Introduction
Multiple left rib fractures, pulmonary contusion, and hemothorax in an elderly man after a motor vehicle accident.
Transaxial, nonenhanced computed tomography scan shows a pneumothorax in a patient in whom the chest radiograph was normal.
Digital subtraction angiogram shows an arteriovenous malformation at the apex of the right lung with contribution from the right subclavian artery, the intercostal arteries (T7-10), and the right internal mammary artery. Drainage of the arteriovenous malformation was via the pulmonary circulation. (See also Images below.)
Digital subtraction angiogram shows an arteriovenous malformation at the apex of the right lung with contribution from the right subclavian artery, the intercostal arteries (T7-10), and the right internal mammary artery. Drainage of the arteriovenous malformation was via the pulmonary circulation. (See also Image above and Image below.)
Digital subtraction angiogram shows an arteriovenous malformation at the apex of the right lung with contribution from the right subclavian artery, the intercostal arteries (T7-10), and the right internal mammary artery. Drainage of the arteriovenous malformation was via the pulmonary circulation. (See also 2 Images above.)
Background
Lung trauma is an important component of thoracic injuries. Thoracic injuries have immense medical and social impact, contributing to as much as 25% of trauma-related deaths and contributing significantly to another 25% of all deaths.
Thoracic trauma is the leading cause of death, morbidity, hospitalization, and disability in Americans from 1 year of age until the middle of the fifth decade of life. Trauma is, therefore, a major national health care problem.
Most thoracic injuries are attributable to road traffic accidents. The incidence of thoracic trauma in the United States is 12 per million per day; 20-25% of deaths resulting from trauma are attributed to thoracic injury. It has been estimated that thoracic trauma is responsible for approximately 16,000 deaths per year in the United States.1,2,3,4
For excellent patient education resources, visit eMedicine's Lung and Airway Center; Back, Ribs, Neck, and Head Center; and Skin, Hair, and Nails Center. Also, see eMedicine's patient education articles Collapsed Lung, Costochondritis, Chest Pain, Puncture Wound, and Lupus (Systemic Lupus Erythematosus).
Thoracic Trauma
Pneumothorax
Cardiac Tamponade
Pathophysiology
Blunt versus penetrating trauma
Chest trauma is traditionally classified as blunt or penetrating. The trauma is classified as blunt when the chest wall remains intact; it is classified as penetrating when the integrity of the chest wall is breached. Traffic accidents (ie, steering-column injuries) are the most common cause of blunt trauma; penetrating trauma may result from stab wounds and bullet and shrapnel injuries.
Blunt trauma
Blunt trauma is more common than penetrating chest injury, accounting for more than 90% of thoracic injuries. Two mechanisms occur in blunt trauma: (1) the direct transfer of energy to the chest wall and thoracic organs, and (2) differential deceleration, experienced by the thoracic organs at the time of the impact. A direct blow to the thoracic wall produces crush and shear injury associated with fractures of soft tissues and bones, such as the ribs. Injury to the thorax in association with substantial pressure may sufficiently increase the intrathoracic pressure so as to cause rupture of gas- or fluid-filled organs.
Injury from deceleration occurs when forward motion of the thorax is abruptly stopped while the intrathoracic viscera continue to move forward, as in a steering-column injury. In deceleration injury, the visceral structures not bound to the chest wall move forward until they are halted by the inner surface of the thoracic wall in a second, internal collision or until the stresses created by the motion exceed tolerance of the tissue, causing injury.
Ribs may be fractured at the point of impact, and damage to the underlying lung may produce lung bruising or puncture. The ribs usually become fairly stable within 10 days to 2 weeks. Firm healing with callus formation is seen after about 6 weeks.
Penetrating trauma
Penetrating injury is usually the result of the abrupt, direct application of a mechanical force to a focal area. A knife or projectile, for example, produces tissue damage by stretching and crushing; injury is usually confined to tissues in the path of penetration. The severity of the internal injury depends on the organ penetrated and on how vital the organ is.
The degree of injury also depends on the biomechanics of the penetrating projectile. Factors determining the degree of injury include the efficiency with which energy is transferred from the object to the body tissues. Other factors that dictate the severity of injury include the physical characteristics of the weapon, such as its velocity, size of impact face, and deformability, and the density of the body tissues penetrated. The velocity of the penetrating projectile is the single most important factor that determines the severity of the wound.
Knives usually produce limited injury because knives are low-velocity projectiles. Knife wounds are confined to the areas that have been penetrated. Knife wounds are usually well tolerated; even in cases involving the stabbing of the heart, the patient often survives when given prompt medical attention.
Bullets are classified as high-velocity projectiles, particularly bullets that achieve velocities faster than 1800-2000 ft/s. High-velocity projectiles cause injuries of similar severity to knife wounds and tissue damage in the path of the penetrating bullet. However, unlike knives, bullets also produce injury in structures adjacent to the bullet path. They produce tissue cavitation and, by producing shock waves, extend the area of tissue damage. Thus, a bullet passing through body tissues not only damages tissues directly in its path but also causes adjacent tissues to extend outward; in doing so, the bullet expands the sphere of injury.
The outward displacement of tissues produces a temporary cavity, the diameter of which may be 20-30 times the diameter of the bullet. Thus, unlike a knife wound, high-velocity bullet wounds produce injury far beyond the flight path of the bullet. Furthermore, the subatmospheric pressure generated within the cavities produced by bullets may suck dirt and debris into the wound, thereby compromising the injury and adding to its severity.
Impalement injuries, in which a large foreign body traverses a body cavity or extremity, produce a life-threatening situation. Impalement is uncommon and is only occasionally reported in the literature. Reports of impalement injuries limited to the thorax are even less common. The heart, great vessels, lungs, and thoracic cage may be impaled. Major impalement injury may involve any part of the body, with each appearing as an anatomically distinct injury. Because the impaling object may penetrate several organs in its path, a complete assessment for life-threatening injuries is important. The cardinal rule of management is to leave the impaling object in situ while the patient is rapidly transported to an operating theater, because it may have a tamponade-like effect on damaged vascular structures. The object should be removed only in a controlled surgical environment.
Complications of lung trauma
Chest-wall injuries, such as rib fractures, may impair breathing because of associated pain. Ventilation and gas exchange may be compromised in this fashion. Direct lung injuries, such as pulmonary contusions, interfere with gas exchange because of the shunting and dead-space ventilation resulting from the presence of blood or fluid-filled alveoli and injured pulmonary microvasculature. Pneumothoraces and hemothoraces are space-occupying lesions that interfere with gas exchange primarily by compressing otherwise healthy lung parenchyma. A component of direct pulmonary parenchymal injury is frequently found with these etiologies.
Pneumothorax
A frequent complication of chest trauma is a pneumothorax, or the collection of air within the pleural cavity. The lungs are elastic organs that have an inherent tendency to collapse. The pleural space has a negative pressure compared with atmospheric pressure; because the alveolar pressure is always greater than the pleural pressure, a communication between an alveolus and the pleural space results in airflow down the pressure gradient until equilibrium occurs or until the communication is sealed. As the pneumothorax enlarges, the lung becomes smaller. The main complication of this process is a decrease in the vital capacity and in the partial pressure of oxygen. Young, healthy individuals can tolerate these changes fairly well, with minimal changes in vital signs and symptoms. However, persons with underlying lung disease may experience respiratory distress.
Pneumomediastinum
Excessive intra-alveolar pressures may lead to rupture of perivascular alveoli. Air escapes into the perivascular connective tissue, with subsequent dissection into the mediastinum, causing a pneumomediastinum. Air from a pneumomediastinum may then dissect into the visceral, retropharyngeal, and subcutaneous spaces of the neck. From the neck, the subcutaneous compartment is continuous throughout the body; thus, air may be distributed widely.
