Corrosive/Caustic Esophagitis

Clinical

Ingestion of caustic or corrosive agents (i.e. lye, dishwasher detergents, alkali or acidic agents) causes acute and chronic inflammatory changes mostly in the distal two-thirds of the esophagus. Whether the ingestion be accidental or intentional, the alkali agents penetrate the layers of the esophagus and cause severe liquefaction necrosis. Ingested acidic agents cause less damage and mainly cause superficial coagulative necrosis which forms an eschar that prevents further penetration to deeper esophageal layers. There are three characteristic phases of injury in caustic esophagitis: 1) acute necrosis, 2) ulceration-granulation, 3) stricture formation. Patients will present with rapid onset of odynophagia, chest pain, vomiting, and hematemesis.

Radiological findings

Chest and abdominal radiographs should be ordered routinely for patients who have ingested these agents. Chest films may reveal a dilated esophagus or evidence of esophageal perforation. Abdominal films may show pneumoperitoneum secondary to gastric perforation. If perforation is suspected, the study should be followed up by a water-soluble contrast study. In the acute phase, esophagrams may show abnormal esophageal motility with diffuse spasms and poor primary peristalsis. On double contrast studies, shallow ulcers may appear as punctuate, linear, or serpiginous collections of barium. In severe cases, the esophagus may show diffuse narrowing with an irregular contour. Chronically, cicatrisation and fibrosis may lead to the development of strictures 1 to 3 months after the injury. The strictures typically appear as areas of smooth, tapered narrowing in the cervical or upper thoracic esophagus.

Image "A" and "B" both depict ulcerations of the distal esophageal mucosa secondary to lye ingestion. Image "C" depicts irregular narrowing of the esophagus with ulcerations.