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.

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.