Mediastinal air may also track down into the retroperitoneum and other extraperitoneal compartments. If the mediastinal pressure rises abruptly or if decompression in not sufficient, the mediastinal parietal pleura may rupture and cause a pneumothorax (occurring in 10-18% of patients).
Hemothorax
A hemothorax accommodates approximately 40% of the total blood volume. Aspiration of large amounts of blood (>1500 mL) in the initial drainage from the chest tube suggests injury to a major vessel or cardiac rupture. This finding is an indication for thoracotomy.
Bronchial injury
Bronchial or tracheal ruptures are rare consequences of blunt injury (0.4%); they are usually caused by deceleration or in association with compression injury. A bronchial or tracheal rupture may appear as either a pneumothorax that fails to resolve or a persistent air leak through the thoracostomy tube.
Fallen lung
A partial tear or complete transection of the major airways as a result of penetrating or blunt trauma may result in fallen lung. Most of these injuries are related to high-speed road accidents. More than 80% of tracheobronchial ruptures occur within 2.5 cm of the carina.
Two basic mechanisms producing major airway disruption in blunt trauma have been implicated: The first is reflex closure of the glottis and compression of the tracheobronchial tree, causing intraluminal pressure to quickly reach a level too high for the airway to sustain. The second is deceleration injury produced by shearing forces; injury results from sudden deceleration and rotation of the lung on the relatively fixed carina.
Lung contusion
A lung contusion represents a bruise of the lung. It is usually caused by blunt trauma. Following blunt trauma, such as that produced by a deceleration or blast injury, a pressure wave compresses the thoracic cavity, injuring the underlying lung. In the young, the pliable thoracic wall usually returns to its initial state, and no rib fracture may occur despite underlying lung injury. In older individuals, rib fractures with underlying lung contusion are common.
A lung contusion is usually a combination of alveolar hemorrhage with interstitial hemorrhage and edema. Most patients have minimal respiratory deficit as a result of the injury. Extensive contusions may result in respiratory difficulty or progress to acute respiratory distress syndrome.
Lung laceration
Pulmonary lacerations are tears in the lung parenchyma. If the laceration fills with blood, a spherical hematoma forms. If it fills with air, a traumatic pneumatocele or air cyst forms. If blood and air are present, an air-fluid level may be seen.
Aortic injury
An aortic rupture is usually placed at the isthmus just distal to the left subclavian artery. Approximately 80-90% of patients with rupture of the thoracic aorta die before reaching the hospital. Surviving patients who reach the hospital may have minimal if any symptoms. After cardiovascular stabilization, emergency surgery is necessary.
Blunt cardiac injury
A variety of injuries may follow blunt trauma to the heart. These include myocardial concussion, contusion, and myocardial rupture. By virtue of their anterior position in the thorax, the right atrium and ventricle are the chambers most frequently injured. The next most commonly injured structures are the left atrium and the left ventricle. The survival rate for patients with a 1-chamber rupture is about 40%. Invariably, a 2-chamber rupture is a mortal injury.
Pericardial tamponade
Cardiac rupture, aortic disruption, or myocardial contusion without rupture may cause pericardial tamponade. The diagnosis of pericardial tamponade is usually suspected clinically when persistent hypotension cannot be explained on the basis of hemorrhage, tension pneumothorax, or hemothorax. Neck vein distention is an important physical sign, but it may be masked by the cervical collar. Urgent pericardial drainage with the patient under local anesthesia should be considered and may be curative.
Diaphragmatic rupture
Symptoms similar to a pneumothorax may develop from a diaphragmatic rupture, because lung compression may cause hypoxemia. Intubation and mechanical ventilation may be needed for adequate oxygenation. Hemothorax may be caused by a ruptured spleen.
Esophageal tears
Esophageal tears are estimated to occur in 1% of patients with blunt trauma, but they are far more common with penetrating or iatrogenic trauma. Esophageal rupture carries a high mortality rate; death occurs as a result of rapidly developing mediastinitis. Survival improves dramatically if the esophageal injury is recognized and treated within 24 hours of its occurrence.
About 82% of esophageal tears caused by blunt trauma occur in the cervical and upper thoracic esophagus. It has been postulated that compression of the esophagus between the sternum and vertebral column is the mechanism of injury. Tears may also occur in the distal esophagus just above the gastroesophageal junction along the left posterolateral wall. The mechanism of injury in this setting is probably similar to that of spontaneous rupture in Boerhaave syndrome, when esophageal pressures rise against a closed glottis.
Iatrogenic lung complications
Iatrogenic tracheal rupture is a serious complication with potentially high postoperative mortality (mortality is mostly the result of the underlying disease). Early surgical repair is a preferred treatment. The incidence of tracheobronchial rupture is lower in children than in adults, with a ratio of 1:10.
Blunt trauma is the most common cause, although tracheobronchial rupture may occur as a complication of tracheotomy or bronchoscopy. Because most patients with severe blunt or penetrating trauma are treated in an emergency setting before imaging is performed, iatrogenic injury from placement of catheters, chest tubes, endotracheal tubes, feeding tubes, pacemaker electrodes, and counter pulsation balloons is common. Simple radiologic procedures, such as chest radiography and fluoroscopy, permit diagnosis of unsuspected and clinically silent complications.
Clinically important iatrogenic trauma to the lung is associated with the increasing use of overpressure ventilation. Experimental evidence shows that for patients with interstitial emphysema, the lung may be damaged with peak pressures as low as 40 cm water. The chest radiograph may show an early pathognomonic finding of perivascular air collections. The respirator treatment should then be adjusted to avoid pneumomediastinum and pneumothorax. Follow-up chest radiography after these procedures is important.
Other lung injuries or illnesses
Iatrogenic intrathoracic trauma may occur after procedures such as lung biopsy and thoracentesis, among others. Mechanical ventilation with positive end-expiratory pressure predisposes the patient to the development of barotrauma and pneumothorax. Thoracic injuries may result from the inhalation of toxic and inert substances; blast; and radiation.
Iatrogenic trauma
Thoracostomy tubes in a traumatized patient are often placed in an emergency setting. It is common for chest tubes to be positioned improperly. The tubes may be improperly positioned in extrathoracic, intraparenchymal, mediastinal, or intrafissural locations (26-58%). Misplaced chest tubes may cause intercostal artery lacerations, liver lacerations, splenic injuries, and diaphragmatic tears. Extrathoracic, mediastinal, and intraparenchymal chest tubes require immediate repositioning or replacement.
The significance of chest tubes within the fissure is controversial, although development of empyema with intrafissural chest tubes has been reported. Computed tomography (CT) is more accurate than portable anteroposterior (AP) chest radiography in identifying malpositioned chest tubes in the patient with trauma.
Drug-induced lung disease
Drug-induced lung disease is a relatively common condition. Many mechanisms are involved; some are dose related, whereas others result from a hypersensitivity reaction that requires prior sensitization. It is often impossible to predict who will develop lung disease in association with drug treatment.
The clinical and radiographic changes in drug-induced disease are nonspecific. Many drugs may produce a similar clinical picture, and individual drugs may cause different types of reactions. Chest radiographs and CT scans must be correlated with the patient's clinical history and drug history; the patient's response to alterations in therapy; and laboratory data.
