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Diagnosis: Spontaneous Pneumothorax

Wiler, Jennifer L. MD, MBA

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Emergency Medicine News: May 2008 - Volume 30 - Issue 5 - p 14
doi: 10.1097/01.EEM.0000319591.77170.89

    A pneumothorax occurs when air collects between the chest wall (pleural space) and lung, with resulting lung collapse on the affected side. It is often the result of trauma or lung disease, but can occur spontaneously. Approximately 8,600 individuals develop primary spontaneous pneumothorax (SP) in the United States per year. The incidence is substantially higher in men than women (6:1), with the peak age of onset being the early 20s and rare after 40. One to two percent of neonates can develop pneumothoraces, but those tend to be secondary to meconium aspiration, infection, or positive pressure ventilation.

    Risk factors for SP include chronic obstructive pulmonary disease, subpleural blebs, smoking, Marfan syndrome, α1-antitrypsin deficiency, homocystinuria, thoracic endometriosis, cystic fibrosis, pyogenic infections, pulmonary fibrosis, pulmonary tuberculosis, cancer, positive pressure ventilation, and family history of SP. (Curr Opin Pulm Med 2006;12[4]:268.) Radiographic and thoracoscopic examinations of patients with primary SP often reveal subtle underlying lung abnormalities including blebs, bullae, and cysts. (N Engl J Med 2000;342:868.)

    The risk of SP is related to the amount and duration of cigarette smoking. (Chest 1987;92[6]:1009.) The relative risk of pneumothorax is seven times higher in light smokers (1–12 cigarettes/day), 21 times higher in moderate smokers (13–22 cigarettes/day), and more than 80 times higher in heavy smokers (>22 cigarettes/day).(Chest 1987;92:1009.)

    Primary SP usually occurs when the patient is at rest (Eur J Respir Dis 1987;71[3]:181), and has been noted to occur in patients with a body habitus taller and thinner than the average person. (Am J Surg 1964;108:772.) Patients typically complain of acute onset pleuritic chest pain and dyspnea, with the intensity of symptoms depending on the volume of lung collapse. They may appear anxious or fatigued. On physical examination, the patient may be tachycardic, tachypnic, or hypoxemic, and appear in respiratory distress or have mental status changes. On the affected side, patients may have hyperressonant percussion, decreased breath sounds, and decreased chest excursion. Subcutaneous emphysema may be appreciated on the overlying chest wall or tracking into the neck.

    Tension pneumothoraces complicate approximately one to two percent of idiopathic spontaneous pneumothorax cases. Patients with tension pneumothorax can present with hemodynamic instablity, tracheal deviation, jugular venous distention, and significant hypoxia.

    Chest x-ray is the gold standard for making the diagnosis radiographically. Inspiratory and expiratory films have not been shown to be superior to standard inspiratory views. (Am J Roentgenol 1996;166[2]:313.) Radiographic findings include visualizing the ipsilateral lung margin as a radiolucent line that parallels the chest wall and a deep sulcus sign (lucency of the lateral costophrenic angle extending toward the hypochondrium). The abnormally deepened lateral costophrenic angle may have a sharp, angular appearance. (Radiology 2003;228:415.) Air typically tracks to nondependent areas of the chest cavity, if not trapped by loculations. A pneumothorax is typically best appreciated at the lung apex in upright films. Approximately 2.5 cm from the chest wall edge to the collapsed lung margin correlates with a 30 percent lung collapse. Computerized tomography is more sensitve than chest radiography, and can be helpful in identifying small pneumothoraces and underlying lung disease. Transillumination with increased light transmission on the affected side may be helpful for diagnosis in neonates.

    The treatment options for an SP depend on the patient's clinical condition, the amount of lung collapsed, and the patient's history of previous SP. Any patients with concern for or verification of a tension pneumothorax require emergent needle decompression on the affected side with a large bore angiocath. All patients should receive supplemental oxygen, preferably by high-flow face mask. Clinically stable patients with a small pneumothorax (<3cm from lung to chest wall) should do well with supplemental oxygen and at least six hours of observation. After that time, if a repeat chest radiograph demonstrates resolution of the pneumothorax, the patient can be safely discharged home.


    Without supplemental oxygen, the rate of lung expansion is approximately 1.25 percent per 24 hours. This improves substantially (sixfold) if humidified 100 percent oxygen is administered. (Pediatrics 1963;32:816.) Patients with a large pneumothorax can be treated with simple aspiration or intercostal thoracostomy tube. Pleurodesis via thoracostomy tube should be considered nonemergently for patients with recurrent SP. This is obviously not performed in the ED. Patients in whom a thoracostomy tube is placed should have a specialist consultation.

    A recent Cochrane review concluded that “there is no significant difference between simple aspiration and intercostal tube drainage with regard to immediate success rate, early failure rate, duration of hospitalization, one-year success rate, and number of patients requiring pleurodesis at one year. Simple aspiration is associated with a reduction in the percent of patients hospitalized when compared with intercostal tube drainage.” (Cochrane Database of Systematic Reviews 2008; Issue 1.) The risk of a recurrent SP is as high as 50 percent, and typically occurs within the first year. (Thorax 1997;52[9]:805.) Prognosis depends on the underlying etiology, but is generally good for simple SP. Complications, however, can include pneumomediastinum, pneumopericardium, pneumoperitoneum, hemopneumothorax, pulmonary edema, empyema, bronchopulmonary fistula, and cardiorespiratory arrest.

    This patient had a thoracostomy tube placed in the ED. During hospitalization, his pneumothorax resolved, but he was incidentally found to have advanced pancreatic cancer.

    © 2008 Lippincott Williams & Wilkins, Inc.