While the most common cause of hyperammonemic (HA) coma is hepatic disorder, other rare etiologies to be considered include congenital causes, drug induced states, portosystemic shunts, and urinary tract infections with urea-splitting organisms. HA usually results from one of the following three mechanisms: A relative excessive nitrogen load on a normal functioning liver via the portal circulation (e.g., parenteral nutrition in a patient with urea cycle defect); ammonia bypassing liver (e.g., congenital vascular malformations, portal hypertension in cirrhotic patients); or from impaired ammonia metabolism. Herein, we describe a case of HA coma secondary to an interplay of multiple psychiatric drugs mainly sodium valproate and probably an added effect by the lithium-induced hypothyroidism/myxedema.
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