S.190-199]

24. S.198(6). Cognizance of marital rape not to be taken by court if wife is <18 y
and >1 y has elapsed from the date of commission of offence – ch 25.

Chapter XXIII: Evidence in Inquiries and Trials [S.272-299]

25. S.273 - Victim of rape or other sexual offences if <18 y, not to be confronted
with the accused – ch 25
26. S.291 - Evidence of a doctor recorded in court can be used in other trials –
ch 1.
27. S.292 - Written reports of mint officers etc accepted as such – ch 1.
28. S.293 - Reports of certain Government scientific experts admissible without
oral evidence – ch 1.

Chapter XXIV: General provisions as to enquiries and trials [S.300-327]

29. S.300. Person once convicted or acquitted not to be tried for same offence
[Res judicata] – ch 2.
30. S.309(1). In some cases of rape, inquiry or trial shall be completed within 2
months – ch 25.
31. S.327(2). The enquiry into and trial of rape shall be conducted in camera –
ch 25.
32. S.327(3). Proceedings of trial of rape not to be published without previous
permission of court – ch 25.

Chapter XXVII - The Judgment [S.353-365]

33. S.357B - Additional compensation by state to be given over and above the
fine paid by convicted person in cases of gang rape and vitriolage – ch 25.
34. S.357C - All hospitals, whether Govt or private to provide immediate first-
aid or medical treatment free of cost to any victim of rape and vitriolage – ch
 25.

Chapter XXVIII: Submission of Death Sentences for confirmation [S.366-371]

35. S.366(1) CrPC. Sentence of death passed by Sessions court must be
submitted to High Court for confirmation – ch 1.

Chapter XXXII: Execution, Suspension, Remission And Commutation Of

Sentences [Memory Aid Ea Sy Ra Ce] [S.413-435]
36. S.416. Commutation of capital sentence on pregnant woman – ch 24.
37. S.433(b) . Power to commute sentence — Appropriate Govt may commute
life imprisonment to 14 y. Ch 1. Pl also see S.55, IPC.

III. IEA [INDIAN EVIDENCE ACT]

Chapter II – Of the relevancy of facts [s5-55]

1. S.6. Res gestae – ch 1.
2. S.32(1)Q. Dying declaration – ch 1.
3. S.35 – Public records made in performance of official duties are acceptable in
court of law – ch 1.
4. S.45Q. Expert witness – ch 1.
Memory Aid 4: Two important sections are consecutive numbers
S.44, IPC - Injury
S.45, IEA - Expert Witness

Chapter IV – Of oral evidence [S.59-60]

5. S.60. Author of a book not to be called in a court as witness – ch 1.

Chapter V: Of Documentary Evidence [S.61-90A]

6. S.62. Primary evidence – ch 1.
7. S.63. Secondary evidence – ch 1.
8. S.74. Definition of public documents – These are the documents forming the
acts or records of the acts (i) of the sovereign authority (ii) of official bodies
and tribunals, and (iii) of public officers, legislative, judicial and executive of
any part of India or of the Commonwealth, or of a foreign country - ch 1.
9. S.76. Certified copies of public documents – Must be given by public officers
 having custody of such documents – ch 1.
10. S.78. How certain public documents can be proved in a court of law.

Chapter VII - Burden of proof [S.101-114A]

11. S.105 - Burden of proving that case of accused comes within general
exceptions of Ch IV of IPC – ch 28.
12. S.107Q. Presumption of life – ch 9.
13. S.108Q. Presumption of death – ch 9.
14. S.112. Period of Legitimacy of child – ch 24.
15. S.113A. Presumption as to abetment of suicide by a married woman – ch 11.
16. S.113B. Presumption as to dowry death – ch 11.
17. S.114AQ. Presumption of absence of consent in certain cases of rape – ch
25.

