Nandhini

EFFECT OF INTRAVENOUS DEXMEDETOMIDINE
ON PROLONGING SPINAL ANESTHESIA, A

RANDOMISED CONTROLLED STUDY
Submitted to
THE TAMILNADU DR.M.G.R

MEDICAL UNIVERSITY
in partial fulfillment of regulations

for award of the degree of
M.D (ANESTHESIOLOGY)
BRANCH – X
ESIC MEDICAL COLLEGE & PGIMSR

K.K.NAGAR ,CHENNAI
THE TAMILNADU DR. M.G.R MEDICAL UNIVERSITY

CHENNAI, TAMILNADU
APRIL 2015
BONAFIDE CERTIFICATE
This is to certify that the dissertation named “EFFECT OF
INTRAVENOUS DEXMEDETOMIDINE ON PROLONGING SPINAL
ANESTHESIA, A RANDOMISED CONTROLLED STUDY” is a bonafide
work performed by Dr.T.S.Nandhini, post graduate student, Department of
Anaesthesiology, ESIC Medical College & PGIMSR, Chennai-78, under my
guidance and supervision in fulfillment of regulations of The Tamilnadu Dr.
M.G.R Medical University for the award of M.D. Degree during the academic year
2012-2015.
GUIDE: CO-GUIDE:
Dr. K.Radhika, M.D., Prof. Dr. Kamalini Sridharan

Associate Professor, M.D., D.A,
Department of Anaesthesiology, Professor and Head,
ESIC Medical College & PGIMSR Department of Anaesthesiology,
Chennai -78 ESIC Medical College & PGIMSR
Chennai -78
ENDORSEMENT BY THE DEAN/
THE HEAD OF THE INSTITUTION
This is to certify that this dissertation titled “EFFECT OF
ANESTHESIA, A RANDOMISED CONTROLLED STUDY” submitted by
Dr.T.S.Nandhini, appearing for M.D Degree Branch – X ANAESTHSIOLOGY
examination in April 2015 is a bonafide record of work done by her under my
direct guidance and supervision in partial fulfillment of the regulations of
Tamilnadu Dr.M.G.R Medical University, Chennai. I forward this to the
Tamilnadu Dr. M.G.R Medical University, Chennai Tamilnadu, India.
DEAN
Dr. SRIKUMARI DAMODARAM,
M.S,M.Ch(SGE), M.A.M.S.,
F.A.C.S., F.I.C.S., F.M.M.C
ESIC Medical College and PGIMSR
K.K.Nagar, Chennai-78
DATE:
PLACE: K.K. Nagar

DECLARATION
I solemnly declare that this dissertation entitled “EFFECT OF
ANESTHESIA, A RANDOMISED CONTROLLED STUDY” has been
conducted by me at ESIC Medical College & PGIMSR, Chennai, under the
guidance and supervision of Prof.Dr.KAMALINI SRIDHARAN, M.D., and
Dr.K.RADHIKA, M.D., Department of Anesthesiology, ESIC Medical College &
PGIMSR, Chennai. This dissertation is submitted to The Tamil Nadu Dr. M.G.R.
Medical University, Chennai in partial fulfillment of the University regulations
for the award of the degree of M.D. Branch X (Anesthesiology).
Date:
Place:Chennai (Dr.T.S.Nandhini)
ACKNOWLEDGEMENTS
It is my immense pleasure to thank everybody who contributed in

compilation of this study.
I convey my sincere regards to my guide Dr. K.RADHIKA, M.D., for her

scholarly guidance, dynamic interest, clinical acumen and constructive criticism.
Her considerable time and effort enabled me to give this study its final shape.
I acknowledge my heartfelt gratitude to my co-guide

Prof.KAMALINI SRIDHARAN, M.D., D.A., who provided invaluable
suggestions, patience, guidance, inspiration and encouragement to help me
perform better.
I would also like thank Dr.T.K.RENUKA DEVI, M.D.,DGO., HOD of the
Department of obstetrics and gynecology, who had permitted to do the study on
their patients.
I am grateful in every possible way to the Specialists, Medical Officers,
Senior Residents and the postgraduates of the Department of Anesthesiology for
helping me to conduct the study in the theatre.
Many thanks in particular to the statistician Dr.ARUNA PATIL, Ph.D., for
her guidance regarding the sample size and data analysis.

Iam thankful to the institutional ethical committee for their guidance and
approval for the study.
I also thank the theatre personnel for their help. I would like to thank all the
patients for their participation and cooperation.
I am thankful to my parents for their blessings for their unconditional love,
support and time.
Dr. T.S.Nandhini
CONTENTS
Page
Sl.No. Title
No.
1. Introduction 1
2. Aim of the study 6
3. Objectives 7
4. Review of Literature 8
5. Pharmacology of Dexmedetomidine 21
6. Pharmacology of Bupivacaine 44
7. Anatomy of Spinal Anesthesia 52
8 Physiology of Spinal Anesthesia 55
9. Materials & Methods 67
10. Results & Analysis 77
11. Discussion 95
12. Conclusion 104
13. Bibliography
14. Annexure
ABSTRACT
BACKGROUND AND OBJECTIVES
The aim of this study was to evaluate the effect of intravenous dexmedetomidine
on prolongation of spinal anesthesia.
METHODS
Study population comprised of 100 patients scheduled for abdominal/vaginal
hysterectomy under spinal anesthesia. 100 adult patients classified as ASA 1 or 2
were studied. Patients were randomly assigned to one of the two groups
In Group-D patients received hyperbaric intrathecal bupivacaine anesthesia
3.5ml 0.5% (17.5 mg) and intravenous Dexmedetomidine 0.5micro grams/Kg
in10 ml normal saline over 10 minutes after initiation of spinal block.
In Group C patients received hyperbaric bupivacaine anaesthesia 3.5 ml 0.5%
(17.5mg) and intravenous normal saline 10 ml over 10 minutes.
RESULTS
The time for the motor block to become B0 was 243±17.0 minutes in the
study group and in the control group it was 211.2±16.7 minutes The total time
for sensory level to reach S1 was 255±8.6in the study group while it was
210.8±33,1 in the control group. The time for two dermatome regression from the
maximal level was 125.2±17.5minutes in the study group and 94.6±18.9 in the
control group. This proved the significant prolongation of motor block, sensory
block, sensory block to regress from the maximal level in the study group with a p
value of 0.001***.
CONCLUSION
Dexmedetomidine in the dose of 0.5 microgram/kg given as single intravenous
dose to patients who underwent abdominal/vaginal hysterectomy under spinal
anesthesia significantly prolonged the duration of sensory and motor blockade and
also caused arousable sedation.

INTRODUCTION
Spinal anesthesia is a well known technique of regional anesthesia and is
always considered as a safe option to general anesthesia when the surgical site
is located to the lower extremities, perineum or lower abdomen[1]. Spinal
anesthesia produces intense sensory, motor and sympathetic blockade with
significantly lesser concentration of local anesthetics when compared to other
modes of regional anesthesia. Although the operating site is anesthetized and the
patient cannot appreciate pain, he or she remains awake during the whole
procedure which contributes to mental stress ranging from mild to severe
depending on the patient’s mentality.
Spinal anesthesia has many advantages like low cost, reduced risk of
aspiration even in patients who are considered to be full stomach and reduced
blood loss. There is relaxation of abdominal muscles and this facilitates surgical
approach. The main limitation of spinal anesthesia is that it is limited in duration.
The patient’s anxiety adds to the technical difficulties.
Usually spinal anesthesia with hyperbaric bupivacaine lasts for 2 to 2.5
hours.[2]. To extend the duration of spinal anesthesia adjuvants like opiods,
epinephrine and neostigmine are added to local anesthetics and instilled into the
subarachnoid space. These added substances have their own advantages and
disadvantages.
Sedation in adequate dose during neuraxial block alleviates the anxiety of
the patient[3]. When the patient is relaxed ,the surgeon finds it easy to operate[4].
Under sedation ,patients should be able to respond to command and maintain a
patent airway with minimal oxygen supplementation.
Two commonly used drugs for sedation are propofol and midazolam.
Intravenous propofol in the dose of 0.2to 0.3 mg/kg is used for sedation. This
produces a rapid decline in the level of consciousness. With a continuous
infusion of propofol both the cardiovascular and respiratory function are
depressed to a considerable extent. The newer water soluble benzodiazepine,
midazolam given in the dose of 0.03mg/kg has a quick onset of action. But,
recovery is slow.
In day to day practice although we use midazolam and propofol for sedating
patients, they are vulnerable to cause significant reduction in blood pressure and
respiratory function. This effect can sometimes be deleterious to the patient. Hence
there has been always a search for the ideal sedative which can be used to relieve
anxiety.
The newer drug Dexmedetomidine is a more specific alpha 2 adrenoreceptor
agonist. It causes analgesia, sedation and sympatholysis. Food and Drug
Administration (FDA) approved the use of dexmedetomidine in 1999 for short-
term sedation and analgesia (<24 hours) in the intensive care unit. It is becoming
very popular because it maintains hemodynamic stability and does not cause
significant respiratory depression.
2-adrenergic receptor ( 2-AR) agonists have been used in varied clinical
situations because of their actions which include sedation, analgesia, anxiolysis,
perioperative sympatholysis, cardiovascular stabilizing effects, reduced anesthetic
requirements, and preservation of respiratory function.
Many studies are available in the literature which prove the efficacy of
clonidine ,a first generation alpha2 agonist to prolong spinal anesthesia whether
administered by intravenous or intrathecal route.[2][5] Clonidine is also known to
decrease the anesthetic requirements in general anesthesia[6] .
Dexmedetomidine being a second generation alpha2 agonist is more specific
for alpha2 receptors. Dexmedetomidine acts on the locusceruleus area of brain

stem which is concerned with modulation of sleep and respiratory control. This
results in sedation without respiratory depression.
Dexmedetomidine has all the properties of an ideal sedative. There is a
hypothesis that by its actions in the substantia gelatinosa in the spinal cord (spinal
action)and locus ceruleus in the brain (supra spinal action) dexmedetomidine can
prolong spinal anesthesia. This is the basis of its antinociceptive action.[7]Studies
have been conducted to prove that dexmedetomidine when given intravenously or

[8][9][10]
intrathecally prolongs the duration of spinal anesthesia.
In this study we investigated the effect of a single intravenous dose of
dexmedetomidine on hyperbaric bupivacaine spinal anesthesia. In addition to
prolonging the duration of spinal anesthesia, dexmedetomidine causes a decrease
in stress response, heart rate and blood pressure by lowering secretion of
catecholamines. This can be of great value in the perioperative period during
which most of the vulnerable hemodynamic variations occur due to stress.

AIM OF THE STUDY
AIM OF THE STUDY
The main aim of this study was to investigate the effect of a single dose of
0.5micrograms/kg of dexmedetomidine administered intravenously over 10
minutes after initiation of neuraxial block, on prolonging duration of sensory
and motor block in hyperbaric bupivacaine spinal anesthesia. Proper approval
from the Institutional ethical board was obtained and the study was conducted
over a period of six months.

OBJECTIVES
PRIMARY OUTCOME
Total duration of both sensory and motor blockade after hyperbaric
bupivacaine anesthesia was studied.
SECONDARY OUTCOME
Grade of sedation
REVIEW OF LITERATURE
Aantaa , Kanto J, Kallio A et al[11] had done a study in patients undergoing
minor gynecologic surgery . Nineteen women who had been posted for
dilatation and curettage of the uterus were given dexmedetomidine in the dose of
0.5 micrograms/kg fifteen minutes before induction and another set of 20 patients
received saline in the same frame. Anesthetic induction was given with
thiopental. The maintenance of anesthesia was with N2O/O2 (70/30%) and with
incremental doses of thiopentone sodium . In their study they had observed that
“The total amount of thiopental required to maintain patient in a good plane of
anesthesia for performing the procedure was reduced by approximately 30%, in
the group that had received dexmedetomidine”. They had observed that the
recovery from anesthesia was much better with dexmedetomidine as measured by
the visual analogue scale. They measured the concentration of norepinephrine and
found a 56%reduction in concentration of nor epinephrine because of the
sympatholysis caused by dexmedetomidine. They had observed moderate
decrease in systolic and diastolic blood pressure after dexmedetomidine
administration. The authors concluded that “Premedication with dexmedetomidine
decreased thiopental anesthetic requirements and also improved the recovery from
anesthesia with no serious hemodynamic compromise”.

Khaled Taha[12] had done a study in 60 patients evaluating analgesic
,sedative and hemodynamic effects of Dexmedetomidine following major
abdominal surgeries. It was a randomized ,double blinded comparative study with
morphine. All surgeries were under general anesthesia. Twenty minutes before
surgery random allocation of groups was done. One group received
dexmedetomidine as intravenous infusion 4 microgram/kg/hr for 15 minutes and a
maintenance dose for 3 hours at the rate of 0.4 microgram/kg/hour. Another group
received a single dose of morphine 0.07mg/kg. All patient received patient
controlled analgesia with morphine. They concluded that “There was significant
decrease in the total PCA morphine in the dexmedetomidine group”. The author
had emphasized that cardiovascular effects of dexmedetomidine could be
beneficial in patients with ischemic or non ischemic heart disease. The authors
had concluded that “The cardiovascular protective profile and the lack of
respiratory depression makes dexmedetomidine a suitable drug for post operative
analgesia after major abdominal surgeries”.
[8]
Kanazi GE, Aouad MT, Jabbour-Khoury SI et al, did a prospective,
double-blinded study on 60 patients posted for transurethral resection of prostate
or bladder tumor under spinal anesthesia. Patients were allocated to three groups
randomly. Patients in Group 1 were given hyperbaric bupivacaine 12 mg.

Patients in group 2 were given 12 mg of bupivacaine supplemented with
dexmedetomidine 3 microgram . Patients in group 3 were given 12 mg of
bupivacaine supplemented with clonidine 30 microgram. .The onset time for peak
sensory and motor levels, and the sensory and motor block regression time were
recorded.. The authors concluded that “Dexmedetomidine (3 microgram) or
clonidine (30 microgram), when added to intrathecal bupivacaine, produces a
similar prolongation in the duration of the motor and sensory block with preserved
hemodynamic stability and lack of sedation”.
Murat Teikin, kati I,Yakup et al[13] had done a double-blind, prospective
study in 60 patients classified as American Society of Anesthesiologists grade I to
II who were posted for lower abdominal, anorectal, lower extremity surgery
under spinal anesthesia. Patients were assigned to 1 of 2 groups. All patients
received prilocaine 2% for spinal anesthesia. After 10 minutes patients in group 1
received a loading dose of dexmedetomidine 1 g/kg IV, followed by a
maintenance dose of 0.4 g/kg / h for 50 minutes; group 2 (control) received the
same amount of physiologic saline in the same time schedule. Hemodynamic
parameters were also assessed. They concluded that “Intravenous
dexmedetomidine significantly prolonged the duration of spinal anesthesia and
provided a significantly higher level of sedation compared to placebo and was
well tolerated by all patients.”

