Anatomy and Pathophysiology

Subcutaneous emphysema in the presence of chest wall trauma usually indicates a more serious thoracic injury. Although the presence of air in the tissues is a benign condition, in the context of chest trauma it usually represents serious injury to any air-containing structure within the thorax. Air enters the tissues either extrapleurally or intrapleurally. Extrapleural tears in the tracheobronchial tree allow air to leak into the mediastinum and soft tissues of the anterior neck, producing a pneumomediastinum, which rarely may progress to a tension pneumomediastinum. This most often occurs in patients who are undergoing positive-pressure ventilation and have a pneumopericardium visible on chest x-ray examination. They may also have Hamman’s crunch, which is a crackling sound with each heartbeat, heard on cardiac auscultation. Intrapleural lesions, however, usually produce a pneumothorax by allowing air to escape the lung through the visceral pleura into the pleural space and then through the parietal pleura into the thoracic wall.

An esophageal tear resulting from Boerhaave’s syndrome or penetrating injury may also produce a pneumomediastinum manifested by subcutaneous emphysema over the supraclavicular area and anterior neck. An additional cause of subcutaneous emphysema, which may or may not be indicative of intrathoracic injury, is found immediately adjacent to a penetrating wound of the thorax. A small amount of air may be introduced into the adjacent subcutaneous tissues from the outside at the time of penetration. However, it is assumed that this is secondary to a pneumothorax or pneumomediastinum, and appropriate diagnostic and therapeutic maneuvers to rule out or treat the intrathoracic injury should be carried out.

The presence of localized subcutaneous emphysema over the chest wall in the presence of blunt trauma is usually indicative of the presence of a traumatic pneumothorax, whereas the presence of subcutaneous emphysema over the supraclavicular area and anterior neck usually indicates a pneumomediastinum.

Management

Tension pneumothorax is considered and treated appropriately. If a tension pneumopericardium is suspected, then immediate pericardiocentesis with aspiration of air from the pericardial space may be lifesaving.

Although subcutaneous emphysema is a benign condition, massive accumulations can be uncomfortable to the patient. The underlying cause, such as pneumothorax, ruptured bronchus, or ruptured esophagus, is treated appropriately. Benign pneumomediastinum secondary to a Valsalva maneuver is treated with observation and high-flow oxygen to facilitate the reabsorption of nitrogen from tissues because the volume of nitrogen causes the discomfort.

Epidemiology

Pulmonary contusion is reported to be present in 30 to 75% of patients with significant blunt chest trauma, most often from MVCs with rapid deceleration.¹ Pulmonary contusion can also be caused by high-velocity missile wounds and the high-energy shock waves of an explosion in air or water. Pulmonary contusion is the most common significant chest injury in children, and it is most commonly caused by an MVC or an automobile versus pedestrian accident.²¹

Anatomy and Pathophysiology

Pulmonary contusion is a direct bruise of the lung parenchyma followed by alveolar edema and hemorrhage but without an accompanying pulmonary laceration, as first described by Morgagni in 1761.²⁶

The early diagnosis of pulmonary contusion is important if treatment is to be successful. The onset may be insidious, and therefore it should be suspected from the history of the mechanism of injury rather than the initial chest radiograph. Great force is required to produce pulmonary contusion, such as from a fall from height, an MVC, and other forms of significant trauma.

Clinical Features

The clinical manifestations include dyspnea, tachypnea, cyanosis, tachycardia, hypotension, and chest wall bruising. There are no specific signs for pulmonary contusion, but hemoptysis may be seen sometime during the patient’s course, and moist rales or absent breath sounds may be heard on auscultation. Palpation of the chest wall commonly reveals fractured ribs. If flail chest is discovered, pulmonary contusion is commonly present.

Surprisingly, many of the worst contusions occur in patients without rib fractures. It has been theorized that the more elastic chest wall, as in younger individuals, transmits increased force to the thoracic contents. Although isolated pulmonary contusions can exist, they are associated with extrathoracic injuries in the majority of patients.²⁷

Diagnostic Strategies

Care is taken not to focus exclusively on more dramatic injuries at the expense of failing to recognize the evolving pulmonary contusion. This is particularly true with the initial x-ray studies when overlying rib fracture, pneumothorax, aspiration pneumonitis, or poor radiograph quality may mask the contusion.

Typical radiographic findings begin to appear within minutes of injury and range from patchy, irregular, alveolar infiltrate to frank consolidation (Fig. 45-4). Usually, these changes are present on the initial examination, and they are almost always present within 6 hours. The rapidity of changes on chest x-ray visualization usually correlates with the severity of the contusion. Pulmonary contusion should be differentiated from acute respiratory distress syndrome (ARDS), with which it is often confused because the radiographic appearance of the two conditions may be similar. The contusion usually manifests within minutes of the initial injury, is usually localized to a segment or a lobe, is often apparent on the initial chest study, and tends to last 48 to 72 hours. ARDS is diffuse, and its development is usually delayed, with onset typically between 24 and 72 hours after injury.²⁸

The increased frequency of CT scans for blunt trauma patients has resulted in a corresponding increase in the diagnosis of pulmonary contusion. CT scans have been shown to detect twice as many pulmonary contusions as plain radiographs.⁷ Some authors suggest that pulmonary contusions visible only on CT scan and not on plain radiographs may not be clinically significant.²⁹

Chest CT scan is particularly valuable to identify a pulmonary contusion in the acute phase after injury because plain chest x-ray films have a low sensitivity.⁷ Although CT scan may not be necessary to make the diagnosis of a pulmonary contusion that is evident on plain chest radiography, it may be helpful to further define the extent of the contusion and to identify other thoracic injuries. Infectious complications, sternoclavicular joint dislocation, pneumothorax, misplaced endotracheal tube, intraperitoneal air, and vertebral fracture have all been identified by CT scan in the trauma patient. Occult pulmonary contusions are those that are visible only on CT scan, not plain radiographs, and usually involve more than 20% of the lung volume. These “occult” pulmonary contusions are not associated with a worse clinical outcome as compared with blunt trauma patients without pulmonary contusion.²⁹ Patients with pulmonary contusion visible on both conventional chest radiographs and the CT scan frequently have a higher contusion volume and a worse outcome than patients with occult pulmonary contusion. Thus pulmonary contusions that are visible on plain chest radiographs have a higher morbidity and mortality and should therefore receive special medical attention as compared with contusions only seen on the chest CT scan.

Arterial blood gases may be helpful in making the diagnosis of pulmonary contusion because most patients are hypoxemic at the time of admission. A low partial pressure of oxygen (PO₂) alone may be reason to suspect pulmonary contusion. A widening alveolar-arterial oxygen difference indicates a decreasing pulmonary diffusion capacity of the patient’s contused lung, and it is one of the earliest and most accurate means of assessing the current status, progress, and prognosis.

Management

Treatment for pulmonary contusion is primarily supportive.²⁹ When only one lung has been severely contused and has caused significant hypoxemia, consideration should be given to intubating and ventilating each lung separately with a dual-lumen endotracheal tube and two ventilators. This allows for the difference in compliance between the injured and the normal lung and prevents hyperexpansion of one lung and gradual collapse of the other.³⁰ As with flail chest, however, intubation and mechanical ventilation should be avoided if possible because they are associated with an increase in morbidity, including pneumonia, sepsis, pneumothorax, hypercoagulability, and longer hospitalization.³¹ The need for mechanical ventilation increases significantly when the area of pulmonary contusion exceeds 20% of total lung volume.³²

Certain patients may benefit from a trial of noninvasive positive-pressure ventilation with BPAP or CPAP to avoid intubation and mechanical ventilation. In those patients most severely injured with extensive pulmonary contusions and the development of ARDS with severe hypoxia refractory to conventional therapy, some small studies suggest a possible role for extracorporeal membrane oxygenation.³³

Certain procedures may ameliorate the pulmonary contusion, including the restriction of intravenous fluids to maintain intravascular volume within strict limits and aggressive supportive care consisting of vigorous tracheobronchial toilet, suctioning, and pain relief. These maneuvers may preclude the need for ventilator support and allow a more selective approach to flail chest and pulmonary contusion.

