The object of this study was to evaluate retrospectively the incidence and severity of heparin-induced thrombocytopenia (HIT)-related complications in patients undergoing cardiopulmonary bypass.

The object of this study was to evaluate retrospectively the incidence and severity of heparin-induced thrombocytopenia (HIT)-related complications in patients undergoing cardiopulmonary bypass. We reviewed the records of 1500 consecutive patients who underwent cardiopulmonary bypass between August 1987 and December 1991 at Thomas Jefferson University Hospital. During this period of time, there were 1155 coronary artery bypass graft operations (77 percent); 225 valve replacements and repairs, or the one and the other (15 percent); 60 combination coronary artery bypass graft or valve operations, or the one and the other (4 percent); and 60 miscellaneous deeds (4 percent). Although not all patients with postoperative complications were proofed for the HIT antibody, 11 patients (075 percent) were diagnosed with HIT. There were 17 complications in these 5 men and 6 women including 6 cases of ischemic limbs which required amputation, 4 thumps 2 instances of saphenous vein graft occlusion with resulting myocardial infarction, 2 cases of pulmonary emboli, 1 case of phlegmasia cerulea dolens, and 2 deaths. The complications occurr an average of 36 days postoperatively, with a range of affair of 1 to 11 days postoperatively. The mean nadir platelet account at the time of recognition was 123000/[mmsup3] (range 32000 to 193000/[mmsup3]) with 9 of 11 patients (818 percent) having holds greater than 100,000/[mm.sup.3]. There was, however, a mean percent decrease in the platelet consider of 50 percent (range, 31 to 75 percent) from the time of first front to heparin to the time of recognition of HIT. In our patients, HIT was not related to the symbol duration of treatment with or amount of heparin, or to pretreatment with aspirin.

(Chest 1993; 104:1436-40)

Since its discovery in 1916 by dint of McLean,[1] heparin has had extensive clinical applications, including the prevention and treatment of venous thrombosis and pulmonary embolism, pat myocardial infarction, preventing thrombosis after coronary artery thrombolysis or angioplasty, atrial fibrillation with embolization, peripheral arterial embolization, disseminated intravascular coagulation, fetal shooting retardation, and so on.[2] Heparin also has been invaluable in the unfolding and use of extracorporeal devices so as the heart-lung machine, cell-saver devices, hemodialysis, as well as for an expansive list of clinical and experimental laboratory uses.

Heparin-induced thrombocytopenia (HIT) come abouts when specific heparin-dependent antibodies attach to platelet membranes, causing platelet activation. The aggregation and degranulation of platelets during this proces be the effect in a variety of clinical scenarios ranging from asymptomatic thrombocytopenia to devastating intravascular coagulation.

The final cause of our study was to evaluate the incidence and severity of HIT-related complications in patients undergoing cardiopulmonary bypass. A further review of the literature will be discussed with particular emphasis in succession early recognition and treatment of patients suspected of having HIT.

Materials and Methods

We leadershiped a retrospective study of 1500 consecutive patients undergoing cardiopulmonary bypass between August 1987 and December 1991 at Thomas Jefferson University Hospital to evaluate the morbidity and mortality of similar patients when the diagnosis of HIT is made postoperatively. During this time, there was no systematic investigation of platelet judges in postoperative patients. Early in the reported period, a diagnosis of HIT was considered when a thromboembolic complication occurr in association with a decrease in the platelet enumerate Later, a diagnosis of HIT was considered in any patient with a thromboembolic complication following cardiopulmonary bypass. The diagnostic proof used to detect the carriage of the anti-platelet antibody was the two-point [C.sup.14]-serotonin platelet release proof described by Sheridan et al.[3]

In order to assess normal platelet accounts in patients following cardiopulmonary bypass, the platelet holds of 100 additional consecutive patients with no evidence of HIT were studied. the two the nadir and the percent ear-ring in the platelet count were determined.

Results

During the subject of attention period, there were 1,155 coronary artery bypass graft operations (77 percent) 225 valve replacements or repairs, or one as well as the other (15 percent); 60 combination coronary artery bypass graft and valve operations (4 percent); and 60 miscellaneous measures (4 percent). Cardiopulmonary bypass was performed with clear prime and moderate systemic hypothermia. All patients received bovine lung heparin during cardiopulmonary bypass; however, all prior frontage to heparin, including during cardiac catheterization, was with porcine mucosal heparin. Postoperative heparin frontage such as in heparin flushes, was also with porcine mucosal heparin.

Eleven of 1500 patients (075 percent) were diagnosed as having HIT, including 5 men (45 percent) and 6 (55 percent) women All 11 patients had exposore to heparin while onward another service prior to cardiopulmonary bypass from a variety of sources, including heparin flushes, subcutaneous heparin, heparin-coated pulmonary artery catheters, and cardiac catheterization. The mean time from initial outlook to heparin to time of cardiopulmonary bypass was 45 days, with a range of 3 to 10 days. No patients were suspected of having HIT preoperatively, since there was no significant change in their platelet cast ups during this time nor were there any thromboembolic conclusions prior to surgery. Six of 11 patients (55 percent) were receiving aspirin immediately prior to surgery and 5 of 11 patients (45 percent) had no fresh exposure to aspirin. All 6 patients taking aspirin received a daily dose of 325 mg of aspirin for a minimum of 1 week prior to surgery

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