[Downloaded free from http://www.aeronline.org on Wednesday, December 25, 2019, IP: 189.40.103.

218]

Original Article

The Effectiveness of Intravenous Dexmedetomidine on

Perioperative Hemodynamics, Analgesic Requirement, and
Side Effects Profile in Patients Undergoing Laparoscopic
Surgery Under General Anesthesia
Vinayak Panchgar, Akshaya N. Shetti1, H. B. Sunitha2, Vithal K. Dhulkhed3, A. V. Nadkarni3
Departments of Anesthesiology and Critical Care and 2Obstetrics and Gynecology, Gadag Medical College, Gadag, Karnataka, 1Department of Anesthesiology and
Critical Care, Rural Medical College, Pravara Institute of Medical Sciences, Loni (Bk), Ahmednagar, Maharashtra, 3Department of Anesthesiology and Critical Care,
Krishna Institute of Medical Sciences, Karad, Maharashtra, India

Abstract
Background: There is an upward surge in the use of laparoscopic surgeries due to various advantages when compared to open surgeries.
Major advantages are, due to small incisions which are cosmetically acceptable and most of them are now daycare procedures. Problem
of economic burden and hospital bed occupancy has been overcome with laparoscopic surgeries. All these advantages are not free from
disadvantages, as hemodynamic changes such as hypertension; tachycardia and other surgical‑related complications are commonly observed
intraoperatively. Dexmedetomidine is one of the α2 agonist drugs which acts at both supraspinal and spinal level and modulate the transmission
of nociceptive signals in the central nervous system. The basic effect of dexmedetomidine on the cardiovascular system is to decrease the heart
rate and systemic vascular resistance with additional feature of opioid sparing effect. This drug has become an ideal adjuvant during general
anesthesia, especially when stress is expected. Hence, the drug was studied in laparoscopic surgeries. Aims and Objectives: (a) To study the
effect of dexmedetomidine on hemodynamic parameters during perioperative period in patients undergoing laparoscopic surgery. (b) To study
the postoperative sedation score and analgesic requirement. (c) To study the side effect profile of dexmedetomidine. Settings and Design:
Randomized double blind controlled trial. Subjects and Methods: After obtaining the Institutional Ethical Clearance, the study was conducted.
Forty patients of American Society of Anesthesiologists Class I and II were enrolled in this randomized study. The patients were randomly
divided into two groups; group normal saline (NS) and group dexmedetomidine. Patient received either NS or dexmedetomidine in group NS
and group dexmedetomidine, respectively, depending upon the allocation. The infusion rate was adjusted according to; loading dose (1 µg/kg)
over 10 min and maintenance dose (0.5 µg/kg/h) and perioperative hemodynamics was recorded. Routine general anesthesia was administered
in all the patients with conventional technique without deviating from institutional protocols. Postoperatively, Rasmsay sedation score, time
taken for request of first analgesic dose, and side effects if any were recorded. Statistical Analysis Used: The categorical factors are represented
by the number and frequency (%) of cases. The continuous variables are represented by measures of central frequency and standard deviation.
The statistical analysis was done by using unpaired t‑test and Chi‑square. P < 0.05 was considered statistically significant. Results: Significant
hemodynamic changes are observed in NS group during laryngoscopy, intubation, during pneumoperitoneum formation, and during extubation.
Hemodynamic stress response in dexmedetomidine group was significantly attenuated. Analgesic requirement during postoperative 24 h were
much less in dexmedetomidine group when compared to NS group. No significant side effects were noted except for bradycardia; which was
observed in two cases of dexmedetomidine group. Conclusion: Dexmedetomidine infusion in the dose of 1 µg/kg body weight as bolus
over 10 min and 0.5 µg/kg/h intraoperatively as maintenance dose controlled the hemodynamic stress response in patients undergoing
laparoscopic surgery. Use of dexmedetomidine extends the pain
free period postoperatively and thereby reducing total analgesic
Address for correspondence: Dr. Akshaya N. Shetti,
requirement. Thus, dexmedetomidine can be utilized as an ideal Associate Professor, Department of Anesthesiology and Critical Care, Rural
anesthetic adjuvant during laparoscopic surgeries. Medical College, Loni, Ahmednagar, Maharashtra, India.
E‑mail: aksnsdr@gmail.com
Keywords: Analgesia, dexmedetomidine, laparoscopic surgery,
sedation, α2 agonist
This is an open access article distributed under the terms of the Creative
Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows
others to remix, tweak, and build upon the work non-commercially, as long as the
Access this article online author is credited and the new creations are licensed under the identical terms.
Quick Response Code: For reprints contact: reprints@medknow.com
Website:
www.aeronline.org
How to cite this article: Panchgar V, Shetti AN, Sunitha HB,
Dhulkhed VK, Nadkarni AV. The effectiveness of intravenous
DOI: dexmedetomidine on perioperative hemodynamics, analgesic requirement,
10.4103/0259-1162.200232 and side effects profile in patients undergoing laparoscopic surgery under
general anesthesia. Anesth Essays Res 2017;11:72-7.