Menon DV, Wang Z, Fadel PJ, Arbique D, [14] et al, had done a study to
determine whether cocaine's sympathomimetic actions could be reversed by
dexmedetomidine which is a alpha2 agonist. They had conducted a study in 22
healthy cocaine-naïve humans. Intranasal cocaine [2 mg/k g] was given to all the
subjects ,and then they were divided into two groups. One group received
intravenous dexmedetomidine and the other group received intravenous saline. The
parameters studied were sympathetic neuronal activity (SNA)measured by
microneurography, skin vascular resistance as measured by laser doppler
velocitometry ,heart rate and mean arterial pressure. They had observed that in the
group that received dexmedetomidine there was no increase in sympathetic
neuronal activity ,skin vascular resistance heart rate blood pressure.
Dexmedetomidine abolished these increases, whereas intravenous saline was
without effect. The authors had concluded that “Dexmedetomidine was effective
in blocking sympathomimetic actions of cocaine”.
Al-Mustafa MM, Badran IZ, Abu-Ali HM, et al,[10] did a study in 48 patients
who underwent transurethral resection of prostate, trans urethral resection of
bladder tumor under spinal anesthesia. In that study they had randomly allocated
patients into 2 equal groups after spinal isobaric bupivacaine 12.5mg. One group
received intravenously a loading dose of dexmedetomidine 1 microgram/kg over
10 minutes and a maintenance of 0.5 micrograms /kg/hour. Another group
received normal saline in the same frame. The regression time to reach S1 sensory
level, Bromage scale 0, hemodynamic changes during surgery and level of
sedation were studied. In their study they had concluded that “Dexmedetomidine
given by intravenous administration prolonged the sensory and motor blocks of
bupivacaine spinal anesthesia with good sedation effect and hemodynamic
stability”. They had assessed motor level using Bromage scale, sedation using
Ramsay sedation scale and time for regression to S1 dermatome.
[9]
Kaya FN, Yavascaoglu B, Turker G et al had done a study to compare
intravenous dexmedetomidine with midazolam and placebo on spinal block
duration, analgesia, and sedation in patients undergoing transurethral resection of
the prostate. In this double-blind randomized placebo-controlled trial, 75 American
Society of Anesthesiologists' I and II patients were divided into 3 groups .One
group received dexmedetomidine 0.5 microgram / kg, Second group received
midazolam 0.05 mg / kg and the third group received saline intravenously before
spinal anesthesia. All patients received bupivacaine 0.5% 15 mg intrathecally. In
their study they had observed that the duration of motor block was similar in all
groups. Dexmedetomidine also increased the time to first request for postoperative
analgesia (P < 0.01 ) and decreased analgesic requirements. The maximum
Ramsay sedation score was greater in the dexmedetomidine and midazolam groups
than in the saline group (P < 0.001). They had concluded that “Intravenous
dexmedetomidine, but not midazolam, prolonged spinal bupivacaine anesthesia”.

[15]
Ok HG, Baek SH, Baik SW, Kim HK et al, had done a study to
determine the optimal dose of dexmedetomidine that can be given for sedation
during spinal anesthesia. In their study they had emphasized on the need of
sedation in patients under spinal anesthesia. They had selected one hundred and
twenty eight patients, aged 20-70 years who underwent surgery under spinal
anesthesia. After spinal anesthesia was initiated with hyperbaric bupivacaine (13
mg), dexmedetomidine (1 µg/kg)as loading dose intravenously was administered
over 10 min for all the patients .After that patients were divided into 3 groups and
followed by the maintenance infusion which differed in each group. Group A
comprising of 33 patients received normal saline, Group B comprising of 35
patients received dexmedetomidine in the dose of 0.2 µg/kg/hr, and Group C with
39 patients received dexmedetomidine in the dose of 0.4 µg/kg/hr. Heart rate,
blood pressure, and the bispectral index score (BIS) were monitored and noted
during the operation. In the recovery room, modified aldrete score (MAS) was
measured. They had concluded that “The loading dose (1 µg/kg/10 min) of
dexmedetomidine was sufficient for sedation for surgery of less than 60 min done
under spinal anesthesia. This should be followed by a maintenance dose of
dexmedetomidine (0.2 µg/kg/hr) for surgeries which last for 90 min”.
[16]
Annamalai A, Singh S, Singh A, Mahrous DE et al, had done a study in
ninety ASA1 or 2 patients posted for surgeries below umbilicus under spinal
anesthesia. Patients had been double blind randomized in to three groups. One
group received normal saline 10 ml over 10 minutes before spinal anesthesia.
Second group received dexmedetomidine 1 microgram/kg through intravenous
route 10 minutes before spinal anesthesia. Third group received dexmedetomidine
1 microgram/kg via intravenous route 10 minutes after spinal anesthesia. All the
patients had been advised to take tablet alprozolam 0.25mg and tab ranitidine
150 mg on the previous night and on the day of surgery. They concluded that
dexmedetomidine through intravenous route prolonged spinal “sensory blockade
in both the groups irrespective of the timing whether it was given before or after
spinal anesthesia. The onset of post operative pain was delayed in the group which
received dexmedetomidine”. The authors further concluded that “The patients in
the dexmedetomidine group needed lesser doses of post operative analgesic than
the other group”.
Jia Song, Woong-Mo Kim et al,[17] had done a study in 45 ASA1 or 2
patients who underwent surgery under spinal anesthesia. In that study they had
given dexmedetomidine in three different doses to evaluate the hemodynamic
changes and their main aim was to get the optimal dose of dexmedetomidine. All
patients were given a loading dose of dexmedetomidine 1 microgram/kg. Then the
patients were divided randomly into one of the 3 groups for maintenance dose.
One group received dexmedetomidine in the dose of 0.25 microgram/kg/hr, second
group received dexmedetomidine in the dose of 0.5 microgram/kg /hr and the third
group received dexmedetomidine in the dose of 0.75microgram/kg/hr .They had

clearly stated that patients were able to remain calm after sedation with
dexmedetomidine. They had stressed on the need of adequate sedation if the
advantages of spinal anesthesia are to be fully appreciated. In their conclusion Jia
song et al had stated about the incidence of hypotension as the dose increased.
They had emphasized on the fact that “To minimize the risk of hemodynamic
instability a maintenance dose of 0.25micrograms/Kg/h r may be most
appropriate”.
SS Harsoor, D Devika Rani, Bhavana et al[18] did a study to determine the
effects of intravenous dexmedetomidine on sensory, motor, haemodynamic
parameters and sedation after spinal anesthesia. 50 patients posted for infra
umblical and lower limb surgeries under neuraxial blockade were selected and
divided into 2 groups. Group D received dexmedetomidine in the dose of 0.5
mcg/kg intravenously bolus over 10 min prior to spinal , followed by an infusion
of dexmedetomidine 0.5 mcg/kg/h for the duration of the surgery. Group C
received similar volume of normal saline infusion. They concluded that
“Administration of intravenous dexmedetomidine during spinal anesthesia
hastened the onset of sensory block and prolonged the duration of sensory and
motor block with satisfactory arousable sedation”.
[19]
Abdallah FW1, Abrishami A, Brull et al, had evaluated whether
intravenous dexmedetomidine can prolong the duration of sensory block

associated with spinal anesthesia. The parameters assessed by the authors were
duration of sensory and motor block, onset time for sensory and motor block,
postoperative pain scores, time to first analgesic request, total analgesic
requirement and side effects. A total of 364 patients were analyzed from 7
randomized controlled trials. The authors had concluded that “When intravenous
dexmedetomidine accompanied spinal anesthesia, sensory block duration was
prolonged by about 34% , motor block duration was prolonged by about 17%, and
time to first analgesic request was increased by 53% with a significant p value”.
They had stated that there was increased incidence of bradycardia in
dexmedetomidine group. They had concluded that “Intravenous dexmedetomidine
prolonged the duration of sensory block, motor block, and time to first analgesic
request associated with spinal anesthesia.”
Seung Hwan Jung et al[20] had done a study in sixty adult patients who
were scheduled for lower extremity surgery under spinal anesthesia. Patients were
randomly allocated to one of three groups and administered hyperbaric intrathecal
bupivacaine 12 mg. After 5 minutes of spinal anesthesia, patients in groups 1
were administered normal saline 10 ml intravenously, patients in group 2 were
given intravenous dexmedetomidine 0.25 microgram/kg, and the third group
received dexmedetomidine i.v 0.5 microgram/kg over 10-minutesThey
concluded that “The single-dose intravenous dexmedetomidine 0.25–0.5 g/kg,
administered 5 min after intrathecal hyperbaric bupivacaine, improved the

duration of spinal anesthesia without significant side effects”. They stated that this
effect on spinal anesthesia could be seen even when dexmedetomidine is
administered several minutes after spinal anesthesia.
Reddy VS, Nawaz Ahmed Shaik and Venkatsiva Janga[21] had compared
the efficacy of intravenous dexmedetomidine with clonidine and placebo on
spinal blockade duration, analgesic effect post operatively and sedation in patients
undergoing surgery under bupivacaine neuraxial block. 75 patients of the ASA I
or II, scheduled for orthopedic lower limb surgery under spinal anesthesia, were
randomly divided into three groups each group consisting of 25 patients. Group 1
received dexmedetomidine 0.5 microgram/kg/hr, group 2 received clonidine 1.0
microgram/kg/hr and placebo group 3 received 10 ml of normal saline
intravenously before subarachnoid anesthesia with 15 mg of 0.5% hyperbaric
bupivacaine They concluded that “Premedication with intravenous
dexmedetomidine was better than clonidine for intraoperative sedation and
postoperative analgesia during spinal anesthesia with hyperbaric bupivacaine”.
[22]
Dinesh CN, Sai Tej NA, Yatish B et al, had done a study to evaluate
the effects caused by intravenous dexmedetomidine on spinal anesthesia with
0.5% of hyperbaric bupivacaine. One hundred patient posted for elective surgeries
under spinal anesthesia were randomized into two groups of 50 each. After
subarachnoid block with 0.5% hyperbaric bupivacaine 3 ml, patients in

dexmedetomidine group were given a loading dose of dexmedetomidine 1
microgram/kg of intravenously over 10 min followed by a drip in the dose of 0.5
microgram/kg/hour as maintenance till the end of surgery, whereas patients in
control group received an equivalent quantity of normal saline. In their study they
concluded that “Intravenous dexmedetomidine prolonged the duration of sensory
and motor block of hyperbaric bupivacaine spinal anesthesia”. The authors had
observed that the occurrence of bradycardia was higher when intravenous
dexmedetomidine was used in bupivacaine spinal anesthesia.
Park SH, Shin YD, Yu HJ, Bae JH, et al[23] had compared the effects caused
by two different doses of intravenous dexmedetomidine in elderly patients during
spinal anesthesia. They had selected 45 elderly patients ( 60 years) classified as
ASA1 or II who were posted for transurethral resection of the prostate or
transurethral resection of the bladder tumor and the patients were divided
randomly into three treatment groups. The group 1 received dexmedetomidine in
the dose of 0.5 µg/kg while the second group received dexmedetomidine 1 µg/kg
intravenous injection over 10 min before anesthetic induction. The Control group
received normal saline. Comparison was done regarding the maximum sensory
block level, extension of anesthesia, degree of motor block, sedation level and
complications. They had concluded that “There was not much of difference in the
groups on achieving the maximum level of sensory block and motor block. But the
total time of sensory block was significantly longer in group which received
dexmedetomidine 1microgram/kg than in the control group”. There was significant
increase in bradycardia in the patients who received dexmedetomidine. No
complications such as hypotension, nausea, tremor, and hypoxia was reported by
them .
DEXMEDETOMIDINE –PHARMACOLOGY
Dexmedetomidine is the dextrorotatory S-enantiomer of medetomidine,
which is widely used in veterinary practice[24].
Chemically, Dexmedetomidine is (S)-4-[1-(2,3-dimethylphenyl) ethyl]-3H-
imidazole
CHEMICAL FORMULA is C13H16N2[11][12]
Structure of dexmedetomidine
Clonidine, the first generation alpha 2 agonist has been in use for many
years. It is used as an antihypertensive by oral route. When given intrathecally, it
prolongs the duration of spinal anesthesia[2]. Intravenously it decreases anesthetic
requirements. Dexmedetomidine is a newer drug in the same group and has many
advantages when compared to clonidine.
Differences between clonidine and dexmedetomidine[25][26]

CLONIDINE DEXMEDETOMIDINE
It was first synthesized in 1960s Dexmedetomidine was first
produced in 1980s
Started to use clinically as Approved for clinical use as
antihypertensive in 1966. analgesic and sedative in 1999.
Alpha2;Alpha1 receptor binding Alpha2;Alpha1 receptor binding
ratio is 220:1. ratio is 1620:1
Acts as a partial agonist at alpha Acts as a full agonist at alpha
receptor. receptor.
Octanol /buffer partial coefficient Octanol /buffer partial coefficient
is 0.8. is 2.8.It is 3.5 fold more lipophilic
than clonidine.
Plasma half life is 9-11.5 hours. Plasma half life is 2-2.25 hours.
It is 50% bound to proteins. It is 94%bound to proteins.
Elimination half life is 8 hours. Elimination half life is 2 hours.
Distribution half life >10 minutes. Distribution half life is 5 minutes.
It has been proved that there is It has been proved that there is
50% reduction in MAC of 90% reduction in MAC of
inhalational agents when clonidine inhalational agents when
is used. dexmedetomidine is used.
ALPHA 2 ADRENORECEPTOR
Schematic representation of alpha2

Adrenoreceptor
The prime sympathetic neurotransmitter nor adrenaline and the most
important adrenal medullary hormone adrenaline mediate their central and
peripheral actions through a special type of receptors called adrenergic receptors.
Adrenergic receptors are abundantly present in nearly all peripheral tissues
and in the neurons of the central nervous system. [27] There are three types of
adrenergic receptors. They are alpha1,alpha2,and beta receptors. These
adrenergic receptors are one among cell surface receptors that arbitrate their
actions through guanine nucleotide binding proteins [G-Proteins][26].

