Tension pneumothorax is a clinical diagnosis that should be considered in any patient with shock and respiratory distress. Treatment should not be delayed for radiologic confirmation.
Appropriate treatment of a tension pneumothorax is a needle thoracostomy, followed by tube thoracostomy.
Unless a pneumothorax is spontaneous, small (<20%), minimally symptomatic, and primary, definitive treatment is tube thoracostomy.
Pneumothorax is an accumulation of air within the pleural space. Spontaneous pneumothorax is acquired in the absence of trauma. A primary spontaneous pneumothorax is found in patients without underlying pulmonary pathology. A secondary spontaneous pneumothorax is found in patients with underlying lung disease and damage to the alveolar-pleural barrier (most commonly seen with chronic obstructive pulmonary disease [COPD] or asthma).
Spontaneous primary pneumothoraces have the greatest incidence of occurrence in young adults. They are more common in males than females (6:1), greater height-weight ratios, and smokers. Smoking is the most important modifiable risk factor, with a lifetime risk of 12% compared with 0.1% in nonsmokers. Spontaneous secondary pneumothoraces are most common in patients older than 40 years with COPD. Recurrence rates range from 30–45%.
The parietal pleura lines the thoracic cavity and closely adheres to the visceral pleura, which surrounds the lungs. The potential area between these 2 layers is known as the pleural space. If air accumulates within this potential space, the pressure causes the thoracic cavity to expand and the lung to collapse, creating a pneumothorax. Secondary spontaneous pneumothoraces are the result of a damaged alveolar-pleural barrier or underlying lung problems that cause an increase in intrabronchial pressures. Tension pneumothoraces occur when air enters the pleural space on inspiration but cannot escape on expiration (known as ball-valve effect). There is progressive accumulation of air in the pleural space, resulting in collapse of the affected lung and shift of the mediastinal structures to the opposite side. This ultimately causes compression of the contralateral lung, impairment of venous return, decreased cardiac output, and signs of cardiovascular collapse requiring immediate intervention with a needle thoracostomy.
Symptoms can vary, but are predicated on the pneumothorax size, rate of formation, and cardiorespiratory reserve. A typical history includes a sudden onset of ipsilateral pleuritic chest pain and/or dyspnea with a nonproductive cough. Patients, however, range from clinically silent to agitated, restless, altered mental status, and/or cardiac arrest if severe respiratory compromise is present.
The physical examination can range from unremarkable to a patient in shock. Vital signs typically include a mild tachycardia and tachypnea, although only 5% of patients have a respiratory rate greater than 24. Findings on the lung examination may be subtle if there is a small pneumothorax. Decreased breath sounds occur in 85%, whereas hyperresonance to percussion occurs in less than 33%. Patients with tension pneumothorax present in extremis with hypotension, cyanosis, severe respiratory distress, and tracheal deviation to the contralateral side.
