Endotracheal Tubes

On the chest radiograph, the position of an endotracheal tube (ETT) is determined by the location of the tube’s tip in relation to the carina with respect to the position of the patient’s chin. With the chin in the neutral position, the tip of the ETT should be 3 to 7 cm above the carina (Figure 57-1). Alternatively, the tip of the ETT should project over the T3 or T4 vertebral body, because the carina is located between T5 and T7 on anteroposterior radiographs in most individuals. Neck flexion and extension can result in 2 cm of downward or upward displacement, respectively, of the ETT.¹⁹ Projection of the anterior portion of the mandible over the lower cervical spine indicates neck flexion, whereas an unobscured cervical spine indicates neck extension.

Figure 57-1 Typical normal line and tube positions. Note expected positions of endotracheal tube (superimposed over T3 vertebral body [arrowhead]), central venous catheter (in the origin of superior vena cava [arrow]), and nasogastric tube (in stomach [double arrows]).

The most common complication of ETT placement is inadvertent intubation of the right main bronchus (Figure 57-2) because of its shallower angle of departure from the trachea compared to the left main bronchus. Esophageal placement of the ETT can occur, although this is usually detected on physical examination. Radiographic findings of esophageal intubation include direct visualization of the ETT lateral to the tracheal wall, gaseous distention of the stomach, and displacement of the trachea by an overdistended balloon cuff.

Figure 57-2 Anteroposterior chest radiograph shows endotracheal tube (arrows) extending into bronchus intermedius, with resulting collapse of left lung and right upper lobe from hypoventilation.

Tracheostomy Tubes

The tip of a tracheostomy tube should be several centimeters above the carina, and the tube’s diameter should be approximately two-thirds that of the trachea.²⁰ Unlike ETTs, chin position does not affect tracheostomy tube position. Air is commonly seen in the subcutaneous tissue of the neck and upper mediastinum immediately after tracheostomy tube placement and should resolve over time. Pneumothorax and mediastinal hematoma, the latter manifesting as a dense mediastinum with full, convex margins, are more worrisome complications of tracheostomy tube placement that should not be overlooked.

Central Venous Catheters

Central venous catheters are inserted from an internal jugular (IJ), subclavian (SC), or femoral approach. The optimal location of an IJ or SC catheter tip is within the superior vena cava downstream of the central venous valves. On the anteroposterior chest radiograph, the origin of the superior vena cava usually lies to the right of midline at the level of the first intercostal space (see Figure 57-1).²¹ The catheter tip should remain proximal to the right atrium to reduce the risk of arrhythmias, myocardial perforation, or cardiac tamponade. Portable chest radiographs should be obtained immediately after central venous catheter placement to determine catheter position and identify any complications such as pneumothorax, vessel perforation (Figure 57-3), cardiac perforation, retained or fragmented catheter, or a knotted catheter.

Figure 57-3 Complications of intravenous catheter placement. A, Right internal jugular (IJ) catheter (arrow) is lateral to right mediastinal margin (arrowheads), indicating catheter is extravascular. B, Twelve hours later, a pleural fluid collection has developed from inadvertent infusion of saline into right pleural space (arrows). C, In another patient, a peripherally inserted central catheter (PICC) line is malpositioned, with tip in internal jugular vein (arrow).

Peripherally Inserted Central Catheters

Peripherally inserted central catheters (PICCs) are relatively new devices gaining widespread acceptance for long-term central venous access. The catheters are small, 2 to 5 French, and are placed into the superior vena cava through a large upper-extremity vein. PICCs may be difficult to identify on bedside chest radiographs because of their small size and faint opacity. They are also more susceptible to displacement than other intravenous catheters, owing to increased flexibility of the material (see Figure 57-3).

Pulmonary Artery Catheters

Pulmonary artery catheters measure intracardiac and intrapulmonary pressures reflecting volume status, cardiac function, and vascular tone. Their use is declining in many ICUs because recent studies demonstrate limited utility in affecting patient outcomes in a variety of clinical settings.^22,23 Nevertheless, when they are used, accurate placement is critical for proper interpretation. The catheters are usually introduced via an internal jugular or subclavian approach; less commonly they may be inserted through the femoral vein. They then traverse the central venous system into the right ventricle, through the pulmonic valve into the main, then right (less commonly left) pulmonary artery, then “wedge” in a proximal interlobar artery. If the tip extends beyond these larger arteries (Figure 57-4), pulmonary infarction from occlusion of the pulmonary vessel or development of a pseudoaneurysm can ensue. The balloon at the catheter tip should be inflated only during placement or when obtaining pressure measurements, so an inflated balloon should never be present on a portable chest radiograph. Complications are similar to those that occur with other central venous catheters but also include pulmonary vascular perforation and pulmonary hemorrhage.

