Symptoms include cough (with or without sputum), fever, chills, fatigue and malaise. Chest pain may be present, especially if there is pleural involvement. The elderly may present with confusion or other cognitive dysfunction. Clinically, pneumonia is classified as community acquired, hospital acquired, or ventilator dependent. On radiographs and CT, pneumonias are usually described as lobar pneumonia, bronchopneumonia, or intersitial pneumonia.

Lobar pneumonia typically shows dense opacification of a lobe or segment with little or no associated volume loss. They typically begin in the periphery and spread to adjacent alveoli via direct intra-alveolar connections (pores of Kohn and canals of Lambert). Airways appear outlined as dark tubular structures within otherwise opacified lung parenchyma (air-bronchograms). Lobar pneumonias are delimited by the pleural surfaces, which permits localization on radiographs. Common causative organisms include Streptococcus pneumoniae, Haemophilus influenzae, and Klebsiella pneumoniae.

Lobar pneumonia. Dense homogeneous consolidation of the right middle lobe lateral segment and portions of the medial segment.

Bronchopneumonia involves the airspaces of the lung in patches around the bronchi or bronchioles. This pattern is associated with Staphylococcus aureus, Streptococcus pneumoniae, Pseudomonas, tuberculosis, and Enterobacter. On CT, tiny soft tissue density nodules can be seen at the ends of bronchioles and create the appearance of a budding tree.

In bronchopneumonia due to post primary tuberculosis, the nidus of primary infection, usually in the apex, ruptures into a bronchus and spreads through the tracheobronchial tree to other regions of the lung. Resulting parenchymal destruction and residual scarring may result in cavity formation.

Many different organisms can produce radiographic findings of bronchopneumonia, and sputum and blood cultures may be necessary for precise diagnosis and management. Empiric treatment is directed by clinical parameters such as severity of illness, immunologic status, and whether the infection was community-acquired, hospital-acquired, or in a ventilated patient.

Bronchopneumonia. Heterogeneous airspace opacity predominantly involving the left lower lobe. The lingula is not involved, as the left heart border is sharply visible on the frontal radiograph.

Acute interstitial pneumonia is an idiopathic disease characterized by fever, and shortness of breath that progresses rapidly to hypoxia and respiratory distress/failure. It is due to severe diffuse alveolar damage from activation of the inflammatory cascade acutely, with later fibrotic changes. Acute interstitial pneumonia is indistinguishable from ARDS on imaging studies and demonstrates bilateral airspace consolidation and ground glass opacities. Cardiogenic pulmonary edema can have a similar appearance and should be excluded.

Aspiration pneumonia is the consequence of a direct chemical insult to the lung parenchyma by an aspirated solid or liquid material. The clinical presentation depends on the chronicity as well as the volume and pH of the aspirated contents. Several populations at risk include alcoholics, those undergoing general anesthesia, prolonged hospitalization, and mechanical ventilation. Aspiration pneumonia preferentially involves the posterior segments of the upper lobes and superior segments of the lower lobes, which are dependent regions, particularly in the supine patient.

Aspiration pneumonia in two different patients. Right upper and lower lobe consolidation (left image). Bilateral upper lobe/superior segment lower lobe heterogeneous consolidation (right image).

Pneumonia may be indistinguishable from, or superimposed upon many other conditions that result in lung opacity. These include pulmonary edema, pulmonary hemorrhage, lung contusion (in the setting of trauma), metastatic neoplasm and chemical pneumonitis.

Segmental embolus. Lateral basal segment right lower lobe embolus with associated wedge-shaped peripheral opacity corresponding to a small pulmonary infarct.

Occasionally large emboli can obstruct the central pulmonary arteries (saddle embolus) and severely compromise air exchange and circulatory function, in which case, the clinical presentation may include circulatory collapse.

Central “saddle” embolus. Large clot within the right and left main pulmonary arteries.

