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A 62-year-old woman is hospitalized for intravenous antibiotic treatment of a left lobar pneumonia. An initial complete blood count shows a hemoglobin of 12.2 g/dL, a platelet count of 283 x 103/mm3, and a white cell count of 18.2 x 103/mm3. During her hospitalization, she is immobile and is started on subcutaneous heparin to prevent deep vein thromboses. 5 days after the initiation of subcutaneous heparin, her platelet count drops to 100 x 103/mm3 then normalizes over the next 4 days. What is the most likely diagnosis?
A. Type I heparin induced thrombocytopenia
B. Type II heparin induced thrombocytopenia
C. Asplenia
D. Idiopathic thrombocytopenic purpura
E. Bernard-Soulier syndrome
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Choice (A) is the correct answer. Type I heparin induced thrombocytopenia is a non-immune mediated thrombocytopenia associated with heparin. Patients develop a mild to moderate thrombocytopenia that resolves after several days without discontinuation of heparin. Type II heparin induced thrombocytopenia (Choice B) is immune mediated and is more severe than type I. The pathophysiology of type II heparin induced thrombocytopenia is as follows: heparin binds to platelet factor 4 (PF4), which induces an antibody response. Antibodies, primarily IgG antibodies, bind to the heparin/PF4 molecule to form an immune complex. The immune complex binds to platelet surface membranes, which results in platelet activation, aggregation, and causes a consumptive thrombocytopenia. Activated platelets release more PF4 and results in a vicious cycle. In addition, immune complexes bind to endothelial cells and cause endothelial injury. Thrombus formation and disseminated intravascular coagulation can result. Asplenia (Choice C) is associated with a thrombocytosis, not a thrombocytopenia. Idiopathic thrombocytopenia purpura (Choice D) is an immune-mediated disease that causes platelet destruction as a result of autoantibodies against platelets. Bernhard-Soulier syndrome (Choice E) is caused by a deficiency of glycoprotein Ib. It is characterized by easy bruising, epistaxis, menorrhagia, and GI bleeds. Thrombocytopenia is often present, and large platelets are seen on peripheral smear. Bleeding time is increased. Bernard-Soulier platelets do not aggregate in the presence of ristocetin.
