Pulmonary barotrauma may also be diagnosed clinically, particularly in patients with extensive subcutaneous emphysema. In such cases, chest computed tomography may be required for diagnosis. Further, pneumothorax and pneumomediastinum may be obscured by the presence of extensive subcutaneous emphysema. Plain chest radiography is first line, though in mechanically ventilated patients, free air may accumulate in atypical locations due to supine or semi-recumbent positioning. For patients who develop pneumothorax or pneumomediastinum, pulmonary barotrauma is typically diagnosed via imaging. Įarly recognition of pulmonary barotrauma is essential for prevention of hemodynamic and respiratory collapse. Decreased compliance is typical of ARDS, pneumonia, and interstitial lung disease, whereas hyperinflation is seen in COPD and asthma. Disease processes associated with reduced lung compliance and/or dynamic lung hyperinflation increase the risk for development of pulmonary barotrauma. However, underlying pulmonary disease is also typically present in patients who develop this complication. Positive-pressure mechanical ventilation is the most important risk factor leading to the development of pulmonary barotrauma. The incidence in ARDS patients is approximately 10%. The incidence of pulmonary barotrauma is estimated between 2% and 10% and varies based on the presence of underlying pulmonary disease. The consequences of an extrapulmonary air leak include subcutaneous emphysema, pneumothorax, pneumomediastinum, and pneumoperitoneum. Pulmonary barotrauma is caused by alveolar rupture in the setting of elevated trans-alveolar pressures. Four weeks after admission, the patient was terminally extubated and expired. ![]() However, she developed progressive lung injury related to severe ARDS, which was refractory to salvage therapies, including deep sedation, neuromuscular paralysis, prone positioning, high-dose glucocorticoids, and inhaled epoprostenol. Consequently, the patient was managed conservatively with lung-protective mechanical ventilation and remained hemodynamically stable. However, direct airway trauma, particularly related to endotracheal tube removal by the patient, could not be entirely excluded.Īlthough manifestations of the patient’s pulmonary barotrauma were apparent clinically and radiographically, her hemodynamic status and pulmonary mechanics were unaffected. The extensive pulmonary barotrauma was presumed due to alveolar rupture, precipitated by reduced lung compliance, which is characteristic of severe ARDS. Radiographic ( Figure 1) and computed tomographic ( Figure 2, Figure 3A and Figure 3B) imaging following re-intubation demonstrated diffuse subcutaneous emphysema, a large pneumomediastinum, and a small, right-sided pneumothorax. This rapidly progressed to overt distention of her face, neck, trunk, and extremities. Shortly after re-intubation, the patient had evidence of pulmonary barotrauma, with mild crepitus in her chest. Thus, she was electively re-intubated and mechanically ventilated on Hospital Day 11. She was initially supported with non-invasive positive pressure ventilation, but she developed recurrent, progressive, hypoxemic respiratory failure. During a standard interruption of sedation on Hospital Day 5, the patient self-extubated. The patient was intubated and mechanically ventilated for management of hypoxemic respiratory failure. Comparison of treatments proved difficult and it was concluded that, although most cases would probably respond satisfactorily to 2.8 bar (2100 mm Hg) of oxygen, there were no compelling reasons for altering the current treatment practice of beginning treatment of acute cases with a 30-min period at 6.0 bar (165 fsw) before returning to 2.8 bar (60 fsw) to complete the therapy.A 57-year-old woman with chronic obstructive pulmonary disease (COPD), decompensated cirrhosis, and hepatopulmonary syndrome developed severe acute respiratory distress syndrome (ARDS) of presumed viral etiology. Increasing the time to treatment reduced the likelihood of cure. ![]() The remaining cures occurred in equal numbers during decompression and after surfacing. An overall success rate of 65% was seen with 62% of cures occurring within 25 min of arrival at pressure. The 89 treated cases of AGE (including 2 iatrogenic cases) were used to study the efficacy of different treatments. Half of AGE cases improved spontaneously, including 21% which recovered completely. ![]() Details of presentation and precipitating factors were analysed. There were 23 cases of uncomplicated PBT and 117 cases of cerebral arterial gas embolism (AGE), of which 58 had respiratory manifestations. A review of case records spanning 20 years revealed 140 cases of decompression pulmonary barotrauma (PBT) in divers.
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