Drug-induced lung disease may manifest in a variety of forms:
- Allergic-type reactions: asthma, hypersensitivity pneumonitis, or eosinophilic pneumonia
- Cough or bronchitis caused by inflammation of the air sacs, pneumonitis, or pulmonary infiltrate
- Interstitial fibrosis
- Noncardiogenic pulmonary edema
- Alveolar hemorrhage
- Pleural effusion
- Lung vasculitis
- Mediastinal inflammation
- Hilar/mediastinal lymphadenopathy
- Respiratory failure
- Granulomatous lung disease
- Drug-induced systemic lupus erythematosus
Direct toxicity
Lung toxicity has been described in association with the use of many drugs, such as amiodarone, angiotensin-converting enzyme (ACE) inhibitors, and retinoid acid. However, lung toxicity is particularly common with cytotoxic agents, such as bleomycin, busulfan, and carmustine. In many cases, the toxicity is dose related. The toxicity may be accentuated by other factors, such as increasing patient age, decreased renal function, radiation therapy, oxygen therapy, and other associated cytotoxic drug therapy.
The pathologic changes are those of increased permeability of the alveolar sacs, which causes pulmonary edema and leads to diffuse alveolar damage. This is followed by interstitial pulmonary fibrosis. Pulmonary fibrosis develops as a chronic, insidious disease.
The radiologic features are those of diffuse lung opacities in a reticular or reticulonodular pattern, or airspace consolidation, mainly seen at the lung bases. High-resolution CT scanning more effectively shows the reticular or reticulonodular pattern and airspace consolidation. High-resolution CT scanning also depicts ground-glass attenuation, which is often associated with intralobular lines, traction bronchiectasis, traction bronchiolectasis, and honeycombing.
Hypersensitivity reaction
A hypersensitivity reaction affecting the lungs may occur after exposure to a variety of drugs and extrinsic agents. Sulfasalazine is the drug most frequently associated with hypersensitivity reactions. Drug-related hypersensitivity is not dose related and requires prior sensitization to the drug. The reaction is a result of interactions between the drug and humeral antibodies or sensitized lymphocytes.
Fever, peripheral eosinophilia, and asthmatic dyspnea are the usual clinical features. The radiographic findings are those of bilateral peripheral areas of fleeting airspace consolidation. Lung parenchymal changes are similar to those of acute or chronic eosinophilic pneumonia. Most patients generally respond to withdrawal of the drug, although some patients may need steroid therapy.
Pulmonary edema
Noncardiogenic pulmonary edema may occur as a complication of the use of a variety of drugs, especially when cytotoxic agents, such as interleukin, methotrexate, cytosine, and arabinosine, are used. Pulmonary edema characteristically occurs within hours of use of the drug. The radiologic and clinical features may be indistinguishable from those of cardiogenic edema.
Pulmonary hemorrhage
Pulmonary hemorrhage is most commonly associated with anticoagulant therapy or drug-induced thrombocythemia, but it has also been reported with the use of nitrofurantoin, quinidine, oxyphenbutazone, and penicillamine. In rare cases, pulmonary hemorrhage is associated with pulmonary renal syndrome similar to Goodpasture syndrome. Hemoptysis is a common manifestation. The radiologic appearance consists of diffuse patchy areas of airspace consolidation, which may be extensive and severe.
Lupus erythematosus syndrome
Drug-induced systemic lupus erythematosus may be associated with procainamides, hydralazine, isoniazid, or phenytoin. Most patients test positive for the presence of antinuclear antibodies. The clinical and radiologic manifestations of drug-induced systemic lupus erythematosus do not differ from those of the idiopathic form of systemic lupus erythematosus. Pleural effusion, often with concomitant pericardial effusion, is a common manifestation. Subsegmental atelectasis and basilar consolidation are typical radiographic findings.
Pulmonary granulomas
Pulmonary granulomas may develop as a result of complications from the use of a variety of drugs, such as methotrexate and nitrofurantoin. Histologically, the granulomas are composed of macrophages. Granulomatous reaction may also occur as a complication of the long-term aspiration of mineral oils, which form chronic conglomerate masses in the basilar aspects of the lungs. Pulmonary granulomas are a known complication when a particulate suspending agent for oral use (eg, talc) is deliberately or accidentally injected intravenously.
Bronchiolitis obliterans
Bronchiolitis obliterans is a frequent complication of penicillamine therapy prescribed for rheumatoid arthritis.
Lipoid pneumonia
Lipoid pneumonia may occur as a complication of accidental aspiration of mineral or vegetable oil. Mineral or vegetable oils are often used as laxatives or lubricants, which may be aspirated on a long-term basis. The risk is especially great in elderly patients who have difficulty swallowing or who have hiatal hernias; in such patients, night reflux may be aspirated.
Radiation pneumonitis and fibrosis
When the normal lung is exposed to irradiation, 2 well-recognized adverse effects may follow: pneumonitis and fibrosis. Radiation pneumonitis occurs during the acute injury phase, typically within the first 6 months after treatment. Lung injury is initiated within the irradiation field, resulting in damage at the capillary-alveolar level, with collagen deposition occurring in the alveolar wall and alveolar spaces. The characteristic histologic finding in patients with radiation pneumonitis is a prominent inflammatory cell infiltrate in the alveoli and in the pulmonary interstitium.
Radiation-induced lung fibrosis occurs months to years after irradiation. Its pathogenesis is less well defined than that of radiation pneumonitis, although some evidence suggests that cytokines and growth factors play a role. The target cells of radiation injury in the lung are thought to be type II pneumocytes, which are found in the alveoli, and vascular endothelial cells; inflammatory cell infiltrates play an accessory role. Once the target cells sustain injury, the recruitment of inflammatory cells in the alveolar interstitium contributes to the acute inflammatory response, the subsequent deposition of collagen in the lung, and the development of noncompliant lungs.
Acute respiratory distress syndrome
Acute respiratory distress syndrome (ARDS) is a term used for severe acute respiratory failure of diverse etiology. The associated morbidity and mortality rates are high (50-70%). Regardless of etiology, the basic pathogenesis of ARDS is a systemic inflammatory response that leads to a diffuse inflammatory process involving both lungs. The result is diffuse alveolar and endothelial damage with increased pulmonary capillary permeability and excessive extravascular water accumulation in the lung.
ARDS is associated with a variety of serious illnesses. It is most commonly associated with sepsis and multiple organ failure. The clinical presentation is that of progressive hypoxemia; pulmonary edema, which is radiographically evident; decreased lung compliance; and pulmonary hypertension. There is no specific treatment of ARDS, and its management remains supportive. Therapeutic goals include resolution of underlying conditions, the maintenance of acceptable gas exchange and tissue oxygenation, and the prevention of iatrogenic lung injury.
Gas embolism
Gas embolism is an uncommon complication of lung injury, decompression sickness, surgery, or the accidental infusion of gas during various diagnostic procedures. Iatrogenic gas embolism is often not considered or recognized. As a result, mortality and morbidity rates may be high. Gas embolism must always be considered in the differential diagnosis when a patient presents with unexplained neurologic symptoms in the appropriate clinical setting. Hyperbaric oxygen treatment may be lifesaving.
Fat-embolism syndrome
The clinical fat-embolism syndrome, a rare condition that is characterized by progressive pulmonary insufficiency, cerebral dysfunction, and petechiae, is typically associated with severe skeletal injuries. Fat droplets appear in the circulating blood and embolize to the capillaries of the lungs and other organs. Whether fat droplets are of mechanical or chemical origin remains controversial. These fat droplets cause mechanical occlusion of lung capillaries, followed by chemical changes associated with hydrolysis of the neutral fat to free fatty acids. The free fatty acids produce a toxic and inflammatory reaction resulting in pulmonary edema, hemorrhage, and microatelectasis.5
The clinical and radiographic abnormalities appear after an initial 12- to 72-hour latent period. The chest radiographic findings, which are nonspecific, consist of bilateral patchy or diffuse alveolar and interstitial lung densities. Aggressive management has markedly improved the survival rate, and mortality is now rare.
