NATIONAL BOARD OF EXAMINATIONS NEW DELHI

THESIS PROTOCOL

Name of the candidate: Dr. Kishor Kumar

Subject: Neurosurgery

Date of joining :8thFeb 2010

Hospital/Institute : Apollo hospital, Jubilee hills,Hyderabad

Guide :Dr.Rahul Lath Mch. DNB(Neurosurgery), Apollo Hospital

Title of the thesis :Predictors of sepsis in severe head injury A prospective study

1.1 INTRODUCTION Head injuries are leading cause of death in young .Of the patients who succumb, 50% of patient with severe head injury die immediately 1,30% with in the first few days2 and 20% much later,mainly as a result of sepsis.While prognostication of acute severe head injury can be done using the Glasgow coma score3, there are hardly any studies that predict the development of sepsis in head injury.This pilot aims to identi fy factors that cause sepsis in a head injured patient. . 1.2 REVIEW OF LITERATURE Sepsis leading to multi organ dysfunction is the major cause of death in survivors following severe traumatic brain injury 4. Non neurological organ dysfuction independent of severity of neurological injury was reported by Zygun et al and he concluded that these are are independently assiociated with poor outcome5.In astudy by E G Mckeating et al 6 ,they found that there are increased levels of pre inflammatory substances in blood with in the first 48 hours following trauma.They also found that prolonged elevation of these pro inflammatory agents (especially IL-6) increased the risk of systemic inflammatory response syndrome(SIRS) and adult respiratory distress syndrome(ARDS).Development of multi organ dysfunction was found in the absence of usual etiologic agent like infection or systemic injury in the setting of traumatic brain injury as reported by David Zygun5. Apart from this various other factors also contribute to development of sepsis multi organ dysfunction following traumatic brain injury.Significantly modifiable factors that were studied are hypoxia,hypercapnia,hypotension hypovolumia and coagulopathy 7,8,9,10.Though hypoxia,hyprcapnia,hypotension and hypovolaemia can all be caused by sepsis, sepsis perse has not been studied in patient with severe head injury.

1.3 AIMS AND OBJECTIVES OF STUDY

y To study the out come of patients severe head injury with sepsis.

1.4 Materials and Methods

y Hospital admitted patients above 18 yrs diagnosed with severe head injury on the basis of GCS(<8) 3. y Sepsis is a systemic inflammatory response to a bacterial infection and is common complication during the course of treatment of patients with multiple trauma and major surgery.in severe sepsis, the inflammatory response leads to multiple organ failure that can result in death. Multiple organ dysfunction in sepsis is now considered the most common cause of death in non-coronary critical care units. In fact, sepsis is one of the top 10 or 12 causes of death in the general population 4 y Sepsis is a significant complication in any patient and is a particular problem in the ICU due to the illness of the patient population and the invasive nature of many treatments and monitoring devices. In a study by j piek et al11,elimination of sepsis would shift an estimated 1.5% of all patients from an unfavorable to a favorable outcome category. Due to its multifactorial nature and many venues of origin, sepsis is particularly difficult to prevent 12. y Fundamental techniques for prevention include screening studies such as surveillance pulmonary' cultures, careful attention to invasive monitors and vascular access lines for early evidence of local infection, and possibly, systemic nutritional support in order to increase the patient's immunological competency. y When prevention is unsuccessful, management of sepsis requires rapid diagnosis and treatment. It is important to keep m mind that some of the more occult sources for bacteremia, such as sinusitis, can easily be overlooked in the head-injured patient13. Early diagnosis may be particularly difficult in the patient treated with high-dose barbiturates

for intracranial hypertension.The mild hypothermia and systemic anergy often seen in these patients makes it more critical to recognize the secondary indicators of sepsis, such as progressive thrombocytopenia, hyperglycemia, and unexplained cardiovascular hyperdynamism with low sequential vascular response and a falling arteriovenous oxygen content difference14. Unfortunately, the first recognized sign of sepsis in such patients is often septic shock. This adds the morbidity of hypotension to the patient's complication profile, further increasing the detrimental effects of sepsis.

SAMPLE SIZE :
. 400

Patients of severe head injury .

METHODS:

We performed a prospective cohort study at Apollo healthy city centre, the tertiary care trauma center servicing south India. All patients above 18 years of age and older with severe traumatic brain injury (sTBI) and intensive care unit length of stay > 48 hours between Feb 1, 2009 and April 31, 2016 were included. Non-neurologic organ dysfunction was measured by the SOFA and APACHEII scoring systems. This study demonstrates that the prevention or effective early treatment of sepsis would have a salutary role in improving the outco me from head injury. This area of study represents fertile ground for innovative strategies to improve the overalloutcome of severe head injury.

INCLUSION CRITERIA

1.All patients above 18 years of age with severe head injury are included in the study

EXCLUSION CRITERA

1.Patients below 18 years of age and above 80 years of age. 2.patients with quadriplegia due to spinal cord injury after trauma.

COMPOSITION OF CLINICAL ETHICS COMMITTEE :

1) Dr. SudhirNaik, MD, DM 2)Dr.V K Bhargava, MD

Sr. Consultant Cardiologist, Chairman of Ethics committee Sr.Consultant Physician.

3)Dr. MeenaTrehan, MD 4)Dr. N RaghupathiRao, MS

Paed.CardiacAnesthetist. Sr.Consultant Surgeon.

APPROVAL OF CHAIRMAN OF CLINICAL ETHICS COMMITTEE .

