BAL is a procedure considered to have a low incidence of complications and has not been associated with pneumothorax in patients with interstitial lung disease. The pathophysiology of BAL-induced pneumothorax is not clear, but presumably is related to the associated airway obstruction, with impaired pressure equilibration of entrapped intra-alveolar gases, interstitial dissection of air, and, finally, decompression into the pleural cavity. Pneumothorax and hydropneumothorax have been reported to occur in patients with pulmonary alveolar proteinosis following whole lung BAL. The unit volume of “alveolar flooding would be similar in subsegmental BAL and total lung lavage. Upwards of 40 to 60 percent of BAL fluid is not removed by suctioning, depending on the severity of the destructive parenchymal process. The retained fluid may promote local gas trapping as a consequence of the loss of the protective decompression mechanism of collateral ventilation acting via channels at both the alveolar and bronchiolar levels. Collateral flow has been previously reported to be impaired in the dog lung when water is injected into a lobe. Also, obstruction of sublobar segments at low lung volumes in animal models results in a greater outward acting stress on the alveolar wall (alveolar pressure gradient) as a result of pulmonary interdependence. The potential significance of these factors in the pathogenesis of pneumothroax would be further enhanced with BAL of a subsegment of the middle lobe, as done in this case, since there is only a single interface with another segment. canadian neightbor pharmacy
The role of interstitial emphysema in pneumothorax formation has been defined in both the laboratory and clinical setting. It has been shown by others as well that it is the transpulmonic pressure gradient due to inadequate venting, rather than the absolute intrathoracic pressure, which is responsible for interstitial air accumulation. In addition, inflammation allows for the escape (leakage) of air at less than the usual critical pressure gradient of the epithelial barrier, which in normal lungs is approximately 40 cm H20.n Bronchoscopy, with its concurrent cough, aside from producing shearing forces altering the topographic pressure profile along the pleural surface, causes this pressure gradient to be exceeded as intrathoracic pressures as high as 150 mmHg are produced. The apparent innocuous coughing, as occurred in this patient, thus represents a very real determinant of the occurrence of pneumothorax.
Finally, consideration must be given to the increase in surface tension resulting from the removal of surfactant from lavaged alveoli. It is suggested that the combination of increased hydrostatic and surface forces exerted on an already structurally compromised parenchyma secondary to pneumonia predisposes to the dissection of air and pneumothorax development, an entity that may be termed infectious interstitial emphysema.
These adverse consequences of BAL, including fluid retention, obliteration of collateral communications, and increased forces, dictate the careful monitoring of patients who undergo FOB and BAL, with an expiratory chest x-ray film should there be signs or symptoms of pneumothorax.