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J R Soc Med. 2006 April; 99(4): 170.
PMCID: PMC1420789

Cannabis, pneumothorax and lung bullae

Author's reply

Clinical and pathological entities have diagnostic `frames'.1 For pneumothorax we use clinical and radiological features; tuberculosis is framed by the infecting agent; and lung cancer is defined by its histological features. `Bong lung' grabs our attention2 but it leaves something to be desired as a diagnostic frame. In our review we did two things: defined exactly what entities we were writing about and sought evidence specific to each.

Pneumothorax and pneumomediastinum have separate aetiologies. They infrequently co-exist. We see pneumothorax in about 150 patients a year. In the younger group, we find the characteristic apical lung blebs.3 They are from the lung and rarely cause surgical emphysema unless the parietal pleura is breached with a chest drain. In pneumomediastinum, the air is from the gastrointestinal tract or the proximal airways, tracking along the bronchi. Only in severe instances, such as ruptured oesophagus, does it burst through the mediastinal pleura. Pneumomediastinum always merits attention because of the terrible consequences of ruptured oesophagus. It can occur following severe sneezing and Ambu Bag resuscitation due to high pressure breeching the pharyngeal mucosa. This fits well with the report from Houston, Texas 30 years ago.4

Lung bullae (the subject of our review) are quite different again. They are chronic, degenerative and progressive. We used the prospective study of 241 cannabis smokers5 cautiously, to draw the weak inference that if an excess of lung bullae had been seen on the X-ray (which would be a normal part of preparation for bronchoscopy) they would have been mentioned. If there were better evidence we would have cited it.

With reference to a list of conditions Dr Gill writes `... there are too many reports for this to be a coincidence'. For what to be coincidental with what? The case reports include a gallimaufry of acute mechanical and chronic degenerative manifestations with little distinction made between aetiology specific to cannabinoids, the effects of other smoke, or the self-induced pressure changes. Perhaps `bong lung' sums it up.

References

1. Rosenberg CE, Golden Janet. Framing Disease: Studies in Cultural History. New Brunswick: Rutgers University Press, 1992
2. Gill A. Bong lung: regular smokers of cannabis show relatively distinctive histologic changes that predispose to pneumothorax. Am J Surg Pathol 2005;29: 980-2 [PubMed]
3. Tan C. The management of (spontaneous) pneumothorax. In: Treasure T, Keogh SB, Hunt I, Pagano D, eds. The Evidence for Cardiothoracic Surgery. London: tfm, 2005: 107-18
4. Mattox KL. Pneumomediastinum in heroin and marijuana users. J Am Coll Emerg Physicians 1976;5: 26-8 [PubMed]
5. Fligiel SE, Roth MD, Kleerup EC, Barsky SH, Simmons MS, Tashkin DP. Tracheobronchial histopathology in habitual smokers of cocaine, marijuana, and/or tobacco. Chest 1997;112: 319-26 [PubMed]

Articles from Journal of the Royal Society of Medicine are provided here courtesy of Royal Society of Medicine Press