Thoracic Trauma

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Chapter 45

Thoracic Trauma


Thoracic injury directly accounts for 20 to 25% of deaths from trauma, resulting in more than 16,000 deaths annually in the United States. The most common cause of injuries leading to accidental death in the United States is motor vehicle collisions (MVCs) in which immediate deaths are often caused by rupture of the myocardial wall or the thoracic aorta. Early deaths (within the first 30 minutes to 3 hours) resulting from thoracic trauma are often preventable. Causes of these include tension pneumothorax, cardiac tamponade, airway obstruction, and uncontrolled hemorrhage. Because these problems are often reversible or may be temporized nonoperatively, it is vital that emergency physicians be thoroughly familiar with their pathophysiology, clinical presentation, diagnosis, and treatment.1

Approximately 75% of patients with thoracic trauma can be managed expectantly with simple tube thoracostomy and volume resuscitation. Therefore initial care and disposition of these patients is usually performed by emergency physicians. Definitive care of these patients is often multidisciplinary in nature, involving trauma surgeons, cardiothoracic surgeons, and intensivists. Improvement in the understanding of the underlying physiologic mechanisms involved, the advancement of newer imaging modalities, minimally invasive approaches, and pharmacologic therapy contribute to decreasing the morbidity and mortality of these injured patients. The role of multidetector helical computed tomography (CT) scanning in the evaluation of trauma patients continues to expand. Although CT scans provide much greater diagnostic sensitivity than plain radiography, the precise indications for CT scanning in trauma patients remain unclear. Concerns regarding cost, contrast-induced nephrotoxicity, and cumulative radiation exposure to the thorax have been mounting.2

Injuries to the lung parenchyma are common in severely injured patients and include contusion, laceration, and hematoma.1 Hemothorax and pneumothorax are also common injuries in patients with thoracic trauma. Treatment of these injuries has changed during the past decade primarily because of advances in diagnostic imaging techniques and an increased understanding of the pathophysiology.

Chest Wall Injury


Among victims sustaining thoracic trauma, approximately 50% will have chest wall injury: 10% minor, 35% major, and 5% flail chest injuries.1 Chest wall injuries are not always obvious and can easily be overlooked during the initial evaluation.

Rib Fracture


Simple rib fractures are the most common form of significant chest injury, accounting for more than half the cases of blunt trauma.1 The susceptibility to rib fracture increases with age. The importance of this injury is not the fracture itself but rather the associated potential complications, particularly pneumothorax, hemothorax, pulmonary contusions, and post-traumatic pneumonia. Rib fractures in children signify serious trauma to the thorax and have a high incidence of underlying injury.

Anatomy and Pathophysiology

Ribs usually break at the point of impact or at the posterior angle or posterolateral area, which is structurally the weakest area. The fourth through ninth ribs are most commonly involved. Ribs 1 to 3 are relatively protected, and ribs 9 to 12 are more mobile at the anterior end. This confers the relative resistance to fracture of the “high” and “low” ribs. Fractures occur more commonly in adults than in children, and this is attributed to the relative inelasticity of the older chest wall compared with the more compliant chest wall in children.

The true danger of rib fracture involves not the rib itself but the potential for penetrating injury to the pleura, lung, liver, or spleen. Fractures of ribs 9 to 11 are associated with intra-abdominal injury. Patients with right-sided rib fractures are almost three times more likely to have a hepatic injury, and patients with left-sided rib fractures are almost four times more likely to have a splenic injury.3 Fractures of ribs 1 to 3 may indicate severe intrathoracic injury. The presence of two or more rib fractures at any level is associated with a higher incidence of internal injuries. Elderly patients with multiple rib fractures have a greater incidence of pneumonia and a higher mortality compared with patients younger than age 65 years.46 To prevent a minor injury from developing into a serious complication, these fractures should be diagnosed rapidly and treated expectantly.

