Severe hypokalemia and rebound hyperkalemia due to barbiturate coma

What is it about?

Objectives: 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. Methods: 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. Results: No potassium disturbance occurred in 14 patients. Seventeen patients developed mild-moderate hypokalemia (2.6–3.5 mEq/L), and 6 patients developed severe hypokalemia(<2.5 mEq/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 hypokalemia (p < 0.001). Four of 6 patients with severe hypokalemia developed rebound hyperkalemia exceeding 6 mEq/L following the cessation of barbiturate infusion. The nadir potassium concentration was 1.5 mEq/L and the highest value was 6.8 mEq/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 and8 respectively. Conclusions: 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 overtime may be advantageous in the management of severe serum potassium disturbances.

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