Ischemic Stroke and Bilateral Pulmonary Embolism in COVID-19: COVID-Associated Coagulopathy or Heparin-Induced Thrombocytopenia

IF 1.3 Q4 HEMATOLOGY
S. Soliman, Medhat Ghaly
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引用次数: 4

Abstract

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/mm3 to 43,000/mm3, 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.
COVID-19缺血性卒中和双侧肺栓塞:COVID-19相关凝血功能障碍或肝素诱导的血小板减少症
2019冠状病毒病(COVID-19)发病机制的一个主要特征是血栓形成频率高,主要是肺栓塞(PE)。抗凝治疗是治疗的重要组成部分。肝素用于抗凝可能增加肝素诱导的血小板减少(HIT)的风险,这是一种潜在的致命并发症,表现为血小板减少伴或不伴血栓形成。我们报告一名69岁未接种疫苗的女性重症COVID-19肺炎患者。最初的实验室调查是显著的血小板减少和低d -二聚体水平。她最初开始使用依诺肝素,然后是未分离肝素。住院第8天,患者出现左侧面部下垂和构音障碍,并发现大脑中动脉近端有非闭塞性血栓和双侧肺栓塞。她接受静脉溶栓治疗并输注肝素。住院第13天,血小板计数从12万/mm3降至4.3万/mm3,提示HIT可疑。停用肝素,开始使用氟达肝素。3天后,HIT抗体测试返回阳性,然后血清素释放试验阳性证实了诊断。出院时,她被转移到阿哌沙班完成3个月的抗凝治疗诱发性PE。该病例代表了HIT在COVID-19患者中的诊断挑战。肝素输注后血小板减少应引起临床对HIT的怀疑,这允许适当停止肝素产品并开始使用替代抗凝剂以限制破坏性并发症。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和动脉血栓形成事件的COVID-19患者报告。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of hematology
Journal of hematology HEMATOLOGY-
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