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Pulmonary contusion and flail chest are the two most common anatomic complications of major blunt chest trauma. Each will directly alter pulmonary physiology in a specific and unique fashion, and thus contribute to pulmonary dysfunction and failure after trauma. Pulmonary contusion was probably first described by Morgagni in the 18th century, but Laurent’s description in the Lancet in 18831 appears to be the first to recognize the possibility that plasticity of the chest wall, most notably in the young, can allow injury to the underlying lungs without disruption of the bony thorax. Conversely, flail chest is predominantly a disease of the elderly, with most patients being in the sixth decade of life and beyond and older patients having the worst outcomes.24 Pulmonary contusion and flail chest commonly coexist but their degree of association changes and they may exist entirely separately under specific circumstances in specific patient groups. Yet because of their close association, their effects on pulmonary pathophysiology are often confused. Such confusion can lead to misapplication of studies aimed at one entity or the other and eventually to inappropriate treatment.


Pulmonary hemorrhage and contusion were noted to be common at autopsy of patients dying from battlefield and blast injuries during World War I.5,6 Similar findings were noted in World War II,7,8 and the term “pulmonary concussion” appears to have been coined by Hadfield describing civilian injuries from bomb blasts sustained during the Battle of Britain.9 Reports in the 1960s first noted that pulmonary contusions occurred frequently after civilian motor vehicular trauma and were seen in up to 10% of thoracic injuries.10

Currently, the incidence of “pulmonary contusion” varies markedly depending on how aggressively it is sought and diagnosed. In some large series, about 15% of major blunt injuries11 are found to have a pulmonary contusion. Using closer computed tomography (CT) evaluation, up to 25% of patients with chest trauma may be noted to have some form of contusion.12 Yet a 10-year registry review of approximately 20,000 blunt trauma patients seen at the New Jersey State Trauma Center in Newark performed in preparation for this review showed that only 2.6% of all patients arriving at our Level I trauma center were diagnosed as having a pulmonary contusion.

So the “denominator” patient population examined will clearly affect the disease incidence reported in administrative databases, as will the tendency to identify and report less severe injuries. Yet our experience over the last several years indeed shows that the diagnosis of pulmonary contusion is increasing alongside our increased use of CT diagnosis for chest trauma (Figure 1).

The extent to which these previously subclinical injuries will turn out to predispose patients to complications remains to be seen, but these considerations suggest that future scaling systems for thoracic trauma will need to take into account the fact that modern imaging may find contusions that are either physiologically insignificant or that may “prime” the lung for secondary injury rather than lead to immediate dysfunction.

The relative frequency of flail chest as compared with pulmonary contusion will also vary depending upon the denominator population. Pediatric reviews find that the majority of major thoracic trauma presents with pulmonary contusions whereas flail chest is very rare, even where multiple fractures exist.13,14 In contrast, in a large contemporary descriptive series examining adult blunt chest trauma, flail chest was diagnosed in about half of all patients with significant pulmonary contusions.11 Moreover, the diagnosis of flail chest is often missed or delayed in sicker patients that require mechanical ventilation.4 This results from the synchronous expansion of the lungs and “splinting” of the chest wall by positive intrathoracic pressure. Thus, it is clear that the proportions change and flail chest becomes increasingly common with advancing age and brittleness of the thoracic cage. Consequently, the frail elderly frequently sustain a flail chest with relatively minor chest trauma and little or no pulmonary contusion. Similarly, flail chest has been reported in newborns with osteogenesis imperfecta.15

Physical Mechanisms of Injury

The overwhelming majority of significant blunt chest trauma in civilian life occurs as a result of motor vehicle crashes and motor vehicle versus pedestrian injuries. Falls are another common cause of pulmonary contusion and flail chest. Thoracic compression injuries are not as common as vehicular trauma and falls, and although they may produce similar syndromes, the slower speed of impact makes contusion less likely than flail chest. Rather, these patients may manifest traumatic asphyxia. In military practice, blast injuries from high explosives can occur both in air and underwater. These produce specific and recognizable diffuse contusion patterns resulting from the concentration of energy at interfaces between denser tissues and tissues that contain gas, like the lung and bowel. Although these injuries have been rare in civilian life for the last 60 years, the advent of international terrorism as a mode of political action within the last 10 years has led to a resurgence of such injuries in civilian life—first in the Middle East, and now in the West.16