72 © 2017 Anesthesia: Essays and Researches | Published by Wolters Kluwer - Medknow

[Downloaded free from http://www.aeronline.org on Wednesday, December 25, 2019, IP: 189.40.103.218]
Panchgar, et al.: Dexmedetomidine in laparoscopic surgery
Introduction
Laparoscopic surgery or key hole surgeries are very popular
nowadays due to various advantages such as the shorter
length of stay in the hospital, lesser postoperative pain,
and cosmetically appealing.[1] Recently, dexmedetomidine,
a newer α2 agonist, has been introduced in Indian market.
Dexmedetomidine was initially permitted to use in the
Intensive Care Unit sedation, but now it is commonly used as
an anesthetic adjuvant due to its distinct properties.[2] Various
doses and routes of administration of dexmedetomidine have
been tried successfully in anesthesia practice.[3‑5] During
laparoscopic surgeries because of pneumoperitoneum, various
pathophysiological changes may occur in the patient. These
changes are mainly rise in systemic and pulmonary vascular
resistance, rise in heart rate, and decrease in the cardiac
output. Position of the patient during the laparoscopic surgery
also adds up for these pathophysiological changes further
compromising the hemodynamics.[6] Certain steps in anesthesia
such as laryngoscopy, intubation, and extubation also causes
the stimulation of sympathetic nervous system leading to
unacceptable hemodynamic changes. Various drugs such as
opioids, beta blockers, and centrally acting sympatholytics
have been tried to attenuate such stress response. Various
studies have been conducted to know the effectiveness of
dexmedetomidine in various doses for the prevention of
stress‑induced hemodynamic changes.[7,8] Dexmedetomidine
has been used in routine anesthesia practice and studies have
shown that there is a reduction of requirement of induction
agents and opioids during perioperative period.[2,9] Though the
clonidine is α2 agonist and has the property of sympatholytic,
dexmedetomidine is more specific for α2 receptors when
compared to it.[10] We therefore carried out this study with
the primary aim of assessing the hemodynamic response
and secondary aims of assessing sedation and analgesia
requirement in first 24 h of postoperative recovery following
intravenous infusion of dexmedetomidine in patients
undergoing laparoscopic surgery under general anesthesia.
Subjects and Methods
After obtaining approval by the Institutional Ethics Committee,
written informed consent was taken from all forty patients who
satisfied the inclusion criteria. All these patients were posted
for laparoscopic surgery under general anesthesia.
Inclusion criteria
Age groups between 18 and 65 years, either sex, American
Society of Anesthesiologists physical status Class I or II,
posted for laparoscopic surgery under general anesthesia were
included in this study.
Exclusion criteria
Patients with decreased autonomic control such as the elderly,
diabetic patients, patients with cardiovascular pathology,
pregnant or lactating women, patients unwilling to participate
in the study were excluded from the study.
Anesthesia: Essays and Researches  ¦  Volume 11  ¦  Issue 1  ¦  January-March 2017
All the patients were fasted adequately, premedicated with tablet
