A clinicopathologic study of hepatic dysfunction following shock.
Nineteen patients who had profound hypotensive shock were studied to correlate the light and electron microscopic appearances of the liver with the clinical and biochemical evidence of hepatic dysfunction. Despite the multiple etiologic factors that can result in jaundice in these patients, a fluctuating pattern occurs which enables the correlation of a bilirubin peak with the predominating etiologic factor. Immediately after shock, there was enzymatic and light and electron microscopic evidence of hepatocellular damage, resulting in a  jaundice peak on the eighth to tenth day after the shock episode. This was followed by repair and regeneration of the liver as well as an increase in cholestatic enzyme levels. Later, bilirubin peaks occurred when hepatocellular function was further decreased or overloaded against this background of dysfunction related to the episode of shock. Recovery of hepatic function could continue or be delayed by intercurrent disease, particularly systemic infection. Support of hepatic function, similar to that available for pulmonary and renal failure may, in the future, be used to effect the prognosis of these patients.
D001663:Bilirubin / Q000097:blood; D006801:Humans; D007565:Jaundice / Q000201:enzymology / Q000473:pathology*; D008099:Liver / Q000473:pathology* / Q000503:physiopathology / Q000648:ultrastructure; D008107:Liver Diseases / Q000473:pathology; D011446:Prospective Studies; D012771:Shock, Hemorrhagic / Q000473:pathology* / Q000503:physiopathology
D001663:Bilirubin