Alpha2 receptors are again subdivided into 3 subtypes
alpha2A,alpha2B,alpha2C[28].They have individual patterns of tissue distribution in
the two types of nervous system.
ALPHA 2A are found in Locus ceruleus of brain,
nor adrenergic cell body regions,
spleen, pancreas,
kidney, blood vessels, urethra,
thrombocytes.
ALPHA2B are found in Kidney, placenta, liver smooth
muscle of blood vessel ,thalamus
ALPHA2C are found in Central nervous system
There are two mechanisms of action of alpha2 receptor agonists. When the
alpha2 receptor is activated, calcium entry into the nerve terminal is decreased and
this action is responsible for the inhibitory effect on catecholamine
secretion[24][29]. N-type voltage-gated calcium channels are directly involved in
this particular action. G0 proteins mediate this action.

Alpha2 receptor stimulation also inhibits the enzyme adenylate cyclase.
Adenylate cyclase is the key enzyme which is responsible for the production of
3,5-cyclic adenosine monophosphate . The net result is decreased availability of 3
5 cyclic AMP, which is a second messenger.
Specific cyclic AMP-dependent kinases alter the phosphorylation status of
target proteins. Due to decreased levels of 3,5,cyclic AMP , major alterations
occur in the ion channel activity[26]. This results in hyperpolarization of the cell
membrane. Thus neuronal firing is suppressed to a great extent. Activation of G1-
protein gated potassium channels on the cell surface causes hyperpolarization of
membrane which in turn decrease the firing rate of excitable cells in the central
nervous system.
Activation of the 2adrenoceptor present in the presynaptic regions leads to
the reduction in the release of neurotransmitter nor epinephrine. Because of the
decreased concentration of the prime neurotransmitter, cell signals are not
propagated. This leads to decreased sympathetic activity and reduction in blood
pressure and heart rate.
Dexmedetomidine, a single drug can produce all these effects and thus
avoiding much complicated multiple drug therapy. In multiple drug therapy many
drugs belonging to different classes are usually given to produce all these
beneficial effects.
Till date ,there is no clear mention of the mechanism by which alpha 2
agonist cause analgesia. Most likely postulated mechanisms include supraspinal
action in the locus ceruleus and spinal action in the substantia gelatinosa that
modulate the transmission of nociceptive signals in the central nervous system [29].
Drugs may perform action at any of these sites resulting in analgesia.
By the result of all these actions neither the nerve can fire nor it can
propagate signal to the neighboring cells. Ultimately, this results in analgesia by
central, spinal and peripheral mechanisms. The net result is a considerable
reduction in the stimulation and propagation of nervous signals.
Action in the brain stem
Alpha2 receptors are present in highest densities in the locus ceruleus[12]
the chief noradrenergic nucleus in the brain . The locus ceruleus is one of the
important centers which control vigilance. The hypnotic and sedative effects of
alpha2 adrenergic receptor is due to the action on the locus ceruleus [26] [29].
The locus ceruleus is also the place of origin for the descending
medullospinal noradrenergic pathway , which is mainly involved in nociceptive

transmission. This may be the reason for the anti nociceptive action of
dexmedetomidine.
The ratios of 2 1 activity is 1620:1 for dexmedetomidine and 220:1 for
clonidine. Therefore dexmedetomidine is a more suitable sedative and analgesic
agent than clonidine.
Spinal action of dexmedetomidine
Besides actions in the locus ceruleus of the brain stem, dexmedetomidine
causes direct stimulation of alpha2 receptors in the spinal cord. The alpha2
receptors are found in abundance in the substantia gelatinosa of the dorsal horn
of the spinal cord .On stimulation , these receptors inhibit the firing of neurons
accountable for nociception perceived by A type and C type fibers [10][24][25][29].
Release of substance P is also inhibited. This spinal mechanism is responsible for
dexmedetomidine action when used epidurally and when administered as an
intravenous drug .
Dexmedetomidine causes sedation which resembles physiological sleep
without causing respiratory depression.

Diagram Showing Physiological Response To Alpha2 Receptor Stimulation
Type of receptor Physiological functions and responses of

alpha receptors
Alpha 2A Presynaptic inhibition of neurotransmitter

release
Sedation and anaesthesia
Analgesia
Bradycardia and hypotension
Regulation of blood glucose and insulin
homeostatasis
Hypothermia
Inhibition of epileptic seizures
Decrease in intraocular pressure.
Inhibition of gastrointestinal motility
Alpha2B Vascular smooth muscle contraction

Hypertension
Placental angiogenesis
Alpha2C Presynaptic inhibition of catecholamine
release.
Modulation of motor behavior, vascular
smooth muscle contraction, Controlled
balance of dopamine and serotonin release in
the brain.
Pharmacokinetics of Dexmedetomidine
Absorption
Dexmedetomidine is not orally active. The conventional route of
administration of dexmedetomidine is intravenous route. Dexmedetomidine shows
good bioavailability when administered via other routes such as intranasal,
intramuscular, buccal, sublingual, intragastric, neuraxial, regional,
intraarticular[24].
Distribution
In elimination phase the half life is 2-3 hours. The steady state volume of
distribution is 118 liters.
Protein binding
Dexmedetomidine is 94%protein bound. Hepatic impairment slightly
decreases the fraction bound to plasma proteins. In vitro studies conclude that
dexmedetomidine does not displace phenytoin, warfarin, propanolol, theophyline,
digoxin from plasma proteins. Pharmacokinetics of dexmedetomidine does not
change with age, sex or in patients with renal failure[26].
Metabolism
DEX undergoes (> 95%) biotransformation in liver into inactive
metabolites. Direct N-glucuronidation is the main pathway of metabolism and
glucuronides are the important circulatory and urinary metabolites of
dexmedetomidine[24]. Hydroxylation and oxidation are the minor pathways. It is a
must to decrease the dose of dexmedetomidine in patients with hepatic failure,
because the half life is prolonged in hepatic failure . The half life of
dexmedetomidine is 7.5 hours in hepatic failure whereas the elimination half-life
in healthy patients is approximately 2 hours.
In clinical doses ,dexomedetomidine acts as a decongestant and as an
antisialagogue. It also has antishivering and antiemetic effects. Added benefits of

dexmedetomidine include less respiratory depression when compared to other
drugs with additional benefits of cardioprotection, neuroprotection and
renoprotection.
Adverse Effects
The commonly seen side effects of dexmedetomidine are bradycardia,
hypotension and dry mouth. Both bradycardia and hypotension respond promptly
to anticholinergics and vasopressors respectively.
Transient hypertension is seen when given in large doses( due to peripheral
alpha2 B receptor stimulation). Other reported side effects include nausea,
vomiting, atrial fibrillation, pyrexia, chills, pleural effusion, pulmonary edema,
atelectasis, hyperglycemia, hypocalcaemia, acidosis. After administration for more
than 24 hours as an infusion , sensitization and up regulation of receptors occur.
After abrupt discontinuation, a withdrawal syndrome of nervousness, agitation,
severe headaches, and emergency hypertensive crisis can occur[26].
Dexmedetomidine is contraindicated in patients with advanced heart block
and ventricular dysfunction. FDA has classified it as a category C risk in
pregnancy. Hence the drug should be used with caution in pregnancy.

PHARMACODYNAMICS Effects on the
respiratory & cardiovascular system;
Activation of alpha 2 receptors leads to dose dependent reduction in
catecholamine level (up to 89%)[26].Due to inhibition of sympathetic medullary
vasomotor center, bradycardia and hypotension occur.
In the respiratory centre alpha2 receptors do not have any active role and
so, dexmedetomidine (up to 8 nanogram/ml), has minimal effects on the
respiratory system[24]. Hence, dexmedetomidine does not cause respiratory
depression.
Dexmedetomidine does not have any direct action on the myocardium[26].
After administering it rapidly in a larger dose (>1 microgram/kg), a biphasic
response on BP is seen. There is an initial short hypertensive phase mediated by
peripheral alpha2B adrenergic receptor stimulation. Subsequent hypotension is
mediated by presynaptic 2A adrenergic receptors. The direct action on the
peripheral vascular smooth muscle causing usually lasts for 10 minutes.
Dexmedetomidine causes dose dependent decrease in the vasoconstriction
and shivering thresholds.
The postulated neuro protective action of dexmedetomidine

Dexmedetomidine reduces cerebral blood flow and cerebral metabolic
requirement of oxygen . There are many studies which suggest that
neuroprotective action is achieved by reducing the levels of circulating and brain
catecholamines[26]. Thus it causes balancing of the ratio between cerebral oxygen
supplies and demand . It reduces excitation levels, and improves the perfusion in
the ischemic penumbra[26]. It reduces glutamate levels responsible for brain cell
injury. This suggests the application of dexmedetomidine in head injury patients to
enhance cerebral perfusion.
The postulated renoprotective action of dexmedetomidine
Its renoprotective effects include inhibition of renin release, increased
glomerular filtration, and increased secretion of sodium and water in the kidney.
These actions are probably mediated through peripheral alpha2 receptors.
Antagonism of actions by Atipamezole
After continous infusion is stopped, dexmedetomidine has a rapid and
predictable offset of action. Though not orally active, Atipamezole[30](antisedan) is
considered to be an effective antagonist for reversing psychomotor disturbance
and vigilance caused by dexmedetomidine. Both dexmedetomidine and
Atipamezole show linear pharmacokinetics . The elimination half-lives of the
two drugs is approximately 2 hours. This is a clear benefit while considering the
promising clinical applications for long term use of dexmedetomidine in intensive
care unit.Any adverse effect can be countered by Atipamezole.
Clinical actions of dexmedetomidine
Centrally mediated actions of dexmedetomidine
Bradycardia and hypotension
Sedation, anxiolysis ,hypnosis
Analgesia
Peripherally mediated actions of dexmedetomidine
Decrease of GI secretions, salivary secretion and decreased gastro
intestinal peristaltic movement.
Contraction of smooth muscle including blood vessels .
Renin release is reduced by the inhibition of rennin angiotensin system.
Glomerular filtration rate (GFR) is increased. Sodium excretion and water
excretion is enhanced. All these effects contribute to the diuretic effect of
dexmedetomidine.
Significant reduction in intra-ocular pressure
Decreased release of insulin from the pancreas .
Reduced platelet aggregation
Shivering threshold is decreased approximately by 2ºC.

Clinical Applications of dexmedetomidine
Peri-operative uses of dexmedetomidine
1.Attenuation of intubation response
Dexmedetomidine decreases stress response to tracheal
intubation/extubation when given in the dose of 1 microgram /kg with lesser doses
not being effective. It has analgesic sparing effect which lasts up to 24 hour[31].
2.As an adjuvant to GA
Dexmedetomidine boosts the anesthetic effects of all anesthetic agents
despite the method of administration (intravenous, volatile or regional block). It
has minimum alveolar concentration (MAC) reducing and opioid sparing
properties, which results in decreased use of inhalation anesthetics and
opioids[32][33].
The reduction in myocardial oxygen demand and rate pressure product
reduce myocardial ischemia and infarction which is very beneficial for cardiac
patients. When used in obstructive sleep apnoea and in morbidly obese patients, it
does not cause any cardio-respiratory depression and helps in faster,
neuromuscular recovery[34]. In literature search, case reports are available stating

the use of dexmedetomidine as an anesthetic adjuvant intraoperatively in
reducing episodes of abrupt hypertension that occurs during manipulation of the
tumor in surgery for pheochromocytoma .
3.As an agent for producing Controlled hypotension
In the literature there are many studies which say that dexmedetomidine is
equally potent as remifentanil and esmolol in controlled hypotension application.
The parameters studied were intraoperative bleeding, preoperative hemodynamics,
lactate levels[24].
4.As an adjuvant to regional anesthesia
Researchers are doing intense search to find an ideal adjuvant to regional
anesthesia . The alpha 2 adrenergic agonists, in particular dexmedetomidine has
both analgesic and sedative actions. 3 g DEX and 30 g clonidine are equipotent
intrathecally. The addition of 5 g of intrathecal dexmedetomidine prolonged the
post-operative analgesic effect of ropivacaine by 8 hours[25].
5.As an adjuvant in peripheral nerve block
Dexmedetomidine (in the dose of 0.5 microgram/kg)when added to
bupivacaine in nerve blocks prolongs the duration of sensory block, and decreases
tourniquet pain.
6. The role of dexmedetomidine in Cardiac anesthesia-
In American Heart Association (AHA) guideline 2002 2-adrenoceptor
agonist has been mentioned as a grade IIb agent . They are particularly of use in
situations when –blockers are contraindicated. In the human physiology
hemodynamic, sympathetic activity and renal function are closely interrelated.
Dexmedetomidine induced sympatholysis might attenuate harmful hemodynamic
events responsible for deterioration of renal function in patients undergoing
elective CABG with extracorporeal circulation[24].
7. The role of dexmedetomidine in Neuroanesthesia-
Anesthesia for awake craniotomy which needs cooperation of patients
presents a challenge to the anesthesiologist. Common side effects associated with
conventionally used neuroleptanalgesia are drowsiness, respiratory depression,
agitation and intra operative seizure. Using dexmedetomidine we can achieve a
level of sedation and analgesia to complete the neuropsychiatric testing for
electrocorticography ,for the mapping of the cortical language area, for bone flap
removal, and to perform an awake tumor resection [35].
8. The role of dexmedetomidine in monitored anesthesia care

Dexmedetomidine is an ideal agent for many procedures like fiberoptic
bronchoscopy, ophthalmic procedures ,head and neck procedures, ,vascular
surgeries and dental procedures. Dexmedetomidine provides better patient
satisfaction, less respiratory depression and less opiod requirements. Intraocular
pressure is decreased by dexmedetomidine which is an added advantage in
ophthalmic procedures. Intravenous dexmedetomidine in the dose of
0.6microgram/kg prevented the rise of intraocular pressure after suxamethonium.
9.As Post operative analgesic
Its wide safety margins and respiratory function preservation allows
continued use of dexmedetomidine in extubated patients. It decreases the
incidence of nausea and vomiting postoperatively. Dexmedetomidine when added
to morphine in patient controlled analgesia has been proved to increase post
operative analgesia .
10. The role of dexmedetomidine in Intensive care unit
Sedation plays an important role in intensive care. The sleep induced by
dexmedetomidine mimics normal sleep and this is an advantage during weaning
from mechanical ventilation.
Reduced stay in intensive care unit, decreased duration of ventilation,
haemodynamic stability and reduced agitation are the proven advantages of

dexmedetomidine. Dexmedetomidine need not be stopped and the sedation can be
maintained following tracheal extubation[36, 37]

. Dexmedetomidine is an
alternative in patients developing tolerance to opiods.

