Tugulan Carmen, Chang Donald D, Bates Michael J
Section of Cardiothoracic Surgery, Department of Surgery, Ochsner Clinic Foundation, New Orleans, LA.
The University of Queensland Faculty of Medicine, Ochsner Clinical School, New Orleans, LA.
Ochsner J. 2021 Summer;21(2):200-204. doi: 10.31486/toj.20.0007.
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%. 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. 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.
肝素诱导的血小板减少症(HIT)是一种罕见的自身免疫反应,表现为接触肝素后血小板计数下降,并可能伴有危及生命的血栓形成。由于心脏手术患者肝素暴露时间延长,他们有发生HIT的风险,发生率为0.1%至3%。一名65岁男性,患有严重二尖瓣反流,术前射血分数为20%至25%,接受了二尖瓣生物瓣置换术及冠状动脉旁路移植术。术后第1天开始使用肝素抗凝。呼吸衰竭导致机械通气时间延长且持续肝素化,无法启动华法林治疗。患者使用肝素期间,术后第2天血小板计数下降,然后在术后第7天稳步上升至术前水平以上。术后第10天,患者血小板计数急剧下降,术后第13天出现急性股总动脉闭塞,需要进行取栓术。术中经食管超声心动图显示二尖瓣生物瓣上有大量血栓负荷。肝素诱导的血小板抗体和血清素释放试验呈阳性,确诊为HIT。停用肝素并开始使用阿加曲班。患者在术后第18天再次接受生物瓣二尖瓣置换术,术中使用比伐卢定。尽管HIT得到缓解,但患者发生了败血症,于术后第59天死亡。对于接受体外循环的患者,HIT的诊断具有挑战性。术后最初72小时内血小板计数通常会下降40%至60%,非特异性抗血小板因子4/肝素抗体形成的频率很高。这些发现可能掩盖HIT的早期迹象并延迟诊断。