1

What are the consequences of thoracic trauma?

Of the 112,000 annual deaths caused by unintentional injuries, almost half result from motor vehicle–related trauma, which carries a high risk of chest injury. Similarly, of the 55,000 deaths caused by intentional injuries, 20,000 are also likely to involve injuries to the chest. It is estimated that 12%–21% of all trauma deaths result primarily from blunt and penetrating chest injury. For each chest trauma–related death, there are approximately 100 nonfatal thoracic injuries. Not all intrathoracic organs are at equal risk of injury. The chest wall (50%–71%) and lungs (21%–26%) are the most commonly involved structures. The heart (7%–9%), aorta and great vessels (4%), esophagus (7%), and diaphragm (0.5%–7%) are less likely to be injured.

The immediate threat to life also varies with different thoracic organ injuries. Immediately life-threatening injuries include major airway trauma with airway obstruction, tension pneumothorax, open pneumothorax, cardiac tamponade, massive hemothorax, and free rupture of the thoracic great vessels. Potentially life-threatening injuries include partial tracheal disruption, contained rupture of the great vessels, myocardial contusion, valvular or septal injuries, pulmonary contusion, esophageal disruption, and diaphragmatic tear. Flail chest can be immediately or potentially life-threatening depending on the severity of associated hypoxemia. Risk factors for mortality after blunt chest trauma are patient age >65 years; three or more rib fractures; preexisting diseases, particularly involving the cardiopulmonary system; and pneumonia developing after injury.

Although cardiothoracic trauma is a major contributor to all trauma mortality, it coexists in 80% of cases with other injuries that commonly require major surgery. Some serious thoracic organ injuries may be clinically silent, and active suspicion and sophisticated diagnostic measures may be required to detect them. Physiologic derangements from chest injuries are multi-dimensional, including pulmonary failure, hemorrhage, and cardiac dysfunction, and coexist in varying combinations and severity. Some clinicians use the term “thoracic shock” to describe chest injury–induced physiologic derangements ( Figure 75-1 ). Individually or in combination, each of these physiologic abnormalities can interfere with oxygen delivery, consumption, and extraction. They can potentially shift oxygen use from a flow-independent to a flow-dependent state, with associated anaerobic tissue metabolism and lactic acidosis.

Schematic depiction of the pathophysiology of chest injury.

2

How are traumatic pneumothorax and hemothorax managed in patients undergoing laparotomy for splenic injury?

Pneumothorax and hemothorax are the most frequent consequences of chest injury and require timely recognition and treatment. They can occur after both penetrating and blunt chest trauma. Both can result from laceration of visceral pleura by sharp objects during assaults or by fractured ribs. However, pneumothorax may also occur after blunt chest trauma without rib fracture. The mechanism of this injury relates to sudden elevation of alveolar pressures, producing alveolar rupture with entry of air into the interstitial space, mediastinum, and visceral pleura.

Concerns about exacerbating spine injuries or producing adverse hemodynamic changes preclude obtaining a chest radiograph in the sitting position, which is required for the diagnosis of a pneumothorax and recognition of the magnitude of a hemothorax. For these reasons, although supine chest radiographs are obtained routinely in all patients with major trauma, additional measures may be necessary to diagnose pneumothorax and hemothorax when their presence is suspected. CT scan of the chest obtained in the supine position is highly specific, so even a small amount of air in the pleural cavity can be recognized by this method.

In some instances, an undiagnosed pneumothorax may enlarge during surgery for associated injuries. Tension pneumothoraces can result in severe hemodynamic and oxygenation abnormalities that can be lethal. Our approach is to place a chest tube for all patients with a diagnosis of pneumothorax and in need of mechanical ventilation for any reason. Not all clinicians agree with this approach. It has been demonstrated that by using CT, the size of a traumatic pneumothorax may be classified as miniscule or limited anteriorly and anterolaterally. In most of these patients, chest tubes may not be indicated, even during mechanical ventilation, if close observation with appropriate monitoring is provided. However, during emergency surgery, such observation and monitoring may not be easy to achieve.

