Thiopental Pharmacokinetics in Patients with Cirrhosis

The Risk of Surgery in Patients With Liver Disease

“…Although the metabolism of thiopental is decreased in patients with cirrhosis, plasma protein binding of thiopental is also decreased, so that total body clearance of the drug is unaltered in cirrhosis. 13 Rare instances of usually cholestatic hepatotoxicity caused by benzodiazepines or barbiturates, including a syndrome of fever, hepatitis, lymphadenopathy, eosinophilia, and dermatitis, are no more likely in patients with liver disease than in those without liver disease. 14 Chlorpromazine has a more depressant effect on the central nervous system in patients with liver dysfunction than in healthy subjects.…”

The volatile anesthetics, halothane, enflurane and isoflurane, influence the distribution of thiopental in man differently

“…An inhibition of the thiopental metabolism by halothane with a consequent increase of the T-values cannot be considered as the causc of this phenomenon since, first: thiopental is extracted by the liver only to a small extent (9) so that changes of liver functions in general are negligible for its early distribution phase; second: changes in the metabolism of thiopental cannot be responsible in this period (0-15 min) since they take place very slowly. Furthermore, studies in patients with liver cirrhosis showed that thiopental pharmacokinetics (V,., C1, tip) were inlluenced only slightly, despite the hepatic-dependent route of elimination for this thiobarbiturate (17). I t seems most likely that specific eirects of halothane on the cardiovascular system or on the tissue perfiision rate are responsible for this interaction which was not observed during anesthesia with enflurane or isollurane.…”

A Survey of Current Practice and Attitudes Surrounding the Use of Ancillary Tests in the Diagnosis of Brainstem Death in Neurocritical Care Units in the UK

“…It may be difficult to predict a mathematical model, as thiopentone exhibits large intra-patient and inter-patient variability due to patient age, obesity, renal and hepatic dysfunction, and hepatic enzyme induction. Several studies [4][5][6] investigating the effect of renal and hepatic dysfunction on the pharmacokinetics and pharmacodynamics of thiopentone highlight the complexity of predicting thiopentone elimination where organ dysfunction co-exists, as is common in the intensive care population. The measurement of serum thiopentone levels remains the only robust means of excluding residual drug effect.…”