|Year : 2016 | Volume
| Issue : 2 | Page : 273-277
Single dose intravenous dexmedetomidine prolongs spinal anesthesia with hyperbaric bupivacaine
Jyotsna Kubre1, Ashish Sethi2, Mamta Mahobia2, Deeksha Bindal3, Neeraj Narang2, Anudeep Saxena4
1 Department of Anaesthesiology and Critical Care, All India Institute of Medical Sciences, Bhopal, Madhya Pradesh, India
2 Department of Anaesthesiology and Critical Care, N.S.C.B. Medical College, Jabalpur, Madhya Pradesh, India
3 Department of Anaesthesiology, S.M.S. Medical College, Jaipur, Rajasthan, India
4 Department of Critical Care and Emergency Medicine, Sir Ganga Ram Hospital, New Delhi, India
|Date of Web Publication||26-Apr-2016|
Department of Anaesthesiology and Critical Care, AIIMS, Saket Nagar, Bhopal, Madhya Pradesh
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background and Introduction: Spinal block, a known technique to obtain anaesthesia for infraumblical surgeries. Now physician have advantage of using adjuvant to prolong the effect of intrathecal block, which can be given either intravenously or intrathecally, dexmedetomidine is one of them. We studied effect of intravenous dexmedetomidine for prolongation of duration of intrathecal block of 0.5% bupivacaine block.
Objective: To evaluate the effect of intravenous dexmedetomidine on sensory regression, hemodynamic profile, level of sedation and postoperative analgesia.
Methodology: 60 patients of ASA grade I and II posted for elective infraumblical surgeries were included in the study and randomly allocated into two groups. Group D recieved intrathecal 0.5% bupivacaine heavy, followed by infusion of intravenous dexmedetomidine 0.5mic/kg over 10 min, patients in group C received intrathecal 0.5% bupivacaine heavy 3ml followed by infusion of same volume of normal saline as placebo.
Results: Two segment regression of sensory block was achieved at 139.0 ± 13.797 in group D whereas in group C it was only 96.67 ± 7.649min, the total duration of analgesia achieved in both study groups was 234.67 ± 7.649min and 164.17 ± 6.170min respectively in group D and group C. The time at which first analgesic was given to the patients when VAS >3 achieved that is in group D at 234.67 ± 7.649min and in group C at 164.17 ± 6.170min. Inj diclofenac sodium 75mg intramuscular was used as rescue analgesic.
Keywords: Intravenous dexmedetomidine, postoperative analgesia, sensory regression,spinal block
|How to cite this article:|
Kubre J, Sethi A, Mahobia M, Bindal D, Narang N, Saxena A. Single dose intravenous dexmedetomidine prolongs spinal anesthesia with hyperbaric bupivacaine. Anesth Essays Res 2016;10:273-7
|How to cite this URL:|
Kubre J, Sethi A, Mahobia M, Bindal D, Narang N, Saxena A. Single dose intravenous dexmedetomidine prolongs spinal anesthesia with hyperbaric bupivacaine. Anesth Essays Res [serial online] 2016 [cited 2021 Apr 19];10:273-7. Available from: https://www.aeronline.org/text.asp?2016/10/2/273/174465
| Introduction|| |
Spinal anesthesia is a unique technique to provide sensory and motor blockade in the large part of the body with a lesser amount of drug, hence very popular for infraumbilical surgeries. Usually, without any additive one can achieve 60–90 min anesthesia with a spinal block.
Nowadays, anesthetists are fortunate enough to have agents that can be used either intrathecally or intravenously to enhance the efficacy and duration of the block they are called adjuvants. Some of the drugs that were previously used are epinephrine, magnesium sulphate, fentanyl, midazolam, clonidine,,,, nowadays dexmedetomidine is trending.
Dexmedetomidine was a newer congener of clonidine, a dextro isomer of medetomidine, first introduced for short-term Intensive Care Unit sedation in 1999, is having 8 times more selectivity to α2-adrenergic receptors than clonidine which might permit its application in relatively high doses for sedation and analgesia without any unwanted vascular effects from activation of α1 receptors. Dexmedetomidine is rapidly emerging drug as an adjuvant to general anesthesia, regional anesthesia, spinal anesthesia, during monitored anesthesia care, as premedication and for postoperative sedation and analgesia.