Figure 57-4 Tip of Swan-Ganz catheter extends into right lower lobe pulmonary artery. In this location, risk of vessel injury increases.

Intraaortic Balloon Pumps

Intraaortic balloon pumps (IABPs) assist left ventricular function in patients with severe left ventricular dysfunction, usually after myocardial infarction. They are essentially balloons approximately 16 cm in length that are inflated during systole to reduce afterload and augment coronary artery perfusion. IABPs are inserted into the common femoral artery and advanced into the descending thoracic aorta. On the frontal chest radiograph, the tip of the balloon should be visible within the descending thoracic aorta just distal to the origin of the left subclavian artery, typically at the level of aortic arch. A more upstream location of the balloon can result in occlusion of the subclavian and vertebral arteries, whereas a more downstream location can lead to occlusion of the mesenteric and renal arteries. IABPs can migrate, so position should be reassessed on subsequent chest radiographs.

Thoracostomy Tubes

Thoracostomy tubes are placed in the pleural space to drain fluid or air. On a chest radiograph, the side port of a thoracostomy tube is marked by a disruption in the radiographically opaque line and should be located medial to the inner margin of the ribs. A malpositioned thoracostomy tube is often suspected when the tube does not drain as expected. It may not be inserted into the pleural space at all but instead tunnel through the subcutaneous soft tissues. Alternatively, the tip may lie within a pulmonary fissure, or rarely within the lung parenchyma. Subcutaneous placement can be very difficult to ascertain on chest radiograph, and an intrafissural location can only be suspected when the tube follows the course of one of the pulmonary fissures. The cross-sectional nature of CT scans provides an advantage to accurately identify the course of a thoracostomy tube and its relationship to abnormal air or fluid collections (Figure 57-5).

Figure 57-5 Malpositioned thoracostomy tube after bedside placement. A, Anteroposterior chest radiograph shows bilateral thoracostomy tubes (arrows) with tips and side ports projecting over lungs. B, Computed tomography shows left thoracostomy tube (double arrows) is in posterior chest wall. Right thoracostomy tube (single arrow) is in satisfactory position. C, In a different patient, a small-bore, curved “pigtail” catheter is appropriately placed for drainage of a right pleural effusion.

Enteric Tubes

Enteric tubes are placed into the stomach or proximal small bowel via a transoral or transnasal approach and come in a variety of sizes and configurations (see Figure 57-1). These tubes are frequently placed in ICU patients, especially those who are endotracheally intubated. Although the best position for feeding tubes is controversial, placement distal to the pylorus may decrease the risk of aspiration.²⁴ Usually, enteric tube position is easily determined by a chest or abdominal radiograph, although they may occasionally be obscured by excess soft tissue in obese patients. These tubes can coil in the pharynx or esophagus, putting the patient at risk for aspiration if tube feeds are initiated. Inadvertent insertion into the tracheobronchial tree (Figure 57-6) and esophageal perforation are rare but have more serious consequences.

Figure 57-6 Distal-weighted enteric feeding tube (arrow) extending into right lower lobe bronchus.

Cardiogenic Pulmonary Edema

Several conditions can cause the pattern of homogenous lung opacity that represents, or mimics, pulmonary edema. The classic appearance of cardiogenic pulmonary edema is that of bilateral perihilar fluffy opacities, sometimes called a butterfly or bat-wing pattern, in association with an enlarged heart, engorgement of central pulmonary veins, interstitial edema, and vascular redistribution or cephalization of vessels (Figure 57-7). Pleural effusions may also be present. The opacities associated with cardiogenic pulmonary edema can fluctuate rapidly, a clue to its diagnosis. However, this classic appearance is rare in the ICU. The bat-wing pattern is seen in few patients with pulmonary edema; opacities may be asymmetrical due to variations in patient position and underlying cardiopulmonary disease, such as emphysema or mitral valve insufficiency. In addition, cephalization of the vasculature is not a very useful marker of edema in supine ICU patients. Finally, some patients, particularly those with milder disease or chronically elevated left ventricular pressures, may only have more subtle radiographic findings, such as peribronchial cuffing and indistinct vessels.^25,26 Serial measurements of vascular pedicle width may be a useful adjunct indication of intravascular volume status in these patients.²⁷

Figure 57-7 Cardiogenic pulmonary edema in a 54-year-old man with acute myocardial infarction. Chest radiograph shows an enlarged cardiac silhouette with bibasilar opacities and diffuse septal thickening in both lungs. Note Kerley’s A (arrowheads) and Kerley’s B lines (arrows).