Chapter IX – Of witnesses [S.118-134]

18. S.118. Who may testify – ch 1.
19. S.119. Dumb witnesses – ch 1.

Chapter X: Of The Examination Of Witnesses [S135-166]

20. S.137. Examination in chief – ch 1.
21. S.138. Order of examinations – ch 1.
22. S.141. Leading questions – ch 1.
23. S.142. When LQs can not be asked – ch 1.
24. S.143. When LQs may be asked – ch 1.
25. S.154. Leading questions by party to his own witness – ch 1.
26. S.157. Victim survives after making a dying declaration – witness must give
oral evidence. D/dec used only or corroboration – ch 1.
27. S.159. Refreshing memory by witness during examination is allowed – ch 1.
28. S.160. Testimony from documents prepared by witness – ch 1.
29. S.161. Right of the adverse party as to writing used by witness to refresh
memory – ch 1.

IV. MEDICOLEGALLY IMPORTANT ACTS AND RULES

1. Biomedical waste (Management and Handling) Rules 1998.
2. Consumer Protection Act 1986 – Ch 2.
3. Cantonments Act, 2006– Ch 2.
4. Children Act 1960 – Provides for the care, protection, maintenance, welfare,
training, education and rehabilitation of neglected or delinquent children and
for the trial of delinquent children in the Union territories.
5. Clinical Establishments Act 2010 - ch 2
6. Drugs and Cosmetics Act 1940 – ch 31
7. Dentists Act 1948 - ch 2
8. Dock Workers (safety, health and welfare) Act 1986
9. Drugs and Magic Remedies (Objectionable advertisement) Act 1954
10. Drug Control Act 1950
11. Epidemic Diseases Act 1897
12. Employees’ State Insurance Act 1948
13. Environment Protection Act 1986
14. Factories Act 1948
15. Fatal Accidents Act 1855
16. Homeopathy Central Council Act 1973 - ch 2
17. Information Technology Act 2000 – ch 25 [Shakti Mills Gang rape case]
18. Insecticides Act 1968
19. Indian Majority Act 1875
20. Indian Medicine Central Council Act, 1970 - ch 2
21. Indian Medical Council Act, 1956 - ch 2
22. Indian Medical Degrees Act 1916 - ch 2
23. Leprosy Act 1898
24. Indian Medical Degrees Act 1916
25. Indian Medical Council Act 1956
Indian Nursing Council Act - ch 2
26. Maternity Benefit Act 1961
27. Mental Health Act 1987- ch 28
28. Minimum Wages Act 1948
29. Medical Council of India Regulations - ch 2
30. Medical Termination of Pregnancy Act 1971
31. Mines Act 1952
32. Motor Vehicles Act 1988
33. Personal Injuries (Emergency Provisions) Act 1962
34. Personal Injuries (Compensation, Insurance) Act 1963
35. Pharmacy Act 1948 - ch 2
36. Poisons Act 1919
37. Preconception and prenatal Diagnostic Techniques (Regulations and
Prevention of misuse) Act 1994
38. Protection of Human Rights Act 1993
39. Registration of Births and Death Act 1969
40. Transplantation of Human Organs Act 1994
41. Vaccination Act 1880
42. Workmen’s Compensation Act 1923

Appendix 2: Important Values

Regarding Fatal Doses etc
Q in superscript denotes a possible theory or viva question.

I. COMMON NAMES AND ACTIVE PRINCIPLES OF

POISONOUS PLANTS
1 Only the most well known common names are given here. For an exhaustive list of ALL common names,
please refer to the concerned chapter.
2 Only the most common active principles are given here. For an exhaustive list of ALL active principles,
please refer to the concerned chapter.

II. FATAL DOSE, FATAL PERIODS AND ANTIDOTES IN A

NUTSHELL
Appendix 3: Weights and Measurements
of Organs
Appendix 4: Common Mistakes in Some
Books
Enumerated below are common mistakes given in some books. For proper explanation
of why the information is incorrect, pl refer to chapter number mentioned.