Trauma is the most common cause of mortality in childhood. Although most fatalities are a result of head injuries, the thorax is often involved in major injuries, including motor vehicle-related trauma. The most common manifestations of thoracic trauma are rib fractures. Injuries of the lungs or mediastinum can be life-threatening. Intentional trauma is an important cause of rib fractures in infants and young children.

Thoracic trauma is classified as penetrating versus nonpenetrating. Specific intrathoracic injuries include contusion; pulmonary laceration; traumatic pneumatocele; hematoma; hemothorax; pneumothorax; tracheobronchial disruption; injury of the thoracic aorta; esophageal perforation; thoracic duct rupture; rupture of the diaphragm; and cardiac injury. Pulmonary laceration is an integral component of the mechanism of injury with pulmonary contusion, pulmonary hematoma, and pulmonary cyst or pneumatocele.¹

Pulmonary contusion is the most common lung abnormality in children suffering chest trauma. Pulmonary contusion is extravasation of blood into the lung parenchyma. Typically, radiographic manifestations of pulmonary contusion are present within a few hours of the injury. There is subsequent rapid improvement, with diminished opacification within 1 to 2 days and complete clearing within several days after the injury. In comparison to standard radiographs, CT provides greater sensitivity for the early detection and characterization of pulmonary contusion.^2,3

The imaging appearance of pulmonary contusion ranges from homogeneous consolidation to irregular mixed airspace densities (Figures 6-1 and 6-2). Air bronchograms are frequently present. The consolidation does not conform to lobes or segments. Contrecoup injury can result in contusion of the lung contralateral to the trauma. In children, there is a propensity for a pulmonary contusion to be located posteriorly or posteromedially, and to have a nonsegmental crescentic shape. This pattern may be related to the relatively compliant anterior chest wall in children.⁴

An intraparenchymal hematoma of the lung can occur with either penetrating or nonpenetrating mechanisms of injury. The lesion usually occurs in association with a laceration of the lung. The hematoma is most often located in the region of the greatest injury force. A parenchymal lung hematoma is demonstrated radiographically as a homogeneous, well-circumscribed mass, most often located in the peripheral aspect of the lung. An air–fluid level can occur. There is nearly always a surrounding contusion, which may initially obscure the underlying hematoma. CT offers greater sensitivity and specificity than standard radiographs for the diagnosis of a parenchymal hematoma (Figure 6-3).⁵

As with a hematoma, a traumatic pneumatocele is usually associated with a pulmonary laceration that allows localized escape of air and blood into the lung tissue. The compliance of the pediatric chest wall may make children more prone than adults to the development of traumatic pneumatocele. Traumatic pneumatoceles are most often located in the subpleural region.

The radiographic appearance of a traumatic pneumatocele is that of a completely or partially air-filled structure (Figure 6-4). The size, shape, and number of cysts vary greatly between patients. On initial radiographs, a surrounding contusion may obscure a small pneumatocele. Rapid enlargement of a traumatic pneumatocele may occur in patients undergoing mechanical ventilation.²

Pneumothorax is a common sequela of penetrating or blunt thoracic injuries. This finding can occur in conjunction with pulmonary laceration, traumatic pneumatocele, rib fracture, or tracheobronchial fracture.

Hemothorax is common with severe chest injuries. The blood can originate from the chest wall, the lung or the mediastinal vessels. Some patients have concomitant mediastinal hemorrhage. Visualization of an interface between the opacified pleural space and adjacent aerated lung or pneumothorax serves to confirm the presence of pleural fluid in a patient with extensive intrathoracic opacification (Figure 6-5).

Lung torsion is a rare traumatic abnormality that can occur as a result of sudden compression injury of the thorax. The most common mechanism in children is related to crushing of the thorax by the wheel of a vehicle. Traumatic lung torsion most often involves the upper lobe, and consists of flipping of the lobe so that the apex is directed inferiorly. Torsion of a lobe or an entire lung can also occur following thoracic surgery or in patients with a large pneumothorax. Radiographs show alteration of the normal bronchovascular anatomy. There may be hilar displacement. The involved portion of the lung is usually opacified and atelectatic. If standard radiographs are equivocal, CT is diagnostic.