Another area of controversy in the management of pulmonary contusions is the appropriate use of crystalloid versus colloid solutions in resuscitation of the multiply injured patient with suspected contusion. Because of the potential for colloid sequestration within the pulmonary alveoli as a result of capillary leak, colloids are not recommended for use in treating these patients.

Pneumonia is the most common complication of pulmonary contusions, and it significantly worsens the prognosis. It develops insidiously, especially in patients treated with prophylactic antibiotics. Antibiotics should be reserved for use with specific organisms rather than given prophylactically.

Epidemiology

Pneumothorax, which is the accumulation of air in the pleural space, is a common complication of chest trauma. It is reported to be present in 15 to 50% of patients who sustain significant chest trauma, and it is invariably present in those with transpleural penetrating injuries.¹

Anatomy and Pathophysiology

Pneumothorax can be divided into three types depending on whether air has direct access to the pleural cavity: simple, communicating, and tension. A pneumothorax is considered simple (Fig. 45-5) when there is no communication with the atmosphere or any shift of the mediastinum or hemidiaphragm resulting from the accumulation of air. It can be graded according to the degree of collapse as visualized on the chest radiograph. A small pneumothorax occupies 15% or less of the pleural cavity, a moderate one 15 to 60%, and a large pneumothorax more than 60%. Traumatic pneumothorax is most often caused by a fractured rib that is driven inward, lacerating the pleura. It may also occur without a fracture when the impact is delivered at full inspiration with the glottis closed, leading to a tremendous increase in intra-alveolar pressure and the subsequent rupture of the alveoli. A penetrating injury, such as a gunshot or stab wound, may also produce a simple pneumothorax if there is no free communication with the atmosphere (Fig. 45-6).

Clinical Features

Shortness of breath and chest pain are the most common presenting complaints of pneumothorax. The patient’s appearance is highly variable, ranging from acutely ill with cyanosis and tachypnea to misleadingly healthy. The signs and symptoms are not always correlated with the degree of pneumothorax. The physical examination may reveal decreased or absent breath sounds and hyper-resonance over the involved side as well as subcutaneous emphysema, but small pneumothoraces may not be detectable on physical examination.

Patients with tension pneumothorax become acutely ill within minutes and develop severe cardiovascular and respiratory distress. They are dyspneic, agitated, restless, cyanotic, tachycardic, and hypotensive and display decreasing mental activity. The cardinal signs of tension pneumothorax are tachycardia, jugular venous distention (JVD), and absent breath sounds on the ipsilateral side. However, JVD may not reliably be present with massive blood loss. Hypotension will not occur as early as hypoxia and may represent a preterminal event.

Diagnostic Strategies

Because intrapleural air tends to collect at the apex of the lung, the initial chest radiograph should be an upright full inspiratory film if the patient’s condition permits. An upright film will often reveal small pleural effusions that are not visible on supine films, and it also allows better visualization of the mediastinum. Although the chest radiograph has traditionally been the preferred initial study for diagnosing a simple pneumothorax, emerging literature suggests that a simple pneumothorax can be identified during the initial US examination of the trauma patient as part of the extended focused assessment with sonography in trauma (E-FAST) examination. Because FAST is becoming part of the routine initial evaluation of trauma patients, evaluation for the presence of a pneumothorax should be included in this rapid bedside examination, especially because this is performed before chest radiography. In fact, several studies have found that the US has greater sensitivity for pneumothorax than chest radiography.34–36

If a pneumothorax is suspected but not visualized on the initial inspiratory film, an expiratory film should be obtained because it makes the pneumothorax more apparent by reducing the lung volume. Notably, as many as one third of initial chest x-ray films will not detect a pneumothorax in trauma patients.⁷ Although it is not recommended as a primary method of diagnosing pneumothorax, CT is very sensitive in finding small pneumothoraces even in supine patients. When CT scans are obtained to evaluate the abdomen, it may be helpful to take a few low cuts into the chest to exclude the presence of a small pneumothorax.

Occult Pneumothorax

A pneumothorax that is absent on the initial chest radiograph but is identified on subsequent chest or abdominal CT is called an occult pneumothorax. Occult pneumothorax is being diagnosed more frequently given the increased use of CT.37,38 Studies have found rates as high as 75% for diagnosis on CT scan of occult pneumothorax that was absent on initial chest radiographs (Fig. 45-10).^7,37–39

The diagnosis and treatment of tension pneumothorax should not be delayed. Although tension pneumothorax usually occurs dramatically, the clinical diagnosis is occasionally obscure, and chest x-ray examination may be required to suggest the diagnosis, particularly in patients on mechanical ventilation. This film will show complete lung collapse and shift of the mediastinum to the opposite side. Ideally, the diagnosis and treatment should be completed without a chest x-ray examination because the delay in obtaining this radiograph may adversely affect patient outcome. As previously stated, tension pneumothorax will typically cause significant hemodynamic compromise and therefore remains a clinical diagnosis.

Management

In the setting of penetrating trauma in which the patient is asymptomatic and the initial chest x-ray study is negative, the patient can be safely observed and the x-ray examination repeated. Previously, it was thought that if the patient was still asymptomatic and the radiograph negative after 6 hours, the patient could be discharged. Recent experience indicates that 3 hours is probably effective and safe for observation, with repeat x-ray film before discharge for patients with penetrating trauma.⁴⁰ Patients with blunt trauma in whom clinical suspicion for pneumothorax is high should still undergo a 6-hour delayed chest x-ray examination before discharge. However, if the stable patient undergoes initial screening chest CT that is negative for pneumothorax or hemothorax, the literature suggests that obtaining a delayed chest x-ray film is unnecessary, and these patients may be discharged from the ED.⁴¹

Epidemiology

Hemothorax, which is the accumulation of blood in the pleural space after blunt or penetrating chest trauma, is a common complication that may produce hypovolemic shock and dangerously reduce vital capacity. It is commonly associated with pneumothorax (25% of cases) as well as extrathoracic injuries (73% of cases).⁵⁰

Anatomy and Pathophysiology

Hemorrhage from injured lung parenchyma is the most common cause of hemothorax, but this tends to be self-limited unless there is a major laceration. Specific vessels are less often the source of hemorrhage, with intercostal and internal mammary arteries causing hemothorax more often than hilar or great vessels. Bleeding from the intercostal arteries may be brisk, however, because they branch directly from the aorta.

Management

Close monitoring of the initial and ongoing rate of blood loss is performed. Immediate drainage of more than 1500 mL of blood from the pleural cavity is usually considered an indication for urgent thoracotomy. Perhaps even more predictive of the need for thoracotomy is a continued output of at least 200 mL/hr for 3 hours. General considerations for urgent thoracotomy are outlined in Box 45-2.⁵¹

Clinical Features

Depending on the rate and quantity of hemorrhage, varying degrees of hypovolemic shock will be manifested. Tactile fremitus is decreased, and breath sounds are diminished or absent.

