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

PURPOSE: There have been case reports of hypokalaemia and hyperkalaemia on induction and cessation of thiopentone barbiturate coma for refractory intracranial hypertension, respectively. However, the incidence and characteristics are not well described.

METHODS

We performed a retrospective review of all patients who received thiopentone barbiturate therapy for refractory intracranial hypertension during an 18-month period from January 2004 to June 2005 in our neurosurgical intensive care unit (ICU).

RESULTS

During this time period, 47 patients received thiopentone barbiturate therapy for refractory intracranial hypertension. Forty-two (89.4%) patients developed hypokalaemia after induction of barbiturate therapy. The median time to onset of hypokalaemia was 11 (6-23) h and time to nadir of serum potassium levels was 25 (15-41) h. Sixteen (34%) patients developed hyperkalaemia on weaning of barbiturate therapy. The peak serum potassium levels developed 31 (28-56) h after cessation. All patients who developed hyperkalaemia had been hypokalaemic previously. The mean potassium replaced during hypokalaemia was higher in patients who developed hyperkalaemia compared to those who did not (230 ± 135 vs. 66 ± 70, p < 0.001).

CONCLUSIONS

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.