diazepam 10 mg and tablet ranitidine 150 mg on the night before
surgery and on the morning of surgery. In the operation theater,
patient’s oxygen saturation by pulse oximetry, noninvasive
blood pressure, respiratory rate, and electrocardiogram
were monitored. A wide bore 18‑gauge intravenous line
was secured and infusion of ringer lactates at the rate 10 ml/
kg/h started. Inside the operation room, the patient received
injection fentanyl 1 µg/kg and injection midazolam 0.05 mg/
kg, intravenously. Preparation of drug: The study drug was
prepared by a senior resident who was not involved in the study.
Both observer as well as patients was blinded from the study.
In dexmedetomidine group; Ampoule containing 200 mcg of
dexmedetomidine was diluted with normal saline (NS) in a 50 ml
syringe to achieve a final concentration of 4 mcg/ml. In saline
group; 50 ml syringe was loaded with 50 ml of NS. Depending
upon randomization, patients received either dexmedetomidine
or NS. Infusion was set for loading dose (1 µg/kg), which was
infused over 10 min using syringe pump. As soon as the loading
dose is over, rate of infusion in syringe pump was adjusted to
precalculated rate for maintenance dose (0.5 µg/kg/h).
Ten minutes after the administration of study drug, patients
were preoxygenated with 100% oxygen for 3 min and
induced with injection thiopentone 5 mg/kg intravenously.
The intubation was facilitated by intravenous administration
of injection succinyl choline 1.5 mg/kg. The anesthesia was
maintained with oxygen, nitrous oxide 1:1 ratio, injection
vecuronium (0.1 mg/kg), and sevoflurane (dial setting range
between 1.5 and 2) using circle system. The patients were
put on mechanically ventilator, and setting was adjusted in
such a way that the end‑tidal concentration of carbon dioxide
was maintained between 35 and 45 mmHg. Throughout the
procedure, intra‑abdominal pressure was maintained between
12 and 14 mmHg. Any fall in heart rate <60/min is considered
as bradycardia and treated with intravenous injection atropine
0.6 mg. Any fall in blood pressure more than 20% of baseline is
considered as hypotension and initially treated with 200 ml of
bolus ringer lactate fluid. If there was no improvement in blood
pressure, then it was treated with injection mephentermine
6 mg intravenously.
At the end of operation, the infusion of study drug, nitrous
oxide, and sevoflurane were stopped. The reversal was done
with injection glycopyrrolate 0.008 mg/kg and injection
neostigmine 0.05 mg/kg intravenously. Extubation was carried
out once the patient met all the extubation criteria.
Monitoring of parameters, i.e., heart rate, systolic blood
pressure (SBP), diastolic blood pressure (DBP), mean
arterial blood pressure (MAP) were noted at, before the start
of infusion, 10 min after starting the infusion, immediately
after induction, after laryngoscopy, and intubation at 1, 3,
and 5 min. Data collected at the time of pneumoperitoneum,
i.e., 1 min, 15 min, and 30 min and then every 15 min. After
extubation, postoperatively 0, 15, 30, and 60 min, the vitals
were recorded. Sedation was assessed by Ramsay sedation
73
[Downloaded free from http://www.aeronline.org on Wednesday, December 25, 2019, IP: 189.40.103.218]

