Secondary Logo

Journal Logo

Acute Gastric Perforation after Acid Ingestion

Gün, Feryal; Abbasoğlu, Latif; Çelik, Alaaddin

Journal of Pediatric Gastroenterology and Nutrition: September 2002 - Volume 35 - Issue 3 - p 360-362
Case Reports

Gastric outlet obstruction is a common late result after acid ingestion; early complications, such as gastric necrosis or perforations are unusual. This is a report of a patient with the history of strong acid ingestion who underwent total gastrectomy due to perforation and extensive necrosis of the stomach.

Istanbul University, Istanbul Medical School, Department of Pediatric Surgery, Turkey

Received November 15, 2001; accepted April 16, 2002.

Correspondence to Feryal Gün, Hareket Ordusu sok. Isil apt. No: 12/17 Bahçelievler, Istanbul, 34590 Turkey (e-mail:

Back to Top | Article Outline


Corrosive injury after ingestion of caustic household products is a common problem in children (1,2). The ingestion of alkalies primarily damages oropharynx and esophagus whereas the injury form ingestion of strong acids usually involves the distal part of the esophagus and stomach (2,3). The acid pools in the antrum and causes gastric outlet obstruction more commonly because of cicatricial antral stenosis (1,4). Concentrated acids, if swallowed in large amounts, may even lead to early perforation of the stomach if it is in a fasting state (2–4). We report a case of acute gastric perforation due to acid ingestion and discuss its clinical presentation, course, and management.

Back to Top | Article Outline


A 2-year-old boy was admitted to our unit 2 hours after ingesting an unknown amount of scale dissolvent (25% nitric acid). He was lethargic. His respirations were shallow and he was vomiting blood. His vital signs were temperature, 36°C; pulse rate, 154/min; respiratory rate, 40/min; and blood pressure, 110/60 mm Hg. On physical examination, there were erythemas of the lips and oropharynx, and first- and second-degree skin burn on the neck. Abdominal examination revealed tenderness and voluntary guarding. Laboratory studies disclosed the following values: WBC count, 34,100 /mm3; hemoglobin, 8.6 g/dl; glucose, 520 mg/dl; Na, 127 mEq/L. Arterial blood gas values showed pH, 7.11; pO2, 133 mm Hg; and pCO2, 55 mm Hg. Renal, hepatic, and pancreatic function test results were within normal limits. An abdominal roentgenogram showed free air under the diaphragm suggesting a perforation in the gastrointestinal tract. He experienced a respiratory arrest. He was intubated, intravenous antibiotics were given and he was transported to the operating room immediately.

Laparotomy revealed extensive gastric necrosis on both the anterior and posterior walls with a linear perforation of 4 to 5 cm along the greater curvature starting from fundus of the stomach (Fig. 1). The esophagogastric junction was not damaged. A total gastrectomy was performed, remodeling the gastrointestinal tract by anastomosing the distal end of the esophagus to the jejunum with a Braun anastomosis, and closing the duodenal stump. The resected stomach measured 9 cm in length and 6 cm in width. The mucosa was dark brown and black in color. Microscopic sections of stomach showed extensive areas of necrosis and edema. On the second postoperative day, weaning from mechanical ventilation was achieved. He was given total parenteral nutrition for 10 days. On the seventh day, barium meal revealed a satisfactory esophago-jejunal anastomosis, and oral feeding was started and well tolerated (Fig. 2). However, at the end of the first month a stricture was detected at the anastomotic region which was dilated. He is currently asymptomatic, 18 months after the dilatation.

FIG. 1.

FIG. 1.

FIG. 2.

FIG. 2.

Back to Top | Article Outline


Acidic substance ingestion is less common in children than alkali ingestion. The acidic products ingested are usually household cleaning substances. In contrast with alkaline caustics that damage the esophagus and usually spare the stomach, acidic solutions frequently pass through the esophagus without causing mucosal injury but producing coagulation necrosis of the stomach as in a thermal burn (1,2). Although the esophagus is usually spared after acid ingestion due to rapid transit and the resistance of squamous epithelium, isolated cases of esophageal acid injury have been reported (4,5). Acid ingestion may induce pyloric spasm and produces antral mucosal edema, inflammation, and finally pyloric stricture due to extensive fibrosis (2–4,6). Gastric burns caused by alkali corrosives have also been reported (7).

The extent and the severity of corrosive gastric injury is directly related to the concentration and amount of acidic substance as well as the length of time in the stomach, and to the amount of gastric content at the time of ingestion (1,4,6,8). The most-frequently encountered acidic substances are hydrochloric acid, sulfuric acid, or, as in our case, nitric acid.

Strong acids reaching the stomach may cause perforation and peritonitis in 24 to 48 hours if a large volume is involved and if the organ is empty (2,3,9). In our case, perforation appeared 2 hours after ingestion.

An immediate total gastrectomy may be indicated, as in our case, if there is perforation or extensive necrosis of the stomach wall (2–4,7,10). Otherwise, these patients should be kept under close observation and fiberoptic endoscopy is performed to determine the extent of the damage (1,6). Total gastrectomy in children is more troublesome than in adults because of side effects such as anemia, vitamin B12 deficiency, and growth retardation (11,12). Our patient is doing well so far with respect to these complications.

Back to Top | Article Outline


1. Çiftci AO, Šenocak ME, Büyükpamukçu N, Hiçsönmez A. Gastric outlet obstruction due to corrosive ingestion: incidence and outcome. Pediatr Surg Int 1999; 15:88–91.
2. Cochran ST, Fonkalsrud EW, Gyepes MT. Complete obstruction of the gastric antrum in children following acid ingestion. Arch Surg 1978; 113:308–10.
3. Zamir O, Hod G, Lernau OZ et al. Corrosive injury to the stomach due to acid ingestion. Am Surg 1985; 51:170–2.
4. Chong GC, Beahrs OH, Payne SW. Management of corrosive gastritis due to ingested acid. Mayo Clin Proc 1974; 49:861–5.
5. Nicosia JF, Thornton JP, Folk FA, Saletta JD. Surgical management of corrosive gastric injuries. Ann Surg 1974; 180:139–43.
6. Lowe JE, Graham DY, Boisaubin EV, Lanza FL. Corrosive injury to the stomach: The natural history and role of fiberoptic endoscopy. Am J Surg 1979; 137:803–6.
7. Tekant G, Eroglu E, Erdoğan E et al. Corrosive injury-induced gastric outlet obstruction: A changing spectrum of agents and treatment. J Pediatr Surg 2001, 36:1004–7.
8. Chodak GW, Passaro E. Acid ingestion need for gastric resection. JAMA 1978; 239:225–6.
9. Gillis DA, Higgins G, Kennedy R. Gastric damage from ingested acid in children. J Pediatr Surg 1985; 20:494–6.
10. Cattan P, Munoz-Bongrand N, Berney T et al. Extensive abdominal surgery after caustic ingestion. Ann Surg 2000; 231:519–23.
11. Yamataka A, Pringle KC, Wyete J. A case of zinc chloride ingestion. J Pediatr Surg 1998; 33:660–2.
12. Davenport M, Hossie GP, Tasker RC et al. Long-term effects of gastric transposition in children: a physiological study. J Pediatr Surg 1996; 31:588–93.

Acid ingestion; Gastric perforation; Gastrectomy

© 2002 Lippincott Williams & Wilkins, Inc.