Книги по МРТ КТ на английском языке / Advanced Imaging of the Abdomen - Jovitas Skucas

An esophageal carcinoma is generally first detected either with a barium study or endoscopy, while tumor invasion is evaluated with CT or endoscopic US. Because many of these tumors are hypervascular compared to normal esophageal tissues, postcontrast multidetector CT imaging during the arterial phase also appears useful for initial tumor detection, although currently little data are available in the literature to provide guidance.

Esophagography remains an excellent tool both for diagnosis and follow-up of an esophageal carcinoma. A double-contrast technique and meticulous attention to detail are necessary.

At times an early superficial carcinoma presents as an isolated focus of nodularity identified with a double-contrast esophagram. The differential diagnosis of such a finding includes Barrett’s esophagus, focal esophagitis, or even focal glycogenic acanthosis. A more extensive carcinoma is readily detected by a double-contrast barium study, but a biopsy is generally necessary to establish the diagnosis (Fig. 1.17).

Adenocarcinomas tend to have a nodular outline, and a technically high-quality study is necessary to detect smaller tumors (Fig. 1.18). Even when advanced, they tend to infiltrate intramurally, and a bulky intraluminal mass is found only in a minority (Fig. 1.19). Varicoid adenocarcinomas in the distal esophagus mimic varices, but unlike varices, these serpiginous cancers do not change shape and size with degree of esophageal lumen distention, and

B

Figure 1.17. Squamous cell carcinoma in mid-esophagus. A: CT identifies a poorly enhancing tumor infiltrating the esophagus (arrow). (Courtesy of Arunas Gasparaitis, M.D., University of Chicago.) B: Ulcerated carcinoma in mid-esophagus (arrow) in another patient.

most experienced radiologists readily differentiate these two conditions (Fig. 1.20). Adenocarcinomas developing in a setting of Barrett’s esophagus typically have an initial flat or plaque-like, irregular appearance and tend to be difficult to detect.

Staging

Squamous Cell Carcinoma: The tumor, node, metastasis (TNM) system is used for staging

Figure 1.18. Polypoid adenocarcinoma in mid-esophagus (arrows).

esophageal carcinomas (Table 1.4). Information obtained from imaging is combined with other data to achieve a preoperative stage useful for subsequent prognosis and therapy. From an immediate surgical viewpoint, however, a primary

Figure 1.19. Distal esophageal adenocarcinoma. CT reveals diffuse infiltration of surrounding tissues (arrow).

concern is not staging but whether a tumor is resectable or not.

Preoperative imaging is used to detect local and metastatic spread. Computed tomography complements rather than competes with endoscopy and barium studies, which are primarily diagnostic rather than staging modalities. Arterial phase multislice CT shows most tumors to be hypervascular to surrounding normal soft tissues; CT detects tumor intralu-

Table 1.4. Tumor, node, metastasis (TNM) staging of esophageal tumors

Primary tumor:

Lymph nodes:

Nx Regional lymph nodes cannot be assessed N0 No regional lymph node metastasis

N1 Regional lymph node metastasis

Distant metastasis:

Mx Distant metastasis cannot be assessed M0 No distant metastasis

M1 Distant metastasis

Source: From the AJCC Cancer Staging Manual, 6th edition (2002), published by Springer-Verlag, New York, NY, used with permission of the American Joint Committee on Cancer (AJCC), Chicago, IL.

minal extension, invasion, or displacement of tissue planes and blood vessels, obliteration of normal fat planes, and lymph node enlargement. The CT signs pointing toward irresectability are tumor-to-aorta contact angle >45 degrees; obliteration of the fat pad between the tumor, aorta, and spine; and tracheal invasion. Unfortunately, these signs have a high falsepositive rate and they should be interpreted judiciously. Some of these patients are cachectic, however, and have little fat that can serve as a landmark.

A CT-specific staging system is used by some to gauge intramural extension and adjacent structure involvement. Intravascular contrast defines major adjacent vessels. A lymph node transverse diameter of 10mm or more is one criterion used to gauge lymph node metastases, but the results are disappointing. Analysis of 7218 resected lymph nodes in patients with esophageal carcinoma revealed that only 28% of

ADVANCED IMAGING OF THE ABDOMEN

histopathologically proven nodes containing metastases were ≥10mm in size, whereas 35% of metastatic nodes were 5 to 10mm,and 36% were <5mm (61); looking at the reverse, of resected nonmetastatic lymph nodes 7% were >10mm and the authors concluded that CT cannot assess whether mediastinal lymph nodes are affected. Current data indicate that CT cannot reliably identify nodal involvement. It is useful, however, in detecting extensive spread.