Dexmedetomidine is an excellent drug for sedation in intubated as well as non-intubated patients in critical care and for short procedures. Sleep induced with dexmedetomidine is termed as cooperative sleep, and the drug does not disturb the sleep architecture, as well as, the respiratory drive. Taking the advantage of these properties, we decided to study the effects of dexmedetomidine by administrating it intravenously in association with the subarachnoid block.
Dexmedetomidine is a selective α2 agonist; these receptors are found in many sites throughout the body including central nervous system (CNS), spinal, and peripheral tissues. In CNS, the highest densities of α2 receptors are found in the locus ceruleus, an important modulator of vigilance. Presynaptic activation of the α2A-adrenoceptors in the locus ceruleus inhibits the release of norepinephrine (NE) and results in the sedative and hypnotic effects. Furthermore, the locus ceruleus is the site of origin for the descending medullospinal noradrenergic pathway. Stimulation of the α2-adrenoceptors in this area terminates the propagation of pain signals leading to analgesia. At the spinal cord, stimulation of α2 receptors at the substantia gelatinosa of the dorsal horn leads to inhibition of the firing of nociceptive neurons and inhibition of the release of substance P. Furthermore, the α2-adrenoceptors located at the nerve endings have a possible role in the analgesic mechanisms of α2 agonists by preventing NE release. The spinal mechanism is the principal mechanism for the analgesic action of dexmedetomidine even though there is a clear evidence for both a supraspinal and peripheral sites of action. As it is a much known fact that dexmedetomidine is used as a bolus dose followed by continuous infusion, in our study, we have tried to bring out the same effect with single dose over 10 min, as it does with infusion.
Aims and objective
To evaluate the effect of intravenous dexmedetomidine on the duration of sensory block (regression to S1), hemodynamic profile, the level of sedation and postoperative analgesia (time when the first analgesic given and total analgesic consumption in 24 h).
| Materials and Methods|| |
This study was conducted following approval of the Ethics Committee (dated 22/09/2011) and after obtaining written informed consent from patients scheduled to undergo elective infraumblical surgeries, duration of the study was from 30/09/2011 to 30/09/2012.
Selection of cases
- Patients posted for infraumbilical surgeries of American Society of Anesthesiologists (ASA) Class I-II
- Belongs to age group of 25–60 years.
- All contraindication to spinal analgesia including bleeding diathesis, infection at the puncture site, spinal deformity, patient on anticoagulants, preexisting neurological deficits in lower extremities
- Patients on α2-adrenergic receptors antagonists, calcium channel blockers, or angiotensin-converting enzyme inhibitors
- Patients are having cardiac rhythm abnormalities.
A double-blind, randomized, placebo-controlled study was done on 60 ASA Grades I and II patients who were randomly selected and assigned to one of the two groups (D-dexmedetomidine group) and (C-control group). Each group contained 30 patients scheduled to undergo infraumbilical surgeries. Patients in the study group received dexmedetomidine infusion 0.5 μg/kg over 10 min and patients in the control group received saline infusion over 10 min, 45 min after spinal anesthesia with bupivacaine 0.5% 15 mg (n = 30 per group).
Preparation of infusion
Two milliliters of injection dexmedetomidine, diluted in 48 ml of normal saline; hence, the concentration of the drug in the solution is 4 μg/ml. The infusion was prepared by an independent senior resident who was not involved in the subsequent phases of the study. Thus, both the resident conducting the case as well as the patient was not aware of the assigned group in all the cases.
All patients were prehydrated with 10 ml/kg of Ringer's lactate solution through 18-gauge, intravenous cannula. Standard monitoring done, which includes noninvasive blood pressure (BP), electrocardiography, heart rate (HR), and oxygen (O2) saturation. All patients were supplemented with 4 L/min of O2 by simple face mask. Subarachnoid block with 3 ml of 0.5% bupivacaine was performed in the L3–L4 interspace using a 25-gauge Quincke's spinal needle with the patient in the sitting position.
