ANNALS OF SURGERY Vol. 180 AUGUST 1974 No. 2 Surgical Management of Corrosive Gastric In juries JON F. NICOSIA, M.D., JOSEPH P. THORNTON, M.D., FRANK A. FOLK, M.D., JOHN D. SALETTA, M.D. Four cases of extensive corrosive gastric injury requiring surgical treatment are presented. Appropriate management of this life-threatening entity requires an awareness of its subtle presentation plus a well planned surgical approach. From the Division of General Surgery, Cook County Hospital, Chicago, Illinois bile were noted oozing through the wound. At this time the patient admitted that prior to his first admission he had accidentally ingested a large quantity of liquid drain cleaner which contained contain alkalis which frequently cause esophageal burns and sulfuric acid. At reexploration the entire gastric mucosa was found to be strictures, and only occasionally produce gastric injury. with multiple areas of full thickness necrosis. The gangrenous, In contrast, acid ingestions usually spare the esophagus pyloroplasty had disrupted and was the site of bile leakage. The but often burn the stomach. external surface of the esophagus and duodenum appeared norThe following reports represent our personal experi- mal. A total gastrectomy, splenectomy, tube duodenostomy, cloence with four cases of extensive gastric burns resulting sure of the distal esophagus, feeding jejunostomy and doublecervical esophagostomy were performed (Fig. 1). from the ingestion of corrosive materials and requiring barrelled The course was prolonged and complicated by postoperative acute and long termiurgical management. intraperitoneal abscesses requiring surgical drainage. Seven weeks M OST INGESTED CORROSIVE SUBSTANCES Case Reports Case 1.. J. F., a 30-year-old man, was admitted to Cook County Hospital on September 9, 1968 with a history of hematemesis and melena beginning four hours prior to admission. He related a recent heavy alcohol intake but denied previous gastrointestinal bleeding. His bleeding stopped spontaneously, and upper gastrointestinal X-rays were interpreted as normal. The patient was discharged one week later with a presumptive, diagnosis of alcoholic gastritis. The following day he returned, again vomiting blood. On this occasion the bleeding persisted, and during the next four days he received eight units of whole blood. At exploratory laparotomy an edematous, hyperemic, friable gastric mucosa with absent rugal folds was noted. A diagnosis of alcoholic gastritis was presumed, and a vagotomy and pyloroplasty were performed. Postoperatively, bleeding continued and on the second postoperative day air and Submitted for publication August 30, 1973. Reprint requests: John D. Saletta, M.D., Chairman, Division of General Surgery, Cook County Hospital, 1825 West Harrison Street, Chicago, Illinois 60612. 139 following the second operation, with the patient's sepsis eradicated and his nutrition maintained via jejunostomy feedings, he was discharged. Prior to discharge, esophagoscopy revealed normal esophageal mucosa without stricture or ulceration. Three months later, a transabdominal end to side esophagojejunostomy and jejunojejunostomy were performed (Fig. 2). The following month the cervical esophagostomy was closed. At discharge the patient's weight was 108 pounds, whereas, prior to his illness, he weighed 180 pounds. Eighteen months later the patient was readmitted because of vague postprandial epigastric distress. His weight at that time was 145 pounds. A complete work-up, including an upper gastrointestinal series and esophagoscopy were within normal limits. At followup 2% years postoperatively, the patient remained asymptomatic. Case 2. T. M., a 22-year-old woman, was admitted to Cook County Hospital on September 20, 1968, after ingestion of an unknown amount of crystalline lye. Although the patient complained of mild abdominal pain, she had no oropharyngeal burns or abdominal tenderness. On the fourth hospital day the patient suddenly developed severe abdominal pain with signs of peritonitis. At exploratory laparotomy the entire stomach was found to be necrotic without free perforation. Although the external sur- NICOSIA AND OTHERS 140 8 6 Fic. 1. Schematic drawing of / l / m a patient J. F., following total gastrectomy and splenectomy. Note the diverting cervical esophagostomy, Ann. Surg. * August 1974 } / l- tube duodenos- tomy, and feeding } jejunostomy. FIG. 3. Schematic drawing of