询问既往SARS-CoV-2感染史在评估间质性肺疾病新诊断中的重要性

E. Stuewe, S. Kher
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引用次数: 0

摘要

简介:约30%的严重急性呼吸综合征(SARS)和中东呼吸综合征(MERS)患者在急性疾病后出现持续的肺部异常。然而,SARS冠状病毒2 (SARS- cov -2)感染是否会导致长期肺部并发症尚不清楚。我们提出了我们的经验与患者的新诊断间质性肺疾病(ILD)在大流行。病例:一名61岁男性,有高血压和阻塞性睡眠呼吸暂停病史,于2020年3月出现急性发作的咳嗽和呼吸困难。由于当地公共卫生部门的居家咨询,该患者最初没有接受COVID-19检测。咳嗽消退,但呼吸困难持续存在。2个月后复查SARS-CoV-2聚合酶链反应阴性。由于持续的呼吸困难,在症状出现5个月后进行了胸部CT检查,显示上下肺弥漫性,轻度胸膜下网状结节性混浊,与ILD有关(图1)。肺功能测试(PFT)显示肺活量和肺体积正常,气体交换轻度受损。对ILD病因的研究,包括对暴露和风湿病血清学的评估,没有显著意义。检测到SARS-CoV-2 IgG抗体(25.9 AU/ml,正常1.00 AU/ml), IgM未检出。其他原因的呼吸困难检查包括超声心动图、CT肺血管造影和通气灌注扫描,未发现结构性心脏病或血栓栓塞性疾病的证据。讨论:考虑到没有其他ILD的病因,我们的患者在3月份有急性COVID-19感染,并在随后的几个月中发展为继发性ILD是最合理的。先前对SARS和MERS患者的研究发现,肺纤维化和PFT异常在感染后持续数月。因此,对于已知COVID-19感染史的患者,应警惕肺部疾病症状。与上述病例一样,另一个诊断挑战在于出现新发ILD但未确诊COVID-19的患者,特别是考虑到在大流行的早期阶段获得检测的机会有限。在这些患者中,我们建议进行全面的病史检查,包括筛查提示先前病毒综合征的症状,特别是相关的嗅觉缺失或记忆障碍,这可能表明有COVID-19感染史。另一种选择是考虑血清学检测,但鉴于缺乏支持证据,而且可能出现假阳性和假阴性,必须谨慎解释这种检测。
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Importance of Eliciting History of Prior SARS-CoV-2 Infection in Evaluation of New Diagnosis of Interstitial Lung Disease
Introduction: About 30% of patients with severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) had persisting lung abnormalities after acute illness. However, little is known whether SARS coronavirus 2 (SARS-CoV-2) infection will cause long-term pulmonary complications. We present our experience with a patient with a new diagnosis of interstitial lung disease (ILD) during the pandemic. Case: A 61-year-old man with history of hypertension and obstructive sleep apnea developed acute onset cough and dyspnea in March 2020. The patient was not initially tested for COVID-19 because of the local department of public health's stay-at-home advisory. Cough resolved but dyspnea persisted. Two months later, polymerase chain reaction for SARS-CoV-2 was checked and was negative. Due to ongoing dyspnea, a CT chest was performed 5 months after symptom onset and showed diffuse, mild sub-pleural reticulonodular opacities in upper and lower lungs, concerning for ILD (Figure 1). Pulmonary function testing (PFT) showed normal spirometry and lung volumes, and mild impairment in gas exchange. Work up for causes of ILD, including assessment for exposures and serologies for rheumatologic disease, was unremarkable. IgG antibody for SARS-CoV-2 was detected (25.9 AU/ml;normal<1.00 AU/ml);IgM was undetectable. Work up for other causes of dyspnea included an echocardiogram, CT pulmonary angiogram, and ventilation-perfusion scan that revealed no evidence of structural heart disease or thromboembolic disease. Discussion: Given no other etiology of ILD was identified, it is most plausible that our patient had acute COVID-19 infection in March and developed secondary ILD over the ensuing months. Previous studies of patients with SARS and MERS have found occurrences of pulmonary fibrosis and PFT abnormalities persisting many months after onset of infection. Thus, it is prudent to be vigilant for symptoms of lung disease in patients with a known history of COVID-19 infection. An additional diagnostic challenge, as with the case above, lies with patients who present with new onset ILD but without a confirmation of COVID-19, particularly given the limited access to testing in the early stages of the pandemic. In these patients, we suggest a thorough history that includes screening for symptoms suggestive of prior viral syndromes, particularly with associated anosmia or dysgeusia, that can point to a history of COVID-19 infection. Another option is consideration of serologic testing, although such tests must be interpreted with caution in view of the paucity of supporting evidence and the possibility of both false-positives and false-negatives.
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