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Case Report

Acute Gastric Perforation after Acid Ingestion

Feryal Gun, Latif Abbasoglu, Alaaddin Celik

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

ABSTRACTGastric outlet obstruction is a common late result after acidingestion; early complications, such as gastric necrosis or per-forations are unusual. This is a report of a patient with thehistory of strong acid ingestion who underwent total gastrec-

tomy due to perforation and extensive necrosis of the stomach.JPGN 35:360362, 2002. Key Words: Acid ingestionGastric perforationGastrectomy. 2002 Lippincott Willi-ams & Wilkins, Inc.

INTRODUCTION

Corrosive injury after ingestion of caustic householdproducts is a common problem in children (1,2). Theingestion of alkalies primarily damages oropharynx andesophagus whereas the injury form ingestion of strongacids usually involves the distal part of the esophagusand stomach (2,3). The acid pools in the antrum andcauses gastric outlet obstruction more commonly be-cause of cicatricial antral stenosis (1,4). Concentratedacids, if swallowed in large amounts, may even lead toearly perforation of the stomach if it is in a fasting state

(24). We report a case of acute gastric perforation dueto acid ingestion and discuss its clinical presentation,course, and management.

CASE REPORT

A 2-year-old boy was admitted to our unit 2 hoursafter ingesting an unknown amount of scale dissolvent(25% nitric acid). He was lethargic. His respirations wereshallow and he was vomiting blood. His vital signs weretemperature, 36C; pulse rate, 154/min; respiratory rate,40/min; and blood pressure, 110/60 mm Hg. On physicalexamination, there were erythemas of the lips and oro-

pharynx, and first- and second-degree skin burn on theneck. Abdominal examination revealed tenderness andvoluntary guarding. Laboratory studies disclosed the fol-lowing values: WBC count, 34,100 /mm3; hemoglobin,

8.6 g/dl; glucose, 520 mg/dl; Na, 127 mEq/L. Arterialblood gas values showed pH, 7.11; pO2, 133 mm Hg; andpCO2, 55 mm Hg. Renal, hepatic, and pancreatic func-tion test results were within normal limits. An abdominalroentgenogram showed free air under the diaphragm sug-gesting a perforation in the gastrointestinal tract. He ex-perienced a respiratory arrest. He was intubated, intrave-nous antibiotics were given and he was transported to theoperating room immediately.

Laparotomy revealed extensive gastric necrosis onboth the anterior and posterior walls with a linear perfo-ration of 4 to 5 cm along the greater curvature startingfrom fundus of the stomach (Fig. 1). The esophagogas-tric junction was not damaged. A total gastrectomy wasperformed, remodeling the gastrointestinal tract by anas-tomosing the distal end of the esophagus to the jejunumwith a Braun anastomosis, and closing the duodenalstump. The resected stomach measured 9 cm in lengthand 6 cm in width. The mucosa was dark brown andblack in color. Microscopic sections of stomach showedextensive areas of necrosis and edema. On the secondpostoperative day, weaning from mechanical ventilationwas achieved. He was given total parenteral nutrition for10 days. On the seventh day, barium meal revealed asatisfactory esophago-jejunal anastomosis, and oral feed-ing was started and well tolerated (Fig. 2). However, atthe end of the first month a stricture was detected at theanastomotic region which was dilated. He is currentlyasymptomatic, 18 months after the dilatation.

DISCUSSION

Acidic substance ingestion is less common in childrenthan alkali ingestion. The acidic products ingested are

Received November 15, 2001; accepted April 16, 2002.Correspondence to Feryal Gun, Hareket Ordusu sok. Isil apt. No:

12/17 Bahcel ievler, Istanbul, 34590 Turkey (e-mail: [email protected]).

Journal of Pediatric Gastroenterology and Nutrition35:360362 September 2002 Lippincott Williams & Wilkins, Inc., Philadelphia

360 DOI: 10.1097/01.MPG.0000024972.12621.D1


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usually household cleaning substances. In contrast withalkaline caustics that damage the esophagus and usuallyspare the stomach, acidic solutions frequently passthrough the esophagus without causing mucosal injurybut producing coagulation necrosis of the stomach as ina thermal burn (1,2). Although the esophagus is usuallyspared after acid ingestion due to rapid transit and theresistance of squamous epithelium, isolated cases ofesophageal acid injury have been reported (4,5). Acidingestion may induce pyloric spasm and produces antralmucosal edema, inflammation, and finally pyloric stric-ture due to extensive fibrosis (24,6). Gastric burnscaused by alkali corrosives have also been reported (7).

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

Strong acids reaching the stomach may cause perfo-ration and peritonitis in 24 to 48 hours if a large volumeis 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, asin our case, if there is perforation or extensive necrosis ofthe stomach wall (24,7,10). Otherwise, these patientsshould be kept under close observation and fiberopticendoscopy is performed to determine the extent of thedamage (1,6). Total gastrectomy in children is moretroublesome than in adults because of side effects such asanemia, vitamin B

12deficiency, and growth retardation

(11,12). Our patient is doing well so far with respect tothese complications.

REFERENCES

1. Ciftci AO, Senocak ME, Buyukpamukcu N, Hicsonmez A. Gastricoutlet obstruction due to corrosive ingestion: incidence and out-come. Pediatr Surg Int 1999;15:8891.

2. Cochran ST, Fonkalsrud EW, Gyepes MT. Complete obstructionof the gastric antrum in children following acid ingestion. ArchSurg 1978;113:30810.

FIG. 1. Extensive necrotic areas and perforation site of the stom-ach.

FIG. 2. Barium meal showing patent esophagojejunal anastomo-sis.

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3. Zamir O, Hod G, Lernau OZ et al. Corrosive injury to the stomachdue to acid ingestion. Am Surg 1985;51:1702.

4. Chong GC, Beahrs OH, Payne SW. Management of corrosive gas-tritis due to ingested acid. Mayo Clin Proc 1974;49:8615.

5. Nicosia JF, Thornton JP, Folk FA, Saletta JD. Surgical manage-ment of corrosive gastric injuries. Ann Surg 1974;180:13943.

6. Lowe JE, Graham DY, Boisaubin EV, Lanza FL. Corrosive injuryto the stomach: The natural history and role of fiberoptic endos-

copy. Am J Surg 1979;137:8036.7. Tekant G, Eroglu E, Erdogan E et al. Corrosive injury-induced

gastric outlet obstruction: A changing spectrum of agents and treat-ment. J Pediatr Surg 2001, 36:10047.

8. Chodak GW, Passaro E. Acid ingestion need for gastric resection.JAMA 1978;239:2256.

9. Gillis DA, Higgins G, Kennedy R. Gastric damage from ingestedacid in children. J Pediatr Surg 1985;20:4946.

10. Cattan P, Munoz-Bongrand N, Berney T et al. Extensive abdomi-nal surgery after caustic ingestion. Ann Surg 2000;231:51923.

11. Yamataka A, Pringle KC, Wyete J. A case of zinc chloride inges-

tion. J Pediatr Surg 1998;33:6602.12. Davenport M, Hossie GP, Tasker RC et al. Long-term effects of

gastric transposition in children: a physiological study. J PediatrSurg 1996;31:58893.

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