As HIT typically begins 5-10 days after starting therapy with heparin, it follows that the length of heparin treatment can influence the risk for HIT, e.g., a 10-14 day course of UFH is far more likely to result in clinical HIT than a 1 day treatment period (>2% vs. 0.02%, i.e., an OR of ~100). Of note, there is evidence that the risk of HIT begins to decline after 10 days of uninterrupted heparin use (see Fig. 1C, Chapter 2). In a large study of postoperative orthopedic surgical patients receiving postoperative heparin prophylaxis, no patient developed HIT antibodies after day 10, even though many patients received heparin for up to 14 days (Warkentin et al., 1995). These data are consistent with a "point exposure" model for risk of HIT in this patient population, such as a brief time shortly after surgery, when high circulating PF4 levels coincide with the first few sc heparin injections. However, even if HIT antibody formation occurs during the day 5-10 window period, thrombocytopenia itself can occur somewhat later, particularly if a larger dose of heparin is given, or UFH is substituted for LMWH. The characteristic timing of HIT should assist clinicians in focusing their platelet count monitoring for HIT during the critical time period, so that the early diagnosis of HIT is improved (see Section VI).
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