The identification and management of heparin-induced thrombocytopenia in the vascular patient

Abstract

Heparin-induced thrombocytopenia (HIT) is a serious, acquired, prothrombotic disorder caused by an antibody response to the heparin-platelet factor 4 complex, which can precipitate arterial as well as venous thromboembolic complications. HIT should be suspected in patients exposed to heparin who present with an unexplained thrombosis or a significant drop in platelet count, or both. Once HIT is suspected or identified, there are specific approaches to its diagnosis and management, with emphasis on removal of all heparin compounds and administration of alternative nonheparin anticoagulants. Generally, HIT is a self-limiting syndrome that resolves when the antibody titers disappear. Patients should be anticoagulated for up to 6 months, depending on the clinical scenario; however, the management of patients with remote or recent HIT requiring a vascular procedure requires special considerations.

Differential profiles of thrombin inhibitors (heparin, hirudin, bivalirudin, and dabigatran) in the thrombin generation assay and thromboelastography in vitro

“…Heparin is an antithrombin-dependent, indirect, and nonspecific inhibitor for thrombin and has been used to treat various thrombotic diseases in medical/ surgical patients in the past [5]. However, heparin usage is limited by its potential serious side-effect, heparininduced thrombocytopenia (HIT) [7]. Hirudin and bivalirudin are bivalent direct thrombin inhibitors that have high affinity and high specificity for thrombin [8].…”

Low-molecular weight heparin associated multiple digital necrosis in a patient as a result of heparin-induced thrombocytopenia syndrome

“…In the management of a patient with HITS, unfractionated heparin and LMWH should be discontinued, including heparin-coated intravascular catheters [ 6 ]. Except the evidence of clinical bleeding, in the treatment of acute HITS, the platelet transfusions are contraindicated because platelet transfusions can increase the risk of thrombosis [ 5 , 6 ]. The risk of bleeding in these patients is low [ 5 ].…”

Clinical and economic burden of heparin-induced thrombocytopenia in hospitalized patients undergoing percutaneous peripheral arterial interventions

“…2 Thus, PPAI patients are at risk of developing HIT due to the need for repeated heparin exposure. 3 Besides, when HIT occurs after PPAI, the presence of an injured vascular endothelium due to angioplasty, stenting, or atherectomy provides a thrombogenic surface that is at high risk for HIT-induced thrombosis. 3 Therefore, PPAI patients with HIT can experience significant morbidities including pulmonary embolism, acute renal failure, stroke, and acute myocardial infarction.…”

“…3 Besides, when HIT occurs after PPAI, the presence of an injured vascular endothelium due to angioplasty, stenting, or atherectomy provides a thrombogenic surface that is at high risk for HIT-induced thrombosis. 3 Therefore, PPAI patients with HIT can experience significant morbidities including pulmonary embolism, acute renal failure, stroke, and acute myocardial infarction. 1 However, contemporary data on the financial burden, morbidity, and mortality of HIT after PPAI are scarce.…”