Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2009-11-25
pubmed:abstractText
The declaration of brain death requires a standardized clinical neurologic examination and, importantly, the resolution of the underlying cause. Because sedative and anesthetic agents can closely mimic brain death, intoxications must be ruled out. Aspects of brain stem function, particularly the pupillary responses to light, remain intact in most cases of poisonings. Intoxications that cause a condition that fully mimics brain death have only been described in cases of intoxications with tricyclic antidepressants and barbiturates so far. We report the case of a 19-year-old man who presented with severe confusion and developed a deep coma over the next hours. Clinical examination revealed absence of all brain stem reflexes including missing pupillary responses to light. Blood analysis revealed a valproic acid intoxication with levels of 12,430 micromol/L (normal, 350-700 micromol/L) with concomitant severe hyperammonemia of 500 micromol/L (normal, <30 micromol/L), and treatment was initiated including the administration of L-carnitine and a continuous venovenous hemodiafiltration. Brain edema as the cause of absent brain stem reflexes was ruled out twice by computed tomography. After normalization of the serum levels, the patient had a full clinical recovery.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1532-8171
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1177.e5-6
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Valproic acid intoxication imitating brain death.
pubmed:affiliation
Medical Intensive Care Unit, University Hospital Zurich, Raemistrasse 100, CH 8091 Zurich, Switzerland.
pubmed:publicationType
Journal Article, Case Reports