Foreign-body aspiration into the tracheobronchial tree is a common occurrence in infants and young children. Children younger than 3 years of age are most commonly involved. The classic symptoms include cough, choking, cyanosis, and an abrupt onset of wheezing. Gagging and/or vomiting sometimes occur. Infants may suffer cyanosis or brief episodes of apnea. The size of the foreign body, the location within the tracheobronchial tree, and the severity of airway obstruction largely determine the specific pattern of symptoms. Approximately 80% of airway foreign bodies are located in a main bronchus. Some patients with a tracheobronchial foreign body are mistakenly diagnosed with asthma or respiratory infection. The proper diagnosis is suggested by the typical rapid onset of symptoms, although there are occasional patients who present with chronic or recurrent pulmonary infections because of the long-standing presence of a foreign body. In general, wheezing in a young child with no known pulmonary disease should be considered as suspicious of foreign-body aspiration, particularly when the wheezing is unilateral.^6,7

With prompt, spontaneous expulsion or bronchoscopic removal of an airway foreign body, there are usually no long-term untoward effects. However, foreign-body aspiration can be a life-threatening event, and carries the potential for severe permanent lung damage. Most affected patients begin coughing immediately after the aspiration event. In the absence of prompt diagnosis and therapy, there may be subsequent improvement in the clinical findings, despite the persistence of the foreign body. Coughing and wheezing are still common symptoms of a chronic foreign body, however. Recurrent pneumonias can occur.

Potential findings on chest radiographs of children with airway foreign-body aspiration include air trapping, consolidation, atelectasis, unilateral overaeration, and bilateral overaeration. Only approximately 10% of aspirated foreign bodies in children are radiopaque (Figure 6-6). Unless the foreign body is radiographically visible, the most specific imaging finding is unilateral air trapping. Occasionally, narrowing or irregularity of the bronchial air column is visible. A mainstem bronchus foreign body is the most common cause of unilateral hyperinflation in children. This is the result of a ball-valve obstruction of the bronchus that permits air to enter the lung, but impedes outflow. Collateral air drift may also contribute to the hyperinflation, as airflow through the pores of Kohn and canals of Lambert is unidirectional toward the alveolus. Radiographs show a hyperlucent lung, with contralateral mediastinal shift. The unilateral air trapping is best demonstrated on an expiration view (Figures 6-7 and 6-8). In children unable to cooperate for an expiration view, decubitus views and chest fluoroscopy are useful options. A technically adequate expiration radiograph is essential when there is a clinical question of an airway foreign body, as standard inspiration views of the chest are frequently normal. If the diagnosis is delayed, atelectasis frequently develops distal to the foreign body. Pneumonia may eventually occur.⁸

Chest radiographs, including expiration views, are normal in up to 30% of children with a foreign body in the tracheobronchial tree. Bronchoscopy is usually the next step for patients with a documented or suspected airway foreign body. Children with a suspected tracheobronchial foreign body and normal or inconclusive standard radiographic examinations can also be studied with helical CT. The greater sensitivity for tissue characterization provided by CT sometimes allows direct visualization of the foreign body (Figure 6-9). Secondary parenchymal changes are usually present in the portion of the lung served by the airway: hyperaeration, atelectasis, or consolidation. With a long-standing foreign body, CT may demonstrate bronchiectasis, bronchial wall thickening, bronchial stenosis, or hilar lymphadenopathy. CT virtual bronchoscopy can be utilized to demonstrate a foreign body in a larger airway.^9,10

Tracheobronchial injuries in pediatric trauma patients are rare, but potentially devastating. Many trauma victims with tracheobronchial injuries die before or soon after hospital arrival. In others, the clinical findings can be subtle or nonspecific. Injury severity ranges from a small laceration to complete airway disruption. Clinical manifestations of concomitant injuries to other important neck and chest structures can interfere with a prompt diagnosis of airway trauma.^11,12

With blunt chest trauma, fractures of the bronchi are much more common than those of the trachea. Bronchial tears are most often located within a mainstem bronchus. The tear is oriented parallel to the cartilage rings. The right mainstem bronchus is more frequently affected than the left. Tracheal tears caused by blunt thoracic trauma are usually horizontal and located just above the carina. Tears in the cervical trachea caused by blunt trauma to the neck most often involve the membranous portion of the trachea and follow a vertical course.^13,14

