J Clin Gastroenterol 2003;37(2):119124.

2003 Lippincott Williams & Wilkins, Inc.

Clinical Reviews Therapeutic Recommendations

Corrosive Ingestion in Adults

Kovil Ramasamy, MD, and Vivek V. Gumaste, MD, MRCP(I), FACG
Abstract
Ingestion of a corrosive substance can produce severe injury to the gastrointestinal tract and can even result in death. The degree and extent of damage depends on several factors like the type of substance, the morphologic form of the agent, the quantity, and the intent. In the acute stage, perforation and necrosis may occur. Long-term complications include stricture formation in the esophagus, antral stenosis and the development of esophageal carcinoma. Endoscopy should be attempted and can be safely performed in most cases to assess the extent of damage. Procedurerelated perforation is rare. Stricture formation is more common in patients with second and third degree burns. Corticosteroids may help prevent stricture formation. Esophageal carcinoma may develop beginning 30 to 40 years after the time of injury. Key Words: lye ingestion, corrosives, sodium hydroxide

ccording to the annual report of the American Association of Poison Control, there were 206,636 cases of human exposure to cleaning substances (which include acids and alkalis) in 2000. Twenty-seven of these cases (the majority being instances of ingestion) resulted in death.1 Although children account for 80% of accidental ingestion,2 ingestion in adults is more often suicidal in intent and therefore tends to be more serious. Corrosive agents produce extensive damage to the gastrointestinal tract, which may result in perforation and death in the acute phase. Long term complications include stricture formation and the development of esophageal carcinoma.

Most commonly used household bleaches contain hydrogen peroxide (3%), sodium hypochlorite or low concentrations of sodium hydroxide (1%), and are mild to moderate irritants with a pH ranging from 10.8 to 11.4.3 Accidental ingestion produces minimal injury to the gastrointestinal tract; long-term damage including stricture formation is rare. However, the ingestion of large quantities of bleach may be associated with serious damage. Unlike bleaches, drain cleaners are more dangerous. Drain cleaners contain sodium hydroxide in concentrations ranging from 4% to 54% and the crystalline variety tends to contain a higher concentration of sodium hydroxide than the liquid form. These agents can produce severe harm to the gastrointestinal tract including perforation. Stricture formation is consistently seen with ingestion of drain cleaners. Automatic dishwasher detergents contain sodium phosphate or tripolyphosphate that are also powerful corrosive agents.1 Clinitest and denture cleaning tablets contain sodium hydroxide and these can cause major esophageal injuries because their solid form prolongs the duration of contact with the mucosa.4 Hair relaxer, a commercially available alkaline product, is another agent implicated in caustic ingestion. Although these products produce extensive facial injury and oral burns, significant esophageal damage has not been reported.5 Acids Acid ingestion tends to occur less frequently in the United States (<5%) but appears to be more common in countries like India where hydrochloric acid and sulfuric acid are easily accessible.6 In the United States, acids are generally available as toilet bowel cleaners (sulfuric, hydrochloric), anti rust compounds (hydrochloric, oxalic, hydrofluoric), battery fluids (sulfuric), and swimming pool cleaners (hydrochloric). PATHOPHYSIOLOGY Solutions with a pH of less than 2 or greater then 12 are highly corrosive. Alkali produces liquefaction necrosis.2 A 22.5% solution of NaOH in contact with the esophagus for 10 seconds and 30% NaOH for 1 second can produce a full thickness injury.2 Thrombosis of small vessels and production of heat exacerbate the initial corrosive injury. Tissue 119

SUBSTANCES Corrosives can be alkaline in nature or acids. Lye is a general term used for alkali found in cleaning agents. Alkalis Alkaline material accounts for most cases of caustic ingestion in western countries.2 Alkalis can be found in a variety of cleaning agents, drain openers, bleaches, toilet bowl cleaners, and detergents (Table 1).

From The Department of Medicine, Mount Sinai Services, City Hospital Center at Elmhurst, New York and the Mount Sinai School of Medicine of the City University of New York, New York. Address correspondence and reprint requests to Dr. Vivek V. Gumaste, Division of Gastroenterology, Mount Sinai Services at Elmhurst, 79-01 Broadway, Elmhurst, New York, NY 11373, USA.