A negative serum D-dimer effectively excludes pulmonary embolism in patients with low to moderate pretest probability, based on a collection of clinical findings known as the Wells criteria:

Wells Criteria for Prediction of Pulmonary Embolism

Clinical signs and symptoms of DVT + 3

PE is #1 diagnosis OR equally likely + 3

Heart rate > 100 + 1.5

Immobilization at least 3 days OR

surgery in the previous 4 weeks + 1.5

Previous, objectively diagnosed PE or DVT + 1.5

Hemoptysis +1

Malignancy w/ treatment within 6 months or palliative +1

Risk

< 2 low risk (1.3% incidence)

2-6 Intermediate risk (16.2% incidence)

>6 high risk (37.5% incidence)

Patients who are considered to be at high clinical risk, and those low to moderate risk who have an elevated D-dimer, should undergo CT angiography optimized for pulmonary arterial opacification. When positive, CT demonstrates central nonenhancing thrombus surrounded by contrast material. If right heart pressure is increased, the ventricular septum may appear straightened or bowed toward the left ventricle and contrast may reflux into the hepatic veins.

Increased right heart pressures due to large pulmonary embolus. The right ventricle is enlarged with straightening of the intraventricular septum.

Chest radiographs in patients with pulmonary emboli are typically normal or nonspecifically abnormal. Atelectasis, pleural effusions, or small peripheral opacities are sometimes encountered, but they can be seen in many other conditions.

Lower-extremity deep venous thrombosis (DVT) is a common disorder with predisposing factors that include immobilization, prior DVT, recent surgery, hypercoagulable syndromes, indwelling central venous catheter, increased estrogen state, and malignancy. Clinical findings include pain in the calf or thigh, unilateral leg edema, and warmth or tenderness. Ultrasound is most frequently used to differentiate DVT from other clinically similar entities such as cellulitis, ruptured Baker cyst, superficial thrombophlebitis, chronic thrombosis, and venous insufficiency, all of which can cause lower-extremity edema.

The single most reliable diagnostic finding is a non-compressible deep lower extremity vein. Other ultrasound findings include intraluminal thrombus, an enlarged vein, absent color flow signal, absent respiratory variation, and absent response to Valsalva maneuver or squeezing of the calf.

Deep venous thrombosis. Echogenic material fills and expands the superficial femoral vein. In the images on the right, the appearance of the proximal superficial femoral vein without (left) and with (right) compression are identical.

Deep venous thrombosis management includes treatment with low-molecular-weight heparin and analgesic pain control. Treatment of acute PE involves correction of hypoxemia with supplemental oxygen and immediate initiation of anticoagulation. Rarely, patients with hemodynamic compromise may require thrombolytic therapy or embolectomy.

Thoracic aortic dissections are classified by their point of origin, and this determines treatment and prognosis. Stanford type A dissections begin in the ascending aorta and may or may not extend into the descending thoracic aorta. These are managed surgically or by endovascular repair due to their high rate of fatal complications, which include acute aortic regurgitation, rupture into the mediastinum or pleural space, and cardiac tamponade from rupture into the pericardium. Stanford type B dissections arise beyond the left subclavian artery origin, do not require surgery, and are managed by aggressive blood pressure control.

Type A aortic dissection. Unopacified blood and thrombus fills the larger false lumen of a proximal aortic dissection with associated mediastinal hematoma.

Type B aortic dissection. Acute hyperdense intramural hemorrhage surrounds the descending aorta on nonenhanced chest CT. CT angiogram at the level of the upper abdomen shows that the celiac trunk arises from the smaller true lumen.

Patients typically present with sudden, severe chest pain that radiates to the back. Occlusion of branch vessels may result in symptoms of renal, mesenteric or cerebral ischemia.

Urgent CT evaluation is indicated and should include a nonenhanced scan to identify hyperdense intramural or extra-aortic hematoma followed by arterial phase contrast examination. This permits identification of the true and false (intramural) lumens of the dissected aorta, as well as any branch occlusion, intraluminal thrombus, or focal dilatation.

Abdominal radiographs are generally not indicated and are often normal, but they may show aortic calcifications or aneurysm and, if compared with a prior examination, interval aortic enlargement or contour change.

Nontraumatic aortic rupture occurs in the setting of aortic dissection, aneurysm, coarctation, atherosclerosis, inflammation, mycotic disease, or erosion by an adjacent malignant tumor. Most such patients die from catastrophic blood loss, but some may survive to present to the emergency department with chest pain, hypotension and dyspnea.