Dr. SudhirNaik, MD, DM Sr. Consultant cardiologist Chairman of Ethics Committee

5. LIST OF REFERENCES

1. Greenwald BD, Burnett DM, Miller MA (March 2003). "Congenital and acquired brain injury. 1. Brain injury: epidemiology and pathophysiology". Archives of Physical Medicine and Rehabilitation 84 (3 Suppl 1): S3 7. doi:10.1053/apmr.2003.50052 . PMID 12708551. 2.Park E, Bell JD, Baker AJ (April 2008). "Traumatic brain injury: Can the consequences be stopped?". Canadian Medical Association Journal 178 (9): 1163 70. doi:10.1503/cmaj.080282. PMC 2292762. PMID 18427091. 3. TeasdaleG, Jennett B: Assessment of coma and impaired consciousness. A practical scale. Lancet 2:81-84, 1974. 4. The Effect of Recombinant Human Erythropoietin (rHuEPO) on Microcircualtory Alteration in Intensive Care Unit Patients With Severe Sepsis and Septic Shock 5.David Zygun,LV Cberthiaume,Kevin laupland John Kotbeek and Christopha Doig SOFA is superior score forthe determination of non neurologicalorgandysfunction in patient of severe traumatic brain injury.Critical care 2006 10:r115doi:1186/cc5007. 6.E G Mckeating and PJD Andrews cytokinens and adhesion molecule in acute brain injury .British Journal of anaesthesia 1998:80 77 -84. 7.Mikhail J:The trauma traid of death:Hypothermia,acidosis and coagulopathy.AACNClin issues 1999:10:85-94. 8.ClaridgeJA,CrebtreeTD,Pelletet SJ et al:Persistent occult hypoperfusion is associated with a significant increase in infection rate and mortality in major trauma patient.J.trauma 2000:48:8 -14. 9.SegerMJ.DiephuisJC,VanKesternRG,etal :Hypothermia in trauma patient,infallchirurg 1998:101:742 -749. 10.JeremitskyE,OmertL,DunhamM,etal,Herbingeres of poor oucome the day after severe brain injury:Hypothermia.hypoxia,hypoperffusion.J.Trauma 2003:54 312 -319. 11. J Neurosurg 77:901-907, 1992 Extracranial complications of severe head injury Jurgen Piek, M.D., Randai.L M. Chesnut, M.D., Lawrence F. Marshall, M.D., Mar jan Van Berkum-Clark, R.N., Melville R. Klauber, PH.D., Barbara A. Blunt', M.P.H., Howard M. Eisenberg, M.D., John A. Jane, M.D.,Anthony Marmarou, PH.D., and Mary a. Foulkes, PH.D

12. 25. Hosmer DW, Lemeshow S: Applied Logistic Regression.New York: John Wiley & Sons, 1989 13. Chesnut RM, Marshall LF, Bowers -Marshall S: Medical management of elevated intracranial pressure, in Cooper PR (ed): Head Injury, ed 3. Baltimore: Williams & Wilkins, 1992, pp 225-246 14. Jennett B, Bond M: Assessment of outcome after severe brain damage. A practical scale. Lancet 1:480-484, 1975
COMPOSITION OF SCIENTIFIC (THESIS) COMMITTEE :

1) Dr. SantoshRamakrishnan,

Consultant Endocrinologist. MD,DM Chairman of Thesis Committee.

2) Dr. Suneetha Reddy, MD

Sr. Consultant, Infectious Diseases.

3) Dr.Obul Reddy

Principal, Apollo Institute of Hospital Administration.

4) Dr. T.Srinivas Reddy

Group Director of Medical Education, Apollo Hospitals.

5) Dr. Swarnalatha, MD

HOD of Histopathology.

6) Dr. Suhasini, MD

HOD of Biochemistry.

APPROVAL OF CHAIRMAN OF THESIS COMMITTEE.

Dr. Santosh Ramakrishnan, MD, DM. Consultant Endocrinologist. Chairman of Thesis Committee.

NAME OF THE CANDIDATE

Dr Kishorkumar

SIGNATURE OF THE CANDIDATE :

NAME OF THE GUIDE

: Dr. Rahul Lath Consultant Neurosurgeon, Apollo Health City, Hyderabad.

SIGNATURE:

HEAD OF THE DEPARTMENT

: Dr. AlokRanjan Sr.Consultant and HOD Department of Neurosurgery. Apollo Health City, Hyderabad.

SIGNATURE:

HEAD OF THE INSTITUTION

: Dr. T. Srinivas Reddy, Director of Medical Education, Apollo Health City, Hyderabad.

SIGNATURE:

1.8 APPROVAL OF SCIENTIFIC COMMITTEE AND ITS COMPOSITION

(SIGNATURE OF CANDIDATE) (SIGNATURE OF GUIDE) (HEAD OF DEPARTMENT)

STUDY PROFORMA
A PROSPECTIVE COHORT STUDY OF THE PREDICTORS OF SEPSIS IN SEVERE HEAD INJURY.

PATIENT DETAILS:
Name: Tel: Age: Sex: Address: Occuption:

HOSPITAL DETAILS:
Date of addmission: Ip no. Date of dicharge:

PRESENTATION FEATURES:
GCS at presentation: MAP at presentation : Spo2 at presentation : CT SCAN FINDINGS: HTN/DM/CAD/Immunisuppresent: SURGERY- Yes/No. APACHEII at 24 hrs Maximum: SOFA Score: OTHER INJURIES: Procalcitonin Maximum: Sepsis/Septis shock/Sepsis with MODS; Which organs are effected: Vasopressors: Dialysis: Max creatinine:

INTENSIVE CARE UNIT DETAILS

OUT COME AT 3 MONTH.