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MD Consult: Books: Goldman: Cecil Medicine: ESOPHAGITIS

Goldman: Cecil Medicine, 23rd ed.

Copyright © 2007 Saunders, An Imprint of Elsevier


   Infectious Esophagitis


Infectious esophagitis occurs principally, but not exclusively, in immunocompromised patients, usually from cancer chemotherapy, post-transplant antirejection medication, and acquired immunodeficiency syndrome (AIDS) (especially with CD4 counts <200 mm3) ( Chapter 416 ). Candida albicans ( Chapter 359 ), herpes simplex virus type 1 (HSV-1) ( Chapter 397 ), and CMV ( Chapter 399 ) are the most common causes, and coinfection with more than one agent may occur. In AIDS, CMV esophagitis may coexist with CMV retinitis or colitis.

   Clinical Manifestations

Odynophagia is characteristic and may be severe. Dysphagia, weight loss, and gastrointestinal bleeding are common. Complications are infrequent but may include tracheobronchial fistula, perforation, and hemorrhage. Esophageal candidiasis in AIDS is associated with oral candidiasis (thrush) in only about two thirds of cases, and HSV esophagitis is associated with oral herpetic lesions in about a third of cases. In an immunocompetent host, infectious esophagitis is primarily due to HSV or Candida.


On barium swallow, a “shaggy” mucosa suggests Candida; numerous small, volcanic-shaped ulcers suggest HSV; and large, deep linear ulcers suggest CMV (or HIV). Multiple biopsies of ulcerated areas with routine histologic evaluation provide a definitive diagnosis. Candida esophagitis is characterized on endoscopy by numerous small white-yellow mucosal plaques containing microorganisms, inflammatory cells, and necrotic mucosa ( Fig. 140-4A ). Positive brushings and biopsy demonstrate Candida pseudohyphae with periodic acid–Schiff reagent or special silver stains. HSV esophagitis on endoscopy begins as numerous vesicles that ulcerate to yield small (<2 cm), shallow, volcano-shaped ulcers (see Fig. 140-4B ). A positive biopsy specimen from the ulcer edge demonstrates the characteristic cytopathic effect of HSV within squamous epithelial cells—eosinophilic intranuclear occlusions. CMV esophagitis is characterized by large (>2 cm), deep, often linear ulcers; a positive biopsy specimen from the ulcer base demonstrates the characteristic cytopathic effect of CMV within fibroblasts and endothelial cells—basophilic intranuclear inclusions.

FIGURE 140-4  Infectious esophagitis in patients with acquired immunodeficiency syndrome. A, Esophageal candidiasis. The multiple small white plaques of Candida are seen on the background of abnormally reddened esophageal mucosa. Patients with esophageal candidiasis may also have a smaller number of plaques or a more or less confluent white coating of the mucosa (which must not be confused with a coating of barium if the patient has recently undergone a barium study). B, Herpes simplex ulceration of the lower esophagus. Note the multiple shallow ulcers in the lower part of the esophagus. This appearance is not diagnostic of herpes simplex infection because a similar appearance may be seen with other causes of ulceration, including some drugs (such as potassium supplements). The presence of vesicles in the mucosa (not shown here) is virtually diagnostic of herpes simplex.  (From Forbes CD, Jackson WF: Color Atlas and Text of Clinical Medicine, 3rd ed. London, Mosby, 2003.)


In non-AIDS patients, Candida esophagitis may be treated with oral nystatin, 1 to 3 million units four times a day, or clotrimazole, 100-mg tablets dissolved in the mouth three to five times a day, but patients with AIDS require an azole antifungal such as oral or intravenous fluconazole, 100 to 200 mg/day for 10 to 14 days ( Chapter 413 ). Ketoconazole and itraconazole are also effective but, unlike fluconazole, require normal gastric acidity for absorption. In resistant cases, intravenous caspofungin, 50 mg/day (after a 70-mg loading dose), or low-dose intravenous amphotericin, 0.3 to 0.5 mg/kg/day, for 10 to 14 days is effective. HSV esophagitis is treated with a nucleoside analogue such as acyclovir, 200 to 400 mg orally five times a day or 250 mg/m2 intravenously every 8 hours for 2 weeks. Valacyclovir and famciclovir are alternatives; for resistant cases, intravenous foscarnet, 60 mg/kg every 8 hours for 2 to 4 weeks, is effective. CMV esophagitis is treated with intravenous ganciclovir, 5 mg/kg every 12 hours for 2 to 4 weeks; for resistant cases, foscarnet is administered intravenously at 60 mg/kg every 8 hours for 2 to 4 weeks. Idiopathic HIV-associated ulcers are treated with prednisone, 40 mg/day, tapering by 10 mg/wk for 1 month; thalidomide, 200 mg/day, may also be effective. Because relapse of all forms of infectious esophagitis is common in immunocompromised patients, maintenance therapy may be required.

   Other Causes of Esophagitis

   Alkaline Reflux Esophagitis

Alkaline reflux esophagitis is an uncommon and poorly defined clinical entity that develops in the setting of repeated and prolonged contact of the esophageal epithelium with nonacidic gastric or intestinal contents, usually in subjects with a destroyed pylorus after total gastrectomy or a Billroth II gastroenterostomy. Treatment is with bile salt–binding or mucosal-coating agents such as cholestyramine, sucralfate, or colloidal bismuth. Surgical fundoplication (intact stomach) or creation of a Roux-en-Y limb (after gastrectomy) is performed in refractory cases.

