| 8. Nonreflux-Induced Esophagitis | page 110 |
8.1 Infectious Esophagitis
Bacteria rarely cause primary esophageal infection, although the esophagus can be involved secondarily by direct extension from the lung. The two most common forms of infectious esophagitis are caused by Candida and herpes. Other viruses (e.g., CMV, HIV) and fungi can also cause esophagitis; however, this is uncommon and almost invariably associated with immunosuppression.
| 8.1.1 CANDIDA ESOPHAGITIS | page 111 |
This is by far the most common form of infectious esophagitis. Usually there is a predisposing cause, such as diabetes mellitus, antibiotic therapy or some form of immunocompromise. The patient may be asymptomatic. Not all patients will have associated oral thrush. More commonly, however, patients present with odynophagia, retrosternal chest pain and/or dysphagia. Severe cases can be complicated by bleeding, a stricture and sinus tract formation with secondary lung abscess. Barium x-rays reveal an irregular granular or even cobblestone appearance to the esophageal mucosa. Approximately 25% of patients will have a normal barium esophagogram; for this reason, endoscopy with biopsy and brushing are required to make the diagnosis. The typical endoscopic appearance is the presence of small raised whitish plaques. When the plaques are removed the underlying mucosa is seen to be erythematous and friable. Specimens obtained by biopsy or brush cytology should be cultured and examined microscopically for the presence of typical Candida yeast with pseudohyphae formation. Most patients can be treated with oral nystatin (luminal treatment); however, more extensive disease, especially if the patient is immunocompromised, may require systemic treatment with either ketoconazole or fluconazole. Amphotericin B is required if there is evidence of systemic spread.
| 8.1.2 HERPES SIMPLEX ESOPHAGITIS |
Next to Candida, this is the most common form of infectious esophagitis. The clinical presentation is much the same as with Candida esophagitis. There may also be constitutional symptoms of a viral upper respiratory tract infection preceding the esophageal symptoms. Herpetic mouth or skin lesions may also develop. This infection occurs most frequently in immunosuppressed patients, but also develops sporadically in healthy young adults. Endoscopy with biopsy and brush cytology is required to confirm the diagnosis. The pathognomonic finding is the eosinophilic "Cowdry's Type A" intranuclear inclusion body. Herpetic esophagitis is self-limiting in immunocompetent individuals; specific treatment is not indicated. Symptoms of odynophagia often respond to a combination of antacids mixed with viscous Xylocaine®. In severely immunocompromised patients, intravenous acyclovir treatment should be instituted.
| 8.2 Esophagitis Associated with Immune-Mediated Disease | page 112 |
Rarely, esophagitis can occur in association with Crohn's disease or Behçet's syndrome. The typical lesion is scattered aphthous-type ulcerations, although severe transmural involvement with stricture formation can occur. The esophagus can also be severely involved in pemphigoid, in pemphigus and in epidermolysis bullosa.
Esophagitis occurs in as many as one-third of patients who develop chronic graft-versus-host disease after bone marrow transplantation. The typical lesion is a generalized epithelial desquamation of the upper and middle esophagus. There may be associated ring-like narrowings or strictures due to submucosal fibrosis. A nonspecific esophageal motor disorder may also develop and result in superimposed reflux esophagitis because of poor esophageal clearing. Sarcoidosis and eosinophilic gastroenteritis are two other immune-mediated diseases that (rarely) cause esophageal inflammation.
| 8.3 Chemical-Induced Esophagitis | page 112 |
8.3.1 CAUSTIC CHEMICAL INGESTION
Strong acids or alkalis ingested accidentally or as a suicidal gesture cause marked esophagitis. Alkali tends to be more injurious to the esophageal mucosa than acid and produces liquefaction necrosis as well as thermal burns (due to heat release when the alkali is hydrated by gut secretions). Acids tend to produce superficial coagulation necrosis and eschar formation. Typically the patient develops immediate chest pain and odynophagia. Oral burns also may produce local pain and drooling. There may be respiratory symptoms such as stridor, dyspnea and hoarseness if the airway is contaminated. Symptoms alone do not permit accurate prediction of the presence or absence of esophageal injury; therefore early diagnostic endoscopy should be considered in most patients. Clearly, endoscopy should not be performed if there is evidence of esophageal perforation. In the management of these patients, it is imperative to maintain an adequate airway. Oral intake must be stopped and intravenous fluids administered. Empiric treatment classically has involved antibiotics and corticosteroids, but there is no good evidence documenting the efficacy of this approach. Patients who survive the acute phase of the injury are at risk of developing strictures because of the intense collagen deposition associated with healing. This often requires repeated esophageal dilation to maintain luminal patency.
Lye-induced injury increases the risk of developing squamous cell carcinoma of the esophagus. Typically there is a 30- to 50-year lag time before the development of cancer. For this reason any patient with previous lye injury and new esophageal symptoms should be promptly investigated. The extent of the risk is such that periodic endoscopic surveillance is not indicated.
| 8.3.2 PILL-INDUCED ESOPHAGITIS | page 113 |
A large number of oral agents can cause localized esophageal injury. The antibiotic doxycycline and the anticholinergic emepronium bromide are two of the most common culprits. Nonsteroidal anti-inflammatory drugs and slow-release forms of potassium chloride are also frequently implicated. Patients with this type of injury typically take their medication with a small amount of water and then immediately lie down to go to bed. They may then wake up several hours later with severe retrosternal chest pain and odynophagia. Capsules and tablets are notorious for being transported through the esophagus quite poorly unless adequate amounts of fluid are ingested at the same time. This is an important point to remember in counseling all patients who take medicines at bedtime. Rarely, the medication becomes lodged and causes a deep esophageal ulcer with perforation. More commonly the ulceration is superficial and heals in a few weeks. Late stricture formation may occur. Patients with esophageal motility disorders are particularly prone to this complication.
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When included in the field of irradiation the esophagus becomes inflamed in up to 80% of patients receiving therapeutic radiation for cancer. The risk of esophagitis is greater if there is concomitant chemotherapy. The patients typically develop chest pain, dysphagia and odynophagia shortly after the initiation of therapy. This can be a serious problem in such patients, who are already often severely malnourished. Late stricture formation is a well-recognized complication.
