Flail Chest and Pulmonary Contusion

 Flail chest refers to the mechanically unstable thorax that is due to blunt trauma, most frequently from motor vehicle collision and severe falls. Instability and paradoxical thoracic movement are enhanced by double fractures of multiple ribs, often cited as three or more in sequence. However, the pulmonary problems of flail chest do not occur in isolation, and physiologic circumstances are often worsened by pulmonary contusion and other intrathoracic injuries. Thus, in addition to the risk of respiratory failure due to ineffective ventilation (hypercarbic), the patient may have an increased alveolar-arterial gradient progressing to hypoxemic respiratory failure. Recognition is based on the history and radiographic evidence of thoracic trauma; paradoxical movement (in with inspiration, out with expiration), which may be subtle and overlooked; increasing respiratory distress; and worsening gas exchange. Treatment should be conservative in most cases. Pain control is important; systemic narcotics may have deleterious respiratory effects and can be minimized with the use of intercostal nerve blocks and epidural morphine. The evidence supporting surgical fixation of the flail segment is scant, as is the evidence for prophylactic positive pressure ventilation by ETT (and there is no demonstrable reduction in mortality). Oxygen is administered for hypoxemia. Overt respiratory failure is treated with mechanical ventilation. In some centers, noninvasive positive pressure ventilation by nasal or full-face mask is used to reduce work of breathing when physical signs point to impending respiratory failure, but evidence to support this approach is largely lacking.

Pulmonary contusion may complicate flail chest or it may occur in isolation. It occurs in a significantly large minority of patients with severe blunt trauma to the chest. Chest x-ray (CXR) and CT show alveolar infiltrate, which is generally confluent and does not respect lobar boundaries. Appearance of radiographic abnormalities may be delayed for hours. The gas-exchange abnormalities are those of hypoxemia owing to V/Q mismatch, sometimes reaching the severity of true shunt. Treatment is supportive. Oxygen is administered, fluid is given judiciously to avoid increased alveolar edema, and narcotics are administered to reduce splinting. Good-lung-down positioning may improve oxygenation. In a minority, positive pressure ventilation is required, which may be noninvasive ventilation in mild cases and endotracheal ventilation in the more severely affected, with positive end-expiratory pressure.