Diagnostic Strategies

Although clinical impression and physical findings are sensitive, they are not specific and are therefore unreliable for making an accurate diagnosis. Chest x-ray films often do not demonstrate the presence of rib fractures but are of greatest value in suggesting significant intrathoracic and mediastinal injuries. Although the upright posteroanterior chest radiograph has a higher yield in detecting rib fractures or their complications compared with other views, CT scans are significantly more effective than chest x-ray examination in detecting rib fractures (Fig. 45-1).7 Rib series and expiratory, oblique, and cone-down views should not be used routinely. However, if simple rib fractures are strongly suspected or recognized on a clinical basis, there is no need to routinely obtain a CT scan unless other intrathoracic pathology needs to be studied.

Nonetheless, x-ray studies are often ordered, even though 50% of single-rib fractures are not seen on the initial x-ray film. A CT scan should be considered based on the mechanism of injury, physical examination, hemodynamic and respiratory parameters, abnormal findings on chest x-ray examination (especially widened mediastinum), or clinical evidence of multiple rib fractures, especially of the lower ribs (which may herald a splenic or hepatic injury).


Treatment of patients with acute rib fractures is based on adequate pain relief and the maintenance of pulmonary function. Oral pain medications are usually sufficient for young and healthy patients. Continuing daily activities and deep breathing should be stressed to ensure ventilation and prevent atelectasis. It is helpful to advise patients to take their pain medications and wait 30 to 45 minutes before performing deep breathing exercises, perhaps with an incentive spirometer. Pain relief should be effective or patients will not maintain activity. Binders, belts, and other restrictive devices should not be used because although they can decrease pain, they also promote hypoventilation with subsequent atelectasis and pneumonia.

The greater the number of fractured ribs, the higher the mortality and morbidity rates. Patients with three or more fractured ribs, despite the lack of other traumatic injuries, should likely be hospitalized to receive aggressive pulmonary therapy and appropriate effective analgesia. Elderly patients with six or more fractured ribs should be treated in intensive care units owing to high morbidity and mortality. Older patients will probably require narcotic preparations, but care should be taken to avoid oversedation because of the potential for respiratory failure.8

Multiple rib fractures in trauma patients are associated with significant morbidity and mortality. Intercostal nerve blocks with a long-acting anesthetic such as bupivacaine with epinephrine may relieve symptoms up to 12 hours with excellent results. Such nerve blocks are achieved by administration of 1 or 2% lidocaine or 0.25% bupivacaine along the inferior rib margin several centimeters posterior to the site of the fracture. One rib above and one rib below the fractured rib should also be blocked for optimal analgesia. Other alternatives for hospitalized patients include patient-controlled analgesia, parenteral opiates, and thoracic epidural analgesia.9

Sternal Fracture

Anatomy and Pathophysiology

Sternal fracture usually results from the diagonal strap of a seat belt restraining the upper part of the sternum. During rapid deceleration from a frontal impact, the forward thrust of the body against the fixed seat belt across the sternum results in a fracture at that location. The location of the sternal fracture varies depending on the position of the belt, patient size, the magnitude of the impact, and the vector of the forces.

Similarly, depending on patient age, the likelihood of sternal fracture is variable. In general, sternal fractures are more common in older patients than in younger patients, and they are slightly more common in women than in men. It is believed that the more elastic and pliable chest wall of younger people allows more efficient transmission of kinetic energy to the underlying mediastinum. Although skeletal injury is less likely to occur in younger patients, damage to soft tissue structures underneath is greater. In older patients, the energy of impact is dissipated in the sternum, resulting in fewer intrathoracic injuries but a higher frequency of sternal fractures. Multiple rib fractures and lung contusion are concomitant injuries in more than 10% of diagnosed sternal fractures.

The natural history of a nondisplaced sternal fracture is contrary to intuition. It had been thought that the magnitude of the forces required to fracture the sternum must be associated with significant trauma to the mediastinal structures. However, isolated sternal fractures are relatively benign, with low mortality (<1%) and low intrathoracic morbidity.11

Cardiac complications, such as myocardial contusion, occur in 1.5 to 6% of cases. There is no association between sternal fracture and aortic rupture. Spinal fractures are seen in less than 10% of cases and rib fractures in 21%.12 Although sternal fractures may occur in the context of major blunt chest trauma, the presence of a sternal fracture does not imply other major life-threatening conditions. However, associated mediastinal injuries should be considered.