COMPARISON OF SEDATIVES COMMONLY USED IN ICU
11.The role of dexmedetomidine in pediatrics
We can avoid unnecessary needle pricks and reduce the dose of opiods by
using dexmedetomidine through noninvasive routes (intranasal,
buccal). The pharmacokinetics of dexmedetomidine in infants and children is
more or less similar to that in adults. In pediatrics the main upcoming role of
dexmedetomidine is to prevent emergence delirium [36][37]. In children, it is used
in various applications including procedural-sedation, sedation for mechanical
ventilation, for preventing emergence delirium. Dexmedetomidine via intravenous
route or intramuscular route has been used to sedate children for procedures
without stimulation like MRI and CT scan. In children the dose required for bolus
is 2to3 microgram/kg and for infusion is 2 g/kg/hour. The combination of
dexmedetomidine and ketamine makes pharmacologic sense as the two

medications have the potential to balance the hemodynamic and adverse effects
which make both a very effective combination. Khaled Al Zaben et al had
reported the use of dexmedetomidine (5-10 g /kg/h) as the main anesthetic ,
supplemented by incremental propofol dose (100 g/kg/min)for three children
with tracheomalacia [24].
12.The role of dexmedetomidine in Obstetric anesthesia
In view of its high lipophilic nature ,dexmedetomidine is retained in the
placental tissue and this results in less foetal transfer and a reduced incidence of
fetal bradycardia. Continuous intravenous dexmedetomidine infusion is being
used as an adjuvant to opioids in labour analgesia[24]. Dexmedetomidine has an
antinociceptive effect to visceral pain. Dexmedetomidine also provides
hemodynamic stability, anxiolysis. Dexmedtomidine causes stimulation of uterine
contraction which is a beneficial effect in parturient mothers.
Caution about loading dose
Most of the adverse events associated with use of dexmedetomidine occur
during or briefly after loading of the drug. Multiple studies have demonstrated that
by omitting or reducing the loading dose, adverse effects can be

reduced. Although, avoiding the loading dose may prevent erratic hemodynamic
effects ,it may cause delay in onset of action and time to reach steady state.
BUPIVACAINE IN SPINAL ANESTHESIA
Basic pharmacology of bupivacaine;
Molecular Formula: C18H28N2O
Average mass: 288.427704 Da
Chemical name;
(2S)-1-Butyl-N-(2,6-dimethylphenyl)-piperidinecarboxamide
Chemical structure;
Bupivacaine is a long acting spinal anesthetic .Other long acting local
anesthetics are tetracaine and levo bupivacaine.
Amide type-Bupivacaine and Levo bupivacaine.
Onset time-5to 10 minutes.
Total duration of spinal block-90-120 minutes.
MECHANISM OF ACTION OF BUPIVACAINE
All local anesthetics block sodium channels and block entry of sodium into
the cells thereby preventing depolarization. So the nerve cannot get depolarized
and the signal is not propagated. In spinal anesthesia we commonly use hyperbaric
bupivacaine.
BARICITY OF THE SOLUTION; Baricity determines the spread of local
anesthetic in the spinal space and is equal to the density of the local anesthetic
divided by the density of the CSF at 370 c.
The density of cerebrospinal fluid is less than 1.0069. In spinal anesthetics baricity
is mentioned in comparison to that of cerebrospinal fluid.
HYPOBARIC SOLUTION
When the solution of the drug has a density lesser than cerebrospinal fluid ,it
is called hypobaric bupivacaine. Hypobaric bupivacaine is produced when we boil
bupivacaine to 370c. These solutions tend to spread upwards against gravity. It is
of use particularly in fracture hip when the patient has to lie in a lateral position
with the operating site positioned above.
ISOBARIC SOLUTION
Isobaric solution of tetracaine is produced by adding nymphanoid crystals to
cerebrospinal fluid. Isobaric bupivacaine is also available. The height of the block
is dependent on the total milligram of the drug instilled in to the subarachnoid
space. Isobaric bupivacaine is available in the concentration of 0.5% and 0.75%.
HYPERBARIC SOLUTION
Hyperbaric bupivacaine is available in the concentration of 0.5% and 0.75%
in dextrose 8.25%. It is widely used. The height of block is more dependant on the
position of the patient after the block.
SADDLE BLOCK
Make the patient sit. The local anesthetic gets concentrated in the sacral
area.
HEAD DOWN POSITION
More concentrated in the thoraco lumbar region.
LATERAL POSITION
Dense block on the dependant side.
FACTORS DETERMINING THE CHARACTER OF BLOCK
Potency of the spinal anesthetic is related to the lipid solubility.
The total duration of action of the anesthetic is more related to the
protein binding.
The onset of action is related to the availability of the drug in the base
form.
Lipid solubility determines the potency of the anesthetics. Low lipid
soluble medications need to be given in higher concentrations of local anesthesia
to obtain the expected nerve blockade. High lipid solubility can elicit anesthesia
at low concentrations. Protein binding determines the duration of action of the
anesthetic. Higher proportions of protein binding results in longer duration of
action.
pKa of a solution
The pKa of a local anesthetic is defined as the pH at which ionized and
nonionized forms are present in equal concentrations in solution. pKa of

bupivacaine is 8.1.This is important because the nonionized easily diffuses across
the lipophilic nerve sheath and acts on the sodium channels in the nerve
membrane. The onset of action is more dependant on the amount of the medication
available in the base form. All local anesthetics obey the rule that “If the pKa is
lower , the onset of action is faster”.
The fate of local anesthetics in the Subarachnoid Space
Pharmacokinetics of local anesthetic consist of uptake and elimination of
the drug. Four factors play a role in the uptake of local anesthetics from the
cerebrospinal fluid into neuronal tissue.
The factors are
(1) concentration of the dug in cerebrospinal fluid,
(2) surface area of neurons present in CSF,
(3) lipid content of neurons,
(4) vascularity of the nervous tissue.
The uptake of local anesthetic is most dense at the site of highest
concentration in the CSF and is decreased proportionately upwards and
downwards from this point.
Local anesthetics in the subarachnoid space are taken up both by the nerve
roots and the spinal cord. If the surface area of the nerve root is high , the the
uptake of local anesthetic is greater.

There are two postulated mechanisms for the uptake of local anesthetics in
the spinal cord.
The first method is by simple diffusion from the CSF to the pia mater and
thence into the spinal cord, which is comparatively a slow process. Only the
superficial layer of the spinal cord is affected by diffusion of local anesthetics.
The second method of uptake of the drug is by extension into the Virchow–
Robin spaces , which are the layers of pia mater that surround the vasculature that
penetrate the central nervous system. The spaces of Virchow–Robin are inter
connected with the neuronal clefts which surround nerve cell bodies in the spinal
cord and penetrate through to the deeper areas of the spinal cord.
The intensity of anesthetic effect depends on the
1.Diameter of the nerve fibers
2.Myelination of the nerve fibers.
3.conduction velocity
Order of affection of fibres in spinal anesthesia
1.Sympathetic neurons
2.Pain
3.Temperature
4.Touch
5.Proprioception
6.Tone of skeletal muscles
Spread of local anesthetic in the subarachnoid space depends upon
1. Attributed to the properties of the drug
Baricity of the drug
Dose given
Volume of the entire solution
Specific gravity of the solution
2.Patient characteristics
Position of the patient during and after injection
Height of the patient which alters anatomy of the spinal column.
Decrease in CSF volume which plays a major part when there is increased
intra abdominal pressure due to increased weight, pregnancy, etc.
3.Technique
Injection site and the direction of the bevel of the needle.

FUNCTIONAL ANATOMY OF SPINAL BLOCKADE
Five ligaments hold the spinal column together.
They are;
1.supraspinous ligaments connect the apices of spinous processes
2.Inter spinous ligaments connect the spinous processes.
3.Ligamentum flavum connect the lamina above and below.
4.Anterior longitudinal ligament connect the vertebral bodies.
5.Posterior longitudinal ligament connect the vertebral bodies.
Important dermatomal levels
The tenth thoracic (T10) dermatome -Umbilicus.
The sixth thoracic (T6) dermatome -Xiphoid.
The fourth thoracic (T4) dermatome- Nipples

Dermatomal levels needed for various surgeries
Procedure Dermatomal Level
For Upper abdominal surgery T4
Intestinal, gynecologic, urologic T6
surgery
Transurethral resection of the T1O
prostate
Vaginal delivery of a fetus, and T10
hip surgery
Lower leg surgery L1
Foot and ankle surgery L2
Perineal and anal surgery S2 to S5 (saddle block)
Absolute contraindications to spinal anesthesia:
When there is Patient refusal
Presence of Sepsis at the site
Severe Hypovolemia
Coagulopathy
Indeterminate neurologic disease

Increased intracranial pressure
Relative contraindications
Infection distant from the site of injection
Duration of surgery is not known.

PHYSIOLOGY OF SPINAL ANESTHESIA
Cardiovascular changes after spinal anesthesia
Spinal anesthesia causes sympathectomy. So major hemodynamic changes
occur during spinal anesthesia. Sympathetic flow is thoraco lumbar flow. The
height of the block determines the extent of blockade of sympathetic system. So
hypotension and bradycardia, the important effects of sympathetic blockade are
common after spinal anesthesia.
Hypotension is caused due to both arteriolar dilatation and veno dilatation.
Veno dilatation is more than arteriolar dilatation. Pre load to the heart mainly
depends on the position of the patient after spinal anesthesia. Veins above the heart
cause increase in venous return whereas veins below the heart cause pooling of
blood.
Bradycardia occurs due to sympathetic blockade of cardio accelerator fibers.
Bradycardia is exaggerated in young people and in patients and in patients who are
on betablockers for a long time.
Risk factors for causing exaggerated hypotensive response after spinal
anesthesia
1.Volme contracted state(Hypovolemia)
2.History of Hypertension
3.High Level of sensory block
4. Age more than 40 years
5.Obesity,elevated BMI
6.Combination of general and spinal anesthesia
7.Addition of adjuvants like phenylephrine to the local anesthetic
8.History of Chronic alcohol consumption
Decreased venous return can be treated by
Crystalloid infusion
Trendelenburg position
Combined alpha and beta adrenergic agonist like ephedrine.
Excessive crystalloid infusion can result in cardiac failure and pulmonary
edema. It may necessitate catheterization of bladder also.
Head down position should be restricted to 200 down. Inclination more than
this can decrease cerebral perfusion due to increased pressure in the internal
jugular vein.
The Bezold Jarisch reflex
This is a cardio inhibitory reflex. It may occur after central neuraxial
blockade.
Classical triad consists of
Bradycardia
Hypotension
Cardio vascular collapse.
Bezold Jarisch reflex is not a vaso vagal reflex.
Changes in respiratory system after spinal anesthesia
Pulmonary function is not altered much after spinal anesthesia. Lung
volumes, dead space, arterial blood gas, minute ventilation and shunt fraction do
not change to a great extent after spinal anesthesia. The main effect seen is
paralysis of intercostal and abdominal muscles which result in decrease in peak
expiratory flow.
Patients with obstructive pulmonary disease who depend on accessory
muscles for effective ventilation can show a reduction in respiratory function
after spinal anesthesia.
Patients with normal respiratory function may experience dysnoea
sometimes. If they are able to vocalize properly ,there will not be any respiratory
compromise.
Minimal oxygen supplementation is a must in spinal anesthesia.

Changes in gastrointestinal system after spinal anesthesia
Gastro intestinal system receives sympathetic fibres from T6 toL2.
Due to unopposed vagal activity ,the following changes occur
Relaxation of sphincters
2.Increase in secretions.
3.contraction of bowel
These changes usually lead to nausea. So, atropine is more beneficial in combating
nausea after spinal anesthesia.
Changes in hepatobiliary system after spinal anesthesia
Hepatic blood flow is predominantly related to arterial blood flow. Spinal
anesthesia decreases venous return. Pre load is decreased. Hence arterial pressure
and cardiac output get reduced. As arterial blood supply is decreased, total blood
flow to the liver decreases after spinal anesthesia. Hepatic blood flow
predominantly depends on the mean arterial pressure. If mean arterial pressure
(MAP) is maintained , hepatic blood flow is maintained.
Patients with liver diseases should be carefully monitored and mean arterial
pressure should be maintained with in normal limits. In patients with liver disease
either regional or general anesthesia can be given, as long as the MAP is kept close
to baseline.
AUTOREGULATION OF RENAL BLOOD FLOW
Autoregulation of blood flow to the kidney is well maintained above a mean
arterial pressure of 50 mm Hg.Renal blood flow is decreased when the mean
arterial pressure becomes lower than 50 mm Hg.
EQUIPMENTS FOR SPINAL ANETHESIA;
1.Spinal tray
a.sponge holding forceps
b.sterile gauzes
c.bowl
d.sterile drapes
2.Spinal Needle
Spinal needle consists of a needle and a close fitting removable stylet.
Different types available are;
a. Quinke’s needle
b. Sprotte’s needle Pencil point needles
c. Whitaker’s needle
Needles are available in gauges of 29,27,25,23.
POSITION OF THE PATIENT
Proper positioning is essential for technical ease and a resultant successful
block. A trained technician should be present to keep the patient in optimal
position.
The different positions are
1.Lateral decubitus position.
2.Sitting position.
3.Prone position in rectal, perineal and lumbar surgeries if the patient needs to
be in that position during surgery.

Patient In Sitting Posture
Technique of lumbar puncture
Appropriate monitors must be connected.
Airway and resuscitation equipments are kept available.
Oxygen supplementation for all patients.
Skin is cleaned with sterile cleaning solution
The area is draped with a sterile central hole towel.
A small wheal of local anesthetic,2% lignocaine is injected at the site of
insertion.
The various approaches are;

1. Midline approach.
2. Paramedian approach
3. Taylor’s approach.
MIDLINE APPROACH
1. Iliac crests are palpated .The line between the two iliac crests intersects
L4 vertebra or L4-L5 space.
2. Palpate the interspace and the spinal needle is inserted.
3. The spinal needle passes through the following structures;
a.Skin
b.Subcutaneous tissue
c.Supraspinous ligament
d.Inter spinous ligament.
e.Ligamentum flavum.
f.Epidural space.
g.Duramater
h.Arachnoid mater
2.Paramedian or lateral approach
Two methods are available
First method is
The needle is inserted 1 cm lateral to the spinous process.
First structure to be felt is usually ligamentum flavum.
Then the needle is directed towards the midline.
Second method is
The needle is inserted 1 cm lateral and inferior to the interspace.
Lamina is encountered.
Walk through the lamina and enter the sub arachnoid space
PARAMEDIAN APPROACH OF LUMBAR PUNCTURE
3.TAYLOR APPROACH
A paramedian approach in which the needle is directed toward the L5-S1
interspace.
L5-S1 interspace is the largest space and can be tried if other methods fail.
It can be done in any position namely lateral decubitus, sitting or prone.
The needle is inserted at a point 1 cm medial and inferior to the posterior
superior iliac spine, then angled cephalad 45–55 degrees.
The needle is directed medially to reach the midline at the L5 spinous
process. The first significant resistance is the ligamentum flavum, and then the
dura mater is punctured.

