Hyperammonemic coma - Barking up the wrong tree

Doron Rimar, Eti Kruzel-Davila, Guy Dori, Elzbieta Baron, Haim Bitterman

Research output: Contribution to journalArticlepeer-review

Abstract

Hepatic encephalopathy and myxedema coma share clinical features: coma, ascites, anemia, impaired liver functions, and a "metabolic" electroencephalogram (EEG). Hyperammonemia, a hallmark of hepatic encephalopathy, has also been described in hypothyroidism. Differentiation between the 2 conditions, recognition of their possible coexistence, and the consequent therapeutic implications are of utmost importance. We describe a case of an 82-year-old woman with a history of mild chronic liver disease who presented with hyperammonemic coma unresponsive to conventional therapy. Further investigation disclosed severe hypothyroidism. Thyroid hormone replacement resulted in gain of consciousness and normalization of hyperammonemia. In patients with an elevated ammonia level, altered mental status, and liver disease, who do not have a clear inciting event for liver disease decompensation, overwhelming evidence of hepatic decompensation, or who do not respond to appropriate therapy for hepatic encephalopathy, hypothyroidism should be considered and evaluated.

Original languageEnglish
Pages (from-to)549-552
Number of pages4
JournalJournal of General Internal Medicine
Volume22
Issue number4
DOIs
StatePublished - Apr 2007
Externally publishedYes

Keywords

  • Autoimmune hepatitis
  • Autoimmune polyglandular syndrome type 2
  • Hepatic encephalopathy
  • Hyperammonemia
  • Myxedema coma
  • Urea cycle

ASJC Scopus subject areas

  • Internal Medicine

Fingerprint

Dive into the research topics of 'Hyperammonemic coma - Barking up the wrong tree'. Together they form a unique fingerprint.

Cite this