Corrosive esophagitis and stricture
Corrosive esophagitis and stricture: Excerpt from Professional Guide to Diseases (Eighth Edition)
Corrosive esophagitis is inflammation and damage to the esophagus after ingestion of a caustic chemical. Similar to a burn, this injury may be temporary or may lead to permanent stricture (narrowing or stenosis) of the esophagus that’s correctable only through surgery. Severe injury can quickly lead to esophageal perforation, mediastinitis, and death from infection, shock, and massive hemorrhage (due to aortic perforation).
Causes and incidence
The most common chemical injury to the esophagus follows the ingestion of lye or other strong alkali; ingestion of strong acids is less common. The type and amount of chemical ingested determine the severity and location of the damage. In children, household chemical ingestion is accidental; in adults, it’s usually a suicide attempt or gesture. The chemical may damage only the mucosa or submucosa or it may damage all layers of the esophagus.
Esophageal tissue damage occurs in three phases: the acute phase, consisting of edema and inflammation; the latent phase, with ulceration, exudation, and tissue sloughing; and the chronic phase, in which there is diffuse scarring.
Gastroesophageal reflux disease accounts for 70% to 80% of all cases of esophageal stricture. Postoperative strictures account for 10% of all cases, and corrosive strictures account for less than 5% of all cases. Peptic strictures are 10 times more common in Whites than in Blacks and Asians and two to three times more common in men than in women.
Signs and symptoms
Effects vary from none at all to intense pain in the mouth and anterior chest, marked salivation, inability to swallow, and tachypnea. Bloody vomitus containing pieces of esophageal tissue signals severe damage. Signs of esophageal perforation and mediastinitis, especially crepitation, indicate destruction of the entire esophagus. Inability to speak implies laryngeal damage.
The acute phase subsides in 3 to 4 days, enabling the patient to eat again. Fever suggests secondary infection. Symptoms of dysphagia return if stricture develops, usually within weeks; rarely, stricture is delayed and develops several years after the injury.
Diagnosis
CONFIRMING DIAGNOSIS A history of chemical ingestion and physical examination revealing oropharyngeal burns (including white membranes and edema of the soft palate and uvula) usually confirm the diagnosis.
The type and amount of the chemical ingested must be identified; this may be done by examining the container of the ingested material or by calling the poison control center.
Two procedures are helpful in evaluating the severity of the injury:
❑ Endoscopy (in the first 24 hours after ingestion) delineates the extent and location of the esophageal injury and assesses the depth of the burn. This procedure may also be performed a week after ingestion to assess stricture development.
❑ Barium swallow (1 week after ingestion and every 3 weeks thereafter) may identify segmental spasm or fistula, but doesn’t always show mucosal injury.
Treatment
Conservative treatment of corrosive esophagitis and stricture includes monitoring the patient’s condition; early endoscopy; administering corticosteroids, such as prednisone and hydrocortisone, to control inflammation and inhibit fibrosis; and using a broad-spectrum antibiotic, such as ampicillin, to protect the corticosteroid-immunosuppressed patient against infection by his own mouth flora.
Treatment may also include bougienage, a procedure in which a slender, flexible, cylindrical instrument called a bougie is passed into the esophagus to dilate it and minimize stricture. Some physicians begin bougienage immediately and continue it regularly to maintain a patent lumen and prevent stricture; others delay it for a week to avoid the risk of esophageal perforation.
Surgery is necessary immediately for esophageal perforation or later to correct stricture untreatable with bougienage. Corrective surgery may involve transplanting a piece of the colon to the damaged esophagus. However, even after surgery, stricture may recur at the site of the anastomosis.
Supportive treatment includes I.V. therapy to replace fluids or total parenteral nutrition while the patient can’t swallow, gradually progressing to clear liquids and a soft diet.
Special considerations
If you’re the first health care professional to see the patient who has ingested a corrosive chemical, the quality of your emergency care will be critical. To meet this challenge, follow these important guidelines:
❑ Don’t induce vomiting or lavage because this will expose the esophagus and oropharynx to additional injury.
❑ Don’t perform gastric lavage because the corrosive chemical may cause further damage to the mucous membrane of the GI lining.
❑ Provide vigorous support of vital functions, as needed, such as oxygen, mechanical ventilation, administration of I.V. fluids, and treatment for shock, depending on the severity of the injury.
❑ Carefully observe and record intake and output.
❑ Before X-rays and endoscopy, explain the procedure to the patient to lessen anxiety during the tests and to obtain cooperation.
❑ Because the adult who has ingested a corrosive agent has usually done so with suicidal intent, assist him and his family in seeking psychological counseling. Monitor the patient according to facility protocol if the attempt was a suicide.
❑ Provide emotional support for parents whose child has ingested a chemical. They’ll be distraught and may feel guilty about the accident. After the emergency and without emphasizing blame, teach appropriate preventive measures, such as locking accessible cabinets and keeping all corrosive agents out of a child’s reach.
❑ Encourage long-term follow-up because of the increased risk of squamous cell carcinoma.
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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