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Functional testing for HIT antibodies is not standardized and is technically challenging. 1 The platelet aggregation assay, which we use at our institution, is far less sensitive than the serotonin release assay35 and a negative result can therefore be potentially misleading because of the low sensitivity of the assay. 8) can also manifest thrombosis,33–35 we elected to make treatment decisions based on positive ELISA results without regard to a specific cutoff value. 35 We recognize that our report has important limitations: the data are retrospective; it is a small series with no randomization of therapy or comparison to treatment strategies, and the report is not powered or 34 designed to demonstrate risks or benefits of the plasmapheresis procedure compared with heparin anticoagulation alone or a heparin alternative; and the small size of our study population also precludes any meaningful conclusions about safety or efficacy.

Administration of a saline bolus rather than a simulated test dose), the baseline period before any drug injection allowed each subject to serve as his or her own control. There was no stimulation or alteration in anesthetic depth during the baseline or study periods, thus no reason to suppose that physiologic changes measured were due to anything other than the administration of the simulated test dose. The previous studies using this methodology have all shown that false-positive findings do not occur under these conditions.

Current American College of Chest Physicians guidelines recommend that patients with a history of HIT should not be reexposed to heparin until antibody levels are undetectable. For this reason, we elected to pursue a conservative approach reducing antibody levels to the lowest level achievable rather than subjecting patients to an unknown risk of disease exacerbation. Although it would be optimal to select patients for plasmapheresis based on results of functional assays, this approach is often not practical.