One limitation of endoscopic US in staging esophageal cancers is that often the probe cannot be passed through a carcinoma and the full extent of a tumor cannot be assessed. Also, more distant involvement cannot be evaluated. Endoscopic US often does suggest whether a carcinoma is limited to the mucosa or submucosa, or extends into adjacent tissues. Using endoscopic US criteria, a blinded evaluation of patients with esophageal malignancy attempted to differentiate between tumors limited to the esophageal wall (T1-2) and extraesophageal (T3-4) involvement (62); the accuracy of muscularis disruption and tumor border irregularity was low in differentiating between intraand extraesophageal disease. On the other hand, tumor maximal thickness was accurate in predicting extraesophageal extension; tumors limited to the esophagus measured 8 ± 1mm, but extraesophageal tumors had a thickness of 16 ± 2mm.

In a multicenter retrospective study of 79 patients with invasive (T4) esophageal carcinoma, endoscopic US accuracy was 88% in detecting tumor invasion, whereas CT accuracy was 44% (p = .0002) (63); of interest is that in this group of invasive cancers (consisting of both adenocarcinomas and squamous cell carcinomas), overall mortality was not significantly different whether surgery was performed or not.

Gauging lymph node involvement by endoscopic US is problematic. Although some studies have reached a nodal staging sensitivity of 92% (64), others have achieved staging sensitivities of only 60% to 80%. Nevertheless, endoscopic US is more accurate than CT in staging node invasion.

More proximal esophageal squamous cell carcinomas metastasize to cervical lymph nodes. Neck US using a 7.5- or 10-MHz transducer appears useful, keeping in mind that US simply detects lymph nodes, and nodes above a certain

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size, such as 5mm or so in their long dimension, are assumed to be metastatic. Some studies use a short-to-long node dimension ratio >0.5 as an indicator of metastasis.

In patients with an intrathoracic esophageal squamous cell carcinoma, 1.5 T, T1-weighted sagittal MRI could not detect lesions subsequently found to be less than stage T2 (65); detected T3 lesions had a mean diameter of 25mm, whereas T4 lesions were 34mm. Nevertheless, future MRI staging of esophageal cancers appears promising. Thus in evaluating depth of mural invasion, T2-weighted MRI (at 1.5 T) agreed in 95% of patients with suspected superficial esophageal carcinoma with final histopathologic evaluation (66); in 5% of specimens MRI staging was higher.

Positron emission tomography has a role in staging both esophageal squamous cell carcinoma and adenocarcinoma. Its spatial resolution is insufficient to evaluate local extension, but it is often more specific than CT or US in detecting nodal involvement, keeping in mind that activity in a primary tumor can mask adjacent lymph node uptake. In 36 patients with a newly diagnosed esophageal cancer, 18F-FDG PET detected abnormal uptake in all (67); in those undergoing a curative esophagectomy, PET and CT correctly identified extent of nodal involvement in 76% and 45% of patients,respectively. The current primary role for PET is in excluding stage IV disease and in following patients postresection. One should keep in mind that esophagitis and adjacent inflammation result in a false-positive PET scan,and this study thus should be obtained only several months or longer after radiation therapy or resection.

Although thoracoscopic staging has been proposed, it is not widely employed.

Adenocarcinoma: Compared to postoperative staging, endoscopic US correctly staged tumor depth invasion in 87% of patients compared to 40% for CT (68) (Fig. 1.21). It was also significantly more accurate (73%) than CT (33%) in staging node invasion. Even if the endoscope probe could not pass through a tumor stricture, US is able to stage. Falsepositive findings are due to edema or fibrosis, whereas scattered infiltration accounts for falsenegative ones.

Lymph node metastasis is uncommon if an adenocarcinoma is limited to the mucosa, is present in <20% of patients when a cancer

extends to the submucosa, and increases further with deeper tumor extension (Fig. 1.22).

Complications

Esophageal neoplasms necrose and fistulize to adjacent structures, including trachea and major bronchi (Fig. 1.23). Imaging detection of tumor invasion into the tracheoesophageal fat plane increases the likelihood of future tracheoesophageal fistula formation. Unusual ones include an esophagosubarachnoid fistula (69) and even lower extremity subcutaneous emphysema, with psoas muscles presumably serving as a pathway (70).

