Infants with heparin-induced thrombocytopenia (HIT) represent a challenging and high-risk group of patients when they require cardiopulmonary bypass (CPB). Bivalirudin offers many potential pharmacologic advantages over other nonheparin anticoagulants for such patients. We describe our protocol for the use of bivalirudin in a 5-month-old infant undergoing stage 2 Norwood for hypoplastic left heart syndrome. The patient was a 5- month-old, 6-kg infant who developed HIT after a bowel resection complicating initial Norwood stage 1. After sternotomy and dissection had been redone, the child received an initial dose of bivalirudin of 1.0 mg/kg and 0.5 mg/kg 5 min later. The CPB circuit was primed with 50 mg/kg bivalirudn/400 cc volume. With the initiation of CPB, a continuous infusion of 2.5 mg/kg bivalirudin was begun. Activated clotting time (ACT) was targeted for over 400 s, with an examination prior to bypass and each 15 min thereafter. Bivalirudin was discontinued with separation from bypass and during modified ultrafiltration (MUF). The ACT was 286 s after the initial 1 mg/kg bolus and 597 s after the second 0.5 mg/kg bolus and initiation of CPB. At a rate of 2.5 mg/kg/min, ACT ranged between 461 and 597 s. At the completion of MUF, the ACT was 316 s. The ACT was 214 s 20 min after MUF. No clots were noted in the CPB circuit, and good hemostasis was achieved within 10 min after MUF was completed. Incision to closure time was 160 min; time from completion of MUF to sternal closure was 30 min. Post-MUF, 60 cc of processed cell saver blood was reinfused, and no clotting factors were required. Chest tube output was 10, 10, 3, and 4 ccs, respectively, at hours 1-4 post operation. Bivalirudin provides effective anticoagulation in infants requiring CPB in the presence of HIT. Bivalirudin's efficacy is effectively monitored by ACT, and, after CPB, its short half-life and ability to be ultrafiltered facilitate the ability to achieve hemostasis in a timely fashion.
A 4-year-old boy had a 15-mm atrial septal defect repaired percutaneously with use of an Amplatzer Septal Occluder. At age 16 years, he presented with a week's history of fever, chills, dyspnea, fatigue, and malaise. Cultures grew methicillin-sensitive Staphylococcus aureus. A transesophageal echocardiogram showed a 1.25 × 1.5-cm pedunculated mass on the left aspect of the atrial septum just superior to the mitral valve, and a smaller vegetation on the right inferior medial aspect of the septum. At surgery, visual examination of both sides of the septum revealed granulation tissue, the pedunculated mass, the small vegetation, and exposed metal wires that suggested incomplete endothelialization of the occluder. We removed the occluder and patched the septal defect. The patient returned to full activity after 4 months and was asymptomatic 3 years postoperatively. Our report reinforces the need for further investigation into prosthetic device endothelialization, endocarditis prophylaxis, and recommended levels of physical activity in patients whose devices might be incompletely endothelialized. In addition to reporting our patient's case, we review the medical literature on this topic.
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