Curtis and associates reviewed the clinical course and radiographs of 30 patients with fat-embolism syndrome.6 All 30 patients displayed the syndrome's classic triad of neurologic dysfunction, respiratory insufficiency, and petechiae. Responses to embolized fat were noted in 3 patients. The hyperacute response was demonstrated in 2 patients with paradoxical embolization of fat to the systemic circulation. A classic response, with transient respiratory compromise and variable radiographic findings, was found in 18 patients. Two deaths in the classical response group were considered to be the result of massive pulmonary emboli. For the remaining 10 patients, findings on chest radiography were compatible with pulmonary edema in the clinical setting of ARDS. The degree of respiratory dysfunction and pulmonary damage in members of this third group correlated with the development of disseminated intravascular coagulation.
Traumatic asphyxia
Traumatic asphyxia is unique to the pediatric population; it commonly results from blunt compressing thoracic trauma, with sudden airway obstruction and abrupt retrograde high pressure in the superior vena cava. For children with traumatic asphyxia, the clinical presentation is dramatic; it is characterized by cervical and facial petechial hemorrhages or cyanosis associated with vascular engorgement and subconjunctival hemorrhage. Despite the alarming presentation, the prognosis is good. Central nervous system injuries, pulmonary contusions, and intra-abdominal injuries are common associated injuries.
Lung hernia
Lung hernia is a rare complication of lung trauma or inadequate healing from recent or remote thoracic surgery, although a congenital variety has been reported. Most patients with a lung hernia present with acute respiratory symptoms. Awareness of the clinical and radiologic appearance of lung hernia helps prevent confusing it with other conditions, such as subcutaneous emphysema, chest tumor, pneumothorax, or a focus of infection.
Frequency
United States
Blunt chest trauma accounts for 100,000 hospital admissions per year in the United States. Chest injuries are the third most frequent type of injury occurring in high-speed motor vehicle accidents.
The age-adjusted incidence of primary spontaneous pneumothorax is 7.4 cases per 100,000 men and 1.2 cases per 100,000 women. The age-adjusted incidence of secondary spontaneous pneumothorax is 6.3 cases per 100,000 men and 2 cases per 100,000 women. The incidence of iatrogenic pneumothorax is not known, but it is probably higher than those of primary and secondary spontaneous pneumothoraces combined. Pneumomediastinum occurs in approximately 1 per 10,000 hospital admissions.
International
No accurate data are available on the incidence of lung trauma internationally.
Mortality/Morbidity
In the United States, thoracic trauma accounts for about 25% of all trauma deaths.7 Overall, the mortality rate for persons who suffer thoracic trauma is approximately 10%. Chest injuries cause 25% of trauma deaths in the United States. Many of these deaths could be prevented with prompt diagnosis and treatment. Among patients who are transferred to the operating room within 24 hours of admission, the incidence of blunt thoracic trauma has been reported to be as high as 62.5%.8
In a 5-year Canadian study of patients admitted to an urban trauma unit, 96.3% had sustained blunt trauma; the remaining 3.7% were injured with a penetrating mechanism. The causes of blunt injuries were attributed to motor vehicle accidents (70%), suicides (10%), falls (8%), homicides (7%), and others (5%). The incidence of thoracic trauma was 46%. For patients with thoracic injuries, the mortality rate was 15.7%; for those without thoracic injuries, it was 12.8%.9
A spontaneous pneumothorax is a benign condition; however, deaths have been rarely reported. Secondary spontaneous pneumothoraces may be life threatening, depending on the severity of the underlying disease and the size of the pneumothorax. Compared with similar patients without pneumothorax, age-matched patients with chronic obstructive pulmonary disease have a 3.5-fold increase in relative mortality when a spontaneous pneumothorax occurs.
Mortality rates in patients with chronic obstructive pulmonary disease and spontaneous pneumothorax vary in the range of 1-17%. Iatrogenic pneumothorax may cause substantial morbidity and, rarely, death.
A number of long-term sequelae may follow unrecognized bronchial tears; these sequelae include bronchial stenosis, bronchomalacia, and recurrent atelectasis or pneumonia of the affected lobe. Strictures also may follow repairs of bronchial tears.
Thoracic aorta rupture occurs in persons experiencing severe decelerating forces, such as occur in high-speed car accidents or a fall from a great height. These injuries are associated with a high mortality rate. Aortic transection causes 16% of all deaths from automobile accidents. Of patients sustaining an aortic transection, 85% die before reaching the hospital. Of the remaining short-term survivors, 50% die within 24 hours.
Race
There is no racial predilection for lung trauma.
Sex
Although exact figures are not available, lung trauma is more common in men than in women.
Age
Persons of any age may suffer thoracic trauma, although it typically affects the young. It is the leading cause of death during the first 3 decades of life. Injury accounts for more than 50% of deaths in children; it is the third leading cause of death, after cancer and arteriosclerosis, in all age groups.
Anatomy
Anatomy and physiology of the lung
The lung is a complex organ composed primarily of air sacs, or alveoli, enmeshed within a rich blood supply. The lungs receive the entire output of the right ventricle. Lung trauma has the potential to cause significant systemic pathophysiologic conditions as a result of interference with gas exchange or significant blood loss if major pulmonary vessels are injured. Injury to surrounding or supporting structures in the chest may compromise lung function as well.
The major physiologic functions of the lung include the uptake and diffusion of oxygen to restore acceptable oxygen tension of blood returning to the systemic circulation, and the offloading and elimination of carbon dioxide and other gaseous by-products of metabolism that arrive via the pulmonary arteries.
Host-tissue characteristics and lung trauma
Host-tissue characteristics, especially the prestress state, are important in determining the type and extent of injury. In experimental settings, myocardial damage is more likely to occur when the impact occurs during systole rather than diastole. Rib fractures are more common in the elderly, who have inelastic bones, than in children, who have more elastic ribs. Therefore, the young may undergo substantial intrathoracic injury without incurring rib fractures, whereas in the elderly, simple trauma may cause rib fractures.
Tissue characteristics are an important determinant of the susceptibility of tissue to injury. The most important determinant is tissue density. Bones and muscles tend to absorb a large amount of kinetic energy from projectiles passing through them. This process decreases the likelihood of damage to deeper organs, but the absorbed energy produces significant muscle and skeletal damage. Because the lungs are porous, elastic projectiles pass through the lungs unimpaired, so that injury to the lungs with high-velocity projectiles is limited to the projectile path.
The major threat from high-velocity projectiles is to other intrathoracic vital organs, such as major vessels, myocardium, the esophagus, and organs that do not tolerate penetrating trauma, as well as to the lungs.
Fractures of the upper 3 ribs may be associated with injury to the major vessels. Fractures of the lower ribs should raise suspicion of injury to the liver, spleen, or diaphragm. Because of the compliance of the chest wall in the young, severe intrathoracic injury may occur without associated rib fractures.
Presentation
Physical examination
Symptoms of chest trauma are variable and primarily depend on the thoracic organ that has been traumatized or that has taken the brunt of traumatic impact. Most patients with significant trauma present with shock. In cases of trauma to the chest, as from a motor vehicle accident or other injury, hemoptysis may occur immediately after the incident or later.
Rib fractures should be taken in context. Fractures of the upper 3 ribs are highly suggestive of injury to the major vessels. Fractures of the lower ribs should raise suspicion of injury to the liver, spleen, or diaphragm. Because of the compliance of the chest wall in the young, severe intrathoracic injury may occur without associated rib fractures. In the presence of a rib fracture, the underlying lung should be examined for contusion, laceration, hemothorax, or pneumothorax. Multiple rib fractures may cause a flail segment.
Patients with multiple rib fractures may harbor a subclinical pneumothorax and may require prophylactic thoracostomy. Indications of a bronchial or tracheal rupture include the following: a pneumothorax that persists despite adequate placement of chest tubes; increasing subcutaneous emphysema; pneumomediastinum; or a pneumothorax.
