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Intraoperative air leak site detection in spontaneous pneumothorax through carbon dioxide insufflation during thoracoscopic surgery.


  • 影响因子:3.18
  • DOI:10.1007/s00464-019-06768-0
  • 作者列表:"Kang DY
  • 发表时间:2020-01-01

BACKGROUND:Although thoracoscopic surgery is commonly performed in patients with a pneumothorax and persistent air leak, it is still difficult to identify a definite air leak site during thoracoscopic surgery. The purpose of this study was to determine the safety, efficacy, and feasibility of intraoperative air leak site detection in spontaneous pneumothorax through low-pressure carbon dioxide (CO2) insufflation during thoracoscopic surgery. METHODS:Of 54 patients who underwent thoracoscopic pneumothorax operations between March 2017 and March 2018, 22 pneumothorax patients underwent surgery for a persistent air leak. All patients were intubated with a single- or double-lumen endotracheal tube for general anesthesia. Three-port thoracoscopic surgery was performed, and CO2 was insufflated into the thoracic cavity at a pressure of 3-5 mmHg under two-lung ventilation to ensure visibility for video-assisted thoracoscopic surgery (VATS) and identification of the air leak site. RESULTS:Air leak sites were identified in all but one patient under CO2 insufflation. No intraoperative or postoperative adverse effects associated with CO2 insufflation were observed. The operative time was 37.8 ± 14.9 min (range 20-66 min), and the chest tube was removed after an average 2.7 ± 0.7 postoperative days (range 2-4 days). Patients were discharged after an average 4.1 ± 0.9 postoperative days (range 3-6 days). Postoperative recurrence was confirmed in 3 patients during 12.0 ± 4.0 months (range 5-16 months) of follow-up. CONCLUSION:A method to detect an air leak site during VATS for pneumothorax using low-pressure CO2 appears to be safe, effective, and feasible.


背景: 虽然胸腔镜手术通常用于气胸和持续性漏气的患者,但在胸腔镜手术中仍然难以确定明确的漏气部位。本研究的目的是确定胸腔镜手术中通过低压二氧化碳 (CO2) 吹气检测自发性气胸术中漏气部位的安全性、有效性和可行性。 方法: 在 2017年3月至 2018年3月期间接受胸腔镜气胸手术的 54 例患者中,22 例气胸患者因持续漏气而接受手术。所有患者均采用单腔或双腔气管导管插管全身麻醉。进行了三孔胸腔镜手术, 在双肺通气下以 3-5 mmHg 的压力向胸腔内注入 CO2,以确保电视胸腔镜手术 (VATS) 的可视性和空气泄漏部位的识别。 结果: 在 CO2 吹入下,除 1 例患者外,所有患者均发现漏气部位。未观察到与 CO2 吹入相关的术中或术后不良反应。手术时间 37.8 ± 14.9 min (范围 20-66 min), 术后平均 2.7 ± 0.7 天 (范围 2-4 天) 拔除胸管。患者平均术后 4.1 ± 0.9 天 (范围 3-6 天) 出院。在 12.0 ± 4.0 个月 (范围 5-16 个月) 的随访中,3 例患者证实术后复发。 结论: 采用低压 CO2 检测 VATS 气胸漏气部位是安全、有效、可行的。



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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