Severe hypokalemia and rebound hyperkalemia during barbiturate coma in patients with severe traumatic brain injury

To evaluate the incidence of severe potassium disturbances during barbiturate coma therapy in patients with severe traumatic brain injury (TBI), and the characteristics of these patients.

The study comprised 37 patients with severe TBI who were treated for barbiturate coma between 2015 and 2017 in level 3 intensive care units of two hospitals.

No potassium disturbance occurred in 14 patients. Seventeen patients developed mild-moderate hypokalemia (2.6-3.5mEq/L), and 6 patients developed severe hypokalemia (<2.5mEq/L) following the induction of barbiturate therapy. The incidence of mild-to-severe barbiturate-induced hypokalemia was 62.2% and the rate of severe hypokalemia was 16.2%. The mean potassium supply per day during thiopentone therapy was statistically significantly different between patients with mild-to-moderate hypokalemic and those with severe hypokalemic (p<0.001). Four of 6 patients with severe hypokalemia developed rebound hyperkalemia exceeding 6mEq/L following the cessation of barbiturate infusion. The nadir potassium concentration was 1.5mEq/L and the highest value was 6.8mEq/L. The mean time to reach nadir potassium concentrations was 2.8 days. The mortality rate of the 6 patients was 66.7%. Of the 2 survivors of severe hypokalemia, the Glasgow Outcome Scale (GOS) on discharge and the extended GOS one year after the trauma were 5 and 8 respectively.

Severe hypokalemia refractory to medical treatment and rebound hyperkalemia is a serious adverse effect of thiopentone coma therapy in patients with severe TBI. Excessive and aggressive potassium replacement during the barbiturate-induced hypokalemia period must be avoided. Weaning barbiturate treatment over time may be advantageous in the management of severe serum potassium disturbances.