The initial evaluation of patients with hemorrhagic problems involves obtaining a detailed history of bleeding symptoms and analyzing any current hemorrhagic lesions, which most often occur on the skin. The bleeding history forms the basis of the diagnosis and therapy of hemorrhagic disorders.Detailed history: Symptoms: epistaxis, gingival bleeding, easy bruising, hematuria, menorrhagia, hemarthrosis, neonatal bleeding, gastrointestinal bleeding, and prolonged bleeding after laceration.
A medication history is incomplete without specific questions concerning aspirin, herbal remedies, dietary supplements, or medications available without prescription that may affect coagulation or platelet function because patients may not recognize these agents as medications. Similarly, it is important to inquire about vitamin tablets that may contain vitamin K in patients taking oral anticoagulants. Hormone replacement therapy and birth control pills can also affect hemostasis.
Family history: Symptoms, response to hemostatic challenge (siblings, parents, aunts, uncles, grandparents).
A constellation of hemorrhagic symptoms, rather than any single symptom, is most helpful in suggesting the etiology of the disorder. Thus, spontaneous hemarthroses and muscle hemorrhages are highly suggestive of severe hemophilia, whereas epistaxis, gingival bleeding, and menorrhagia are more commonly found in patients with thrombocytopenia, platelet disorders, or Von Willebrand disease.
Although obtaining a complete bleeding history may seem tedious, it is well worth the effort because the patient’s previous responses to hemostatic challenges are much better predictors of the patient’s likelihood of bleeding excessively than are the patient’s routine laboratory values.
In general there is strong consensus on the central role of the bleeding history in evaluating hemostatic risk.
Complete physical examination: Signs consistent with past coagulopathy include petechiae, ecchymoses, hematomas, arthropathy, muscle atrophy, synovitis/joint effusion. The location of a bruise may offer indirect evidence of its relationship to trauma. The vast majority of traumatic events occur on exposed sites such as the arms and legs. Therefore, if the patient suffers repeated bruises on unexposed sites on the trunk or back, these are more likely to be either spontaneous or in response to minimal trauma. Patients with diffuse intravascular coagulation, hyperfibrinolysis, thrombocytopenia, or qualitative platelet disorders characteristically bleed for a long time after venipuncture, whereas patients with coagulation disorders do not. Delayed bleeding, however, may occur in the latter group.
Virtually all of the prolonged venipuncture bleeding can be prevented, or at least minimized, by applying direct pressure to the venipuncture site for at least five minutes and then observing the uncovered site for at least one minute for evidence of continual bleeding.
Laboratory evaluation: Initial screening tests: Complete blood count (CBC): quantitative assessments of platelets.
Bleeding time: prolonged with impaired platelet function, platelet counts reduced below 80,000-100.000/mm3 or impaired vascular integrity. Platelet function analyzer in response to ADP and to epinephrine, often prolonged with impaired platelet function.
Coagulation factor screening test (from a laboratory perspective the coagulation system is divided into: intrinsic pathway, extrinsic pathway, and common pathway), is useful for conceptualizing in vitro laboratory testing.
Prothrombin time (PT) assesses the extrinsic system. Normal value: 10-12”, Partial thromboplastin time (PTT) assay (assesses the intrinsic system). 25-35”, and common confirmatory coagulation assays: – fibrinogen: quantitative measurement of fibrinogen are useful when both the PT and PTT are prolonged. Thrombin time: prolonged when fibrinogen is reduced or abnormal, in the presence of inhibitors (fibrin degradation products, D dimers). Useful when PT and PTT are prolonged.
In coagulation, lab mixing studies are performed following addition of normal plasma to patient plasma. Normalization indicates a clotting factor deficiency that was corrected by addition of normal plasma. Continued prolongation indicates presence of coagulation inhibitor. Clotting factor activity assays: performed to identity clotting factor deficiency if mixing studies normalize. Urea clot lysis assay: useful screen for FXIII deficiency. In the absence of fibrin cross linkage by FXIII, a clot will degrade with incubation in 5 M urea.