Mediastinal hematomas, whether or not they are related to aortic injuries, can be life-threatening. The dual problem of acute blood loss and sudden alterations in cardiopulmonary physiology can result in hemodynamic deterioration. In addition to circulatory collapse from exsanguination, mediastinal hematomas can cause death from compression of adjacent structures.

Diagnostic Strategies

Most sternal fractures are transverse, and a lateral radiographic view is often diagnostic. These fractures can be missed radiographically because a lateral plain chest x-ray film is not usually obtained during the initial trauma evaluation. Furthermore, plain films are sometimes inconclusive. Even if the sternal fracture is diagnosed by plain radiographs, the extent of the injury is often underappreciated. The advent of helical CT, especially with three-dimensional images of the skeletal system, has resulted in markedly improved diagnosis of sternal fractures. Emerging literature suggests that ultrasound (US) may be more sensitive than plain radiography.13

Although most nondisplaced sternal fractures are not associated with significant intrathoracic injuries, a conservative approach is to obtain a chest CT scan to rule out any other pathology. This may be clinically important in determining the best management of the sternal fracture in terms of conservative management versus surgical fixation.14 Chest CT also helps to rule out any associated mediastinal injuries. A 12-lead electrocardiogram (ECG) should also be obtained during the initial evaluation.

Flail Chest

Anatomy and Pathophysiology

Flail chest results when three or more adjacent ribs are fractured at two points, allowing a freely moving segment of the chest wall to move in paradoxical motion (Fig. 45-2). It can also occur with costochondral separation or vertical sternal fracture in combination with rib fractures. Because of its common association with pulmonary contusion, it is one of the most serious chest wall injuries (Fig. 45-3).

The physiology of respiration is adversely affected by flail chest in a number of ways. The paradoxical motion of the chest wall is the hallmark of this condition, with the flail segment moving inward with inspiration and outward with expiration. Underlying pulmonary contusion is considered to be the major cause of respiratory insufficiency with flail chest. In addition, the pain of the injury causes muscular splinting with resultant atelectasis, hypoxemia, and decreased cardiac output.


Out-of-hospital or emergency department (ED) stabilization of the flail segment by positioning the person with the injured side down or placing a sandbag on the affected segments has been abandoned. These interventions actually inhibit expansion of the chest and increase atelectasis of the injured lung. Oxygen should be administered, cardiac and oximetry monitors applied if available, and the patient observed for signs of an associated injury such as tension pneumothorax. A 12-lead ECG and cardiac enzymes should be obtained, with consideration given to obtaining an echocardiogram for significant dysrhythmias, high-grade blocks, or hemodynamic instability unexplained by other causes such as hemorrhage.

The outcome of flail chest injury is a function of associated injuries. Because many different physiologic mechanisms have been implicated in flail chest, there is no consensus about hospital treatment. The cornerstones of therapy include aggressive pulmonary physiotherapy, effective analgesia, selective use of endotracheal intubation and mechanical ventilation, and close observation for respiratory compromise.

Respiratory decompensation is the primary indication for endotracheal intubation and mechanical ventilation for patients with flail chest. Obvious problems, such as hemopneumothorax or severe pain, should be corrected before intubation and ventilation are presumed necessary. In fact, in the awake and cooperative patient, noninvasive continuous positive airway pressure (CPAP) by mask may obviate the need for intubation.16 In general, the most conservative methods for maintaining adequate oxygenation and preventing complications should be used. Adequate analgesia is of paramount importance in patient recovery and may contribute to the return of normal respiratory mechanics.