The clinical signs of pneumothorax in anesthetized patients receiving positive pressure ventilation include elevation of peak airway pressure, decreased lung compliance, decreasing oxygen saturation, and decreased breath sounds on the affected side. In extremis, severe hypotension and possibly cardiac arrest can ensue. Chest radiographs can provide the diagnosis even in the supine position if the amount of intrapleural air is large enough; however, chest x-rays may be difficult or impossible to obtain during emergency surgery.

Without a radiologically confirmed diagnosis, placement of a 14-gauge needle between the fourth and fifth ribs (the fourth intercostal space) in the midaxillary line, the thinnest region of the chest wall even in obese patients, may be indicated for unstable patients. Nevertheless, atelectasis, bronchial obstruction, or migration of intraabdominal contents into the chest through a traumatic diaphragmatic defect can mimic the clinical findings of pneumothorax and lead to unnecessary chest tube placement. Sonographic diagnosis of pneumothorax has gained some recognition more recently. Normally, when the lung is imaged by a 3.5- to 7.5-MHz ultrasound probe, sliding of the pleura beneath the chest wall during inspiration and expiration produces multiple echodense spots that originate from the surface of the lungs and project across the lung. These spots are termed comet-tail artifacts. In the presence of a pneumothorax, air between the chest wall and the visceral pleura prevents the appearance of comet-tail artifacts. Ultrasonography may be more sensitive than an anteroposterior chest x-ray for diagnosis of pneumothorax or hemothorax.

Hemothorax may also cause hemorrhagic shock, mediastinal shift, and airway management difficulties. Placement of a large-bore (28F–38F) chest tube in the early phase of management, especially after penetrating injury, provides information about the rate of bleeding and often prevents development of fibrin clot over the lung surface, which may restrict lung expansion and require decortication later. Antibiotic coverage should be provided for the next 24 hours.

The volume and rate of blood drained via the chest tube determine the necessity for video-assisted thoracoscopy or thoracotomy. Drainage of >1200 mL of blood on placement of the tube, continuing drainage of >200 mL/hour for 4 hours, or >100 mL/hour for 4 hours in patients >60 years are indications for surgical intervention. Other indications for emergency surgery include significant hypotension or tachycardia or both, persistent “white lung” on the chest radiograph in the presence of a properly placed chest tube, difficult ventilation, pericardial tamponade, massive air leak into the chest tube, major tracheal or bronchial injury, and cardiac or great vessel injury. Important management aspects of traumatic pneumothorax and hemothorax are summarized in Box 75-1 .

3

What are the mechanisms of morbidity and mortality from flail chest?

Flail chest is defined as fracture of several ribs at two or more sites or disarticulation of two or more ribs from their cartilaginous attachments to the sternum in addition to fractures. The resulting respiratory impairment may lead to arterial hypoxemia or hypercarbia or both. Two mechanisms are involved: paradoxical ventilation and pulmonary contusion. Paradoxical chest wall motion—manifested by “caving” of the flail segment on inspiration and “bulging” on exhalation—is dyssynchronous with movement of the uninjured chest wall and diaphragm. By itself, a flail segment may increase the work of breathing, but it usually is not the primary cause of acute respiratory failure unless there is a coexisting pneumothorax from injury to the underlying pleura. The pendelluft effect, a pendulum like motion of gas from one lung to the other during respiration as a result of inequality of pressures between the two hemithoraces, does not seem to be a significant cause of respiratory impairment either. The primary cause of morbidity and mortality after blunt chest trauma is believed to be severe pulmonary contusion. An increase in elastic recoil from this cause makes it difficult to expand the lung during inspiration in spontaneously breathing patients, which not only increases the work of breathing but also causes a decrease in functional residual capacity and lung compliance that may not return to normal for several weeks. All of these events result in exaggeration of paradoxical chest wall movement.

Pulmonary contusion may be present in 30% of adult patients sustaining multiple trauma with injury severity scores >25. Rapid deceleration with a change in velocity (ΔV) >45 mph, seen during free falls or major motor vehicle accidents, is the primary mechanism of pulmonary contusion in civilian trauma. In the military setting, shock waves from explosions and high-speed projectiles are responsible for pulmonary contusion.

