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Table of Contents  
Year : 2014  |  Volume : 8  |  Issue : 2  |  Page : 175-178  

Prolongation of subarachnoid block by intravenous dexmedetomidine for sub umbilical surgical procedures: A prospective control study

1 Department of Anaesthesiology and Critical Care, N. S. C. B. Subharti Medical College, Swami Vivekananda Subharti University, Subhartipuram, Meerut, Uttar Pradesh, India
2 Department of Radio-diagnosis, Imaging and Interventional Radiology, N. S. C. B. Subharti Medical College, Swami Vivekananda Subharti University, Subhartipuram, Meerut, Uttar Pradesh, India

Date of Web Publication16-Jun-2014

Correspondence Address:
Prof. Kumkum Gupta
108, Chanakyapuri, Shastri Nagar, Meerut - 250 004, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0259-1162.134494

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Background: Intravenous dexmedetomidine is used as adjuvant during general anesthesia due to its sedative and analgesic effects. The present study was aimed to evaluate the effects of intravenous dexmedetomidine on sensory and motor block characteristics, hemodynamic parameters and sedation during subarachnoid block.
Materials and Methods: In this double-blind randomized placebo control study, 60 patients of American Society of Anesthesiologist I and II were randomized into two groups by computer generated table. Patients of Group D administered intravenous dexmedetomidine 0.5 μg/kg and patients of Group C received similar volume of normal saline, administered after 20 min of subarachnoid block with 0.5% hyperbaric bupivacaine. The cephalic level of sensory block, total duration of sensory analgesia and motor block were recorded. Sedation scores using Ramsey Sedation Score (RSS) and hemodynamic changes were also assessed.
Results: Demographic profile, duration of surgery and cephalic level of sensory block were comparable. The time for two segments regression was 142.35 ± 30.7 min in Group D, longer than Group C (98.54 ± 23.2 min). Duration of sensory blockade was 259.7 ± 46.8 min in the Group D versus 216.4 ± 31.4 min in Group C (P < 0.001). The mean duration of motor blockade showed no statistically significant difference between groups. There was clinically significant decrease in heart rate and blood pressure in patients of Group D. The RSS was higher (arousable sedation) in patients of Group D. No respiratory depression was observed.
Conclusion: Intravenous dexmedetomidine in dosage of 0.5 μg/kg, administered after 20 min of subarachnoid block prolonged the duration of sensory and motor blockade with arousable sedation.

Keywords: Bupivacaine, dexmedetomidine, intravenous, subarachnoid block

How to cite this article:
Gupta K, Tiwari V, Gupta PK, Pandey MN, Agarwal S, Arora A. Prolongation of subarachnoid block by intravenous dexmedetomidine for sub umbilical surgical procedures: A prospective control study. Anesth Essays Res 2014;8:175-8

How to cite this URL:
Gupta K, Tiwari V, Gupta PK, Pandey MN, Agarwal S, Arora A. Prolongation of subarachnoid block by intravenous dexmedetomidine for sub umbilical surgical procedures: A prospective control study. Anesth Essays Res [serial online] 2014 [cited 2021 Apr 15];8:175-8. Available from:

   Introduction Top

Subarachnoid block is a common regional anesthetic technique for sub umbilical surgical procedures. The intrathecal 0.5% hyperbaric bupivacaine is appropriate for surgeries lasting for about 120 min. To prolong the duration of analgesia and enhance the spinal anesthetic efficacy, the adjuvants from different pharmacological classes of drugs have been studied. Adjuvants during spinal anesthesia reduce the dose requirements of local anesthetic agents and hence their side-effects. [1],[2] Opioids have attained an integral role as a spinal anesthetic adjuvant, but its addition to local anesthetic solution may lead to pruritus and respiratory depression. [3] Clonidine, α2-adrenergic agonist, has been used widely intrathecally and intravenously after subarachnoid block to prolong the sensory and motor blockade without any such adverse effects. [4]

Dexmedetomidine, the highly selective α2-adrenergic agonist, is used as premedication during general anesthesia due to its sedative and analgesic effects. Dexmedetomidine exert its analgesic action both at the spinal and supraspinal levels. [5] Although synergistic interaction between intrathecal dexmedetomidine and local anesthetics has been observed in previous studies [6],[7] but there are not much clinical data regarding the effects of intravenous dexmedetomidine on the duration of sensory and motor block of spinal anesthesia.

