Valopric Acid Intoxication Induced Hyperammonemic Encephalopathy in Setting of a Normal Liver Function

Mohammed Salhab

doi:10.4172/2161-0495.1000208

Abstract

We present a case of acute valoproic acid intoxication induced hyperammonemia encephalopathy and coma in a young man with a remarkably normal liver function test. L-Carnitine was used in addition to supportive management. Patient mental status improved within 24 hours and VPA and ammonia levels were declining until normalized. Serial liver function tests, including the synthetic functions, were performed and they were only remarkable for mildly elevated aspartate aminotransferase on presentation and were normal throughout the admission course.

Highlights

Valproic acid (VPA, valproate), has been used as an anticonvulsant and mood-stabilizing drug, mainly in the treatment of epilepsy and bipolar disorder
Other complications caused by Valoproic acid (VPA) toxicity include nausea, vomiting, mild toxic hepatitis, anion gap metabolic acidosis, hypernatremia, agitation and hyperammonemia
Laboratory data were significant for elevation of serum VPA level to 1400 μg/ml, ammonia level was 40 μmol/liter, mildly elevated aspartate aminotransferase (44 U/L) and severe hypokalemia (2.4 mEq/L) with anion gap metabolic acidosis

Summary

Introduction

Valproic acid (VPA, valproate), has been used as an anticonvulsant and mood-stabilizing drug, mainly in the treatment of epilepsy and bipolar disorder. LFT: Liver Function Test; VPA: Valoproic acid. Patients who ingest greater than 200 mg/kg of VPA and/or have serum concentrations greater than 180 mg/L (1260 μmol/L) usually develop some degree of central nervous system depression. Other complications caused by VPA toxicity include nausea, vomiting, mild toxic hepatitis, anion gap metabolic acidosis, hypernatremia, agitation and hyperammonemia.

Results

Conclusion