• J Y Jung, C Lee, H Ro, H S Kim, K W Joo, Y Kim, C Ahn, J S Han, S Kim, and K-H Oh.
• Division of Nephrology, Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea.
• Clin Nephrol. 2009 Mar 1;71(3):333-7.

ObjectiveTo report a sequential occurrence of life-threatening hypokalemia and rebound hyperkalemia following barbiturate coma therapy.Case HistoryA 53-year-old man was admitted to the division of nephrology due to sudden development of severe hypokalemia. The patient had been treated following a clinical diagnosis of traumatic subarachnoid hemorrhage and subdural hematoma. Barbiturate coma therapy had been performed on this patient. He developed fatal hypokalemia 10 hours after the start of thiopental administration which did not respond to potassium supplementation. The lowest potassium level following barbiturate coma therapy was 1.0 mmol/l. Severe bradycardia and cardiac arrest developed, which necessitated cardiac massage and treatment with epinephrine and atropine. He recovered from cardiac arrest. When thiopental infusion was suddenly stopped, the potassium level increased to 8.9 mmol/l, which required quick administration of calcium gluconate and infusion of glucose solution mixed with regular insulin. Despite such management, he developed asystole. After direct current cardioversion and emergency hemodialysis, he recovered from cardiac arrest and his serum potassium level was stabilized.ConclusionWe recommend that clinicians must be aware of the potential occurrence of severe hypokalemia, which is rare but fatal, following barbiturate coma therapy. Rebound hyperkalemia, which is fatal, may also occur following cessation of thiopental infusion. Clinicians should also be aware of this potential complication. Further studies are needed to elucidate the precise mechanism of this clinical event.

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