Pneumothorax

Henri G. Colt

The pleural space is located between the visceral pleura surrounding the lung and the parietal pleura lining the inside of the rib cage and is occupied by a small amount of lubricating pleural fluid. Pleural pressure is negative compared with atmospheric pressure, which helps maintain lung inflation. If the parietal or visceral pleura is breached and the pleural space is exposed to atmospheric (positive) pressure, air enters the pleural space (i.e., pneumothorax occurs), and the lung collapses inward toward the mediastinum. Any condition that impairs the structural integrity of either pleural membrane can produce a pneumothorax. This entity presents a true healthcare problem, affecting more than 20,000 individuals each year in the United States and costing more than $130 million in healthcare expenditures. The prognosis and management depend on the underlying cause. Pneumothorax is often categorized as (1) idiopathic or spontaneous, (2) iatrogenic, or (3) traumatic. Within each category, pneumothoraces can be either uncomplicated (usually unaccompanied by symptoms or prolonged air leak) or complicated (accompanied by symptoms, radiographic evidence of mediastinal shift, bleeding, or prolonged air leak). Pneumothorax can also be categorized as “primary” (no underlying lung disease, estimated to occur in 18 to 28 per 100,000 men each year in Great Britain), and “secondary” (presence of underlying lung disease). Primary spontaneous pneumothorax has an estimated yearly incidence of 6 per 100,000 in men and 2 per 100,000 in women. It rarely produces a prolonged air leak. Secondary spontaneous pneumothorax, on the other hand, especially in patients with chronic obstructive pulmonary disease (COPD) occurs in approximately 26 per 100,000 persons per year. Extrapolated to the entire population, this results in about 4,500 cases each year in the United States. At least 20% of these patients will have prolonged air leaks encompassing greater risk of increased morbidity, prolonged hospital stays, and increased used of healthcare resources.

In regard to anatomic abnormalities and other possible risk factors for pneumothorax, smoking has been identified as being associated with a 12% increased risk as compared to 0.1% risk for nonsmoking healthy men. Patients with spontaneous pneumothorax also tend to be taller, suggesting that greater distending pressures at the apex of the lung as compared to the base of the lung might be a contributing factor, especially for the development of apical blebs. Indeed, subapical blebs and bullae have been noticed during thoracoscopy and by computed tomography (CT) in a majority of patients with primary spontaneous pneumothorax, although no significant correlation has been found between existence of these abnormalities and the need to remove them by stapler resection to prevent recurrence. Pleural porosities invisible to white light but detectable on autofluorescent examination, as well as inflammation-mediated small airways obstruction with emphysema-like changes are also suggested etiologic mechanisms. Overall, the risk of recurrence after a primary spontaneous pneumothorax is about 50%. The absence of recurrence in about 50%, and the absence of a firm cause and effect relationship between unruptured blebs or bullae noted on CT scan, makes treatment decisions problematic. Risks for recurrence is increased in the presence of underlying disease such as COPD and pulmonary fibrosis, and age greater than 60 years, but contrary to what was once believed, physical activity has not been identified as a risk factor.

Spontaneous (idiopathic) pneumothorax (SP) occurs in patients without a history of any event known to cause pneumothorax (e.g., trauma or intervention). It generally occurs unexpectedly in an apparently healthy individual. Patients usually have no evidence of bullous lung disease on radiographic, thoracoscopic, or open surgical examination. Spontaneous pneumothoraces should be categorized as secondary, however, when abnormal lung parenchyma is noted, either from underlying lung disease or by identifying bulla or blebs during radiographic or direct examination.

At least two different mechanisms can lead to spontaneous pneumothorax. One is a visceral pleural tear (i.e., a bronchopleural fistula) caused by rupture of a subpleural bleb or bulla or by a parenchymal process that erodes through the visceral pleura (e.g., necrotizing pneumonia). Blebs are found in up to 90% of patients with presumed primary pneumothorax. Another mechanism is partial bronchial obstruction that acts as a check valve. Subsequent progressive hyperinflation of distal air spaces occurs until air eventually dissects along bronchovascular spaces into the hilus and mediastinum, leading to pneumomediastinum. From there, air can also dissect through fascial planes in the neck, resulting in subcutaneous emphysema, or through visceral pleura into one (usually the right) or both pleural cavities, resulting in pneumothorax.

