We Can Just Stop the Heparin

Now that awareness and recognition of HIT are increasing, this myth may be generating the most harm. When Warkentin and Kelton (1996) followed up 62 patients with serologically confirmed "isolated HIT" (HIT with no thrombosis) whose UFH had been stopped, and in whom either no anticoagulant or warfarin was initiated or continued, 53% developed new clots, usually in the first 2 wk; in 3 (5%), the new clot was manifest as sudden death. Other case series have confirmed the high risk for new thromboemboli after heparin is stopped (Wallis et al., 1999; Lewis et al., 2001). Indeed, it seems wise to investigate systematically the lower limbs for DVT when isolated HIT is diagnosed. In getting physicians thinking beyond paradox 4 that stopping the drug will end the danger, one will also confront the "minor paradox" that prophylactic doses of anticoagulation will not suffice in isolated HIT (Farner et al., 2001; Warkentin, 2001; Kodityal et al., 2003) and the myth that HIT with thrombosis is somehow a different disorder than HIT without thrombosis—the only real difference is that clots have not yet appeared in the latter. Continuing to promulgate type I and type II HIT terminology (see Chapter 1) further confuses physicians into believing that some cases of true HIT are benign and do not require intervention (Rice, 2004). My colleagues and I see case after case of new devastating thromboses appear after doctors have recognized HIT and stopped the heparin, but failed to institute an alternative anticoagulant; only then do they consult a hematologist. We have seen many clots emerge after the platelet count has recovered to normal.

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