Patients present with sudden onset of dyspnea, chest pain, and cough. Cyanosis, mediastinal shift, an enlarged ipsilateral hemothorax, decreased chest expansion, hyperresonance, and decreased breath sounds are characteristic physical findings.
Tension pneumothorax is present when the air leak is progressive. Venous return decreases, resulting in decreasing blood pressure, tachycardia, worsening shortness of breath, and hypoxemia.
Rupture of the trachea or major bronchi is a serious injury; the overall mortality rate is estimated to be at least 50%. About 80% of the ruptures of bronchi are within 2.5 cm of the carina. The usual signs of tracheobronchial disruption are hemoptysis, dyspnea, subcutaneous and mediastinal emphysema, and, occasionally, cyanosis.
Esophageal injuries are rare with blunt trauma; penetrating trauma more often causes esophageal perforating injury. Esophageal perforation is lethal if it goes unrecognized because it is often associated with mediastinitis. Patients often complain of sudden, sharp epigastric pain that radiates to the interscapular area. Dyspnea, cyanosis, and shock are late symptoms.
Monitoring and testing
Prolonged observation in a monitored setting is usually not required for patients with suspected myocardial contusion. Patients with a normal electrocardiogram (ECG) and a normal echocardiogram are usually discharged home after 12 hours of monitoring. Cardiac complications are rare in cases of cardiac contusion, particularly in the young.
Biochemical tests, such as determinations of creatine kinase–MB isoenzyme levels, may be nondiagnostic. Cardiac troponin I, a more specific agent for myocardial damage, has not been evaluated. Echocardiography is useful for detecting wall-motion abnormalities and pericardial effusions. In combination with abnormal creatine kinase–MB levels, this may be predictive of complications. Radionuclide angiographic results also may be predictive of complication. Thallium scanning may depict areas of decreased perfusion but are not useful in differentiating an acute lesion from a preexisting lesion.
Injury scoring
The abbreviated injury scale (AIS) and the injury severity score (ISS) are accurate methods for quantifying trauma severity and have many potential applications. The ability to predict morbidity and mortality from trauma by using injury severity scoring is an obvious application. Such scores may be used to inform patients and their families if they desire to know the prognosis and apply the knowledge to end-of-life decision making and resource allocations. However, there is always uncertainty in predicting trauma mortality and morbidity in an individual patient. Decisions for individual patients should never be made solely on the basis of a statistically derived ISS. A variety of anatomic and physiologic trauma scores are used alone or in combination to score the severity of injuries.10
The AIS is an anatomic scoring system first introduced in 1969. Since then, it has been revised several times with regard to survival so that it now provides a reasonably accurate means of ranking the severity of injury. A scaling committee of the Association for the Advancement of Automotive Medicine (AAAM) monitors the AIS. The AIS is used to score traumatic injuries in terms of the anatomic location and severity of the injury. Each traumatic injury is assigned a 7-digit number, with the last number representing the severity of the injury to be used in tabulating the ISS. AIS numbers may be found in the AIS Dictionary, distributed by the AAAM.
The ISS is an anatomic scoring system but only recognizes the highest AIS in each of the 6 body regions: head, face, chest, abdomen, extremities, and external. The ISS is used to assess survivability; its results are often compared with various benchmarks (eg, ISS versus length of stay and ISS versus mortality). Only the highest AIS score in each body region is used. The scores for the 3 most severely injured body regions are squared and added to produce the ISS.
Injuries are scored on a scale of 1-6, with 1 being minor, 5 being severe, and 6 being lethal. This score represents the threat to life associated with an injury and is not meant to represent a comprehensive measure of severity. The AIS is not an injury scale in that the difference between an AIS score of 1 and a score of 2 is not the same as that between 4 and 5. The AIS scale and the organ injury scales of the American Association for the Surgery of Trauma have many similarities.
AIS scores for injury are as follows:
- Minor
- Moderate
- Severe
- Serious
- Critical
- Not survivable
Prognosis
The presence of respiratory distress is ominous. About 50% of trauma patients presenting to the emergency department in respiratory distress die. Mortality for those with both respiratory distress and shock is 75%.
Preferred Examination
Clinical examination
The first priority in cases of thoracic trauma is the provision of effective therapeutic measures to minimize trauma-related deaths and morbidity. Imaging is not indicated until the airway, breathing, and circulation (ABC) have been secured and stabilized.
The initial approach to chest trauma is clinical evaluation, which starts with a thorough examination of the chest after the airway is controlled. Severe internal injury may be present without external tenderness. A chest radiograph is obtained for every patient who has significant trauma.
Imaging examination
Imaging has little if any role in the initial treatment of a critically ill and hemodynamically unstable patient. In many patients, urgent exploratory thoracotomy or laparotomy may take precedence over imaging, whereas in others, diagnosis and treatment are frequently combined with tube thoracostomy or pericardiocentesis. Imaging studies are an essential part of thoracic trauma care once the patient is stabilized.11,12,13,14
Ultrasonography, CT, and magnetic resonance imaging (MRI) may all demonstrate pericardial effusions and hemopericardium, but they are rarely indicated in a patient with acute traumatic tamponade. The roles of CT, MRI, and transesophageal sonography in the evaluation of aortic injuries have not been clearly defined, although multisection CT scanning is increasingly used for diagnosis.
The diagnosis is generally obvious with standard chest radiography or CT, but more subtle signs require careful analysis of CT images and examination with MRI in some situations.
Radiography
Chest radiography is indicated in virtually every trauma patient; a series of radiographs are generally obtained to assess the progress and complications of the trauma. They are also used to look for malpositioned lines and tubes; in the stress and confusion of an emergency department inadequate and inappropriate placement of lines and tubes is common.
A chest radiograph is usually performed initially in the acute setting. Findings on a chest radiograph include pneumothorax (which is difficult to see on a supine image), pneumomediastinum, airspace shadowing (resulting from pulmonary contusion), and pleural hematoma. CT is better for assessing most of these lesions.
Repeat chest radiographs are obtained after any invasive intervention, such as intubation or placement of the central venous pressure catheter or chest tube. Iatrogenic lung trauma may occur after lung biopsy, thoracentesis, cauterization, and other procedures. Mechanical ventilation predisposes the patient to barotrauma and pneumothorax. Lung injuries may result from the inhalation of toxic and inert substances, as well as in association with blast or radiation.
Computed tomography
Advancements in CT imaging have changed the management of blunt lung trauma and permitted the detection of blood in bronchi and interstitial air or blood with greater accuracy. Many centers now screen patients with chest trauma for aortic injuries by using contrast-enhanced CT. CT scans also demonstrate injuries to the lung, pleura, mediastinum, and chest wall better than plain radiographs do. Many serious thoracic injuries may be overlooked on initial chest radiographs; these include tracheobronchial tears, diaphragmatic rupture, esophageal tears, thoracic spine injuries, chest wall and seat-belt injuries, lung contusion, cardiac injuries, pneumothorax, hemothorax, and chest tube complications.
CT images demonstrate fractures of the vertebral bodies with great accuracy and readily show the relationship of fractured fragments and displaced disk material to the cord. Sagittal and coronal reconstructions may provide further exquisite detail.
Echocardiography and ultrasonography
Conventional echocardiography has long been used to image the heart, the pericardial space, and the ascending aorta. Transesophageal ultrasonography is an excellent modality for visualizing the aortic arch and the descending aorta and may be used at the patient's bedside.
Angiography
Conventional or digital subtraction angiography remains the criterion standard for depicting traumatic aortic rupture and aortic pseudoaneurysm.
