Management of bronchopleural fistula in patients on mechanical ventilation
- Andrew M Luks, MD
Andrew M Luks, MD
- Associate Professor - Division of Pulmonary and Critical Care Medicine
- Department of Medicine, University of Washington
When a pneumothorax is detected in a mechanically ventilated patient, air is evacuated from the pleural space by inserting a chest tube and applying external suction. The evacuated air is seen as bubbling through the water seal of the drainage device. Air may continue to leak into the pleural space for minutes to hours, but it will eventually stop in most cases. The bubbling ceases once the lung is fully reinflated and no further air leaks into the pleural space.
A bronchopleural fistula (BPF) exists if the bubbling continues for 24 hours or more. It is indicative of a persistent air leak into the pleural space. Most are small and consist of only a few bubbles escaping through the water seal of the drainage device in synchrony with the inspiratory phase of the ventilator. However, a few leaks are larger and persist through both inspiration and expiration; the volume of such leaks may reach several hundred milliliters per breath.
Although BPF was encountered not infrequently 30 years ago in patients with the acute respiratory distress syndrome (ARDS), in the current era of low tidal volumes and lung-protective ventilation it has become rare as a complication associated with mechanical ventilation. Nonetheless, it remains desirable for clinicians to be familiar with BPF, as it can occur in critically ill patients, and to have an approach to its assessment and management. Assessment and management of a BPF in the setting of mechanical ventilation are reviewed here [1,2]. The pathogenesis, management, and outcomes of BPF following lung surgery are discussed separately [3,4]. (See "Sequelae and complications of pneumonectomy" and "Lung volume reduction surgery in COPD".)
There are many potential causes of bronchopleural fistula (BPF) in mechanically ventilated patients. These include airway disruption or alveolar rupture prior to the initiation of mechanical ventilation (eg, trauma, surgery), laceration of the airway or visceral pleura during mechanical ventilation (eg, central line placement, thoracentesis), and spontaneous alveolar rupture (eg, a complication of the underlying disease or mechanical ventilation). The potential causes of BPF are listed in the table (table 1).
Alveolar rupture due to mechanical ventilation appears to be a consequence of alveolar overdistension due to an excessive inflation volume, more than a consequence of increased airway pressure. This was shown by an animal study in which a high peak inflation volume without increased airway pressure caused alveolar injury, whereas high airway pressure without an increased inflation volume did not cause alveolar injury . The former conditions were created by high tidal volume external negative-pressure ventilation, while the latter conditions were created by strapping the chest and not allowing it to expand despite high inflation pressure. This animal data is supported by the observation that humans frequently have high airway pressures (eg, coughing, bronchospasm without air trapping), but alveolar rupture rarely results. In light of this evidence, the term "volutrauma" is a more accurate description of the pathogenesis of a pneumothorax as a complication of mechanical ventilation than "barotrauma" . The likelihood of volutrauma is increased in the presence of acute lung injury . (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults" and "Inflammatory mechanisms of lung injury during mechanical ventilation".)
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