Panchgar, et al.: Dexmedetomidine in laparoscopic surgery

score (RSS) at 1, 15, 30, 60, and 120 min, postoperatively.
The time to first rescue analgesic requirement and the total
amount of analgesic drugs required during the first 24  h
postoperatively were noted down. For rescue analgesia
injection diclofenac sodium 1.5 mg/kg was intramuscularly
administered when visual analogue score was more than 5.
Throughout the study, patients were also observed for any
adverse effects such as arrhythmias, respiratory depression.
Results
There were no significant differences found between both the
groups with respect to demographic parameters such as age,
height, weight, and gender. The duration of anesthesia and type
of surgery were comparable between both groups.
As shown in Table 1, the values for mean SBP before starting
the infusion were comparable in both groups. The mean SBP in
group NS did not show any significant change till laryngoscopy
and intubation. The mean SBP showed significant rise at
laryngoscopy, intubation, during pneumoperitoneum, and after
extubation. The values returned to preoperative level by about
45 min after extubation.
On the other hand, in group dexmedetomidine, the mean SBP
significantly decreased during laryngoscopy, intubation, and
during pneumoperitoneum. Even after extubation, there was
a significant decrease in mean SBP. The values returned to
preinfusion level after 45 min of extubation.
The values for mean DBP before starting the infusion
were comparable in both the groups [Table 2]. In saline
group, the mean DBP did not show any significant change
till laryngoscopy and intubation. There was a significant
rise in mean DBP at laryngoscopy and intubation, during
pneumoperitoneum, and extubation. The values returned to
preoperative level by about 45 min after extubation. On the
other hand, in dexmedetomidine group, there was a significant
fall in mean DBP values which were actually lesser than
preinfusion values after 10 min drug infusion. The fall was
significant even after laryngoscopy and tracheal intubation,
during pneumoperitoneum in comparison with preinfusion
values. But the mean DBP was equal to preinfusion values
after extubation. There was better control of DBP in group
dexmedetomidine compared to Group NS.
Table 3 shows the values of MAP recorded during various
steps. Before starting the infusion MAP were comparable in
both the groups. After starting saline infusion in group NS,
it did not show any significant change till laryngoscopy
and intubation. A highly significant rise in MAP is noted at
laryngoscopy and intubation. Significant rise in MAP while
creation of pneumoperitoneum and after extubation. The
MAP values came down to preoperative level by about 30 min
after extubation. On the other hand, in dexmedetomidine group,
mean MAP  values were significantly less than preinfusion
values after 10  min of drug infusion and significantly less
after laryngoscopy, tracheal intubation, pneumoperitoneum,
and extubation.
Table 4 shows the postoperative RSS in both the groups.
When compared to both the groups, the maximum RSS of the
three was seen in NS group, and in group dexmedetomidine,
it was four. None of the patients had a RSS of five or six in
either group. In group NS, 10% of patient had RSS of three at
1st min and 15th min of postextubation. In dexmedetomidine
group, 15% of patient had RSS of four and 10% had RSS of

Table 1: Comparison of mean systolic blood pressure

Time Group normal saline Group dexmedetomidine t Intergroup (P)
Before IV infusion 125.5±7.9 120.7±27.3 0.755 >0.05
10 min after starting infusion 123±6.6 118±6.7 2.378 <0.05*
After induction 119±6.5 112.1±9.4 2.700 <0.05*
After laryngoscopy and intubation (min)
1 138.7±4.2 116.1±11.6 8.192 <0.001**
3 133.2±7.5 116.1±6.4 4.591 <0.001**
5 131.7±4.3 112.5±11.2 4.528 <0.001**
After pneumoperitoneum (min)
1 128.9±6.4 116.3±10.0 4.068 <0.001**
15 127.1±9.9 115.6±10.4 3.582 <0.001**
30 124±8.2 115.1±10.6 2.970 <0.05*
45 123.8±5.4 118±9.7 2.336 <0.05*
60 124.1±5.3 119.6±13.2 1.415 >0.05
After extubation (min)
1 133.8±5.2 123.4±9.4 4.330 <0.001**
15 129.6±1.2 123.9±8.8 2.870 <0.05*
30 127.8±2.9 120.4±7.5 4.116 <0.001**
45 123.8±6.2 121.7±7.6 0.9575 >0.05
60 121.2±6.8 114.9±24.4 1.112 >0.05
*Significant, **Highly significant. IV=Intravenous

74 Anesthesia: Essays and Researches  ¦  Volume 11  ¦  Issue 1  ¦  January-March 2017

[Downloaded free from http://www.aeronline.org on Wednesday, December 25, 2019, IP: 189.40.103.218]

