Читать книгу The Esophagus - Группа авторов - Страница 187

Esophageal carcinoma comprises about 1% of all cancers in the United States and 7% of all gastrointestinal tumors [123]. Patients with esophageal carcinoma usually present with dysphagia, but this is a late finding that generally develops only after the tumor has invaded periesophageal lymphatics or other mediastinal structures. As a result, most patients have advanced, unresectable lesions at the time of diagnosis, with overall five‐year survival rates of less than 10% [123]. Histologically, about 50% of these tumors are squamous cell carcinomas, and the remaining 50% are adenocarcinomas [123].

Unlike squamous cell carcinomas of the esophagus, adenocarcinomas virtually always arise on a background of Barrett’s mucosa in the esophagus. The reported prevalence of adenocarcinoma in patients with Barrett’s esophagus is about 10% [123]. Studies using incidence rather than prevalence data indicate that the relative risk of adenocarcinoma developing in patients with Barrett’s esophagus may be 30–40 times greater than that in the general population [124].

Figure 6.52 Drug‐induced stricture. Double‐contrast view shows a smooth, tapered stricture (arrows) in the upper thoracic esophagus caused by previous potassium chloride ingestion.

Early esophageal cancer is defined histologically as cancer limited to the mucosa or submucosa without lymph node metastases. Unlike advanced carcinoma, early esophageal cancer is a readily curable lesion with five‐year survival rates of about 90% [123]. As mentioned previously, early diagnosis of esophageal cancer is usually limited by the late onset of symptoms in patients with this disease. In a minority of patients, however, dysphagia or upper gastrointestinal bleeding develops while the tumor is still at an early stage. Patients with early adenocarcinoma arising in Barrett’s mucosa may also seek medical attention because of their underlying reflux disease, so some early esophageal cancers may be detected fortuitously in patients with reflux symptoms [123].

Double‐contrast esophagography has a sensitivity of greater than 95% in detecting esophageal cancer [125], a figure comparable to the reported endoscopic sensitivity of 95–100% when multiple brushings and biopsy specimens are obtained [123]. Early esophageal cancers are usually small, protruding lesions less than 3.5 cm in diameter. These tumors may be manifested on double‐contrast studies by plaque‐like lesions (often containing a flat central ulcer) (Figure 6.63), by sessile polyps with a smooth or slightly lobulated contour, or by focal irregularity of the esophageal wall [123, 126]. Early adenocarcinomas in Barrett’s esophagus may also be manifested by a localized area of wall flattening or irregularity within a pre‐existing peptic stricture [123] (Figure 6.64). Superficial spreading carcinoma is another form of early esophageal cancer characterized on double‐contrast studies by a confluent area of poorly defined mucosal nodules or plaques that merge with one another [123, 126] (Figure 6.65). Although these lesions can sometimes be confused with focal Candida esophagitis, the plaques in candidiasis tend to be discrete lesions with normal intervening mucosa, whereas the nodules in superficial spreading carcinoma tend to coalesce, producing a continuous area of disease.

Figure 6.53 Eosinophilic esophagitis with a “ringed esophagus.” Double‐contrast view shows a smooth, tapered stricture in the upper thoracic esophagus with distinctive ring‐like indentations (arrows) in the region of the stricture.

Figure 6.54 Eosinophilic esophagitis with a small‐caliber esophagus. Prone single‐contrast view shows a long segment of narrowing involving the entire thoracic esophagus with smooth contours and a mean diameter of less than 20 mm. Also note a small hiatal hernia (arrow).

Figure 6.55 Lichen planus with a small‐caliber esophagus. Prone single‐contrast view shows diffuse narrowing of the entire thoracic esophagus indistinguishable from that in eosinophilic esophagitis (see Figure 6.54). The clinical history is therefore critical for differentiating these conditions.

Source: Reproduced from Rauschecker AM, Levine MS, Whitson MJ, et al. [108], with permission.

Figure 6.56 Radiation injury to the esophagus. (A) Double‐contrast view shows decreased distensibility of the mid esophagus and a granular appearance of the mucosa caused by acute radiation esophagitis. (B) Double‐contrast view from a follow‐up study six months later shows a smooth, tapered area of narrowing in the mid esophagus due to the development of a radiation stricture.

Source: Reproduced from Levine [110], with permission.

Figure 6.57 Chronic lye stricture. Double‐contrast view shows a long stricture in the mid and distal esophagus caused by extensive scarring and fibrosis from lye ingestion many years earlier.

Advanced esophageal carcinomas usually appear on barium studies as infiltrating, polypoid, ulcerative, or, less commonly, varicoid lesions [123]. Infiltrating carcinomas are manifested by irregular luminal narrowing with mucosal nodularity or ulceration and abrupt, often shelf‐like borders (Figure 6.66). Polypoid carcinomas appear as lobulated intraluminal masses (Figure 6.67). Primary ulcerative carcinomas are manifested by a giant meniscoid ulcer surrounded by a radiolucent rind of tumor [127] (Figure 6.68). Finally, varicoid carcinomas are those in which submucosal spread of tumor produces thickened, tortuous longitudinal defects, mimicking the appearance of varices [128]. However, varicoid tumors have a fixed configuration, whereas varices tend to change in size and shape at fluoroscopy. Also, varices rarely cause dysphagia because they are soft and compressible. Thus, it is usually possible to differentiate varices from varicoid tumors on the basis of the clinical and radiographic findings.

Squamous cell carcinomas and adenocarcinomas of the esophagus cannot be reliably differentiated on esophagography. Nevertheless, squamous cell carcinomas tend to involve the upper or mid esophagus, whereas adenocarcinomas are located predominantly in the distal esophagus (Figure 6.69). Unlike squamous cell carcinomas, esophageal adenocarcinomas also have a marked tendency to invade the gastric cardia or fundus, comprising as many as 50% of all malignant tumors involving the GEJ [129, 130].

Figure 6.58 Squamous papilloma. Single‐contrast view shows a small, lobulated mass (arrows) in the distal esophagus. A small esophageal cancer could produce similar findings.

Esophageal carcinomas tend to metastasize to other parts of the esophagus via a rich network of submucosal lymphatic channels. These lymphatic metastases may appear as polypoid, plaque‐like, or ulcerated lesions separated from the primary lesion by normal intervening mucosa [123]. Tumor may also spread subdiaphragmatically to the proximal portion of the stomach via submucosal esophageal lymphatic vessels. These metastases to the gastric cardia and fundus may appear as large submucosal masses, often containing central areas of ulceration [131].

Appropriate treatment strategies for esophageal carcinoma depend on accurate staging of the tumor. Various imaging techniques such as CT, MRI, and endoscopic sonography are used for staging esophageal carcinoma [123]. The tumor stage is assessed by evaluating the depth of esophageal wall invasion and the presence or absence of lymphatic or distant metastases.

Figure 6.59 Glycogenic acanthosis. Double‐contrast view shows multiple small, rounded plaques and nodules in the mid esophagus. Although Candida esophagitis could produce similar findings, this elderly patient was not immunocompromised and had no esophageal symptoms. The clinical history therefore is extremely helpful for differentiating these conditions.

Source: Reproduced from Levine MS. Radiology of the esophagus. Philadelphia: WB Saunders; 1989, with permission.