Heparin‐Induced Thrombocytopenia: Treatment Options and Special Considerations

Abstract

Heparin-induced thrombocytopenia (HIT) is an immune-mediated adverse effect that typically manifests several days after the start of heparin therapy, although both rapid- and delayed-onset HIT have been described. Its most serious complication is thrombosis. Although not all patients develop thrombosis, it can be life threatening. The risk of developing HIT is related to many factors, including the type of heparin product administered, route of administration, duration of therapy, patient population, and previous exposure to heparin. The diagnosis of HIT is typically based on clinical presentation, exposure to heparin, and presence of thrombocytopenia with or without thrombosis. Antigen and activation laboratory assays are available to support the diagnosis of HIT. However, because of the limited sensitivity and specificity of these assays, bedside probability scales for HIT were developed. When HIT is suspected, prompt cessation of all heparin therapy is necessary, along with initiation of alternative anticoagulant therapy. Two direct thrombin inhibitors--argatroban and lepirudin--are approved for the management of HIT in the United States, and bivalirudin is approved for use in patients with HIT who are undergoing percutaneous coronary intervention. Other agents, although not approved to manage HIT, have also been used; however, their role in therapy requires further evaluation. A comprehensive HIT management strategy involves the evaluation of numerous factors. Many patients, including those undergoing coronary artery bypass surgery, those with acute coronary syndromes, those with hepatic or renal insufficiency, and children, require special attention. Clinicians must become familiar with the available information on this serious adverse effect and its treatment so that optimum patient management strategies may be formulated.

Case studies in anticoagulation management

“…Limited data is available for transitioning a patient from argatroban to UFH [23,24]. Argatroban was discontinued and an UFH IV bolus of 2,500 units (46 units/ kg) was given 4 h later.…”

“…Clinicians need to be aware of falsely elevated INR results with non-heparin anticoagulants, creating difficulty with therapeutic dosing of warfarin [24]. A bridging protocol from thrombin inhibitor to warfarin has been recently published [23].…”

Venous Thromboembolism in Neonates, Children and Patients with Chronic Renal Disease – Special Considerations

“…The target activated partial thromboplastin time for both lepirudin and bivalirudin is 1.5 to 2.5 times baseline and argatroban 1.5 to 3 times baseline, which may be different from the range specified for unfractionated heparin. (Dager, 2007;Kiser,2008).…”

Clinical Experience with Argatroban for Heparin-Induced Thrombocytopenia in a Large Teaching Hospital

“…1 Although HIT may not develop until several days after initiation of heparin therapy, it may occur within 24 h in patients who have been exposed to heparin within the previous 90 days. [1][2][3] Furthermore, between 13% and 15% of all HIT cases present 9 to 40 days after discontinuation of heparin. 3 HIT predisposes patients to venous and arterial thrombosis and is associated with a mortality rate of 10% to 30%.…”

“…[1][2][3] Furthermore, between 13% and 15% of all HIT cases present 9 to 40 days after discontinuation of heparin. 3 HIT predisposes patients to venous and arterial thrombosis and is associated with a mortality rate of 10% to 30%. 1,4 This condition may be treated with a direct thrombin inhibitor, such as argatroban.…”