Clamping trials prior to thoracostomy tube removal and the need for subsequent invasive pleural drainage.
- 作者列表："Becker JC","Zakaluzny SA","Keller BA","Galante JM","Utter GH
BACKGROUND:There is little evidence supporting or refuting clamping trials, a period of clamping thoracostomy tubes prior to removal. We sought to evaluate whether clamping trials reduce the need for subsequent pleural drainage procedures. METHODS:We conducted a retrospective cohort study of trauma patients who underwent tube thoracostomy during 2009-2015. We compared patients who underwent clamping trials to those who did not, adjusting for confounders. The primary outcome was subsequent ipsilateral pleural drainage within 30 days. RESULTS:We evaluated 214 clamping trial and 285 control patients. Only two of 214 patients failed their clamping trial and none developed a tension pneumothorax [0.0% (95% CI 0.0-1.7%)]. Clamping trials were associated with fewer pleural drainage procedures [13 (6%) vs. 33 (12%); adjusted OR 0.41 (95% CI 0.20-0.84)]. CONCLUSIONS:A clamping trial prior to thoracostomy tube removal seems to be safe and was associated with less likelihood of a subsequent pleural drainage procedure.
背景: 很少有证据支持或反驳钳夹试验，即在取出前夹闭胸腔造瘘管一段时间。我们试图评估钳夹试验是否减少了后续胸膜引流手术的需要。 方法: 我们对 2009-2015 年期间接受管状胸廓造口术的创伤患者进行了一项回顾性队列研究。我们比较了接受钳夹试验的患者与未接受钳夹试验的患者，调整了混杂因素。主要结局是 30 天内随后同侧胸腔引流。 结果: 我们评估了 214 例钳夹试验和 285 例对照患者。214 例患者中只有 2 例钳夹试验失败，无一例发生张力性气胸 [0.0% (95% CI 0.0-1.7%)]。钳夹试验与较少的胸膜引流程序相关 [13 (6%) vs.33 (12%); 调整后的 OR 0.41 (95% CI 0.20-0.84)]。 结论: 在拔除胸腔造瘘管之前进行钳夹试验似乎是安全的，并且与随后进行胸腔引流手术的可能性较小相关。
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.
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.
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.