This suggests that risk factors predisposing to barotrauma are a severe underlying lung disease, which seriously affects alveoli and all factors predisposing to hyperinflation: high transpulmonary pressure (airway pressure minus the pleural pressure), high tidal volumes, high intrinsic PEEP. In case of mediastinal parietal rupture pneumothorax is appeared.Īll barotrauma forms come from rupture of a hyperinflated alveolus and air leak into the surrounding tissues and spaces.
The air can be decompressed both retroperitoneally and intraperitoneally (pneumoperitoneum). When adequate air is accumulated in mediastinum, it is decompressed along cervical fascial planes into the subcutaneous tissues and subcutaneous emphysema is formed. Air can be introduced along the perivascular sheaths into the mediastinum and pneumomediastinum or pneumopericardium are present. When an overdistended alveolus ruptures, air is diffused into the perivascular adventitia, resulting in PIE. The two terms-barotrauma and volutrauma-reflect the two sides of the same phenomenon: the lung injury due to a large distending volume and/or to a high airway pressure ( 10- 19).Ĭlinical manifestations of barotrauma include pneumothorax, pulmonary interstitial emphysema (PIE), subcutaneous emphysema, pneumoperitoneum, pneumomediastinum or pneumopericardium, air embolisation, tension lung cysts, and hyperinflated left lower lobe. Volutrauma is the term that describes ultrastructural lung injury due to overdistention occurring during mechanical ventilation. Nevertheless, it seems that not only pressure, but high lung volume and lung hyperinflation as well, play a major role in barotrauma aetiology. According to the etymology, barotrauma refers only to high pressures. VALI and VILI can be divided into macrobarotrauma (the form of radiologically detected barotrauma) and microbarotrauma, with diffuse lung injury and possible injury of other organs due to release of inflammatory mediators-biotrauma. This is described as ventilator associated lung injury (VALI) or ventilator induced lung injury (VILI). The implementation of positive pressure ventilation predisposes an already affected lung-when certain limits are overcome-to injury. It is defined as the presence of extraalveolar air in locations, where it is not normally found in patients receiving mechanical ventilation ( 1- 9). Barotrauma must be considered as complication of the use of positive pressures in a tissue, where normal air movement is mainly passive. While human being is created, as other creatures, to breathe with a mechanism based on negative pressures, the patient on mechanical ventilation is ventilated with positive pressures, which is not physiological. Intubation and mechanical ventilation are common but aggressive therapeutic manoeuvres in anesthesia or in ICU setting. Keywords: Barotrauma pneumothorax ICU ventilation Interviews with Outstanding Guest Editors.
Policy of Dealing with Allegations of Research Misconduct.Policy of Screening for Plagiarism Process.Other mechanisms than hypophase dilution or inactivation by proteins may account for surfactant dysfunction in barotrauma. Conclusion : Surfactant and BAL are equally effective in correcting the pulmonary dysfunction associated with barotrauma without affecting the degree of pulmonary edema.
Results of the animals who survived the entire 2 hours is presented. The same post mortem studies were performed in 5 additional animals who did not undergo prior mechanical ventilation (normal). Lung wet and dry weights and hemoglobin content were measured and from those extravascular lung water was calculated (Qwl/kg). Lung functional residual capacity (FRC) was measured by water displacement. After sacrifice, from the static pressure volume curve was derived a numerical index of stability of lung expansion (Gruenwald index) as well as the deflation lung compliance (Cmax). All animals were attempted to be ventilated for 2 hours (tidal volume 6-7 ml/kg, FiO 2: 100%) and arterial blood gases, vascular and airway pressures serially measured. Each treatment was given immediately (E) or 1hour (L) following the hyperventilation sequence. The animals were then randomized to exogenous surfactant (SFCT)(Infasurf™, 100 mg/kg phospholipids), bronchoalveolar lavage (BAL) with dilute surfactant (30 ml/kg, 10mg/ml phospholipids) or no treatment (Control). Barotrauma was produced in 39 rats by 20' of mechanical ventilation at an inflating pressure of 45 cmH 2O (tidal volume: 44 ± 1 ml/kg). To assess whether lung injury produced by baro/volutrauma results in surfactant inactivation we compared the effect of treatment with exogenous surfactant or bronchoalveolar lavage with dilute surfactant following trauma induced pulmonary edema.
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