The pathophysiology of pulmonary contusion involves several mechanisms. The lung contains gas/fluid interfaces and is vulnerable to alveolar disruption. Also, the low-density alveoli may be stripped during impact by higher density hilar tissues. Finally, alveoli compressed during the impact overexpand immediately afterward. Direct laceration of lung parenchyma by inward displacement of fractured ribs or chest wall compression also can occur.

The pathology of lung contusion involves interstitial and intraalveolar hemorrhage, alveolar disruption, and atelectasis. Although these changes begin within a few minutes after injury, they may take 4 hours to complete. Respiratory function, appearance of plain chest radiographs, and arterial blood gases deteriorate gradually within the first few hours after injury. Increased mucus production, decreased clearance, and impaired surfactant production contribute to the respiratory findings produced by intraalveolar bleeding, ventilation/perfusion ( ) mismatching, intrapulmonary shunting, and pulmonary edema. Hypoxemia, wheezing, hemoptysis, hypercarbia, and a rapid respiratory rate with shallow breathing are the main clinical symptoms in spontaneously breathing patients. As a defense mechanism in most instances, hypoxic pulmonary vasoconstriction in the injured lung limits the severity of hypoxemia. However, in patients unable to exert this mechanism, hypoxia may be severe. Generally, age >45 years, preexisting diseases, higher injury severity score, and large fluid volumes predict increased morbidity and mortality.

Pulmonary contusions, if not complicated by inflammation, resolve within a few days. However, when inflammation develops, the likelihood of acute respiratory distress syndrome (ARDS) and pneumonia increases with serious clinical consequences. The long-term outlook after pulmonary dysfunction in patients with flail chest uncomplicated by pulmonary contusion is excellent, generally with complete recovery. The presence of pulmonary contusion, especially when complicated by ARDS or pneumonia, increases the likelihood of long-term pulmonary dysfunction for at least 6 months.

4

What are the management options for flail chest and pulmonary contusion?

Diagnosis

The presence of a flail segment suggests underlying pulmonary contusion, but if breaths are rapid and shallow, this sign may not be evident. However, neither the extent of the flail nor the number of ribs fractured accurately predicts respiratory failure. Chest wall bruising, rib cage deformities, and crepitus or pain or both during palpation of the thorax suggest rib fractures or dislocation even in the presence of a normal chest radiograph, which may not detect cartilaginous injuries and fractures of poorly calcified ribs. The initial film often does not show underlying lung injury because pulmonary edema appears late. If present, a focal infiltrate beneath multiple rib fractures confirms the diagnosis of pulmonary contusion. Clinical signs, such as dyspnea, tachypnea, intercostal muscle retraction, and use of accessory muscles, suggest underlying lung pathology. Monitoring with pulse oximetry in the initial stage is useful only if the patient is breathing room air. Supplemental oxygen administration may mask inadequate ventilation, delaying diagnosis and treatment to restore functional residual capacity and lung compliance toward normal. Likewise, arterial blood gases measured with the patient breathing room air may be useful. Managing these patients without supplemental oxygen necessitates direct observation by a physician or other qualified person. The usual pattern is a progressive decrease in arterial oxygen (PaO ₂ ) and increase in arterial carbon dioxide (PaCO ₂ ) tensions, resulting in a decrease in pH (i.e., respiratory acidosis). When patients need emergency surgery, as our patient required a splenectomy, hypoxemia and hypercarbia often develop intraoperatively. Frequent intraoperative arterial blood gas measurements should be obtained.

Although arterial hypoxemia may precede radiographic abnormalities, it may not reflect the size of the contusion because blood flow to the injured lung is restricted by hypoxic pulmonary vasoconstriction. A PaO ₂ /FiO ₂ <300 after initial resuscitation is considered a risk factor for developing subsequent acute respiratory failure. Because plain chest radiography underestimates contusion volume, CT scans are used for quantifying the contusion size. Patients with a contusion >28% of total lung volume are very likely to require mechanical ventilation, and patients with contusion volumes >20% of total lung volume frequently develop ARDS and pneumonia ( Figure 75-2 ). Although CT is the standard method of diagnosis, patients who are too unstable to be transported to a CT unit may benefit from ultrasound evaluation. Ultrasound may be valuable for detecting rib fractures, pneumothorax, and contusions, although it cannot determine contusion volume. The presence of multiple comet-tail artifacts at the parietal-visceral pleural interface and replacement of the normal transverse A-line pattern by vertical B-lines suggest pulmonary contusion ( Figure 75-3 ). With any of the imaging techniques described, confusion may arise in differentiating contusion from aspiration, atelectasis, hemothorax, fluid overload, transfusion-related acute lung injury, and pulmonary emboli.

