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Secondary tension pneumothorax in a COVID-19 pneumonia patient: a case report

新型冠状病毒肺炎继发张力性气胸 1 例

  • 影响因子:2.48
  • DOI:10.1007/s15010-020-01457-w
  • 作者列表:"Spiro, Judith E.","Sisovic, Snezana","Ockert, Ben","Böcker, Wolfgang","Siebenbürger, Georg
  • 发表时间:2020-06-18

Purpose Especially in elderly and multimorbid patients, Coronavirus Disease 2019 (COVID-19) may result in severe pneumonia and secondary complications. Recent studies showed pneumothorax in rare cases, but tension pneumothorax has only been reported once. Case presentation A 47-year-old male was admitted to the emergency department with fever, dry cough and sore throat for the last 14 days as well as acute stenocardia and shortage of breath. Sputum testing (polymerase chain reaction, PCR) confirmed SARS-CoV-2 infection. Initial computed tomography (CT) showed bipulmonary groundglass opacities and consolidations with peripheral distribution. Hospitalization with supportive therapy (azithromycin) as well as non-invasive oxygenation led to a stabilization of the patient. After 5 days, sputum testing was negative and IgA/IgG antibody titres were positive for SARS-CoV-2. The patient was discharged after 7 days. On the 11th day, the patient realized pronounced dyspnoea after coughing and presented to the emergency department again. CT showed a right-sided tension pneumothorax, which was relieved by a chest drain (Buelau) via mini open thoracotomy. Negative pressure therapy resulted in regression of the pneumothorax and the patient was discharged after 9 days of treatment. Conclusion Treating physicians should be aware that COVID-19 patients might develop severe secondary pulmonary complications such as acute tension pneumothorax. Level of evidence V


目的冠状病毒病 2019 (新型冠状病毒肺炎) 可导致重症肺炎和继发性并发症,尤其是老年人和多发病。最近的研究显示气胸在极少数情况下,但张力性气胸只有一次报道。病例报告: 一名 47 岁男性因发热、干咳、咽喉痛持续 14 天,以及急性心绞痛和呼吸不足而入住急诊科。痰检测 (聚合酶链反应,PCR) 证实 SARS-CoV-2 感染。初始计算机断层扫描 (CT) 显示双肺磨玻璃影和周围分布的巩固。住院支持治疗 (阿奇霉素) 以及无创氧合导致患者稳定。5 天后痰检阴性,IgA/IgG 抗体滴度阳性 SARS-CoV-2。患者 7 天后出院。第 11 天,患者咳嗽后出现明显的呼吸困难,再次就诊于急诊科。CT 显示右侧张力性气胸,经小切口开胸胸腔引流 (Buelau) 缓解。负压治疗导致气胸消退,治疗 9 天后出院。结论内科医师应注意新型冠状病毒肺炎患者可能发生急性张力性气胸等严重的继发性肺部并发症。证据级别 V



作者列表:["De Cunto G","Brancaleone V","Riemma MA","Cerqua I","Vellecco V","Spaziano G","Cavarra E","Bartalesi B","D'Agostino B","Lungarella G","Cirino G","Lucattelli M","Roviezzo F"]

METHODS:BACKGROUND AND PURPOSE:A critical role for sphingosine kinase/sphingosine-1-phosphate (S1P) pathway in the control of airway function has been demonstrated in respiratory diseases. Here, we address S1P contribution in a mouse model of mild chronic obstructive pulmonary disease (COPD). EXPERIMENTAL APPROACH:C57BL/6J mice have been exposed to room air or cigarette smoke up to 11 months and killed at different time points. Functional and molecular studies have been performed. KEY RESULTS:Cigarette smoke caused emphysematous changes throughout the lung parenchyma coupled to a progressive collagen deposition in both peribronchiolar and peribronchial areas. The high and low airways showed an increased reactivity to cholinergic stimulation and α-smooth muscle actin overexpression. Similarly, an increase in airway reactivity and lung resistances following S1P challenge occurred in smoking mice. A high expression of S1P, Sph-K2 , and S1P receptors (S1P2 and S1P3 ) has been detected in the lung of smoking mice. Sphingosine kinases inhibition reversed the increased cholinergic response in airways of smoking mice. CONCLUSIONS AND IMPLICATIONS:S1P signalling up-regulation follows the disease progression in smoking mice and is involved in the development of airway hyperresponsiveness. Our study defines a therapeutic potential for S1P inhibitors in management of airways hyperresponsiveness associated to emphysema in smokers with both asthma and COPD.

