Soliman Sara, Ghaly Medhat
Department of Internal Medicine, Waterbury Hospital, Waterbury, CT, USA.
Department of Internal Medicine, Yale School of Medicine, CT, USA.
J Hematol. 2022 Feb;11(1):40-44. doi: 10.14740/jh956. Epub 2022 Feb 26.
A main feature of coronavirus disease 2019 (COVID-19) pathogenesis is the high frequency of thrombosis, predominantly pulmonary embolism (PE). Anticoagulation therapy is a crucial part of the management. Heparin use for anticoagulation could increase the risk of heparin-induced thrombocytopenia (HIT), a potentially fatal complication that presents with thrombocytopenia with or without thrombosis. We present a 69-year-old unvaccinated female patient with severe COVID-19 pneumonia. Initial laboratory investigation was significant for thrombocytopenia and low D-dimer levels. She was initially started on enoxaparin followed by unfractionated heparin. On hospital day 8, she developed left facial droop and dysarthria and was found to have non-occlusive thrombus in proximal middle cerebral artery as well as bilateral pulmonary emboli. She received intravenous thrombolysis followed by heparin infusion. On day 13 of hospitalization, platelet count dropped from 120,000/mm to 43,000/mm, raising suspicion of HIT. Heparin was stopped and fondaparinux was started. After 3 days, HIT antibody testing returned positive, then a positive serotonin release assay confirmed the diagnosis. On discharge, she was transitioned to apixaban to complete 3 months of anticoagulation for provoked PE. This case represents the diagnostic challenge of HIT in COVID-19 patients. Thrombocytopenia after heparin infusion should raise clinical suspicion of HIT, which allows appropriate discontinuation of heparin products and initiation of alternative anticoagulants to limit devastating complications. To our knowledge, this is the first case report of a COVID-19 patient presenting with venous thrombosis as well as arterial thrombotic event in the context of underlying HIT.
2019冠状病毒病(COVID-19)发病机制的一个主要特征是血栓形成的频率很高,主要是肺栓塞(PE)。抗凝治疗是管理的关键部分。使用肝素进行抗凝可能会增加肝素诱导的血小板减少症(HIT)的风险,这是一种潜在的致命并发症,可出现血小板减少,伴或不伴有血栓形成。我们报告一名69岁未接种疫苗的女性患者,患有严重的COVID-19肺炎。初始实验室检查显示血小板减少和D-二聚体水平低。她最初开始使用依诺肝素,随后使用普通肝素。住院第8天,她出现左侧面部下垂和构音障碍,发现大脑中动脉近端有非闭塞性血栓以及双侧肺栓塞。她接受了静脉溶栓治疗,随后进行肝素输注。住院第13天,血小板计数从120,000/mm降至43,000/mm,引发了对HIT的怀疑。停用肝素并开始使用磺达肝癸钠。3天后,HIT抗体检测呈阳性,随后阳性血清素释放试验确诊。出院时,她改用阿哌沙班,完成3个月的抗凝治疗,以治疗诱因明确的PE。该病例代表了COVID-19患者中HIT的诊断挑战。肝素输注后出现血小板减少应引起临床对HIT的怀疑,这有助于适当停用肝素产品并启动替代抗凝剂,以限制严重并发症。据我们所知,这是第一例在潜在HIT背景下出现静脉血栓形成以及动脉血栓事件的COVID-19患者的病例报告。