Pneumothorax occurs when free air enters the potential space between the visceral and parietal pleura. Primary pneumothoraces occur without clinically apparent lung disease, either spontaneously or from penetration of the intrapleural space by trauma. Secondary pneumothoraces occur in patients with underlying lung disease.
The incidence of primary spontaneous pneumothorax is 10 to 18 cases for men and 2 to 5 cases for women per 100,000 population.1 Associated factors include cigarette smoking, male gender, mitral valve prolapse, Marfan's syndrome, and changes in ambient pressure. Familial patterns also suggest an inherited association.2 Physical activity or exertion can precipitate but is not a common pneumothorax-triggering factor. Traumatic pneumothoraces are subdivided into iatrogenic and noniatrogenic. Noniatrogenic pneumothoraces will be further discussed in the chapter titled "Pulmonary Trauma."
Causes of secondary spontaneous pneumothorax are listed in Table 1. Chronic obstructive pulmonary disease remains the most common cause.3 Pneumothorax occurs in 5% of patients with acquired immunodeficiency syndrome, is associated with subpleural necrosis by Pneumocystis infection, and carries a high mortality. Because of necrosis of lung tissue and continued air leak, simple aspiration fails in this group of patients. Hemopneumothorax occurs in 2% to 7% of patients with secondary pneumothorax and, if associated with a large amount of blood in the pleural cavity, can be life threatening.4–7 Treating the underlying disease may help decrease the risk of future pneumothorax.
Table 1 Causes of Secondary Pneumothorax |Favorite Table|Download (.pdf)
Table 1 Causes of Secondary Pneumothorax
Chronic obstructive pulmonary disease
Cystic fibrosis (8%–20% will develop one in lifetime)
Interstitial lung disease
Human immunodeficiency virus infection, Pneumocystis pneumonia
Bacterial pneumonia, necrotizing
Connective tissue disease
Primary lung or metastatic disease
Under normal conditions, the parietal and visceral pleura are in close apposition. The pleural space is negatively pressured at −5 mm Hg with fluctuations of 6 to 8 mm Hg between inspiration and expiration. The inherent tendency of the chest wall is to expand and for the lungs to collapse from elastic recoil. With the loss of the normal negative pressure in the pleural space that "adheres" the visceral pleura (lungs) to the parietal pleura (ribs), the affected lung collapses. A primary spontaneous pneumothorax occurs when a subpleural bleb ruptures, disrupting pleural integrity. Rupture in primary spontaneous pneumothoraces usually involves the lung apex.6–8 In secondary spontaneous pneumothoraces, disruption of the visceral pleura occurs secondary to underlying pulmonary disease processes.
Once there is a break in the visceral pleura, air travels down a pressure gradient into the intrapleural space, until pressure equilibrium occurs with partial or total lung collapse. Altered ventilation–perfusion relationships and decreased vital capacity contribute to dyspnea and hypoxemia. If air continues to enter the pleural space, intrapleural pressure becomes positive. Tension pneumothorax develops as ...