Diagnostic Strategies

The upright chest radiograph remains the primary diagnostic study in the acute evaluation of hemothorax. A hemothorax is noted as meniscus of fluid blunting the costophrenic angle and tracking up the pleural margins of the chest wall when viewed on the upright chest x-ray film. Blunting of the costophrenic angles on upright chest radiograph requires at least 200 to 300 mL of fluid. The supine view chest film is less accurate, and it may be more difficult to make the diagnosis with the patient in this position. Unfortunately, this is often the only film available because of the patient’s unstable condition. In the supine patient, blood layers posteriorly, creating a diffuse haziness that can be rather subtle, depending on the volume of the hemothorax (Fig. 45-11).With a massive hemothorax, the large volume of blood can create a tension hemothorax, with signs and symptoms of both obstructive and hemorrhagic shock (Fig. 45-12).

As is the case with pneumothoraces, US has much greater sensitivity than chest radiography in the detection of a small hemothorax, but CT scanning has the highest sensitivity, with some studies reporting up to a 25% incidence of hemothoraces diagnosed by CT that were not detected on chest radiography (Fig. 45-13).⁷ Perhaps more important, almost half of these occult hemothoraces underwent drainage with tube thoracostomy.⁵² Furthermore, one drawback of ultrasonography for the identification of traumatic hemothorax is that associated injuries readily seen on chest radiographs in the trauma patient, such as fractures or a widened mediastinum, are not readily identifiable on chest ultrasonography (Fig. 45-14). However, chest radiography and early bedside ultrasonography usually detect clinically significant hemothoraces and should routinely be performed. Delayed hemothorax may be associated with significant morbidity because the residual blood may serve as a nidus for the development of empyema or fibrothorax.

Management

Treatment of hemothorax consists of restoring the circulating blood volume, controlling the airway as necessary, and evacuating the accumulated blood. Tube thoracostomy allows constant monitoring of the blood loss, and serial chest radiographs help monitor lung reexpansion. A large-bore tube (36-F to 40-F) should be inserted in the fifth interspace at the anterior axillary line and connected to underwater seal drainage and suction (20-30 mL H₂O).

Although small hemothoraces may be observed in stable patients, a moderate hemothorax or any hemothorax in an unstable or symptomatic patient requires tube thoracostomy. Severe or persistent hemorrhage requires thoracostomy or open thoracotomy. Studies are required to better delineate the size of a hemothorax detected on CT scan that requires tube thoracostomy drainage.

Autotransfusion has been successfully used in tube thoracostomy. Recent simplification and commercial availability of the equipment have made autotransfusion feasible in most EDs. Autotransfusion also eliminates the risk of incompatibility reactions and transmission of certain diseases such as hepatitis C. Because the majority of blood loss occurs immediately after tube thoracostomy placement, autotransfusion apparatus should be immediately available in the ED.

As a result of the increasing frequency of chest CT scans, it has been found that there may be a greater frequency of misplaced thoracostomy tubes than is evident on conventional chest radiographs. Almost 25% of patients in one series subsequently required operative intervention as a result of complications from penetration of the lung parenchyma from tube thoracostomies.⁵³ However, the true incidence of complications that require some surgical intervention remains unknown (Fig. 45-15).

Although beyond the scope of emergency medicine, mention is made of the role of thoracoscopy. Video-assisted thoracic surgery (VATS) is particularly useful for evaluation and evacuation of retained hemothorax, control of bleeding from intercostal vessels, and diagnosis and repair of diaphragmatic injuries.54,55 As surgeons gain more experience with the technique, VATS will likely become more widely used for other indications as well, given the decreased morbidity and length of hospital stay compared with open thoracotomy.⁵⁶

Epidemiology

Blunt cardiac injury usually results from high-speed MVCs in which the chest wall strikes the steering wheel. Other causes, such as falls from heights, crushing injuries, blast injuries, and direct blows, are less common. The significance of blunt injuries as a cause of myocardial or cardiac contusion was described more than 50 years ago by Bright and Beck.⁶⁹ Nevertheless, the diagnosis of a blunt injury to the heart remains elusive because of the usual concomitant serious injuries to other body organs and, more important, because there is no gold standard for making the diagnosis.

The importance of detecting blunt myocardial injury lies in the recognition of associated potentially fatal complications. Life-threatening dysrhythmias, conduction abnormalities, congestive heart failure, cardiogenic shock, hemopericardium with tamponade, cardiac rupture, valvular rupture, intraventricular thrombi, thromboembolic phenomena, coronary artery occlusion, ventricular aneurysms, and constrictive pericarditis have all been reported as complications.

Anatomy and Pathophysiology

Blunt cardiac trauma may be viewed as part of a continuous spectrum (i.e., myocardial concussion, contusion, infarction, and rupture).⁷⁰ Myocardial concussion occurs when a blunt injury to the interior chest produces a “stun” response in the myocardium. No permanent cellular injury occurs, but transient clinical effects may result. Myocardial contusion is the least severe form of injury that can be demonstrated pathologically. Cellular injury occurs with extravasation of red blood cells into the muscle wall, along with localized myocardial cellular necrosis. Permanent myocardial damage is rare.⁷¹ Traumatic myocardial infarction (MI) results from either direct trauma to the coronary arteries or a severe contusion of the myocardium, leading to irreversible cellular injury and ultimately cell death. Direct injury to the coronary arteries via laceration, thrombosis, or spasm is thought to be the most common mechanism for traumatic MI. Cardiac rupture is obviously the most severe form of blunt cardiac injury.

Epidemiology

Myocardial contusion has been a diagnosis describing a very poorly understood and nebulous condition. Decades of research and widely varied clinical practice have failed to produce a consensus regarding its diagnosis, complication rate, and proper disposition. The incidence of myocardial contusion varies from 3 to 55% in reported series of severe closed-chest trauma, depending on the criteria used for establishing the diagnosis.74,75

Anatomy and Pathophysiology

Several mechanisms have been postulated by which the heart may be injured in cases of blunt trauma. A direct blow to the chest transmits energy through the ribs to the spine. When a large force is applied to the chest wall over an extended period, the sternum is displaced posteriorly and the heart is compressed between the sternum and vertebrae or an elevated diaphragm. Either can result in cardiac injury. Increased intrathoracic pressure from a direct blow to the chest may contribute to the injury. In addition, compression of the abdomen and pelvis may displace abdominal viscera upward and result in cardiac injury.

A myocardial contusion is histologically characterized by intramyocardial hemorrhage, edema, and necrosis of myocardial muscle cells. These histologic findings are similar to those seen in acute MI. An accumulation of edema and cellular infiltrate in the wall of the heart may cause a decrease in ventricular compliance, resulting in cardiac dysfunction.

Most myocardial contusions heal spontaneously, with resolution of cellular infiltrate and hemorrhage leading to scar formation. Small pericardial effusions occur in more than 50% of cases of contusion, usually during the second week. These are probably caused by pericardial irritation, and they neither imply significant cardiac injury nor increase the risk of tamponade, and they require no therapy such as pericardiocentesis. A fibrinous reaction at the contusion site may also occur, resulting in pain, a friction rub, and adhesion to the pericardium. In a few cases, the reabsorption of the hematoma is accompanied by necrosis of the ventricular wall, which may result in a delayed rupture of the myocardium or a scarred and weakened area with subsequent development of a ventricular aneurysm. If necrosis occurs, it will usually be manifested in the second week after injury and is one of the causes of delayed sudden death after blunt trauma to the chest. However, this is a rare phenomenon.

Clinical Features

Myocardial contusion manifests clinically as a spectrum of injuries of varying severity. Although the majority of patients with myocardial contusion have external signs of thoracic trauma (e.g., contusions, abrasions, palpable crepitus, rib fractures, or visible flail segments), the absence of thoracic lesions decreases the suspicion but never excludes cardiac injury. Other associated injuries may include pulmonary contusion, pneumothorax, hemothorax, external fracture, and great vessel injury. The most sensitive but least specific sign of myocardial contusion is sinus tachycardia, which is present in approximately 70% of patients with documented myocardial contusions and is a very common vital sign in trauma patients. A reduction in cardiac output, which can be clinically insignificant or manifest as pronounced cardiogenic shock, may occur in patients with significant cardiac contusion.

