Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

A pouch can no longer be recognized on a postoperative barium study, although after the endoscopic Dohlman procedure a pouch does persist.

Killian-Jamieson Diverticula

Lateral hypopharyngeal pouches, also called

Killian-Jamieson diverticula, are uncommon. Most are asymptomatic, with an occasional one resulting in dysphagia. They tend not to be associated with aspiration.

These diverticula are detected with a frontalview pharyngogram. A pseudo–Valsalva maneuver aids in identifying them. Unilateral left-sided diverticula are more common than bilateral or right-sided ones (116).

(Pseudo)diverticulosis

Occasionally encountered are multiple small diverticular-like outpouchings. Etiology of this condition, commonly called intramural esophageal pseudodiverticulosis, is unknown. These outpouchings are believed to represent dilated esophageal submucosal glands, probably induced by underlying inflammation. They have developed distal to a benign stricture, in esophageal candidiasis, have been described in vigorous achalasia, are associated with an esophageal carcinoma, and have developed following laser therapy. These outpouchings resolved after radiation therapy for cancer.

Dysphagia is inconstant.

Associated intramural tracking is rather common, especially in patients with diffuse pseudodiverticulosis (117).

Intramural pseudodiverticulosis is readily diagnosed with a barium esophagram. In some patients it is localized, whereas in others it extends diffusely throughout the esophagus. Endoscopy may not detect it because the luminal communications tend to be rather narrow.

Fistula

Some acute perforations (discussed in the previous sections on trauma) evolve into fistulas. Most acquired esophageal fistulas in adults are associated with a malignancy. Nonmalignant

Figure 1.35. Esophagocutaneous fistula. A catheter was threaded into a sinus tract on the patient’s back (arrow); injected contrast outlines the esophagus.

fistulas are secondary to erosion by tubes, esophageal or adjacent inflammation/infection, related to surgery, or sequelae of prior perforation (Fig. 1.35).

A tracheoesophageal fistula developed secondary to ingestion of a disk battery (118).

Vascular Lesions

Dieulafoy Lesions

Dieulafoy esophageal lesions are uncommon. These arteriovenous malformations may bleed, with the patient presenting with massive hematemesis.

Varices

Clinical

Portal hypertension is discussed in more detail in Chapter 17.

In cirrhotic patients with portal hypertension, esophageal varices are the most common site for portosystemic shunting. Most varices eventually drain into the azygos or hemiazygos veins.

ESOPHAGUS

Variceal bleeding tends to develop when the portal pressure gradient (portal vein pressure minus inferior vena caval pressure) is above 12mm Hg. This is not an absolute value, of course, and some patients bleed at lower portal pressure gradients.

Imaging

An initial assessment should include a portal vein study, together with its major branches. Ultrasonography, including color Doppler US, identifies portal vein blood flow, establishes patency, and detects any portal thrombi.

Both barium studies and CT readily detect esophageal varices (Fig. 1.36). Their comparable accuracy is not known. Varices are readily apparent on contrast-enhanced CT; unenhanced, they tend to mimic adenopathy. Computed tomography also detects deeper perforating veins in the distal esophagus that interconnect paraesophageal veins with submucosal veins, a finding also identified by endoscopic US, although bleeding is usually from more superficial ones. Presumably the perforating veins play a role in variceal recurrence after sclerotherapy.

Transabdominal US is not often used to detect esophageal varices, yet in 47 patients with cirrhosis or idiopathic portal hypertension US achieved a respectable 93% sensitivity and 82% specificity when an esophageal wall thickness of at least 5mm or an irregular wall outline were used as criteria for esophageal varices (119). Another US findings of varices includes hepatofugal venous flow identified by Doppler US.

Senior radiologists undoubtedly remember being taught that subtle esophageal varices are best identified not at the gastroesophageal junction (high pressure zone) but slightly more proximally. Endoscopic US confirms this observation. Endoscopic US also measures size of esophageal varices and wall thickness, but limitations exist; in particular, small varices are difficult to identify with endoscopic US.

