Acute pulmonary embolism (PE) is the third most common cause of cardiovascular death, with an average incidence in the USA of 1 per 1,000 persons. Approximately 300,000 patients die from PE each year. The most common signs and symptoms at the time of presentation include dyspnea, pleuritic chest pain, tachypnea, and tachycardia [1]. The classic clinical triad of chest pain, dyspnea, and hemoptysis is only seen in a minority of patients. Common risk factors for PE include acute medial illness, prolonged immobilization, malignancy, and orthopedic surgery.

The chest radiograph is usually the first imaging examination obtained in the evaluation of patients presenting with chest pain and can be used to detect other potential causes of symptoms mimicking PE, including pneumonia, pulmonary edema, and pneumothorax. Several classic radiographic signs of PE have been described, but are infrequently encountered. These include Westermark’s sign, which is increased lucency of all or portion of a lung secondary to decreased vascular flow in the setting of obstructive PE. Hampton’s hump is a peripheral, wedge-shaped opacity that may represent pulmonary infarction in the setting of PE [2].

Ventilation-perfusion scintigraphy is performed with the intravenous injection and inhalation of radiopharmaceuticals for the purpose of identifying PE. It is most valuable in the setting of a normal chest radiograph, as pulmonary parenchymal disease limits its sensitivity and specificity. The presence of a ventilation-perfusion mismatch, or a defect on the perfusion study only, is suggestive of PE. The Prospective Investigation of Pulmonary Embolism II (PIOPED II) interpretation scheme is used in the reporting of the ventilation-perfusion scan. The diagnostic categories include normal, very low probability, low probability, intermediate probability, and high probability. Many patients have scans between low and high probability and require additional testing for diagnosis [3].

Pulmonary angiography has traditionally been considered the gold standard examination to evaluate for PE. However, multidetector computed tomography (MDCT) with intravenous contrast has now surpassed angiography and is the primary modality utilized for diagnosis of PE in most institutions. Factors contributing to the effectiveness of CT over pulmonary angiography include widespread availability and fast scan times. Additionally, ventilation-perfusion scintigraphy and pulmonary angiography do not accurately demonstrate subsegmental PE. In addition to demonstrating PE within the main, lobar, and segmental PE, MDCT is more accurate in identifying PE affecting the subsegmental pulmonary arteries. In addition to identifying PE, CT can evaluate the remainder of the chest for abnormalities such as pneumonia, pulmonary edema, and pneumothorax. The most common finding on contrast-enhanced CT is hypodense filling defects within opacified pulmonary artery branches (Fig. 23.1) [4]. Saddle emboli, or pulmonary emboli bridging the main pulmonary arteries, may be seen. Abrupt vessel cutoff and complete occlusion may be identified. Cardiac dysfunction in the setting of massive acute PE may manifest as enlargement of the right atrium and ventricle, straightening of the interventricular septum, or bowing of the interventricular septum towards the left ventricle (Fig. 23.2) [5]. The most common finding within the lung parenchyma in patients with PE is atelectasis. Pulmonary infarction may be seen within the peripheral aspects of the lung parenchyma and typically manifests as wedge-shaped ground glass or mixed ground glass and solid opacities (Fig. 23.3). A thickened vessel may be seen extending to the margin of the opacity. Infarction is more common in patients with impaired collateral circulation and pulmonary venous hypertension. Pleural effusions may also be present [6].

Esophageal perforation is a potentially life-threatening phenomenon. The most common etiology of esophageal perforation is iatrogenic, usually associated with endoscopic instrumentation and thoracic surgery. The rate of perforation associated with endoscopy has been estimated at approximately 1 per 1,000. In one series, perforation was iatrogenic in 55 % of cases. Traumatic perforation is most common within the cervical portion of the thoracic esophagus, which is the narrowest portion. Other etiologies include spontaneous perforation (Boerhaave’s syndrome) in 15 %, foreign body in 14 %, and blunt or penetrating trauma in 10 %. Underlying esophageal disease, such as esophagitis or malignancy, appears to place patients at an increased risk of rupture [7].

Boerhaave’s syndrome or spontaneous esophageal perforation is a rare phenomenon, affecting approximately one per 6,000 patients [7]. Perforation is typically due to an episode of violent vomiting. In this scenario, the posterior esophagus ruptures, usually near the crus of the left hemidiaphragm. The most common clinical symptoms include history of vomiting, chest pain, and fever. Subcutaneous emphysema may be present on physical examination [7, 8]. The role of conventional chest radiography in the assessment of esophageal perforation is limited, and initial radiographs may be normal. The most common abnormalities are characterized as indirect signs of esophageal perforation and include pneumomediastinum, pneumothorax, and pleural effusion (Fig. 23.4) [7, 8].

Pneumomediastinum may appear as visualization of the white pleural line adjacent to the mediastinum, areas of radiolucency in the soft tissues, and focal air collections within the mediastinum and retrosternal region. The “continuous diaphragm sign,” a linear collection of air along the diaphragm, and “V sign” of Naclerio, a collection of air along the left paraspinal region above the left hemidiaphragm, are ­well-described signs of pneumomediastinum that are rarely seen. CT is definitive in demonstrating the presence of pneumomediastinum, pneumothorax, and pleural effusion complicating esophageal perforation.

If oral contrast material is used at the time of CT imaging, extravasation of contrast from the esophageal lumen into the mediastinum or pleura may be present (Fig. 23.5). Eso­phagography had previously been considered the initial examination of choice in the evaluation of uncomplicated esophageal disease. In the event of esophageal perforation, esophagography should be performed with water-soluble contrast material, which is rapidly absorbed by the mediastinum. However, water-soluble contrast material should not enter the tracheobronchial tree, as its hyperosmolar composition may result in pulmonary edema. Contrast esophagography may demonstrate extravasation of intraluminal contrast material into the mediastinum or pleura (Fig. 23.6). However, false-negative results may be encountered 10 % of the time [7].