Patients who experience thoracic trauma may present with life-threatening injuries such as a pneumothorax, hemothorax, traumatic air embolism, cardiac tamponade, major airway injury, aortic rupture, myocardial rupture, and flail chest (Figure 29-1).^1-7

A pneumothorax occurs from an injury to the chest wall or lung. As the patient inspires, gas enters the pleural space, where it is trapped. When a one-way valve mechanism occurs at the site of injury, intrapleural pressure increases with each respiratory cycle. Eventually, the ipsilateral lung is compressed and displaced to the opposite side causing a tension pneumothorax. In a tension pneumothorax, kinking of the major vessels entering the heart, decreased venous return, and hypotension occur.⁸ A hemothorax also occurs after blunt or penetrating thoracic trauma. The diagnosis is confirmed by placement of a chest tube and drainage of blood from the thoracic cavity. A double-lumen tube can be used for lung isolation to prevent further hypoxia (Figure 29-2).

There is paradoxical motion of the chest wall in patients with a flail chest. After rib injury, free-floating segments of a loose chest wall move in response to pleural pressure instead of the mechanical positions of the rest of the chest wall. Compromised lung mechanics make inspiration difficult and lead to a pulmonary contusion as a loose chest wall collides with underlying lung tissue.

In patients who present with stridor or subcutaneous emphysema, major airway injury should be considered.⁹ There should be a low threshold to intubate patients with suspected injury of the airway. Endotracheal intubation can be difficult when there are changes in the anatomy of the airway. Damage to the bronchial tree can lead to the development of a bronchovenous fistula resulting in a massive air embolus. The presentation of this process may be delayed and unmasked by positive-pressure ventilation.

Almost all patients with an aortic or myocardial rupture die prior to transfer to the intensive care unit (ICU).^3,10

Multiple mechanisms contribute to respiratory failure after a burn injury. Most commonly, toxins contained in smoke injure and inflame the airway. Upper airway edema may completely obstruct the airway, and lower airway edema may close small airways and lead to pneumonia. Patients at risk may have stridor, wheezing, hoarseness, facial burns, or carbonaceous sputum, but these signs are not always present. In many cases, fiberoptic bronchoscopy may be necessary to reveal inhalation injury. If inhalation injury is suspected, the airway should be secured promptly by endotracheal intubation, as the progress of edema is unpredictable and may worsen with fluid resuscitation.

Intubation is considered in trauma patients who present with diminished mental status and the inability to maintain an airway or clear secretions. Patients with a Glasgow Coma Scale (GCS) score ≤ 8 may be intubated to prevent secondary cerebral injury from hypoxemia or hypercapnia.¹¹ Additional indications for tracheal intubation after trauma include cardiopulmonary arrest, elevated intracranial pressure, acute hypoxemia, and transport to a less-monitored situation.

Inadequate analgesia causes splinting and respiratory compromise and may lead to mechanical ventilation of the patient’s lungs. Cautious use of opioid analgesics is advised in patients whose lungs are not mechanically ventilated. Thoracic epidural analgesia with continuous infusion of local anesthesia in the epidural space effectively prevents pulmonary splinting from rib fractures.^12,13 Placement of an epidural catheter is contraindicated in patients who are coagulopathic or suffer from head injury. An anesthesiologist should be consulted to place a thoracic epidural catheter. Repeated intercostal nerve blockade (Figure 29-4) anesthetizes the nerves of the chest wall without sedation. Disadvantages of this technique include the need for repeat injections and the risk of local anesthetic toxicity from intravascular uptake of medications.

The differential diagnosis for respiratory failure 2 days after thoracic injury includes pleural effusion; pulmonary contusion; pneumonia; recurrent pneumothorax from a dislodged thoracostomy tube; splinting with atelectasis; pericardial effusion with tamponade, cardiac contusion, and myocardial stunning; and congestive heart failure in the setting of fluid mobilization after trauma. Her unilateral findings of decreased breath sounds and egophony suggest pulmonary contusion and pneumonia.

Twenty-five percent of patients who suffer from blunt force thoracic trauma are diagnosed with a pulmonary contusion.¹⁴ Contusions develop over 24 to 48 hours, worsen with time, and resolve within 2 weeks. Initial chest radiography may be unremarkable or show unilateral infiltrates from capillary leak and edema (Figure 29-5). Compared with chest radiography, CT scans have a higher sensitivity (Figure 29-6).¹⁵

Complications of pulmonary contusions are common. Pulmonary contusion may progress to parenchymal lung injury or noncardiogenic pulmonary edema (Figure 29-7). Noncardiogenic pulmonary edema results from increased permeability of the alveolar capillary membrane, creating a capillary leak syndrome with exudation of water and protein into the alveolar space. In its most dramatic form, it presents as the acute onset of a massive outpouring of proteinaceous fluid from the endotracheal tube. Noncardiogenic pulmonary edema is distinguished from cardiac failure by the finding of normal or low left atrial or pulmonary artery wedge pressures and a high protein concentration in the edema fluid (albumin concentration ≥ 90% than that of serum albumin).

Pneumonia occurs after airway edema obstructs the airway. Chest radiography may not be diagnostic in the setting of a preexisting opacification from the pulmonary contusion. Prophylactic antibiotics are not recommended in the treatment of pulmonary contusions, but aggressive treatment of pneumonia after presumptive diagnosis is warranted since it is a prime cause of increased morbidity and mortality.