In patients with Child-Pugh class A cirrhosis without ascites, an increased renal resistive index (>0.7), measured by duplex Doppler US, significantly correlates with the presence of esophageal varices (120).

T2-weighted MRI using an esophageal receiver probe is an alternate method of evaluating not only esophageal but also periesophageal varices. Magnetic resonance angiography (MRA) also identifies both esophageal

and gastric varices. It is also useful in detecting variceal recurrence after sclerotherapy.

Therapy

Medical

An initial approach in cirrhotic patients is drug therapy to reduce portal hypertension and thus reduce risk of variceal bleeding, with the most widely used being beta-blockers (medical and surgical therapies of bleeding esophageal varices are discussed in more detail in Chapter 17). Vasopressin infusion is often used as initial therapy for acute variceal bleeding.

On a chronic basis, medical therapy, sclerotherapy, varix ligation, or TIPS significantly reduces the risk of recurrent bleeding. Differences in mortality, however, have been variable. In selected patients liver transplantation is a consideration. Recommendations for use of these various therapies abound in the clinical literature.

Sclerotherapy

In many institutions endoscopic sclerotherapy is the initial therapy for acute esophageal variceal bleeding. A number of studies confirm that the risk of rebleeding and mortality are significantly reduced by sclerotherapy, but success in arresting acute variceal bleeding is not universally achieved. Sclerotherapy and medical therapy probably have similar mortalities. Endoscopic therapy fails in about 15%.

Most often sclerotherapy is performed in a setting of portal hypertension due to cirrhosis, but esophageal varices in patients with noncirrhotic portal fibrosis have also been effectively treated. Sclerotherapy is readily performed in children.

Endoscopic US appears useful in evaluating and following varices after both sclerotherapy and ligation. Presence and size of residual paraesophageal varices can be evaluated.

Is it possible to gauge whether esophageal varices will recur after endoscopic sclerotherapy? The answer depends to some degree on whether other collateral channels are present. Presence or development of other portosystemic collaterals protects to some degree against recurrent esophageal varices after sclerotherapy. Also, a portal pressure increase or

ADVANCED IMAGING OF THE ABDOMEN

splenomegaly developing after sclerotherapy indicates an increased risk for variceal recurrence.

Contrast-enhanced CT postsclerotherapy reveals an enhancing and thickened esophageal wall. The involved esophageal segment is distorted and narrowed. Edema, mediastinal effusion, and pleural effusion develop in some patients.

Intramural thickening and disappearance of submucosal varices and extramural collaterals are endoscopic US findings after sclerotherapy. Ultrasonography determines whether adequate variceal thrombosis was induced by sclerotherapy.

Barium studies and scintigraphy reveal uncoordinated peristaltic contractions and a marked increase in esophageal transit time shortly after sclerotherapy. Many of these patients also develop transient gastroesophageal reflux. These peristaltic abnormalities presumably are due to a sclerotherapy-induced chemical esophagitis, possibly accentuated by peptic esophagitis. In fact, most rebleeding after sclerotherapy is believed to be secondary to esophageal ulcerations related to sclerotherapy. These ulcers are difficult to detect because of underlying distortion. They heal either with no sequelae or progress to strictures, with an occasional one evolving into a sinus tract, an esophagotracheal or esophagopleural fistula, or even an abscess.

The effect of sclerotherapy on esophageal motility appears to be more complex than described above and probably is multifactorial. Thus amplitude of esophageal peristaltic contractions also increase after TIPS, yet resting lower esophageal sphincter pressure is similar before and after TIPS (121); TIPS thus improves esophageal motor function without inducing gastroesophageal reflux.

Sclerotherapy does not increase the risk of developing portal vein thrombosis, but patients with portal hypertension and varices are at increased risk for developing bacterial peritonitis, and sclerotherapy appears to accentuate this risk.

Several patients with esophageal varices, treated by sclerotherapy, later developed a carcinoma near the gastroesophageal junction and at sclerotherapy sites (122,123); whether this is a coincidence or whether sclerotherapy is indeed carcinogenic is speculation.

