Reply to Albert and Dhooria et al.

From the Authors:

The recent research in spontaneous pneumothorax has stimulated unprecedented interest in the subject, as emphasized in our editorial (1). Healthy discussions (like the review by Walker and colleagues [2] and our editorial [1]) and insightful comments, such as those from Dr. Albert and Dr. Dhooria and colleagues, are welcomed, add to the momentum, and generate novel hypotheses to be explored.

The suggestion by Dr. Albert to consider factors affecting interstitial pressure in the pathophysiology and treatment of pneumothorax is on the basis of the idea that air may leak from the lung into the interstitial space, enter the mediastinum and subsequently appear in the pleural cavity. This idea has also been cited in high-profile reviews (3).

Direct and indirect evidence in animal models suggests that interstitial pressure of healthy lungs (approximately −10 to −12 cmH₂O at functional residual capacity) is considerably lower than pleural pressure because of the powerful lymphatic pump. As such, there certainly appears to be a higher pressure gradient for air to leak from alveoli to interstitial spaces than to the pleural space (4, 5). However, elastance of the extracellular matrix in the interstitium is high because of the mechanical resistance of proteoglycans, so interstitial pressure rises rapidly to above atmospheric pressure with fluid loading or hypoxia (6, 7). This may limit the capacity of the interstitial space to act as a conduit for air between the alveoli and mediastinum. We are unaware of comparable data in humans.

We also note that in patients with spontaneous pneumothorax, residual air in the mediastinum (of any volume) is exceedingly rare, even on computed tomography scans. These observations suggest that air leak from alveoli to interstitial spaces is unlikely to be a common cause of spontaneous pneumothorax.

We also thank Dhooria and colleagues for their proposed algorithm. We support clinical algorithms that minimize unnecessary chest tube insertions. We advocate the findings of the PSP (primary spontaneous pneumothorax) randomized trial (8), which convincingly showed that most (85%) patients with PSP do not require aspiration or drainage, on the proviso that the pneumothorax does not enlarge on a repeat radiograph after 4 hours and vital signs are stable. Insertion of a chest tube significantly increased the risk of prolonged air leak, time in hospital, need for surgery, and serious adverse events compared with the patients managed conservatively. The trial included patients with moderate to large pneumothorax (median 64% of hemithorax), and we apply this regularly in our practice, even to patients with complete pneumothorax (9). It is important to note that most patients with PSP are much more troubled by pain than breathlessness.

An interval chest radiograph is a useful alternative to determine if the air leak is ongoing without interventions. Simple aspiration has been shown to be at least as effective as chest tube insertion (10). Another recent randomized trial (11) showed that an ambulatory device (incorporating an 8F catheter attached to a one-way Heimlich valve and fluid collection chamber) is useful for community management of patients who may have an ongoing air leak without connecting to an underwater seal bottle. Hence conventional chest tube insertion and underwater seal bottle management should only be necessary for a minority of patients.