TY - CHAP M1 - Book, Section TI - Fragmentation Hemolytic Anemia A1 - Baker, Kelty R. A1 - Moake, Joel A2 - Kaushansky, Kenneth A2 - Prchal, Josef T. A2 - Burns, Linda J. A2 - Lichtman, Marshall A. A2 - Levi, Marcel A2 - Linch, David C. Y1 - 2021 N1 - T2 - Williams Hematology, 10e AB - SUMMARYErythrocyte fragmentation and hemolysis occur when red cells are forced through partial vascular occlusions or over abnormal vascular surfaces at high shear stress. “Split” red cells, or schistocytes, are prominent on blood films under these conditions, and considerable quantities of lactate dehydrogenase are released into the blood from traumatized red cells. In the high-flow (high-shear) microvascular (arteriolar or capillary) or arterial circulation, partial vascular obstructions are caused by platelet aggregates in the systemic microvasculature during episodes of thrombotic thrombocytopenic purpura by platelet-fibrin thrombi in the renal microvasculature in the hemolytic uremic syndrome and by malfunction of a cardiac prosthetic valve in valve-related hemolysis. Less-extensive red cell fragmentation, hemolysis, and schistocytosis occur under conditions of more moderate vascular occlusion or endothelial surface abnormalities, sometimes under conditions of lower shear stress. These latter entities include excessive platelet aggregation, fibrin polymer formation, and secondary fibrinolysis in the arterial or venous microcirculation (eg, disseminated intravascular coagulation); in the placental vasculature in preeclampsia or eclampsia and the syndrome of hemolysis, elevated liver enzymes and low platelets (HELLP) in march hemoglobinuria; and in giant cavernous hemangiomas (the Kasabach-Merritt phenomenon). SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/29 UR - accessmedicine.mhmedical.com/content.aspx?aid=1180482399 ER -