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aPulmonary embolism (PE) occurred on postoperative day 8, in association with a platelet count fall of 41%, from 378 (postoperative peak) to 224x109/L. The platelet count began to fall on day 7. The case illustrates why it is wrong to use the preoperative platelet count value as the "baseline," as the fall in platelet count from 227 (preoperative [day -1]) to 224 (day 7) would be considered trivial, even though HIT-associated pulmonary embolism occurred. The preoperative (day -1) and first three postoperative days should be censored in the interpretation of platelet counts in HIT. In this patient, the abrupt fall in platelet count from 227 to 98 (day 0) is expected (heart surgery). This patient was treated successfully with danaparoid sodium (D.S.), with longer-term anticoagulation with warfarin. The patient's clinical course is also shown in Fig. 4B in Chapter 11. Abbreviations-. D.S., danaparoid sodium; HIT, heparin-induced thrombocytopenia; PE, pulmonary embolism; UFH, unfractionated heparin.

FIGURE 7 "Iceberg" model of HIT: Model A indicates that thrombosis occurs in patients who develop HIT antibody formation and thrombocytopenia. This model is supported by clinical data. In contrast, model B indicates the possibility of HIT antibody formation contributing to thrombosis without the intermediary process of thrombocytopenia. Although anecdotal experience suggests occasional patients consistent with model B, controlled studies indicate that HIT antibody formation without thrombocytopenia does not have an increased frequency of thrombosis, compared with controls (Warkentin et al., 1995, 2003). Note that thrombocytopenia is broadly defined and includes patients with large relative falls in the platelet count, even if the platelet nadir is >150 x 109/L. Abbreviation: HIT, heparin-induced thrombocytopenia. Source: From Warkentin, 1999.

FIGURE 7 "Iceberg" model of HIT: Model A indicates that thrombosis occurs in patients who develop HIT antibody formation and thrombocytopenia. This model is supported by clinical data. In contrast, model B indicates the possibility of HIT antibody formation contributing to thrombosis without the intermediary process of thrombocytopenia. Although anecdotal experience suggests occasional patients consistent with model B, controlled studies indicate that HIT antibody formation without thrombocytopenia does not have an increased frequency of thrombosis, compared with controls (Warkentin et al., 1995, 2003). Note that thrombocytopenia is broadly defined and includes patients with large relative falls in the platelet count, even if the platelet nadir is >150 x 109/L. Abbreviation: HIT, heparin-induced thrombocytopenia. Source: From Warkentin, 1999.

the frequency and the severity of thrombotic complications increase somewhat in relation to the magnitude of the platelet count decline, whether quantitated in relative or absolute terms (Warkentin et al., 2003; Greinacher et al., 2005b; Lewis et al., 2006).

Platelet Count Recovery Following Discontinuation of Heparin

The median time to platelet count recovery to more than 150 X 109/L after stopping heparin administration is about 4 days, although several more days may be required for the platelet count to reach a stable plateau. In patients with very severe HIT, the platelet count may take 2 wk or more to recover (Warkentin, 1998a). Unlike nonimmune heparin-associated thrombocytopenia, the platelet count will generally not recover in patients with HIT unless the heparin is discontinued.

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