All blunt injuries result from the physical transfer of energy to the patient, but because of the rigidity of the bony thorax, all pulmonary contusions and most flail chest injuries are high-energy injuries, with the primary exception being occasional chest wall injuries in the frail elderly. Thus, they are seen primarily in motor vehicular trauma, perhaps most classically where unrestrained drivers strike the steering column. Pedestrian trauma and falls from a distance are frequent causes. Interpersonal violence leading to blows with blunt objects or kicking are occasional causes of pulmonary contusion. Flail chest however, is rare in our experience, first because assaults are most common in young adults and second because biomechanically they are unlikely to result in segmental injuries of multiple contiguous ribs. The physician should also bear in mind that rib fractures in infants and small children occur most commonly as a result of child abuse, and that any rib fracture in a child is a marker for severe trauma.17

The transfer of energy typically leads directly to hemorrhage into the lung. Pulmonary lacerations are uncommon but can occur (Figure 2) and in our experience are seen with increasing frequency when routine CT imaging is used. On rare occasions, tangential gunshot injuries will cause contusions of the underlying pulmonary parenchyma without actually entering and lacerating the lung. These injuries are usually very limited in their extent and cause little or no physiologic effects. Another potential mechanism of pulmonary dysfunction after trauma is the activation of pulmonary vascular endothelium by percussive cellular deformation per se. This phenomenon is much better documented in cerebrovascular endothelial beds,18,19 but it is likely to exist in the pulmonary bed as well (see Figure 2).

Mechanisms of Physiologic Injury

Studies done toward the end of World War I suggested that blast injury predominantly resulted in pulmonary hemorrhage,5 and it was felt that pulmonary failure reflected the effects of blood filling the air spaces. Whereas this effect undoubtedly contributes to the increased pulmonary shunting (Qs/Qt) seen after injury, many other pathophysiologic processes are at work. There is now little doubt that the majority of pulmonary dysfunction seen after chest trauma results from secondary injury processes rather than direct injury to the lung. It is most convenient to divide the various pathophysiologic influences on pulmonary function into those that result in increased Qs/Qt and hypoxemia, and those that alter the work of breathing and can lead to ventilatory failure. Either can result from chest wall or parenchymal pathology. It is important to note that associated intrapleural collections of air and blood may also impact mechanical chest wall function and pulmonary aeration as well as systemic hemodynamic performance, although these considerations are outside the scope of this review.

Shunting and Hypoxemia

Systemic shock and ischemia/reperfusion (I/R) are well-known activators of immune system attacks on the lung, causing shunting and hypoxia. This is perhaps most clearly evident in lung transplantation,20 but is also seen in systemic I/R21 as well as intestinal I/R.22 All will activate the innate immune system and cause systemic inflammatory response syndrome (SIRS), which contributes to acute lung injury (ALI) and pulmonary dysfunction after chest trauma. Inadequately treated pain resulting from chest wall injury and splinting is a common cause of splinting and hypoventilation. The resultant atelectasis is a common cause of increased Qs/Qt and hypoxemia after trauma. The use of mechanical ventilation, although necessary, can result in ventilator-induced lung injury (VILI) through a number of mechanisms.23 Immunologic injury can be induced by leukocytes in the presence activating cytokines, resulting in increased lung water and decreased diffusion capacity of the lung (DL). Thus, secondary immune attack on the “primed” lung can be initiated by pneumonia, shock, injudicious ventilation strategies, or the release of cytokines into the circulation, as may happen in long-bone fixation.24,25

Increased Work of Breathing and Ventilatory Failure

Ventilatory failure, hypercarbia, and respiratory acidosis after injury are most commonly the result of increased work of breathing. Such increases in work of breathing seen are typically multifactorial. Chest wall injuries can lead to decreased compliance of the chest wall as well as deficits in neuromuscular chest wall function. The pain and splinting associated with chest wall injuries will also lead to decreased tidal volume. Because decreased tidal volume per se results in relatively increased anatomic dead space (Vd/Vt), patients with chest injuries need to increase minute ventilation simply to achieve normal alveolar ventilation. This can be difficult or impossible to achieve in the presence of musculoskeletal chest wall dysfunction.