The present prospective double-blind randomized control study was aimed to evaluate the effect of intravenous dexmedetomidine on sensory and motor block characteristics, hemodynamic changes and sedation during subarachnoid block.

   Materials and Methods Top

After approval of Institutional Ethical Committee and written informed consent, this prospective double blind randomized control study enrolled 60 adult patients of physical status American Society of Anesthesiologist (ASA) I and II of both genders, aged range from 25 to 65 years with body weight 55-85 kg and height 150-165 cm, scheduled for sub umbilical surgical procedures under subarachnoid block from August 2012 to September 2013. All patients were subjected to pre-anesthetic assessment and patients with history of severe cardiac diseases, hypertension, chronic obstructive respiratory disease, metabolic or endocrinal disorders, neurologic or renal dysfunction, bleeding or coagulation disorder, allergy to local anesthetic amides, infection at the site of lumber puncture, deformed spine or refusal to technique were excluded from the study.

Patients were randomized into two equal groups of 30 patients each according to computer generated number. Patients of Group D (study drug group) administered intravenous dexmedetomidine in a dose of 0.5 μg/kg and patients of Group C (control group) received normal saline. The study drug was premixed to a total volume of 10 ml and was administered intravenously over a period of 10 min as a single dose, 20 min after subarachnoid block with 0.5% hyperbaric bupivacaine, by an anesthesiologist not involved in the study.

On arrival to operation-theater, baseline vital parameters of heart rate, systemic arterial blood pressure, pulse oximetry and electrocardiography were recorded. All patients were pre-hydrated with 10 ml/kg Ringer lactate solution before initiation of the subarachnoid block. Under all aseptic condition, the subarachnoid block was established with an intrathecal injection of 3.5 ml 0.5% hyperbaric bupivacaine (17.5 mg) in a sitting position at the L2-3 or L3-4 interspace through midline approach using a 25 G Quincke spinal needle. All patients received oxygen 5 l/min via a face mask throughout the surgical procedure. The patient and the anesthesiologist were blinded to the treatment group and all recordings were performed by an anesthesiologist, who was blinded to randomization schedule.

The sensory block was assessed by pinprick method at 2 min intervals until the maximum level of the block was achieved and at 5 min interval subsequently. The motor blockade was evaluated bilaterally by modified Bromage scale (0-3): 0-Full movement, no power impairment, 1-Unable to raise extended leg at hip, 2-Unable to flex the knee, 3-No motor activity. Onset of motor block was considered when complete loss of motor power was achieved.

The onset time of sensory and motor blockade at T10 dermatome, maximum cephalic dermatome level of sensory block, the two dermatome regression time to reach S1 sensory level and time taken to achieve complete recovery from motor blockade were assessed. Post-operatively the sensory and motor block levels were assessed at 15 min intervals until normal sensation returned. Total duration of analgesia was defined as time from administration of subarachnoid block until the first complaint of pain. Injection diclofenac 75 mg intramuscular was used as rescue analgesic.

The systemic arterial blood pressure, heart rate, pulse oximetry and electrocardiography were recorded at base line, after subarachnoid block at 3 min interval until 20 min and then at 5 min interval until the end of surgery and thereafter at every 15 min in the first post-operative hour followed by every half hourly for next 3 h. For the present study, hypotension was defined as systolic blood pressure <100 mm Hg and was treated primarily by increasing the intravenous crystalloid infusion rate and additionally with vasoactive drugs, if required. Bradycardia was defined as heart rate <60 beats/min and was treated with atropine.

The level of sedation was evaluated intra-operatively using Ramsey Sedation Score (RSS): 1-Patient anxious, agitated or restless; 2-Patient co-operative, oriented and tranquil; 3-Patient responds to verbal commands; 4-Asleep with brisk response; 5-Asleep with sluggish response; 6-Asleep with no response. All sedation scores were recorded considering the time of start infusion of study drug as time zero. Intra-operatively any analgesic requirement, respiratory depression, nausea, vomiting and post-spinal shivering or any drug induced side-effects were noted and managed accordingly. An anesthesiologist, who blinded to the study drug used, documented all the parameters.