The possibility of an airway injury should be considered in all patients who suffer blunt or penetrating trauma to the neck or upper chest. Potential clinical and radiographic manifestations of airway trauma include respiratory distress, extraluminal air in the neck or mediastinum, pneumothorax, hemoptysis, and cyanosis. A pneumothorax that does not resolve with thoracostomy tube drainage is a strong indicator of a bronchial or mediastinal tracheal injury and active air leak. Complete bronchial disruption is accompanied by ipsilateral lung collapse. Intraluminal granulation tissue or a fibrotic stricture because of a bronchial injury can cause delayed symptoms.¹⁵

The most important radiographic indicator of a possible airway injury is the presence of air in the soft tissues of the neck, mediastinum, or pleural space. This finding is, however, nonspecific. The diagnosis of an airway injury is usually established with bronchoscopy.¹⁶ CT, particularly using a thin-section helical technique, also serves a role in the detection and characterization of injuries of the trachea and main bronchi. The diagnostic imaging approach to these children should also be undertaken with consideration of the potential injuries to structures adjacent to the airway, such as the esophagus and carotid arteries. With airway injury, CT shows irregularity or disruption of the wall, usually with adjacent extraluminal air. Fluid, clotted blood or other debris may be present within the airway. Later in the course of the process, CT serves to detect posttraumatic strictures.¹⁷

Aspiration Pneumonia

Aspiration pneumonia refers to acute pulmonary alterations caused by aspiration of food, oropharyngeal secretions, or gastric contents. The type and amount of material that is aspirated, the presence of underlying lung pathology, and the chronicity of the aspiration determine the clinical and radiographic manifestations. Material with a high or low pH causes a marked inflammatory response in the lung, even in the absence of microorganisms. Children with anatomic or functional abnormalities of the pharynx or esophagus are at risk for aspiration, particularly when there is a coexistent neurological abnormality. Medical conditions that predispose patients to aspiration pneumonia include neuromuscular swallowing dysfunction, laryngotracheal cleft, esophageal obstruction, tracheoesophageal fistula, and severe gastroesophageal reflux.

Aspiration pneumonia most commonly occurs in the posterior segments of the upper lobes and the superior segments of the lower lobes. In infants, there is a predilection for involvement of the right upper lobe. An extensive, patchy bronchopneumonic pattern may be observed in patients following massive aspiration of gastric acid or water.⁸

Chronic Pulmonary Aspiration

Chronic pulmonary aspiration refers to chronic or recurrent lung pathology caused by repeated episodes of aspiration of food, refluxed gastric contents, and/or saliva. Potential causes of chronic pulmonary aspiration overlap those of acute aspiration pneumonia: dysphagia, neurological impairment, severe gastroesophageal reflux, and tracheoesophageal fistula. Chronic aspiration of acidic gastric contents causes airway mucosal injury. This may eventually lead to fibrotic and granulomatous changes in the interstitial tissues of the lungs. The typical symptoms of chronic pulmonary aspiration include chronic or recurrent coughing and wheezing, as well as recurrent pneumonias. Infants with chronic aspiration may have stridor and manifestations of failure to thrive.

Radiographs of children with chronic pulmonary aspiration show peribronchial thickening and linear streaks of subsegmental atelectasis and scarring in the central portions of the lungs. There is usually coexistent hyperinflation, although neurologically impaired children may have underinflated lungs. Potential findings on high-resolution CT include bronchial thickening, centrilobular (tree-in-bud) opacities, air trapping, and bronchiectasis.

Hydrocarbon Aspiration

The ingestion of hydrocarbons is a common type of childhood poisoning, and is the most common cause of chemical pneumonia in children. Hydrocarbons are present in many household products, including solvents, fuels, and cleaning agents. The lungs are usually the most severely involved organs in patients with substantial hydrocarbon aspiration, and approximately 75% of children who present to emergency departments with a history of hydrocarbon ingestion develop radiographic evidence of pneumonia. Other commonly involved organ systems include the central nervous system, GI tract, heart, and kidneys. Hydrocarbon aspiration is a common cause of exogenous lipoid pneumonia; that is, accumulation of lipids in the alveoli because of inhalation or aspiration of animal fat, vegetable oil, or petroleum products.¹⁸

In most instances, coughing and vomiting immediately follow the ingestion of hydrocarbon. With substantial pulmonary aspiration, respiratory symptoms develop within several hours; the onset of pulmonary symptoms may be delayed by 12 to 24 hours with less-extensive aspiration. The radiographic findings are frequently of greater severity than the clinical presentation. Findings on physical examination include dyspnea, basilar rales, and diminished resonance on chest percussion. Children with severe hydrocarbon aspiration may develop fever, lethargy, or coma.

