Lenz K, Kleinberger G, Druml W, Laggner A
Leber Magen Darm. 1982 Oct;12(5):198-202.
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.
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.
在不同病因的严重休克患者中已观察到肝脏的缺氧性中央小叶坏死。在许多情况下，由于临床症状不明显且谷丙转氨酶（SGPT）水平在疾病过程中升高较晚，诊断无法确立。维也纳医学院医学系重症监护病房在10年内共治疗了3788例患者；在此期间仅发现32例休克所致肝损伤。31例因SGPT水平大幅升高而确诊，5例经肝活检证实，仅1例通过活检确诊。SGPT活性的中位数为1160 U/l，乳酸浓度为7.5 mmol/l。18例患者的休克由急性心肌梗死引起，4例由肺梗死引起，3例由心脏和肺部疾病引起。4例有心脏瓣膜病变，1例有心肌炎，1例有急性胰腺炎，1例有失血性休克。死亡率为78.1%。中心静脉压与SGPT最高水平之间无相关性。然而，凝血酶原时间与肌酐清除率之间存在相关性。
在严重休克中，典型的肝脏病变可能作为休克的并发症出现，这种并发症是由于血流减少导致肝细胞中央小叶坏死。