ESOPHAGUS

Ligation

Similar to sclerotherapy, endoscopic band ligation of a varix is effective therapy. Nevertheless, there are differences. Summarizing the published data, endoscopic variceal sclerotherapy and ligation appear equally effective in arresting an acute bleed; ligation requires fewer treatment sessions and is associated with fewer complications, but ligation has a higher variceal recurrence rate than sclerotherapy. A number of investigators believe that ligation should be the first choice therapy for esophageal varices.

After endoscopic variceal ligation an entrapped varix undergoes thrombosis, sloughing, and surrounding fibrosis.

Imaging shortly after ligation reveals ligated varices as smooth nodules that do not change shape, thus distinguishing them from typical varices. Their appearance does mimic other esophageal tumors, but a history of ligation aids in differentiation.

Endoscopic variceal ligation also leads to increased peristaltic activity and prolonged lower esophageal sphincter relaxation.

Other Procedures

Patients with portal hypertension and esophageal varices have also been treated, by TIPS, esophageal transection and devascularization, and by a number of portocaval anastomoses. Embolization of esophageal varices and other endovascular occlusion techniques had a greater role in the past and have been supplanted to a large extent by TIPS. To cite one example of embolization, hematemesis from esophagojejunal varices 5 years after total gastrectomy and Roux-en-Y esophagojejunostomy for carcinoma was treated by embolization after percutaneous transhepatic portography showed that these varices were supplied by an ascending jejunal vein (124) (Fig. 1.37).

Immunosuppression

AIDS

Infection

Dysphagia and odynophagia are common in patients infected with the immunodeficiency virus. The most common infection is candidiasis. If an esophagram reveals ulcerations, infection by cytomegalovirus or herpes simplex should be suspected. The HIV infection per se may result in esophageal ulcers. More than one cause is not uncommon. The specific agent responsible for ulcerations should be sought because therapy is specific. Idiopathic ulcers are treated with steroids.

An occasional AIDS patient with odynophagia develops giant esophageal ulcers. Fragments believed to represent HIV virus are obtained from some of these giant ulcers, which tend to be long and shallow, and some are surrounded by a rim of soft tissue.

Candidiasis

With increasing severity of Candida infection, initial discrete scattered plaques coalesce and narrow the esophageal lumen; these plaques consist primarily of desquamated squamous epithelium and inflammatory cells, Candida sp., and superimposed bacterial infection. Although ulcers are a common finding in Candida esophagitis, most are not due to Candida alone. Untreated, Candida esophagitis can progress to stenosis.

Viral

Cytomegalovirus esophageal infection is not uncommon in immunocompetent patients. A common finding consists of well-circumscribed multiple, large, but shallow discrete ulcers, although at times inflammation resembles a carcinoma. An occasional ulcer evolves into a bronchoesophageal fistula. Occasionally a cytomegalovirus ulcer heals spontaneously.

In distinction to cytomegalovirus infection, herpes ulcers tend to be small,at times even pinpoint, and multiple in otherwise normalappearing mucosa (Fig. 1.38). Simultaneous herpes and Candida esophagitis is not uncom-

ADVANCED IMAGING OF THE ABDOMEN

mon and results in a diffuse and irregular appearance.

The HIV esophagitis results in large shallow ulcers and, in absence of other predisposing causes, such a finding should suggest AIDS.

Imaging appearance of cytomegalovirus and HIV esophagitis is similar, and biopsy or mucosal brushing is necessary to differentiate between them (HIV esophagitis is one of exclusion).

Other

Similar to infections at other body sites, these patients are prone to develop unusual esophageal infections. Esophageal involvement with tuberculosis, actinomycosis, mucormycosis, and leishmaniasis has been reported (Fig. 1.39). Actinomyces superinfection of a cytomegalovirus ulcer has led to numerous sinus tracts.

Microorganisms are identified in about half of esophageal biopsies from AIDS patients with clinical esophagitis.Acid-fast bacilli should be searched for; in some of these patients no underlying giant cells are detected.