Patients without respiratory compromise generally do well without ventilatory assistance. Several studies have found that patients treated with intercostal nerve blocks or high segmental epidural analgesia, oxygen, intensive chest physiotherapy, careful fluid management, and CPAP, with intubation reserved for patients in whom this therapy fails, have shorter hospital courses, fewer complications, and lower mortality rates.17 Avoidance of endotracheal intubation, particularly prolonged intubation, is important in preventing pulmonary morbidity because intubation increases the risk of pneumonia.18

There is also evidence that early operative internal fixation of the flail segment results in a speedier recovery, decreased complications, and better cosmetic and functional results, and that it is cost-effective. Indications for open fixation for flail chest include patients who are unable to be weaned from the ventilator secondary to the mechanics of flail chest, persistent pain, severe chest wall instability, and a progressive decline in pulmonary functions.15,19

The patient with flail chest should be treated in the ED as if pulmonary contusion exists regardless of whether mechanical ventilation is used. The mortality rate associated with flail chest is between 8 and 35% and is directly related to the underlying and associated injuries. However, unilateral flail chest was reported to be infrequently associated with death in one large series.20 Those who recover from flail chest may develop long-term disability with dyspnea, chronic thoracic pain, and exercise intolerance.

Nonpenetrating Ballistic Injury


Many law enforcement officers, emergency medical services personnel, and private security guards wear lightweight synthetic body armor for protection against gunshot injury. In addition, there have been a number of reports of armed robbers wearing such vests in anticipation of exchanging gunfire with police or security personnel.21 These vests are “bullet resistant” rather than “bulletproof,” depending on the weapon being used against them. They are composed of many different combinations of synthetic fibers such as Kevlar.

Another type of nonpenetrating ballistic injury is caused by rubber bullets and beanbag shotgun shells. Rubber bullets have been used for many years by police agencies throughout the world for crowd dispersal and for nonlethal use of force. Beanbag shotgun shells are nylon bags filled with pellets, which are fired from a standard shotgun. Both of these projectiles have the potential to cause serious injury despite their classification of “nonmetal” or “less-than-lethal” use of force.22


It is recommended that all victims of nonpenetrating ballistic injury be observed closely, with overnight observation considered. This is particularly true for injuries over the abdomen, where serial examinations in coordination with CT scanning will help to detect internal injuries that may manifest in a delayed manner.23 Use of protective body armor has resulted in significantly improved survival rates and has dramatically decreased the need for surgical intervention in those protected by it. In addition, “less-than-lethal“ projectiles, such as rubber bullets and beanbag shotgun shells, offer law enforcement an alternative to conventional weapons that are considered “use of deadly force.” However, the possibility of an underlying injury resulting from this form of nonpenetrating ballistic injury should not be underestimated.

Traumatic Asphyxia

Clinical Features

Traumatic asphyxia is characterized by a deep violet color of the skin of the head and neck, bilateral subconjunctival hemorrhages, petechiae, and facial edema. Stagnation develops from capillary atony and dilation, and as the blood desaturates, purplish discoloration of the skin occurs.24 Although the appearance of these patients can be quite dramatic, the condition is usually benign and self-limited if the heavy object was removed before any hypoxic complications such as anoxic encephalopathy occurred.25

Diagnostic Strategies

The clinical significance lies with the possibility of intrathoracic injury from the violent force necessary to produce traumatic asphyxia. Chest wall and pulmonary injuries are most common. If the patient’s examination and chest x-ray film show worrisome features, CT scanning of the chest should be performed.

Disturbance of vision has been attributed both to retinal hemorrhage, which is generally a permanent injury, and to retinal edema, which may cause transient changes in vision. One third of these patients lose consciousness, usually at the time of injury. Intracranial hemorrhages are rare, probably because of the shock-absorbing ability of the venous sinuses, but CT scan of the head should be done in patients with neurologic complaints. Neurologic manifestations typically clear within 24 to 48 hours, and long-term sequelae are uncommon.25

Pulmonary Injuries

Subcutaneous Emphysema

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.

Pulmonary Contusion


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

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.


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.


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).

Communicating Pneumothorax.: A communicating pneumothorax (Fig. 45-7) is associated with a defect in the chest wall and most commonly occurs in combat injuries. In the civilian sector, this injury is typically secondary to shotgun wounds. Air can sometimes be heard flowing sonorously in and out of the defect, prompting the term “sucking chest wound.” The loss of chest wall integrity causes the involved lung to paradoxically collapse on inspiration and expand slightly on expiration, forcing air in and out of the wound. This results in a large functional dead space for the normal lung and, together with the loss of ventilation of the involved lung, produces a severe ventilatory disturbance.