Neurogenic Pulmonary Edema

Neurogenic pulmonary edema can occur in the setting of any cerebral insult, including intracranial hemorrhage or mass, head trauma, stroke, seizures, or infection. Elevated microvascular pressure and increased vascular permeability in the lung both appear to play a role in its development.²⁸ Neurogenic pulmonary edema can develop within hours after the neurologic insult or several days later. On the chest radiograph, neurogenic edema usually manifests as a diffuse, homogeneous pulmonary opacity similar to that of cardiogenic edema, but without an enlarged cardiac silhouette and often without the indistinct vessels that suggest engorgement. (Figure 57-8). Occasionally, opacities may have a focal distribution reflecting gravity, patient position, and heterogeneity in pulmonary venous pressure. Rapid clearing of the lungs within days of resolution of the neurologic insult is characteristic, in contrast to other forms of noncardiogenic pulmonary edema in which opacity can persist.²⁸ It is important to note that some patients with neurologic injury are treated with large volumes of intravenous fluid, which may complicate the interpretation of pulmonary edema opacities on the chest radiograph.

Figure 57-8 Neurogenic pulmonary edema in patient with large left middle cerebral artery stroke. Chest radiograph shows diffuse opacities similar to cardiogenic pulmonary edema, predominantly in the bases. Note normal cardiac silhouette. Echocardiogram confirmed absence of impaired cardiac function.

Acute Lung Injury and Acute Respiratory Distress Syndrome

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common in medical and surgical ICU patients and have a high mortality.^29–31 They are clinical syndromes defined by hypoxemia and diffuse bilateral lung opacities in the absence of left atrial hypertension.³² Both result from a massive inflammatory reaction in the lungs incited by a variety of causes, and they are radiographically indistinguishable. The severity of hypoxemia alone differentiates the two, with ARDS the more severe manifestation. In the acute phase of ARDS, diffuse ill-defined opacities often predominate in the periphery of the lungs. As the disease progresses, the entire hemithorax can become opacified on chest radiographs (Figure 57-9), although CT typically demonstrates heterogeneity in lung aeration. This finding has led to much discussion regarding appropriate ventilator management of ARDS to balance alveolar recruitment while avoiding hyperinflation of spared lung tissue (see Chapter 58). During the subacute phase (5 to 10 days later), proliferation of endothelial cells and fibroblasts leads to a pattern of progressive lung destruction. Some patients recover from ARDS without any residual deficit in pulmonary function, but others progress to a chronic phase several weeks after the initial lung injury and have permanent respiratory sequelae. Fibrosis and focal emphysema are usually evident on these patients’ radiographs or CT scans.

Figure 57-9 A 22-year-old man with clinical sepsis developed hypoxia 2 days after admission. Anteroposterior chest radiograph shows diffuse lung opacity with normal heart size, consistent with noncardiogenic pulmonary edema or acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Also note pneumothorax in left costophrenic sulcus (arrow).

Fat Embolism Syndrome

This syndrome is a rare but serious complication of recent severe fracture, usually of a long bone, and is characterized by pulmonary, cerebral, and cutaneous manifestations 12 to 72 hours after the injury. In mild cases, the chest radiograph often shows no abnormality. In more severe cases, the initial chest radiograph may be normal, but within 12 to 72 hours, airspace and interstitial opacities develop that resemble other causes of pulmonary edema (Figure 57-10), then resolve 10 to 14 days later in the absence of superimposed disease.³³ CT scans are often not performed in these patients, but when available, variable findings including focal or diffuse areas of consolidation or “ground-glass” appearance and small nodules have all been described.^34,35 Rarely, filling defects from fat emboli in pulmonary arteries are reported.³⁶ The history of fracture, associated nonpulmonary symptoms such as a petechial rash, and delay in onset of radiographic opacities are all clues to distinguish fat embolism syndrome from other causes of a pulmonary edema pattern on chest radiographs.