Diagnostic Strategies

Significant controversy exists regarding the importance and manner of establishing the diagnosis of myocardial contusion in otherwise hemodynamically stable patients.⁷⁶

Even when the diagnosis of a myocardial contusion is considered, confirming the diagnosis without a true gold standard is problematic. Clinical evidence is often nonspecific, especially in the setting of multiple trauma. Patients may have dysrhythmias or ST wave changes caused by significant hypoxia as a result of pulmonary injuries or blood loss, which resolve once the hypoxemia or blood loss has been corrected. Likewise, severe intracranial injury, electrolyte abnormalities, and excessive vagal or sympathetic tone may give rise to dysrhythmias or an abnormal ECG. Under these conditions, ECG abnormalities may not represent true myocardial damage. On the contrary, they may cause one to overlook the potential for traumatic cardiac injury. One large series of blunt trauma patients found that blunt cardiac injury was a significant risk factor for cardiac dysrhythmia.⁷⁶

Because myocardial contusion cannot be positively identified short of biopsy or autopsy, there is much confusion regarding the role of the various laboratory and imaging studies used to diagnose myocardial injury. Multiple studies using cardiac biomarkers have been unhelpful in establishing or excluding the diagnosis. Furthermore, the vast majority of myocardial contusions probably do not cause clinically significant complications. Based on mechanism alone, the relative risk of a life-threatening dysrhythmia is far too low to warrant routine admission to rule out myocardial contusion in all patients with blunt chest trauma. Several studies suggest that very few patients diagnosed with myocardial contusion develop cardiac complications requiring therapeutic intervention or a change in management. Therefore a routine cardiac workup is not indicated in most blunt thoracic trauma victims.⁷⁷ The usefulness of diagnostic studies is to identify patients at low risk who can be safely discharged from the ED and not to diagnose the presence of a myocardial contusion.

Diagnostic strategies that have been used to “diagnose” myocardial contusion and assess the risk of complications and the need for admission include ECG, biochemical cardiac markers (serum creatine kinase [CK-MB] isoenzyme levels or troponin levels), two-dimensional echocardiography, and CT scan.

Management

Appropriate workup and treatment of the patient with suspected myocardial contusion begins with accurate out-of-hospital evaluation. Paramedics should observe and relay information to the ED concerning mechanism of injury, status of the motor vehicle, steering wheel and dashboard damage, use of seat belts and air bags, speed of the vehicle before the accident, and position of the patient when found. Pertinent clinical data to be recorded include vital signs, level of consciousness, cardiac rhythm, and the presence of chest wall trauma.

The value of admitting and carefully monitoring patients with suspected mild (i.e., hemodynamically asymptomatic) cardiac contusions is not supported. The latest studies do suggest that troponin levels are very helpful in risk stratification of patients suspected of having myocardial contusion.77,80,81 One such strategy is to perform emergent echocardiography for all severely injured patients with hemodynamic instability who are suspected to have structural damage to the heart and/or great vessels. Elevated troponin levels or ECG abnormalities indicate a higher risk of developing cardiac complications. A similar recommendation exists for severely injured patients with a sternal fracture, although the presence of an isolated sternal fracture is not necessarily a sign of cardiac injury. Increased troponin levels or ECG abnormalities indicate a higher risk of developing cardiac complications. Further investigation, including echocardiography, serial ECGs, and serial troponin levels, is recommended.

In patients who have minor injuries and are otherwise asymptomatic, elevated troponin levels and minor ECG abnormalities do not necessarily indicate a clinically significant myocardial contusion. Very few of these patients will develop complications. However, normal troponin levels (4-6 hours after injury) along with normal (or unchanged) ECGs correlate with minimal risk of cardiac complications. Therefore in-hospital monitoring may be limited to those patients with significant, acute ECG abnormalities, elevated troponin concentrations, or both. Serial ECGs and troponin levels should be obtained until the results return to normal.

Echocardiography is rarely required in this low-risk subset of patients who have minor injuries and are otherwise asymptomatic. If the patient’s clinical status deteriorates or there is inconsistency between the troponin levels and ECG changes, echocardiography can be very useful to rule out structurally significant myocardial injuries, which may include wall motion or valvular abnormalities.

On admission, treatment of a suspected myocardial contusion should be similar to that of an MI: intravenous line, cardiac monitoring, and administration of oxygen and analgesic agents. Dysrhythmias should be treated with appropriate medications as per current Advanced Cardiac Life Support guidelines.⁸² No data exist to support prophylactic pharmacologic agents for dysrhythmia suppression. Measures should be taken to treat and prevent any conditions that increase myocardial irritability (e.g., metabolic acidosis). Thrombolytic agents and aspirin are contraindicated in the setting of acute trauma. In rare instances there may be an acute MI associated with trauma, which can arise from lacerations or blunt injury to the coronary arteries. These cases should be managed by percutaneous coronary intervention (PCI), with cardiothoracic surgery for definitive repair as indicated.

In the setting of depressed cardiac output caused by myocardial contusion, judicious fluid administration is required. Dobutamine may be useful after optimal preload is ensured. Intra-aortic balloon counterpulsation has been used successfully in refractory cardiogenic shock. The priority is to be certain that the decreased cardiac output is not the result of other undiagnosed injuries, particularly aortic rupture.

Prognosis

The prognosis of a patient with myocardial contusion depends on the character and magnitude of the initial trauma, the size and location of the contusion, the preexisting condition of the coronary arteries, and, most important, any other organ trauma and its complications. Major morbidity and mortality correlate most closely with the number of associated serious injuries. Recovery without complications is the usual course.

Epidemiology

High-speed MVCs are responsible for most cases of traumatic myocardial rupture. Myocardial rupture is almost always immediately fatal and accounts for 15% of fatal thoracic injuries. It has been estimated that blunt cardiac rupture accounts for 5% of the 50,000 annual highway deaths in the United States.¹ In various series, the incidence of cardiac rupture in cases of blunt chest trauma ranges from 0.5 to 2%.⁸³ The most common cause of death in cases of nonpenetrating cardiac injuries is myocardial rupture. Approximately one third of these patients have multiple chamber rupture, and one fourth have an associated ascending aortic rupture. Bright and Beck reviewed 152 autopsy cases of traumatic cardiac ruptures and found that 20% of patients survived 30 minutes or more, which would have allowed them to reach the operating room had the problem been recognized.⁶⁹ The first report of successful repair of blunt cardiac rupture was published in 1955 and involved a patient with right atrial rupture.⁸⁴

Anatomy and Pathophysiology

The chambers most commonly involved in cardiac rupture are the ventricles, with right ventricular rupture being most common. Ruptures of the atria are less common, with right atrial rupture being more common than left. Multiple chamber involvement occurs in 20% of patients.⁸³ Twenty percent of nonsurvivors have concomitant aortic rupture.

A rupture occurs during closure of the outflow track when there is ventricular compression of blood-filled chambers by a pressure sufficient to rupture the chamber wall, septum, or valve. This is the most likely mechanism for ventricular rupture when injury occurs in diastole or early systole concomitant with maximal ventricular distention. The atria are most susceptible to rupture by sudden compression in late systole when these chambers are maximally distended with venous blood and the atrial ventricular valves are closed. Other proposed mechanisms of rupture include (1) deceleration shearing stresses acting on the “fixed” attachment of the inferior and superior vena cava at the right atrium; (2) upward displacement of blood and abdominal viscera from blunt abdominal injury that causes a sudden increase in intracardiac pressure; (3) direct compression of the heart between the sternum and vertebral bodies; (4) laceration from a fractured rib or sternum; and (5) complications of a myocardial contusion, necrosis, and subsequent cardiac rupture.