As in traumatic aortic rupture, portable chest radiographs show a widened abnormal mediastinal contour. Indistinct aortic knob, widened paratracheal stripe, and depression of the left main bronchus are sometimes seen. CT is diagnostic and identifies aortic intramural hematoma, mediastinal pleural hematoma, hemopericardium, and other aortic abnormalities including dissection or pseudoaneurysm. Treatment requires urgent surgical intervention via open or endovascular repair.

Nontraumatic aortic rupture due to ascending aortic (type A) dissection. Comparison radiograph from a prior admission shows baseline mild cardiomegaly. Portable examination obtained in the emergency department for evaluation of acute chest pain shows interval enlargement of the cardiac contour with marked ascending aortic widening.

Further reading and reference

Aortic Dissection (National Library of Medicine-StatPearls)

Alcoholism and acute over-eating are risk factors. The typical patient is a man between the ages of 50 and 70 with chest pain and subcutaneous emphysema following an episode of forceful retching or vomiting. Dyspnea, blood-stained vomitus, and, in severe cases, hypovolemic shock may be present.

Consequences include hydropneumothorax, mediastinitis, empyema, pericarditis, sepsis and shock. Overall mortality is ~ 30%. A delay in diagnosis and treatment increases mortality significantly; 50% after 24 hours, and 90% after 48 hours. Treatment consists of early surgical repair and drainage.

Pneumomediastinum, sometimes with cervical subcutaneous emphysema, and left pleural effusion are the radiographic hallmarks of Boerhaave syndrome. CT shows focal distal esophageal wall thickening, mediastinal fluid, pneumomediastinum, and pleural effusion. Esophagogram with water-soluble contrast material is diagnostic and demonstrates contrast extravasation into the mediastinum and/or pleural space just proximal to the esophageal hiatus.

Esophageal rupture after vomiting. Subcutaneous emphysema, pneumomediastinum, and left pleural effusion. Gastrografin esophagogram shows extensive extravasation of contrast into the mediastinum and pleural space.

Esophageal rupture after vomiting. Radiograph and CT show pneumomediastinum, lower cervical soft tissue emphysema, and left pleural effusion. Esophagram demonstrates distal esophageal defect and extravasation of contrast.

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Barium esophagram shows a dilated distal esophagus, aperistalsis, and absent lower esophageal sphincter relaxation, evidenced by a “bird’s beak” appearance to the stenotic gastroesophageal junction. Plain chest radiographs are rarely diagnostic, but the food-filled distended esophagus or a mediastinal air-fluid level may be seen. The gastric air bubble may be small or absent. Esophagoscopy with manometry can be performed to document increased sphincter pressure and exclude complicating esophagitis or neoplasm.

Achalasia. The mediastinum is widened, with a double cardiac shadow along the right heart border. The esophagus is expanded and filled with granular material corresponding to retained food/fluid.

Achalasia. Double cardiac shadow along the lower right heart border on frontal radiograph with retrocardiac density on lateral view. CT and esophagram show gross esophageal dilatation proximal to stenosis (“bird beak”) at the gastroesophageal junction. Incidental barium aspiration.

Treatment aims to reduce lower esophageal sphincter pressure by surgical myotomy, dilation, or endoscopic injection of botulinum toxin.

Patients with laceration of all three layers of the aortic wall invariably exsanguinate before reaching a hospital. If a patient with traumatic aortic injury survives to reach the emergency room, it is because the tear is transverse rather than longitudinal and the outer layer of the aorta (adventitia) remains intact.

Signs of a juxta-aortic hematoma on supine portable radiographs include mediastinal widening, indistinct margins, poor aortic contour definition, a widened paratracheal stripe, pleural effusion, caudal displacement of the right mainstem bronchus, and rightward displacement of an oro- or nasogastric tube. Many patients will have no mediastinal abnormality on portable chest radiograph.

Traumatic aortic injury (11-story fall). Marked upper mediastinal widening with sharply-defined lateral border. Bilateral airspace opacities indicate pulmonary contusion or aspiration. Left scapular body fracture.

