Pneumothorax is a collection of air within the pleural space; after trauma, pneumothorax is most commonly caused by a rib fracture tearing the visceral pleura of the lung, allowing air to escape during inspiration. Penetrating injuries (e.g., stab wounds, gunshot wounds) also frequently produce a pneumothorax via this mechanism. In these cases of penetrating trauma, 80% of patients will also have blood in the pleural space. Pneumothorax is usually identiﬁed on chest radiographs, although it may also be seen during chest or abdominal computed tomography scanning or during ultrasound examination of the abdomen after trauma (focal assessment with sonography for trauma [FAST] examination).
Other causes of traumatic pneumothorax include inadvertant puncture of the lung during central venous access or thoracentesis. The lung can also be ruptured by excessive positive airway pressure during mechanical ventilation, termed barotrauma. Spontaneous pneumo- thorax is usually caused by a ruptured bleb that is often precipitated by coughing. Irrespective of the cause, when the pleural pressure exceeds the normal subatmospheric pressure, the elastic recoil of the lung results in partial collapse. If air continues to ﬂow into the pleural space, the lung collapses entirely and can no longer serve to exchange oxygen (O2) and carbon dioxide (CO2). A one-way valve typically occurs on the lung surface, and air is forced into the pleural space with each breath, which progressively increases the intrapleural pressure and may result in escape of air into the subcutaneous tissues, manifesting as diffuse upper torso swelling and palpable crepitus. Ultimately, if the intrapleural pressure continues to increase, a tension pneumothorax develops. This condition may occur rapidly when the patient is ventilated mechanically, increasing the airway pressure. Eventually, the pressure within the pleural cavity can shift the mediastinum and impede blood return to the right heart. Thus, clinical manifestations of tension pneumothorax reﬂect progressive impairment of pulmonary and myocardial function.
Patients with a tension pneumothorax become dyspneic or hypoxic if ventilated mechanically, with cyanosis and distended neck veins. Hyperresonance and lack of breath sounds on the involved side of the thorax cement the diagnosis without the need for radiographic conﬁrmation. Electrocardiographic changes include (1) rightward shift in the QRS axis, (2) diminution in the QRS amplitude, and (3) inversion of precordial T waves. Tension pneumothorax is a life-threatening emergency, and the air must be urgently released from the pleural cavity. If it is clinically suspected in a patient who is unstable, immediate treatment is indicated without any further diagnostic tests. In an intubated patient in the prehospital setting, air can be vented with a large-bore needle via the anterior second intercostal space in the midclavicular line. Subsequent deﬁnitive treatment with tube thoracostomy should follow. In the hospital, a tube thoracostomy is usually done via the ﬁfth intercostal space at the anterior axillary line. Under these dire circumstances, the tube should be placed expeditiously using primarily a scalpel and scissors. After a limited chest wall preparation and local anesthesia, a 2-cm incision should be made into the intercostal space and the chest entered directly using heavy scissors. The tube should then be directed into the posterior sulcus to optimize subsequent drainage of blood or other pleural ﬂuid.
Alternatively, air can accumulate within the pleural space because of an external wound that violates the parietal pleural, exposing it to the atmosphere. This form of pneumothorax is usually self-limited because the skin edges and adjacent chest wall soft tissue seal the opening. The notable exception is open chest wounds, in which the chest wall defect is sufﬁciently large to remain open, permitting air to move freely in both directions. Open pneumothoraces are usually caused by high-energy gunshot wounds (e.g., close-range shotgun wounds) or impalement during motor vehicle crashes. An open pneumothorax is often referred to as a sucking chest wound because of the sound made as a relatively large volume of air moves through the defect with respiratory effort. The lung on the involved side collapses upon exposure to atmospheric pressure, rendering it nonfunctional. Additionally, because air passes more easily into the chest on inspiration than it exits during expiration, an element of tension pneumothorax with mediastinal shift occurs. Ultimately, this impedes blood return to the heart, leading to clinical signs of cardiac as well as pulmonary dysfunction.
Prehospital management of an open pneumothorax is a partially occlusive dressing in which one corner of the bandage is free to permit escape of pleural air under pressure. In the hospital, treatment consists of applying a completely occlusive dressing, usually of petroleum gauze, followed by standard tube thoracostomy. Although a slash wound may occasionally be managed deﬁnitively in the emergency department, most patients with an open pneumothorax warrant prompt operative care for associated visceral injury as well as chest wall reconstruction. One approach to extension chest wall defects is cephalad transposition of the diaphragm.