Dyskalaemia associated with thiopentone barbiturate coma for refractory intracranial hypertension: a case series

Abstract

Hypokalaemia and hyperkalaemia are frequently associated with induction and cessation of thiopentone barbiturate coma. Serum potassium levels must be monitored vigilantly. Patients who develop hypokalaemia and receive large potassium replacement may be at greater risk of hyperkalaemia on cessation.

Prevalence of severe hypokalaemia in patients with traumatic brain injury

“…Thus, it seems highly unlikely that mannitol administration alone caused the profound electrolyte disorders, although it may have been a contributing factor in some patients. Barbiturate and hypothermia therapy is recommended for control of refractory intracranial hypertension [20] and associated with hypokalaemia [21] and hypophosphataemia [22,23], but they were not used in our population.…”

Year in review in Intensive Care Medicine 2011: I. Nephrology, epidemiology, nutrition and therapeutics, neurology, ethical and legal issues, experimentals

“…However, the real incidence and characteristics of dyskalaemia during and after barbiturate coma have not been well described. Ng et al [55] performed a retrospective review of all 47 patients who received barbiturate therapy for refractory HICP during an 18-month period in a neurosurgical ICU. 89.4% of the barbiturate patients’ cohort developed hypokalaemia after the induction of barbiturate therapy.…”

Life-Threatening Dyskalaemia after Barbiturate Coma Therapy: The Strategy of Management

“…In another recent retrospective study, Ng et al reported that 89.4% of patients on thiopentone BCT for refractory intracranial hypertension developed hypokalaemia after induction of the therapy and severe hypokalaemia was reported in only 23.4% of patients. In this study, 34% of patients developed hyperkalaemia during the weaning of BCT (4).…”

“…This report suggested that a lower potassium replacement target threshold of 3.0 mmol/l might be appropriate in the absence of cardiac arrhythmias. Controlled weaning of BCT, instead of abrupt termination, was recommended, and frequent serum potassium monitoring up to 72 hours following cessation is warranted (4). In other reports that applied hyperkalaemia event following the cessation of BCT may be due to the reduction of barbiturateinduced Na + -K + -ATPase activity, resulting in extracellular potassium redistribution (5).…”