CT in arterial phase should be performed in patients with reported high-energy injury mechanism or who have upper rib, sternal, or scapular fractures on portable radiograph. A normal thoracic CT reliably excludes great vessel injury and can differentiate true aortic disruption from venous mediastinal hematoma by identifying direct findings of aortic injury: pseudoaneurysm, intimal flap, mural thrombus, arterial contrast extravasation, and focal change in aortic contour (“pseudocoarctation”).

Traumatic aortic injury with large hemothorax.  Portable supine radiograph shows widened, ill-defined upper mediastinum. The left hemithorax is opacified. The orogastric tube is displaced to the right. Postcontrast CT demonstrates a large left hemothorax and hemomediastinum. A small aortic pseudoaneurysm is visible adjacent to the left pulmonary artery on the axial image. Sagittal reformations show an associated aortic intramural hematoma, intimal flap, and pseudocoarctation.

Massive hemothorax (> 1 liter) is due to arterial or large venous injury and presents with clinical signs of shock and hypoperfusion. It is a surgical emergency due to potential heart and great vessel tamponade from the accumulated blood, acute hypovolemic shock, and hypoxia from lung collapse.

Hemothorax (stab wound). Massive left intrapleural fluid collection with compressed adjacent lung, contralateral mediastinal shift, and depression of the ipsilateral hemidiaphragm.

Supine chest radiographic findings are often subtle, depending on the volume of blood. Hazy increased density of the involved hemithorax with preserved vessel definition may be seen in smaller posterior hemothoraces. Large amounts of blood can fill the pleural space lateral to the lung and appear as a dense crescent-shaped collection.

Hemothorax (stab wound). Supine radiograph with hazy opacification of the left hemithorax and preservation of the right heart border. CT shows large left posterior blood collection, with lower lobe compressive atelectasis.

CT with arterial-phase contrast enhancement is diagnostic; acute blood products have an attenuation of 35–70 HU, and layering of intrapleural fluid with different densities due to combinations of clot, blood cells, and serum can be seen. In addition, arterial phase CT evaluates the integrity of the great vessels, detects of any foci of arterial extravasation that may be amenable to embolotherapy, and identifies concomitant pneumothorax as well as any other visceral injuries.

Hemopneumothorax (bicyclist struck by car). Moderate right pneumothorax, small hemothorax with lower lobe compressive atelectasis.

Initial management is by placement of a chest tube, which permits evacuation of clot, re-expansion of the collapsed lung, and effective tamponade of low-pressure bleeding. Definitive surgical management depends on the nature of the injury and source of hemorrhage.

The most common imaging findings are pneumomediastinum and pneumothorax. Persistent pneumothorax after chest tube placement and suction is the hallmark of a major bronchial injury. With complete bronchial transection, the ipsilateral lung falls to the dependent (usually posterior) portion of the hemithorax; the “fallen lung” sign.

Bronchial rupture. The right lung is collapsed about the hilum and inferiorly positioned in the chest. Large right pneumothorax

Bronchial rupture. Persistent large pneumothorax following chest tube placement.

Chest CT can identify the exact site of the tear as a focal or a circumferential defect in the tracheal or bronchial wall. Other imaging findings include airway contour deformity, extraluminal endotracheal tube tip position, herniation or overdistension of the balloon, pneumomediastinum, and deep cervical soft tissue emphysema.

Smoking is the most common risk factor for spontaneous pneumothorax, which is usually due to rupture of a subpleural bulla. Primary pneumothorax typically occurs in persons under the age of 35 and is not associated with underlying lung disease. Secondary pneumothorax can occur in the settings of chronic obstructive pulmonary disease, asthma, cystic fibrosis, interstitial lung disease, malignancy, and specific diseases that cause lung cyst formation; lymphangioleiomyomatosis, and Birt-Hogg-Dube syndrome. In women, spontaneous pneumothorax can coincide with menses and is due to intrathoracic endometrial deposits. This is referred to as catamenial pneumothorax.

Patients typically present with acute pleuritic chest pain and dyspnea, but many are only minimally symptomatic.

