Jamil Aayla K, Alam Amit, Youssef Ronnie M, Felius Joost, van Zyl Johanna S, Gottlieb Robert L
Baylor Scott & White Research Institute, Dallas, TX.
College of Medicine, Texas A&M Health Science Center, Dallas, TX.
Mayo Clin Proc Innov Qual Outcomes. 2021 Oct;5(5):827-834. doi: 10.1016/j.mayocpiqo.2021.05.009. Epub 2021 Aug 25.
To determine whether the apparent excess incidence of pneumothorax and pneumomediastinum in patients with coronavirus disease 2019 (COVID-19) is explained adequately by iatrogenic causes vs reflecting sequelae of severe acute respiratory syndrome coronavirus 2 infection.
We retrospectively reviewed patients within our health care system from March 15, 2020, through May 31, 2020, who had a diagnosis of pneumothorax or pneumomediastinum during hospitalization for confirmed COVID-19 infection with attention to timing of pneumothorax and pneumomediastinum; presence, laterality, and placement, or attempts at central lines; and presence of mechanical ventilation before the event.
We report clinical data and outcomes from 9 hospitalized patients with COVID-19 who developed pneumothorax and/or pneumomediastinum among more than 1200 hospitalized patients admitted within our hospital system early in the pandemic. Many events were inexplicable by iatrogenic needle injury, including 1 spontaneous case without central line access or mechanical ventilation. One occurred before central line placement, 2 in patients with only a peripherally inserted central line, and 1 contralateral to a classic central line. Three of these 9 patients died of complications of COVID-19 during their hospital stay.
With COVID-19 affecting the peripheral lung pneumocytes, patients are vulnerable to develop pneumothorax or pneumomediastinum irrespective of their central line access site. We hypothesize that COVID-19 hyperinflammation, coupled with the viral tropism that includes avid involvement of peripheral lung pneumocytes, induces a predisposition to peripheral bronchoalveolar communication and consequent viral hyperinflammatory-triggered pneumothorax and pneumomediastinum.
确定2019冠状病毒病（COVID-19）患者气胸和纵隔气肿的明显超额发病率是由医源性原因充分解释，还是反映了严重急性呼吸综合征冠状病毒2感染的后遗症。
我们回顾性分析了2020年3月15日至2020年5月31日在我们医疗系统内确诊为COVID-19感染并住院期间诊断为气胸或纵隔气肿的患者，关注气胸和纵隔气肿的发生时间；中心静脉置管的存在、侧别和位置，或置管尝试；以及事件发生前是否存在机械通气。
我们报告了在疫情早期我们医院系统收治的1200多名住院患者中，9例COVID-19住院患者发生气胸和/或纵隔气肿的临床数据和结局。许多事件无法用医源性针刺伤解释，包括1例无中心静脉置管或机械通气的自发病例。1例发生在中心静脉置管前，2例仅为外周静脉置入中心静脉导管的患者，1例与经典中心静脉置管对侧。这9例患者中有3例在住院期间死于COVID-19并发症。
由于COVID-19影响外周肺上皮细胞，无论中心静脉置管部位如何，患者都易发生气胸或纵隔气肿。我们推测，COVID-19的过度炎症反应，加上病毒嗜性（包括对外周肺上皮细胞的大量侵袭），导致外周支气管肺泡相通的易感性增加，进而引发病毒超炎症反应触发的气胸和纵隔气肿。