patient T. M., showing a substernal colon bypass, utilizing the descending colon interosed between the cervical esophagus and proximal jejunum. The extensively strictured intrathoracic esophagus has not been removed. face of the esophagus and duodenum appeared normal, the esophageal mucosa was gangrenous. Because of the patient's precarious condition, extension of the operation to include resection of the esophagus was deemed inadvisable. Consequently, a total gastrectomy, closure of the necrotic distal esophagus, cervical esophagostomy, tube duodenostomy and jejunostomy were performed. The patient made an uncomplicated recovery and her nutrition was maintained with hyperalimentation and jejunostomy feedings. Three months later a substernal colon bypass procedure was performed utilizing the descending colon interposed between the cervical esophagus and proximal jejunum (Fig. 3). Postoperatively, a suture line disruption of the proximal esophago-colostomy resulted in a salivary fistula. The patient has subsequently been lost to followup. Case 3. G. J., a 23-year-old man, ingested an unknown amount of liquid drain cleaner containing sulfuric acid, approximately four hours prior to admission on December 31, 1971. He was seen at another hospital, where gastric lavage was performed prior to transfer to the Cook County Hospital. On admission, he was intoxicated and complained of burning abdominal and substernal pain. He had swollen parched lips and multiple burned areas on the buccal mucosa. There was no abdominal tenderness. Moist rales and rhonchi were auscultated throughout both lung fields. The patient was managed with intravenous fluids, parenteral antibiotics and nothing by mouth. His chest X-ray revealed bilateral patchy infiltrates, but there was no evidene of free air on either the upright chest or abdominal X-rays. Parenteral steroids were administered as adjunctive therapy for presumed chemical aspiration pneumonitis and a tracheostomy was performed. Nine days after admission the patient developed abdominal tenderness and signs of peritonitis. At exploratory laparotomy a liter of foul-smelling, bile-stained fluid was found in the peritoneal cavity. The entire stomach and duodenum were necrotic with multiple free perforations, necessitating a total gastrectomy and pancreatoduodenectomy. The distal end of the esophagus was closed and a cervical esophagostomy was constructed. A choledochojejunostomy and feeding jejunostomy were performed and the remaining pancreas was oversewn with separate ligation of the pancreatic duct (Fig. 4). The patient developed progressive pulmonary insufficiency and expired on the second postoperative day. Case 4. S.W., a 26-year-old male, was admitted to Cook County on April 4, 1973, after ingesting liquid drain cleaner which contained sulfuric acid. Superficial burns were noted on the patient's tongue and posterior pharynx. Examination of his abdomen revealed minimal left upper quadrant tenderness without evidence of peritonitis. Six days after admission the patient had several episodes of hematemesis during a 24-hour period; however, blood replace- Hospital ment was not required. On May 21, 1973, he began vomiting after meals. An upper gastrointestinal X-ray revealed partial stricture of the distal onethird of the esophagus as well as antral stenosis and ulceration (Figs. 5 and 6). At operation, the distal antral mucosa was observed to be replaced by granulation tissue and a 1 cm ulceration was present on the posterior antral wall. The pre-pyloric region was markedly stenotic, permitting passage of a 3 mm probe (Fig. 7). The operative procedure consisted of a 40% distal gastrectomy with a Billroth I gastroduodenostomy, plus a gastrostomy for subsequent retrograde esophageal dilations. FIG. 4. Schematic drawing of \ ,9-? / / FIG. 2. Schematic drawing of patient J. F., following esophagojejunostomy and jejunojejun- ostomy. The tube duodenostomy gas been removed but the feedhsing jejunostomy and cervical esophagostomy remain. patient G. J., following total gastrectomy and pancreatoduodenectomy. Note the cervical esophagostomy, closure of the proximal jejunum, end to side choledochojejunostomy, feeding jejunostomy. The and re- sected end of the remaining pancreas has been oversewn. Vol. 180 * No. 2 CORROSIVE GASTRIC INJURIES 141 The patient's postoperative course has been uneventful. He is currently eating without difficulty. Discussion Gastric