Pleural Disease

Foundations

Anatomy and Physiology

Anatomically, the visceral and parietal pleura lie in close approximation with only potential space between them. Normally, the intrapleural pressure remains negative during inspiration, meaning that it is slightly less than atmospheric pressure. The alveolar walls and visceral pleura form a barrier that separates the intrapleural and intraalveolar space and maintains the transpulmonary pressure gradient. When this barrier is disrupted, air enters the pleural space until either the pleural defect is sealed or until the intraalveolar and the intrapleural pressures equalize. In primary spontaneous pneumothorax, the alveolar-pleural barrier is disrupted when a subpleural bleb or bulla ruptures into the pleura space. Blebs are small subpleural thin-walled air-containing pockets that can easily rupture. Increased intrabronchial pressures and intraalveolar pressures generated by bronchospasm and intrinsic positive end expiratory pressure (PEEP) can play a role in the rupture of these blebs. In secondary spontaneous pneumothorax, underlying lung disease and chronic inflammation can also weaken the alveolar-pleural barrier and lead to rupture of blebs.

When negative intrapleural pressure is lost, the ipsilateral lung collapses. A large pneumothorax can result in a restrictive ventilation impairment with reduced vital capacity, functional residual capacity, and total lung capacity. Shunting of blood through poorly ventilated atelectatic lung tissue may lead to acute hypoxemia, but this effect is a late finding because it is mitigated by compensatory hypoxic vasoconstriction in the collapsed lung.

In tension pneumothorax, the alveolar-pleural defect acts as a one-way valve, allowing air to pass into the intrapleural space during inspiration and trapping the air in the pleural space during expiration ( Fig. 63.1 ). This leads to progressive accumulation of intrapleural air and increasing intrapleural pressure, causing mediastinal shift and compression of the mediastinal venous structures and the contralateral lung. This leads to worsening hypoxemia and can impair venous return to the heart. Untreated, tension pneumothorax progresses to cardiovascular collapse and death.

Clinical Features

Symptoms of primary spontaneous pneumothorax are similar in adults and children. Symptoms often begin suddenly with ipsilateral pleuritic chest pain and dyspnea. Over time, the pain may evolve to a dull steady ache. Although dyspnea is common, it may not be severe in the absence of underlying lung disease or tension pneumothorax. Symptoms are often mild, and patients may wait several days before seeking medical attention. Without treatment, symptoms may spontaneously resolve within 24 to 72 hours, even though the pneumothorax may still be present.

Physical exam findings often correlate with the degree of symptoms. Sinus tachycardia is the most common early physical exam finding. With a large pneumothorax, hypoxia and decreased breath sounds with hyperresonance to percussion may be present. In children, breath sounds are distributed throughout the thorax, which makes unilateral breath sounds more challenging to identify. Other classic physical exam findings include unilateral hemithorax enlargement, unequal chest wall movement with exhalation, absent tactile fremitus, and inferior displacement of the liver or spleen (on the affected side). Absence of these findings does not exclude pneumothorax, and imaging should be obtained when pneumothorax is suspected. In children, routine chest radiography is not recommended in all cases of chest pain, but it should be performed if history or physical examination findings suggest that pneumothorax may be present.

Symptoms of tension pneumothorax include hypoxia, increased work of breathing, and tachycardia. Hypotension is a late finding. Distention of the jugular veins is common but may be difficult to detect. Displacement of the trachea is also a classically described sign but is usually a late finding. Absence of tracheal deviation does not rule out tension. Complete cardiovascular collapse, including cardiac arrest, may occur in tension pneumothorax if intervention is delayed.

In secondary spontaneous pneumothorax, the severity of signs and symptoms are related to both the size of the pneumothorax and the degree of underlying lung disease. Because of poor pulmonary reserve, dyspnea is nearly universal, even in the setting of a small pneumothorax. Symptoms are unlikely to resolve on their own. Physical exam findings such as hyperexpansion and distant breath sounds often overlap considerably with the findings of underlying lung disease, which makes clinical diagnosis difficult. The diagnosis of pneumothorax should be considered whenever a patient with COPD or other significant underlying lung disease has increasing dyspnea, and for this reason chest radiography is recommended in all patients with exacerbations of chronic lung disease.