A Case of Valproic-Acid Induced Hyperammonemic Encephalopathy

Abstract

Valproic acid (VPA), an antiepileptic medication, is known to cause hyperammonemia, which may be asymptomatic or can present with encephalopathy. VPA-induced hyperammonemic encephalopathy (VHE) is a serious but reversible condition, which requires high clinical suspicion for diagnosis. It may occur acutely or after chronic use of VPA. We present the case of a 44-year-old male who was on long-term VPA therapy for a seizure disorder. He presented to the emergency department with the complaint of two episodes of seizures two days before admission. On arrival, the patient was confused and tearful and was unable to recollect the events leading to the seizure. The initial complete metabolic panel, liver function tests, urinalysis, and serum VPA levels were observed to be normal. However, there was a marked elevation in ammonia levels. VPA was suspected to be the inciting agent of hyperammonemic encephalopathy, and, therefore, it was discontinued. The patient was started on oral lactulose and prescribed a different antiseizure medication (i.e., lamotrigine). His ammonia levels decreased gradually, and his condition improved. Thus, it was concluded that the patient had developed VHE. At the time of discharge, he was stable and had no confusion or seizures. This case report evaluates his presentation and discusses the possible pathogenesis of VHE.

Valproic Acid–Associated Hyperammonemia

“…Manual search of reference lists and gray literature did not identify additional studies. After screening and assessing for eligibility, 240 studies were included with the remaining articles being excluded for meeting the exclusion criteria 6,7,12–245 . Among the excluded 350 articles, 37 were literature reviews, 5 were pharmacokinetically related, 41 were VPA overdose related, and 267 articles were unable to clearly answer our objectives listed.…”