Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by uncontrolled proliferation of myeloid blast cells in the bone marrow, leading to pancytopenia, infectious complications, and a high risk of bleeding. Hemorrhagic syndrome is a major contributor to early mortality, particularly during the first 60 days of induction therapy, and is defined by the combination of severe thrombocytopenia, platelet dysfunction, coagulopathy, and disseminated intravascular coagulation (DIC). Quantitative platelet deficiency increases the risk of spontaneous bleeding, whereas platelet dysfunction, including impaired activation and aggregation, significantly influences the severity and frequency of hemorrhagic events regardless of platelet count. DIC in AML develops as a consequence of coagulation system hyperactivation, endothelial injury, and increased expression of procoagulant molecules by leukemic blasts. Diagnosis is based on the ISTH scoring system and dynamic monitoring of laboratory parameters such as platelet count, prothrombin time, fibrinogen, and D-dimer. Molecular genetic factors, particularly KMT2A translocations, further increase the risk of severe bleeding and DIC by promoting a procoagulant state and stimulating hyperfibrinolysis, complicating standard prophylactic strategies.

Risk stratification for severe bleeding includes assessment of the international normalized ratio, platelet count, coagulation parameters, and clinical features such as leukocytosis, extramedullary disease, and concomitant infections. Particularly severe hemorrhagic complications occur in acute promyelocytic leukemia, where coagulopathy is combined with marked hyperfibrinolysis, requiring immediate initiation of specific therapy, transfusion support, and close monitoring of key hemostatic parameters.

Modern approaches to the prevention and management of hemorrhagic syndrome in AML should be comprehensive and include prophylactic and therapeutic platelet transfusions, maintenance of fibrinogen and coagulation factors, selective use of antifibrinolytic agents, consideration of platelet transfusion refractoriness, and early integration of targeted therapies. Early molecular screening and personalized monitoring protocols may reduce the incidence and severity of bleeding, improve treatment efficacy, and enhance survival, particularly in patients with a high hemorrhagic risk profile.

Keywords: review, acute myeloid leukemia, hemorrhagic syndrome, bleeding, thrombocytopenia, hemostasis, disseminated intravascular coagulation (DIC).