Because of the nature of the mechanisms involved in cardiac rupture, associated multisystem injuries are common. More than 70% of reported survivors of myocardial rupture have other major associated injuries, including pulmonary contusions, liver and spleen lacerations, closed head injuries, and major fractures. Twenty percent of nonsurvivors have concomitant aortic ruptures.⁸³

The immediate ability of the patient to survive cardiac rupture depends on the integrity of the pericardium. Two thirds of patients with cardiac rupture have an intact pericardium and are protected from immediate exsanguination. These patients may survive for variable periods but eventually develop significant hemopericardium and pericardial tamponade. One third of patients with cardiac rupture have associated pericardial tears and succumb promptly to exsanguination.

Occasionally, patients survive if the pericardial tear is small or the rupture is small enough to seal itself. A small pericardial laceration may allow partial and intermittent release of tamponade while still controlling bleeding. In one series of patients with confirmed myocardial rupture, 40% of patients had isolated rupture of the right atrium. The overall mortality rate was 81%, with none of the patients with two-chamber rupture, ventricular rupture, or absence of vital signs on arrival at the ED surviving.⁸³

Clinical Features

The clinical presentation of a patient who has sustained a myocardial rupture is usually that of cardiac tamponade or severe hemorrhage. Rarely, a patient is seen with a large hemothorax, hypotension, and hypovolemia, suggesting rupture with associated pericardial tear. A patient with an intact pericardial sac and developing tamponade displays physical findings of tamponade, usually with subsequent clinical deterioration. Initial inspection of the torso may reveal little more than a bruised area over the sternum or no external physical evidence. More often, however, signs of significant chest trauma or other associated injuries will be present, indicating a mechanism of injury that could result in myocardial rupture. Auscultation may reveal a harsh murmur, known as a “bruit de moulin,” which sounds like a splashing mill wheel. This is caused by pneumopericardium.

In a review of survivors of myocardial rupture, common symptoms and signs included hypotension (100%); elevated CVP (95%); tachycardia (89%); distended neck veins (80%); cyanosis of the head, neck, arms, and upper chest (76%); unresponsiveness (74%); distant heart sounds (61%); and associated chest injuries (50%).83–86

The following findings are suggestive of pericardial rupture:

Diagnostic Strategies

Early use of ED US may facilitate the early diagnosis of cardiac rupture and pericardial tamponade.⁸⁷ The combination of shock and jugular venous distention (or an elevated CVP) in a patient with blunt chest trauma should immediately suggest pericardial tamponade. However, in patients with coexistent hemorrhage from other injuries, JVD may be absent. Other considerations include tension pneumothorax, right ventricular myocardial contusion, superior vena cava obstruction, and ruptured tricuspid valve. Sonographic visualization of pericardial fluid in this setting should be followed by emergent thoracotomy (Fig. 45-17).

A chest radiograph should be obtained immediately in all cases of acute, blunt chest injuries. Although this study usually does not help diagnose cases of myocardial rupture, it notes the presence of other intrathoracic injuries (e.g., hemothorax, pneumothorax, and signs of possible aortic dissection). An increase in the size of the cardiac silhouette more commonly reflects preexisting disease or valvular incompetence with chamber enlargement caused by increased filling pressures. ECG changes may occur with myocardial injury, but these are often nonspecific for myocardial rupture. Early use of bedside echocardiography in the ED should be performed in any case of suspected cardiac rupture, pericardial tamponade, a previously undiagnosed murmur, or shock unexplained by other causes (e.g., exsanguination).

Management

When nonhospital medical personnel evaluate a patient who has sustained blunt chest trauma, they should concentrate on rapid transport and pay attention for any signs of pericardial tamponade. En route to the hospital, the possibility of a tension pneumothorax should be considered as well.

In the ED, treatment of patients with a myocardial rupture is directed toward immediate decompression of cardiac tamponade and control of hemorrhage. Pericardiocentesis may be effective in cases of a small rupture, but it is usually performed as a diagnostic or temporizing therapeutic procedure until surgical correction can be undertaken. Emergency thoracotomy and pericardiotomy may be required in the ED if the patient has rapidly deteriorating vital signs or a cardiac arrest. After emergency thoracotomy and pericardiotomy, the myocardial rupture should be controlled until the patient can be transported to the operating room for definitive repair. Hemorrhage from a ruptured atrium can often be controlled by finger occlusion or application of a vascular clamp. Insertion of a Foley catheter through the defect, followed by inflation of the balloon and traction on the catheter, may also control the bleeding. Ventricular rupture can usually be controlled by direct digital pressure or by suturing with nonabsorbable vascular sutures.

Cardiopulmonary bypass is commonly required in only 10% of successful repairs of myocardial rupture.⁸³ Therefore, for patients with suspected myocardial rupture, it is appropriate to undertake emergency thoracotomy in institutions that have qualified surgeons but no immediate access to cardiopulmonary bypass.

Prognosis

Reported survival rates for patients with myocardial rupture and an intact pericardium vary widely. Although only a small number of survivors of ventricular rupture had been previously reported,81,82,84 a small case series reported that four out of a total of five patients with blunt cardiac rupture who arrived at the ED with vital signs ultimately survived.⁸⁵ Most survivors of cardiac rupture are patients with atrial rupture, including one patient with multiple atrial tears. Most undergo surgical repair within 3 or 4 hours of injury. Approximately 60% of successful repairs have been performed more than 60 minutes after injury.

Clinical Features

The clinical presentation of these patients depends on which valve or septum is involved and whether coincident cardiac injuries are present. A complete rupture of the mitral valve usually results in immediate death. The clinical presentation of an incomplete rupture depends on the hemodynamic state of the patient. Cardiogenic shock is common. Findings of acute mitral insufficiency and rapidly developing pulmonary edema are usually predominant. A loud, harsh diastolic murmur with frank left heart failure suggests acute aortic insufficiency. If the patient is in a low output state, the associated thrills and murmurs of aortic or mitral insufficiency may not be appreciated. The signs and symptoms of tricuspid insufficiency that follow a rupture of that valve may be less dramatic or even minimal. Examination may reveal only a diastolic murmur and prominent V waves of the jugular venous pulsations.

Patients with isolated septal defects may have minimal symptoms of exertional dyspnea or severe progressive shock and pulmonary edema, depending on the size and location of the defect. Dysrhythmias and conduction defects are rare because the lower muscular septum is principally involved. The typical holosystolic murmur along the left sternal border is an important clue in diagnosing a ventricular septal defect, but it may not appear for days or months after the injury. Serial echocardiography and ultimately cardiac catheterization for both valvular and septal defects are necessary for a definitive diagnosis.

Management

The therapy selected depends primarily on how well the patient tolerates the insult. Many years may elapse before operative treatment is required. In cases of ventricular septal defects, a period of observation is valuable because there have been reports of the spontaneous closure of traumatic ventricular septal defects months after the injury when the defects and resultant shunt are small. Medical therapy commonly relieves the symptoms of congestive failure, but intractable or progressive heart failure or the development of pulmonary hypertension usually indicates the need for surgery.

Epidemiology

The reported incidence of acute pericardial tamponade is approximately 2% in patients with penetrating trauma to the chest and upper abdomen; it is rarely seen after blunt chest trauma. It occurs more commonly with stab wounds than with gunshot wounds, and 60 to 80% of patients with stab wounds involving the heart develop tamponade.⁸⁹ Patients with acute pericardial tamponade can deteriorate in minutes, but many can be saved if proper steps are taken.