Some neoplastic fistulas are iatrogenic. These tissues are friable, and even passage of a feeding tube can result in a perforation and fistula.

Therapy

Therapeutic options available for cure consist of surgical resection, at times in combination with radiotherapy or chemotherapy. Combined chemoand radiation therapy before esophagectomy for invasive esophageal or gastroesophageal junction cancer did not influence distant metastases but did control local recurrence, achieving a 5-year local tumor control rate of 90%, compared to 64% after esophagectomy only (71); on the other hand, postoperative mortality was 16% in the chemoand radiation therapy group versus 6% after esophagectomy only.

Some surgeons recommend esophagectomy to all patients able to withstand resection, keeping in mind that such an approach provides no survival benefit; only those patients who are too ill for surgery are referred to palliation, an approach of questionable value.

For cure: Flat esophageal carcinomas and areas of dysplasia are amenable to endoscopic mucosal strip resection. This procedure holds promise as long as a lesion is limited in depth. In general, survival does not depend on tumor location within the esophagus.

Photodynamic therapy cures most early squamous cell carcinomas (Tis and T1a) of the esophagus (72).

Traditional therapy for squamous cell esophageal carcinomas involves resection (where applicable), radiation therapy, and chemotherapy. Patients with stage I and II

28

A

C

E

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B

D

Figure 1.21. Esophageal endosonography. A: Image of superficial cancer of gastric cardia (arrows). The outer hyperechoic layer, representing muscularis propria, is intact. B: T1 tumor with an intact outer hypoechoic layer. C: Cancer invading muscularis propria. The outer hyperechoic layer is discontinuous and this tumor is thus stage T2. D: Tumor invading beyond the serosa; it is thus stage T3. Enlarged nodes were also present. E: Gastric cardia tumor extends through serosa and invades diaphragm (arrows).The tumor is thus stage T4. (Courtesy of Eric François, M.D., Centre AntoineLacassagne, Nice, France.)

Figure 1.22. Endosonography reveals numerous hypoechoic nodes surrounding the esophagus, (Courtesy of Eric François, M.D., Centre Antoine-Lacassagne, Nice, France.)

cancer achieve greater 5-year survival either with surgery only or surgery plus adjuvant chemoradiotherapy than with primary radiation therapy only.

Either a transhiatal esophagectomy or a transthoracic approach is used to resect a distal esophageal or gastric cardia adenocarcinoma. Both techniques appear to be equally safe and have comparable complications and survival rates.

The 5-year survival for patients undergoing resection of an esophageal adenocarcinoma, without postoperative residual tumor and without lymph node involvement, is about 60–70%.

Computed tomography using a negative oral contrast agent and endoscopy appear comparable in evaluating the response to chemotherapy

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Figure 1.23. Cancer ulcerating into carinal lymph nodes (arrow).

of gastroesophageal junction adenocarcinomas

(3).

Although of limited application, transjugular intrahepatic portosystemic shunting (TIPS) can relieve portal hypertension in a cirrhotic patient with esophageal varices and an esophageal adenocarcinoma, allowing subsequent cancer therapy.

Palliation: Therapy of patients with cancer invading adjacent structures is controversial. Palliation of dysphagia in most patients with either squamous cell carcinoma or adenocarcinoma consists of stenting, radiotherapy, laser therapy, or serial dilation of the malignant stricture. Some centers report prolonged survival after chemotherapy, radiotherapy, and esophagectomy combined with regional node dissection.

Indications for stenting an inoperable esophageal carcinoma are obstruction or fistula. The procedure of choice for an inoperable carcinoma, especially in underdeveloped countries, is often a plastic stent inserted under endoscopic guidance without general anesthesia and requiring only a short hospital stay (73).

Numerous commercial stents are available and new ones continue to be introduced. These

stents are inserted using either endoscopic or fluoroscopic guidance. Self-expanding metal stents provide dysphagia palliation for a majority of patients. Covered stents provide better long-term palliation than uncovered stents. Comparing Wallstents and knitted nitinol stents, a multicenter study found that proce- dure-related mortality, early complication rate, and severe persistent pain after stent placement were higher with Wallstents (74); on the other hand, stent dysfunction, reintervention rate, and cost were lower in the Wallstent patients. Mean survival time of patients with malignant dysphagia is longer with covered than with uncovered stents.