After performing the spinal block vital signs were recorded every 2 min initially, and every 5 min thereafter. Forty-five minutes after the subarachnoid block, dexmedetomidine group (Group D) received dexmedetomidine infusion 0.5 μg/kg over 10 min, and the control group (Group C) received the same volume of normal saline infusion over 10 min.
Onset, height, duration, and regression of sensory block (two segment regression) were assessed with an ice cube and by the loss of pinprick sensations. Sensory block was assessed every 2 min for the first 10 min and thereafter every 5 min during surgery. Before giving the study drug or placebo, the sensory level was recorded. In the postanesthesia care unit (PACU), the sensory level was recorded every 15 min for the next 4 h or regression to S1 level, after which the patient was shifted to the ward.
The level of sedation was evaluated intraoperatively and postoperatively every 15 min using Ramsay level of sedation scale [Table 1].
All sedation score was recorded considering the time of injecting dexmedetomidine.
If sensory levels of anesthesia were not equal bilaterally, we used the higher level for the statistical analysis. Patients were discharged from the PACU to the ward after sensory regression to the S1 segment.
Postoperative pain was assessed using visual analog scale (VAS), every 15 min until the first analgesic given, and 4 hourly for the next 24 h, rescue analgesia was given in the form of injection diclofenac sodium 75 mg intramuscular (IM) when VAS score was more than 3.
For the purpose of this study, hypotension was systolic BP of <90 mmHg and if was treated with a bolus administration of 300 ml of lactated Ringer's solution over 10 min and 6 mg of intravenous ephedrine. Bradycardia was defined as HR <50 beats/min, and if persist treated with 0.6 mg of intravenous atropine.
The data of this study were recorded into the computers and after its proper validation, check for error, coding, and decoding were compiled and analyzed using the statistical programming software Statistical Package for the Social Sciences - SPSS Statistics version 17.0.0 (SPSS Inc., Chicago, Illinois, USA). All the data were analyzed using Student's t-test in this study and P < 0.05 was considered significant.
| Results|| |
All the patients of Group D and Group C were comparable demographically [Table 2], [Table 3], [Table 4]. Time of onset and of sensory and motor block was also comparable in both the groups as we have given the study drug after 45 min of the subarachnoid block, the height of sensory block was also comparable. The two segment regression time in Group D was 139.00 ± 13.797 min whereas in Group C it is only 96.67 ± 7.649 min. Hence, we found a highly significant difference in two segment regression time in both groups with P < 0.0001 (t-test).
The time at which the first analgesic was requested was 234.67 ± 7.649 min in Group D and 164.17 ± 6.170 min in Group C injection diclofenac sodium was used as rescue analgesic. P < 0.0001 (t-test).
Total number of doses of analgesic given as injection diclofenac sodium 75 mg (IM), in Group D was 2 ± 0.000 doses and in Group C was 2.90 ± 0.305 doses, which was highly significant as P < 0.0001 (t-test).
Twenty-four patients out of 30 in Group D achieved sedation score of 3 and in Group C 20 patients achieved a score of 2, rest of them were fully awake.
| Discussion|| |
As sympatholysis is the hallmark feature of central neuraxial blockade, more so after subarachnoid block and dexmedetomidine also leads to significant hypotension and bradycardia, so in our study we kept the timing of administration of dexmedetomidine after the peak of the hemodynamic response due to intrathecal bupivacaine was over, by giving dexmedetomidine infusion 45 min  after intrathecal block with 0.5% bupivacaine.
In previous studies, dexmedetomidine group had bradycardia compared to the control group, which is similar to the findings of other studies Whizar-Lugo et al. in which higher proportion of patients in the dexmedetomidine group required atropine compared to the control group, as was also reported in other studies Tekin et al. and Hong et al. Contrary to above studies, Al-Mustafa et al. reported no significant difference in atropine requirement between dexmedetomidine and control groups.