Spontaneous pneumothorax due to apical bullae. Small bilateral subpleural cysts at both lung apices predispose to spontaneous pneumothorax.

On upright PA radiographs, a fine, dense line corresponds to the visceral pleura and divides the lucent, air-filled lung from air in the pleural space. Pulmonary vessels and other lung markings are not visible lateral to the visceral-pleural line. The heart and mediastinum are often normal in position but may be displaced to the opposite side in tension pneumothorax.

Tension pneumothorax. Left pneumothorax and pneumomediastinum (arrows). Subtle visceral-pleural line.

Tension pneumothorax. Same patient as above with left pneumothorax and pneumomediastinum. Mild left to right mediastinal shift.

Supine, portable radiographs obtained in trauma patients often do not show pneumothoraces even when present, partly because air in the pleural space lies anterior, rather than lateral to the lung, and the pleura is imaged en face rather than tangentially. Thoracic hyperlucency that extends over the lateral costophrenic angle and upper abdomen is referred to as the “deep sulcus” sign and is a useful but indirect finding in acute trauma.

Deep sulcus sign on supine portable radiograph. Initial study (left) shows diffuse bilateral airspace opacity due to cardiogenic edema. Subsequent supine radiograph (right) shows left sided pneumothorax with deep sulcus sign.

Ultrasound can identify pneumothorax in the trauma setting, but findings are often subtle. The normal lung shows mobile dotlike echoes as the visceral pleura moves against the parietal pleura with respiration. In pneumothorax these mobile echoes are not seen.

Skin folds can simulate the appearance of a pneumothorax and are seen exclusively on portable AP chest radiographs. When the detecting plate is placed behind the patient, redundant skin can fold against the plate, causing an air–soft tissue interface external to the patient and will appear as a dense edge against more lucent lung usually containing visible peripheral vessels.

In patients with hypoxia or vascular collapse, treatment should not be delayed while awaiting chest radiograph. A 14–16 gauge intravenous catheter can be inserted, either in the second anterior intercostal space in the midclavicular line or in the fifth intercostal space on the anterior axillary line, before a larger chest tube can be placed.

The right hemidiaphragm is elevated and the liver has herniated into the thoracic cavity with leftward tracheal and mediastinal shift. A right hepatic lobe laceration is present.

Blunt impact, with abrupt elevation of intra-abdominal pressure sometimes results in diaphragmatic rupture, more commonly on the left side. Abdominal viscera can herniate through the defect, and result in acute or delayed bowel obstruction, which may occur years after the primary injury. In patients on mechanical ventilation, positive intrathoraci pressure can prevent herniation and make early diagnosis more difficult.

Penetrating trauma to the back or upper abdomen can also result in diaphragm laceration, but the defect is usually smaller than tears resulting from blunt trauma.

In both cases, the integrity of the diaphragm should be carefully assessed, particularly in the ventiated patient and in any patient with penetrating trauma that may traverse the diaphragm. Remote laceration is a consideration in any patient with acute bowel obstruction and a past history of torso trauma.

CT is the optimal imaging technique, although plain radiographs and ultrasound may also be diagnostic. Direct imaging signs include diaphragmatic discontinuity, waistlike constriction of herniated viscus (collar sign), and the dependent viscera sign, in which abdominal viscera appear to contact the posterior thoracic wall. Indirect findings include hemidiaphragm elevation  > 4 cm, a nasogastic tube that does not descend below the expected position of the gastroesophageal junction, diaphragmatic thickening, injury on both sides of the diaphragm, or hemothorax without obvious thoracic injury.

Penetrating injuries are less likely than blunt injuries to result in organ herniation, as the diaphragmatic defect is typically smaller (1 cm for penetrating injury compared with 5–6 cm in blunt trauma)

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Sternal fractures are a marker of high-energy impact and are seen in approximately 8% of patients with blunt thoracic trauma. Retrosternal hematoma, myocardial contusion, coronary artery tear, aortic laceration, and tracheobronchial tear are potential associated injuries.