Panchgar, et al.: Dexmedetomidine in laparoscopic surgery

four at 1st and 15th min of postextubation period, respectively. The mean time for rescue analgesia in Group NS was 50 min
In dexmedetomidine group, 60 min after extubation around and all patients from this group received rescue analgesia.
80% of patients were having RSS of two. However, in dexmedetomidine group, mean time for the need
of rescue analgesia was 360 min. The cumulative analgesic dose
requirement in 24 h of postoperative period was 195 mg in NS
Table 2: Comparison of mean diastolic blood pressure
group, 90 mg in dexmedetomidine group. The adverse event
Time Group Group t P like bradycardia was observed in dexmedetomidine group in
normal dexmedetomidine two patients. There was no such incidence noticed in the NS
saline
group. In this study, incidence of dryness of mouth was 5% in
Before IV infusion 76.7±5.8 79.9±6.3 1.664 >0.05
both the group. There was no statistically significant dryness of
10 min after 82.9±6.1 78.8±4.2 0.5846 <0.05*
starting infusion
mouth was observed in both the groups. There was no adverse
1 min after 79.2±5.5 73.7±7.6 2.608 <0.05* incidence of respiratory depression; nausea and vomiting were
induction noted in either group.
After laryngoscopy
and intubation
(min) Discussion
1 93.9±5.0 77.2±8.7 7.443 <0.001** In 1947, Booker et al. studied the acute effects of abdominal
3 90.2±4.7 74.1±4.7 10.83 <0.001** pressure changes. [11] Hemodynamic changes are mainly
5 84.1±8.1 74.0±8.6 3.823 <0.001** observed in a patient who is undergoing laparoscopic surgery
After during intubation, pneumoperitoneum, reverse trendelenburg
pneumoperitoneum
position, and while extubation.[12] All these changes are well
(min)
1 83.5±8.2 74.2±5.8 4.141 <0.001**
tolerated in patients with normal cardiovascular function.
15 81.6±10.4 73.6±6.7 2.892 <0.001** One of the advantages of injection dexmedetomidine is that,
30 80.1±7.3 72.8±6.2 3.409 <0.001** it significantly reduces the release of catecholamine thus
45 77.2±6.7 77.4±7.1 0.091 >0.05 attenuating increase in systemic vascular resistance and heart
60 73.5±4.5 82.4±22.8 1.713 >0.05 rate. The adverse hemodynamic changes can be abolished with
After extubation dexmedetomidine infusion and thus preventing complications.
(min)
1 86.2±4.9 76.6±7.7 4.704 <0.001** Dexmedetomidine, as said before, is a highly selective α2
15 78.6±8.0 76.1±7.4 1.026 <0.05* adrenergic agonist with sedative, anxiolytic, and analgesic,
30 77.2±8.9 71.6±3.2 2.648 <0.05* sympatholytic, and antihypertensive effects. Activation of
45 72.4±6.0 73.1±5.1 0.397 >0.05 α2 adrenergic receptors in the brain and spinal cord inhibits
60 72.2±5.4 76.7±9.0 1.917 >0.05 neuronal firing leading to hypotension, bradycardia, and
*Significant, **Highly significant. IV=Intravenous sedoanalgesia. The presynaptic activation of α2 adrenergic

Table 3: Comparison of mean arterial blood pressure

Time Group normal saline Group dexmedetomidine t Intergroup (P)
Before IV infusion 96.2±11.1 97.6±9.6 0.426 >0.05
10 min after starting infusion 94±8.1 88±7.9 2.372 <0.05*
After induction 90±7.4 82.9±7.0 3.117 <0.05*
After laryngoscopy and intubation (min)
1 108.8±6.6 86.9±10.8 7.738 <0.001**
3 102.8±4.7 85.6±5.0 11.2 <0.001**
5 101.5±4.9 82.6±7.7 9.261 <0.001**
After pneumoperitoneum (min)
1 97.8±7.4 84.6±6.4 6.034 <0.001**
15 94.9±9.4 85.1±7.0 3.739 <0.001**
30 91.1±9.3 84.1±7.3 2.648 <0.05*
45 88.6±6.1 87.7±7.7 0.409 >0.05
60 87.6±6.1 88.6±13.2 0.307 >0.05
After extubation (min)
1 105.7±9.9 89.7±10.4 4.983 <0.001**
15 98.8±8.8 89.3±10.1 3.172 <0.05*
30 92.7±9.3 85±6.8 3.416 <0.05*
45 88±8.1 85±6 1.342 >0.05
60 86.4±7.2 83.4±7.2 1.318 >0.05
*Significant, **Highly significant. IV=Intravenous

Anesthesia: Essays and Researches  ¦  Volume 11  ¦  Issue 1  ¦  January-March 2017 75

[Downloaded free from http://www.aeronline.org on Wednesday, December 25, 2019, IP: 189.40.103.218]