Tension Pneumothorax.: The progressive accumulation of air under pressure within the pleural cavity, with shift of the mediastinum to the opposite hemithorax and compression of the contralateral lung and great vessels, is the constellations of findings in tension pneumothorax (Figs. 45-8 and 45-9). It occurs when the injury acts like a one-way valve, prevents free bilateral communication with the atmosphere, and leads to a progressive increase of intrapleural pressure. Air enters on inspiration but cannot exit with expiration. The resulting shift of mediastinal contents compresses the vena cava and distorts the cavoatrial junction, leading to decreased diastolic filling of the heart and subsequent decreased cardiac output. These changes result in the rapid onset of hypoxia, acidosis, and shock.


Figure 45-9 Resolution of the tension pneumothorax shown in Figure 45-7 with placement of a left-sided tube thoracostomy.

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).7,3739

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.


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

Simple Pneumothorax.: Treatment of a simple pneumothorax depends on its cause and size. Most advocate treating a traumatic pneumothorax with a chest tube to correct any respiratory compromise; treatment with a chest tube is generally thought to be safer than observation in these patients. Small pneumothoraces (i.e., <15%), whether spontaneous or traumatic, have been treated with hospitalization and careful observation if the patient is otherwise healthy and symptom free, if the patient does not need anesthesia or positive-pressure ventilation, and the pneumothorax is not increasing in size.

Isolated apical pneumothoraces of less than 25% may be observed in patients with stab wounds. This conservative method seldom has application in multisystem trauma, and a chest tube should be inserted immediately on any signs of deterioration. Some suggest that because it is small and lacks symptoms, occult traumatic pneumothorax found only on CT scan can be managed with observation and does not need treatment. Studies indicate that these injuries can be handled as small but initially detectable pneumothoraces, with observation in hemodynamically stable patients without symptoms. The data regarding the frequency with which patients with occult pneumothorax on mechanical ventilation will require tube thoracostomy are conflicting.42–44 However, an occult pneumothorax may be observed in a stable patient even if he or she is placed on positive-pressure ventilation.44

Any moderate to large pneumothorax should be treated with a chest tube. The indications for tube thoracostomy (chest tube) are listed in Box 45-1. The preferred site for insertion is the fourth or fifth intercostal space at the midaxillary line. If the tube is positioned posteriorly and directed toward the apex, it can effectively remove both air and fluid. This lateral placement of the tube is preferred not only because it is more efficient but also because it does not produce an easily visible cosmetic defect, as does the anterior site at the second interspace at the midclavicular line. With multisystem trauma, an adequate size chest tube (36-F to 40-F in adults and 16-F to 32-F in children) should be used, particularly in cases of major trauma, when hemothorax is likely to occur.

Care is taken to be certain the vent holes along the side of the tube are all inside the chest cavity. A radiopaque line along the side of the tube with interruptions at these drainage holes helps greatly in radiographically interpreting tube position. The tube should be attached to a water seal drainage system that allows reexpansion of the pneumothorax. If there is significant air leak or a large hemothorax, the tube may be connected to a source of constant vacuum at 20 to 30 cm H2O for more rapid reexpansion.

Tube thoracostomy does have some potentially serious complications, including the formation of a hemothorax, pulmonary edema, bronchopleural fistula, pleural leaks, empyema, subcutaneous emphysema, infection, intercostal artery laceration, contralateral pneumothorax, and parenchymal injury.45–47 To reduce the incidence of empyema and pneumonitis, current recommendations include the administration of empirical antibiotics with all tube thoracostomy placements.48 Pneumothoraces that have been present for more than 3 days should be reexpanded gradually without suction to avoid reexpansion pulmonary edema.