In order to detect a 30 min difference in mean duration of sensory block between the group for type 1 error of 0.01 and power of 90% to ensure statistically significant results, the minimum sample size required was 23 patients in each group. However, we included 30 patients in each group, assuming 5% drop out rate for better validation of results. The recorded data are presented in tabulated form as mean ± standard deviation and was analyzed using Statgraphics Centurion (Statpoint Technologies, Inc). The demographic data for categorical variables were compared using Chi-square test and statistical significance in mean difference was done by using Student's t-test. P < 0.05 was considered to be statistically significant.

   Results Top

The study was successfully completed on all 60 patients and all patients were co-operative with subsequent assessments of block characteristics and sedation. The demographic data were comparable between the groups for age, weight, height, sex, ASA physical status and duration of surgical procedures [Table 1].
Table 1: Demographic profile of patients

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There was no significant difference in the mean onset time of sensory analgesia at T10 dermatome and onset of motor blockade between the groups. The maximum level of cephalic spread of sensory blockade was comparable between the groups. The time required for two segment regression was significantly prolonged in Group D (124.35 ± 30.7) when compared with Group C (98.54 ± 23.2), P < 0.05. The mean duration of analgesia was significantly prolonged in Group D (259.70 ± 46.87 min vs. 216.40 ± 31.43 min in Group C, P < 0.001). Complete regression of motor blockade took longer time in Group D (189.34 ± 34.78 min vs. 168.67 ± 41.86 min in Group C) with no statistically significant difference. The motor blockade was of shorter duration in both groups when compared with sensory analgesia [Table 2].
Table 2: Sensory and motor blockade characteristics

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The basal hemodynamic parameters of heart rate and systemic blood pressure were comparable between the groups. Intra-operatively after dexmedetomidine infusion there was a clinically and statistically significant decrease in heart rate in patients of Group D and persisted to be lower for 90 min. Only two patients of Group C and nine patients of Group D required intravenous atropine administration. Similar trend was observed in systolic blood pressure. Hypotension was observed in five patients of Group C and seven patients of Group D and managed with an increased rate of intravenous Ringer lactate infusion and mephentermine 6-12 mg. Post-operatively, the heart rate was comparable between the groups but the systolic blood pressure continued to be clinically lower in patients Group D for the initial 60 min [Table 3].
Table 3: Intra-operative and post-operative adverse events

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The maximum mean RSS of 3.78 ± 0.47 was achieved after 20 min of intravenous dexmedetomidine in patients of Group D, while it was less than 2 in patients of Group C. However, RSS was comparable in both groups in the post-operative period. The respiratory depression was not observed in any patient, though respiratory rate was lower in Group D but oxygen saturation (SpO 2 ) was comparable between both groups.

Intra-operative shivering was observed in seven patients of Group C while only two patients of Group D showed shivering of lesser intensity. No significant complication occurred after use of intravenous infusion of dexmedetomidine in our study and no patient complaint of any neurological symptoms [Table 3].

   Discussion Top

Intravenous dexmedetomidine prolonged the duration of bupivacaine induced sensory blockade during subarachnoid block and increased the time for the first request of analgesic for post-operative pain relief. Dexmedetomidine was well tolerated and provided clinically effective but arousable sedation without any respiratory depression. No systemic and neurotoxic adverse effects of dexmedetomidine were observed in any patient during the study.

Dexmedetomidine is pharmacologically related to clonidine and has been shown to produce sedation by binding to α2-receptors in the locus coeruleus. The locus coeruleus and the dorsal raphe are important central neural structures where it acts producing sedation and analgesia. The effect seems to be mediated through both presynaptic and the post-synaptic α2-receptors. [8] The results of our study indicate that infusion of dexmedetomidine enhanced the duration of sensory analgesia, may be due to activation of α2-receptor induced inhibition of nociceptive impulse transmission. Studies by Al-Mustafa et al. and Reddy et al. also observed similar findings in their study. [9],[10]

It is recommended to administer dexmedetomidine over more than 20 min as rapid or bolus intravenous administration might produce sudden hypertension and bradycardia until the central sympathetic effects dominates, resulting in a decrease of systemic blood pressure and heart rate from baseline. Most of the studies have noted bradycardia with incidence varying from 30% to 40% sometimes requiring treatment with atropine. No biphasic change or significant cardiovascular variability occurred as dexmedetomidine 0.5 μg/kg was given over 10 min and sufficient pre-hydration in this study.