Magnetic resonance imaging
MRI has many advantages over CT in the evaluation of patients with suspected dorsal spine injuries. It provides excellent detail of intervertebral disks, spinal ligaments, paravertebral soft tissues, and other spinal contents (eg, cord and nerve roots). MRI is particularly useful in evaluating patients with spinal cord injury without radiographic abnormality (SCIWORA) syndrome. MRIs show cord edema or hematoma, which may account for any neurologic deficit the patient may have.
Nuclear medicine study
Thallium and multigated acquisition isotope scans are useful for assessing myocardial damage. Similarly, technetium-99m diphosphonate may be used to assess fracture sites when radiographs are negative and patients are symptomatic.
Limitations of Techniques
Each method of imaging has advantages and pitfalls in accordance with the type of injury.
Radiography
Portable AP radiographs have several limitations when the images are obtained in an emergency situation with the patient in a supine position. Expiratory artifacts and the magnification effect of a short beam distance may make the mediastinum appear widened. Injuries involving the diaphragm are often missed, and preexisting diaphragmatic eventrations or an elevated hemidiaphragm may mimic diaphragmatic injuries.
Radiographic findings associated with aortic transection are nonspecific. They may be seen in a variety of other mediastinal or chest wall injuries, including nonaortic vascular injuries, fractures of the sternum, vertebral fractures, and esophageal rupture. Predictions regarding the presence of mediastinal hemorrhage on supine portable chest radiographs in the setting of trauma are inaccurate. Plain imaging findings of thoracic spinal fractures are often subtle and are difficult to identify because of the limited quality of many trauma radiographs.
Computed tomography
Because of a dramatic reduction in motion and beam-hardening artifacts and significant improvement of spatial resolution, especially along the z-axis, helical and multisection CT scanning allows better demonstration of the most subtle signs of thoracic trauma, such as a focal indentation of the liver or a right-sided collar sign. In addition, helical and multisection CT is a useful tools in the evaluation of patients with multiple traumatic injuries.
Patients with severe trauma are often difficult to scan with CT because of resuscitative equipment.
CT is an excellent modality, but patients are required to receive contrast agents and be transported from the protected resuscitation area to the radiology suite. Therefore, CT scanning is difficult to perform in hemodynamically unstable patients.
Magnetic resonance imaging
MRI is expensive and is not universally available in emergency departments. Also, MRI often cannot be used in patients with ferromagnetic foreign bodies or some types of prosthetic cardiac valves, as well as in those with claustrophobia. MRI should be performed only in patients when MRI-compatible resuscitation equipment is readily available. Ultrasonography is operator dependent and may cause some aortic injuries to be missed.
MRI with breath-hold acquisition permits good visualization of diaphragmatic abnormalities, but this technique cannot be performed in emergency situations. MRI offers a major advantage in exploring the cord, disks, and ligaments and in looking for a hematoma. Nevertheless, the indication is carefully weighed in patients with multiple trauma because of monitoring difficulties during the examination, which may be long. MRI is an important diagnostic and prognostic tool in patients with thoracolumbar compression–type fractures.
Ultrasonography
Because ultrasonography is unique in being portable, rapid, and noninvasive, it is particularly suited to the trauma setting and offers immediate feedback that may be incorporated into the management plan for the patient.
Nuclear medicine study
Findings on radionuclide scans are nonspecific.
Angiography
Angiography is invasive and may cause small aortic tears to be missed. Iodinated contrast media are nephrotoxic and pose a risk of anaphylaxis.
More on Thorax, Trauma |
 Overview: Thorax, Trauma |
| Imaging: Thorax, Trauma |
| Follow-up: Thorax, Trauma |
| Multimedia: Thorax, Trauma |
| References |
| Next Page » |
References
Anthoine D, Vaillant G, Martinet Y. [Diagnostic pitfalls, artefacts and difficulties of thoracic radiography]. Rev Pneumol Clin. 1990;46(6):251-9. [Medline].
Collins J. Chest wall trauma. J Thorac Imaging. Apr 2000;15(2):112-9. [Medline].
Fabian TC, Croce MA, Minard G. Current issues in trauma. Curr Probl Surg. Dec 2002;39(12):1160-244. [Medline].
Reuter M. Trauma of the chest. Eur Radiol. 1996;6(5):707-16. [Medline].
Batra P. The fat embolism syndrome. J Thorac Imaging. Jul 1987;2(3):12-7. [Medline].
Curtis AM, Knowles GD, Putman CE. The three syndromes of fat embolism: pulmonary manifestations. Yale J Biol Med. Mar-Apr 1979;52(2):149-57. [Medline].
Jones KW. Thoracic trauma. Surg Clin North Am. Aug 1980;60(4):957-81. [Medline].
Devitt JH, McLean RF, Koch JP. Anaesthetic management of acute blunt thoracic trauma. Can J Anaesth. May 1991;38(4 Pt 1):506-10. [Medline].
Hill AB, Fleiszer DM, Brown RA. Chest trauma in a Canadian urban setting—implications for trauma research in Canada. J Trauma. Jul 1991;31(7):971-3. [Medline].
Esme H, Solak O, Yurumez Y, et al. The prognostic importance of trauma scoring systems for blunt thoracic trauma. Thorac Cardiovasc Surg. Apr 2007;55(3):190-5. [Medline].
De Wever W, Bogaert J, Verschakelen J. Radiology of lung trauma. JBR-BTR. Aug 2000;83(4):167-73. [Medline].
Gavelli G, Canini R, Bertaccini P. Traumatic injuries: imaging of thoracic injuries. Eur Radiol. Jun 2002;12(6):1273-94. [Medline].
Hall A, Johnson K. The imaging of paediatric thoracic trauma. Paediatr Respir Rev. Sep 2002;3(3):241-7. [Medline].
Stark P, Jacobson F. Radiology of thoracic trauma. Curr Opin Radiol. Oct 1992;4(5):87-93.
Rowan KR, Kirkpatrick AW, Liu D. Traumatic pneumothorax detection with thoracic US: correlation with chest radiography and CT—initial experience. Radiology. Oct 2002;225(1):210-4. [Medline]. [Full Text].
Hehir MD, Hollands MJ, Deane SA. The accuracy of the first chest X-ray in the trauma patient. Aust N Z J Surg. Jul 1990;60(7):529-32. [Medline].
Gayer G, Rozenman J, Hoffmann C. CT diagnosis of malpositioned chest tubes. Br J Radiol. Jul 2000;73(871):786-90. [Medline]. [Full Text].
Omert L, Yeaney WW, Protetch J. Efficacy of thoracic computerized tomography in blunt chest trauma. Am Surg. Jul 2001;67(7):660-4. [Medline].
Shang XL, Zhang YZ, Zhang XL. Diagnoses of bronchus and lung trauma by computed tomography and X-ray examination in 37 cases: a comparative study. Di Yi Jun Yi Da Xue Xue Bao. Apr 2002;22(4):380-1. [Medline].
Tack D, Defrance P, Delcour C. The CT fallen-lung sign. Eur Radiol. 2000;10(5):719-21. [Medline].
Tack D, Widelec J, De Maertelaer V. Comparison between low-dose and standard-dose multidetector CT in patients with suspected chronic sinusitis. AJR Am J Roentgenol. Oct 2003;181(4):939-44. [Medline]. [Full Text].
Wintermark M, Schnyder P, Wicky S. Blunt traumatic rupture of a mainstem bronchus: spiral CT demonstration of the "fallen lung" sign. Eur Radiol. 2001;11(3):409-11. [Medline].
Zissin R, Shapiro-Feinberg M, Rozenman J. CT findings of the chest in adults with aspirated foreign bodies. Eur Radiol. 2001;11(4):606-11. [Medline].
