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The abnormal presence of air in the pleural cavity, separating the visceral from the parietal pleura, is known as pneumothorax. Tra­ditionally, pneumothorax has been classified as having occurred spontaneously or as a result of trauma. Spontaneous pneumothorax can occur in a background of clinically normal lungs (primary spontaneous pneumothorax [PSP]) or in the setting of underlying lung disease (secondary spontaneous pneumothorax [SSP]). Since underlying anatomic lung abnormalities (subpleural blebs) are often identified in PSP,1–3 it is now believed that the majority of PSPs occur in the setting of occult lung disease. Nevertheless, this method of classification is still common in practice.

Traumatic pneumothorax results from a disruption of the structural integrity of the lung, chest wall, esophagus, trachea, or bronchi secondary to either blunt or penetrating trauma to the chest. It can also occur as a consequence of diagnostic or therapeutic procedures such as central-line insertions, thoracentesis, or mechanical ventilation, in which case it is referred to as iatrogenic pneumothorax.


As noted above, air does not normally exist within the pleural space. During both inspiration and expiration, the pressure within the pleural space is negative with respect to the alveolar pressure. This pressure gradient is called transpulmonary pressure, which results from the tendency of the lung to collapse (elastic recoil) and of the chest wall to expand. This negative pressure is not uniform throughout the pleural space, causing a greater distention of the alveoli at the apex of the lung secondary to higher negative pressure (Fig. 79-1). A gradient of 0.25 cm of water per centimeter of vertical distance can be measured between the apex and the base of the lung. The pleural pressure is also negative compared with the atmospheric pressure (760 mm Hg at sea level during end inspiration); nevertheless, the pressure gradient still favors net movement of alveolar air into the capillaries (average pressure of all gases in capillaries is 706 mm Hg) and not into the pleural space. Under normal circumstances, most individuals do not generate a net negative inspiratory force of −54 mm Hg.4

Figure 79-1

Transpulmonary pressure changes related to lung zone.

The presence of air in the pleural cavity is thought to occur by one of three events: a communication between the pleura and the alveolus, a communication between the atmosphere and the pleural space, or the presence of a gas-producing organism within the pleura.4 When a communication develops between an alveolus and the pleural space, air will move from the alveolus into the pleural space until there is equalization of pressure or until the communication is sealed. The same happens with a communication between the chest wall and the pleural cavity. The greater the amount of air that enters the pleural cavity, the more the lung collapses. ...

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