Figure 57-10 A 33-year-old man presented with a left femur fracture and clinical fat embolism syndrome. Initial chest radiograph was normal. A, Seventy-two hours later, diffuse pulmonary opacity developed without an enlarged cardiac silhouette, coinciding with dyspnea, altered level of consciousness, and diffuse petechiae. B, Computed tomography image (same day) shows geographic appearance of ground-glass opacity in both lungs, consistent with noncardiogenic pulmonary edema.

Unilateral Pulmonary Edema Pattern

Postpneumonectomy pulmonary edema is described later. Reexpansion pulmonary edema (RPE) rarely follows treatment of pneumothorax or pleural effusion. It is more likely to occur if the lung has been chronically collapsed, if large volumes of air or pleural fluid (greater than 1 L) are removed rapidly, or pleural pressure drops below −20 cm H₂O.³⁷ Recent studies call these absolute numbers into question, however.³⁸ Usually within a few hours after evacuation of air or fluid, patients develop symptoms such as cough, dyspnea, and tachypnea; hypotension due to third-spacing of edema fluid in the affected lung has been described. Chest imaging reveals diffuse homogeneous opacity on the affected side, and in rare cases, the contralateral lung may also demonstrate opacities.

Aspiration

Patients with a decreased level of consciousness are at risk for aspiration. These include neurologic or neurosurgical patients who have suffered a stroke, head injury, or seizure, as well as medical or surgical patients who have esophageal disorders, altered mental status, or who have been pharmacologically sedated. The clinical severity and radiographic appearance of aspiration depend on both the amount and composition of aspirated fluid. Radiographically, aspiration can result in unilateral or bilateral lobar or multilobar opacities. Opacities tend to be in the dependent portions of the lungs, including the posterior segments of the upper lobes and the superior and posterior basilar segments of the lower lobes (Figure 57-11). Occasionally, aspirated particulate matter or foreign bodies can obstruct the airways and cause volume loss.

Figure 57-11 A 49-year-old man presented with seizure and witnessed aspiration. A, Initial anteroposterior chest radiograph is normal. B, Twenty-four hours later, patchy left lower lobe opacity (arrow) has developed, consistent with aspiration pneumonia. Note increased opacity behind heart.

Pneumonia

The radiographic hallmark of community-acquired bacterial pneumonia (CAP) is lung consolidation with air bronchograms in a segmental, lobar, or (less commonly) diffuse distribution (Figure 57-12). In comparison, the majority of patients with healthcare-associated or nosocomial pneumonia (HCAP), including ventilator-associated pneumonia, are more likely to have bilateral multilobar disease.³⁹ Radiographs typically demonstrate bronchopneumonia characterized by patchy peribronchial opacities, bronchial wall thickening, and sometimes volume loss.

Figure 57-12 A 30-year-old man presented with Klebsiella pneumoniae infection. A, Initial chest radiograph shows right upper lobe opacity consistent with lobar pneumonia. B, Two days later, right lung is nearly completely consolidated, showing rapid spread of infection. Tube and line are in expected location. Pacing pad is superimposing on right chest.

CT scanning is unnecessary in most patients with community-acquired pneumonia and a typical chest radiograph as described; in such patients, a given radiographic pattern is poorly predictive of a specific causative organism.⁴⁰ CT scans may be helpful for patients whose chest radiographs are atypical or have nonresolving opacities, patients who are immunosuppressed, or patients who may require invasive procedures such as bronchoscopy. In these cases, CT can provide additional anatomic detail that may assist in identifying a pathogen or noninfectious etiology, or in guiding interventions. Ground-glass opacities are nonspecific, but airspace disease including consolidation and air bronchograms suggests bacterial, mycoplasma, or fungal pneumonia. Centrilobular nodules are infrequently found in bacterial pneumonia and instead suggest mycoplasma, fungal, or viral infection (Figure 57-13).

Figure 57-13 A 45-year-old woman with heart transplant and varicella pneumonia. Computed tomography shows multiple small lung nodules (arrows) and patchy foci of ground-glass opacity (arrowheads). A small left pleural effusion is present (curved arrow).

