RT Book, Section
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.
SR Print(0)
ID 1180482399
T1 Fragmentation Hemolytic Anemia
T2 Williams Hematology, 10e
YR 2021
FD 2021
PB McGraw-Hill Education
PP New York, NY
SN 9781260464122
LK hemonc.mhmedical.com/content.aspx?aid=1180482399
RD 2024/04/16
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).