   Pill-Induced Esophagitis

Pill-induced esophagitis commonly develops in patients, particularly the elderly, who are taking medication improperly (i.e., while supine or with too little liquid). It also occurs in patients with a preexisting abnormality, such as a stricture, diverticulum, or motor disorder. Pills adhere to the esophageal mucosa and cause necrosis and ulceration by the topical release of caustic medication. Among the common offenders are doxycycline, tetracycline, vitamin C, potassium chloride, nonsteroidal anti-inflammatory drugs, quinidine, alendronate and other bisphosphonates ( Chapter 27 ), and iron ( Chapter 162 ). Odynophagia is characteristic and commonly accompanied by dysphagia. Ulceration may lead to hemorrhage, perforation, and stricture. Upper endoscopy is indicated in nonobvious cases to exclude infectious esophagitis. Discontinuation of the offending medication and treatment with sucralfate suspension (1 g orally four times a day for 1 to 2 weeks) or a cocktail (equal parts viscous lidocaine, antacid, and diphenhydramine [Benadryl]) may control the symptoms. Once-a-day PPI therapy is useful to prevent aggravation by reflux. Education about the proper method of taking medication may prevent recurrence.

   Radiation Esophagitis

Radiation esophagitis occurs after chest radiation therapy at dose levels that exceed 30 Gy (3000 rad) ( Chapter 192 ). At levels higher than 60 Gy, severe esophagitis and ulceration can develop and lead to hemorrhage, perforation, or fistula. Concomitant chemotherapy with cytotoxic agents (e.g., doxorubicin [Adriamycin]) can potentiate radiation injury. Substernal pain, odynophagia, and dysphagia are typical. Barium swallow and endoscopy can demonstrate the extent and severity of mucosal inflammation, ulceration, and luminal narrowing; endoscopy has the added benefit of biopsy for exclusion of infectious esophagitis. A liquid diet or intravenous fluids plus the treatments described for pill-induced esophagitis are helpful. Strictures may require bougienage for dilation or even esophagectomy with colonic or jejunal interposition.

   Eosinophilic Esophagitis

Eosinophilic esophagitis is an uncommon, immunologically mediated entity that is being recognized with increasing frequency in children and adults aged 20 to 40 years. It has a 3 : 1 male-to-female predominance, and half the patients have asthma, skin reactions, and peripheral eosinophilia. The disease is due to food allergy and can be manifested as chest pain or heartburn, but solid food dysphagia and food impaction are characteristic. Endoscopic findings range from grossly normal to a corrugated, inflamed, eroded, or fibrotic esophagus in which a single- or multiple-ringed (feline) esophagus or a stiff, narrowed, noncompliant organ is often produced. Esophageal biopsy is diagnostic with high (>15 to 20 per high-power field) concentrations of mucosal eosinophils ( Fig. 140-5 ). The presence of a dense collagen network within the lamina propria accounts for the rigidity and propensity to fracture (tear) on bougienage. Skin testing and a radioallergosorbent assay (RAST) for allergy should be performed to identify and remove the offending agent or agents—the most common being seafood, nuts, milk, eggs, and soy. Dietary changes or therapy with oral cromolyn (100 to 200 mg four times daily), an H1-antagonist (e.g., chlorpheniramine, 4 mg four times daily) plus an H2-antagonist (e.g., cimetidine, 300 mg four times daily), glucocorticoids (topical fluticasone propionate, 220 μg per puff, two puffs swallowed twice to four times daily), or a leukotriene receptor antagonist (montelukast, maintenance dose of 20 to 40 mg/day) may control symptoms, but relapse is common after cessation of therapy. Monoclonal antibodies to interleukin-5 are being investigated as therapy because this cytokine mediates the esophageal eosinophilia.

FIGURE 140-5  Eosinophilic esophagitis. Infiltration of the esophageal epithelium with large numbers of eosinophils, more than 15 to 20 per high-power field, is diagnostic of the condition.  (From Castell DO, Richter JE [eds]: The Esophagus, 4th ed. Philadelphia, Lippincott Williams & Wilkins, 2004.)

   Caustic Esophagitis

Caustic esophagitis ( Chapter 111 ) occurs from accidental ingestion in children and from suicidal attempts in adults. Among the more common materials ingested are drain cleaners (sodium hydroxide), bleach (sodium hypochlorite), detergents (sodium tripolyphosphates), and disc batteries (sodium hydroxide). Sodium hydroxide (lye) produces liquefaction necrosis on contact with the oropharynx and esophagus and thus has the potential to cause acute ulceration, perforation, and later stricture formation. When perforation is excluded by contrast (diatrizoate [Gastrografin] and, if negative, barium) swallows, endoscopy may be of value to assess the esophageal injury, but passage of the scope beyond an area of severe injury is not recommended to avoid perforation. Emergency esophagogastrectomy is indicated for free perforation and mediastinitis. In the absence of these complications, esophagitis is treated supportively with intravenous fluids and prophylactic antibiotics. Steroids in tapering dosage are often given but are without proven efficacy. A feeding tube is passed under direct vision to provide nutrition and a means for later dilation of a tight stricture. When strictures are complex and respond poorly to dilation, intestinal or colonic interposition should be considered to restore oral intake.

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