Chest radiography and CT may also show complications of pneumonia. Cavitation can occur in some bacterial infections, particularly in nosocomial pneumonia or immunocompromised patients, and may progress to larger abscess or pneumatocele formation. Pleural effusions are also more common in nosocomial pneumonia; a minority will become complicated and may develop into empyema (see later discussion).³⁹

Septic Emboli

Septic emboli to the lungs come from a variety of sources, including infected right heart valves, peripheral and pelvic thrombophlebitis, and infected intravenous catheters. The usual radiographic findings of septic emboli are bilateral ill-defined nodules, predominantly in the lung periphery. These opacities classically develop at different times and show features of different stages of evolution; they often cavitate and may develop into larger abscesses. On CT, multiple lung cavitary and noncavitary nodules and wedge-shaped subpleural areas of consolidation are the usual findings (Figure 57-14).

Figure 57-14 A 46-year-old intravenous drug abuser presented with septic emboli. A, Bedside chest radiograph shows multiple bilateral peripheral opacities, some of which are cavitary. B, Computed tomography shows multiple peripheral well-defined pulmonary nodules.

Pneumonectomy

Radiographs obtained immediately after pneumonectomy normally show midline position of the mediastinum and gas filling the pneumonectomy space. Over the first few days, the ipsilateral hemidiaphragm elevates, and fluid begins to accumulate within the pneumonectomy space as the gas is resorbed. In most cases, one-half to two-thirds of the hemithorax fills within the first week, and the remainder over the next several weeks to months.⁴¹ The mediastinum shifts toward the operative side as the remaining lung hyperinflates and herniates across the midline, anterior to the heart. The degree of mediastinal displacement depends primarily on the compliance and the degree of hyperinflation of the remaining lung. Appropriate mediastinal displacement is the most reliable indicator of a normal course after pneumonectomy. Failure of the mediastinum to shift to the operative side indicates an abnormality in the pneumonectomy cavity such as bronchopleural fistula, hemothorax, or empyema. Postoperative complications of pneumonectomy can occur early (within a few days of surgery) or late; in this review, we will focus on the early complications.

Postpneumonectomy pulmonary edema is an uncommon condition with a high mortality rate, due at least in part to an increase in pulmonary capillary permeability. Radiographic features can be mild, with peribronchial cuffing and ill-defined vascular structures. In more severe cases, the pattern is identical to that of ARDS. Bronchopleural fistula is another infrequent but life-threatening complication of pneumonectomy, which manifests with dyspnea and sometimes hemoptysis. Both pulmonary edema and bronchopleural fistula are more common after right pneumonectomy; in the latter case, the shorter length of the bronchial stump predisposes to leakage. Radiographic findings of bronchopleural fistula include persistent pneumothorax or subcutaneous and mediastinal emphysema after surgery, a decrease in height of more than 1.5 cm of the gas-fluid level in the pneumonectomy cavity, and mediastinal shift away from the operative side rather than toward it (Figure 57-15).

Figure 57-15 Serial chest radiographs after right pneumonectomy show development of a bronchopleural fistula. A, Supine view obtained the day after surgery shows fluid in right hemithorax and rightward deviation of mediastinum, as expected. Tube and line are in expected positions. B, Four days later, mediastinum is now shifted to the left, and several lucencies have developed in right hemithorax. C, Two weeks after pneumectomy, upright posteroanterior radiograph shows gas-fluid level (arrows) and leftward mediastinal deviation, opposite of what is expected, consistent with bronchopleural fistula from a stump leak.

Lobectomy

After uncomplicated lobectomy, the chest radiograph can show rotation and hyperinflation of the remaining lobe(s), change in the orientation of the remaining bronchovascular structures, linear atelectasis, and/or development of pleural effusion. Reorientation of the remaining bronchovascular anatomy should not be confused with atelectasis. Complications of lobectomy occur with less frequency than with pneumonectomy but are similar. In addition, lung torsion, which has a high mortality rate, occurs rarely and manifests as rapid opacification of a lobe or lung associated with unusual configuration of the hilum. Anastomotic suture lines are evident when the fissure incompletely divides the lung into lobes.

Pulmonary Contusion

Contusion is the most common lung injury after blunt chest trauma, occurring in up to 70% of patients.⁴² It is characterized by leakage of blood into the pulmonary interstitium and alveolar spaces and clinically presents with dyspnea, tachycardia, and hypoxia. On chest radiographs, the contusion manifests as pulmonary opacity in a nonanatomic distribution, in contrast to the usual segmental or lobar distribution of pneumonia or atelectasis. Contusion usually occurs in the lung periphery deep to the site of chest wall impact, although it is sometimes seen opposite the location of the injury owing to a contrecoup effect. The timing of the developing opacity on the chest radiograph suggests the diagnosis in the setting of acute trauma, presenting within the first several hours after injury and resolving within 14 days. CT is more sensitive than chest radiography for detecting pulmonary contusion as well as associated chest wall injuries.^43,44 The appearance on CT of lung contusion ranges from patchy, ground-glass opacity to dense consolidation in a nonsegmental distribution, often sparing 1 to 2 mm of subpleural lung (Figure 57-16).

