J Korean Neurosurg Soc.  2015 Aug;58(2):159-162. 10.3340/jkns.2015.58.2.159.

Valproic Acid-Induced Hyperammonemic Encephalopathy as a Cause of Neurologic Deterioration after Unruptured Aneurysm Surgery

Affiliations
  • 1Department of Neurosurgery, Hanyang University Guri Hospital, Hanyang University College of Medicine, Guri, Korea. kjm2323@hanyang.ac.kr

Abstract

Neurological deficits after brain surgery are not uncommon, and correct and prompt differential diagnosis is essential to initiate appropriate treatment. We describe a patient suffering from loss of consciousness due to hyperammonemia, following valproic acid treatment after surgery for an unruptured cerebral aneurysm. A 57-year-old female patient underwent successful aneurysmal neck clipping to correct an unruptured aneurysm. Her postoperative course was good, and she received anti-epileptic therapy (valproic acid) and a soft diet. Within a few days the patient experienced mental deterioration. Her serum valproic acid reached toxic levels (149.40 mg/L), and serum ammonia was fifteen times the upper normal limit (553 mmol/L; normal range, 9-33 mmol/L). After discontinuation of valproic acid and with conservative treatment, the patient recovered without any complications. Valproate-induced hyperammonemic encephalopathy is an unusual but serious neurosurgical complication, and should not be disregarded as a possible cause of neurological deficits after neurovascular surgery. Early diagnosis is crucial, as discontinuation of valproic acid therapy can prevent serious complications, including death.

Keyword

Hyperammonemia; Valproic acid; Encephalopathy

MeSH Terms

Ammonia
Aneurysm*
Brain
Diagnosis, Differential
Diet
Early Diagnosis
Female
Humans
Hyperammonemia
Intracranial Aneurysm
Middle Aged
Neck
Reference Values
Unconsciousness
Valproic Acid
Ammonia
Valproic Acid

Figure

  • Fig. 1 Preoperative three dimensional computer tomographic angiography (3-D CTA) demonstrating postero-medially directed aneurysm with broad neck and multi-lobulated sac. Aneurysm sac is located in the carotid cave portion of the left proximal internal cerebral artery. A : View from the top. B : View from the right top.

  • Fig. 2 Postoperative left three dimensional digital subtraction angiography (3-D DSA) (A and B). Demonstrating complete obliteration of carotid cave aneurysm sac with preservation of ophthalmic artery using two fenestrated clips. A : Anterior-oblique view. B : Medial view. Postoperative conventional DSA (C and D) demonstrating mild narrowing of the internal cerebral artery at the clipping portion. However, no definite vasospasm is observed at the whole left cerebral vascular trees. C : Anterior-posterior view. D : Lateral view.


Reference

1. Chou HF, Yang RC, Chen CY, Jong YJ. Valproate-induced hyperammonemic encephalopathy. Pediatr Neonatol. 2008; 49:201–204. PMID: 19133574.
Article
2. DeWolfe JL, Knowlton RC, Beasley MT, Cofield S, Faught E, Limdi NA. Hyperammonemia following intravenous valproate loading. Epilepsy Res. 2009; 85:65–71. PMID: 19299111.
Article
3. Eubanks AL, Aguirre B, Bourgeois JA. Severe acute hyperammonemia after brief exposure to valproate. Psychosomatics. 2008; 49:82–83. PMID: 18212182.
Article
4. Felipo V, Butterworth RF. Neurobiology of ammonia. Prog Neurobiol. 2002; 67:259–279. PMID: 12207972.
Article
5. Garg R, Sunder RA. Valproate-induced hyperammonemia and seizures : perioperative concerns. Paediatr Anaesth. 2011; 21:1084–1085. PMID: 21981101.
6. Hamer HM, Knake S, Schomburg U, Rosenow F. Valproate-induced hyperammonemic encephalopathy in the presence of topiramate. Neurology. 2000; 54:230–232. PMID: 10636156.
Article
7. Segura-Bruna N, Rodriguez-Campello A, Puente V, Roquer J. Valproate-induced hyperammonemic encephalopathy. Acta Neurol Scand. 2006; 114:1–7. PMID: 16774619.
Article
8. Tsai MF, Chen CY. Valproate-induced hyperammonemic encephalopathy treated by hemodialysis. Ren Fail. 2008; 30:822–824. PMID: 18791959.
Article
9. Verrotti A, Trotta D, Morgese G, Chiarelli F. Valproate-induced hyperammonemic encephalopathy. Metab Brain Dis. 2002; 17:367–373. PMID: 12602513.
Full Text Links
  • JKNS
Actions
Cited
CITED
export Copy
Close
Share
  • Twitter
  • Facebook
Similar articles
Copyright © 2024 by Korean Association of Medical Journal Editors. All rights reserved.     E-mail: koreamed@kamje.or.kr