In addition to treating strictures, covered metallic stents also are effective in treating inoperable malignant perforations and tracheoesophageal fistulas. Both covered Wallstents and Gianturco stents are popular. A contrast study shortly after the procedure evaluates stent position with respect to the fistula. Therapy with Wallstent endoprostheses or Gianturco stents of esophagorespiratory fistulas or perforations in patients with unresectable esophageal cancer led to closure of 90% of fistulas and all perforations (75).

What is the effect of a magnetic field on various metallic stents? Magnetic resonance imaging quality was not degraded by the titanium alloy Ultraflex stent and nitinol covered Wallstent (76); stainless steel Gianturco stent and modified Gianturco stent have an appreciable attraction force and torque. In particular, the Gianturco stent is pulled toward the head with a force 7¥ gravity, although whether this is enough of a risk for dislodgment is unknown. In addition, the stainless steel Gianturco stents produce gross artifacts around the stent.

Stent-related delayed complications tend to be more common than immediate complications and consist of recurrent fistula, tumor ingrowth, and tracheal compression by tumor (Fig. 1.24). Complications appear to be similar regardless of whether a stent is used primarily to treat a stricture or to bypass a fistula (Table 1.5). Gastroesophageal reflux is common if the stent straddles the gastroesophageal junction; at times resultant esophagitis is sufficiently severe to mimic an obstruction. Tumor ingrowth and overgrowth after stenting result in recurrent dysphagia and can be treated by balloon dilation or insertion of a second stent. Stents

Figure 1.24. Tygon tube perforation (arrow). Most common site of perforation is at the proximal sleeve.

do migrate proximally and distally, although migration is less of a problem with newer stents. Covered stents tend to migrate more often than uncovered stents; on the other hand, tumor ingrowth occurs with uncovered stents. Stent erosion into adjacent tissues is not uncommon, with most perforations occurring at stent ends.

A nitinol stent broke spontaneously shortly after insertion, and another one broke after

Table 1.5. Complications of esophageal stenting

Reflux

Aspiration

Food impaction

Perforation

Benign strictures at stent edges

Esophagorespiratory fistula

Esophagovenous intravasation

Aortoesophageal fistula

Stent migration

Stent fracture

Stent invagination

Stent twisting/torsion

Tumor ingrowth or overgrowth

Massive hemorrhage

Death

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laser therapy for tumor ingrowth, possibly due to thermal overload during laser therapy (77); electrocoagulation and laser use should be used with caution around a stent. Another nitinol stent invaginated after initial expansion and shortened to about two thirds of its length, allowing tumor overgrowth (78).

Endoscopic laser therapy is useful in palliating some of these cancers, and reopening rates of >90% can be achieved. Survival did not differ in patients with stages III and IV squamous cell carcinoma whether they underwent esophagectomy or endoscopic laser therapy (79); patients undergoing laser therapy did have a shorter hospital stay, although sequential retreatments are necessary. Complications of laser therapy include esophagotracheal fistulas and hemorrhage. There have been incidents of procedurerelated mortality. A prospective randomized trial found that in patients with inoperable esophageal cancer dysphagia palliation was substantially better with stenting than with endoscopic laser therapy (80).

Tumor response to radiotherapy or chemotherapy is estimated by measuring residual tumor size. Tumor volume can be calculated from CT scans by combining adjacent measured tumor areas on each 1-cm slice. The accuracy of this method is similar to results obtained from resected tumor weight and water displacement measurements.

Complications of Therapy: A gastroesophageal anastomotic leak is not uncommon after cancer resection. Most of these leaks are detected by a barium study shortly after surgery, and most smaller ones are managed medically and close spontaneously. Larger ones or those not healing with conservative therapy are amenable to esophageal stenting. In one study, immediate leak occlusion was evident after stenting, and clinical healing occurred in 93% of patients, with a median healing time of 6 days (81).

An esophageal mucocele developed after surgical bypass due to continued secretions in the excluded esophagus (82).

Recurrence/Metastasis

Local recurrence manifest as dysphagia and generally implies extensive disease (Fig. 1.25).

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Figure 1.25. Recurrent cancer at gastroesophageal anastomosis. A gastric cardia adenocarcinoma had been resected previously.

Typical metastases are to mediastinal, cervical, and abdominal lymph nodes.

Endoscopic US is an option for early detection of locally recurrent cancer. A study of patients followed by endosonography found that two thirds of patients were still asymptomatic when US detected recurrence (83).

