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HEMORRHAGE is a frequent and often major complication in patients with acute leukemia. In addition to thrombocytopenia and its resulting coagulation defects disturbances of the hemostatic mechanism have been described in such patients.1 These include qualitative platelet defects2 3 4 and the presence of a fibrinolytic system and hypofibrinogenemia.5 , 6 Fever, which is presumably due to bacterial infection, has been found to be related to bleeding in patients with acute leukemia.6 , 7 This may result from the anticoagulant effect of bacterial polysaccharide demonstrated in vitro.8 Capillary damage resulting from lysins,9 anoxemia or leukemic infiltration has been postulated.10 Although any or all of these disturbances . . .
Gaydos et al. (1962) studied this question.