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Case Reports
. 2021;26(2):210-212.
doi: 10.5863/1551-6776-26.2.210. Epub 2021 Feb 15.

Valproate-Induced Hyperammonemic Encephalopathy Following Accidental Ingestion in a Toddler

Moftah Alhagamhmad, Aisha Elarwah, Alia Alhassony, Shirin Alougly, Hamza Milad, Aziza Dehoam, Suliman Elbrgathy, Nuri Shembesh, Emhemed Mousa, Abdulhamid ElShiky
Case Reports

Valproate-Induced Hyperammonemic Encephalopathy Following Accidental Ingestion in a Toddler

Moftah Alhagamhmad et al. J Pediatr Pharmacol Ther. 2021.

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.

Keywords: accidental ingestion; adverse effect; case report; encephalopathy; hyperammonemia; infant; valproic acid.

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Conflict of interest statement

Disclosure. The authors declare no conflict or financial interest in any product or service mentioned in the manuscript, including grants, equipment, medications, employment, gift, and honoraria. The authors had full access to all patient information in this report and take responsibility for the integrity and accuracy of the report.

Figures

Figure.
Figure.
Mechanistic basis of valproate induced hyperammonemic encephalopathy.
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References

    1. Mugada V, Kakarparthy R, Ayinampudi BK et al. Sodium valproate induced Stevens Johnson syndrome and hepatitis in a pediatric patient: a case report. T J Res Med Sci. 2016;4(7):3058–3060.
    1. Henry TR. The history of valproate in clinical neuroscience. Psychopharmacol Bull. 2003;37(suppl 2):5–16. - PubMed
    1. Dinçer M, Akgün A, Bodur Ş et al. Hyperammonemic encephalopathy without hepatic dysfunction due to treatment with valproate: four cases and a mini review. Psych Clin Psychopharmacol. 2018;28(4):448–460.
    1. Abraham TC, James G, Thomas A et al. Sodium valproate induced hyperammonemia with normal liver function: a case report. J Pharmac Sci Res. 2017;9(6):818–823.
    1. Gerstner T, Buesing D, Longin E et al. Valproic acid induced encephalopathy–19 new cases in Germany from 1994 to 2003–a side effect associated to VPA-therapy not only in young children. Seizure. 2006;15(6):443–448. - PubMed

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