Panchgar, et al.: Dexmedetomidine in laparoscopic surgery

Table 4: Comparison of postoperative Ramsay sedation score

Group Time after extubation (min) Number of patients (%)
RSS 1 RSS 2 RSS 3 RSS 4 RSS 5 RSS 6
Group normal saline 1 12 (60) 6 (30) 2 (10) 0 0 0
15 6 (30) 12 (60) 2 (10) 0 0 0
30 8 (40) 12 (60) 0 0 0 0
45 14 (70) 6 (30) 0 0 0 0
60 16 (80) 4 (20) 0 0 0 0
Group dexmedetomidine 1 0 7 (35) 10 (50) 3 (15) 0 0
15 2 (10) 5 (25) 11 (55) 2 (10) 0 0
30 3 (15) 9 (45) 8 (40) 0 0 0
45 4 (20) 15 (25) 1 (5) 0 0 0
60 4 (20) 16 (80) 0 0 0 0
RSS=Ramsay sedation score

receptors inhibits the release of norepinephrine. Effects of
hemodynamics changes are mainly mediated by outflow
inhibition of central sympathetic system.
The two groups under study were comparable to each other
with respect to age, gender, and weight, duration of surgery,
and anesthesia. The results of our study show that, in NS group,
there was a significant rise in mean pulse rate, SBP, DBP, and
MAP following laryngoscopy, intubation, pneumoperitoneum,
and after extubation. These results are in consistent with
the study conducted by authors Bhattacharjee et al., Keniya
et al., and Tufanogullari et al.[5,8,13] The suppression of the
sympathoadrenal response was seen in dexmedetomidine
group as it was observed in a study conducted by Scheinin
et al.[9] Dexmedetomidine is a highly selective α2 adrenergic
agonist. The mechanism of action is mainly on three types
of α2 receptors. The α2A, α2B, and α2C receptors are found in
brain and spinal cord. The resultant action of dexmedetomidine
is sedation, anxiolysis, analgesia, and sympatholysis.
Dexmedetomidine has been found to reduce both intraoperative
and postoperative opioid requirement due to its opioid sparing
effect.[14,15] In our study, we observed, an increase in the time to
receive first rescue analgesia in dexmedetomidine group when
compared to NS group. The mean time for rescue analgesia in
Group NS was 50 min and all patients received rescue analgesia.
However, in dexmedetomidine group, mean time for the need
of rescue analgesia was 360 min. The cumulative analgesic
dose requirement in 24 h of postoperative period was 195 mg
in NS group, 90 mg in dexmedetomidine group. Suggesting
there was a decrease in total analgesic requirements in first
24 h postoperatively in patient receiving dexmedetomidine.
Similar results are observed by Manne et al. in a study where
the different doses of dexmedetomidine were compared with
placebo.[6]
Stimulation of α2A and α2C receptors in which are seen in locus
coeruleus causes sedation. Whereas action of dexmedetomidine
on similar receptors located in spinal cord causes analgesia.
Hypotension and bradycardia are mainly due to its action on
α2A receptors of brain stem situated in vasomotor center.
In our study, RSS[16] was recorded once patient was taken
inside and postoperatively after extubation at 1, 15, 30, 45,
60 min. The mean sedation score 1 min after patient is taken
inside the operation theatre were 1.6 ± 0.5 in group NS and
1.4 ± 0.5 in dexmedetomidine group. Thus, the sedation
scores were equal in both the groups. Ten minutes after
the infusion of drug dexmedetomidine, the mean score in
dexmedetomidine group was 2.9 ± 0.3, whereas in NS group,
it was 1.9  ±  0.3; hence there was highly significant higher
sedation scores in dexmedetomidine group. Immediately
after extubation and during postoperative period, i.e., till 1 h,
significantly higher sedation scores noted in dexmedetomidine
group. We followed RSS as described in Table 5. Majority of
the patients in group NS had the score of one but in group
dexmedetomidine majority of the patients had score of three.
And five patients had sedation score of four. The sedation
caused by dexmedetomidine is mainly does dependent.[17] The
dexmedetomidine has similar properties of clonidine but with
more affinity toward its receptor and absence of respiratory
depression.[18] Complication such as respiratory depression
was not observed in any of the group. In our study, we did
observe episode of bradycardia intraoperatively in two patients
of dexmedetomidine group and were treated by injecting
injection atropine 0.6 mg intravenously. None of the patient in
the NS group had bradycardia. Possible reason for such a low
incidence rate of bradycardia might be due to slow infusion of
bolus.[19] Our study results are comparable to those of Bekker
et al., in which the author observed no statistically significant
increase in the incidence of bradycardia in dexmedetomidine
group.[20] The incidence of the bradycardia is more common
in young adults in whom the bolus dexmedetomidine
administered rapidly.[21]
The incidence of dryness of mouth was 5% in both the group.
There was no statistically significant dryness of mouth was
observed in both the groups. The results are in consistent
with the study conducted by Parikh et al.[22] In this study,
none of our patients had nausea or vomiting in either group.
In a study conducted by Bakri et al. showed the incidence of
nausea and vomiting significantly decreases as effectively