In a young, otherwise healthy individual without radiographic evidence of lung disease, SP usually results from the rupture of subpleural apical blebs or bullae. The peak incidence is between the ages of 20 and 30 with a 4:1 male predominance, and as mentioned previously, with a predilection for tall, thin individuals. The incidence of SP has been reported to be increased in cigarette smokers, but this remains controversial. Interestingly, most patients who smoke continue to do so after a first episode of pneumothorax, even though the recurrence rate is more than 50% during the first 4 years after a first episode.

In most cases, symptoms develop at rest; however, onset can be associated with strenuous activity in up to 20% of cases and with a forceful cough or sneeze in at least 5%. Spontaneous pneumothorax should always convey a high index of suspicion for the presence of intrinsic lung disease, particularly if pneumomediastinum also is present. Among the lung conditions often associated with pneumothorax are emphysema (particularly bullous emphysema), diffuse interstitial processes (e.g., eosinophilic granuloma, sarcoidosis, usual interstitial pneumonia, desquamative interstitial pneumonia, and the pneumoconioses), necrotizing pneumonias (including tuberculosis), endometriosis (catamenial pneumothorax in women during menses), and acquired immune deficiency syndrome (related to malnutrition or Pneumocystis carinii pneumonia and associated with prolonged air leaks and decreased survival).

Iatrogenic pneumothorax most commonly occurs after invasive thoracic procedures, such as thoracentesis, transbronchial lung biopsy, and subclavian vein catheterization; however, it also can complicate virtually any invasive procedure involving the neck or abdomen (e.g., liver biopsy, transtracheal aspiration, intercostal nerve block, and even acupuncture). A very infrequent cause may be tracheotomy, where iatrogenic tracheal laceration should be suspected in the presence of otherwise unexplained pneumothorax, pneumomediastinum, or even pneumoperitoneum. Iatrogenic pneumothorax can complicate positive pressure ventilation and, in this setting, can be life threatening. The mechanism is usually a combination of partial bronchial obstruction caused by edema, secretions, and check-valve air entry leading to progressive alveolar expansion and rupture.

Traumatic pneumothorax can occur in the setting of penetrating or nonpenetrating chest trauma. The former generally presents no diagnostic problem; however, the latter should prompt a careful search for rib fracture, bronchial rupture, and esophageal injury. Rib fractures are associated with tears of the visceral pleura and pneumothorax; bronchial rupture is associated with deceleration injury; and esophageal rupture is often associated with mediastinal air entry. Pneumothorax can also result from abdominal trauma (e.g., abdominal stab wound, bullet wound) and diaphragmatic tears.

The clinical manifestations of pneumothorax depend on its size, the clinical context in which it occurs, and the mechanism(s) involved. Chest pain and dyspnea are common presenting symptoms. The pain is usually of sudden onset and initially pleuritic in character. After a few hours, it often changes to a dull ache, and spontaneous resolution of the pain can occur within 2 to 3 days. At least 10% of patients do not experience pain. Dyspnea occurs in 80%, often with spontaneous resolution within 24 hours despite persistence of the pneumothorax. Prominent coughing occurs in 10%; occasionally, it is the major or only symptom. Less than 5% of patients are asymptomatic. Symptoms can be transient and do not always correlate well with the radiographic size of the pneumothorax.

The most common physical findings are tachypnea, splinting, and decreased inspiratory expansion of the involved hemithorax, a tympanitic percussion note, decreased fremitus, and decreased breath sounds on the involved side. In patients with a check-valve mechanism, the initial complaint of substernal pressure or discomfort is often interpreted as cardiac in origin. Subsequently, the patient can experience chest pain, dyspnea, and relief of the substernal symptoms if pneumothorax or decompression into cervical subcutaneous tissues occurs. Mediastinal emphysema can be detected on auscultation by the presence of a mediastinal crunch (Hamman sign) coincident with cardiac systole and diastole. Similarly, subcutaneous emphysema may be noted on palpation of the anterior chest, axilla, shoulders, and neck. Subcutaneous infiltration of air may not always be readily visible, but can often be felt. Dyspnea can be exaggerated and persistent when underlying lung disease is present. In severely traumatized or mechanically ventilated patients, symptoms and signs can be obscured or difficult to interpret. This also is the case in patients with emphysema who have severe hyperinflation and diminished breath sounds. An electrocardiogram may show nonspecific ST–T wave changes and axis shifts, suggesting myocardial or thromboembolic disease.

Only gold members can continue reading. Log In or Register to continue