Use Of Heparin For Cpb In Patients With A Previous History Of

An intriguing option for patients with a history of HIT, but in whom HIT antibodies can no longer be detected, is to consider reexposure to UFH for CPB, and to avoid heparin completely both before surgery (e.g., at heart catheterization) and in the postoperative period. This approach has been used successfully (Makhoul et al., 1987; Potzsch et al., 2000; Selleng et al., 2001; Warkentin and Kelton, 2001), and is based on the following rationale. First, HIT antibodies are transient, and are usually not detectable after several weeks or a few months following an episode of HIT (see Chapter 2). Thus, no immediate problems would be expected in a patient without residual HIT antibodies. Second, it appears that a minimum of 5 days are required before clinically significant levels of HIT antibodies are generated following any episode of heparin treatment (Warkentin and Kelton, 2001). In the event that a recurrent immune response to PF4-heparin is induced by reexposure to heparin during CPB, it is unlikely that the newly generated antibodies will contact exogenously administered heparin. As a consequence, platelet activation by HIT antibodies should not occur, and thus the thrombotic risk should not be increased. Potzsch et al. (2000) reported 10 patients with a documented history of HIT, but no detectable HIT antibodies at the time of the proposed surgery, who thus underwent CPB anticoagulation with heparin. In none of the 10 patients was a thromboembolic complication or prolonged thrombocytopenia observed. Further, no increase in anti-PF4/heparin antibody concentrations occurred during 10-day follow-up. These data are consistent with the findings of Warkentin and Kelton (2001), who also observed no evidence for a rapid "anamnestic" type of immune response when heparin reexposure was used

FIGURE 1 Algorithm for decision making for alternative anticoagulation in HIT patients. "Negative" testing for HIT antibodies includes a weak (gray zone) enzyme immunoassay result plus a negative functional test using washed platelets, such as the serotonin release assay or heparin-induced platelet activation assay (see Chapter 10). Abbreviations: CPB, cardiopulmonary bypass; OPCAB, off-pump coronary artery bypass; UFH, unfractionated heparin.

FIGURE 1 Algorithm for decision making for alternative anticoagulation in HIT patients. "Negative" testing for HIT antibodies includes a weak (gray zone) enzyme immunoassay result plus a negative functional test using washed platelets, such as the serotonin release assay or heparin-induced platelet activation assay (see Chapter 10). Abbreviations: CPB, cardiopulmonary bypass; OPCAB, off-pump coronary artery bypass; UFH, unfractionated heparin.

as a strategy for intraoperative anticoagulation for cardiac and vascular surgery in patients with previous HIT.

We recommend that HIT antibody-negative patients with a history of HIT who require CPB for heart surgery should be treated according to established heparin protocols (Fig. 1). The use of heparin should be restricted to the operative period itself; if necessary, postoperative anticoagulation should be achieved with an alternative anticoagulant (see Chapters 12-17).

Testing for HIT antibodies in patients with a history of HIT before anticipated heparin reexposure at heart surgery should be performed using one or more sensitive tests (see Chapter 10). Particularly in cardiac surgical centers where there is limited experience with non-heparin anticoagulation for CPB, risk-benefit considerations strongly favor a brief use of heparin for these patients. For example, a patient who developed near-fatal CPB circuit thrombosis during danaparoid anticoagulation had had HIT 11 yr earlier and had no detectable HIT antibodies at the time danaparoid was used (Grocott et al., 1997).

Studies using enzyme immunoassays show that the frequency of anti-PF4/ heparin antibody formation following heart surgery (Visentin et al., 1996; Bauer et al., 1997; Warkentin and Sheppard, 2006) is as high as 70% (see Chapter 3). Even with the washed platelet serotonin-release assay, platelet-activating antibodies are detected in 13-20% of patients (Bauer et al., 1997; Warkentin et al., 2000). However, despite this high seroconversion rate, only about 1-3% of patients who receive further postoperative anticoagulation with UFH develop HIT. Currently, there is no convincing evidence that patients who form anti-PF4/heparin antibodies in the absence of thrombocytopenia are at increased risk for thrombosis (Bauer et al., 1997; Trossaert et al., 1998; Warkentin et al., 2000). However, postoperative cardiac surgical patients who develop clinical HIT appear to be at increased risk for both venous and arterial thrombotic events (Walls et al., 1990; Van Dyck et al., 1996; Pouplard et al., 1999). Therefore, if HIT is clinically highly suspected or confirmed, an alternative non-heparin anticoagulant should be initiated (see Chapter 12).

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