Anatomy and Pathophysiology

The primary feature of a pericardial tamponade is an increase in intrapericardial pressure and volume. As the volume of the pericardial fluid encroaches on the capacity of the atria and ventricles to fill adequately, ventricular filling is mechanically limited, and thus the stroke volume is reduced. This results in decreased cardiac output and ultimately diminished arterial systolic blood pressure and decreased pulse pressure. As little as 60 to 100 mL of blood and clots in the pericardium may produce the clinical picture of tamponade. Concomitantly, CVP rises because of the mechanical backup of blood into the vena cava.

Several compensatory mechanisms then occur. The heart rate and total peripheral resistance rise in an attempt to maintain adequate cardiac output and blood pressure. A less effective compensatory response, resulting in a greater rise in CVP, is an increase in venomotor tone caused by contractions of the smooth muscles within the wall of the vena cava.

The diagnosis of pericardial tamponade should be suspected in any patient who has sustained a penetrating wound or blunt trauma to the thorax or upper abdomen. One is never certain of the trajectory of the bullet or the length, force, and direction of a knife thrust on initial evaluation. Obviously, wounds directly over the precordium and epigastrium are more likely to produce a cardiac injury resulting in tamponade than those in the posterior or lateral thorax. Nevertheless, it is assumed that a penetrating wound, particularly a gunshot wound, anywhere in the thorax or upper abdomen may have injured the heart. Rapid bedside echocardiography, performed as part of the standard FAST examination, easily detects a pericardial effusion causing cardiac tamponade.91,92

Clinical Features

Patients with cardiac tamponade may initially appear deceptively stable if the rate of bleeding into the pericardial space is slow or if the pericardial wound allows intermittent decompression. Other patients may complain primarily of difficulty breathing, which suggests pulmonary rather than cardiac pathology.

The physical findings of pericardial tamponade are hypotension, distended neck veins, and, rarely, distant or muffled heart tones.⁹³ This so-called Beck’s triad is sometimes difficult to demonstrate clinically, especially in the midst of a major resuscitation with concomitant hypovolemia, when the neck veins may be flat.⁹¹ Although the most reliable signs of pericardial tamponade are an elevated CVP (>15 cm H₂O) in association with hypotension and tachycardia, bedside echocardiography performed as part of the FAST examination rapidly identifies pericardial tamponade and has largely replaced the use of CVP measurements to make the diagnosis. Echocardiography also distinguishes pericardial tamponade versus tension pneumothorax when the triad of elevated CVP, hypotension, and tachycardia is present.

Acute pericardial tamponade may be seen with three distinct clinical pictures. If the hemorrhage is confined to the pericardial space, the patient is initially normotensive but will have a tachycardia and elevated CVP. If untreated, most of these patients go on to develop hypotension. If significant hemorrhage has occurred outside the pericardial sac, either through a tear in the pericardium or from associated trauma, the clinical picture is that of hypovolemic shock with hypotension, tachycardia, and a low CVP. If the CVP rises to a level of 15 to 20 cm H₂O with volume replacement and hypotension and tachycardia persist, the presence of a pericardial tamponade is considered. Also considered are other causes, such as a tension pneumothorax, Valsalva maneuver, or pulmonary edema secondary to fluid overload.

The third clinical picture is that of an intermittently decompressing tamponade. In this case, intermittent hemorrhage from the intrapericardial space occurs, decompressing and partially relieving the tamponade. The clinical picture may wax and wane depending on the intrapericardial pressure and volume and total blood loss. In general, this condition is compatible with a longer survival than are the first two clinical presentations.

Pulsus paradoxus is defined as an excessive drop in systolic blood pressure during the inspiratory phase of the normal respiratory cycle. This sign may be an additional clue to the presence of pericardial tamponade, but it is often difficult to measure during an intensive resuscitation or in the presence of shock.

Diagnostic Strategies

Management

Prognosis

After penetrating wounds to the heart, several factors adversely affect survival, including gunshot wound mechanisms and wounds that involve the left ventricle, multiple cardiac chambers, intrapericardial great vessels, or one or more coronary arteries. The factors favorable to survival include stab wound mechanisms with minor perforations, isolated right ventricular wounds, a systolic blood pressure greater than 50 mm Hg on arrival at the ED, and the presence of cardiac tamponade.

Survival rates after EDT have been correlated with the mechanism and location of injury, field and transport times, the duration of arrest, and the physiologic status of the patient in the out-of-hospital and hospital settings. Although reported survival rates after EDT vary widely, they are consistently higher in victims with isolated cardiac injuries secondary to stab wounds versus gunshot wounds.99–102,104

A meta-analysis of the literature found that EDT had an overall survival rate of 7.4%, with normal neurologic outcomes noted in 92.4% of surviving patients. Survival rates according to mechanism of injury were 9% for penetrating injuries and 1% for blunt injuries. When penetrating injuries were further separated, the survival rates were 17% for stab wounds and 4% for gunshot wounds. The presence of pericardial tamponade is a favorable prognostic finding.105,106

Epidemiology

Blunt aortic injury is a life-threatening injury, usually resulting from sudden deceleration, usually from automobile crashes. Other mechanisms of injury include pedestrians struck by automobiles, motorcycle crashes, airplane crashes, and falls from heights.¹⁰⁷ In an analysis of automobile crash data, the impact was most often head-on (72%), followed by side impact (24%) and rear impact (4%).¹⁰⁸ Despite the improvement in and increased use of restraint systems, the overall incidence of blunt aortic injury associated with fatal automobile crashes has remained unchanged over the past decade.¹⁰⁹

Blunt aortic injury includes a spectrum of lesions, ranging from a small intimal tear to frank rupture, which usually cause rapid lethal hemorrhage. The most common sites of injury are the aortic isthmus and the ascending aorta just proximal to the origin of the brachiocephalic vessels.¹⁰⁷ Sixty percent to 90% of patients with blunt aortic injury die at the site of accident or within hours of hospital admission.^109,110 However, an increasing number of patients arrive at a treatment facility because of improvement in out-of-hospital care, more aggressive resuscitation in the field, and rapid transportation to a trauma center. The early survival rate of such patients depends on the initial resuscitation and/or the timeliness and correct choice of the diagnostic procedures. A rapid and accurate diagnosis is thus mandatory to optimize treatment and maximize patient survival.

Anatomy and Pathophysiology

Blunt aortic injury encompasses various histologic lesions. Minor blunt aortic injuries (grade 1, intramural hematoma or limited intimal flap) and major blunt aortic injuries (grade 2, subadventitial rupture or modification of the geometric shape of the aorta; and grade 3, aortic transection with active bleeding or aortic obstruction with ischemia) can be differentiated by TEE. Whereas minor blunt aortic injuries appear to have a good prognosis, major blunt aortic injuries involve the entire depth of both the intimal and the medial layers and may lead to adventitial rupture, resulting in sudden death at the scene of the accident or during the first hours of hospitalization.¹¹¹

Several theories about the mechanism of aortic rupture have predominated in the literature. The descending thoracic aorta is relatively fixed and immobile because of its tethering by intercostal arteries and the ligamentum arteriosum. With sudden deceleration, the more mobile aortic arch swings forward, producing a shearing force or “whiplash effect” on the aorta at the isthmus. A bending stress at the isthmus, created by sudden lateral oblique chest compression, may also result in rupture by causing flexion of the aortic arch on the left mainstem bronchus and the pulmonary artery. It has been suggested that the forces created by the whiplash effect or lateral oblique compression may not be sufficient to provoke aortic tears. It is now postulated that those injuries may be caused by inferior and posterior rotation of anterior thoracic osseous structures (manubrium, first rib, and medial clavicles), pinching and shearing the interposed aorta as they strike the vertebral column.

