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Pulmonary contusion and flail chest
Pulmonary contusion was probably first described by Morgagni in the 18th century, but Laurent’s description in The Lancet in 1883 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, patients in the sixth decade of life and beyond are prone to fracture their calcified and less compliant rib cages with notably worse outcomes than younger counterparts. Pulmonary contusion and flail chest therefore coexist variably, but their effects on pulmonary pathophysiology are distinct. Confusion between these two clinical entities can therefore lead to misapplication of studies aimed at one entity or the other with the potential for suboptimal management and outcomes.
Incidence
Pulmonary hemorrhage and contusion were first noted at autopsy of patients dying from battlefield and blast injuries during World War I. Similar findings were noted in World War II, and the term “pulmonary concussion” appears to have been coined by Hadfield describing civilian injuries from bomb blasts sustained during the Battle of Britain. In more modern military engagements, blast-associated lung injury continues to represent 3% of the overall injury in Iraq and Afghanistan, and its incidence has been rising secondary to increased utilization of explosive devices.
The incidence of pulmonary contusion in the civilian population varies significantly between studies. Initially described in the 1960s in motor vehicular trauma, rates in early reports were quoted to be 10% of thoracic injuries. A review of the Department of Transportation’s Crash Injury Research and Engineering Network reviewed 2187 passengers involved in frontal and near-side lateral collisions who were evaluated at one of eight participating Level I trauma centers. Just over half (52%) of these passengers sustained blunt chest trauma. Of those, 32% had pulmonary contusion (mean Injury Severity Score [ISS] of 17).
The reported rates of “pulmonary contusion,” however, vary markedly because of multiple factors. For one, modern imaging techniques have doubled the rate of detection of small lung volume contusions compared to “plain” radiography. Second, the age of the “denominator” patient population examined will clearly affect the disease incidence reported in administrative databases. Younger patients, and specifically pediatric patients, have a compliant chest wall compared to older individuals. In chest trauma in the young, compliant chest transmits more energy to the lung parenchyma, rather than distributing the force to the ribs. Studies suggest car occupants younger than age 25 are about 50% more likely to sustain a pulmonary contusion than older occupants, whereas older individuals have almost double the risk of rib fracture.
The relative frequency of flail chest as compared with pulmonary contusion will also vary depending upon the studied population. Pediatric thoracic trauma commonly presents with pulmonary contusions whereas flail chest is very rare, even where multiple fractures are present. One rare exception to this is infants with osteogenesis imperfecta who may manifest their disease with flail chest. Adults, in contrast, have a much higher rate of flail segments. In a large contemporary descriptive series examining adult blunt chest trauma, flail chest was diagnosed in 5% to 13% of chest wall injuries and in 50% of patients with significant pulmonary contusions. Increasing brittleness of the thoracic cage also predisposes the frail elderly to a flail chest with relatively minor chest trauma and little or no associated pulmonary contusion.
Mechanisms of injury
Physical mechanisms of injury
All blunt injuries result from the physical transfer of energy to the patient, but because of the rigidity of the bony thorax, most pulmonary contusions and most flail chest injuries are high-energy injuries, with the primary exception being chest wall injuries in the elderly. 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. Classically, the scenario of injury involves unrestrained drivers striking the steering column. Falls are another common cause of pulmonary contusion and flail chest. Thoracic compression injuries are not as common as vehicular trauma and falls. Although they may produce similar syndromes, the slower speed of impact makes contusion less likely in these injuries than in flail chest. Typically, these patients manifest with traumatic asphyxia. Interpersonal violence, blows with blunt objects, and kicking are occasional causes of pulmonary contusion. Flail chest, however, is less common first owing to the younger demographic involved in such injuries, and second, because biomechanically they are unlikely to result in segmental injuries of multiple contiguous ribs. On rare occasions, tangential gunshot injuries will cause contusions of the underlying pulmonary parenchyma without actually entering the pleural space and lacerating the lung. These injuries are usually very limited in their extent and cause little or no physiologic effect.
The physician should be especially alert to rib fractures in infants and small children as they most commonly occur as a result of child abuse. Any rib fracture in a child is a marker for severe trauma.
As military strategy evolves from conventional engagement to counterinsurgency, improvised explosive devices (IEDs) have become the most common source of injury for American military forces. Blast injuries have four mechanisms of energy transference. Primary blast injuries are directly attributed to the shock wave itself and may occur in the absence of obvious external injury from shrapnel ( secondary injuries), blunt impact ( tertiary injuries), or other blast by-products ( quaternary injuries). The density interface between air-filled body cavities and the tissue parenchyma predisposes to “spallation,” whereby the high-density material transfers its kinetic energy to lower-density surfaces, with the excess energy causing implosion of gas bubbles. “Short-duration” blast injuries such as those from IEDs are generally localized pulmonary injuries. Presumably this is based on shearing of the alveolar surfaces due to resistive differences of the tissue and air interface. “Long-duration” blast injuries transfer a compressive, high-momentum force to the pulmonary parenchyma and are characteristic of larger bombs such as aircraft delivered bombs and vehicle-borne IEDs. The use of ballistic protective vests and body armor increases pulmonary blast tolerance substantially. These injuries are now also seen in civilians as a consequence of terrorism.
Pathophysiology
The transfer of energy to the chest cavity leads directly to edema and hemorrhage of the lung. A shearing force from the inertial differences of the hilum and the lung parenchyma can lead to pulmonary lacerations. Although an uncommon occurrence, lacerations to the lung ( Fig. 1 ) have been diagnosed with increasing frequency with the use of routine computed tomography (CT) imaging. Another potential mechanism of pulmonary dysfunction after trauma is the activation of pulmonary vascular endothelium by percussive cellular deformation. This phenomenon is better documented in cerebrovascular endothelial beds, but it is likely to exist in the pulmonary bed as well (see Fig. 1 ).
