[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. The median time to onset of hypokalaemia was 11 h and the time to nadir of serum potassium levels was 25 h. More importantly, 34% patients developed hyperkalaemia on weaning off barbiturate therapy. All patients who developed hyperkalaemia had previously been hypokalaemic. The mean potassium replaced during hypokalaemia was higher in patients who developed hyperkalaemia compared to those who did not. Therefore, hypokalaemia and hyperkalaemia are frequently associated with induction and cessation of 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. Hyperkalaemia at cessation has been described as cause of cardiac arrest in this population.