Hypokalemia after cessation of the therapeutic barbiturate coma- an unusual complication.indd

Barbiturate coma is one of the treatment modalities used to prevent secondary brain damage in refractory malignant intracranial tension both in traumatic and non-traumatic brain injuries. Complications such as hypotension, myocardial suppression, hepatorenal dysfunction and delayed return of consciousness have been reported following barbiturate coma therapy. In addition, potassium changes have also been reported, in particular hypokalemia during barbiturate coma therapy and a rebound hyperkalemia after cessation of therapy. We however report an unusual complication of refractory hypokalemia occurring after stopping barbiturate therapy. A 24-year-old patient was treated with a thiopentone infusion for management of increased intracranial pressure after severe head injury. The patient developed persistent hypokalemia (1.6 mmol) 8 hours after withdrawing thiopentone infusion. Severe disturbance of plasma potassium balance is a rare but life-threatening complication of therapeutic barbiturate coma. We recommend that clinicians be aware of the potential occurrence of severe hypokalemia, which is rare but fatal, not only during barbiturate coma therapy but also following cessation of thiopentone infusion. We recommend close monitoring of serum potassium during as well as after discontinuing barbiturate coma therapy in order to prevent fatal complications secondary to potassium abnormalities. Further studies are needed to elucidate the precise mechanism of this clinical event. From Singapore General Hospital, Singapore (Sudhakar Subramani and