Heparin-Induced Thrombocytopenia After Mitral Valve Replacement

Abstract

Background: Heparin-induced thrombocytopenia (HIT) is a rare autoimmune reaction that involves a decrease in platelet count following heparin exposure and can be associated with life-threatening thrombosis. Because of their prolonged heparin exposure, patients undergoing cardiac surgery are at risk of HIT, with an incidence of 0.1% to 3%. Case Report: A 65-year-old male with severe mitral regurgitation and preoperative ejection fraction of 20% to 25% underwent mitral valve bioprosthetic replacement with coronary artery bypass graft surgery. Heparin anticoagulation was started on postoperative day (POD) 1. Respiratory failure resulted in prolonged mechanical ventilation and heparinization without the ability to initiate warfarin. While the patient was on heparin, his platelet count declined on POD 2 and then steadily increased to above the preoperative level on POD 7. On POD 10, the patient's platelet count dramatically decreased, and on POD 13 he developed acute common femoral artery occlusion necessitating embolectomy. Intraoperative transesophageal echocardiography revealed heavy thrombus burden across the mitral bioprosthesis. HIT was confirmed with a positive heparin-induced platelet antibody and serotonin release assay. Heparin was stopped and argatroban initiated. The patient underwent reoperative bioprosthetic mitral valve replacement on POD 18 using bivalirudin intraoperatively. Despite resolution of HIT, the patient developed sepsis and died on POD 59. Conclusion: The diagnosis of HIT is challenging in patients who undergo cardiopulmonary bypass. Platelet counts often decrease 40% to 60% during the first 72 hours postoperatively, and the frequency of nonspecific anti-platelet factor 4/heparin antibody formation is high. These findings can mask early signs of HIT and delay diagnosis.

Keywords: Cardiac surgical procedures; heparin; mitral valve; thoracic surgery; thrombocytopenia; thrombocytopenia–heparin-induced.

Figure 1.

Preoperative ultrasound transesophageal echo-cardiography shows the thickened mitral valve obstructing cardiac vascular flow.

Figure 2.

(A) Superior, (B) sagittal, and (C) inferior views of the resected thrombosed mitral valve show the thrombotic debris on the thickened leaflet walls.

Figure 3.

Biphasic morphology of the platelet count trend suggests heparin-induced thrombocytopenia pathology. POD, postoperative day.