组合拳:SARS-CoV-2与急性纤维性肺炎和组织性肺炎

M. Forson, D. Bajaj, V. Ramalingam
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引用次数: 0

摘要

简介:急性纤维性组织性肺炎(AFOP)是一种罕见的肺损伤组织学类型。在COVID-19肺损伤患者中,组织性肺炎(OP)的发生频率可能比人们意识到的要高。本病例报告回顾了1例COVID-19患者AFOP的表现和病程。病例描述:一名49岁男性,有糖尿病和慢性淋巴细胞性淋巴瘤史,服用Venetoclax和Obinutuzumab,表现为发热、用力呼吸困难和干咳,被诊断为COVID-19。他的CT扫描显示广泛的外周为主的斑片状和异质磨玻璃混浊,并伴有纵隔淋巴结病(图A)。他的血清半乳甘露聚糖曲霉指数为4.37,他开始服用伏立康唑。然而,他仍然发热,因此,他进行了经支气管冷冻活检。病理显示间质性t淋巴细胞炎性浸润伴纤维性和组织性肺炎。有增生性细支气管炎和急性肺出血的证据,没有血管炎/毛细血管炎的特征。没有发现恶性肿瘤或微生物的证据。他开始每日使用甲基强的松龙,最初病情有所改善,但随着类固醇逐渐减少,他又发烧,需氧量迅速增加。胸部重复CT扫描显示双侧斑片状实变明显增加,周围有磨砂玻璃影和小叶间隔增厚(“疯狂铺路”)。此时,他需要有创机械通气,随后接受脉搏剂量类固醇治疗3天,然后进行大剂量维持。他好转了,拔管了。然而,他需要高流量的补充氧,并且无法在吸入氧的100%以上断奶,因此,添加了Ruxolitinib。不幸的是,他的低氧血症仍然是难治性的,他出现了突然的心血管衰竭,导致了他的死亡。患者于入院后40天死亡。讨论:了解COVID-19的组织病理学、病程和后遗症至关重要,因为COVID-19的AFOP增加了管理的复杂性。我们的患者在急性呼吸窘迫综合征和机械通气前进行了死前活检,而不是之前的病例报告在长时间机械通气后尸检发现AFOP。值得注意的是,30% - 60%的重症监护SARS冠状病毒患者有OP和AFOP。此外,COVID-19的CT表现与OP相似,这支持了OP是COVID-19肺损伤的潜在模式的可能性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The One-Two Punch: SARS-CoV-2 and Acute Fibrinous and Organizing Pneumonia
Introduction: Acute fibrinous and organizing pneumonia (AFOP) is a rare histological pattern of lung injury. Organizing Pneumonia (OP) may be occurring more frequently than realized in patients with lung injury from COVID-19. This case report reviews the presentation and disease course of AFOP in a patient with COVID-19. Case description:A 49-year-old male with a history of Diabetes Mellitus and Chronic Lymphocytic Lymphoma on Venetoclax and Obinutuzumab presented with fever, exertional dyspnea, and dry cough and was diagnosed with COVID-19. His CT scan showed extensive peripheral predominant patchy and heterogenous ground glass opacities with mediastinal lymphadenopathy (Image A). His serum aspergillus galactomannan index was 4.37 and he was started on voriconazole. He however remained febrile;so, he had a transbronchial cryobiopsy. His pathology revealed marked interstitial T-cell lymphocytic inflammatory infiltrate with fibrinous and organizing pneumonia. There was proliferative bronchiolitis and evidence of acute pulmonary hemorrhage, without features of vasculitis/capillaritis. No evidence of malignancy or organisms were identified. He was started on methylprednisolone daily and he initially improved, however, his fever returned and his oxygen requirements increased rapidly with steroid taper. His repeat chest CT scan showed a marked increase in bilateral patchy areas of consolidation with surrounding areas of ground glass opacity and intralobular septal thickening ("crazy paving") Image B. His infectious work up was extensive but negative. At this point, he required invasive mechanical ventilation;after which he received pulse dose steroids for three days followed by high dose maintenance. He improved and was extubated. However, he required high flow supplemental oxygen and was unable to be weaned past 100% fraction of inspired oxygen;as a result, Ruxolitinib was added. Unfortunately, his hypoxemia remained refractory and he developed sudden cardiovascular collapse which led to his demise. The patient died 40 days after admission. Discussion: Understanding the histopathology, disease course, and sequelae of COVID-19 is of paramount importance, because AFOP in COVID-19 adds complexity to management. Our patient's antemortem biopsy was performed prior to acute respiratory distress syndrome and mechanical ventilation as opposed to previous case reports with post mortem findings of AFOP after prolonged mechanical ventilation. Notably, 30% - 60% of intensive care patients with SARS CoV 1 had OP and AFOP. Additionally, the CT findings of COVID-19 are similar to OP and this lends support to the possibility that OP is an underlying pattern of lung injury in COVID-19.
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