Communicating Pneumothorax.: For a patient with a communicating pneumothorax in the out-of-hospital setting, the defect should be covered immediately, which helps convert the condition to a closed pneumothorax and eliminates the major physiologic abnormality. An occlusive dressing of petrolatum gauze can be applied, but care should be taken because this can convert the injury to a tension pneumothorax, especially in patients who are intubated and undergoing positive-pressure ventilation. The wound should never be packed because the negative pressure during inspiration can suck the dressing into the chest cavity. These considerations are not as important once the patient is in the ED, where endotracheal intubation and tube thoracostomy can be performed. Positive-pressure ventilation can then be started without the fear of producing a tension pneumothorax, and the patient can be prepared for definitive surgical repair.

Tension Pneumothorax.: When the diagnosis of tension pneumothorax is suspected clinically, the pressure should be relieved immediately with needle thoracostomy, which is performed by inserting a large-bore (14-gauge or larger) catheter, at least 5 cm in length, through the second or third interspace anteriorly or the fourth or fifth interspace laterally on the involved side. Recent studies have suggested that some catheters may not be of sufficient length to penetrate the pleural space and that the lateral approach may be preferred. This method can be easily performed in the field or ED, allowing vital signs to improve during transport or preparation for a tube thoracostomy.49

The intubated patient in the ED who is receiving positive-pressure ventilation and external cardiac compressions is at particular risk for developing tension pneumothorax. Fractured ribs from cardiopulmonary resuscitation (CPR) can penetrate lung parenchyma and cause pneumothorax. Positive-pressure ventilation then increases intrapleural pressure and produces a tension pneumothorax. The earliest sign of this complication is an increase in resistance to ventilation. If the patient has vital signs, the blood pressure will fall and the central venous pressure (CVP) will rise. Misplacement of an endotracheal tube does not result in tension pneumothorax but, rather, asymmetry of breath sounds. If tension pneumothorax is suggested, the clinician should proceed with empirical emergent therapy.



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

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).


Figure 45-12 Tension hemothorax.

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.


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

Tracheobronchial Injury

Anatomy and Pathophysiology

Tracheobronchial injuries caused by knife wounds develop almost exclusively from wounds in the cervical trachea, whereas gunshot wounds may damage the tracheobronchial tree at any point. Intrathoracic injury to the tracheobronchial tree occurs most commonly from blunt trauma. These injuries may result from direct blows, shearing stresses, or burst injury. A direct blow to the neck may crush the cervical trachea against the vertebral bodies and transect the tracheal rings or cricoid cartilage. Shear forces on the trachea will produce injury at the carina and the cricoid cartilage, which are its relatively fixed points.

Sudden deceleration of the thoracic cage, as occurs in a decelerating auto accident, pulls the lungs away from the mediastinum, producing traction on the trachea at the carina. When the elasticity of the tracheobronchial tree is exceeded, it ruptures. It has also been suggested that if the glottis is closed at the time of impact, the sudden increase in intrabronchial pressure will rupture the tracheobronchial tree. Regardless of the mechanism, more than 80% of these injuries occur within 2 cm of the carina.

Clinical Features

Massive air leak through a chest tube, hemoptysis, and subcutaneous emphysema should suggest the diagnosis of major airway damage. Subcutaneous emphysema is typically the most common physical finding.57 Auscultation of the heart may reveal Hamman’s crunch if air tracks into the mediastinum. Hamman’s crunch is a crunching, rasping sound that is synchronous with the pulse and is best heard over the precordium. It is the result of the heart beating against air-filled tissues. Patients with tracheobronchial disruption have one of two distinct clinical pictures. In the first group of patients, the wound opens into the pleural space, producing a large pneumothorax. A chest tube fails to evacuate the space and reexpand the lung, and there is continuous bubbling of air in the underwater seal device.

In the second group of patients there is complete transection of the tracheobronchial tree but little or no communication with the pleural space. A pneumothorax is usually not present. The peribronchial tissues support the airway enough to maintain respiration, but within 3 weeks granulation tissue will obstruct the lumen and produce atelectasis. These patients are relatively free of symptoms at the time of injury but weeks later have unexplained atelectasis or pneumonia. Radiographic signs in either group of patients are pneumomediastinum, extensive subcutaneous emphysema (Fig. 45-16), pneumothorax, fracture of the upper ribs (first through fifth), air surrounding the bronchus, and obstruction in the course of an air-filled bronchus.