MEDizzy - A 75-year-old man is hospitalized for treatment of a deep

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A 75-year-old man is hospitalized for treatment of a deep venous thrombosis. He had recently been discharged from the hospital about 2 months ago. At that time, he had been treated for community-acquired pneumonia complicated by acute respiratory failure requiring mechanical ventilation. He was hospitalized for 21 days at that time and was discharged from a rehabilitation facility 2 weeks ago. On the day prior to admission, he developed painful swelling of his left lower extremity. A lower extremity Doppler ultrasound confirmed an occlusive thrombus of his deep femoral vein. After an initial bolus, he is started on a continuous infusion of unfractionated heparin at 1600 U/hr as he has end-stage renal disease on hemodialysis. His activated partial thromboplastin time (aPTT) is maintained in the therapeutic range. On day 5, it is noted that his platelets have fallen from 150,000/μL to 88,000/μL. What is the most appropriate action at this time?

ExplanationHeparin-induced thrombocytopenia (HIT) is a clinical diagnosis that must not be missed because life-threatening thrombosis can occur if not treated appropriately. The cause of HIT is the formation of antibodies to the complex of heparin and platelet factor 4 (PF4). This complex is able to activate platelets, monocytes, and endothelial cells. Many patients exposed to heparin will develop antibodies to the heparin/PF4 complex, but only a few of these will progress to develop thrombocytopenia or thrombocytopenia with thrombosis (HITT). The typical patient will develop evidence of HIT 5–14 days after exposure to heparin, although it can occur within 5 days in individuals exposed to heparin within the previous approximately 100 days, as would be expected in this patient given his recent hospitalization. The nadir platelet count is typically greater than 20,000/μL. When HIT is suspected, one should not delay treatment for laboratory testing as no currently available test has adequate sensitivity or specificity for the diagnosis. The anti-heparin/PF4 antibody test is positive in many individuals who have been exposed to heparin regardless of whether HIT is present. The platelet activation assay is more specifc but less sensitive for HIT. As soon as HIT is suspected, heparin should be discontinued and replaced with an alternative form of anticoagulation to protect against the development of new thromboses. Low-molecular-weight heparins (LMWH) such as enoxaparin are not appropriate treatment options in individuals with HIT. Although heparin is 10 times more likely to cause HIT, LMWHs also cause illness and should not be used. The primary agents used for HIT in the United States are the direct thrombin inhibitors argatroban and lepirudin. Argatroban is the preferred agent for this patient because of his renal failure. The drug is not excreted by the kidneys, and no dosage adjustment is required. In contrast, lepirudin is markedly increased in renal failure, and signifcant dosage adjustment is required. Danaparoid has previously been used frequently for HIT/HITT, but this medication is no longer available in the United States. Other anticoagulants that are used for the treatment of HITT include bivalirudin and fondaparinux, but these are not currently approved by the U.S. FDA for this indication.