.
Complications of spinal anesthesia
A.Local anesthetic induced neurotoxicity and neurological injury.
B.Cardio vascular instability.
C.High blockade.
D.Post dural puncture headache.
E.Transient neurological symptoms more common with lidocaine.
F.Permanent neurological injury.
1. Cauda equina syndrome.

2. Arachnoiditis.
3. Meningitis
4. Spinal hematoma formation.
Factors to be followed to reduce neurological complications
Absolute sterility.
Assurance of normal coagulation parmeters.
Lowest efficient dose of the drug.
Complete neurological examination before spinal anesthesia.
Use of preservative free solution.

MATERIALS AND METHODS
AIM OF THE STUDY
The purpose of this study was to investigate the effect of small single dose
intravenous dexmedetomidine administration on prolonging duration of
hyperbaric bupivacaine spinal anesthesia. Institutional ethical board committee
approval was obtained before the commencement of the study.
Sample size calculation
This study was a prospective randomized controlled study. Study population
comprised of 100 adult patients classified as ASA 1 or 2 who were scheduled for
total abdominal hysterectomy or vaginal hysterectomy under spinal anaesthesia.
INCLUSION CRITERIA
1) ASA grade I-II
2) Age < 60 years
3)Patients who were posted for Total abdominal Hysterectomy and vaginal
hysterectomy under spinal anesthesia.
EXCLUSION CRITERIA
1) Patients on sedatives/opioids/antidepressants in the week prior to
surgery.
2) Patients with morbid obesity.
3) Patients with diabetes and renal disease.
4) Pre-operative baseline heart rate equal to or less than 60/min
5) Pre-operative baseline systolic blood pressure equal to or less than 90
mm Hg.
All patients were examined on the day prior to surgery and pre anesthetic
evaluation chart was checked. Special consideration was given to elicit
hypertension, breathlessness, pain, cough, wheezing ,previous anesthesia and drug
sensitivity. The patient’s weight, height was measured. The nutritional status,
airway assessment, spine examination were also done on the previous day.
A detailed examination of all systems was done. Pre operative routine
investigations such as hematocrit ,renal function tests, complete blood count, blood
grouping, platelet count, chest radiography, electrocardiography were checked
properly.
All patients were informed about the procedure and written consent was
taken. All patients were kept nil per oral for 10 hours and were given
premedication with tablet alprazolam 0.5 milligram, tablet. ranitidine 150
milligrams and tablet metaclopramide 10 milligram on the night before surgery.

After putting the patient on operating table electrocardiography, peripheral
saturation of oxygen (SpO2) and non-invasive blood pressure monitor and all the
basal parameters were recorded. An IV access with 18 gauge cannula and all
patients were preloaded with Ringer lactate solution 10 ml/kg body weight.
Patients were randomly allocated to one of the two groups by slips in box
technique.
Patient was put in lateral decubitus position.Lumbar puncture was
performed at L3-L4 level with Quincke type 25 gauge spinal needle and injection
hyperbaric bupivacaine 17.5 mg was given intrathecally over 30 seconds. If there
was technical difficulty at L3- L4 level ,one more try was given at L2-L3 level
with Quinckes needle25 gauge. If found un successful those patients were
excluded from the study.
In group D patients received hyperbaric intrathecal bupivacaine anesthesia
3.5ml 0.5% (17.5 mg) and intravenous Dexmedetomidine 0.5mcg/Kg in10 ml
normal saline over 10 minutes.
In group C patients received Hyperbaric bupivacaine anaesthesia 3.5 ml
0.5% (17.5mg) and intravenous normal saline 10 ml over 10 minutes.

Vitals were recorded [Heart rate, Non invasive blood pressure monitoring,
pulseoximetry, Respiratory rate] every 5 min till the end of surgery and then every
5 min in post anaesthesia care unit.
MONITORING OF PATIENTS
Hypotension was defined as systolic BP of less than 90 mm Hg or 25%
lesser than the baseline value and was treated with 6 mg of Inj. Mephenteramine
intravenously.
Bradycardia was defined as heart rate <50/min and was treated Inj.
Atropine 0.6 mg.

ASSESSEMENT OF SENSORY BLOCKADE
Sensory blockade was checked with an alcohol swab in mid axillary line .
Sensory blockade was assessed after 5 minutes and there after maximum level of
blockade was noted . After this point surgery was started. Vitals monitored
through out the procedure. At the end of surgery, sensory level was noted. Two
dermatome regression time from the maximal level and regression to level S1was
noted every 20 min post operatively. Time of spinal injection was taken as 0.
ASSESSMENT OF MOTOR LEVEL

Motor level was assessed using Modified Bromage scale[38] at 5th minute and
every 20 min after the end of surgery.
1. BROMAGE0-Able to move hip, knee, ankle.
2. BROMAGE1-Unable to move hip ,but is able to move knee and ankle.
3. BROMAGE2-Unable to move hip and knee but is able to move the ankle.
4. BROMAGE3-Unable to move hip, Knee and ankle.
ASSESSMENT OF SEDATION
Sedation was assessed by Ramsay sedation scale[39] at the 5th minute. Again
sedation was assessed at the end of the surgery. Level of sedation was evaluated
every 20 minutes post operatively for 4 hours.
Ramsay Level of sedation scale.

1. Awake and anxious, agitated, or restless
2. Awake, cooperative, accepting ventilation, oriented, tranquil
3. Awake; responds only to commands
4. Asleep; brisk response to light glabellar tap or loud noise
5. Asleep; sluggish response to light glabellar tap or loud noise
stimulus but does not respond to painful stimulus
6. Asleep; no response to light glabellar tap or loud noise
Patient Posted For Abdominal/Vaginal Hysterctomy Under
Spinal Anesthesia Selected According To Inclusion Criteria
Informed Consent Obtained
Patient Shifted Inside Operation Theatre
WHO Check List Carried Out
Group Alloted By Slips Of Paper In A Box Technique
Pulsoximetry,ECG Leads, NIBP Connected And Vitals
Checked And Recorded
Preloaded With Ringers Lactatate 10ml/Kg

Spinal Block Performed In The Lateral Decubitus
Position
Patient was placed in lateral decubitus position, Quinkes 25 gauge
needle was inserted . Sub arachnoid block performed by giving
0.5% hyperbaric bupivacaine 3.5 ml(17.5 mg) given over 30 seconds.

After Spinal Anesthesia Patient Was Put Back To
Supine Position
group D Group C
(dexmedetomidine group ( control group
selected
Selected randomly)
randomly)
Received
received intravenous
dexmedetomidine Iv normal saline given over 10 minutes
o.5 microgram per kg
given in 10 min
At the 5 th minute sensory block level checked with alcohol swab,motor
block level according to Modified Bromage scale,sedation score as per
Ramsay sedation score and noted in the master chart.
Surgery started vitals monitored continously
If heart rate fell below 50 inj. Atropine0.6 mg was given. If blood
pressure fell below 90/60 inj Mephenteramine 6 Mg Was given.

At The End Of Surgery Sensory Level, Grade Of Motor
Block , Sedation Score Noted
After this sensory level, grade of motor block , sedation score
checked every 20 minutes for 260 minutes. Continous
monitoring of vitals carried on till 260th minute.

RESULTS AND ANALYSIS
100 patients were enrolled in the study ,50 patients were randomly allocated
into the study group and 50 patients to the Control group. All 100 patients
successfully completed the protocol and they were included in the analysis of data.
The demographic data of the patients in the two groups were studied and the
analysis revealed no significant difference in both the groups. In the demographic
data the continuous variables studied were age, body mass index.
DEMOGRAPHIC DATA
Group Statistics
character
groupcode Number Mean Std. Deviation Std. Error Mean
study group 50 48.24 4.792 0.678
Age
control group 50 48.78 4.82 0.682
study group 50 53.64 2.905 0.411
wt
control group 50 53.2 2.399 0.339
study group 50 151.54 3.215 0.455

Height
control group 50 151.38 3.09 0.437
study group 50 23.39 1.67 0.24

BMI
control group 50 23.24 1.41 0.20
GRAPHIC REPRESENTATION OF DEMOGRAPHIC VARIABLES IN
BOTH THE GROUPS
From this graph as the line joining the means of both groups is a straight
line it is clearly evident that both the groups were similar in all the
characteristics like age, height, weight, BMI. As the study was conducted in
abdominal hysterectomy and vaginal hysterectomy only, the type of surgery and
the sex of the patients were not taken for comparison.

DESCRIPTIVE ANALYSIS OF DEMOGRAPHIC VARIABLES
Independent Samples Test

Levene's Test for Equality of Variances t-test for Equality of Means
character
95% Confidence Interval of the Dif erence
F P value t df Sig. (2-tailed) Mean Dif erence Std. Error Dif erence Lower Upper
Equal variances
Age 0.001 0.977 (NS) -0.562 98 0.576(NS) -0.54 0.961 -2.448 1.368
assumed
Equal variances
wt 0.809 0.371 0.826 98 0.411(NS) 0.44 0.533 -0.617 1.497
assumed
Equal variances
Height 0.258 0.612 0.254 98 0.8(NS) 0.16 0.631 -1.091 1.411
assumed
Equal variances
BMI 0.294 0.589 0.482 98 0.631(NS) 0.1487867 0.308793 -0.4640029 0.7615764
assumed
Demographic variables like age, weight, height and BMI were compared
using Levene’s test for equality of variances and independent sample T test The
p value was found not to be significant.

COMPARISON OF HEART RATE IN THE TWO GROUPS
THROUGHOUT THE STUDY PERIOD
Heart Rate STUDY CONTROL
PRE OP 86.44 84
MEAN HR at 5 min 74.14 75.9
MEAN HR at 20 mi 58.64 107
MEAN HR 40min 59.78 72.7
MEAN HR60 min 59.32 70.3
MEAN HR 80min 59.4 75.3
MEAN HR100min 60.6 69.8
MEAN HR120min 57.42 70.68
MEAN HR140min 63.22 77.06
MEAN HR 160min 62.86 74.36
MEAN HR 180min 66.2 70.87
MEAN HR 200min 63.54 77.01
MEAN HR 220min 70.56 82.01
MEAN HR 240min 73.8 85.19
MEAN HR 260min 72.9 78.2

120
100
80
60
40 STUDY
20 CONTROL
0
MEANHR5
MEANHR20
MEAN HR 160
MEAN HR 180
MEAN HR 200
MEAN HR 220
MEAN HR 240
MEAN HR 260
MEAN HR 40
MEAN HR 80
MEAN HR60
MEAN HR100
MEAN HR120
MEAN HR140
PRE OP
GRAPHIC REPRESENTATION OF MEAN HEART RATE THROUGH

OUT THE STUDY PERIOD
It is clearly evident that the mean heart rate pre operatively and 5 minutes
after spinal anesthesia was almost similar inboth the groups. But after this both
intra operatively and post operatively patients in the study group had significantly
lower heart rate than in the control group.

COMPARISON OF MEAN ARTERIAL PRESSURE IN BOTH THE
GROUPS THROUGH OUT THE STUDY PERIOD
Mean arterial pressure Study Control group
group
MEAN MAPat 5 min 90.29 76.6
MEANMAP at 20 min 82.92 84.4
MEAN MAPat 40 min 72.46 86.4
MEANMAPat 60 min 72.74 94.2

100
90
80
70
60
50
40
30 STUDY
20
CONTROL
10
0
MEANMAP20
MEANMAP60
MEANMAP80
MEANMAP100
MEANMAP120
MEANMAP140
MEANMAP160
MEANMAP180
MEANMAP200
MEANMAP220
MEANMAP240
MEANMAP260
MEAN MAP5
MEAN MAP40
GRAPHIC REPRESENTATION OF
MEAN ARTERIAL PRESSURE THROUGH OUT
THE STUDY PERIOD
This graph clearly depicts that the mean arterial pressure was comparatively
low in the study group which received dexmedetomidine than in the control group.
COMPARITIVE STATISTICAL ANALYSIS OF MEAN ARTERIAL
PRESSURE AND MEAN HEART RATE IN THE TWO GROUPS
Levene's Test t-test for

for Equality of Equality of
Variances Means
Sig. (2- Mean

F P value t df
tailed) Difference
Equal
MEANMAP variances 3.01 0.086 -32.98 98 0.0001*** -17.9047619
assumed
Equal
variances
MEANHR 11.41 0.001 -15.79 98 0.0001*** -13.3528571
not
assumed
Levene's Test t-test for
for Equality of Equality of
Variances Means
Sig. (2- Mean

F P value t df
tailed) Difference
Equal
MEANMAP variances 19.8 -0.084 1.387 98 0.0001*** -8.8009523
assumed
Equal
variances
MEANHR 28.2 -0.169 18.57 98 0.0001*** -4.2490475
not
assumed
Both groups were compared in terms of mean arterial pressure and mean
heart rate by independent sample test and Levene’s test for equality of variances
and the p value was found to be highly significant.

COMPARISON OF PATIENTS WHO RECEIVED ATROPINE IN BOTH
THE GROUPS
DEXMEDETOMIDINE
PARAMETER GROUP CONTROL GROUP
NO OF PATIENTS WHO
RECEIVED ATROPINE 10 2
In the dexmedetomidine a total of 10 patients recived atropine while only 2
patients in the control group received atropine.

ASSESSMENT OF MOTOR LEVEL AT 5 MINUTES
Percentage Study group Control group

Number of Percentage Number
patients of
patients
Bromage 3 50 100% 50 100%
At the 5th minute ,before the onset of surgery motor level was checked. All
the patients in both the groups were not able to move the hip and showed Bromage
grade 3. It is clear from this graph that there was no change in achieving the
maximal level in both the groups. Although the onset of motor block was not
compared in our study ,we could not make out any significant difference in both
the groups in the onset of sensory and motor blockade.

ASSESSMENT OF SENSORY LEVEL AT 5 MINUTES
It is evident from the graph that both in the study and control groups the
maximal level of block was the same.

MOTOR BLOCK AT 160 MIN
Motor Dexmedetomidine Control group
block group
At 160 Number Percentage Number Percentage
minutes of of
patients patients
B1 0 0% 8 16%
B2 7 14% 37 74%
B3 43 86% 5 10%
After 160 minutes of spinal anesthesia ,in the study group 43 out of 50
patients were not able to move the hip, knee and ankle .But in the control group,37
out of 50 patients were able to move only the ankle while 8 out of 50 were able to
move knee and ankle. Only 5 patients (10%) had Bromage 3 while 43 patients
(86%) in the study group had Bromage 3.

