Severe cerebral edema in a patient with anasarca and hypernatremia

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

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

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
Pages (from-to)19-22
Number of pages4
JournalClinical Nephrology
Volume37
Issue number1
StatePublished - Jan 1 1992
Externally publishedYes

Fingerprint

Hypernatremia
Brain Edema
Edema
Liver
Intracranial Hypertension
Extracellular Fluid
Blood-Brain Barrier
Liver Transplantation
Blood Vessels
Necrosis
Brain

Keywords

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

ASJC Scopus subject areas

  • Nephrology

Cite this

Wacks, I., Oster, J. R., Roth, D., Norenberg, M. D., Gardner, L. B., Perez, G. O., ... Milgrom, M. (1992). Severe cerebral edema in a patient with anasarca and hypernatremia. Clinical Nephrology, 37(1), 19-22.

Severe cerebral edema in a patient with anasarca and hypernatremia. / Wacks, I.; Oster, J. R.; Roth, David; Norenberg, Michael D; Gardner, L. B.; Perez, G. O.; Burke, George W; Milgrom, M.

In: Clinical Nephrology, Vol. 37, No. 1, 01.01.1992, p. 19-22.

Research output: Contribution to journalArticle

Wacks, I, Oster, JR, Roth, D, Norenberg, MD, Gardner, LB, Perez, GO, Burke, GW & Milgrom, M 1992, 'Severe cerebral edema in a patient with anasarca and hypernatremia', Clinical Nephrology, vol. 37, no. 1, pp. 19-22.
Wacks I, Oster JR, Roth D, Norenberg MD, Gardner LB, Perez GO et al. Severe cerebral edema in a patient with anasarca and hypernatremia. Clinical Nephrology. 1992 Jan 1;37(1):19-22.
Wacks, I. ; Oster, J. R. ; Roth, David ; Norenberg, Michael D ; Gardner, L. B. ; Perez, G. O. ; Burke, George W ; Milgrom, M. / Severe cerebral edema in a patient with anasarca and hypernatremia. In: Clinical Nephrology. 1992 ; Vol. 37, No. 1. pp. 19-22.
@article{10cfb94b258b4c34884809bad937b188,
title = "Severe cerebral edema in a patient with anasarca and hypernatremia",
abstract = "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.",
keywords = "Anasarca, Blood brain barrier, Cerebral edema, Hypernatremia, Hypertonicity",
author = "I. Wacks and Oster, {J. R.} and David Roth and Norenberg, {Michael D} and Gardner, {L. B.} and Perez, {G. O.} and Burke, {George W} and M. Milgrom",
year = "1992",
month = "1",
day = "1",
language = "English",
volume = "37",
pages = "19--22",
journal = "Clinical Nephrology",
issn = "0301-0430",
publisher = "Dustri-Verlag Dr. Karl Feistle",
number = "1",

}

TY - JOUR

T1 - Severe cerebral edema in a patient with anasarca and hypernatremia

AU - Wacks, I.

AU - Oster, J. R.

AU - Roth, David

AU - Norenberg, Michael D

AU - Gardner, L. B.

AU - Perez, G. O.

AU - Burke, George W

AU - Milgrom, M.

PY - 1992/1/1

Y1 - 1992/1/1

N2 - 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.

AB - 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.

KW - Anasarca

KW - Blood brain barrier

KW - Cerebral edema

KW - Hypernatremia

KW - Hypertonicity

UR - http://www.scopus.com/inward/record.url?scp=0026580128&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026580128&partnerID=8YFLogxK

M3 - Article

VL - 37

SP - 19

EP - 22

JO - Clinical Nephrology

JF - Clinical Nephrology

SN - 0301-0430

IS - 1

ER -