Petrovic K, Stojanovic S, Till V, Vucaj-Cirilovic V, Nikolic O, Niciforovic D. [Blunt injuries of the lungs, pleura and chest bone structures: computed tomography contribution]. Med Pregl. Jan-Feb 2008;61(1-2):83-6. [Medline].
Osaki T, Baba T, Matsuura H. Three-dimensional imaging of traumatic multiple fractures of the thorax by multislice computed tomography. Ann Thorac Surg. Jan 2008;85(1):344. [Medline].
Plurad D, Green D, Demetriades D, et al. The increasing use of chest computed tomography for trauma: is it being overutilized?. J Trauma. Mar 2007;62(3):631-5. [Medline].
Traub M, Stevenson M, McEvoy S, et al. The use of chest computed tomography versus chest X-ray in patients with major blunt trauma. Injury. Jan 2007;38(1):43-7. [Medline].
Gavant ML, Menke PG, Fabian T, et al. Blunt traumatic aortic rupture: detection with helical CT of the chest. Radiology. Oct 1995;197(1):125-33. [Medline]. [Full Text].
Bergin D, Ennis R, Keogh C. The "dependent viscera" sign in CT diagnosis of blunt traumaticdiaphragmatic rupture. AJR Am J Roentgenol. Nov 2001;177(5):1137-40. [Medline]. [Full Text].
Huson H, Sais GJ, Amendola MA. Diagnosis of bronchial rupture with MR imaging. J Magn Reson Imaging. Nov-Dec 1993;3(6):919-20. [Medline].
Takahashi N, Murakami J, Murayama S. MR evaluation of intrapulmonary hematoma. J Comput Assist Tomogr. Jan-Feb 1995;19(1):125-7. [Medline].
Tashita H, Inoue R, Goto E. Magnetic resonance imaging for early detection of bronchial foreign bodies. Eur J Pediatr. May 1998;157(5):442. [Medline].
Subhas N, Kline MJ, Moskal MJ, White LM, Recht MP. MRI evaluation of costal cartilage injuries. AJR Am J Roentgenol. Jul 2008;191(1):129-32. [Medline].
Lee TJ, Collins J. MR imaging evaluation of disorders of the chest wall. Magn Reson Imaging Clin N Am. May 2008;16(2):355-79, x. [Medline].
Abu-Zidan FM, Sheikh M, Jadallah F. Blunt abdominal trauma: comparison of ultrasonography and computedtomography in a district general hospital. Australas Radiol. Nov 1999;43(4):440-3. [Medline].
Chan SS. Emergency bedside ultrasound to detect pneumothorax. Acad Emerg Med. Jan 2003;10(1):91-4. [Medline].
Cunningham J, Kirkpatrick AW, Nicolaou S. Enhanced recognition of "lung sliding" with power color Doppler imaging in the diagnosis of pneumothorax. J Trauma. Apr 2002;52(4):769-71. [Medline].
Dulchavsky SA, Schwarz KL, Kirkpatrick AW. Prospective evaluation of thoracic ultrasound in the detection of pneumothorax. J Trauma. Feb 2001;50(2):201-5. [Medline].
Fry WR, Smith RS, Schneider JJ. Ultrasonographic examination of wound tracts. Arch Surg. Jun 1995;130(6):605-7; discussion 608. [Medline].
Johnson SB, Sisley AC. The surgeon''s use of transesophageal echocardiography. Surg Clin North Am. Apr 1998;78(2):311-36.
Mathis G. Thoraxsonography—Part I: Chest wall and pleura. Ultrasound Med Biol. 1997;23(8):1131-9. [Medline].
Sargsyan AE, Hamilton DR, Nicolaou S. Ultrasound evaluation of the magnitude of pneumothorax: a new concept. Am Surg. Mar 2001;67(3):232-5; discussion 235-6. [Medline].
Seale KT, Pou NA, Krivitski N. Quantification of lung microvascular injury with ultrasound. Ann Biomed Eng. May 2002;30(5):671-82. [Medline].
Tilling T, Bouillon B, Schmid A, et al. Ultrasound in blunt abdomino-thoracic trauma. In: Border JF, Allgoewer M, Hansen ST, Reudi TP, eds. Blunt Multiple Trauma. New York, NY: Marcel Dekker;. 1990: 415-33.
Sisley AC, Rozycki GS, Ballard RB. Rapid detection of traumatic effusion using surgeon-performed ultrasonography. J Trauma. Feb 1998;44(2):291-6; discussion 296-7. [Medline].
Fenkl R, von Garrel T, Knaepler H. [Emergency diagnosis of sternum fracture with ultrasound]. Unfallchirurg. Aug 1992;95(8):375-9.
Skarzynski JJ, Slavin JD Jr, Spencer RP. "Matching" ventilation/perfusion images in fat embolization. Clin Nucl Med. Jan 1986;11(1):40-1. [Medline].
Chen MY, Regan JD, D'Amore MJ. Role of angiography in the detection of aortic branch vessel injury after blunt thoracic trauma. J Trauma. Dec 2001;51(6):1166-71; discussion 1172. [Medline].
Ahrar K, Smith DC, Bansal RC. Angiography in blunt thoracic aortic injury. J Trauma. Apr 1997;42(4):665-9. [Medline].
Munoz A, Moreno R, Martin V. Aortography delays surgery of CT proven acute traumatic rupture of the thoracic aorta. Case report. Acta Radiol. Sep 1991;32(5):386-8. [Medline].
Spouge AR, Burrows PE, Armstrong D. Traumatic aortic rupture in the pediatric population. Role of plain film, CT and angiography in the diagnosis. Pediatr Radiol. 1991;21(5):324-8. [Medline].
Sturm JT, Hankins DG, Young G. Thoracic aortography following blunt chest trauma. Am J Emerg Med. Mar 1990;8(2):92-6. [Medline].
von Oppell UO, Beningfield SJ, Odell JA. Cardiac rupture caused by blunt trauma as well as false angiographic aortic rupture. A case report. S Afr Med J. Nov 19 1988;74(10):519-20. [Medline].
Ghayyda SN, Roland D, Cade A. Seat belt associated central line fracture-A previously unreported complication in cystic fibrosis. J Cyst Fibros. May 1 2008;[Medline].
Bergus GR, Barloon TS, Kahn D. An approach to diagnostic imaging of suspected pulmonary embolism. Am Fam Physician. Mar 1996;53(4):1259-66. [Medline].
Bilello JF, Kaups KL, Davis JW. Delayed pulmonary hemorrhage 17 years after gunshot wound to the chest. Ann Thorac Surg. Jun 2001;71(6):2011-3. [Medline].
Bokhari F, Brakenridge S, Nagy K. Prospective evaluation of the sensitivity of physical examination in chest trauma. J Trauma. Dec 2002;53(6):1135-8. [Medline].
Carragher AM, Sulaiman SK, Panesar KJ. Scroto-abdominal impalement injury in a skateboard rider. J Emerg Med. Jul-Aug 1990;8(4):419-21. [Medline].
Cearlock JR, Fontaine AB, Urbaneja A. Endovascular treatment of a posttraumatic bronchial artery pseudoaneurysm. J Vasc Interv Radiol. May-Jun 1995;6(3):495-6. [Medline].
De Waele JJ, Vermassen FE, De Roose J. Bronchial rupture after direct chest trauma in a child. Acta Chir Belg. 2001;101(1):40-1.
Desai SR, Wells AU, Suntharalingam G. Acute respiratory distress syndrome caused by pulmonary and extrapulmonary injury: a comparative CT study. Radiology. Mar 2001;218(3):689-93. [Medline]. [Full Text].
Donaldson B, Ngo-Nonga B. Traumatic pseudoaneurysm of the pulmonary artery: case report and review of the literature. Am Surg. May 2002;68(5):414-6. [Medline].
