Fulminant Hepatic Failure

An Improved Model of Galactosamine-Induced Fulminant Hepatic Failure in the Pig

“…The hallmarks of this condition are acute impairment of liver function, the presence of hepatic encephalopathy, and the absence of preexisting liver disease [35]. It has a very high mortality.…”

Fulminant Hepatic Failure Secondary to Previously Unrecognized Cardiomyopathy

“…FHF typi cally occurs within 8 weeks of the onset of symptoms of liver disease [1], This condition also implies that if survival occurs, hepatocel lular function usually returns to normal with removal of the offending insult [1]. FHF has numerous etiologies including viral hepatitis, various drugs and toxins, Reye's syndrome, Budd-Chiari syndrome, acute fatty liver of pregnancy, Wilson's disease, and prolonged episodes of circulatory insult [1,2], Our pa tient initially had negative viral markers for hepatitis A and B with no risk factors for hep atitis C infection.…”

“…FHF typi cally occurs within 8 weeks of the onset of symptoms of liver disease [1], This condition also implies that if survival occurs, hepatocel lular function usually returns to normal with removal of the offending insult [1]. FHF has numerous etiologies including viral hepatitis, various drugs and toxins, Reye's syndrome, Budd-Chiari syndrome, acute fatty liver of pregnancy, Wilson's disease, and prolonged episodes of circulatory insult [1,2], Our pa tient initially had negative viral markers for hepatitis A and B with no risk factors for hep atitis C infection. The possibility of a non-A, non-B, non-C etiology causing fulminant he patic failure, as has been previously recog nized, was a consideration in his case [3], Prolonged ischemia has been clearly de scribed in the literature as an etiology of FHF [4][5][6][7][8], However, we feel our case is unique in that all other descriptions have involved pa tients with a history of known or suspected cardiac insufficiency, whereas our patient had been a well-conditioned athlete without a his tory or clinical evidence of heart disease on presentation.…”

“…Studies suggest that this increased pressure results in centrilobular cell destruction with subsequent perisinusoidal edema with secondary decreased diffusion of oxygen [1,10], Arterial hypoxemia proba bly contributes to hepatic necrosis, but is less likely to be an important mechanism in its pathogenesis [10,12].…”

Extracorporeal Plasma Perfusion of Cultured Hepatocytes: Effect of Intermittent Perfusion on Hepatocyte Function and Morphology

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support system capable of providing a bridge to either The most promising approaches to developing a tem-liver regeneration or liver transplantation [1,2]. Since porary bioartificial liver support system involve incor-the metabolic abnormalities arising from AHF are not porating cultured primary hepatocytes into an extra-completely understood, there is some uncertainty as to corporeal perfusion device.

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