Corrosive Injury of Stomach

Corrosive injuries of the stomach are not uncommon in developing countries. In these countries, accidental or suicidal ingestion of acids is encountered more often than in developed countries where lye or alkaline corrosives are more frequent. Both accidental ingestion, particularly in children, due to careless storing of chemicals and ingestion with suicidal intent and due to free availability of the caustic agents contribute to their occurrence.

The relative extent of esophageal and gastric involvement largely depends on the nature of the corrosive ingested. Acids affect the stomach more commonly than alkalis, cause mucosal damage by coagulation necrosis, and require a longer duration of contact. However, alkali damage of the stomach has also been reported. Acids are cleared rapidly from the esophagus to the stomach where they pool in the prepyloric area due to corrosive-induced pylorospasm. Prolonged contact with the prepyloric mucosa results in a prepyloric stricture. Strictures can also occur in the antrum, body, or in the pyloroduodenal area. When the volume of the corrosive ingested is large, the entire stomach gets scarred leading to a diffusely contracted stomach. On the other hand, alkalis cause liquefaction necrosis [3], are more viscous, and tend to adhere to the esophageal mucosa with only a relatively small amount reaching the stomach. The extent of esophageal damage is greater with alkalis than acids.

Extensive acute injuries are usually fatal and therefore, the spectrum of acute and chronic gastric injury seen at a tertiary care referral hospital is not reflective of the overall picture as patients with the most severe gastric and esophageal injuries die at peripheral centers.

The spectrum of gastric injury due to corrosives can vary from partial or total gastric mucosal or transmural necrosis to chronic gastric injuries of different types.

Treatment

Laparoscopy is also a useful adjunct in assessing a patient who has a high risk of gastric perforation as seen on endoscopy or in patients with severe esophageal injury in whom an upper gastrointestinal endoscopy to assess the stomach is not feasible. Some authors have advocated routine laparoscopic examination in all injuries of second degree or greater. However, this has not been our practice. There is also a report on the use of a Meckels scan to assess the severity of the gastric injury.

Following an acute injury to the stomach by corrosive ingestion, the initial management is usually conservative. Adherence to the basic tenet of avoiding a gastric lavage in any corrosive poisoning cannot be overemphasized. The patient usually has associated burns to the upper aerodigestive tract which needs attention as well, if required, with a tracheostomy. Attempts at neutralizing the acids or alkalis are ill-advised and the resulting exothermic reaction from the neutralization process may do more harm than good. Similarly, there is not much role for measures to dilute the corrosive with milk, water and so forth, as the definitive extent of the injury is determined within minutes after ingestion.

Emergency surgical intervention is needed if the patient develops any signs of esophageal perforation, peritonitis, or uncontrolled massive hematemesis.