Figure 57-16 A 30-year-old man involved in motor vehicle crash. A, Chest radiograph shows a small lucent area (arrowhead) within an area of left lower lobe opacity (arrows). B, Computed tomography image of chest shows a “cavity” with an air-fluid level (white arrow) in left lower lobe, representing a pulmonary laceration surrounded by pulmonary contusion and hemorrhage (black arrow).

Pulmonary Laceration

Pulmonary laceration is characterized by frank disruption of the lung parenchyma. Radiographic features of pulmonary laceration are often masked on chest radiography by the surrounding contusion during the first few days and are better seen on CT. The appearance will change over time. In the acute phase, the hematoma within the laceration appears as a well-circumscribed, homogeneous area of soft-tissue attenuation. As the hematoma evolves, a round or elliptical gas collection called a pneumatocele becomes more obvious (see Figure 57-16). Most pneumatoceles appear within a few days, but some may develop over several weeks. They can be single or multiple and can be several centimeters in diameter. Resolution occurs over several months.

Parapneumonic Effusion and Empyema

The nature of fluid within the pleural space can be difficult to determine on the chest radiograph. Pleural effusions can be transudative, exudative, purulent (empyema), bloody, or chylous. On the chest radiograph, pleural effusion causes increased opacity in the affected hemithorax, a crescentic opacity interposed between the inner margin of ribs and the lung, and an apical cap. In the setting of pneumonia, lateral decubitus films can often differentiate mobile from loculated fluid collections, with the latter suggesting active infection of the pleural space (empyema). However, loculations and gas within the pleural space, which also suggests frank empyema, are best detected on CT (Figure 57-17). Empyema can also complicate thoracic surgery, usually at least several days after the operation.

Figure 57-17 Coned-down contrast-enhanced computed tomography image of a 74-year-old man with left empyema from ruptured splenic abscess shows a complex pleural collection containing a large amount of gas (asterisk), smaller gas loculations (white arrows), and a loculated liquid component anteriorly (black arrow).

Acute Traumatic Aortic Injury

Tears of the thoracic aorta (Figure 57-20) are caused by acute deceleration injury such as occurs in a high-speed motor vehicle crash or a fall, or as a result of crush injury to the chest. A tear of the thoracic aorta almost always occurs in a transverse orientation, typically at the aortic isthmus. Tears of the ascending aorta or complete transection are nearly universally fatal, but if the adventitia remains intact, a pseudoaneurysm may form, usually with some amount of surrounding hemomediastinum. These may rupture at any time and require immediate surgical intervention.

Figure 57-20 A 35-year-old man was involved in a high-speed motor vehicle crash. A, Anteroposterior chest radiograph shows abnormal contour of mediastinum, obscuration of aortic knob, and rightward displacement of trachea, consistent with mediastinal injury. Note tubes are in satisfactory position. B, Computed tomography shows intimal flap within aortic lumen (black arrow), representing aortic dissection surrounded by mediastinal hematoma (white arrow).

Radiographic abnormalities that suggest aortic injury include a dense mediastinum with convex margins to the lungs, indistinct aortic contours, rightward deviation of the trachea, downward displacement of the left main bronchus, and thickening of the right paratracheal stripe Mediastinal widening is often mentioned as a sign of mediastinal hematoma, but this is an imprecise finding and not specific for aortic injury.^47,48 In patients whose chest radiographs are equivocal or highly suspicious for aortic injury, contrast medium–enhanced CT is indicated. CT findings of acute aortic injury include irregularity of the aortic wall, pseudoaneurysm, abrupt change in aortic caliber, intimal flap, extravasation of contrast material, and periaortic hematoma. Evidence of hemothorax may also be seen, usually on the left, on the chest radiograph or CT.

Tracheobronchial Tree Rupture

Rupture of the tracheobronchial tree is an uncommon consequence of blunt trauma, with bronchial rupture occurring more often than rupture of the trachea.⁴⁹ In bronchial rupture, the injury is usually located in the main bronchus near the carina. Disruption of the trachea typically involves the membranous portion just proximal to the carina.

