The accidental or suicidal ingestion of strong alkali, such as lye, or of acids, such as hydrochloric or carbolic acid, can cause necrosis of the gastric wall, particularly in the prepyloric region. Alkali usually injures the esophagus more severely than the stomach, whereas the reverse tends to occur with acid. The degree of gastric injury varies with the quantity and concentration of irritant ingested and the amount of food present in the stomach. Patients complain of burning of the mouth, throat, and retrosternal area. With gastric injury, there is severe epigastric pain and often vomiting. Perforation, peritonitis, or massive hemorrhage may occur shortly after ingestion of a corrosive agent or may be delayed. Later, scarring may cause esophageal or pyloric stenosis.
If the patient is seen shortly after ingesting a corrosive agent, some clinicians suggest emptying the stomach gently via a small, soft rubber tube. Acid neutralization is not recommended for alkali ingestion because the heat of the ensuing reaction may aggravate the injury. Antacids may be given for acid ingestion after preliminary dilution with milk or water. Intravenous therapy, sedation, analgesia, airway maintenance, and careful observation are instituted. The use of corticosteroids and antibiotics is controversial, but corticosteroids may be helpful if edema threatens the airway and antibiotics may help treat aspiration pneumonia. Visible mouth and pharyngeal burns are not necessarily accompanied by esophageal or gastric injury. Therefore, early, gentle endoscopy with a small-caliber screening endoscope may establish the extent of injury. However, early in the course of acid injury the damage may be missed even endoscopically. If perforation or peritonitis is suspected, laparotomy should be performed and a partial gastrectomy done if full-thickness injury to the wall is found. Surgical treatment may be necessary also for acute massive bleeding or for late obstruction caused by scarring. Parenteral nutrition may be required.