Low-viscosity hydrocarbons (e.g., gasoline, lighter fluid, lamp oil) are much more toxic to the lungs than high-viscosity hydrocarbons (e.g., mineral oil, petroleum jelly). The low-viscosity hydrocarbons pass rapidly from the hypopharynx into the airway and lungs. The low surface tension promotes distribution along the mucous membranes. Hydrocarbons inactivate pulmonary surfactant, resulting in alveolar collapse. Chemical toxicity causes pulmonary edema, inflammation, and hemorrhage. With severe involvement, the pathological findings include bronchial, bronchiolar, and alveolar necrosis, atelectasis, interstitial inflammation, hemorrhagic pulmonary edema, small vessel thrombosis, necrotizing bronchopneumonia, and hyaline membrane formation.

Radiographic manifestations of chemical pneumonitis are evident within 2 hours after pulmonary aspiration of hydrocarbon in 85% of affected children, and are evident within 12 hours in 95%. The most characteristic findings on chest radiographs are coarse or homogeneous lower-lobe parenchymal opacities, with relative sparing of the peripheral aspects of the lungs (Figure 6-10). An alternative radiographic pattern is that of fine parahilar densities resembling the appearance of pulmonary edema; this is less common than the coarse lower-lobe pattern, however. The lungs are often underaerated; focal atelectasis can occur (Figure 6-11). CT demonstrates airspace consolidation and perihilar opacities. The severity of the radiographic findings typically increases over the first few days, after which there is gradual resolution; complete clearing is to be expected by 2 to 3 weeks. Complications of hydrocarbon aspiration pneumonia that can be identified radiographically include pneumothorax, interstitial emphysema, pleural effusion, pneumatoceles, and secondary infectious pneumonia (Figure 6-12).^8,19

Lipoid pneumonia in patients with chronic aspiration can occur because of repeated aspiration of small amounts of oils or fats in foods during swallowing or because of reflux of material from the stomach. Potential symptoms include cough, chest pain, and low-grade fever. Imaging studies show consolidation and/or fibrosis. High-resolution CT sometimes demonstrates ground glass opacities or a crazy-paving pattern.

Near-Drowning and Drowning

Near-drowning is a common cause of morbidity and mortality in children. The clinical, pathophysiologic, and radiographic manifestations of near-drowning are largely determined by the timing and adequacy of resuscitation, the type of water aspirated, any contaminants within the water, and the presence or absence of water entry into the lungs. There is a spectrum of severity of the clinical findings in near-drowning patients that correlates with morbidly and mortality. Minimally affected patients have coughing; auscultation is normal or demonstrates scattered rales. Manifestations of more severe injury include arterial hypotension and acute pulmonary edema. A history of an isolated respiratory arrest in a near-drowning victim caries a substantial risk of mortality, and most patients who suffer cardiopulmonary arrest do not survive. At the other end of the spectrum, breath-holding and/or reflex laryngospasm prevents substantial water aspiration in some near-drowning victims. A rapid complete recovery is possible if effective ventilatory resuscitation is instituted promptly.²⁰

The pathophysiological effects of water aspiration are variable. The aspiration of hypertonic seawater is associated with passage of fluid from the plasma into the alveoli, resulting in hemoconcentration and hypovolemic shock. Pulmonary compliance is diminished, but the fluid-filled alveoli remain perfused. In contradistinction, aspirated freshwater is hypotonic and is rapidly absorbed into the circulation. Freshwater alters the surface tension properties of pulmonary surfactant, and is more likely to cause atelectasis. The presence of foreign material, microorganisms, or toxic chemicals in the aspirated water is also an important factor in determining the pulmonary effects.

The dominant radiographic feature of near-drowning is pulmonary edema. In many patients, this consists of homogeneous or patchy areas of edema that are usually most prominent in the central portions of the lungs (Figures 6-13 and 6-14). More severely affected children have diffuse edema involving the lungs in their entirety. Atelectasis also can occur, particularly if there was particulate material in the aspirated water. Some patients have normal chest x-rays, particularly if no substantial intrapulmonary aspiration occurred. There are occasional near-drowning victims who have a delay in onset of pulmonary edema until 24 to 48 hours after the event. In the absence of a supervening complication, serial radiographs show prompt clearing of the pulmonary opacities. Progressive worsening of the radiographic findings is suggestive of a superimposed pneumonia or pulmonary damage caused by aspirated toxins or foreign material.

