Article Sidebar
Article Details
Issue
Section
Articles
By submitting manuscripts to SAJAA, authors of original articles are assigning copyright to the SA Society of Anaesthesiologists. Authors may use their own work after publication without written permission, provided they acknowledge the original source. Individuals and academic institutions may freely copy and distribute articles published in SAJAA for educational and research purposes without obtaining permission.
Main Article Content
A comparison of induction of anaesthesia using two different propofol preparations
Abstract
Background: Investigators have reported inter-patient variability with regard to propofol dosage for induction of anesthesia, since early dose finding studies. With the arrival of generic formulations of propofol, questions have arisen regarding further variability in dose requirements. Various studies have confirmed that generic propofol preparations are pharmacokinetically and pharmacodynamically equivalent to Diprivan®. Nevertheless a number of practitioners are under the impression that certain generic propofol preparations require greater doses for induction of anaesthesia than does Diprivan®.
Methods: 20 female patients of ASA status I-II, between the ages of 18-55 years, scheduled for routine surgery were randomly allocated to two groups to undergo induction of anaesthesia using two different propofol formulations; Diprivan® and Propofol 1% Fresenius®. Either preparation was administered using a target-controlled infusion of propofol (STEL-TCI) targeting the plasma (central) compartment at a concentration of 6 μg.ml-1, employing the pharmacokinetic parameters of Marsh et al. A processed EEG (bispectral index) was continuously recorded. Loss of consciousness (LOC) was regarded as the moment at which the patient could not keep her eyes open and was confirmed by the absence of an eyelash reflex. At this point propofol administration was discontinued and data were recorded for a further two minutes, before administering an appropriate opioid and/or nitrous oxide/volatile agent and/or muscle relaxant to maintain anaesthesia. Time to LOC after start of propofol administration, and the dose of propofol administered during induction were annotated. Results: There were no demographic differences between the groups. There were no differences between the groups with regard to the mean dose for LOC, time to LOC and to the mean BIS values obtained at the following stages: awake, at LOC, at 1 and 2 minutes after LOC as well as the lowest recorded value.
Conclusions: Our results confirm that the two propofol formulations that we studied, are pharmacologically equivalent with regard to induction of anaesthesia. Other mechanisms can explain the variability in clinical response to bolus administration of propofol. The most important is the recirculatory or “front-end” kinetics of propofol in which cardiac output plays a major role, as well as the rate of drug administration. Emulsion degradation can also influence dose-response and in this regard it should be noted that the addition of foreign substances such as lignocaine, can result in rapid deterioration of the soyabean emulsion.
Methods: 20 female patients of ASA status I-II, between the ages of 18-55 years, scheduled for routine surgery were randomly allocated to two groups to undergo induction of anaesthesia using two different propofol formulations; Diprivan® and Propofol 1% Fresenius®. Either preparation was administered using a target-controlled infusion of propofol (STEL-TCI) targeting the plasma (central) compartment at a concentration of 6 μg.ml-1, employing the pharmacokinetic parameters of Marsh et al. A processed EEG (bispectral index) was continuously recorded. Loss of consciousness (LOC) was regarded as the moment at which the patient could not keep her eyes open and was confirmed by the absence of an eyelash reflex. At this point propofol administration was discontinued and data were recorded for a further two minutes, before administering an appropriate opioid and/or nitrous oxide/volatile agent and/or muscle relaxant to maintain anaesthesia. Time to LOC after start of propofol administration, and the dose of propofol administered during induction were annotated. Results: There were no demographic differences between the groups. There were no differences between the groups with regard to the mean dose for LOC, time to LOC and to the mean BIS values obtained at the following stages: awake, at LOC, at 1 and 2 minutes after LOC as well as the lowest recorded value.
Conclusions: Our results confirm that the two propofol formulations that we studied, are pharmacologically equivalent with regard to induction of anaesthesia. Other mechanisms can explain the variability in clinical response to bolus administration of propofol. The most important is the recirculatory or “front-end” kinetics of propofol in which cardiac output plays a major role, as well as the rate of drug administration. Emulsion degradation can also influence dose-response and in this regard it should be noted that the addition of foreign substances such as lignocaine, can result in rapid deterioration of the soyabean emulsion.
