ABSTRACT
This chapter reviews the physiological parameters determining cerebral blood flow and cerebral metabolism. The mechanism by which coma occurs in hepatic failure remains poorly understood. The absence of macroscopic structural cerebral changes after acute hepatic failure, and the rapid neurological recovery which ensues with improved hepatic function supports a metabolic causation. The common assumption is that the brain is exposed to toxic substances which are present in portal blood when liver function is inadequate, or when portal blood bypasses the liver to enter directly into the systemic circulation. A complete understanding of the pathogenesis of hepatic encephalopathy requires knowledge of the mechanism by which a substance interferes with cerebral function. The situation of fulminant hepatic failure requires separate attention. Although the pathogenesis of encephalopathy in fulminant and in chronic hepatic failure might be expected to be the same, there are several striking differences.
