Most bleeding seen in the emergency department is due to trauma, the result of local wounds, lacerations, or other structural lesions that occur in patients with normal hemostasis. Conversely, bleeding from multiple sites, bleeding from untraumatized sites, delayed bleeding several hours after trauma, and bleeding into deep tissues or joints suggest the possibility of a bleeding disorder. Historical data for the presence of a congenital bleeding disorder include the presence or absence of unusual or abnormal bleeding in the patient and other family members and the possible occurrence of excessive bleeding after dental extractions, surgical procedures, or trauma. Many patients with abnormal bleeding have an acquired disorder, commonly due to liver disease or drug use (particularly ethanol, aspirin, nonsteroidal anti-inflammatory drugs [NSAIDs], warfarin, and antibiotics).
The site of bleeding may provide an indication of the hemostatic abnormality. Mucocutaneous bleeding, including petechiae, ecchymoses, epistaxis, or gastrointestinal, genitourinary, or heavy menstrual bleeding, is characteristic of qualitative or quantitative platelet disorders. Purpura is often associated with thrombocytopenia and commonly indicates a systemic illness. Bleeding into joints and potential spaces, such as between fascial planes and into the retroperitoneum, as well as delayed bleeding, is most commonly associated with coagulation factor deficiencies. Patients who demonstrate both mucocutaneous bleeding and bleeding in deep spaces may have disorders such as disseminated intravascular coagulation (DIC), in which both platelet abnormalities and coagulation factor abnormalities are present. Basic hemostatic tests and clinical evaluation are generally adequate for diagnosis (Table 41–1). Additional hemostatic studies are ordered as indicated (Table 41–2).
Table 41–1. Standard Tests of Hemostasis. |Favorite Table|Download (.pdf)
Table 41–1. Standard Tests of Hemostasis.
|Platelet count||150,000–400,000 platelets/mL||Traumatic bleeding not a serious concern unless platelet count <50,000/μL, and spontaneous bleeding unlikely unless platelet count <10,000/μL.|
|Prothrombin time and international normalized ratio (INR)||11–13 s, depending on reagent; INR 1.0||Tests extrinsic and common pathways: factors VII, X, V, prothrombin, and fibrinogen.|
|Activated partial thromboplastin time||22–34 s, depending on reagent||Tests intrinsic and common pathways: factors XII, XI, IX, VIII, V, prothrombin, and fibrinogen.|
|Fibrinogen level||150–450 mg/dL||Fibrinogen is cleaved by thrombin into fibrin monomer, which then polymerizes into cross-linked fibrin clot.|
|Fibrin degradation products by latex agglutination||<2.5 mg/L, depending on assay methodology||Breakdown products of fibrinogen and fibrin monomer.|
|D-dimer by enzyme-linked immunoassay||<500 μg/L, depending on assay methodology||Breakdown products of cross-linked fibrin.|
Table 41–2. Specialized Tests of Hemostasis. |Favorite Table|Download (.pdf)
Table 41–2. Specialized Tests of Hemostasis.
|Bleeding time||2.5–10 min||Tests interaction between platelets and subendothelium.|
|Thrombin clotting time||10–12 s||Tests conversion of fibrinogen to fibrin monomer.|
|Mixing test||Variable||1:1 mixing of abnormal plasma with normal plasma will correct any single coagulation factor deficiency and normalize PT or PTT. If mixing does not normalize the PT or PIT, a coagulation inhibitor is present.|
|Specific factor assays||60–130% (0.6–1.3 units/mL)||Used to identify specific factor deficiencies.|
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