How I treat patients with a history of heparin-induced thrombocytopenia

Abstract

Heparin-induced thrombocytopenia (HIT) is a relatively common prothrombotic adverse drug reaction of unusual pathogenesis that features platelet-activating immunoglobulin G antibodies. The HIT immune response is remarkably transient, with heparin-dependent antibodies no longer detectable 40 to 100 days (median) after an episode of HIT, depending on the assay performed. Moreover, the minimum interval from an immunizing heparin exposure to the development of HIT is 5 days irrespective of the patient’s previous heparin exposure status or history of HIT. This means that short-term heparin reexposure can be safely performed if platelet-activating antibodies are no longer detectable at reexposure baseline and is recommended when heparin is the clear anticoagulant of choice, such as for cardiac or vascular surgery. The risk of recurrent HIT 1 to 2 weeks after heparin reexposure is ∼2% to 5% and is attributable to formation of delayed-onset (or autoimmune-like) HIT antibodies that activate platelets even in the absence of pharmacologic heparin. Some studies suggest that longer-term heparin reexposure (eg, for chronic hemodialysis) may also be reasonable. However, for other antithrombotic indications that involve patients with a history of HIT (eg, treatment of venous thromboembolism or acute coronary syndrome), preference should be given to non-heparin agents such as fondaparinux, danaparoid, argatroban, bivalirudin, or one of the new direct-acting oral anticoagulants as appropriate.

Plasma exchange for heparin‐induced thrombocytopenia in patients on extracorporeal circuits: A challenging case and a survey of the field

“…The majority of these respondents reported having only treated a single HIT patient in the past year. These data suggest that TPE is currently not widely utilized for patients with HIT despite the growing body of literature supporting its safety and efficacy in the setting of urgent CPB . As more evidence accumulates supporting the utility of TPE for HIT desensitization to allow short‐term heparin exposure, clinical recommendations will likely evolve.…”

“…These data suggest that TPE is currently not widely utilized for patients with HIT despite the growing body of literature supporting its safety and efficacy in the setting of urgent CPB. 31,48 As more evidence accumulates supporting the utility of TPE for HIT desensitization to allow short-term heparin exposure, clinical recommendations will likely evolve. Interestingly four of the 52 survey respondents (7.7%) reported experience with using VAD circuitry for TPE access.…”

Heparin-induced thrombocytopenia: research and clinical updates

“…All the reported cases to date are associated with findings of thrombocytopenia and thrombosis in association with high-titer platelet activating anti-PF4/ heparin antibodies. 22,23 As with delayed-onset HIT, anti-PF4/ heparin antibodies bind to PF4/GAGs on platelets and, thus, have the distinctive feature of heparin-independent platelet activation. Diagnostic criteria for spontaneous HIT have been proposed based on clinical findings of thrombocytopenia and thrombosis without prior heparin exposure, and stringent laboratory criteria that include both serologic assays and functional assays of heparin-dependent platelet activation.…”

Cost-effectiveness of anticoagulants for suspected heparin-induced thrombocytopenia in the United States

“…[14][15][16][17] Expert opinion 3,[18][19][20] and emerging evidence [21][22][23] suggest fondaparinux is a safe and effective alternative agent. This selective factor Xa inhibitor is provided as a daily subcutaneous injection and requires only infrequent laboratory monitoring.…”