Microangiopathic hemolytic anemia is always present and an abnormal blood smear is a major diagnostic criterion. Red blood cell fragmentation is secondary to passage through blood vessels with endothelial damage and fibrin deposition. Because of the common feature of microangiopathic hemolytic anemia, some authors consider HELLP to be a form of thrombotic thrombocytopenic purpura or hemolytic uremic syndrome. Liver
The classic hepatic lesions associated with HELLP include periportal hemorrhage and focal parenchymal necrosis, with hyaline deposits of fibrin and fibrin microthrombi in the sinusoids. These histological findings explain the right upper quadrant or epigastric pain and the elevation in liver enzymes. These enzyme abnormalities do not reflect the severity of histopathological change seen and could justify the need for rapid and aggressive delivery ( Barton.efa/ 1992).
Blood flow obstruction in the sinusoids is the likely cause of liver distension, subcapsular hemorrhage, and hepatic rupture, the most feared complication of HELLP (Wej_n_s_t_ein_.1982). Increased hepatic artery resistance to blood flow has been demonstrated in pre-eclampsia with or without HELLP and is not implicated in the development of the syndrome. Some liver biopsy specimens have shown fat within hepatocytes; an overlap with acute fatty liver has been described, but clinical and histological findings can distinguish this syndrome from HELLP (Barton.eLai 1992).
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