76 Anesthesia: Essays and Researches  ¦  Volume 11  ¦  Issue 1  ¦  January-March 2017

[Downloaded free from http://www.aeronline.org on Wednesday, December 25, 2019, IP: 189.40.103.218]
Panchgar, et al.: Dexmedetomidine in laparoscopic surgery
Table 5: Ramsay sedation score
Score Description
1 Anxious and agitated or restless
2 Cooperative, oriented, tranquil
3 Responds to commands only
4 Asleep with brisk response to glabellar tap
5 Asleep with sluggish response to glabellar tap
6 No response
as dexamethasone in laparoscopic cholecystectomy.[23] This
decrease in incidence of nausea and vomiting is could be due
to opioid sparing effect and lesser requirement of inhaled
anesthetics.[24,25] Other theories states that dexmedetomidine
decreases noradrenergic activity by acting on α2 presynaptic
inhibitory adreno‑receptors in the locus coeruleus. The
reduction in release of catecholamines due to inhibition of
sympathetic outflow is also one of the contributing factors.[26]
Conclusion
Dexmedetomidine infusion in the dose of 1 mcg/kg body
weight as bolus over 10 min and 0.5 µg/kg/h intraoperatively as
maintenance dose controlled the hemodynamic stress response
in patients undergoing laparoscopic surgery under general
anesthesia. Dexmedetomidine increases the pain free period
postoperatively, thus reducing the total analgesic requirement
with minimal side effects and making it as ideal anesthetic
adjuvant in laparoscopic surgeries.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
1. Bruhat MA, Chapron C, Mage G, Pouly JL, Canis M, Wattiez A, et al.
The benefits and risks of laparoscopic surgery. Rev Fr Gynecol Obstet
1993;88:84‑8.
2. Ghodki PS, Thombre SK, Sardesai SP, Harnagle KD. Dexmedetomidine
as an anesthetic adjuvant in laparoscopic surgery: An observational
study using entropy monitoring. J Anaesthesiol Clin Pharmacol
2012;28:334‑8.
3. Feld JM, Hoffman WE, Stechert MM, Hoffman IW, Ananda RC.
Fentanyl or dexmedetomidine combined with desflurane for bariatric
surgery. J Clin Anesth 2006;18:24‑8.
4. Ramsay MA, Saha D, Hebeler RF. Tracheal resection in the
morbidly obese patient: The role of dexmedetomidine. J Clin Anesth
2006;18:452‑4.
5. Tufanogullari B, White PF, Peixoto MP, Kianpour D, Lacour T,
Griffin J, et al. Dexmedetomidine infusion during laparoscopic bariatric
surgery: The effect on recovery outcome variables. Anesth Analg
2008;106:1741‑8.
6. Manne GR, Upadhyay MR, Swadia V. Effects of low dose
dexmedetomidine infusion on haemodynamic stress response, sedation
and post‑operative analgesia requirement in patients undergoing
laparoscopic cholecystectomy. Indian J Anaesth 2014;58:726‑31.
Anesthesia: Essays and Researches  ¦  Volume 11  ¦  Issue 1  ¦  January-March 2017
7. Aho M, Lehtinen AM, Erkola O, Kallio A, Korttila K. The effect
of intravenously administered dexmedetomidine on perioperative
hemodynamics and isoflurane requirements in patients undergoing
abdominal hysterectomy. Anesthesiology 1991;74:997‑1002.
8. Keniya VM, Ladi S, Naphade R. Dexmedetomidine attenuates
sympathoadrenal response to tracheal intubation and reduces
perioperative anaesthetic requirement. Indian J Anaesth 2011;55:352‑7.
9. Scheinin B, Lindgren L, Randell T, Scheinin H, Scheinin M.
Dexmedetomidine attenuates sympathoadrenal responses to tracheal