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作者列表:["Bernstein DM","Toth B","Rogers RA","Kling DE","Kunzendorf P","Phillips JI","Ernst H"]

METHODS::The interim results from this 90-day multi-dose, inhalation toxicology study with life-time post-exposure observation has shown an important fundamental difference in persistence and pathological response in the lung between brake dust derived from brake-pads manufactured with chrysotile, TiO2 or chrysotile alone in comparison to the amphiboles, crocidolite and amosite asbestos. In the brake dust exposure groups no significant pathological response was observed at any time. Slight macrophage accumulation of particles was noted. Wagner-scores, were from 1 to 2 (1 = air-control group) and were similar to the TiO2 group. Chrysotile being biodegradable, shows a weakening of its matrix and breaking into short fibers & particles that can be cleared by alveolar macrophages and continued dissolution. In the chrysotile exposure groups, particle laden macrophage accumulation was noted leading to a slight interstitial inflammatory response (Wagner-score 1-3). There was no peribronchiolar inflammation and occasional very slight interstitial fibrosis. The histopathology and the confocal analyses clearly differentiate the pathological response from amphibole asbestos, crocidolite and amosite, compared to that from the brake dust and chrysotile. Both crocidolite and amosite induced persistent inflammation, microgranulomas, and fibrosis (Wagner-scores 4), which persisted through the post exposure period. The confocal microscopy of the lung and snap-frozen chestwalls quantified the extensive inflammatory response and collagen development in the lung and on the visceral and parietal surfaces. The interim results reported here, provide a clear basis for differentiating the effects from brake dust exposure from those following amphibole asbestos exposure. The subsequent results through life-time post-exposure will follow.

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作者列表:["Zaragosi LE","Deprez M","Barbry P"]

METHODS::The respiratory tract is lined by a pseudo-stratified epithelium from the nose to terminal bronchioles. This first line of defense of the lung against external stress includes five main cell types: basal, suprabasal, club, goblet and multiciliated cells, as well as rare cells such as ionocytes, neuroendocrine and tuft/brush cells. At homeostasis, this epithelium self-renews at low rate but is able of fast regeneration upon damage. Airway epithelial cell lineages during regeneration have been investigated in the mouse by genetic labeling, mainly after injuring the epithelium with noxious agents. From these approaches, basal cells have been identified as progenitors of club, goblet and multiciliated cells, but also of ionocytes and neuroendocrine cells. Single-cell RNA sequencing, coupled to lineage inference algorithms, has independently allowed the establishment of comprehensive pictures of cell lineage relationships in both mouse and human. In line with genetic tracing experiments in mouse trachea, studies using single-cell RNA sequencing (RNAseq) have shown that basal cells first differentiate into club cells, which in turn mature into goblet cells or differentiate into multiciliated cells. In the human airway epithelium, single-cell RNAseq has identified novel intermediate populations such as deuterosomal cells, 'hybrid' mucous-multiciliated cells and progenitors of rare cells. Novel differentiation dynamics, such as a transition from goblet to multiciliated cells have also been discovered. The future of cell lineage relationships in the respiratory tract now resides in the combination of genetic labeling approaches with single-cell RNAseq to establish, in a definitive manner, the hallmarks of cellular lineages in normal and pathological situations.

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