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TABLE 1. Common household corrosives

Product Chlorox Peroxide Tilex mildew remover Electrasol dishwasher detergent Cascade dishwater detergent Comet cleanser Polident powder Drano (liquid) Drano Professional (liquid) Crystal Drano (granular) Liquid Plummer Dow oven cleaner Mister Plumber Lysol toilet cleaner Contents Sodium hypochlorite (5.25%) Hydrogen Peroxide (3%) Sodium hypochlorite (5%), sodium hydroxide (1%) Sodium tripolyphosphates (20%40%) Phosphates (25%50%) Trisodium phosphate (14.5%) Sodium tripolyphosphate (<15%) Sodium hydroxide (9.5%) Sodium hydroxide (32%) Sodium hydroxide (54%) Sodium hydroxide (0.5%2%) Sodium hypochlorite (5%10%) Sodium hydroxide (4%) Sulfuric acid (99.5%) Hydrochloric acid (8.5%)

injury progresses rapidly in the first few minutes but can continue for several hours. Mucosal sloughing occurs 4 to 7 days after the initial injury, and bacterial invasion, inflammatory response, and development of granulation tissue ensue. Because collagen deposition may not begin until the second week, the tensile strength of the healing tissue is low during the first 3 weeks. Many people therefore advocate avoiding endoscopy between 5 to15 days after caustic ingestion.7 Scar retraction begins by the third week and may continue for several months. This results in stricture formation and shortening of the involved segment of the gastrointestinal tract. Shortening of the esophagus alters the LES pressure leading to increased gastroesophageal reflux, which in turn accelerates stricture formation.8 Esophageal injury due to caustic ingestion also produces changes in esophageal motility resulting in low amplitude and nonperistaltic contractions.9 The degree of injury produced depends, to some extent, on the physical form of the alkali. Crystals or solid particles adhere to the mucous membrane making it difficult to swallow and thereby diminishing the injury produced to the esophagus. On the other hand, liquid alkali is easily swallowed, being tasteless and odorless, and is most likely to damage the esophagus and stomach.2 Acid induces coagulation necrosis with eschar formation and this may limit tissue penetration, but this does not appear to be a major variable in determining the extent of injury. Although some earlier studies10,11 indicated that acid preferentially damages the stomach, recent studies6 have reported extensive damage to the esophagus as well. The pathologic classification of caustic injury to the esophagus is similar to classification of burns to the skin and is elaborated in Table 2. The degree of injury correlates directly with stricture formation and mortality. Over 80% of patients with grade 3 burns go on to stricture formation while one-third of those with grade 2 burns may stenose.7

Stricture formation is extremely rare in injuries of the first degree. Mortality is also more common in grade 3 injury.7 CLINICAL PRESENTATION The clinical presentation depends upon the type of the substance, amount, and physical form of the substances. Solid alkali adheres to the mouth and pharynx producing maximum damage to these areas while relatively sparing the esophagus. In contrast the liquid form transits rapidly through the mouth and pharynx and produces its greatest caustic effect on the esophagus.2 Hoarseness and stridor may be seen suggesting laryngeal or epiglottic involvement. Symptoms of esophageal involvement include dysphagia and odynophagia, whereas epigastric pain and hematemesis may be manifestations of stomach involvement. However, the absence of pain does not preclude significant gastrointestinal damage. Sometimes massive hematemesis can occur as a result of an aortoenteric fistula.2 Perforation of the stomach or the esophagus can occur at any time during the first 2 weeks.2 Hence, any change in the clinical condition of the patient such as worsening of abdominal pain or the appearance of chest pain should be promptly investigated by radiologic studies Studies have tried to ascertain whether the presenting signs and symptoms accurately predict esophageal injury. While one study12 claimed that stridor was 100% specific for significant esophageal injury another study13 indicated that no single symptom or group of symptoms could accurately predict esophageal injury. Asymptomatic children with unintentional caustic ingestion usually do not have significant lesions on endoscopy.14 Ten to 30 percent of patients with esophageal burns have no oropharyngeal damage.2 One study reported esophageal injury in 37.5% of patients without oral damage and twentytwo percent of these were grade 2 or 3 lesions.15 Upto16

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TABLE 2. Endoscopic grading of corrosive esophageal injury

Grade 0 Grade 1 Grade 2a Grade 2b Grade 3a Grade 3b Normal findings on endoscopy Edema, hyperemia of mucosa Friability, blisters, hemorrhages, erosions, whitish membranes, exudates and superficial ulcerations Grade 2a plus deep discrete or circumferential ulcerations Small scattered areas of multiple ulcerations and areas of necrosis (brown-black or grayish discoloration) Extensive necrosis