Fauroux B, Clement A, Tournier G. [Pulmonary toxicity of drugs and thoracic irradiation in children]. Rev Mal Respir. Jul 1996;13(3):235-42. [Medline].
Feliciano DV, Rozycki GS. Advances in the diagnosis and treatment of thoracic trauma. Surg Clin North Am. Dec 1999;79(6):1417-29. [Medline].
Filosso PL, Oliaro A, Donati G. Post-traumatic hernia of the lung. Eur J Cardiothorac Surg. Mar 2001;19(3):360. [Medline].
Gelman R, Mirvis SE, Gens D. Diaphragmatic rupture due to blunt trauma: sensitivity of plain chest radiographs. AJR Am J Roentgenol. Jan 1991;156(1):51-7. [Medline].
Ghaye B, Dondelinger RF. Imaging guided thoracic interventions. Eur Respir J. Mar 2001;17(3):507-28. [Medline]. [Full Text].
Glenn C, Bonekat W, Cua A. Lung hernia. Am J Emerg Med. May 1997;15(3):260-2. [Medline].
Gormus N, Ceran S, Aribas OK. Soft-tissue images. Ingestion of a knife into the right mainstem bronchus. Can J Surg. Dec 2002;45(6):447. [Medline]. [Full Text].
Holmes JF, Sokolove PE, Brant WE. A clinical decision rule for identifying children with thoracic injuries after blunt torso trauma. Ann Emerg Med. May 2002;39(5):492-9. [Medline].
Igai H, Okumura N, Ohata K, Matsuoka T, Kameyama K, Nakagawa T. Rapidly expanding extrapleural hematoma. Gen Thorac Cardiovasc Surg. Oct 2008;56(10):515-7. [Medline].
Israel-Biet D, Labrune S, Huchon GJ. Drug-induced lung disease: 1990 review. Eur Respir J. Apr 1991;4(4):465-78. [Medline].
Kaptanoglu M, Dogan K, Nadir A. Tracheobronchial rupture: a considerable risk for young teenagers. Int J Pediatr Otorhinolaryngol. Feb 1 2002;62(2):123-8. [Medline].
Kelly IP, Attwood SE, Quilan W. The management of impalement injury. Injury. Apr 1995;26(3):191-3. [Medline].
Maffessanti M, Bortolotto P, Grotto M. Imaging of pleural diseases. Monaldi Arch Chest Dis. Apr 1996;51(2):138-44. [Medline].
Matejovic M, Novak I, Sramek V. [Acute respiratory distress syndrome]. Cas Lek Cesk. Apr 26 1999;138(9):262-7. [Medline].
Mellem H, Emhjellen S, Horgen O. Pulmonary barotrauma and arterial gas embolism caused by an emphysematous bulla in a SCUBA diver. Aviat Space Environ Med. Jun 1990;61(6):559-62. [Medline].
Moore EE, Cogbill TH, Jurkovich GJ. Organ injury scaling. III: chest wall, abdominal vascular, ureter, bladder, and urethra. J Trauma. Sep 1992;33(3):337-9. [Medline].
Moore EE, Cogbill TH, Jurkovich GJ. Organ injury scaling: spleen and liver (1994 revision). J Trauma. Mar 1995;38(3):323-4. [Medline].
Moore EE, Cogbill TH, Malangoni MA. Organ injury scaling, II: pancreas, duodenum, small bowel, colon, and rectum. J Trauma. Nov 1990;30(11):1427-9. [Medline].
Moore EE, Malangoni MA, Cogbill TH. Organ injury scaling. IV: thoracic vascular, lung, cardiac, and diaphragm. J Trauma. Mar 1994;36(3):299-300. [Medline].
Mortelliti MP, Manning HL. Acute respiratory distress syndrome. Am Fam Physician. May 1 2002;65(9):1823-30. [Medline]. [Full Text].
Munshi IA, Becker EJ, Bean M. Pulmonary parenchymal and bronchial arterial injuries secondary to blunt trauma. J Trauma. Aug 2001;51(2):418. [Medline].
Murthy PS, Ingle VS, George E. Sharp foreign bodies in the tracheobronchial tree. Am J Otolaryngol. Mar-Apr 2001;22(2):154-6. [Medline].
Myers C. Fluid resuscitation. Eur J Emerg Med. Dec 1997;4(4):224-32. [Medline].
Newman B, Oh KS. Iatrogenic tracheobronchial perforation in infants. J Thorac Imaging. Fall 1994;9(4):269-72. [Medline].
Ramchandani S, Bigey P, Szyf M. Genomic structure of the human DNA methyltransferase gene. Biol Chem. Apr-May 1998;379(4-5):535-40. [Medline].
Rose EH. Massive foreign body impalement of the shoulder and chest wall. Ann Plast Surg. May 1990;24(5):451-4. [Medline].
Sahni JK, Mathur NN, Kansal Y. Bronchial foreign body presenting as an accidental radiological finding. Int J Pediatr Otorhinolaryngol. Jul 9 2002;64(3):229-32. [Medline].
Stathopoulos G, Chrysikopoulou E, Kalogeromitros A. Bilateral traumatic pulmonary pseudocysts: case report and literature review. J Trauma. Nov 2002;53(5):993-6.
Swanson KL, Edell ES. Tracheobronchial foreign bodies. Chest Surg Clin N Am. Nov 2001;11(4):861-72. [Medline].
Thor CP, Gabler HC. Methodology for estimating thoracic impact response in frontal crash tests. Biomed Sci Instrum. 2007;43:336-41. [Medline].
Vaslef SN, Dragelin JB, Takla MW. Multiple impalement with survival. Am J Emerg Med. Jan 1997;15(1):70-2. [Medline].
Velmahos GC, Karaiskakis M, Salim A. Normal electrocardiography and serum troponin I levels preclude the presence of clinically significant blunt cardiac injury. J Trauma. Jan 2003;54(1):45-50; discussion 50-1. [Medline].
Watson JM, Goldstein LJ. Golf club shaft impalement: case report of a zone III neck injury. J Trauma. Dec 1996;41(6):1036-8. [Medline].
Weilemann Y, Thali MJ, Kneubuehl BP, Bolliger SA. Correlation between skeletal trauma and energy in falls from great height detected by post-mortem multislice computed tomography (MSCT). Forensic Sci Int. Sep 18 2008;180(2-3):81-5. [Medline].
Wennberg B, Gagliardi G, Sundbom L. Early response of lung in breast cancer irradiation: radiologic densitychanges measured by CT and symptomatic radiation pneumonitis. Int J Radiat Oncol Biol Phys. Apr 1 2002;52(5):1196-206. [Medline].
Wintermark M, Schnyder P. The Macklin effect: a frequent etiology for pneumomediastinum in severeblunt chest trauma. Chest. Aug 2001;120(2):543-7. [Medline]. [Full Text].
Further Reading
Keywords
trauma of the thorax, pulmonary trauma, thoracic trauma, lung injury, pulmonary injury, thoracic injury, pneumothorax, pneumomediastinum, hemothorax, bronchial injury, fallen lung, lung contusion, pulmonary contusion, lung laceration, aortic injury, blunt cardiac injury, pericardial tamponade, diaphragmatic rupture, esophageal tears, iatrogenic lung complications, iatrogenic lung trauma, drug-induced lung disease, lung toxicity, hypersensitivity reaction, pulmonary edema, pulmonary hemorrhage, lupus erythematosus syndrome, pulmonary granulomas, bronchiolitis obliterans, lipoid pneumonia, radiation pneumonitis and fibrosis, acute respiratory distress syndrome, ARDS, gas embolism, gas embolism syndrome, traumatic asphyxia, lung hernia, abbreviated injuryscale, AIS, injury severity score, ISS, rules of 2 s
