Birgens H S, Henriksen J, Matzen P, Poulsen H
Acta Med Scand. 1978;204(5):417-21.
Five patients with severe heart disease developed cardiogenic shock of more than 24 hours' duration. As a sequela to the shock, severe liver affection was demonstrated. Serum aspartate aminotransferases and serum lactate dehydrogenases showed very high activities. The prothrombin-proconvertin index was reduced to less than 25% of the normal. Four of the patients were jaundiced. The condition gave rise to some differential diagnostic problems. Liver biopsies were available from four of the patients, and histological examination of an autopsy specimen of the liver was performed in each case. The liver histology showed centrilobular necrosis and haemorrhage in all patients. It seems that centrilobular fibrosis develops later in the condition. The pathogenesis of this liver affection is probably hypoxic injury to the centrilobular areas of the liver lobule due to reduced liver blood flow.
五名患有严重心脏病的患者发生了持续超过24小时的心源性休克。作为休克的后遗症，出现了严重的肝脏病变。血清天冬氨酸转氨酶和血清乳酸脱氢酶活性非常高。凝血酶原-前转变素指数降至正常的25%以下。其中四名患者出现黄疸。这种情况引发了一些鉴别诊断问题。四名患者有肝活检样本，且对每例患者均进行了肝脏尸检标本的组织学检查。所有患者的肝脏组织学均显示小叶中心坏死和出血。在这种情况下，小叶中心纤维化似乎在后期才会出现。这种肝脏病变的发病机制可能是由于肝血流量减少，导致肝小叶小叶中心区域发生缺氧损伤。
