Acute liver failure pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]
Overview
Pathophysiology
Acute liver failure is caused due to extensive damage to the liver tissue, causing severe compromise of its function. The effects of acute liver failure are due to loss of its metabolic, secretory and regulatory effects. This results in accumulation of toxic substances and causes deleterious effects. The major cause of morbidity and mortality in patients of liver failure is due to the development of cerebral edema which causes altered sensorium and increased intracranial pressure.
Cerebral edema is mediated due to damage to blood brain barrier. Acute liver failure causes increased ammonia concentrations due to failure of detoxification system. This increased ammonia with glutamate of astrocytes of brain gets converted to glutamine with the help of enzyme glutamine synthetase. This accumulation of glutamine in high concentrations causes cerebral edema.
In acute liver failure there is increase in levels of nitric oxide in circulation. This nitric oxide is a potent vasodilator causing disruption of cerebral blood. This disrupts cerebral auto regulation.
Another consequences of liver failure is multiorgan failure due to severe hypotension caused by decreased systemic vascular resistance.
Pathology
In the majority of acute liver failure (ALF) there is widespread hepatocellular necrosis beginning in the centrizonal distribution and progressing towards portal tracts. The degree of parenchymal inflammation is variable and is proportional to duration of disease[1].