Rupture of the ascending aorta just distal to the aortic valve likely occurs through a different mechanism. At the time of rapid deceleration and chest compression, the heart is displaced into the left posterior chest, which causes a shearing stress just above the aortic valve. A sudden increase in intra-aortic pressure, “the waterhammer effect,” may also cause an explosive rupture of the aorta at this location. Involvement of the coronary ostia with coronary artery occlusion may occur in association with tears to the ascending arch. The intraluminal pressure tolerance of the aorta may be exceeded in a high-speed motor vehicle crash. It is likely that a combination of the preceding mechanisms accounts for the multiple aortic ruptures that have been found in 20% of traffic accident victims examined at autopsy.¹⁰⁹

A total of 80 to 90% of aortic tears occur in the descending aorta at the isthmus, just distal to the left subclavian artery (Fig. 45-20).^107,110,111 Less common sites of involvement are the ascending aorta, the distal descending aorta at the level of the diaphragm, the midthoracic descending aorta, and the origin of the left subclavian artery. Although ruptures of the ascending aorta are much less common than those of the descending aorta, they have a 70 to 80% incidence of associated lethal cardiac injuries. This is in contrast to ruptures at the isthmus, which have a 25% incidence of associated cardiac injuries. Lethal cardiac injuries commonly include pericardial tamponade, aortic valve tears, myocardial contusion, or coronary artery injuries. Passenger ejection, pedestrian impact, severe falls, and crush injuries commonly result in ascending thoracic aortic ruptures. Survival long enough to be evaluated in the ED is rare among patients who sustain an ascending aortic rupture.¹¹¹

Aortic rupture may occur from causes other than high-speed MVC deceleration. Rupture has been documented as a complication of external cardiac massage and has been known to occur after fracture-dislocations of the thoracic spine, presumably as a result of direct shearing force. Vertical deceleration injuries resulting from falls can cause a rupture of the ascending aorta by producing an acute lengthening of the ascending aorta. This is the likely mechanism responsible for aortic rupture in the setting of airplane and elevator accidents. Direct kicks by animals, crush injuries, sudden burial by landslide, and air bag deployment have also been reported as causes of aortic rupture. Direct compression of the compliant thorax has been postulated to contribute to aortic rupture in children. Displaced fractures of the sternum, ribs, and clavicle have also been shown to directly lacerate the aorta.

Clinical Features

The possibility of aortic disruption is considered in every patient who sustains a severe deceleration injury, because approximately 30% of surviving patients with blunt aortic injury will die within the first 24 hours without treatment.¹¹² This is especially true if the automobile was moving in excess of 45 mph or if there is evidence of severe blunt force to the chest (e.g., from a damaged steering wheel).¹⁰⁹ In the case of any moderate- or high-speed motor vehicle accident, it is imperative that paramedics carefully evaluate the extent of damage to the vehicle, the complaints of the victims, and the physical manifestations of blunt chest trauma. This information should be promptly relayed to the emergency physician.

Despite the severe nature of the injury, the clinical manifestations of an aortic rupture are often deceptively meager. Associated pulmonary, neurologic, orthopedic, facial, and abdominal injuries are commonly present. Coexisting injuries can mask the signs and symptoms of an aortic injury or divert the physician’s attention away from the more lethal aortic rupture. The absence of any external evidence of a chest injury does not eliminate the possibility of an aortic tear. One third to one half of patients reported in the literature have no external signs of chest trauma.107,111

The most common symptom is interscapular or retrosternal pain. It is often found in nontraumatic aortic dissection but is present in only 25% of patients with a traumatic aortic disruption. Other symptoms described in the literature but uncommonly present include dyspnea resulting from tracheal compression and deviation, stridor or hoarseness caused by compression of the laryngeal nerve, dysphagia caused by esophageal compression, and extremity pain caused by ischemia from decreased arterial flow.

Clinical signs are uncommon and nonspecific. Generalized hypertension, when present, may be an important clinical sign. Sympathetic afferent nerve fibers, located in the area of the aortic isthmus, are capable of causing reflex hypertension as a response to a stretching stimulus. A less common clinical finding is the acute onset of upper extremity hypertension, along with absent or diminished femoral pulses. This pseudocoarctation syndrome has been reported to occur in up to one third of these patients and is attributed to compression of the aortic lumen by a periaortic hematoma.

The presence of a harsh systolic murmur over the precordium or posterior interscapular area may be heard in up to one third of patients. The murmur is thought to result from the turbulent flow across the area of transection. A less commonly encountered physical finding is a swelling at the base of the neck caused by the extravasation of blood from the mediastinum, which results in an increased neck circumference or a pulsatile neck mass. Other clinical signs suggestive of aortic rupture include lower extremity pulse deficit and lower extremity paralysis. Initial chest tube placement output in excess of 750 mL is also suggestive of aortic rupture, especially if the hemothorax is left sided. However, the physical examination is neither sensitive nor specific for aortic injury, preventing accurate diagnosis without ancillary studies.

Diagnostic Strategies

Management

Surgical Techniques

Many surgical techniques have been described since the first successful repair by Passaro and Pace in 1959.¹³¹ In those patients who survive operative repair, paraplegia from spinal cord ischemia has been a significant complication, traditionally affecting as many as 10 to 20% of such patients.^132,133 The major variable thought to be related to spinal cord ischemia and subsequent development of paraplegia has been aortic cross-clamp times.¹³⁴ Blunt aortic injury ranges from a simple tear (usually distal to the origin of the subclavian artery) to complex injuries involving the proximal aorta and branch vessels.

Many surgeons have reported the use of cardiopulmonary bypass techniques in surgical repair to allow for distal spinal cord perfusion with significantly reduced incidence of paraplegia.135,136 This is especially true for patients with complex aortic injuries, for which the aortic cross-clamp times are typically prolonged.¹³⁰

The pathologic condition found dictates the type of repair. A synthetic graft is often required because of extensive tension on the vessel walls or jagged torn ends of the vessel. Data on successful primary repair of aortic disruption are encouraging. The procedure requires less operative time and has a lower potential infection risk, blood loss through a prosthesis is avoided, the possibility of pseudoaneurysm formation is eliminated, and secondary embolism arising from mural thrombosis is avoided. Multiple tears of the descending thoracic aorta have been successfully repaired with the primary suture technique. Direct end-to-end anastomosis appears to be most feasible in the younger population.

For patients who arrive at the hospital alive but who have descending thoracic aortic injuries, the incidence of mortality during surgery ranges from 20 to 30%, and the paraplegia rate is 5 to 7%.132,135,136 Younger patients have the highest survival rate. Mortality is related to the presence or absence of extensive dissection and to the preoperative condition of the patient.

Endovascular Repair

There is a growing body of evidence demonstrating the safety and efficacy of endovascular repair of traumatic aortic tears.137–141 This involves the use of a stent placed through a femoral or iliac artery approach. Preliminary data indicate that success rates and complication rates are comparable if not better than those of traditional open surgical repairs and that the risk of major surgery and subsequent paraplegia from prolonged aortic clamping is significantly reduced with endovascular repair.¹⁴² Emerging literature suggests that endovascular repair with stenting is replacing open repair as the treatment of choice for blunt aortic injury (see Fig. 45-26).^143–148

Iatrogenic

Most esophageal perforations are iatrogenic, most commonly as a complication of instrumentation (59% of all patients).¹⁵² The rigid endoscope is the most common offender, particularly when general anesthesia is used. Although use of the flexible endoscope has made this complication less likely, the total number of perforations has increased as more procedures are performed. Injuries tend to occur near either the cricopharynx or the cervical esophagus as the endoscope is inserted.¹⁵² Endoscopic procedures that are too vigorous in the presence of a corrosive burn or carcinoma are also a common cause of iatrogenic esophageal injury.

