Bleeding is regulated by a complex process involving platelets and the coagulation system (see Chapter 232, “Hemostasis”). Platelet defects typically manifest with petechiae and mucosal bleeding, whereas coagulation defects usually present as spontaneous or excessive hemorrhage. Management of significant acquired bleeding disorders should be discussed with a hematologist because there are often subtleties in diagnosis and treatment.
ACQUIRED PLATELET DEFECTS
Circulating platelets provide the initial defense against bleeding. Acquired platelet disorders may be quantitative (decreased number of circulating platelets) or qualitative (poorly functioning platelets). Both significant thrombocytopenia and qualitative platelet dysfunction are commonly manifested by the presence of nonpalpable petechiae, often most pronounced in the lower extremities and in areas where blood flow is restricted. Other typical findings may include purpura, mucosal bleeding (gingival, epistaxis), menorrhagia, hemoptysis, hematuria, and hematochezia, whereas deep tissue bleeding and hemarthrosis are less common.
Securing circulatory stability is the primary treatment priority in the bleeding patient. Once done, perform the history, physical examination, and directed laboratory testing to define the clinical syndrome. Recent illness, symptoms, and medications are potentially relevant in the patient who appears to have a platelet disorder. Physical examination should assess for additional bleeding sites and the type of bleeding. Assess for lymphadenopathy, splenomegaly, rash, pallor, or jaundice that suggests diagnoses such as leukemia, lymphoma, systemic lupus erythematosus, infectious mononucleosis, or hemolytic anemia.
Quantitative defects that result in thrombocytopenia are caused by decreased production, increased destruction, splenic sequestration, platelet loss, or a combination (Table 233-1).1 The etiologies of thrombocytopenia are diverse, and the pathologic mechanism is not always initially clear. Viral infections may impair thrombopoiesis due to direct infection of the megakaryocyte, toxic effects of viral proteins or cytokines, hemophagocytosis, or production of antibodies that bind to platelets and enhance immune destruction.2 A drug history is important, because many medications have been implicated in causing thrombocytopenia or impairing platelet function (Table 233-2).3-5
TABLE 233-1Pathophysiology of Acquired Thrombocytopenia |Favorite Table|Download (.pdf) TABLE 233-1 Pathophysiology of Acquired Thrombocytopenia
|Mechanism ||Associated Clinical Conditions |
|Decreased platelet production || |
Marrow infiltration (tumor or infection)
Viral infections (rubella, HIV, hepatitis C, others)
Drugs (Table 233-2)
Vitamin B12 and/or folate deficiency
|Increased platelet destruction || |
Thrombotic thrombocytopenic purpura
Disseminated intravascular coagulation
Viral infections (HIV, mumps, varicella, Epstein-Barr virus)
Drugs (Table 233-2)
|Platelet loss || |
Hemodialysis, extracorporeal circulation
|Splenic sequestration ||Sickle cell disease, cirrhosis |
TABLE 233-2Drugs That Produce Thrombocytopenia or Impair Platelet Function |Favorite Table|Download (.pdf) TABLE 233-2 Drugs That Produce Thrombocytopenia or Impair Platelet Function
|Produce Thrombocytopenia* ||Impair Function |
Quinine and quinidine
Ethanol (chronic use)