Role of Clonidine as adjuvant to intrathecal bupivacaine in patients undergoing lower abdominal surgery: A randomized control study

Abstract

Background:Neuraxial anesthesia greatly expands the anesthesiologist armamentarium, providing alternatives to general anesthesia, especially in the lower abdominal surgeries. Clonidine, an alpha-2 adrenergic agonist, has a variety of actions, including potentiation of effects of local anesthetics. This study was undertaken to assess the degree of sensory and motor block and postoperative analgesia provided by low dose (50 mcg) intrathecal clonidine admixed with bupivacaine.Aims:The aim of this study is to establish efficacy and safety of intrathecal clonidine as adjuvant to bupivacaine.Settings and Design:The type of the study was double-blind randomized trial.Materials and Methods:Hundred patients were randomly allocated in two groups, A and B. Group A received bupivacaine 0.5%, 3 ml with placebo (normal saline 0.33 ml) and Group B, bupivacaine 0.5%, 3 ml with clonidine 50 μg (0.33 ml).Statistical Analysis Used:Statistical Package for Social Sciences version 15.0 statistical analysis software.Results:Mean duration of motor block was significantly higher in Group B (280.80 ± 66.88 min) as compared with Group A (183.60 ± 77.06 min). Significant difference in duration of sensory block was noted between Group B (295.20 ± 81.17 min) and Group A (190.80 ± 86.94 min). Duration of postoperative analgesia was significantly higher in Group B as compared to Group A (551.06 ± 133.64 min and 254.80 ± 84.19 min respectively). Mean visual analog scale scores at different time intervals were significantly lower in the study group (except for 4-h time interval), but the control group had better hemodynamic stability as compared with study group.Conclusion:The findings in this study suggested that use of clonidine 50 μg added to bupivacaine for spinal anesthesia effectively increased the duration of sensory block, duration of motor block, and duration of analgesia.

Transmission pathways and mediators as the basis for clinical pharmacology of pain

“…Singh et al [152] studied Clonidine as an adjuvant to Bupivicaine in patients undergoing abdominal surgery. They showed that spinal anesthesia that contained Clonidine and Bupivicaine provided longer-lasting blockade of motor movement and sensation, as well as longer-term analgesia [152] compared to giving Bupivicaine alone.…”

“…Singh et al [152] studied Clonidine as an adjuvant to Bupivicaine in patients undergoing abdominal surgery. They showed that spinal anesthesia that contained Clonidine and Bupivicaine provided longer-lasting blockade of motor movement and sensation, as well as longer-term analgesia [152] compared to giving Bupivicaine alone. Similarly, Sen and Sen [153] found Clonidine to be an effective adjuvant to Bupivicaine and noted that patients who received Clonidine with Bupivicaine waited longer after surgery before requesting additional analgesia.…”

Comparison of two different doses dexmedetomidine as an adjuvant to bupivacaine in sub-arachnoid block for abdominal hysterectomies. A randomized double blinded study.

“…16 Intrathecal clonidine is known for severe hypotension and bradycardia. 17 Compared to clonidine, dexmedetomidine produces optimal hypotension which decreases blood loss during major abdominal surgeries like hysterectomies. 18,19 One study conducted with different doses of intrathecal dexmedetomidine (5 µg, 10 µg, 15 µg and 20 µg) as an adjuvant to assess duration of sensory block, motor block and duration of pain relief concluded that 5 µg and 10 µg are optimal doses.…”

Randomized clinical study comparing safety and efficacy of adjuvant intrathecal clonidine versus normal saline along with bupivacaine anaesthesia in lower limb surgery patients

“…As a result, the dose response for clonidine by neuraxial administration is U shaped with peripheral vasoconstriction from circulating drug concentration at high doses opposing central sympatholysis. 19 In addition, clonidine directly inhibits sympathetic preganglionic neurons in the spinal cord. The degree of clonidine induced hypotension is related to the spinal level of injection.…”

“…The explanation for this could be that α2 agonist induce cellular modification in the ventral horn of spinal cord (motoneuron hyperpolarisation) and facilitate local anaesthetic action. 18,19 Clonidine may cause local vasoconstriction, thereby reducing vascular removal of local anaesthetics surrounding the neural structures. This may also partly explain increased duration of motor blockade associated with clonidine administration.…”