Heparin-Induced Thrombocytopenia Clinical Presentation
- Author: Sancar Eke, MD; Chief Editor: Emmanuel C Besa, MD more...
History
There are 3 characteristic features of heparin-induced thrombocytopenia (HIT) that can distinguish it from other causes of thrombocytopenia: (1) the timing of the onset of thrombocytopenia, a platelet count decrease that begins between days 5 and 14 of beginning heparin treatment; (2) the severity of the thrombocytopenia (usually mild to moderate), with platelet counts only rarely less than 15 x 109/L; and (3) large-vessel venous or arterial thrombosis in association with thrombocytopenia.[22]
Physicians should think of the possibility of heparin-induced thrombocytopenia (HIT) if venous thromboembolism (VTE) develops during or soon after UFH use; if thrombocytopenia is present, alternative anticoagulation should be used until heparin-induced thrombocytopenia (HIT) is excluded.[23] Delayed-onset heparin-induced thrombocytopenia (HIT) develops several days after heparin cessation. In patients with previous heparin exposure, heparin-induced thrombocytopenia (HIT) may have a rapid onset (within hours of reexposure)
Clinical features of heparin-induced thrombocytopenia (HIT) that help distinguish it from other forms of thrombocytopenia include the timing of onset (usually 5-14 d after beginning an immunizing exposure to heparin), the severity of the thrombocytopenia (usually mild to moderate), and the presence of thrombosis or other sequelae.
In one study, 12 patients were described who experienced thrombocytopenia or symptoms of thrombosis an average of 9 days after all heparin was withdrawn.[24] This phenomenon was referred as delayed-onset heparin-induced thrombocytopenia. Delayed-onset heparin-induced thrombocytopenia (HIT) should be considered when a patient presents with thrombosis and unexplained thrombocytopenia up to 3 weeks after the end of heparin therapy.[24]
Physical
Heparin-induced thrombocytopenia (HIT) may present with unusual characteristic sequelae, including warfarin-associated venous limb gangrene, bilateral adrenal hemorrhagic infarction, heparin-induced skin lesions, or acute systemic reactions following an intravenous heparin bolus. In contrast to other drug-induced immune thrombocytopenia syndromes, in general, heparin-induced thrombocytopenia (HIT) is not associated with bleeding.[22]
In addition to the occurrence of thrombocytopenia within the appropriate time frame, a diagnosis of heparin-induced thrombocytopenia (HIT) is suggested by the presence of skin lesions at heparin injection sites and acute systemic reactions including chills, fever, dyspnea, chest pain; flushing may be observed following intravenous heparin administration.[25] Patients with heparin-induced thrombocytopenia (HIT) can also present with DVT, which can progress to limb loss if the use of coumarin leads to severe protein C depletion (coumarin-induced venous limb gangrene).[26]
Causes
Heparin-induced thrombocytopenia (HIT) is caused by antibody formation to heparin-PF4 complexes. A study showed that heparin-induced thrombocytopenia (HIT) is more frequently encountered with UFH compared with LMWH.[15] Case studies have also demonstrated the probability of developing heparin-induced thrombocytopenia (HIT) with minimal heparin exposure via intravascular flushes to maintain the patency of indwelling arterial or venous catheters.[27, 28, 29, 30, 31]
Fondaparinux is a new anticoagulant that catalyzes the inhibition of factor Xa (but not thrombin) by antithrombin, and this results in the inhibition of thrombin generation. A study suggested that fondaparinux may be associated with formation of anti–PF4/heparin antibodies but, in contrast to LMWH, it is unlikely to cause heparin-induced thrombocytopenia (HIT) because of the poor reactivity of antibodies against PF4/fondaparinux.[32]
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