exposed to topical thrombin with a prolonged prothrombin time, which does not correct on a 1:1 mix, should be evaluated for a possible inhibitor against factor V. These same patients may demonstrate a prolonged thrombin time when bovine thrombin is used in the test procedure. The patient thrombin time is normal if human thrombin is used. PLATELET DISORDERS Platelets play a central role in maintaining hemostasis and must be present in adequate number and have normal function. Platelets undergo a complex series of morphological and biochemical changes when activated. Platelets have the ability to bind to non-endothelial surfaces (adhesion), bind to other platelets (aggregation) and secrete substances that are stored in internal granules (secretion). EVALUATION OF PLATELET DISORDERS Platelet count and smear evaluation Platelet Function Screen May be abnormal if platelet count less than 150,000/uL or Hct less than 30% Sample submitted to lab within 1 - 2 hrs of collection or patient comes to lab site for blood collection. Contact Reference Laboratory Services (see below) Platelet aggregation studies May be abnormal if platelet count less than 150,000/uL or Hct less than 30% Patient must not be taking aspirin or NSAID containing medication. Test requires patient to come to UWMC blood draw for blood collection. Please call Reference Laboratory Services at (206) 598-6066 or (800) 713-5198 for assistance and contact the Coagulation Lab at (206) 598-6242 to schedule an aggregation study. Platelet and vascular disorders are characterized by petechiae and/or small superficial ecchymosis, mucosal hemorrhage (e.g. gingival bleeding, GI bleeding, menorrhagia) and immediate profuse bleeding from small cuts. This immediate bleeding distinguishes platelet disorders from a coagulation protein deficiency where the bleeding is typically delayed. Platelet disorders can be quantitative or qualitative. 9 Qualitative platelet disorders can be inherited or acquired and are further classified into disorders of adhesion, aggregation or secretion. The inherited disorders usually have normal platelet counts. The most common adhesion disorder is von Willebrand disease, a quantitative and/or qualitative defect of von Willebrand factor (vWF). vWF serves as a bridge between platelets and collagen, permitting adhesion of platelets to injured vessels. Bernard Soulier is a rare adhesive disorder where the patient’s platelets lack part of the GPIb receptor complex that is required for platelets to bind to von Willebrand factor. This group of patients may present with mild to moderate thrombocytopenia and abnormally large platelets on smear evaluation. The rare inherited aggregation disorders include Glanzmann’s Thrombasthemia (missing or defective fibrinogen receptor, GPIIbIIIa) and afibrinogenemia. Defective secretion disorders include storage pool abnormalities, Wiskott-Aldrich syndrome, Hermansky-Pudlak syndrome and Chediak-Higashi. Of this group, storage pool abnormalities are the most common. Acquired platelet function abnormalities are more common than inherited defects and can be associated with decreased number and/or abnormal function. Drugs such as aspirin, penicillin and alcohol affect platelet function. Uremia, disseminated intravascular coagulation and myeloproliferative disorders are associated with abnormal platelet function as well. Thrombocytopenia can be a result of a production defect, nonimmune destruction, immune platelet destruction or splenic sequestration. The severity of bleeding is usually related to the degree of thrombocytopenia and may be more severe when there is a rapid loss of platelets. Some drugs may cause thrombocytopenia through a variety of mechanisms. Platelet counts usually return to normal within 7-10 days once the offending drug is discontinued. Heparin-induced thrombocytopenia is a potentially life threatening form of acquired immune thrombocytopenia, caused by development of an antibody to the complex of PF4 and heparin on the platelet surface. At the same time, the PF4-heparin complex also binds to the endothelial surface where it is thought to promote potentially life threatening arterial and venous thrombosis. The