Dexmedetomidine does not have any direct effects on the heart. In the coronary circulation, it causes a dose-dependent increase in coronary vascular resistance and O2 extraction, but the supply/demand ratio is unaltered. A biphasic cardiovascular response has been described after the administration of dexmedetomidine. A bolus of 1 μg/kg results in a transient increase in BP and a reflex decrease in HR. This initial response is attributed to the direct effects of β-adrenoceptor stimulation of the vascular smooth muscle. This response can be attenuated by a slow infusion over 10 min, as given in our study, 0.5 μg/kg over 10 min, which resulted in stabilization of the HR and BP 10–15% below baseline values. In this study, changes in pulse rate, systolic, and diastolic BP were similar in both the groups. The decrease in the HR was more evident in Group D but not statistically significant when compared with Group C, and only two patients required atropine for bradycardia, which was comparable with the control group. The lower HR observed in Group D could be explained by the postsynaptic activation of α2-adrenoceptors in the CNS, which results in a decrease in sympathetic activity and circulating levels of catecholamines., Other studies support the finding that the bradycardia caused by dexmedetomidine is long lasting when used as a premedication drug , in these studies dexmedetomidine was given as premedication and in some as continuous infusion ,, throughout the procedure, which lead to hypotension and bradycardia intraoperatively, as well as, postoperatively and which lead to increase drug consumption to overcome these effects, by giving slow infusion and after spinal block when the peak hemodynamic effects of subarachnoid block were already settled we have avoided these complications in our study.
Previous studies have shown that the hypotension caused by dexmedetomidine persists in the intraoperative as well as in the postoperative period. In our patients, there was a fall in mean arterial pressure in Group D as well as in Group C and clinically was not significant. There was no further decrease in the BP after adding intravenous dexmedetomidine to patients with bupivacaine spinal anesthesia. Only two patients in Group D received ephedrine because of fall in systolic BP <90 mmHg, which was statistically not significant and comparable with Group C. Similarly, Al-Mustafa et al., Tekin et al. and Whizar-Lugo et al. reported no significant difference in mean arterial pressures in the dexmedetomidine group.
The mean duration of two segment regression in Group D and Group C was 139.00 ± 13.79 min and 96.67 ± 7.64 min, respectively [Table 5]. The difference in the duration between the groups is statistically significant. This is consistent with the findings reported by Kaya et al. who concluded that intravenous dexmedetomidine, but not midazolam, prolongs bupivacaine spinal anesthesia. Our study also correlates with the study of Al-Mustafa et al. who stated that intravenous dexmedetomidine prolongs bupivacaine spinal analgesia, and also with other two studies., This also correlates with the studies of Hong et al. and Whizar-Lugo et al. Similar observations were also made by Tekin et al.
In our study, the time to first request for postoperative analgesic was significantly prolonged (234.67 ± 7.649 min) and the 24 h mean requirement of analgesics was significantly less in the dexmedetomidine group [Table 6] and [Table 7] compared to the control group that also correlates with the findings reported by Kaya et al. Al-Mustafa et al. and also with Whizar-Lugo et al. Similarly, Hong et al. noticed that postoperative pain intensity was lower and the mean time to first request for postoperative analgesia was longer in the dexmedetomidine group compared to the control group (6.6 vs. 2.1 h). Kaya et al. in their study observed that dexmedetomidine increased the time to the first request for postoperative analgesia and decreased the analgesic requirements. Whizar-Lugo et al. In their study noticed that the time to first request for postoperative analgesic in the dexmedetomidine group was (220 ± 30 min) significantly prolonged as compared to the control group (150 ± 20 min).
Dexmedetomidine does not cause much respiratory depression despite providing good sedation resulting in wide safety margins. Sedation scores in Groups D and C were 3 and 2, respectively [Table 8], sedation produced by dexmedetomidine is different from other sedatives as the patient is easily arousable and remains cooperative. The participation of nonrapid eye movement sleep pathways seems to explain why patients who appear to be “deeply asleep” from dexmedetomidine are relatively easily aroused in much the same way as occurs with natural sleep. This type of sedation is termed “cooperative” or “arousable,” to distinguish it from the sedation induced by drugs acting on the gamma-aminobutyric system, such as midazolam or propofol, which produce a clouding of consciousness.
| Conclusion|| |
Single dose IV dexmedetomidine of 0.5 mcg/kg prolongs the duration of sensory blockad and analgesia and reduces the requirement of analgesics with lesser incidence of bradycardia and hypotension introperatively as well as postoperatively. As well as it produces satisfactory arousable sedation without causing respiratory depression
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Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]