Pathophysiology of brain edema in fulminant hepatic failure, revisited

Authors
Citation
At. Blei, Pathophysiology of brain edema in fulminant hepatic failure, revisited, METAB BRAIN, 16(1-2), 2001, pp. 85-94
Citations number
58
Categorie Soggetti
Neurosciences & Behavoir
Journal title
METABOLIC BRAIN DISEASE
ISSN journal
08857490 → ACNP
Volume
16
Issue
1-2
Year of publication
2001
Pages
85 - 94
Database
ISI
SICI code
0885-7490(200106)16:1-2<85:POBEIF>2.0.ZU;2-C
Abstract
We have proposed a combined osmolar-hemodynamic disturbance to explain the presence of brain edema in fulminant hepatic failure, a major cause of deat h in this disorder. The concept of an osmotic disturbance in the brain, emp hasizing the presence of astrocyte swelling and low-grade cerebral edema, h as been expanded to the entire spectrum of liver disease. The mechanism of cerebral hyperemia in patients with FHF and brain swelling has been studied in experimental models linking hyperammonemia and glutamine generation in astrocytes to the development of this hemodynamic alteration. Measures to c ontrol cerebral hyperemia, such as mild hypothermia, are effective in preve nting the development of brain edema in experimental models as well as intr acranial hypertension in human disease.