ASSESSMENT OF MOTOR BLOCK AFTER 160 MINUTES
Motor block was assessed using modified Bromage scale . This bar diagram
clearly depicts the significant difference in the motor block in both the groups.
ASSESSMENT OF SENSORY BLOCKADE AT 160 MIN
sensory level at 160 min STUDY GROUP CONTROL GROUP

NUMBER PERCENTAGE NUMBER PERCENTAGE
T10 0 0% 17 34%
T12 0 0% 28 56%
T6 24 48% 0 0%
T8 26 52% 5 10%
SENSORY BLOCK AT 160 MINUTE
Sensory block assessed at 160 minutes showed a level of T6 in 48% andT8
in 52% of the patients in the study group . In the control group it was T10 IN 34%
and T12 in 56% of the patient .Only 10% of thr patients in the control group
showed a level of T8.

COMPARISON OF DURATION OF MOTOR BLOCK IN TWO GROUPS
Group Statistics
PARAMETER Std. Std. Error
groups NUMBER Mean
Deviation Mean
DEXMEDETOMIDINE
50 243.6 17.0 2.4
TIME FOR MOTOR GROUP
BLOCK TO BECOME
BROMAGE O CONTROL GROUP 50 211.2 16.7 2.4
The time for the motor block to become B0 was 243±17.0 minutes in
the study group and in the control group it was 211.2±16.7 minutes. This
showed a significant prolongation of motor block in the dexmedetomidine group
with a p value of 0.001***.

95% CI of the
Equal variances F test t test Mean Std. Error
p value p value Lower Upper
assumed value value Difference Difference
TIME FOR MOTOR

BLOCK TO BECOME 0.223 0.638 9.605 0.001*** 32.4 3.373 25.706 39.094
BROMAGE O
COMPARISON OF DURATION OF SENSORY BLOCK IN TWO GROUPS
PARAMETER Group Statistics

groups NUMBER Mean Std. Std.
Deviation Error
Mean
TIME FOR DEXMEDETOMIDINE 50 255.2 8.6 1.2
SENSORY GROUP
LEVEL TO CONTROL GROUP 50 210.8 33.1 4.7
BECOME S1
The total time for sensory level to reach S1 was 255±8.6in the study group
while it was 210.8±33,1 in the control group. This also proved significant
prolongation in the study group with a p value of 0.001***.

95% CI of the
Equal variances F test t test Mean Std. Error
p value p value Lower Upper
assumed value value Difference Difference
TIME FOR SENSORY

7.281 0.008 9.172 0.001*** 44.4 4.841 34.793 54.007
LEVEL TO REACH S1
COMPARISON OF TIME OF TWO DERMATOME REGRESSION IN
TWO GROUPS
Group Statistics
PARAMETER Std. Std. Error
groups NUMBER Mean
Deviation Mean
DEXMEDETOMIDINE
TIME FOR 50 125.2 17.5 2.5
GROUP
REGRESSION FROM
MAXIMAL LEVEL CONTROL GROUP 50 94.6 18.9 2.7
The time for two dermatome regression from the maximal level was
125.2±17.5minutes in the study group and 94.6±18.9 in the control group. This
proved the significant prolongation of sensory block to regress from the maximal
level in the study group with a p value of 0.001 ***.

95% CI of the
F test t test Mean Std. Error
Equal variances assumed p value p value Lower Upper
value value Difference Difference
TIME FOR THE

REGRESSION OF
1.062 0.305 8.403 0.001*** 30.6 3.642 23.373 37.827
SENSORY LEVEL
FROM MAXIMUM
SEDATION LEVEL AT 140 MINUTES
At 140 minutes the patients who received dexmedetomidine remained
calm and sedated with Ramsay sedation grade of 3 or 2.
STUDY GROUP C ONTROL GROUP
Sedation Numberof Percentage Number of Percentage
140 min patients patients
R1 0 0.00% 45 90.00%
R2 12 24.00% 5 10.00%
R3 38 76.00% 0 0.00%
SEDATION SCALE AT 140 MINUTES

DISCUSSION
There has always been immense research to improve the effects of spinal
anesthesia by changing drug regimens and technical methods. Usually adjuvants
are added to hyperbaric bupivacaine and instilled intrathecally to prolong the
anesthetic effects. These adjuvants act perineurally or at different sites in the
spinal cord and exert their antinociceptive action. They prolong anesthesia and
decrease pain in the post operative period.
In the past clonidine, alpha 2 agonist has been used in oral, intrathecal,
intravenous routes to prolong spinal anesthesia. The previous studies have proved
that clonidine 30 micrograms is equivalent to dexmedetomidine 3 micrograms
intrathecally. The proven advantages of dexmedetomidine are minimal
depression of respiration cardioprotection, renoprotection and neuroprotection.
This prospective randomized controlled study conducted in 100 patients
who underwent abdominal/vaginal hysterectomy under spinal anesthesia
demonstrated that dexmedetomidine given in the dose of 0.5 microgram/kg
prolonged the sensory and motor block significantly.
Both the groups were comparable in demographic parameters like age,
weight, height and BMI. The mean age of all the patients in the dexmedetomidine
group was 48.24±4.7.The mean age of the patients in the control group was
48.78±4.82. The mean body mass index for all the patients in dexmedetomidine
group was 23.39±1.67.The mean body mass index for all the patients in the control
group was 23.24±1.41. They were compared using independent sample test and
Levene’s test for equality of variances and the p value was found not significant.
At the 80th minute the average mean arterial pressure in the
dexmedetomidine group was around 72 whereas in the control group it was around
90 . The mean heart rate of all the patients after 40 minutes of spinal
anesthesia was 72 in the control group whereas in the dexmedetomidine group
it was 58.Statistical analysis was done for mean arterial pressure and mean heart
rate and the p value was found to be highly significant. This has proved the fact
that dexmedetomidine has got a definite role in hypotensive anesthesia.
In our study the number of patients who received atropine was more than
in the control group because of bradycardia caused by dexmedetomidine induced
sympatholysis. In the dexmedetomidine group 10 out of 50 patients needed
atropine whereas in the control group only 2 patients needed atropine. This
bradycardia promptly responded to Inj. Atropine 0.6mg intravenously. During our
study there was no other adverse effect of dexmedetomidine observed in the study
group. This may be due to the fact that we had used only moderate dose of
dexmedetomidine as a single intravenous injection given slowly over 10 minutes.
At the fifth minute of spinal anesthesia ,grade of motor level and sensory
level was checked. All the patients in both the groups were not able to move the
hip and showed Bromage 3. All the patients in both the groups had a sensory level
of T4.This showed that there was no difference in achieving the maximum motor
and sensory level in both the groups.
At the 160th minute of spinal anesthesia grade of motor level was Bromage 3
in 43 patients in the dexmedetomidine group(86%). But in the control group only
5 patients(10%) had Bromage grade 3.This demonstrated that there was a
prolongation of motor block in the dexmedetomidine group.
At the 160th minute of spinal anesthesia,24 patients(48%) had a sensory
level of T6 in the dexmedetomidine group. But in the control group no patient had
a sensory level of T6.In the control group,17 patients (34%) had a sensory level of
T10. This was the maximum level seen at 160th minute in the control group.
The time for the motor block to become Bromage grade 0 was
243±17.0 minutes in the dexmedetomidine group and in the control group it
was 211.2±16.7 minutes. This on statistical analysis by independent sample test
and t test for equality of means showed a significant prolongation of motor block
in the dexmedetomidine group with a p value of 0.001***.
Al Mustafa et al. in their study in 48 patients had demonstrated similar
prolongation 199 ± 42.8 min vs. 138.4 ± 31.3 min (P < 0.05). They had given
isobaric bupivacaine 12.5 mg for spinal block In our study the total duration of
motor block was more in both the control and study groups when compared to Al
mustafa et al . This may be due to the fact that we had given hyperbaric
bupivacaine 17.5 mg.
Dinesh et al had done a similar study in 100 patients with 15 mg of
hyperbaric bupivacaine and they had given dexmedetomidine 1 microgram/kg as
a loading dose and 0.5 microgram/kg/hour as maintenance dose. They
demonstrated the regression time to reach the modified Bromage scale 0 was
significantly prolonged in the dexmedetomidine group (220.7 ± 16.5 min)
compared to the control group (131.6 ± 10.5 min).
In our study, the total time for sensory level to reach S1 was 255±17.5in the
study group while it was 210.8±33.1 in the control group. Dinesh et al had
demonstrated that the total duration of sensory blockade was significantly
prolonged in the dexmedetomidine group (269.8 ± 20.7 min) whereas it was 169
minutes in the control group (169.2 ± 12.1) . We had got the almost similar to
the results seen in other studies. Al Mustafa et al., whose study formed the basis
of our dissertation had 261.5 ± 34.8 min in the study group vs. 165.2 ± 31.5 min
in the control group (P < 0.05. Dexmedetomidine group had higher level of
sensory block compared to the control group in our study, similar to the study
results of Kaya et al.
In our study the time for two dermatome regression from the maximal level
was 125.2±17.5minutes in the study group and 94.6±18.9 in the control group.
This proved the significant prolongation of sensory block to regress from the
maximal level in the dexmedetomidine group with a p value of 0.001***. This
showed the prolongation of sensory block by intravenous dexmedetomidine.
Dinesh et al had given 15 mg of hyperbaric bupivacaine . They had given
dexmedetomidine 1 microgram/kg as a loading dose and 0.5 microgram/kg/hour as
maintenance dose. They demonstrated that the mean time for two-dermatomal
regression of sensory block was significantly prolonged in the group that received
dexmedetomidine (137.4 ± 10.9 min) compared to the other group (102.8 ± 14.8).
Sudhesh,K.Harsoor in the article dexmedetomidine a wonder drug has
clearly mentioned about the transient hypertensive response when
dexmedetomidine is given in the dose of 1-4 microgram/kg. Jia Song et al in the
article titled dexmedetomidine for sedation in patients undergoing surgery under
regional anesthesia has clearly mentioned that as the dose increased the incidence
of hypotension also increased. In their study they had given a loading dose of 1
microgram/kg and they had advised that maintenance dose 0.25
microgram/kg/hour may be most appropriate if severe bradycardia and
hypotension have to be avoided. Dexmedetomidine is given intravenously in doses
ranging from 0.1 to 1 g/kg/h but higher doses is usually associated with a
significant incidence of bradycardia and hypotension. Aantaa et al., had concluded
that “The optimal dose of dexmedetomidine for single dose intravenous
premedication in minor surgery has wide safety margins in the range of 0.33 to
0.67 g/kg”. Hence we selected a dose of 0.5 g/kg in our study. While deciding
on the dose of single intravenous dose of dexmedetomidine these articles were
given utmost importance.
We decided on the dose 0.5microgram/kg to be given slowly over 10
minutes so as to avoid side effects and to get the desirable therapeutic effect.
When given intravenously the half life of dexmedetomidine is 2-3 hours. All the
patients were closely monitored for 5 hours. This is a great advantage of
dexmedetomidine over clonidine whose half life is 6-10 hours.
In our study no patient had transient hypertension . The transient
hypertensive response due to peripheral alpha2 receptor stimulation occurs when
dexmedetomidine is given in the dose more than 1 microgram/kg.
Post operatively when the sensory level touched T12-L1 most of our
patients complained of pain with some discomfort. Rescue analgesic Inj.
Paracetamol 1gram intravenously was administered to those patients who
complained.
It is a common practice to sedate patients with midazolam who are under
spinal anesthesia. Kaya etal in their article had compared midazolam and
dexmedetomidine and had clearly explained about the superiority of
dexmedetomidine over midazolam.

Intraoperatively the patients in the study group showed significantly high
sedation scores than in the control group. In their study’ Kaya et al had reported
about the paradoxical reactions of midazolam when given in high doses.
Dexmedetomidine is unique in causing arousable sedation. All patients who
received dexmedetomidine had good sedation score through out the intra
operative period ( Ramsay sedation score R3-R2)compared to the control group .

th
At 140 minute 76% of the patients in dexmedetomidine group remained sedated
with the grading of Ramsay 3.
We had assessed sedation level at the 5th minute and then at the end of
surgery. The average duration of the surgery was around 130 minutes. The peak
action of dexmedetomidine is around 10-20 minutes. We could see the patients
sleeping well when the surgery was going on. Some patients snored but there was
no incidence of desaturation.
All patients in the study and control group were given oxygen at the rate
of 2 liters/minute through ventimask. This clearly demonstrated the nature of
dexmedetomidine in causing arousable sedation without respiratory depression.
As dexmedetomidine do not affect synthesis ,storage or metabolism of
catecholamines its actions can be easily reversed by vasopressors or
anticholinergics. The availability of antagonist Atipamezole with similar
distribution and elimination characteristics is a great advantage for

dexmedetomidine over other anesthetic agents. Atipamezole is of particular use in
reversing the sedative effects of dexmedetomidine. In our study bradycardia
caused by dexmedetomidine promptly responded to anticholinergics.

CONCLUSION
Dexmedetomidine in the dose of 0.5 microgram/kg given as single
intravenous dose to patients who underwent abdominal/vaginal hysterectomy
under spinal anesthesia significantly prolonged the duration of sensory and motor
blockade. There was also significant prolongation of the time for the two segment
dermatome regression in the dexmedetomidine group compared to the control
group. All these effects were achieved without causing deep level of sedation and
with minimal hemodynamic side effects.

