Heparin-platelet factor 4 antibodies in patients presenting to the ED with thrombosis.

BACKGROUND: Patients with heparin-platelet factor 4 (PF4) antibodies, particularly platelet-activating ones, are at risk for heparin-induced thrombocytopenia if administered heparin. We determined the heparin-PF4 antibody prevalence in emergency department (ED) patients presenting with chest pain or symptoms of thrombosis. METHODS: Admission samples from 324 ED patients with chest pain or symptoms of thrombosis were tested for heparin-PF4 antibodies and, if positive, platelet-activating antibodies. RESULTS: Twenty-four (7.4%; 95% confidence interval, 4.8%-10.8%) patients had heparin-PF4 antibodies. Seropositivity occurred in 18 (9.2%) of 196 patients recently (< or =6 months) hospitalized vs 6 (4.7%) of 128 not recently hospitalized (P = .19), and in 16/231 (6.9%) patients with chest pain vs 8/93 (8.6%) with other thrombosis (P = .64). Of 22 seropositive patients retested, 8 (7 recently hospitalized) had platelet-activating antibodies. CONCLUSION: Heparin-PF4 antibody prevalence is 7.4% in ED patients with chest pain or thrombosis, with approximately 1 in 3 seropositive patients having platelet-activating antibodies. Alternative, nonheparin anticoagulation would be prudent in these at-risk patients.

Striking back at heparin-induced thrombocytopenia.

This immune reaction to a common anticoagulant can have devastating consequences. Learn how to recognize who's at risk and how to intervene if trouble hits.

Heparin-induced thrombocytopenia in the emergency department.

We describe 3 patients who presented to the emergency department (ED) with stroke, deep venous thrombosis, or pulmonary embolism and renal failure after undergoing cardiac surgery 7 to 17 days earlier. Their onset of thrombosis after previous heparin exposure was temporally plausible for complications of heparin-induced thrombocytopenia, an immune-mediated thrombotic disorder triggered by heparin. The patients had normal platelet counts at presentation, yet each had circulating heparin-induced thrombocytopenia antibodies that were ultimately confirmed. Two patients had heparin reexposure in the ED, 1 of whom developed thrombocytopenia with new thrombosis and died. Alternative parenteral anticoagulation prevented further thrombosis in 2 patients. Because heparin use can be catastrophic in patients with heparin-induced thrombocytopenia, physicians should be vigilant in suspecting heparin-induced thrombocytopenia in patients with thrombosis after recent hospitalization or heparin exposure. Alternative anticoagulants are available for these at-risk patients.

Comparison of bovine and porcine heparin in heparin antibody formation after cardiac surgery.

BACKGROUND: Heparin-induced thrombocytopenia (HIT) is a potentially devastating complication of heparin therapy. The incidence of clinical HIT after cardiovascular surgery is less than 2%, although asymptomatic antibodies to heparin-platelet factor 4 (PF4) occur more frequently. Bovine heparin is thought to cause more HIT than porcine heparin, although this has never been established for heparin use during coronary artery bypass grafting. We therefore undertook a randomized, prospective study of heparin-PF4 antibody formation in patients undergoing first-time CABG given intraoperative bovine or porcine heparin. METHODS: Two hundred seven patients (108 porcine, 99 bovine) completed the study. Heparin given pre- or postoperatively was always porcine. Platelet counts and heparin-PF4 antibody tests (enzyme-linked immunosorbent assays) were performed preoperatively and daily until postoperative day 7 or discharge if earlier. RESULTS: The overall incidence of heparin-PF4 antibody formation was 42%. Six patients (2.9%) were positive preoperatively, of which, 1 developed clinical HIT. When these were excluded, seroconversion rates were 44 of 99 (44.4%) and 33 of 108 (30.6%) for bovine and porcine heparin, respectively (p = 0.041). Among patients who produced antibodies, most (90% bovine, 85% porcine) seroconverted after postoperative day 2. There were no differences in postoperative platelet counts; only 1 patient developed thrombosis associated with seroconversion, but without developing thrombocytopenia. The seroconversion rates for patients having cardiopulmonary bypass or off-pump surgery were not significantly different. CONCLUSIONS: This study confirms the high frequency of heparin-PF4 antibodies after coronary artery bypass grafting and demonstrates a significantly higher incidence after bovine heparin. However, because some patients may seroconvert after discharge, our study may underestimate the true incidence.

Delayed-onset heparin-induced thrombocytopenia.

BACKGROUND: Heparin-induced thrombocytopenia presents 5 to 12 days after heparin exposure, with or without arterial or venous thromboemboli. Delayed recognition and treatment of heparin-induced thrombocytopenia contribute to poor patient outcomes. OBJECTIVE: To describe and increase awareness of a clinical scenario in which the onset or manifestations of heparin-induced thrombocytopenia are delayed. DESIGN: Retrospective case series. SETTING: Three large urban hospitals (with active cardiovascular surgery programs). PATIENTS: 14 patients seen over a 3-year period in whom heparin-induced thrombocytopenia became apparent on delayed presentation with thromboembolic complications. MEASUREMENTS: Platelet counts, onset of objectively determined thromboembolism, results of heparin-induced platelet factor 4 antibody tests, and outcomes. RESULTS: Patients went home after hospitalizations that had included heparin exposure--in most cases, with no thrombocytopenia recognized--only to return to the hospital (median, day 14) with thromboembolic complications. Thromboemboli were venous (12 patients, 7 with pulmonary emboli) or arterial (4 patients) or both. Platelet counts were mildly decreased in all but 2 patients on second presentation. On readmission, 11 patients received therapeutic heparin, which worsened the patients' clinical condition and, in all 11 cases, decreased the platelet count (mean at readmission, 143 x 10(9) cells/L; mean nadir after heparin re-exposure, 39 x 10(9) cells/L). Results of serologic tests for heparin-induced antibodies were positive in all patients. Subsequent treatments included alternative anticoagulants (11 patients), thrombolytic drugs (3 patients), inferior vena cava filters (3 patients) and, eventually, warfarin (11 patients). Three patients died. CONCLUSIONS: Delayed-onset heparin-induced thrombocytopenia is increasingly being recognized. To avoid disastrous outcomes, physicians must consider heparin-induced thrombocytopenia whenever a recently hospitalized patient returns with thromboembolism; therapy with alternative anticoagulants, not heparin, should be initiated.