Tracheobronchial disruption often causes pneumomediastinum or pneumothorax visible on chest radiographs and/or CT. The “fallen lung” sign (Figure 57-21), indicating complete bronchial disruption, describes the severed and collapsed lung lying against the posterolateral aspect of the chest wall or the diaphragm. Other findings that suggest tracheobronchial injury include a large pneumothorax not responding to percutaneous drainage, or pneumothorax and pneumomediastinum in the absence of pleural effusion. However, it should be noted that pneumomediastinum is not specific for tracheobronchial or esophageal injury after blunt trauma.⁵⁰ Bronchoscopy is usually performed to confirm tracheobronchial injury, although CT with two-dimensional multiplanar reconstruction may prove a useful noninvasive alternative.⁵¹

Figure 57-21 A 22-year-old man was involved in a high-speed motor vehicle crash. A, Anteroposterior chest radiograph shows right pneumothorax, pneumomediastinum, right lung collapse, and subcutaneous emphysema. B, Computed tomography shows tracheal laceration (large arrow), right pneumothorax (asterisk), and collapsed right lung (small arrows) in dependent portion of chest (“fallen lung sign”).

Esophageal Rupture

Acute rupture of the esophagus can occur by iatrogenic means, from blunt chest trauma, or in the setting of severe retching or vomiting (Boerhaave syndrome). Trauma patients are more likely to have an injury in the upper thoracic esophagus, whereas Boerhaave syndrome usually involves the lower third of the esophagus.⁵² Mediastinitis and septic shock rapidly follow esophageal rupture, accounting for the relatively high mortality rate. The radiographic findings of esophageal rupture include a dense mediastinum with convex margins to the lungs, pneumomediastinum, pleural effusion, pneumothorax, and hydropneumothorax. On CT, the area of greatest esophageal thickening often represents the perforation site. CT also provides more detailed information than radiography on developing complications. Contrast esophagography is the standard approach to confirm the diagnosis.

Thoracic Duct Rupture

The most common cause of thoracic duct disruption is iatrogenic injury.⁵³ Thoracic duct injury from blunt chest injury is very rare and is thought to occur with hyperextension of the thoracic spine. Chylothorax, which usually develops several days to weeks after the trauma, is the typical radiographic finding. The delay in development of chylothorax is a clue to the diagnosis, particularly in differentiating it from traumatic hemothorax (see earlier discussion). The injury site is best identified with lymphangiography.

Pulmonary Thromboembolic Disease

Acute pulmonary embolism (PE) is a potentially lethal condition that can be difficult to diagnose clinically because of the nonspecific clinical presentation. Hospitalized patients are at increased risk of developing a PE. Although many imaging tests, including ventilation-perfusion scintigraphy and conventional pulmonary angiography, have been used to diagnose pulmonary embolism, CT pulmonary angiography (CTPA) has emerged as the initial imaging study of choice, given its high sensitivity and specificity and generally good interobserver agreement.^54–57 CTPA has the additional advantage of evaluating the entire thorax for other explanations for cardiopulmonary signs and symptoms. Specifically in ICU patients, CTPA appears to be an accurate diagnostic technique; indirect CT venography (CTV) compares favorably with ultrasound in evaluating venous thrombosis and improves the diagnostic yield of CTPA alone.^57–59 The addition of CTV to PE evaluation protocols is a controversial topic because it requires additional radiation and has not been conclusively demonstrated to improve patient outcomes compared to CTPA alone.⁵⁹ However, this has not yet been well studied in hospitalized or critically ill patients.

Many findings on conventional chest radiographs have been described in patients with pulmonary embolism, but they are inconsistently present and are nonspecific. Features diagnostic of acute pulmonary embolism on CTPA include a partial or complete filling defect in the pulmonary arteries (Figure 57-22). Associated lung abnormalities such as regional oligemia, volume loss, and a wedge-shaped subpleural opacity may also be present.

Figure 57-22 A 46-year-old woman presented with acute shortness of breath and hypoxia. Chest radiograph is normal. A, Chest computed tomography shows a low-attenuation filling defect in left and right main pulmonary arteries (large arrows) and left upper lobe segmental artery (small arrow), representing massive pulmonary embolism. Emboli extend to left and right interlobar arteries (arrows) as well as a left lower lobe segmental artery (arrow), seen in B and C, respectively.