burns often occur following ingestion of corrosive materials, either accidentally by children and alcoholics, or intentionally by emotionally disturbed individuals. On the basis of experimental animal studies and clinical observation, it is well known that acids tend to destroy the stomach and spare the esophagus.23 On the other hand, alkalis usually injure the esophagus and spare the stomach.2 Large amounts of either substance cause severe damage to both organs in approximately 20% of ingestions.'0 The esophageal sparing noted in acid ingestions appears related to the resistance of the esophageal squamous epithelium to acid erosion and rapid esophageal transit time.5 Alkalis are usually prevented from damaging the stomach by the neutralizing effect of the acid normally present in the stomach.24 In most instances, the gastric burn injury is greatest along the lesser curvature and in the pre-pyloric area.21 The explanation for this distribution was provided by Testa in 1938. He introduced caustic soda mixed with barium into the esophagus of dogs and demonstrated by X-ray that the alkali-barium bolus flowed along the lesser curvature, produced severe pylorospasm, and was retained in the pre-pyloric area.23 The extent of gastric injury appears related to the nature, volume, and concentration of corrosives ingested; the length of time they remain in contact with the stomach; the content of the stomach at the time of ingestion; and the relative tonicity of the pyloric sphincter.4 At times only superficial mucosal injuries occur which heal uneventfully. More extensive gastric burns which involve the submucosa and muscularis produce various degrees of deformity including antral stenosis,8"10"12"14,16,19 hourglass strictures,7 22 and rigidity simulating infiltrating gastric carcinoma."1'l3 Elective surgical correction of these deformities may be necessary when signs of gastric outlet obstruction develop. This usually develops between the first and second month post-injury.'4 Partial gastric resection is the procedure of choice.7 Gastroenterostomy without resection has been used for definitive therapy, but the uncertain fate of the burned stomach would appear to be a good indication for its resection.'158,20 In this regard, O'Donnel in 1949 reported a case of gastric carcinoma developing six years following gastroenterostomy for a nitric acid burn which had produced pyloric obstruction.17 In the extensively burned stomach, visceral perforation may occur immediately. More frequently, massive gastrointestinal bleeding or peritonitis are delayed for FIG. 5. Barium esophagogram of patient S.W., taken seven weeks following acid ingestion. Note the incomplete stricture of the distal one-third of the esophagus. FIG. 6. Barium filled distal stomach of patient S.W., seen on an upper gastrointestinal X-ray performed seven weeks following acid ingestion. The complete antral obstruction and posterior ulcer crater are seen. NICOSIA AND OTHERS 142 Ann. Surg. - August 1974 FIG. 7. Intraoperative photograph of the antrum in patient S.W., as seen through a gastrotomy incision. The thickened antral wall as well as the antral stricture, which pennits the passage of a 3 mm probe, can be seen. three to fourteen days, making it imperative that repeated daily abdominal examinations be performed during the first two weeks following corrosive ingestions.3 The frequent absence of oral and esophageal burns may further mask the suspicion of severe injuries to the stomach and duodenum. Initial management should consist of nothing by mouth, antacids per nasogastric tube, antibiotics, intravenous fluids, and blood transfusions when indicated.24 Fiberoptic endoscopy should be performed initially to determine the most proximal level of injury.5 The fiberoptic scope should not be passed beyond the most proximal area of mucosal burn because of the danger of perforation. Developing signs of peritonitis may be masked if steroids are used (Case 3). Gastric lavage or the inducing of emesis is contraindicated, since perforation of the injured organ or tracheobronchial aspiration may occur. Emergent surgery is indicated for hemorrhage, free perforation or peritonitis. Removal of necrotic tissue is essential and may necessitate total gastrectomy, pancreatoduodenectomy and small bowel resection. Attempts at definitive restoration of intestinal continuity should be deferred at the time of emergency surgery as anastomoses