The presence of gas within the pleural space, termed a pneumothorax, is always secondary to disruption of the parietal, visceral, or mediastinal pleura. It may occur as a result of trauma (traumatic pneumothorax) or as a consequence of a ruptured pulmonary subpleural bleb (spontaneous pneumothorax). When pleural gas collects under pressure within the pleural space, as a consequence of a one-way flap valve mechanism, a tension pneumothorax is produced.

Primary spontaneous pneumothorax

This is usually found in young, healthy, adult men: 85 per cent of patients are less than 40 years of age and the male:female ratio is 6:1. The disease has an annual incidence of nine cases per 100 000 population.

Pneumothorax is caused by rupture of acquired subpleural blebs; these are usually found in the pulmonary apices, but occasionally occur in the superior segment of the lower lobes. These blebs have no epithelial lining, and possibly arise from rupture of alveolar walls in the area of the bleb. Apical blebs are found in 85 per cent of adults who undergo thoracotomy. Spontaneous pneumothorax is bilateral in 10 per cent of patients. This is potentially life-threatening, though not usually so. No abnormalities are found at thoracotomy in 15 to 20 per cent of patients, but active pulmonary tuberculosis may subsequently develop in 2 to 3 per cent. The frequency of primary spontaneous pneumothorax increases after each episode: the chance of a second episode is 50 per cent, a third 62 per cent, and a fourth 80 per cent. Most recurrences occur within 2 years of the initial episode. Three-quarters of them are ipsilateral.

Spontaneous pneumothorax is secondary to underlying pulmonary disease in 10 to 20 per cent of patients. Chronic obstructive pulmonary disease, usually productive of bullae formed by progressive destruction of alveolar walls, is the most commonly encountered. These patients tend to be older than average, have compromised pulmonary function, and, because of their limited pulmonary reserve, may experience respiratory failure from the pneumothorax.

Other underlying pulmonary diseases that may cause pneumothorax include interstitial pulmonary disease, pulmonary infections, primary and metastatic neoplasms, and pulmonary emboli. Pneumothorax also occurs in Ehler–Danlos syndrome, Marfan's syndrome, and endometriosis.

There is a 50 per cent recurrence rate for secondary spontaneous pneumothorax. Because of the severe underlying pulmonary disease, the disease is associated with a mortality rate of 16 per cent.

Pneumothorax in the neonate may be associated with hyaline membrane disease, renal malformation, Potter's syndrome, and meconium aspiration. It is also present in children with cystic fibrosis.

A spontaneous pneumothorax may occur during menstruation, usually 48 to 72 h after the beginning of menses. The right hemithorax is affected in 90 per cent of patients. The underlying cause of this condition is unknown.

Blunt or penetrating injuries to the chest wall may produce a sucking wound or may cause fractures of the ribs which then lacerate the lung. Penetrating missiles or a knife may also cause such lacerations. Laryngotracheobronchial or oesophageal injury, whether produced by blunt or penetrating trauma can produce mediastinal emphysema, pleural rupture, and pneumothorax.

Pneumothorax is common following pulmonary resection, and is universal for some time after pneumonectomy. It is also frequently present after resection of smaller amounts of pulmonary parenchyma. Placement of an intercostal catheter to vent the pleural space is routine after such resection. Pneumothorax is occasionally seen after thoracocentesis, either as a consequence of air entering the pleural space through the needle or through the catheter used to drain the pleural space, or secondary to penetration of the visceral pleura when the needle is introduced into the pleural space. Mechanical ventilation, particularly with high airway pressures, may rupture pulmonary parenchyma. Placement of central venous lines for monitoring of parenteral nutrition may also produce pneumothorax if their associated needles and guidewires penetrate the pleura.

Rarely, air may be purposely introduced into the pleural space to assess pleural disease or suspected pleural involvement in patients with pulmonary parenchymal disease.

The dominant symptoms of pneumothorax from any cause are acute pleuritic chest pain on the affected side, and dyspnoea due to pulmonary compression. The severity of symptoms is generally proportional to the magnitude of the pneumothorax, although in patients with multiple trauma, associated injuries may dominate the clinical picture. Mental obtundation from any cause may mask the presence and severity of the pneumothorax.

Absence of breath sounds over the affected hemithorax and, in the presence of a tension pneumothorax, shift of the trachea to the contralateral side, are the physical findings that mark the presence of a pneumothorax.

Although a chest radiograph will usually allow the diagnosis to be clearly established, it may not clearly demonstrate the underlying cause of the pneumothorax. CT scanning of the chest, with ‘lung windows’ is extremely useful in the assessment of the pulmonary parenchyma, chest wall, and mediastinum.

The management of pneumothorax is based on observation, both clinically and with regular chest radiographs, thoracocentesis, and introduction of a catheter into the pleural space through the fifth or sixth intercostal space. Blunt penetration of the intercostal space with a Kelly clamp is less likely to injure the lung than insertion of a sharp trochar. The pleural space should be entered on the upper margin of the rib, to avoid injury to the intercostal neurovascular bundle. All holes in the tube must be located within the pleural space: this must be verified by chest radiographs. Thereafter, the tube is placed to water-seal suction drainage, and the patient is observed until absence of an air leak from the pleural cavity and expansion of the lung have occurred.

Patients who have a post-traumatic pneumothorax and in whom a general endotracheal anaesthesia or in whom tracheal intubation is required for the purpose of intermittent positive pressure ventilation should have an intercostal catheter placed within the affected pleural space promptly. In the presence of a ‘sucking’ wound of the chest, one must assume the presence of pulmonary parenchymal injury. Venting of the pleural space with an intercostal catheter must precede temporary closure of the chest wall wound, in preparation for later operative repair of the defect.

Although a spontaneous pneumothorax may be no more than that, signs of a tension pneumothorax (hypotension, shift of the mediastinum, engorged jugular vein) should lead to venting with an intercostal catheter immediately, prior to all diagnostic studies. On the other hand, if the spontaneous pneumothorax is the first such episode, a minimal pneumothorax in an asymptomatic patient may be managed by observation and by assessment with periodic chest radiographs. Moderate pneumothoraces (greater than 20 per cent lung collapse) should be managed by insertion of an intercostal catheter connected to water-seal suction drainage. If there is a minimal air leak, but with complete lung expansion, a one-way flutter valve (Heimlich valve) may facilitate evacuation of intrathoracic air until cessation of the air leak allows removal of the tube.

A suture of an air leak, dermabrasion of the pleural lining, or parietal pleurectomy is indicated in patients with an air leak that persists for more than 10 days, in those in whom an intercostal catheter with water-seal suction drainage fails to expand the lung because of a massive air leak, and usually recurrent spontaneous pneumothorax, or complications, such as haemothorax, empyema, and chronic pneumothorax. Previous contralateral or bilateral simultaneous pneumothorax is best managed with pleurodesis with access through a median sternotomy. If a specific pulmonary disease which is amenable to operative management is responsible for the pneumothorax, this appropriate operation should be undertaken.

Poor risk patients requiring pleurodesis need to have the lung expanded by closed tube thoracostomy, followed by chemical pleurodesis with tetracycline hydrochloride (20 mg/kg in 50 ml of saline solution). Ascorbic acid in the tetracycline preparation is the active agent, not tetracycline itself.

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