Pathomorphologic Basis of the Severe Viral Hepatitis Ⅱ. Pathological Changes in Extrahepatic Organs
- VernacularTitle:重型病毒性肝炎的病理形态学基础——Ⅱ、肝外脏器病理形态变化
- Author:
Guanghan ZHONG
- Publication Type:Journal Article
- Keywords:
Hepatitis, viral, hnman/complications;
Brain edema;
Pulmonary edema;
Heart enlargement;
Esophageal varises
- From:Journal of Third Military Medical University
1984;0(01):-
- CountryChina
- Language:Chinese
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Abstract:
The report dealt with the pathological changes in the extrahepatic organs from 30 autopsied cases with clinical manifestations of severe viral hepatitis (SAH) . The main findings were epitomized as follows.(1 ) Brain edema with herniation of tonsil cerebelli in 24 (71%) cases among the 27 whose brains were examined. (2) Bilateral pulmonary edema in 20 (43%) cases among the 28 whose lungs were examined. 45% cases of pulmonary edema were complicated by bronchopneumonia, 10% by fungal infection, and 15% by pulmonary hemorrhage. ( 3 ) Cardiac hypertrophy in ( 43% ) cases among the 28 whose hearts were examined. (4) Biliary nephrosis in 22 (92%) cases among the 24 whose kidneys wers examined. ( 5 ) All the 30 cases showed intestinal congestion and edema throughout the 3 laminae of intestinal wall. (6) of 30 cases, 8 (27%) showed esophageal varicosis. Early hepatic cirrhosis was established in half of the cases. (7) of 29 cases, 25 (85%) had ascitis with various amount of transudate ranging from 2000-8000 ml in adults and 300-1500ml in children. (8) of 30 cases, 4 (13%) had subacute phlegmonous colitis. (9) of 30 cases, 3 (10%) were complicated by the generalizad aspergillosis and/or candiasis involving the lungs, brain, heart, kidneys, intestines, et al.It was considered that the alterations in extrahepatic organs should aggravate the primary disease and thus be prone to increase its motality rate. Some of them, such as brain edema might be the direct cause of death. It was thought that two factors might be responsible for the initiation of extrahepatic alterations. ( 1 ) increase in intrahepatic resistance to the portal blood flow which is presumably due to reduction of hepatic microcirculatory beds, and ( 2 ) hypoxemia which is probably due to intrapulmonary vascular shunts in case of hepatic failure. These factors, once established, might in turn trigger off a sequence of pathological events.