Synergistic interaction between dexmedetomidine and local anesthetics has been observed in previous studies. Memiş et al. in their study have reported that addition of 0.5 μg/kg dexmedetomidine to lidocaine for intravenous regional anesthesia shortened sensory and motor block onset times and prolonged the recovery. [11] A study by Coskuner et al. have shown that intravenous administration of dexmedetomidine might prolong the recovery time of the sensory blockade during epidural anesthesia. [12] In addition, compared with the prolongation of the sensory block, the duration of motor block was not affected by dexmedetomidine. In our study, no significant difference was observed between the groups. Kaya et al. have used a single dose of 0.5 μg/kg dexmedetomidine and reported no effect on duration of motor block. [13]

Dexmedetomidine induced intra-operative sedation eliminates the need of additional sedatives, thus provided better conditions for the surgeon and the patient. [14] Our study has demonstrated effective sedation of 3.78 ± 0.47, as observed by Ramsay sedation scale. Slower respiratory rate was not clinically significant enough to be considered as respiratory depression. SpO 2 was maintained equally well in all patients.

Regional anesthesia produces vasodilation, which facilitate core to peripheral redistribution of heat and cause shivering. [15] Dexmedetomidine decreases the thermoregulatory threshold for vasoconstriction and shivering. In our study, only two patients of Group D and seven patients of Group C showed intra-operative shivering, but the intensity of shivering was lesser in patients of Group D.

   Conclusion Top

Intravenous dexmedetomidine in a single dosage of 0.5 μg/kg, administered after 20 min of subarachnoid block, prolonged the duration of sensory and motor blockade with arousable sedation without respiratory depression. It prevented the post-spinal shivering.

   References Top

1.Chilvers CR, Goodwin A, Vaghadia H, Mitchell GW. Selective spinal anesthesia for outpatient laparoscopy. V: Pharmacoeconomic comparison vs general anesthesia. Can J Anaesth 2001;48:279-83.  Back to cited text no. 1
2.Liu SS, McDonald SB. Current issues in spinal anesthesia. Anesthesiology 2001;94:888-906.  Back to cited text no. 2
3.Ozgurel O. Comparison of fentanyl added to ropivacaine or bupivacaine in spinal anesthesia. Reg Anesth Pain Med 2003;28:Abs 89.  Back to cited text no. 3
4.Rhee K, Kang K, Kim J, Jeon Y. Intravenous clonidine prolongs bupivacaine spinal anesthesia. Acta Anaesthesiol Scand 2003;47:1001-5.  Back to cited text no. 4
5.Paris A, Tonner PH. Dexmedetomidine in anaesthesia. Curr Opin Anaesthesiol 2005;18:412-8.  Back to cited text no. 5
6.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.  Back to cited text no. 6
7.Harsoor S, Rani DD, Yalamuru B, Sudheesh K, Nethra S. Effect of supplementation of low dose intravenous dexmedetomidine on characteristics of spinal anaesthesia with hyperbaric bupivacaine. Indian J Anaesth 2013;57:265-9.  Back to cited text no. 7
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8.Gerlach AT, Dasta JF. Dexmedetomidine: An updated review. Ann Pharmacother 2007;41:245-52.  Back to cited text no. 8
9.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.  Back to cited text no. 9
10.Reddy VS, Shaik NA, Donthu B, Reddy Sannala VK, Jangam V. Intravenous dexmedetomidine versus clonidine for prolongation of bupivacaine spinal anesthesia and analgesia: A randomized double-blind study. J Anaesthesiol Clin Pharmacol 2013;29:342-7.  Back to cited text no. 10
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11.Memiº D, Turan A, Karamanlioðlu B, Pamukçu Z, Kurt I. Adding dexmedetomidine to lidocaine for intravenous regional anesthesia. Anesth Analg 2004;98:835-40.  Back to cited text no. 11
12.Coskuner I, Tekin M, Kati I, Yagmur C, Elcicek K. Effects of dexmedetomidine on the duration of anaesthesia and wakefulness in bupivacaine epidural block. Eur J Anaesthesiol 2007;24:535-40.  Back to cited text no. 12
13.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.  Back to cited text no. 13
14.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.  Back to cited text no. 14
15.Moorf M, Khan SA, Jain D, Khan RM, Maroof SM. Evaluation of effect of dexmedetomidine in reducing shivering following epidural anesthesia. Anesthesiology 2004;101:A495.  Back to cited text no. 15


  [Table 1], [Table 2], [Table 3]

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