In this prospective single-blinded randomized control trial, a total of 43 patients were recruited (Figure 1). Distributions of patients in both groups were similar with respect to age, weight, sex, American Society of Anesthesiologists physical status, and duration of surgery. The mean time for two dermatomal regressions was significantly prolonged in group A than B (2.3 ± 0.4 h vs.1.6 ± 0.5 h) with a P value of 0.001. The mean time for regression to S1 dermatome was also significantly prolonged in group A (5.2 ± 0.83 h vs. 4.4 ± 0.87 h) with a P value of 0.01 (Table 1). Percentage of decrease in heart rate at one hour after the subarachnoid block was statistically not significant between groups (27.9 ± 8.7% fall vs. 20.5 ± 8.7% fall). Percentage of systolic blood pressure and mean arterial pressure drop at one hour after subarachnoid block were comparable (Table 2). Glycopyrrolate was administered in 45% of patients in group A and 21% in group B (Figure 2). This was found to be statistically significant with a P value of 0.039. Ephedrine was required for 30% of patients in group A and 13% in group B. This was not statistically significant. Intravenous atropine was not used in any of the patients. There were no incidences of desaturation or excessive sedation observed in either of the group. There were also no delays in shifting patients out of recovery unit noted in the study groups.
Spinal anesthesia is the most common choice of anesthesia for infraumbilical surgeries of short duration. Various intravenous agents like midazolam,5,7,8 propofol,9 butorphanol,10 dexmedetomidine1,11,12 and clonidine13,14 have been used along with spinal anesthesia with the aim of prolonging the duration of the sensory block. Even with an adequate sensorimotor block of a desired dermatomal level, most patients would benefit from anxiolysis and sedation during the surgical period. Recently intravenous dexmedetomidine has been frequently studied for its efficiency in prolonging the duration of the sensorimotor block. Some of the studies have emphasized caution while administering dexmedetomidine due to its association with bradycardia.15 In our study, we compared the efficacy of two intravenous drugs, midazolam and dexmedetomidine, in prolonging the duration of the sensory block of spinal anesthesia and in enhancing patient comfort. We did not find equipotent doses between intravenous dexmedetomidine and intravenous midazolam. We chose doses that were reported to provide adequate levels of sedation. In our study intravenous dexmedetomidine was given five minutes after intrathecal bupivacaine prolonged the time taken for two dermatomal sensory regression from the highest level and regression of blockade to S1 dermatome by 45 minutes. Similar observations were made by Kaya FN et al,7 Rekhi BK et al,5 Bisht S et al16 and Patel VH et al.6 However, in the study by Kaya FN et al,7 there was no significant prolongation of time taken for regression to S1 dermatome between the two groups. This conflict could be explained by the fact that in our study bolus dose of intravenous dexmedetomidine was followed by an infusion till the end of surgery.
Dexmedetomidine provides analgesia through supraspinal effects which are mediated by activation of both pre-synaptic and post-synaptic sympathetic nerve terminal and central nervous system resulting in suppression of noradrenergic neurons.17,18 This analgesic effect is obtained after dexmedetomidine administration irrespective of the route whereas midazolam has no analgesic property following intravenous injection. This could be the reason for prolongation of sensory block in our patients in dexmedetomidine group.
In our study, the incidence of bradycardia was higher in the dexmedetomidine group than midazolam group even though we used a lower bolus dose than used in previous studies.5,6,7 Glycopyrrolate was required for 45% (9of 20) patients in the dexmedetomidine group and 21% (5 of 23) patients in the midazolam group. Similar observations were made by YoonDK et al,4 Rekhi BK et al5 and Bisht S et al.16 However in contrast, no bradycardia was noted in a study by Patel VH et al.5 The initial bolus of dexmedetomidine results in a transient increase of blood pressure and reflex bradycardia. This is explained by its action on ?2 B receptors and was mitigated by a slow infusion over 10 minutes. This was followed by delayed bradycardia which could be due to inhibition of central sympathetic outflow overriding the direct stimulant effect of dexmedetomidine.3
Meta-analysis of 7 randomized control trials19 analyzed a total of 364 patients and concluded that iv dexmedetomidine used along with spinal anesthesia prolonged sensory blockade by 34% and motor blockade by 17%. But dexmedetomidine caused 3.7 fold increase in bradycardia which responded to standard treatment.
The fall in blood pressure from the baseline at one hour was statistically similar in both our groups. Ephedrine was required in 30% of our patients in the dexmedetomidine group and 13% in the midazolam group. Similar observations were made by Rekhi BK et al,5 Bisht S et al16 and Patel VH et al.6 But in a study by Sangma SJN et al11 higher incidences of hypotension was documented. The higher incidence of hypotension could be attributed to the higher bolus and infusion doses of dexmedetomidine used.
In a study by Talakoub et al,20 addition of 30 ?g/kg of intravenous midazolam to lignocaine for spinal anesthesia improved duration of the motor block without causing any side effects. Various previous studies have shown4,5,7,11,16 prolongation of motor blockade when dexmedetomidine was given to patients under subarachnoid block. But we have not looked into this because it was difficult to assess regaining of motor power intraoperatively and most of our patients were mobilized after 12 hours postoperatively as per institutional policy. Similar to previous studies5,6,7,11 we did not encounter excessive sedation or desaturation or delay in shifting out of the recovery unit in any of our patients. As in our study, a lower dexmedetomidine bolus dose followed by an infusion was used, we could provide an adequate level of sedation with better patient comfort without compromising the efficacy in prolonging the duration of sensory blockade of spinal anesthesia.
Limitations of study
The dose of spinal bupivacaine was fixed at 15 mg irrespective of the patient’s height, which could have led to a greater degree of block in short stature individuals. The study drugs were continued till the end of surgery causing some of the patients to receive a higher volume of drugs which could have affected the total duration of the sensory block. We could have used an additional saline placebo group to have a better comparison.
The study can be extended to compare weight based calculated dose versus titrated doses of intravenous dexmedetomidine to maintain an optimal level of sedation and to limit the incidence of bradycardia during spinal anesthesia. A study involving administration of intravenous dexmedetomidine to patients undergoing surgeries under epidural anesthesia can be done, to find out if the requirement of local anesthetics can be reduced.
Intravenous dexmedetomidine prolongs the duration of spinal anesthesia than intravenous midazolam in patients undergoing infraumbilical surgeries. The use of intravenous dexmedetomidine for prolonging spinal anesthesia should be practiced with caution due to a higher incidence of hemodynamic instability. However, these adverse effects were responding well to treatment.