Figure 1.38. Herpes esophagitis in an AIDS patient manifesting with thickened folds and an occasional small ulcer.

Bacillary angiomatosis, due to Rochalimaea henselae infection, causes multiple, diffuse, friable esophageal polyps.

Tumor

The most common esophageal tumors in AIDS patients are Kaposi’s sarcoma and nonHodgkin’s lymphoma (Fig. 1.40). Some lymphomas are primary esophageal and consist of large, ulcerating tumors mimicking a sarcoma. Infection, at times with an unusual organism, coexists with some esophageal lymphomas. The occasional Barrett’s adenocarcinoma may be fortuitous.

An inflammatory fibroid polyp presented as a long submucosal mass in the distal esophagus.

Radiation therapy has been used to treat esophageal malignancies in AIDS patients. These patients appear to have greater sensitivity to radiation therapy than non-AIDS patients.

Posttransplant

Esophageal webs and strictures develop in graft-versus-host disease. These strictures mimic those seen in reflux esophagitis. Large esophageal bulla have been reported in patients after bone marrow transplantation (125);

Figure 1.40. High-grade, large-cell malignant lymphoma in an HIV patient. A barium esophagram reveals an irregular, almost tube-like esophagus containing extensive ulcers. (From Marnejon T, Scoccia V. The coexistence of primary esophageal lymphoma and Candida glabrata esophagitis. Am J Gastroenterol 1997;92:354–356, with permission from Blackwell.)

whether these are due to a superimposed infectious agent or graft-versus-host disease is conjecture.

Postoperative Changes

Pharyngeal Surgery

Postoperative pharyngography is helpful in following patients after oropharyngeal surgery. Considerable variability exists in the imaging findings and a baseline postoperative imaging study is very helpful in these patients (126). Knowledge of the specific surgical procedure performed aids in differentiating postsurgical fibrosis from tumor recurrence.

Transplanted jejunal patches are used to reconstruct oropharyngeal soft tissue defects. Transplant viability is maintained via vascular anastomoses. Tumors tend to recur at patch margins. Needless to say, such transplanted tissue has a complex CT and MRI appearance during follow-up due to the degree of underlying fibrosis, and differentiation from recurrent tumor is difficult. Nevertheless, these imaging studies are especially useful with tumor recurrence beneath a patch, where clinical access is not feasible.

ADVANCED IMAGING OF THE ABDOMEN

Celiac disease became clinically evident in a woman after vagotomy and esophagectomy for hypopharyngeal squamous carcinoma (128); presumably her postoperative hypocalcemia unmasked indolent celiac disease.

An uncommon way of demonstrating an anastomotic leak is with Tc-99m-HIDA scintigraphy.

Examination Complications

The choice of contrast agent to be used in a setting of a suspected esophageal perforation was discussed above (see Perforation).

Endoscopy Related

The most common endoscopy-related complication is perforation. Postprocedure pain is common with a perforation but it sometimes manifests later. Oral contrast for imaging studies should be used with caution until topical anesthesia and sedation wear off. Initially, an esophagram generally has a highest yield, but CT is appropriate once enough time elapses for inflammation or abscess to develop (Fig. 1.41).

Postesophagectomy

Gastric pull-through with a cervical esophagogastric anastomosis is a common procedure. Some patients are not given anything per os until an esophagram has excluded a perforation or obstruction. The study also determines how well the intrathoracic stomach empties. Some surgeons advocate peroral water feeding to detect leaks. Many radiologists use a watersoluble contrast agent for this examination. Because of a potential for aspiration, unless an acute intraperitoneal communication is suspected, I prefer barium as a contrast agent. After major barium aspiration delayed CT identifies thickened interlobular septa, subpleural lines, subpleural cysts and centrilobular nodules with barium particles, findings of mild but silent fibrosis (127).

Some patients develop dysphagia years after colonic interposition. Usually by that time marked colonic redundancy has developed and accounts for dysphagia.

Figure 1.41. Esophageal perforation secondary to endoscopic dilation. Contrast outlines a mid-esophageal cavity (arrow).