Sternal fractures are not visible on supine portable AP chest radiographs, but they can be detected with a true lateral view. In practice, they are usually diagnosed on CT and are most commonly located 2 cm below the sternomanubrial joint. Retrosternal hematoma may be the consequence of great vessel injury or hemorrhage from small vessels; identification of normal fat between a substernal hematoma and the aorta indicates that the hematoma is not due to aortic rupture.

Sternal fracture. The upper portion of the sternal body is depressed by half its width at a point 4 cm distal to the sternal manubrial joint. No visible retrosternal hematoma.

Sternoclavicular dislocation

Sternoclavicular dislocation refers to anterior or posterior displacement of the medial clavicle relative to the sternal manubrium. Posterior dislocation, in which the clavicular head is displaced deep to the manubrium, typically results from a blow to the dorsal shoulder or to the anteromedial clavicle and can be associated with serious morbidity; as the medial clavicular head is driven into the soft tissues of the thoracic inlet, it can impact or injure the trachea, esophagus, recurrent laryngeal nerve, or great vessels. Anterior sternoclavicular dislocation results from a frontal blow to the ipsilateral shoulder, is more common than posterior dislocation, and carries less risk of associated injury.

The sternoclavicular joint is difficult to assess on plain radiographs. CT permits accurate characterization of the dislocation and any hematoma or vascular compromise. Sternal dislocations are usually treated by closed reduction in the absence of associated mediastinal injuries.

Posterior right medial clavicle dislocation. The right medial clavicular head is interposed between the subclavian vein and the right carotid artery. No associated vascular hematoma or definite injury. On coronal images, the right medial clavicle is posterior to the sternal manubrium. The left clavicle articulates normally.

Flail Chest

Flail chest is defined by the presence of five or more adjacent simple rib fractures or more than three segmental rib fractures; it can lead to impaired ventilation and respiratory failure in the trauma patient. The normal thorax increases in volume on inspiration. In flail chest, the affected side, lacking structural support, retracts inward under negative intrapleural pressure as the diaphragm contracts. On expiration, positive intrapleural pressure allows the free-floating segment of fractured ribs to bulge outward, referred to as paradoxical respiration.

Flail chest. The left chest wall is deformed due to segmental left fifth through seventh rib fractures with adjacent opacity. Noncontrast CT reveals depressed segmental rib fractures with adjacent anterior segment left upper lobe pulmonary contusion and laceration. Extensive soft tissue emphysema. Left thoracostomy tube.

Flail chest is extremely painful, and patients display rapid shallow breathing. Hypoxia is usually a consequence of associated pulmonary contusion rather than simple hypoventilation. Management includes supplemental oxygen and analgesics and may require regional nerve blocks or epidural anesthesia in severe cases. Surgical plating of rib fractures is increasingly utilized in chest trauma and  has been shown to reduce pain, pulmonary complications, length of mechanical ventilation, length of overall hospital stay and mortality. Indications include flail chest, chest wall deformity and failure to wean from mechanical ventilation.

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Cardiomediastinal anatomy. On the frontal radiograph, the right heart border corresponds to the right atrium (RA) and superior vena cava/right atrial junction. The left heart border corresponds to the left ventricle (LV). On the lateral radiograph, the anterior border of the heart is made up of the right ventricle (RV) and pulmonary outflow tract (PA), with the inferior and posterior margins formed by the left ventricle, inferior vena cava (IVC), and left atrium (LA). The retrosternal space in adults should be free of soft tissue.

Pulmonary segmental anatomy. The lobar anatomy of the right and left lungs dif- fers; the right lung contains a middle lobe and the left upper lobe contains a roughly analogous lingular segment. On the lateral radiograph, the right and left lungs are superimposed upon each other. Localizing an intrapulmonary mass or lesion requires attention to both frontal and lateral views.

Pulmonary segmental anatomy on CT. Axial images at the levels of the Aortic arch, pulmonary artery, aortic root/left mainstem bronchus, and cardiac chambers. Solid lines denote lobar divisions. Dotted lines indicate segmental borders.

Localization of incidental pulmonary nodule. A 1 cm nodule located between the 5th and 6th posterior ribs on the frontal radiograph is located in the anterior segment of the right upper lobe.

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