Esophageal dilation performed for benign or malignant strictures of the esophagus is the second most common iatrogenic cause of esophageal perforations.¹⁵³ Increasing the dilator size too rapidly during these procedures may lead to perforation. The preexisting fibrotic process that resulted in the stricture tends to scar the surrounding mediastinal tissues, however, limiting free access to the mediastinum provided by many other perforations. In the ED, nasotracheal or nasogastric intubations are the most common causes of iatrogenic perforation, with the perforation usually occurring in the pyriform sinus. In a closed claims analysis published in 1999, esophageal injuries by anesthesiologists were overwhelmingly associated with difficult intubations.¹⁵⁴ Risk factors for a difficult airway include obesity, cervical arthritis, haste, and improper muscle relaxation. Claims involving airways that were classified as “nondifficult” involved other esophageal instrumentation, such as a nasogastric tube, esophageal dilator, or esophageal stethoscope. In all cases, esophageal injuries were more severe than any other type of airway injury sustained during airway maneuvers.

The use of an esophageal obturator airway was also associated with occasional esophageal trauma, specifically midesophageal perforation. Use of the esophageal obturator airway’s successors, the laryngotracheal Combitube and the King airway, do not seem to be associated with trauma more severe than occasional esophageal abrasions or contusions.¹⁵⁵

Several cases of esophageal rupture secondary to compressed air have been reported, including two cases of pharyngoesophageal perforation secondary to gas in carbonated beverages and in tartaric acid–sodium bicarbonate mixtures administered to treat esophageal food impactions. Esophageal perforation has also been caused by placement of a cervical fixation device and secondary to the Heimlich maneuver.

Foreign Bodies

Foreign bodies can cause an esophageal injury by direct laceration, by pressure necrosis, or during endoscopic removal.¹⁵⁶ Small perforations tend to seal without sequelae, but pressure necrosis or lacerating injuries provide ample access to the mediastinum.¹⁵³ Foreign bodies usually lodge in the cervical esophagus, but if a distal stricture is present, this too is a common site. In children younger than 4 years, the cricopharyngeal narrowing is the usual point of foreign body impaction. After age 4 years, most objects pass this region and traverse the remaining normal esophagus. In adults, a foreign body impaction, especially in cases of repeated episodes, raises the possibility of a stricture and warrants further investigation.

In elderly patients, foreign bodies commonly enter the esophagus because of a loss of oral tactile sensation resulting from intoxication or a poorly fitting set of dentures.¹⁵² Inadequate dentures may also lead to the swallowing of large pieces of poorly chewed food. Other esophageal foreign bodies include sharp fish or chicken bones and corn chips that may impale the esophageal wall leading to eventual leakage.

Caustic Burns

Caustic burns of the esophagus occur from intentional or accidental ingestion of acid or alkali. There are two peaks of incidence: 1 to 5 years of age, when ingestion is usually of a small amount of material and accidental, and in the teens and 20s, when larger quantities are ingested during suicide attempts. Symptoms include hematemesis, respiratory distress, vomiting, drooling, or the presence of oropharyngeal lesions on physical examination.¹⁵⁷ Perforation usually occurs during the latent granulation stage of the disease, approximately 4 to 14 days after ingestion.

The liquefaction necrosis classically resulting from strong alkali burns (pH >12) is more likely to cause esophageal perforation than the coagulation necrosis resulting from strong acid burns (pH <2). Individuals ingesting alkali substances with a pH less than 11.5 rarely sustain injuries more serious than superficial mucosal burns. Acid ingestions cause damage more frequently in the stomach than in the esophagus.¹⁵⁷

In treating a patient who has ingested a caustic substance, decontamination should involve only the rinsing of the mouth. Dilution of the substance with milk or water has been suggested; however, further liquid ingestion should be avoided if there is suspicion of perforation. Emesis, gastric lavage, and charcoal should be avoided.¹⁵⁴

Endoscopy within the first 6 to 18 hours may be used to determine the extent of the injury and to guide therapy. Antibiotics are reserved for patients with evidence of perforation, and steroids are suggested by some authors if the burns are circumferential or transmural. Other authors have shown that in the setting of large alkali ingestions, corticosteroids not only did not prevent the formation of esophageal stenosis but also increased the risk of other complications.¹⁵⁷

Although admission after significant ingestion is the rule, some authors suggest that in the setting of accidental ingestion in children and in the absence of symptoms, endoscopy and admission may not be indicated.158,159 Esophagoscopy is commonly undertaken to ascertain the presence or absence of esophageal injury. Advancing the esophagoscope beyond the first burn in the esophagus increases the risk of perforation and is a common iatrogenic cause of esophageal perforation.

Penetrating and Blunt Trauma

Because of its well-protected position posteriorly, esophageal trauma occurs in approximately 5% of patients with injuries to the neck, but only 1% of blunt trauma victims, and it is usually not an isolated injury.¹⁵² Cervical esophageal injuries are the most common because of a lack of protection by the bony thorax, and the trachea is the most common associated site of injury.¹⁵² In some cases, the esophageal injury may be overlooked initially because of the dramatic presentation of a patient with a tracheal injury.

Typical symptoms seen in cervical esophageal injuries include neck pain, dysphagia, cough, voice changes, and hematemesis. Physical findings may include neck tenderness, resistance to flexion, crepitus, or stridor.152,158 In one large series, the most common life-threatening problem in the ED was compromise of the airway. Most of these cases were handled with rapid sequence intubation, but a significant number (12%) of patients required cricothyroidotomy.¹⁵²

If the patient’s condition is stable, a preoperative esophagogram with a water-soluble agent should precede any endoscopy. Although chest and neck radiograph and CT also may be used to diagnose this injury, emergent bedside flexible endoscopy seems to be the test of choice to confirm negative findings on esophagography (especially in the setting of penetrating trauma).¹⁶⁰ Operative repair is indicated in most of these injuries (>90%) and should be done as quickly as possible to avoid the development of fistulae, mediastinitis, or abscess formation.¹⁵⁸

Blunt traumatic injuries to the esophagus occur much less often than penetrating injuries. The pathophysiology and prognosis of blunt injuries to the esophagus are similar to those of spontaneous rupture or emesis. In some cases, rupture of the cervical esophagus has been reported in association with cervical spine fracture.¹⁶¹

Spontaneous Rupture

Spontaneous esophageal rupture, postemetic rupture, and Boerhaave’s syndrome are synonymous terms. This esophageal injury is associated with a poor prognosis because the forces required to rupture the esophagus result in almost instantaneous and massive mediastinal contamination. The distal esophagus is the usual site of injury, with a longitudinal tear occurring in the left posterolateral aspect. More than 80% of these injuries occur in middle-aged men who have ingested alcohol and large meals.

In vitro, a tear similar to that seen in cases of Boerhaave’s syndrome requires a force of 3 to 6 psi, which may be generated in vivo by gastric pressure caused by the reverse peristalsis (seen with emesis) pushing against a closed cricopharyngeal muscle. The role of preexisting gastrointestinal disease in spontaneous rupture of the esophagus is unclear. Some authors emphasize its importance, whereas others report that 80% of esophageal ruptures occur in a previously normal esophagus.¹⁶⁰ Less pressure is required to perforate a diseased esophagus. Approximately 25% of patients with Boerhaave’s syndrome have no history of emesis.¹⁵² Increases in intra-abdominal pressure resulting from blunt trauma, seizures, childbirth, laughing, straining at stool, and heavy lifting have all been reported to cause this injury.

1. Mediastinal air with or without subcutaneous emphysema

2. Left-sided pleural effusion

3. Pneumothorax

4. Widened mediastinum