Severe cerebral edema in a patient with anasarca and hypernatremia

I. Wacks, J. R. Oster, D. Roth, M. Norenberg, L. B. Gardner, G. O. Perez, G. Burke, M. Milgrom

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


We describe a woman whose fatal post-liver transplantation cerebral edema was unexpected and of unusual pathogenesis. Her severe cerebral edema is of considerable pathophysiologic interest: 1) it developed in the setting of marked anasarca and persistent hypernatremia, and 2) although hepatic function was poor, it was not considered sufficiently deranged to induce cerebral edema. Furthermore, there was no histologic evidence of hepatic rejection or antemortem hepatic necrosis. We postulate that an impairment of the blood brain barrier in association with a degree of hepatic dysfunction insufficient by itself to cause cerebral edema permitted the brain interstitial fluid volume to increase pari passu with ECF expansion. Cytotoxic cerebral edema and vascular engorgement may also have contributed to a life-threatening increase in intracranial pressure.

Original languageEnglish (US)
Pages (from-to)19-22
Number of pages4
JournalClinical Nephrology
Issue number1
StatePublished - Jan 1 1992


  • Anasarca
  • Blood brain barrier
  • Cerebral edema
  • Hypernatremia
  • Hypertonicity

ASJC Scopus subject areas

  • Nephrology


Dive into the research topics of 'Severe cerebral edema in a patient with anasarca and hypernatremia'. Together they form a unique fingerprint.

Cite this