Studies from World War I initially proposed that blast injuries predominantly resulted in pulmonary hemorrhage and that pulmonary failure reflected 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. It is most convenient to divide the various pathophysiologic influences on pulmonary function into two categories:
- 1.
Those that result in hypoxemia from increased shunt (Qs/Qt)
- 2.
Injuries that mechanically alter the work of breathing and can lead to ventilatory failure with eventual CO 2 retention and respiratory acidosis
These two physiologic insults often overlap, thus compounding the consequences of pulmonary injury. Furthermore, injury may impact mechanical function of the chest wall, pulmonary aeration, and cardiac performance as it relates to lung perfusion, although these considerations are outside the scope of this review.
Shunting and hypoxemia
Injured, hemorrhagic lung is not the only factor that contributes to V/Q mismatch in the acutely injured chest. Progressive atelectatic shunting often results from splinting from inadequately treated pain, in addition to the chest injury itself. Systemic shock and ischemia/reperfusion (I/R) are well-known activators of immune system attacks on the lung. This is perhaps most clearly evident in lung transplantation, but is also seen in systemic I/R as well as intestinal I/R. 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.
The use of mechanical ventilation, although necessary, can also result in ventilator-induced lung injury (VILI) through a number of mechanisms. Immunologic injury can be induced by leukocytes in the presence of activating cytokines, resulting in increased lung water and decreased diffusion capacity of the lung. Finally, secondary immune attack on the “primed” lung can be initiated by pneumonia, shock, injudicious ventilation strategies, or the release of cytokines or damage-associated molecular patterns (DAMPs) into the circulation, as may happen with systemic trauma or in long-bone fixation.
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 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 lead to decreased tidal volume and a relative increase in anatomic dead space (Vd/Vt). Thus, patients with chest injuries may need to increase minute ventilation simply to achieve normal alveolar ventilation and CO 2 exhalation. This can be difficult or impossible to achieve in the presence of musculoskeletal chest wall dysfunction and pain.
In the presence of a flail chest, “CO 2 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 rebreathing of airway gas would indeed create a pathologic dead space. Yet direct application of this concept to clinical chest injury is simplistic. In practice, elevated shunt fractions and hypoxemia are more common in flail chest than is hypercarbia. Moreover, pendelluft occurs in lung injury even without chest wall instability. This is a result of the heterogeneous viscoelastic properties of the injured lung, which lead to gas movement between lung segments of differing compliance. Clearly, though, flail segments do make ventilation both painful and increasingly inefficient.
Last, in any major trauma the same immune attack on the pulmonary parenchyma that leads to lung injury, ARDS (acute respiratory distress syndrome) and increased Qs/Qt 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.
An extrapulmonary cause of decreased ventilatory compliance that should always be sought in acute situations is abdominal compartmental hypertension. This condition may be difficult to diagnose and should always be suspected when bladder pressures exceed 20 to 25 mm Hg in association with high peak and plateau inspiratory pressure on mechanical ventilation.
Inflammatory lung injury
Deteriorating pulmonary function after chest trauma is commonly related to systemic inflammation after injury. ARDS is the extreme of secondary lung injury after trauma. Such injury is widely believed to result from polymorphonuclear neutrophil–endothelial cell interactions that activate pulmonary capillary endothelial membranes, increasing endothelial permeability, causing interstitial and alveolar edema, and finally resulting in both diminished compliance and gas diffusion. We have recently demonstrated that the interactions of polymorphonuclear neutrophils and endothelial cells can specifically be initiated by the circulation of mitochondrial DAMPs after injury. ARDS is a diagnosis of exclusion when severe hypoxemia exists in the absence of other discrete causes of pulmonary failure such as pneumonia or congestive heart failure. The lung is “primed” for secondary insults after chest trauma and at risk for marked deterioration in the event of secondary insults such as shock, pneumonia, and sepsis. There is increased risk of pneumonia after chest trauma. And, of course, pneumonia can act both as a primary cause of pulmonary dysfunction and as a trigger for sepsis with “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 long-bone fracture fixation. Fractures are reservoirs for inflammatory mediators in the early postinjury period that can be mobilized to the bloodstream by operation and potentially contribute to lung damage. Intracellular DAMPs such as mitochondrial peptides and DNA are generated in high concentration when marrow cavities are reamed and can activate leukocytes as well as endothelial cells. To date, the management of such lung injury is primarily supportive.
Management of lung injury
Before routine clinical use of pulmonary artery catheters and later development of noninvasive methods of circulatory assessment, it was widely believed that fluid overload and subsequent increases in extravascular lung water were the primary cause of pulmonary dysfunction after trauma. Modern concepts challenged that view and emphasized that hypovolemia, systemic hypoperfusion, and I/R can all lead to inflammatory lung injury. Additionally, 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, but this is typically transient with right ventricular dysfunction that resolves quickly. Shock and resuscitation (especially with crystalloids) certainly can expand extravascular water, but pulmonary lymphatics have remarkable reserve to protect the lung from interstitial overload. We therefore stress maintaining euvolemia and circulatory adequacy in patients with chest injuries. In patients with underlying cardiac, renal, or hepatic disease, inotropes, diuretics, or oncotic support may enhance the patient’s Starling curve for optimized hemodynamic function.
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