SL.No. NAME IP NO PRE OP DRUG 20 MIN 40 MIN 60MIN
AGE WEIGHTHEIGHT BMI ASA BP HR AFTER 5 MIN
DIA SYS HR DRUG MOTOR
SENSORY
SEDATION
SYS DIA BP HR DRUG MOTOR
SENSORYSEDATION
BP HR DRUG MOTORSENSORYSEDATION
BP HR
68 BANUMATHY 43 57 154 24.0344 1 22163896 145/90 102 NS 82 124 73 B3 T4 R1 100 70 100/70 89 123/84 73 112/76 71
69 NEELA 44 56 154 23.6128 1 12410869 134/86 99 NS 70 119 68 B3 T4 R1 109 78 126/76 80 120/76 78 112/56 67
70 SUGANTHI 55 55 150 24.4444 1 14411811 144/74 98 DEX 0.5 mcg/Kg78 132 67 B3 T4 R4 98 68 100/67 60 98/72 60 M6 111/77 50
71 MUNIYAMMAL43 50 149 22.5215 1 2288096 110/80 87 DEX 0.5 mcg/Kg80 140 92 B3 T4 R4 99 67 128/88 68 100/78 56 90/56 58
72 PAPPATHY 56 54 154 22.7694 1 16972056 144/74 86 NS 65 98 78 M6 B3 T4 R1 90 78 90/78 70 M6 100/68 67 100/76 70
73 JAYAMALADEVI46 50 150 22.2222 1 43808024 158/84 69 NS 76 109 87 B3 T4 R1 92 68 98/78 67 110/67 76 98/87 78
74 SASIKALA 47 56 143 27.3852 2 20743083 150/100 78 DEX 0.5 mcg/Kg57 108 60 M6 B3 T4 R3 100 89 100/89 56 A0.6 100/80 50 A0.6 100/78 56
75 RAMANI 40 50 154 21.0828 1 15619413 136/84 87 NS 78 110 78 B3 T4 R1 109 78 109/78 69 98/68 76 M6 100/70 78
76 JAYALAKSHMI 42 55 152 23.8054 1 21413547 146/80 87 DEX 0.5 mcg/Kg67 129 70 B3 T4 R4 100 78 100/78 50 A0.6 98/78 54 A0.6 90/50 62
77 GOMATHI 44 50 148 22.8269 1 15931401 130/92 78 DEX 0.5 mcg/Kg65 109 58 B3 T4 R4 122 90 98/78 58 90/78 67 M6 98/78 58
78 ARPUDAM 47 53 149 23.8728 2 16541215 160/80 79 NS 67 110 65 B3 T4 R1 123 89 100/87 78 110/89 77 112/78 66
79 CHINNAPONNU46 54 149 24.3232 1 124/88 76 NS 78 98 65 M6 B3 T4 R1 124 87 100/70 56 100/78 62 110/78 61
80 LILLY 45 55 150 24.4444 1 136/78 77 NS 90 140 87 B3 T4 R3 100 60 116/76 60 106/68 66 99/86 78
81 KAVITHA 46 56 151 24.5603 1 17746051 132/68 79 DEX 0.5 mcg/Kg80 140 92 B3 T4 R4 99 67 128/88 68 100/78 56 90/56 58
82 KUMARI 46 49 148 22.3703 2 21716914 134/69 78 NS 65 98 78 M6 B3 T4 R1 90 78 90/78 70 M6 100/68 67 100/76 70
83 KASTHURI 50 56 150 24.8889 1 21155291 120/80 76 NS 76 109 87 B3 T4 R1 92 68 98/78 67 110/67 76 98/87 78
84 CHANDRA 51 52 152 22.5069 1 11818766 134/67 75 DEX 0.5 mcg/Kg57 108 60 M6 B3 T4 R3 100 89 100/89 56 A0.6 100/80 50 A0.6 100/78 56
85 RAJALAKSHMI 52 53 154 22.3478 1 13871711 122/78 74 NS 78 110 78 B3 T4 R1 109 78 109/78 69 98/68 76 M6 100/70 78
86 AMUL 54 53 155 22.0604 1 16830219 120/78 65 DEX 0.5 mcg/Kg67 129 70 B3 T4 R4 100 78 100/78 50 A0.6 98/78 54 A0.6 90/50 62
87 VIJAYAKSHMI 55 54 156 22.1893 1 20030759 144/89 66 DEX 0.5 mcg/Kg65 109 58 B3 T4 R4 122 90 98/78 58 90/78 67 M6 98/78 58
88 SHANTHI 56 57 153 24.3496 1 21488650 140/80 68 NS 67 110 65 B3 T4 R1 123 89 100/87 78 110/89 77 112/78 66
89 JOTHI 54 56 154 23.6128 1 20513236 136/84 90 NS 78 98 65 M6 B3 T4 R1 124 87 100/70 56 100/78 62 110/78 61
90 GIRIJA 51 55 150 24.4444 1 20816437 136/84 89 NS 90 140 87 B3 T4 R3 100 60 116/76 60 106/68 66 99/86 78
91 CHANDRA 46 56 151 24.5603 1 21925194 146/80 88 NS 78 98 65 M6 B3 T4 R1 123 89 100/70 89 100/78 76 110/78 61
92 MAYA 46 49 148 22.3703 2 14004768 130/92 102 NS 78 122 87 B3 T4 R1 124 87 119/89 98 119/87 77 100/67 76
93 SIVASANKARI 50 56 150 24.8889 1 15067666 134/86 99 NS 82 124 73 B3 T4 R1 100 70 100/70 89 123/84 73 112/76 71
94 MALA 51 52 152 22.5069 1 22500301 144/74 98 NS 70 119 68 B3 T4 R1 109 78 126/76 80 120/76 78 112/56 67
95 MINI 52 53 154 22.3478 1 22180993 122/68 87 DEX 0.5 mcg/Kg78 132 67 B3 T4 R4 98 68 100/67 60 98/72 60 M6 111/77 50
96 KALAVATHY 54 53 155 22.0604 1 20859793 122/78 74 DEX 0.5 mcg/Kg80 140 92 B3 T4 R4 99 67 128/88 68 100/78 56 90/56 58
97 SHAHEEN BEGUM
55 54 156 22.1893 1 10331987 120/78 65 NS 65 98 78 M6 B3 T4 R1 90 78 90/78 70 M6 100/68 67 100/76 70
98 GEETHA 56 57 153 24.3496 1 14292770 144/89 66 NS 76 109 87 B3 T4 R1 92 68 98/78 67 110/67 76 98/87 78
99 CHIMRA 54 56 154 23.6128 1 13335215 140/80 68 DEX 0.5 mcg/Kg57 108 60 M6 B3 T4 R3 100 89 100/89 56 A0.6 100/80 50 A0.6 100/78 56
100 SAGAYAMARY 51 52 152 22.5069 1 16754259 136/84 90 NS 78 110 78 B3 T4 R1 109 78 109/78 69 98/68 76 M6 100/70 78
60MIN 80 MIN 100 MIN 120 MIN 140 MIN 160 MIN
DRUG MOTORSENSORY
SEDATION
BP HR DRUG MOTOR SENSORYSEDATION
BP HR DRUGMOTOR SENSORYSEDATION
BP HR DRUG MOTORSENSORY
SEDATION
110/87 87 122/78 70 132/86 79 B3 T8 R1 110/70 88 B2 T10 R1 112/67 78 B2 T10 R1
M6 110/78 88 112/89 68 110/65 65 B2 T8 R1 128/87 87 B2 T10 R1 112/87 87 B2 T12 R1
A0.6 100/68 60 100/68 60 B3 T4 R3 122/78 50 A0.6 B3 T4 R3 130/80 60 B3 T6 R3 110/78 60 B3 T6 R2
M6 89/56 52 M6 110/78 62 B3 T4 R3 112/67 58 B3 T6 R3 100/78 62 B3 T6 R3 122/82 66 B2 T8 R2
111/87 67 12O/80 70 B3 T6 R1 113/59 67 B3 T8 R1 110/88 77 B3 T10 R1 138/78 78 B2 T12 R1
100/789 78 108/78 68 B3 T4 R1 100/76 77 B3 T8 R1 132/86 77 B3 T10 R1 123/68 79 B2 T12 R1
A0.6 112/67 56 128/86 60 B3 T4 R4 98/78 65 B3 T4 R3 110/65 62 B3 T6 R3 147/98 67 B3 T6 R3
113/78 65 106/68 68 B3 T4 R1 102/70 78 B3 T8 R1 122/78 75 B2 T10 R1 120/80 76 B2 T12 R1
M6 114/69 60 100/76 65 B3 T6 R4 100/70 56 B3 T6 R4 112/67 57 B3 T6 R3 12O/78 50 A0.6 B3 T6 R3
112/56 59 98/67 59 B3 T6 R4 102/76 58 B3 T4 R3 113/59 58 B3 T6 R3 112/80 58 B3 T8 R3
122/78 87 110/87 77 B3 T6 R1 104/67 77 B3 T8 R1 100/76 69 B2 T10 R1 110/78 67 B2 T12 R1
100/76 67 110/80 56 B3 T6 R1 122/78 54 B2 T8 R1 109/78 57 B2 T8 R1 132/87 60 B2 T10 R1
93/58 69 M6 100/68 68 99/70 50 A0.6 B3 T6 R3 100/68 77 B3 T8 R2 110/76 62 B3 T8 R1
M6 89/56 52 M6 110/78 62 B3 T4 R3 112/67 58 B3 T6 R3 100/78 62 B3 T6 R3 122/82 66 B2 T8 R2
111/87 67 12O/80 70 B3 T6 R1 113/59 67 B3 T8 R1 110/88 77 B3 T10 R1 138/78 78 B2 T12 R1
100/789 78 108/78 68 B3 T4 R1 100/76 77 B3 T8 R1 132/86 77 B3 T10 R1 123/68 79 B2 T12 R1
A0.6 112/67 56 128/86 60 B3 T4 R4 98/78 65 B3 T4 R3 110/65 62 B3 T6 R3 147/98 67 B3 T6 R3
113/78 65 106/68 68 B3 T4 R1 102/70 78 B3 T8 R1 122/78 75 B2 T10 R1 120/80 76 B2 T12 R1
M6 114/69 60 100/76 65 B3 T6 R4 100/70 56 B3 T6 R4 112/67 57 B3 T6 R3 12O/78 50 A0.6 B3 T6 R3
112/56 59 98/67 59 B3 T6 R4 102/76 58 B3 T4 R3 113/59 58 B3 T6 R3 112/80 58 B3 T8 R3
122/78 87 110/87 77 B3 T6 R1 104/67 77 B3 T8 R1 100/76 69 B2 T10 R1 110/78 67 B2 T12 R1
100/76 67 110/80 56 B3 T6 R1 122/78 54 B2 T8 R1 109/78 57 B2 T8 R1 132/87 60 B2 T10 R1
93/58 69 M6 100/68 68 99/70 50 A0.6 B3 T6 R3 100/68 77 B3 T8 R2 110/76 62 B3 T8 R1
100/76 67 110/80 76 B3 T6 R1 122/78 78 B2 T8 R1 109/78 81 B2 T10 R1 132/87 71 B2 T10 R1
98/67 78 122/90 78 124/78 80 B2 T8 R1 112/87 80 B2 T10 R1 120/80 77 B1 T10 R1
110/87 87 122/78 70 132/86 79 B3 T8 R1 110/70 88 B2 T10 R1 112/67 78 B2 T10 R1
M6 110/78 88 112/89 68 110/65 65 B2 T8 R1 128/87 87 B2 T10 R1 112/87 87 B2 T12 R1
A0.6 100/68 60 100/68 60 B3 T4 R3 122/78 50 A0.6 B3 T4 R3 130/80 60 B3 T6 R3 110/78 60 B3 T6 R2
M6 89/56 52 M6 110/78 62 B3 T4 R3 112/67 58 B3 T6 R3 100/78 62 B3 T6 R3 122/82 66 B2 T8 R2
111/87 67 12O/80 70 B3 T6 R1 113/59 67 B3 T8 R1 110/88 77 B3 T10 R1 138/78 78 B2 T12 R1
100/789 78 108/78 68 B3 T4 R1 100/76 77 B3 T8 R1 132/86 77 B3 T10 R1 123/68 79 B2 T12 R1
A0.6 112/67 56 128/86 60 B3 T4 R4 98/78 65 B3 T4 R3 110/65 62 B3 T6 R3 147/98 67 B3 T6 R3
113/78 65 106/68 68 B3 T4 R1 102/70 78 B3 T8 R1 122/78 75 B2 T10 R1 120/80 76 B2 T12 R1
180 MIN 200 MIN 220 MIN 240 MIN 260 MIN 280 MIN
BP HR DRUG MOTOR SEDATION
BP HR DRUGMOTOR SENSORY
SEDATION
BP HR DRUG MOTOR SENSORY SEDATION
BP HR DRUGMOTOR SENSORY SEDATION
BP HR DRUGMOTORSENSORYSEDATION
BP HR SPO2
110/78 77 B2 L2 R1 136/84 71 B1 S2 R1 122/78 89 B0 S2 R1 135/87 80 B0 S2 R1 138/89 87 B0 S2 R1
98/76 77 A0.6 B3 T8 R2 130/92 56 B2 T10 R2 136/84 98 B1 L3 R1 136/86 71 B0 S2 R1 124/78 78 B0 S2 R1
132/80 53 B1 L2 R1 128/67 77 B0 S2 R1 132/80 78 B0 L3 R1 128/89 80 B0 S2 R1 132/76 80 B0 S2 R1
109/78 56 B1 L2 R1` 147/98 89 B0 S2 R1 132/80 70 B0 S1 R1 130/80 82 B0 S2 R1 132/76 89 B0 S2 R1
112/87 65 B3 T8 R3 120/80 66 B2 T10 R2 109/78 67 B2 T12 R2 140/88 69 B1 T12 R2 138/89 69 B0 S2 R1
110/70 76 B1 L2 R1 12O/78 76 B0 L4 R1 112/87 80 B0 S2 R1 145/95 98 B0 S2 R1 122/78 78 B0 S2 R1
130/80 51 A0.6 B2 T8 R3 100/60 62 B2 T10 R2 128/87 62 B2 T12 R2 138/89 70 B1 L2 R2 136/84 71 B0 S2 R1
100/78 76 B1 L2 R1 98/67 89 B0 L4 R1 130/80 89 B0 S1 R1 122/78 89 B0 S2 R1 146/80 53 B0 S2 R1
12O/78 65 B2 T12 R1 122/78 66 B1 L2 R1 132/76 68 B1 S1 R1 134/87 69 BO S2 R1 145/95 56 B0 S2 R1
124/78 67 B2 T8 R1 112/76 67 B1 T10 R1 123/89 77 B0 L1 R1 132/76 76 B0 L3 R1 144/86 56 B0 S2 R1
130/80 51 A0.6 B2 T8 R3 100/60 62 B2 T10 R2 128/87 62 B2 T12 R2 138/89 70 B1 L2 R2 136/84 71 B0 S2 R1
100/78 76 B1 L2 R1 98/67 89 B0 L4 R1 130/80 89 B0 S1 R1 122/78 89 B0 S2 R1 146/80 53 B0 S2 R1
12O/78 65 B2 T12 R1 122/78 66 B1 L2 R1 132/76 68 B1 S1 R1 134/87 69 BO S2 R1 145/95 56 B0 S2 R1
124/78 67 B2 T8 R1 112/76 67 B1 T10 R1 123/89 77 B0 L1 R1 132/76 76 B0 L3 R1 144/86 56 B0 S2 R1
12O/78 76 B2 L2 R1 122/78 78 B1 S1 R1 132/76 98 B1 S2 R1 134/87 88 BO S2 R1 145/95 90 B0 S2 R1
280 MIN 300 MIN
DRUG MOTOR SENSORY SEDATION BP HR SPO2 DRUG MOTOR SENSORY SEDATION BP HR SPO2 DRUG MOTOR SENSORY SEDATION BP HR SPO2 DRUG MOTOR SENSORY
SEDATION
BIBLIOGRAPHY
1. Collins VJ. Spinal anaesthesia principles. In: Cann CC, DiRienzi DA, editors.
Principles of Anaesthesiology, General and Regional Anaesthesia. 3rd ed.
Philadelphia: Lea and Febiger; 1993. p. 1484.
2. Brown DL. Spinal epidural and caudal anaesthesia. In: Miller RD, Eriksson LI,
Fleisher LA, Wiener-Kronish GP, Young WL, editors. Millers’ Anaesthesia.
7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010. p. 1624.
3. Hohener D, Blumenthal S, Borgeat A. Sedation and regional anaesthesia in the
adult patient. Br J Anaesth. 2008;100:8–16.
4. De Andres J, Valia JC, Gil A, Bolinches R. Predictors of patient satisfaction
with regional anesthesia. Reg Anesth. 1995;20:498–505.
5. Rhee K, Kang K, Kim J, Jeon Y. Intravenous clonidine prolongs bupivacaine
spinal anesthesia. Acta Anaesthesiol Scand. 2003;47:1001–5.
6. Reves JG, Glass P. Intravenous anesthetics. In: Miller RD, Eriksson LI,
Fleisher LA, Wiener-Kronish GP, Young WL, editors. Miller's Anaesthesia.
7th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2010. p. 756.
7. Jorm CM, Stamford JA. Actions of the hypnotic anaesthetic,
dexmedetomidine, on noradrenaline release and cell firing in rat locus
coeruleus slices. Br J Anaesth. 1993;71:447–9.

