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The abnormal presence of air in the pleural cavity, separating the visceral from the parietal pleura, with subsequent collapse of the adjacent lung, is known as pneumothorax. Traditionally, pneumothorax has been classified as having occurred spontaneously or as a result of trauma. Spontaneous pneumothorax is then further subclassified as having occurred without an apparent cause, in a background of clinically normal lungs (primary spontaneous pneumothorax [PSP]) or having occurred in the setting, and as a consequence of, underlying lung disease (secondary spontaneous pneumothorax [SSP]). Although it is now believed that the majority of PSPs occur in the setting of occult lung disease with underlying anatomical abnormalities such as subpleural blebs, this method of classification is still in common practice.

Traumatic pneumothorax occurs as a result of either blunt or penetrating trauma to the chest with a subsequent disruption of the structural integrity of the lung, chest wall, esophagus, trachea, or bronchi. Iatrogenic pneumothorax is a subtype of traumatic pneumothorax resulting as a consequence of diagnostic or therapeutic procedures such as central-line insertions, thoracentesis, or mechanical ventilation.


As alluded to above, air does not normally exist within the pleural space. The pressure within the pleural space is negative with respect to the alveolar pressure during the entire respiratory cycle. Despite this, air does not enter the pleural space from the alveoli. The reason for this lies in the fact that the partial pressure of all gases in the venous blood averages only 706 mm Hg, thereby driving the net movement of alveolar air (760 mm Hg at sea level during end-inspiration) into the capillaries and not into the pleural space, which would require a pleural pressure lower than 706 mm Hg to pull the air in. Under normal circumstances, most individuals do not generate a net negative inspiratory force of −54 mm Hg.1

The negative pressure in the pleural space results from the inherent tendency for the lung to collapse (elastic recoil) and of the chest wall to expand. The negative intrapleural pressure is not uniform throughout the pleural space; 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. At the apex, the pressure is more negative than at the base, and this pressure difference tends to favor a greater distention of the alveoli located in this region.

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.1 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 ...

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