Correlation of pulmonary contusion volume with subsequent development of ARDS.

(From Miller PR, Croce MA, Bee TK, et al.: ARDS after pulmonary contusion: accurate measurement of contusion volume identifies high-risk patients. J Trauma 51:223, 2001.) ARDS, Adult respiratory distress syndrome.

Ultrasound diagnosis of pulmonary contusion. A, Ultrasound image of the normal lung showing ribs ( r ) and the pleural line ( p ) with A-lines ( asterisks ), which are horizontal reverberation artifacts at equal distances. B, Ultrasound image of the contused lung showing ribs ( r ) and the pleural line ( p ) without A-lines. Instead, there are vertical hyperechoic artifacts known as B-lines ( asterisks ), which arise from the pleural line and erase the normal A-line pattern.

(From , Secko MA: Bedside diagnosis of pulmonary contusion. Pediatr Emerg Care 25:854, 2009.)

Management

As in our case, patients with pulmonary contusion frequently have associated injuries that may or may not require emergency surgery. Management may need to take into account treatment requirements of associated injuries as well. For example, in a bleeding patient, restricting fluids out of a concern for exacerbating pulmonary contusion may have serious consequences. Many patients with rib fractures and pulmonary contusion also have spinal fractures. Administering continuous epidural anesthesia to these patients because of its salutary effect on contusions would be extremely uncomfortable for the patient and may sometimes be associated with worsening of the vertebral injury or causing spinal cord damage.

During the initial phase, simple measures such as oxygen administration by mask to patients who are hypoxic breathing room air and maintaining the uninvolved lung in a dependent position may help improve oxygenation. Patients with intratracheal bleeding may need a double-lumen endotracheal tube or an endobronchial blocker to prevent contamination of the intact lung and possibly to tamponade the bleeding. Ventilation of the intact lung alone may also be useful in patients with complete unilateral contusions. In patients with bilateral contusions presenting with severe hypoxemia, differential lung ventilation via a double-lumen tube should be considered. When hypoxemia is life-threatening, high-frequency jet ventilation or oscillatory ventilation may improve systemic oxygenation effectively. These modes of ventilation may also improve depressed cardiac function caused by concomitant myocardial contusion or ischemia.

Early treatment is crucial. A delay of even a few hours may result in progression of underlying lung pathology with increasing morbidity and mortality. The goal is to decrease elastic recoil and the work of breathing and to improve arterial blood gases without adverse hemodynamic effects. In patients without acute respiratory failure or associated injuries requiring tracheal intubation, this goal can be accomplished by continuous positive airway pressure (CPAP) of 10–15 cm H ₂ O applied by facemask. Noninvasive positive pressure ventilation using titrated bilevel positive airway pressure with both inspiratory (10–12 cm H ₂ O) and expiratory (6 cm H ₂ O) positive pressures can avoid tracheal intubation in more than one half of patients.

Early tracheal intubation and mechanical ventilation with alveolar recruitment maneuvers, the usual practice before 1975, has fallen into disfavor because of a high incidence of tracheobronchitis and pneumonia leading to sepsis, multiorgan failure, and death. At the present time, except in instances when tracheal intubation and mechanical ventilation are necessary (i.e., PaO ₂ <60 mm Hg in room air, <80 mm Hg with supplemental oxygen, and conditions other than thoracic injury), most patients do well with noninvasive positive pressure ventilation. When impending respiratory failure indicates tracheal intubation, airway pressure release ventilation (APRV) may be a reasonable choice. With this mode of ventilation in a spontaneously breathing patient, CPAP is intermittently decreased for short periods with the device shown in Figure 75-4 . In other words, spontaneous breathing is superimposed on mechanical ventilation. In addition to decreased work of breathing, the advantages of this technique over controlled ventilation are improved matching, increased systemic blood flow, lower sedation requirements, greater oxygen delivery, shorter periods of intubation, and decreased risk of pneumonia. In patients with severe life-threatening pulmonary contusion, ARDS, or acute lung injury unresponsive to APRV or routine mechanical ventilation, lung recruitment strategies such as high-frequency inverse ratio ventilation, low tidal volume (6 mL/kg) and titrated positive end expiratory pressure (PEEP) ventilation, permissive hypercapnia, or high-frequency oscillatory ventilation may be considered.

