Some Causes of Excessive Bleeding

Platelet disorders

Decreased number of platelets (quantitative disorder)

Inadequate production (eg, in leukemias, aplastic anemia, and some myelodysplastic syndromes)

Decreased production due to thrombopoietin deficiency related to liver disease

Splenic sequestration (eg, in cirrhosis with congestive splenomegaly)

Increased platelet destruction or consumption (eg, in ITP, DIC, thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome, sepsis, and HIV infection)

Medication-induced destruction (eg, by heparin, quinidine, quinine, sulfonamides, sulfonylureas, or rifampin), quinidine, quinine, sulfonamides, sulfonylureas, or rifampin)

Increased number of platelets (quantitative disorder)

Essential thrombocythemia (bleeding may occur with very high platelet counts)

Inadequate platelet function (qualitative disorder)

v Willebrand disease (inadequate VWF-mediated platelet adhesion)

Medication-induced dysfunction (eg, by aspirin, the P2Y12 inhibitors [cangrelor, clopidogrel, prasugrel, ticagrelor], or NSAIDs), the P2Y12 inhibitors [cangrelor, clopidogrel, prasugrel, ticagrelor], or NSAIDs)

Systemic disorders (uremia; occasionally, myeloproliferative disorders [due to platelet destruction of VWF at very high platelet counts], myelodysplastic syndromes, multiple myeloma)

Coagulation disorders

Acquired

Vitamin K deficiency

Liver disease

Anticoagulation with warfarin, heparin or the direct oral inhibitors of thrombin or factor Xa (eg, apixaban, edoxaban, rivaroxaban)(eg, apixaban, edoxaban, rivaroxaban)

DIC

Hereditary

Hemophilia A (factor VIII deficiency)

Hemophilia B (factor IX deficiency)

Vascular disorders

Acquired

Vitamin C deficiency (scurvy)

Immunoglobulin A–associated vasculitis

Amyloidosis

Hereditary

Systemic rheumatic disorders (eg, Ehlers-Danlos syndrome, osteogenesis imperfecta, Marfan syndrome)

Hereditary hemorrhagic telangiectasia