of edematous friable segments of esophagus, stomach or small bowel are prone to disrupt.3 Following total gastrectomy and closure of the distal esophagus, cervical esophagostomy is recommended for diversion of saliva.6'9 Tube drainage of the distal esophagus without cervical esophagostomy has been inadequate because esophageal stricture, mediastinitis or tracheoesophageal fistulae have developed.' Since the postoperative course may be prolonged, a feeding jejunostomy is nutritionally beneficial and provides either an adjunct or an alternative to intravenous hyperalimentation. Staged reconstruction of intestinal continuity should be performed when the patient's condition warrants. Full recovery can be expected in most patients and nutrition can be maintained with minor adjustments in eating habits plus supplemental vitamins, especially B12, for patients who have undergone total gastrectomy. References 1. Allen, R. E., Thoshinsky, N. K., Stollone, R. J. and Hunt, T. K.: Corrosive Injuries of the Stomach. Arch. Surg., 100: 409, 1970. 2. Ballenger, J. J.: Disease of Nose, Throat, and Ears. Eleventh Edition. Philadelphia, Lea and Febeger, 872-874, 1969. 3. Berry, W. B., Hall, R. A. and Jordan, G. L.: Necrosis of the Entire Stomach Secondary to Ingestion of a Corrosive Acid. Report of a Patient Successfully Treated by Total Gastrectomy. Am. J. Surg., 109:652, 1965. 4. Boikan, W. S. and Singer, H. A.: Gastric Sequelae of Corrosive Poisoning. Arch. Int. Med., 46:342, 1930. 5. Citron, B. P., Pincus, I. V., Geokas, M. D., et al.: Chemical Trauma of the Esophagus and Stomach. Surg. Clin. N. Am., 48: 1303, 1968. 6. Davis, L. L., Raffensperger, J. and Novak, G. M.: Necrosis of the Stomach Secondary to Ingestion of Corrosive Agents. Vol. 180 7. 8. 9. 10. 11. 12. 13. 14. - No. 2 CORROSIVE GASTRIC INJURIES Report of Three Cases Requiring Total Gastrectomy. Chest, 62:48, 1972. Gonzalez, L. L., Zinninger, M. M. and Altemeier, W. A.: Cicatricial Gasric Stenosis Caused by Ingestion of Corrosive Substance. Ann. Surg., 156:84, 1962. Gray, J. K. and Holmes, C. L.: Pyloric Stenosis Caused by Ingestion of Corrosive Substances: Report of Case. Surg. Clin. N. Am., 28:1041, 1948. Gryboski, W., Page, R. and Rush, B. F.: Management of Total Gastric Necrosis Following Lye Ingestion. The Use of Colon to Replace both Esophagus and Stomach. Ann. Surg., 161:469, 1965. Herrington, L. J.: Stenosis of the Gastric Antrum and Proximal Duodenum Resulting from the Ingestion of a Corrosive Agent. Am. J. Surg., 107:580, 1964. Holzbach, R. T.: Corrosive Gastritis Resembling Carcinoma due to Ingestion of Acid. JAMA, 205:883, 1968. Karon, A. B.: The Delayed Gastric Syndrome with Pyloric Stenosis and Achlorhydria Following the Ingestion of Acid -A Definite Clinical Entity. Am. J. Digest. Dis., 7:1041, 1962. Karon, A. B. and Wall, H. C.: Pyloric Stenosis Caused by the Ingestion of a Corrosive Acid Simulating Gastric Carcinoma: Report of a Case. Castroenterology, 17:445, 1951. Marks, I. N., Banks, M. B., Werbeloff, L., Forman, M. B. and Louw, J. H.: The Natural History of Corrosive Gas- 143 Report of Five Cases. Am. J. Digest. Dis., 8:509, 15. Meyer, K. A. and Steigmann, F.: Surgical Treatment of Corrosive Gastritis. Surg. Gynecol. Obstet., 79:306, 1944. 16. Nevin, I. N., Turner, N. W. and Gardner, H. T.: Early and Late Roentgenographic Findings in Corrosive Gastritis. Am. J. Roent., 81:603, 1959. 17. O'Donnell, C. H., Abbott, W. E. and Hirchfeld, J. W.: Surgical Treatment of Corrosive Gastritis. Am. J. Surg., 78:251, tritis: 1963. 1949. 18. Poteshman, N. L.: Corrosive Gastritis due to Hydrochloric Acid Ingestion. Am. J. Roent., 99:182, 1967. 19. Schulenberg, C. A. R.: Corrosive Stricture of the Stomach: Without Involvement of the Esophagus. Lancet, 2:367, 1941. 20. Steigmann, F. and Dolehide, R. A.: Corrosive (Acid) Gastritis Management of Early and Late Cases. N. Engl. J. Med., 254:981, 1956. 21. Strange, D. C., Finneran, J. C. and Shumacker, H. B.: Corrosive Injury of the Stomach. Arch. Surg., 62:350, 1951. 22. Strode, E. C. and Dean, M. L.: Acid Burns of the Stomach. Ann. Surg., 313:801, 1950. 23. Testa, G. F.: Contrilreta Radiologica e Sperimentale alla Studio dell Lesione Esofagee e Gastriche nelle Causticazioni da Alcali. Radiol. Med. Torina, 25:17, 1938. 24. Tucker, A. S. and Gerrish, E. W.: Hydrochloric Acid Burns of the Stomach. JAMA, 174:890, 1960.
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