Left panel, Schematics of the APRV circuit. Right panel, Airway pressure pattern produced by APRV (A) compared with the airway pressure pattern produced by conventional mechanical ventilation (B) . The circuit consists of a flow generator ( F ) that produces continuous positive airway pressure as it exits through a threshold resistor valve ( V1 ). APRV breaths are produced by a timer ( T ) controlled release valve ( R ) in the expiratory limb of the circuit. This valve allows the circuit pressure to decrease intermittently below the continuous positive airway pressure; the level is determined by a second threshold resistor valve ( V2 ). B, Gas source; H, humidifier; P, patient. Note on the right panel spontaneous breathing superimposed on continuous positive airway pressure ( CPAP ) and the opposite inspiration ( I )/expiration ( E ) ratios of APRV and conventional ventilation. APRV can be described as a time-cycled, time-initiated, volume-variable device that limits peak airway pressure ( PAP ).

(Adapted from Räsänen J, Cane RD, Downs JB, et al.: Airway pressure release ventilation during acute lung injury: A prospective multicenter trial. Crit Care Med 19:1234, 1991; and McCunn M, Habashi NM: Airway pressure release ventilation in the acute respiratory distress syndrome following trauma. Int Anesthesiol Clin 40:89, 2002.)

Effective removal of tracheobronchial secretions has a significant effect on outcome. Likewise, monitoring with pulse oximetry, an arterial catheter, and a pulmonary artery catheter when indicated is important. A pulmonary artery catheter can not only guide fluid management, which should be adjusted to the minimum consistent with adequate end-organ perfusion, but it also may aid ventilatory management, as it permits calculation of oxygen delivery and intrapulmonary shunt fraction and thus helps to adjust the optimal level of CPAP.

Supplemental oxygen should be administered judiciously to permit the acquisition of maximal information from the initial oxyhemoglobin saturation with pulse oximetry or arterial blood analysis. Supplemental oxygen has detrimental effects, such as absorption atelectasis, interference with hypoxic pulmonary vasoconstriction in damaged lung regions, decreased mucociliary clearance, free radical formation, and decreased surfactant production.

Although the effect of fluids on pulmonary function in the presence of pulmonary contusion has not been conclusively defined, we believe that overzealous fluid administration may result in an increase in the size of the lung contusion and a decrease in PaO ₂ . Although it is possible to remove excess fluid with diuretics, use of diuretics is associated with electrolyte abnormalities, cardiac dysrhythmias, and hypovolemia. At least during initial resuscitation, the type of fluid used does not seem to affect outcome. Crystalloid solutions are favored because they are less expensive. The initial enthusiasm for hypertonic saline in fluid management of pulmonary contusion has not been substantiated. In the presence of concomitant blunt cardiac injury, complications of pulmonary contusion can easily confuse the clinical picture. In this situation, the best guide to fluid management is transesophageal echocardiography (TEE) or, if TEE is unavailable, pulmonary artery and wedge pressures.

Continuous epidural analgesia is the best pain management technique available for patients with blunt chest trauma. It improves lung function and decreases overall morbidity. However, as mentioned earlier, concomitant spine or other injuries and inability of the patient to consent to the procedure preclude this technique. Continuous thoracic paravertebral block with ultrasound guidance may also be considered as a component of multidimensional pain management. Other modalities, such as parenteral opioids, are not nearly as effective, whereas multiple intercostal blocks are labor-intensive and short-lasting and must be repeated at least twice a day. Important management aspects of flail chest and pulmonary contusion are summarized in Box 75-2 .

BOX 75-2

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