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The term ‘pneumothorax’ was first coined by Itard and then Laennec in 1803 and 1819 respectively,1 and refers to air in the pleural cavity (ie, interspersed between the lung and the chest wall). At that time, most cases of pneumothorax were secondary to tuberculosis, although some were recognised as occurring in otherwise healthy patients (‘pneumothorax simple’). This classification has endured subsequently, with the first modern description of pneumothorax occurring in healthy people (primary spontaneous pneumothorax, PSP) being that of Kjærgaard2 in 1932. It is a significant global health problem, with a reported incidence of 18–28/100 000 cases per annum for men and 1.2–6/100 000 for women.3
Secondary pneumothorax (SSP) is associated with underlying lung disease, in distinction to PSP, although tuberculosis is no longer the commonest underlying lung disease in the developed world. The consequences of a pneumothorax in patients with pre-existing lung disease are significantly greater, and the management is potentially more difficult. Combined hospital admission rates for PSP and SSP in the UK have been reported as 16.7/100 000 for men and 5.8/100 000 for women, with corresponding mortality rates of 1.26/million and 0.62/million per annum between 1991 and 1995.4
With regard to the aetiology of pneumothorax, anatomical abnormalities have been demonstrated, even in the absence of overt underlying lung disease. Subpleural blebs and bullae are found at the lung apices at thoracoscopy and on CT scanning in up to 90% of cases of PSP,5 6 and are thought to play a role. More recent autofluorescence studies7 have revealed pleural porosities in adjacent areas that were invisible with white light. Small airways obstruction, mediated by an influx of inflammatory cells, often characterises pneumothorax and may become manifest in the smaller airways at an earlier stage with ‘emphysema-like changes’ (ELCs).8
Smoking has been implicated in this …