intubation and reduces the need for thiopentone and peroperative
fentanyl. Br J Anaesth 1992;68:126‑31.
10. Hall JE, Uhrich TD, Barney JA, Arain SR, Ebert TJ. Sedative, amnestic,
and analgesic properties of small‑dose dexmedetomidine infusions.
Anesth Analg 2000;90:699‑705.
11. Booker WM, French DM, Molano PA. Further studies on the acute
effects of intra‑abdominal pressure. Am J Physiol 1947;149:292‑8.
12. Mann C, Boccara G, Pouzeratte Y, Eliet J, Serradel‑Le Gal C, Vergnes C,
et al. The relationship among carbon dioxide pneumoperitoneum,
vasopressin release, and hemodynamic changes. Anesth Analg
1999;89:278‑83.
13. Bhattacharjee DP, Nayek SK, Dawn S, Gargi B, Gupta K. Effects of
dexmeditomidine on haemodynamics in patients undergoing laproscopic
cholecystectomy – A comparitive study. J Anaesth Clin Pharmacol
2010;26:45‑8.
14. Lin TF, Yeh YC, Lin FS, Wang YP, Lin CJ, Sun WZ, et al. Effect
of combining dexmedetomidine and morphine for intravenous
patient‑controlled analgesia. Br J Anaesth 2009;102:117‑22.
15. Abdelmageed WM, Elquesny KM, Shabana RI, Abushama HM,
Nassar AM. Analgesic properties of a dexmedetomidine infusion after
uvulopalatopharyngoplasty in patients with obstructive sleep apnea.
Saudi J Anaesth 2011;5:150‑6.
16. Riessen R, Pech R, Tränkle P, Blumenstock G, Haap M. Comparison
of the Ramsay score and the Richmond agitation sedation score for the
measurement of sedation depth. Critical Care 2012;16 Suppl 1:P326.
17. Shehabi Y, Botha JA, Ernest D, Freebairn RC, Reade M, Roberts BL,
et al. Clinical application, the use of dexmedetomidine in intensive care
sedation. Crit Care Shock 2010;13:40‑50.
18. Carollo DS, Nossaman BD, Ramadhyani U. Dexmedetomidine: A
review of clinical applications. Curr Opin Anaesthesiol 2008;21:457‑61.
19. Vora KS, Baranda U, Shah VR, Modi M, Parikh GP, Butala BP. The
effects of dexmedetomidine on attenuation of hemodynamic changes
and there effects as adjuvant in anesthesia during laparoscopic surgeries.
Saudi J Anaesth 2015;9:386‑92.
20. Bekker A, Sturaitis M, Bloom M, Moric M, Golfinos J, Parker E, et al.
The effect of dexmedetomidine on perioperative hemodynamics in
patients undergoing craniotomy. Anesth Analg 2008;107:1340‑7.
21. Lawrence CJ, De Lange S. Effects of a single pre‑operative
dexmedetomidine dose on isoflurane requirements and peri‑operative
haemodynamic stability. Anaesthesia 1997;52:736‑44.
22. Parikh DA, Kolli SN, Karnik HS, Lele SS, Tendolkar BA. A prospective
randomized double‑blind study comparing dexmedetomidine vs.
combination of midazolam‑fentanyl for tympanoplasty surgery
under monitored anesthesia care. J Anaesthesiol Clin Pharmacol
2013;29:173‑8.
23. Bakri MH, Ismail EA, Ibrahim A. Comparison of dexmedetomidine
and dexamethasone for prevention of postoperative nausea and
vomiting after laparoscopic cholecystectomy. Korean J Anesthesiol
2015;68:254‑60.
24. Gurbet A, Basagan‑Mogol E, Turker G, Ugun F, Kaya FN, Ozcan B.
Intraoperative infusion of dexmedetomidine reduces perioperative
analgesic requirements. Can J Anaesth 2006;53:646‑52.
25. Whittington RA, Virág L. Dexmedetomidine‑induced decreases
in accumbal dopamine in the rat are partly mediated via the locus
coeruleus. Anesth Analg 2006;102:448‑55.
26. Watcha MF, White PF. Postoperative nausea and vomiting. Its etiology,
treatment, and prevention. Anesthesiology 1992;77:162‑84.
77