急性COVID-19肺炎并发自发性纵隔气胸1例

N. Sahu, J. Roy, E. Ernst, A. Zamir
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引用次数: 0

摘要

自发性纵隔肺炎是病毒性肺炎中的一种罕见疾病,在持续的COVID-19大流行期间,越来越多地报道了自发性纵隔肺炎。新出现的文献表明,同时伴有气胸和纵隔气肿的COVID-19患者的发病率和死亡率更高。早期认识和了解这些并发症对于改善预后是必要的。我们报告了一例最初被诊断为轻度COVID-19症状的老年男性,随着氧气水平的增加,病情迅速发展,发现有小气胸和纵隔气肿。一名77岁男性,高血压,阻塞性睡眠呼吸暂停,在家持续气道正压通气(CPAP)治疗,1周前通过逆转录酶聚合酶链反应诊断为轻度COVID-19,因呼吸急促加重而就诊于急诊室。患者体温101.5°F,心率103bpm,血压稳定,呼吸频率25次/分钟,环境空气氧饱和度70%。他被安排在下午15点。白细胞计数14k/uL,血红蛋白11.7g/dL, c反应蛋白185 mg/L,前BNP 637pg/mL,铁蛋白802 ng/mL,乳酸2 mmol/L,降钙素原0.84 ng/mL。胸片显示双侧肺叶周围及下肺叶浸润。他开始使用地塞米松、瑞德西韦、抗生素、托珠单抗和依诺肝素。他的CPAP维持并继续吸氧。纵隔气肿,或纵隔空气,有多种病因,分为继发性和自发性。常见的继发原因包括外伤造成的钝性损伤,医源性原因如插管、中央导管和胸部手术,最后,医学条件如间质性肺疾病、哮喘、结缔组织疾病和呼吸道感染可能是其他原因(1)。已经报道了几例COVID-19患者自发性纵隔气肿,然而,确切的病因尚不清楚,因为没有人使用机械通气(2-5)。一种机制可能是由于反复发作的咳嗽引起气道压力增加,导致已经广泛受损的肺泡破裂和近端气体泄漏(2)。根据一份尸检报告,发现肺细胞脱屑和透明膜形成表明早期急性呼吸窘迫综合征(6)。使用CPAP时较高的呼气末正压(呼气末正压)造成的气压创伤可能是另一种机制(7)。进行性COVID-19患者应仔细考虑这些并发症,确保咳嗽抑制、使用止吐剂、利尿剂和低呼气末正压策略,以帮助减轻这种以前罕见的现象。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Spontaneous Pneumomediastinum/Pneumothorax in Acute COVID-19 Pneumonia: A Case Report
Introduction Spontaneous pneumomediastinum, a rare condition in viral pneumonias, has been increasingly reported during the ongoing COVID-19 pandemic. Emerging literature suggests a higher incidence and mortality in COVID-19 patients with both a pneumothorax and pneumomediastinum. Early recognition and understanding of these complications are necessary to improve outcomes. We present a case of an older man initially diagnosed with mild COVID-19 symptoms who quickly progressed with increasing oxygen levels found to have a small pneumothorax and pneumomediastinum. Description A 77-year-old man with hypertension, obstructive sleep apnea on home continuous positive airway pressure (CPAP) therapy, and diagnosis of mild COVID-19 via reverse transcriptase polymerase chain reaction 1-week prior, presented to the emergency department for worsening shortness of breath. He was found to have a temperature of 101.5°F, heart rate of 103bpm, stable blood pressure, respiratory rate of 25 breaths/minute, and oxygen saturation of 70% on ambient air. He was placed on 15lpm mid-flow. Labs were significant for a white blood cell count of 14k/uL, hemoglobin 11.7g/dL, c-reactive protein 185 mg/L, pro- BNP of 637pg/mL, ferritin 802 ng/mL, lactic acid 2 mmol/L, procalcitonin of 0.84 ng/mL. He had a chest x-ray with bilateral perihilar and lower lobe infiltrates. He was started on dexamethasone, remdesivir, antibiotics, tocilizumab, and enoxaparin. His CPAP was held and continued on oxygen therapy. Discussion Pneumomediastinum, or air in the mediastinum, occurs through various etiologies categorized into secondary and spontaneous. Common secondary causes include blunt injuries by trauma, iatrogenic causes such as intubation, central lines, and chest operations, and finally, medical conditions such as interstitial lung disease, asthma, connective tissue disorders, and respiratory infections may be other causes (1). Several cases have been reported with spontaneous pneumomediastinum in patients with COVID-19, however, the exact etiology is unknown as none were placed on mechanical ventilation (2-5). One mechanism is likely due to the repetitive episodes of cough causing increased airway pressure leading to alveolar rupture in already extensively damaged alveoli and proximal gas leakage (2). Based on one autopsy report, there were findings of desquamation of pneumocytes and hyaline membrane formation indicating early acute respiratory distress syndrome (6). In another case series, barotrauma from higher PEEP (positive end-expiratory pressure) with the use of CPAP is potentially another mechanism (7). Careful consideration for these complications should occur in patients with progressive forms of COVID-19, ensuring cough suppression, use of anti-emetics, diuretics and low PEEP strategy to help mitigate this previously rare phenomenon.
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