Heparin-induced thrombocytopenia: clinical manifestations and management strategies.

Thrombocytopenia is a relatively frequent and usually benign clinical complication of heparin therapy. However, some patients receiving heparin and heparin-based products experience an immune-mediated reaction due to the development of heparin-induced antibodies. This reaction leads to a highly specific and paradoxical form of thrombocytopenia, known as type II heparin-induced thrombocytopenia (HIT). Unlike other types of drug-induced thrombocytopenia, HIT promotes thrombosis rather than bleeding; therefore HIT should be suspected in patients who experience thrombotic events despite adequate anticoagulation therapy. Early identification and treatment of HIT can prevent more serious complications associated with this disorder (e.g., exacerbation of venous thromboembolism, limb gangrene, and skin necrosis). Both arterial and venous thrombosis can arise from a single episode of HIT. Routine assessment of platelet counts is necessary with heparin therapy, as a decreased platelet level is usually the only indication of HIT. Although compared with unfractionated heparin, low-molecular-weight heparin therapy is less likely to result in HIT, the use of these agents is contraindicated in HIT patients. Concomitant warfarin therapy is not contraindicated in such patients but must be carefully monitored. Treatment with a direct thrombin inhibitor, such as lepirudin or argatroban, is an effective strategy in reversing the thrombocytopenia associated with HIT and reducing its complications. This article discusses the clinical syndrome of HIT, including pathophysiology, diagnostic criteria, clinical presentations, and current available management strategies in the context of 2 case studies.

Early-onset heparin-induced thrombocytopenia after a 165-day heparin-free interval: case report and review of the literature.

Early- or abrupt-onset immune-mediated heparin-induced thrombocytopenia (HIT) is defined as HIT that occurs less than 5 days after exposure to heparin in patients who have received heparin within the previous 100 days. We identified no reports in the literature of early-onset HIT in patients who had a heparin-free interval longer than 100 days. However, we report a case of early-onset immune-mediated HIT illustrated by a positive HIT result with serotonin release and enzyme-linked immunosorbent assays, and a decrease in platelet count to less than 100 x 10(3)/mm3 with no evidence of thrombosis, approximately 165 days after the patient's last exposure to heparin. We conclude that clinicians should choose alternative forms of anticoagulation in patients with even a remote history of HIT. If clinicians are compelled to reexpose patients to heparin, they should confirm a negative HIT assay result, monitor for clinical signs of HIT, and provide appropriate treatment if HIT is suspected.

Benefits of more aggressive VTE prophylaxis in hospitalized medical patients.

Venous thromboembolism (VTE), which includes both deep vein thrombosis and pulmonary embolism, is a well-known risk in surgical patients, but it is also a significant and often unrecognized source of mortality and morbidity in hospitalized medical patients. The need for routine prophylaxis in the general medical population is increasingly supported.