Rupture of the diaphragm can occur with blunt, crush, or penetrating injuries. There is a predilection for involvement of the left hemidiaphragm. Blunt diaphragmatic rupture is sometimes clinically silent until delayed complications occur. GI strangulation and obstruction because of an unrecognized diaphragmatic herniation carry a substantial risk for mortality. The possibility of blunt diaphragmatic rupture should be considered in the presence of any radiographic finding of this injury, even if equivocal.

With traumatic rupture of the right hemidiaphragm, the liver may herniate into the right hemithorax and simulate elevation of the diaphragm on standard radiographs. On the left, traumatic diaphragmatic rupture is usually accompanied by herniation of gas-containing bowel that is visible on chest radiographs. Strangulation of the herniated viscera is common with diaphragmatic rupture. In some cases, a “collar sign” is demonstrated as a constriction in herniated bowel where it passes through the diaphragm. An abnormal accumulation of pleural fluid is typically present, particularly when strangulation has occurred. Other potential findings include elevation, discontinuity, or nonvisualization of the hemidiaphragm. Pulmonary contusion is common in these patients, as are rib fractures.^21–23

CT offers greater sensitivity and specificity than standard radiographs for the diagnosis of traumatic diaphragmatic rupture (Figure 6-15). CT findings that are strongly associated with a diagnosis of diaphragmatic rupture include diaphragmatic discontinuity, diaphragmatic thickening (the “curled diaphragm” sign), segmental nonvisibility of the diaphragm, intrathoracic herniation of abdominal viscera, elevation of the hemidiaphragm, and concomitant hemothorax and hemoperitoneum. Other potential findings include the collar sign, thoracic fluid abutting intraabdominal viscera, the “dependent viscera” sign, contrast extravasation adjacent to the diaphragm, and a rib fracture adjacent to the diaphragm. As with standard radiographs, the collar sign on CT consists of a waist-like appearance of herniated organs at the level of the diaphragm; this often is best visualized on coronal reformatted images. The dependent viscera sign refers to lack of normal inter-position of the lungs between the subphrenic abdominal organs and the posterior chest wall; that is, the herniated viscera (bowel or solid organs) are no longer supported posteriorly by the injured diaphragm and fall to a dependent position against the posterior ribs. There is a positive dependent viscera sign on the right if the upper one-third of the liver abuts the posterior ribs, and on the left if the stomach or bowel abuts the posterior ribs.^24,25

The most common cause of phrenic nerve paralysis is surgery in the mediastinum. Rarely, the abnormality is idiopathic or a result of a malignant mediastinal tumor. In the neonate, birth injury is the most frequent cause. Phrenic nerve injury after cardiac surgery is a serious complication that often leads to respiratory insufficiency, particularly in patients younger than 2 years of age. Standard radiographs show elevation of the affected hemidiaphragm. Various other conditions can result in this finding, however (Table 6-1). Phrenic nerve paralysis is best confirmed by fluoroscopy or real-time ultrasound, which show paradoxical motion of the hemidiaphragm. As the patient inspires, the paralyzed hemidiaphragm rises while the normal side moves inferiorly; this finding is accentuated by having the patient sniff.^26–29

Direct thermal injury or toxic materials within smoke can produce tracheobronchial and pulmonary injuries. During the first 24 hours after the injury, manifestations of upper-airway edema dominate the clinical picture. The initial appearance of the effects on the lower respiratory tract may not occur until up to 2 days after the injury. Additional pulmonary complications may not become evident until 2 to 5 days after the initial injury. Acute respiratory distress syndrome is a potential complication of inhalational injuries and burns.³⁰

The radiographic findings in patients with thermal injuries of the large airways include subglottic edema and indistinctness of the tracheal wall. Early in the course, chest radiographs may be normal or demonstrate hyperinflation (Figure 6-16). Atelectasis can develop because of mucus plugging of the large bronchi; this usually results in one or more focal opacities that clear within a few days. The most common early radiographic manifestation of severe inhalational injury is pulmonary edema. The edema may involve the interstitium and/or airspaces. These patients are at risk for the development of a superimposed infectious pneumonia. Potential long-term lung sequelae of thermal lung injuries include bronchiectasis, bronchospastic disease, and obliterative bronchiolitis.