8. Kanazi GE, Aouad MT, Jabbour-Khoury SI, Al Jazzar MD, Alameddine MM,
Al-Yaman R, et al. Effect of low-dose dexmedetomidine or clonidine on the
characteristics of bupivacaine spinal block. Acta Anaesthesiol Scand.
2006;50:222–7.
9. Kaya FN, Yavascaoglu B, Turker G, Yildirim A, Gurbet A, Mogol EB, et al.
Intravenous dexmedetomidine, but not midazolam, prolongs bupivacaine
spinal anesthesia. Can J Anaesth.2010;57:39–45.
10.Al-Mustafa MM, Badran IZ, Abu-Ali HM, Al-Barazangi BA, Massad IM, Al-
Ghanem SM. Intravenous dexmedetomidine prolongs bupivacaine spinal
analgesia. Middle East J Anesthesiol. 2009;20:225–31.
11.Aantaa R, Kanto J, Scheinin M, Kallio A, Scheinin H Dexmedetomidine, an
alpha 2-adrenoceptor agonist, reduces anesthetic requirements for patients
undergoing minor gynecologic surgery. Anesthesiology.1990 Aug;73(2)230-5.
12. Khaled Taha Analgesic ,sedative and hemodynamic effects of
Dexmedetomidine following major abdominal surgeries;A randomized ,double
blinded comparative study with morphine .Egyptian journal of hospital
medicine vol 12 113-120.

13.Murat Tekin, MD,1,a Ismail Kati, MD,1 Yakup Tomak, MD,1 and Erol Kisli,
MD2 Effect of Dexmedetomidine IV on the Duration of Spinal Anesthesia
with Prilocaine: A Double-Blind, Prospective Study in Adult Surgical Patients
C urr Ther Res Clin Exp. Sep 2007; 68(5): 313–324
14. Menon DV, Wang Z, Fadel PJ, Arbique D, Leonard D, Li JL, Victor RG,
Vongpatanasin W. Central sympatholysis as a novel countermeasure for
cocaine-induced sympathetic activation and vasoconstriction in humans Am
Coll Cardiol. 20 J 07 Aug 14;50(7):626-33. Epub 2007 Jul 30
15. Ok HG, Baek SH, Baik SW, Kim HK, Shin SW, Kim KH. Optimal dose of
dexmedetomidine for sedation during spinal anesthesiaKorean J Anesthesiol.
2013 May;64(5):426-31.
16.Annamalai A, Singh S, Singh A, Mahrous DE (2013) Can Intravenous
Dexmedetomidine Prolong Bupivacaine Intrathecal Spinal Anesthesia? J
Anesth Clin Res 4:372. doi: 10.4172/2155-6148.
17. Jia Song, Woong-Mo Kim, [...], and Myung Ha Yoon Dexmedetomidine for
sedation of patients undergoing elective surgery under regional anesthesia
Korean J Anesthesiol. Sep 2013; 65(3): 203–208
18.SS Harsoor, D Devika Rani, [...], and SS Nethra Effect of supplementation of
low dose intravenous dexmedetomidine on characteristics of spinal anaesthesia
with hyperbaric bupivacaine I ndian J Anaesth. 2013 May-Jun 57(3): 265–269.

19.Abdallah FW1, Abrishami A, Brull R.The facilitatory effects of intravenous
dexmedetomidine on the duration of spinal anesthesia: a systematic review and
meta-analysis Anesth Analg. 2013 Jul;117(1):271-5.
20.Seung Hwan Jung The effects of single-dose intravenous dexmedetomidine
on hyperbaric bupivacaine spinal anesthesia Journal of AnesthesiaJune
2013, Volume 27, Issue 3, pp 380-384
21.Reddy VS, Shaik NA, Donthu B, Reddy Sadennala VK, Jangam Intravenous
of bupivacaine dexmedetomidine versus clonidine for prolongation spinal
anesthesia.J Anaesthesiol Clin Pharmacol. 2013 Jul; 29(3):342-7.
22.Dinesh CN, Sai Tej NA, Yatish B, Pujari VS, Mohan Kumar RM, Mohan
CV.Effect of intravenous dexmedetomidne on hyperbaric bupivacaine spinal
anesthesia Saudi J Anaesth. 2014 Apr; 8(2):202-8.
23. Park SH, Shin YD, Yu HJ, Bae JH, Yim KH. Comparison of two dosing
schedules of intravenous dexmedetomidine in elderly patients during spinal
anesthesia.KoreanJAnesthesiol. 2014May;66(5):371-6.
24. JyotsanaS.paranjpe Dexmedetomidine;expanding role in anesthesia medical
journal of D.Y.Patil university /jan-mar2013/vol 6/issue
25. Sudheesh K, Harsoor S. Dexmedetomidine in anaesthesia practice: A wonder
drug? Indian J Anaesth. 2011;55:323–4. [PMC free article].

26. Ralph Gertler, MD, H. Cleighton Brown, MD, [...], and Erin N. Silvius, MD
Dexmedetomidine: a novel sedative-analgesic agent Proc (Bayl Univ Med
Cent). Jan 2001; 14(1): 13–21
27. Alquist RP. A study of adrenergic receptors. Am J Physiol. 1948;153:586–589.
28. Drew GM, Whiting SB. Evidence for two distinct types of postsynaptic alpha-
adrenoceptor in vascular smooth muscle in vivo. Br J Pharmacol.
1979;67:207–9
29. Jaakola ML, Salonen M, Lehtinen R, Scheinin H. The analgesic action of
dexmedetomidine – A novel alpha 2-adrenoceptor agonist – In healthy
volunteers. Pain. 1991;46:281–5.
30. Jones JG, Taylor PM. Receptor-specific reversible sedation: dangers of
vascular effects. Anesthesiology. 1999;90:1489–1490.
31. Scheinin B, Lindgren L, Randell T, Scheinin H,Scheinin M. Dexmedetomidine
attenuates sympathoadrenal responses to tracheal intubation and reduces the
need for thiopentone and perioperative fentanyl. Br J.Anaesth.1992;68:126–
131.
32. Aantaa R, Jaakola ML, Kallio A, Kanto J. Reduction of the minimum alveolar
concentration of isoflurane by dexmedetomidine. Anesthesiology.
1997;86:1055–1060.
33. Taittonen MT, Kirvela OA, Aantaa R, Kanto JH. Effect of clonidine and
dexmedetomidine premedication on perioperative oxygen consumption and
haemodynamic state. Br J Anaesth. 1997;78:400–406.
34. Bührer M, Mappes A, Lauber R, Stanski DR, Maitre PO. Dexmedetomidine
decreases thiopental dose requirement and alters distribution
pharmacokinetics. Anesthesiology. 1994;80:1216–1227.
35. Zornow MH, Maze M, Dyck JB, Shafer SL. Dexmedetomidine decreases
cerebral blood flow velocity in humans. J Cereb Blood Flow Metab.
1993;13:350–353.
36. Dexmedetomidine premedication attenuates ketamine-induced
cardiostimulatory effects and postanesthetic deliriumLevänen J1, Mäkelä ML,
Scheinin H.
37.Venn RM, Bradshaw CJ, Spencer R, Brealey D, Caudwell E, Naughton C,
Vedio A, Singer M, Feneck R, Treacher D, Willatts SM, Grounds RM.
Preliminary UK experience of dexmedetomidine, a novel agent for
postoperative sedation in the intensive care unit. Anaesthesia. 1999;54:1136–
1142.
38.Bromage PR, Burfoot MF, Crowell DE, Pettigrew RT. Quality of epidural
blockade. I. influence of physical factors. Br J Anaesth. 1964;36:342–52.
39.Ramsay MA, Savege TM, Simpson BR, Goodwin R. Controlled sedation with
alphaxalone-alphadolone. Br Med J. 1974;2:656–9.

PATIENT CONSENT FORM
Study title
Effect of intravenous dexmedetomidine on prolonging spinal anesthesia, a randomized
controlled study
Study centre : ESI – PGIMSR, K.K.NAGAR, CHENNAI -78
Participant name : Age: Sex:
I confirm that I have understood the purpose of procedure for the above study . I have the
opportunity to ask the question and all my questions and doubts have been answered to my
satisfaction.
I have been explained about the pitfall in the procedure. I have been explained about the
safety, advantage and disadvantage of the technique. I understand that my participation in the study
is voluntary and that I am free to withdraw at anytime without giving any reason.
I understand that investigator, regulatory authorities and the ethics committee will not need
my permission to look at my health records both in respect to current study and any further research
that may be conducted in relation to it, even if I withdraw from the study . I understand that my
identity will not be revealed in any information released to third parties or published , unless as
required under the law . I agree not to restrict the use of any data or results that arise from the study.
I understand that that I will receive drugs intravenously to prolong spinal anesthesia. I will
receive Inj. Dexmedetomidine ,intravenously . I have been explained that the anesthetic technique is
a standard and approved technique. I have been explained that the drug will cause sleep and a
reduction in heart rate. This may help in future research in the field of anesthesia. I consent to
undergo this procedure
Insurance No:
Date: Signature / thumb impression of
Patient
B´ÄUPõÚ J¨¦uÀ £iÁ®
PROFORMA
Name of the patient:
Age:
Sex Wt:
Insurance No: OT:
Diagnosis: Duration of Procedure:
Surgeon: Anaesthetist
PREOPERATIVE DETAILS
ASA Grade Remarks:
vitals
BP Pulse Resp. SpO2 Temp ECG Xray

rate rate
Hb RBS RFT LFT Others
SIGNATURE OF INVESTIGATOR SIGNATURE OF THE PARTICIPANT
WITNESS:

Nandhini

Uploaded by

Copyright:

Available Formats

Nandhini

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Nandhini

Uploaded by

Copyright:

Available Formats

EFFECT OF INTRAVENOUS DEXMEDETOMIDINE

ON PROLONGING SPINAL ANESTHESIA, A

THE TAMILNADU DR.M.G.R

in partial fulfillment of regulations

ESIC MEDICAL COLLEGE & PGIMSR

THE TAMILNADU DR. M.G.R MEDICAL UNIVERSITY

INTRAVENOUS DEXMEDETOMIDINE ON PROLONGING SPINAL

ANESTHESIA, A RANDOMISED CONTROLLED STUDY” is a bonafide

work performed by Dr.T.S.Nandhini, post graduate student, Department of

Anaesthesiology, ESIC Medical College & PGIMSR, Chennai-78, under my

guidance and supervision in fulfillment of regulations of The Tamilnadu Dr.

Dr. K.Radhika, M.D., Prof. Dr. Kamalini Sridharan

Department of Anaesthesiology, Professor and Head,

ESIC Medical College & PGIMSR Department of Anaesthesiology,

Chennai -78 ESIC Medical College & PGIMSR

This is to certify that this dissertation titled “EFFECT OF

INTRAVENOUS DEXMEDETOMIDINE ON PROLONGING SPINAL

ANESTHESIA, A RANDOMISED CONTROLLED STUDY” submitted by

Dr.T.S.Nandhini, appearing for M.D Degree Branch – X ANAESTHSIOLOGY

examination in April 2015 is a bonafide record of work done by her under my

direct guidance and supervision in partial fulfillment of the regulations of

Tamilnadu Dr.M.G.R Medical University, Chennai. I forward this to the

Tamilnadu Dr. M.G.R Medical University, Chennai Tamilnadu, India.

PLACE: K.K. Nagar

I solemnly declare that this dissertation entitled “EFFECT OF

INTRAVENOUS DEXMEDETOMIDINE ON PROLONGING SPINAL

ANESTHESIA, A RANDOMISED CONTROLLED STUDY” has been

conducted by me at ESIC Medical College & PGIMSR, Chennai, under the

guidance and supervision of Prof.Dr.KAMALINI SRIDHARAN, M.D., and

Dr.K.RADHIKA, M.D., Department of Anesthesiology, ESIC Medical College &

Medical University, Chennai in partial fulfillment of the University regulations

for the award of the degree of M.D. Branch X (Anesthesiology).

It is my immense pleasure to thank everybody who contributed in

I convey my sincere regards to my guide Dr. K.RADHIKA, M.D., for her

I acknowledge my heartfelt gratitude to my co-guide

I would also like thank Dr.T.K.RENUKA DEVI, M.D.,DGO., HOD of the

Department of obstetrics and gynecology, who had permitted to do the study on

I am grateful in every possible way to the Specialists, Medical Officers,

Senior Residents and the postgraduates of the Department of Anesthesiology for

helping me to conduct the study in the theatre.

Many thanks in particular to the statistician Dr.ARUNA PATIL, Ph.D., for

her guidance regarding the sample size and data analysis.

approval for the study.

patients for their participation and cooperation.

I am thankful to my parents for their blessings for their unconditional love,

support and time.

2. Aim of the study 6

7. Anatomy of Spinal Anesthesia 52

8 Physiology of Spinal Anesthesia 55

9. Materials & Methods 67

10. Results & Analysis 77

12. Conclusion 104

on prolongation of spinal anesthesia.

Study population comprised of 100 patients scheduled for abdominal/vaginal

hysterectomy under spinal anesthesia. 100 adult patients classified as ASA 1 or 2

In Group-D patients received hyperbaric intrathecal bupivacaine anesthesia

3.5ml 0.5% (17.5 mg) and intravenous Dexmedetomidine 0.5micro grams/Kg

in10 ml normal saline over 10 minutes after initiation of spinal block.

In Group C patients received hyperbaric bupivacaine anaesthesia 3.5 ml 0.5%