[Shock liver].
Hypoxic, central lobular necrosis of the liver has been observed in patients with severe shock of different origin. In many cases diagnosis is not established, since clinical symptoms are unrevealing, and since SGPT levels rise rather late in the course of the disease. 3,788 patients have been treated in the intensive care unit of the Department of Medicine of the Vienna Medical School, within 10 years; liver damage caused by shock has been found during this period only in 32 cases. Diagnosis was established in 31 cases because of highly elevated SGPT levels, and substantiated in 5 cases by liver biopsy; diagnosis was established in one case by biopsy only. The median value of SGPT activity was 1,160 U/l and of lactate concentration 7.5 mmol/l. In 18 patients shock was caused by acute myocardial infarction, in 4 patients by pulmonary infarction and in 3 patients by cardiac as well as pulmonary events. In 4 cases there were heart valve lesions, one case had myocarditis, one case acute pancreatitis and one case hemorrhagic shock. Lethality was 78.1%. There was no correlation between central venous pressure and the maximal SGPT levels. There was however a correlation between prothrombin time and creatinine clearance.


CONCLUSIONS
In severe shock typical lesions of the liver may originate as a complication of shock, this complication being due to reduced blood flow leading to central lobulare necrosis of liver cells.
D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood; D001219:Aspartate Aminotransferases / Q000097:blood; D002496:Central Venous Pressure; D003402:Creatine Kinase / Q000097:blood; D003404:Creatinine / Q000097:blood; D006801:Humans; D007511:Ischemia / Q000201:enzymology*; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008099:Liver / Q000098:blood supply*; D008297:Male; D012769:Shock / Q000150:complications*
D003404:Creatinine; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D003402:Creatine Kinase
Die Schockleber.