ABSTRACT
Clinical manifestations of valproic acid (VPA) toxicity can range from just mild confusion and drowsiness to serious encephalopathy, leading to depressed sensorium and even coma and death. The exact cause(s) of how VPA influences the integrity of brain function remains unknown. Nevertheless, several mechanisms have been postulated including a surge in the blood ammonia concentration. Valproic acid-induced hyperammonemic encephalopathy is a rare yet serious sequalae and that can lead to grave outcomes. We report a case of hyperammonemic encephalopathy with preserved liver function following a moderate VPA intoxication in a toddler, who was successfully managed conservatively. Additionally, we briefly discuss mechanistic basis of VPA toxicity and highlight some of the available potential therapies.