Metastases from an esophageal adenocarcinoma mimicked myositis ossificans (84).

Lymphoma

A primary esophageal lymphoma is rare. Most involvement is secondary, often due to direct spread from mediastinal lymph nodes or stomach. Lymphomas range from polypoid to diffusely infiltrating (Fig. 1.26). An occasional one is primarily intramural and mimics esophageal varices, similar to a varicoid carcinoma.

A lymphoma infiltrating an esophageal squamous cell carcinoma is a rarity; the diagnosis is difficult even for a pathologist because reactive lymphoid infiltration is not uncommon adjacent to a squamous cell carcinoma.

Sarcoma

Some connective tissue tumors are difficult to characterize even with immunohistochemistry, and most authors simply label them as stromal tumors. Whenever possible, however, a specific pathologic diagnosis should be applied to mesenchymal tumors because of differences in therapy and prognosis.

Within the gastrointestinal tract, gastrointestinal stromal tumors (GISTs) are least common in the esophagus and most common in the stomach. These tumors are discussed in more detail in Chapter 2.

Leiomyosarcoma

Although leiomyomas are common in the esophagus, sarcomatous degeneration is not. Most sarcomas present as large bulky tumors varying in size. Their growth rate is variable, although most are slow-growing. The distinction between a leiomyoma and a leiomyosar-

A B

Figure 1.26. Esophageal lymphoma. A: A diffuse infiltrating, ulcerating tumor (arrows) was believed to have been induced by cyclosporin. (Courtesy of Arunas Gasparaitis, M.D., University of Chicago.) B: Recurrent lymphoma presenting as multiple nodules (arrows).

coma is generally made only by the pathologist and even then often with difficulty.

Dysphagia is the usual presentation. An occasional patient manifests with bleeding or pain. Leiomyosarcomas tend to metastasize late in their course.

The vast majority of leiomyosarcomas develop in the esophageal segment containing smooth muscle (i.e., mid-to-distal esophagus). The rare one found more proximally presumably originates either from the vessel wall or muscularis mucosa. Some are sufficiently large that a chest radiograph reveals a mediastinal mass. Squamous cell carcinomas and adenocarcinomas, on the other hand, rarely are sufficiently large at initial presentation to be detected with chest radiography.

Their barium appearance varies from a mostly intramural to a large intraluminal mass. A primarily infiltrating tumor is less common. Larger ones tend to ulcerate. A rare one is pedunculated and occasionally even extends into the stomach. At times a necrotic one communicates with the esophageal lumen, leading to gas and contrast within the tumor.

Computed tomography identifies any exophytic component. These tumors are isointense with skeletal muscle on T1-weighted MRI and hyperintense on T2-weighted MRI.

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Figure 1.27. A carcinosarcoma presents as an expansile intraluminal polyp (arrows). (Courtesy of Arunas Gasparaitis, M.D., University of Chicago.)

Commonly a carcinosarcoma presents as an intraluminal polyp mimicking a fibrovascular polyp (Fig. 1.27).

Other

Although liposarcomas are relatively common throughout the body, they are rare in the esophagus. Some appear polypoid, and imaging suggests a fibrovascular polyp.

A hypopharyngeal liposarcoma grew submucosally into the esophagus (85).

A rare malignant fibrous histiocytoma presents as a soft tissue polyp.

A carcinosarcoma is uncommon in the esophagus. Histologically, these tumors show elements of both squamous cell carcinoma and sarcoma. Histogenesis is believed to involve metaplasia of some carcinomatous cells toward mesenchymal differentiation. Only rarely is a carcinosarcoma a result of simultaneous adjacent tumor development from both epithelial and mesenchymal tissue, identified by distinct immunoreactive and genetic clonalities in the two components.

Melanoma

Melanocytes are normally present in the esophageal epithelium,and primary melanomas develop in the esophagus, albeit rarely. Many esophageal melanomas, however, are metastatic. These are aggressive tumors associated with a poor prognosis regardless of presentation or appearance.

Common presentations are dysphagia or odynophagia; melena is rare.

Primary melanomas range from an exophytic, pedunculated polyp, often bulky, to an infiltrative lesion, generally not obstructing but distending the esophageal lumen (Fig. 1.28). Endoscopic US shows some of these tumors to be smooth-walled, have discrete margins, and have varying echogenicity (86).

Metastatic melanomas tend to be flat and not visualized with barium studies, although CT and US detect any intramural or extrinsic extension.