In the presence of a flail chest, CO2 retention has commonly been attributed to the pendelluft phenomenon, where to-and-fro flow of gas has been postulated to exist between the two hemithoraces in the presence of a unilateral flail segment. This concept is intuitively appealing, and the re-breathing of airway gas does create a pathologic dead space. Yet direct application of this concept to clinical chest injury is probably simplistic. In practice, elevated shunt fractions and hypoxemia are more common in flail chest and in trauma in general than is hypercarbia. Moreover, pendelluft occurs in acute lung injury even without chest wall instability. This results from the heterogeneous viscoelastic properties of the injured lung itself, which leads to gas movements between lung segments of differing compliance.26 Clearly though, flail segments do make ventilation both painful and increasingly inefficient.

Last, in any major trauma with secondary acute lung injury the same immune attack on the pulmonary parenchyma that leads to ALI-ARDS and hypoxemia will also lead to “stiff lungs” and increased work of breathing. Such decreases in pulmonary compliance may persist even after the chest wall has resumed normal configuration and biomechanics. A final, extra-pulmonary cause of decreased pulmonary compliance that should always be sought in acute situations is abdominal compartmental hypertension.

Inflammatory Lung Injury

Deteriorating pulmonary function after chest trauma is commonly related to systemic inflammation after injury. Acute lung injury (ALI) and adult respiratory distress syndrome (ARDS) are terms widely used to reflect the increasing severity of secondary lung injury after trauma. Such injury is widely believed to result from polymorphonuclear neutrophil (PMN)–endothelial cell (EC) interactions that injure pulmonary capillary endothelial membranes, causing interstitial and alveolar edema, and resulting in diminished compliance and gas diffusion. ALI/ARDS are usually defined as a diagnosis of exclusion where hypoxemia exists in the absence of other discrete causes of pulmonary failure such as pneumonia or congestive heart failure. In fact, ALI/ARDS probably exists in all major chest trauma to some extent. Although management of ALI/ARDS is to date supportive, an understanding of the pathogenesis is important because the lung should be understood to be “primed” for secondary insults after chest trauma and at risk for marked deterioration in the event of secondary insults like shock and sepsis. There is increased risk of pneumonia after chest trauma, and pneumonia, of course, can act both as a primary cause of pulmonary dysfunction and as a trigger for “second-hit” organ failure. A special problem is that chest trauma is often accompanied by long-bone fractures and patients with chest injuries are clearly at special risk for pulmonary deterioration after fracture fixation.27 Fractures are reservoirs for inflammatory mediators in the early post-injury period which can be mobilized to the bloodstream by operation and potentially contribute to ALI/ARDS.24,26,28,29 Prospective studies will be needed to determine whether orthopedic management of these patients should be tailored to the protection of lung function.

Extravascular Lung Water

Before the routine clinical use of pulmonary artery (PA) catheters, it was widely believed that fluid overload and subsequent increases in extravascular lung water were the primary cause of pulmonary dysfunction after trauma. In contrast, modern concepts emphasize that hypovolemia, hypoperfusion, and reperfusion can lead to inflammatory organ injury. Also, impaired right-to-left blood flow leads to preferential perfusion of the dependent (West Zone III) lung segments that are poorly ventilated, thus also increasing shunt. Chest injury may be associated with myocardial dysfunction as well, but this is typically right ventricular in nature, and resolves quickly.30 Shock and resuscitation do in fact lead to some expansion of extravascular water, but pulmonary lymphatics protect the lung from interstitial overload remarkably well.31 We therefore stress maintaining euvolemia and circulatory adequacy in patients with chest injuries. In patients with underlying cardiac, renal, or hepatic disease, however, extravascular lung-water accumulation may be a significant issue. These patients may require inotropes, diuretics, or oncotic support.


Physical Examination

The diagnosis of flail chest is best made by visual inspection or palpation of asymmetric chest wall movement in the spontaneously breathing patient. Palpation is often the more sensitive test. It is rapid and informative but is often overlooked. Mobile segments of chest wall and sternum can often be palpated even when not visible on inspection. Clinical flail chest is associated with worse outcomes and greater need for intubation than pulmonary contusion alone.32 Spontaneously breathing patients are often best examined by placing both hands on the two hemithoraces and palpating the symmetry of chest wall motion. Crepitance is also a common finding and point tenderness over the costochondral junctions may point to dislocations or cartilaginous fractures that are not visible on radiographs. Auscultation of the chest is usually suboptimal in trauma, and will play little role in the diagnosis of pulmonary contusion and flail chest except to diminish concern for lesions (such as pneumothoraces) that may deteriorate acutely.