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Normal regulation of bleeding is a complex process involving platelets and the coagulation system (see Chapter 227, Tests of Hemostasis). Bleeding related to platelets usually presents as petechiae and mucosal bleeding, whereas other coagulation defects present as spontaneous or excessive bleeding. In general, management of significant acquired bleeding disorders should be discussed with a hematologist because, at times, there are subtleties in diagnosis and treatment.

Circulating platelets provide an important initial defense against bleeding. Acquired platelet defects can be either quantitative (decreased number of circulating platelets or thrombocytopenia) or qualitative (poorly functioning platelets). Quantitative defects, resulting in thrombocytopenia, are caused by decreased production, increased destruction, splenic sequestration, platelet loss, or a combination of these (Table 228-1).1 A significantly decreased platelet count is commonly manifested by the presence of nonpalpable petechiae. These are most prominent in the lower extremities and in areas where blood flow is restricted. Other findings typical of thrombocytopenia include purpura, mucosal bleeding (gingival, epistaxis), menorrhagia, hemoptysis, hematuria, and hematochezia, whereas deep tissue bleeding is less common.

Table 228-1 Pathophysiology of Acquired Thrombocytopenia

When platelet levels decrease to below 10,000 to 20,000/mm3, the risk of spontaneous bleeding becomes concerning, particularly for intracranial bleeding. Additional risk factors for bleeding include age, comorbid illnesses (i.e., renal disease, liver disease, connective tissue disease, peptic ulcer disease, hypertension), fall risk, and lifestyle activity. With the exception of a few disease processes, platelet transfusion should be considered when counts fall below 10,000 mm3 (higher if other comorbid illnesses are present).2 The cause of the platelet deficiency may also influence the risk of bleeding. At a given platelet level, patients with idiopathic thrombocytopenic purpura (ITP) bleed less than patients with aplastic anemia. Research suggests that the younger platelets present in ITP are more effective in hemostasis due to increased metabolic activity.3

The initial priority in the bleeding patient is securing circulatory stability. Once this is done, the history, physical examination, and directed laboratory testing will define the clinical syndrome. Family history is important, but recent illness, current complaints, and recent medications are likely of greater relevance in the patient who appears to have a platelet disorder. Physical examination should evaluate for additional bleeding sites and, the type of bleeding, and assess the size of the spleen.

A complete blood count (CBC) will establish ...

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