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Clinical Trial
Comparative Study
Journal Article
Randomized Controlled Trial
Enhancement of intrathecal lidocaine by addition of local and systemic clonidine.
Acta Anaesthesiologica Scandinavica 1999 May
BACKGROUND: Enhancement of local anesthetic-produced regional blocks by clonidine seems well established. There are insufficient data about dose-effect relationship of combinations of clonidine with individual agents, efficiency of local versus systemic administration of clonidine, and comparative evaluation of clonidine with vasoconstrictors. Because of unavailability of long-acting local anaesthetics at the time of study, our aim was to evaluate augmentation of lidocaine spinal block with local or systemic clonidine and to compare the results with the efficacy of intrathecal phenylephrine.
METHODS: Ninety pts of age 50-72 yrs with ASA 1-4 physical status, scheduled for open prostatectomies, hysterectomies or ostheosynthesis of fractured hip were randomized to one of 6 treatment groups, 15 pts in each. Patients received intrathecally (L3-L4) either 100 mg of plain lidocaine (group L100); or a mixture of lidocaine 40 and 80 mg with clonidine 100 micrograms (groups L40-C100 and L80-C100); or a combination of lidocaine 40 and 80 mg with clonidine 300 micrograms orally 60 min before spinal puncture (L40-C300 and L80-C300). Addition of intrathecal phenylephrine 5 mg to 80 mg of lidocaine was also investigated (L80-P5).
RESULTS: There were no significant intergroup differences concerning demographic data or type of surgery. All operations (duration up to 150 min) were completed without need for analgesic supplementation. The addition of clonidine resulted in a significant reduction of the onset time of spinal block and prolongation of the duration of sensory and motor blocks compared to plain lidocaine or lidocaine with phenylephrine. In spite of the well-known hypotensive action of alpha 2-agonists, haemodynamic depression only in group L80-C300 was significantly more pronounced than in L100 and L80-P5 groups. The least decrease of BP and minimal need of rescue ephedrine among all patients studied were recorded in the group receiving low dosage of lidocaine with intrathecal clonidine (L40-C100). Sedation occurred in most patients receiving clonidine.
CONCLUSION: Our results indicate that addition of clonidine to lidocaine, irrespective of the route of administration, prolongs the duration of spinal block and permits a reduction of the lidocaine dose needed for a given duration of block. Addition of phenylephrine results in a less pronounced statistically significant prolongation of anaesthesia. The regression of sensory block before restoration of motor function seems to be a specific (and unfortunate) effect of both clonidine and phenylephrine.
METHODS: Ninety pts of age 50-72 yrs with ASA 1-4 physical status, scheduled for open prostatectomies, hysterectomies or ostheosynthesis of fractured hip were randomized to one of 6 treatment groups, 15 pts in each. Patients received intrathecally (L3-L4) either 100 mg of plain lidocaine (group L100); or a mixture of lidocaine 40 and 80 mg with clonidine 100 micrograms (groups L40-C100 and L80-C100); or a combination of lidocaine 40 and 80 mg with clonidine 300 micrograms orally 60 min before spinal puncture (L40-C300 and L80-C300). Addition of intrathecal phenylephrine 5 mg to 80 mg of lidocaine was also investigated (L80-P5).
RESULTS: There were no significant intergroup differences concerning demographic data or type of surgery. All operations (duration up to 150 min) were completed without need for analgesic supplementation. The addition of clonidine resulted in a significant reduction of the onset time of spinal block and prolongation of the duration of sensory and motor blocks compared to plain lidocaine or lidocaine with phenylephrine. In spite of the well-known hypotensive action of alpha 2-agonists, haemodynamic depression only in group L80-C300 was significantly more pronounced than in L100 and L80-P5 groups. The least decrease of BP and minimal need of rescue ephedrine among all patients studied were recorded in the group receiving low dosage of lidocaine with intrathecal clonidine (L40-C100). Sedation occurred in most patients receiving clonidine.
CONCLUSION: Our results indicate that addition of clonidine to lidocaine, irrespective of the route of administration, prolongs the duration of spinal block and permits a reduction of the lidocaine dose needed for a given duration of block. Addition of phenylephrine results in a less pronounced statistically significant prolongation of anaesthesia. The regression of sensory block before restoration of motor function seems to be a specific (and unfortunate) effect of both clonidine and phenylephrine.
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