Spontaneous Pneumothorax

The term pneumothorax was first coined by Jean Marc Gaspard Itard in 1803, when he called attention to five cases in which free air was found in the thorax after trauma. Derived from the Greek words pneuma (air) and thorakos (breastplate or chest), it is an apt description for the accumulation of air in the pleural space that leads to partial or total collapse of the affected lung. The clinical features of pneumothorax were first described in 1819 by René Laennec, who postulated the relationship to preexisting blebs and unprovoked rupture and, hence, the term spontaneous pneumothorax . This pathophysiologic mechanism was confirmed by Kjærgaard in later decades. Today, the classification of pneumothoraces is based on clinical presentation and underlying lung disease. Multiple management strategies range from simple evacuation of air from the pleural space to potential prevention of future pneumothoraces.


Spontaneous pneumothorax (SP) may be termed either a primary or secondary event, dependent on underlying lung disease. Primary spontaneous pneumothorax (PSP) typically occurs in young patients with localized blebs but otherwise normal lungs. Secondary spontaneous pneumothorax (SSP) occurs in patients with marked structural lung disease and directly contributes to SP. Approximately 20,000 new cases of PSP are diagnosed annually in the United States, with an estimated economic impact of $130 million per year in lost wages. The annual estimated incidence of PSP is between 7.4 and 18 cases per 100,000 population among men and between 1.2 and 6 cases per 100,000 population among women. Patients prone to PSP are usually tall and thin and between 10 and 30 years of age. A significant factor is cigarette smoking, which can increase the risk of PSP by a factor as high as 20.

SSP develops as a complication of underlying lung disease, most commonly chronic obstructive pulmonary disease (COPD). The annual incidence of SSP is approximately 6.3 cases per 100,000 population among men and 2 cases per 100,000 population among women. The peak incidence occurs between the ages of 60 and 65 years.


PSP manifests without forewarning signs or symptoms and is most likely caused by rupture of a subpleural bleb. This premise is based on cumulative results of patients undergoing computed tomography (CT), which demonstrated subpleural blebs in as many as 80%. Surgical experience confirmed the presence of bullae in more than 75% of patients who underwent video-assisted thoracoscopic surgery (VATS) and thoracotomy. Recent research may indicate a more diffuse pathologic etiology than simple bleb rupture. Fluorescein-enhanced pathologic assay of resected lung tissue in PSP patients reveals significant inflammatory changes and potential air-leak sites remote from blebs and other visible abnormalities.

After the first episode of PSP, recurrence varies, ranging from 16% to 54%. Most studies indicate an average of 30%. Recent research indicates that the presence of subpleural blebs on high-resolution CT confers a recurrence risk of up to 68.1%, whereas the absence of blebs carries a recurrence risk of only 6.1%. Most recurrences develop between 6 months and 2 years after the initial episode. Men who are tall and have a history of smoking are at the greatest risk of recurrence. Counseling for smoking cessation should be strongly encouraged. After the second episode of PSP, the likelihood of recurrence increases markedly and can reach as high as 83%.

Clinical Presentation

PSP typically manifests with sudden pleuritic chest pain and dyspnea. Classic findings on physical examination include diminished breath sounds, hyperresonance, and fremitus; however, patients with small pneumothoraces may have normal findings on physical examination. Most patients with PSP are stable, primarily because of their young age and otherwise normal lung function. Patients with SSP are more likely to present with respiratory distress, a result of respiratory compromise caused by SP superimposed on preexisting lung disease. Whereas tension SP is unusual, indicators include tachycardia, cyanosis, and hypotension.


Chest radiography is the most common diagnostic tool for SP. A thin pleural line can be identified that has been displaced from the chest wall. A small SP may be difficult to identify on plain radiography; an expiratory view may prove more beneficial in determining the presence of SP. Frequently, attempts are made to measure the size of the SP as a percentage of the hemithorax it occupies, although this method is typically inaccurate. On occasion, a giant bulla can mimic a pneumothorax. Subtle lines demarcate a bulla, which tends to be surrounded by thickened visceral pleura. In addition, a pleural line can frequently be seen with lung markings visible beyond the suspected bulla (double wall sign).

Controversy exists about the significance of routine chest CT to evaluate for subpleural blebs. Proponents contend that identification of large or multiple subpleural blebs on CT is an indication for early surgical intervention to prevent recurrence. Opponents of this principle argue that management should not be influenced by these findings alone. Although CT is seldom required for routine diagnosis of SP, when subpleural blebs are diagnosed on CT, recurrence rates are high and some will elect early intervention such as bleb resection.

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