70% of patients with oropharyngeal burns do not have significant damage to the esophagus. Injuries of the oropharynx are therefore not a reliable index of damage to esophagus. No one sign or group of signs was 100% accurate in predicting positive or negative endoscopies. Late Sequelae 1. Stricture formation may become symptomatic within 3 months or may even manifest a year later.2 Ingestion of liquid lye is most likely to induce stricture formation than solid crystals. Lye induced strictures tend to be long (Fig. 1).2 Indwelling nasogastric tube may also contribute to the increased formation of long strictures. 2. Gastric outlet obstruction: Symptoms of early satiety and weight loss may suggest gastric outlet obstruction. This tends to occur less frequently than stricture formation, being noted in only 4 of 214 patients in 1 study.17 This complication may be seen within 5 or 6 weeks or may present for the first time after several years.2 Although initially thought to be a specific complication of acid ingestion, it can also occur with lye injury to the stomach.18 3. Esophageal carcinoma is a well-known sequel of lye ingestion.2 The latent period between the time of ingestion and the development of carcinoma may be as long as 58 years. There is a 1000- to 3000-fold increase in the incidence of esophageal carcinoma after lye ingestion, and up to 3% of patients with carcinoma of the esophagus may have history of caustic ingestion. Most lesions occur at the level of the carina. Patients with carcinoma of the esophagus due to lye ingestion may have a better prognosis than other patients, as they tend to be younger and tend to have earlier symptoms.2 4. Gastric carcinoma is a rare occurrence in patients with a history of caustic injury.2 MANAGEMENT Pre Hospital Measures Gastric lavage and induced emesis are contraindicated because re-exposure of the esophagus to the corrosive agent tends to produce additional injury. Milk and water have been used as antidotes but their effectiveness has not been proven. Furthermore heat generated by the chemical reaction may increase the damage. Milk may also obscure

subsequent endoscopy. Activated charcoal is also contraindicated for the same reason. Radiologic Studies In the acute phase, a plain chest radiograph may reveal air in the mediastinum suggesting esophageal perforation. Likewise free air under the diaphragm may indicate gastric perforation. If it is necessary to confirm perforation, the classic teaching is that a water-soluble agent like hypaque or gastrograffin should be used as they are less of an irritant to the mediastinum and peritoneal cavity compared with barium sulfate. However, some investigators feel that both

FIGURE 1. UGI series showing a long esophageal stricture in a patient with history of lye ingestion.

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are equally irritants.19 Endoscopy is the diagnostic procedure of choice in the absence of perforation. Barium studies may be helpful as a follow-up measure and for the evaluation of complications. In fact, barium sulfate is the preferred contrast agent for an anatomically intact but scarred gastrointestinal tract. It is radio opaque, provides greater radiographic details than water-soluble contrast agents, and is relatively nonirritant to the pulmonary tissues in case it is aspirated into the lungs. Endoscopy (Table 3) The oropharynx needs to be first examined by laryngoscopy. A supraglottic or epiglottic burn with erythema and edema formation may be a harbinger of airway obstruction and should be seen as an indication for early endotracheal intubation or tracheostomy. A third degree burn of the hypopharynx is a contraindication for endoscopy. Indications There are no strict guidelines as to who needs endoscopy and who does not. However the following factors may be taken into account when making the decision. (a) Substance. Household bleach ingestion in asymptomatic children does not warrant endoscopy.20 Similarly endoscopy may not be necessary in asymptomatic children who have ingested hair relaxer.21 (b) Quantity. Ingestion of larger quantities of corrosives is usually associated with greater damage. Although it is difficult to exactly quantify the amount, a cupful may be associated with significant injury while a teaspoonful may not. (c) Intention. Serious damage is noted when the intent is suicidal and endoscopy is usually indicated in such circumstances. (d) Symptoms. Persistent symptoms also warrant endoscopic examination. Timing Some previous studies have tried to stipulate the timing of endoscopy indicating when it should be done and when it should not be done. Endoscopy can be performed preferably within 12 hours and generally not later than 24 hours alTABLE 3. Endoscopic management
1. Initial endoscopy should be performed as soon as possible as long as the patient is stable and there is no evidence of perforation. 2. Third degree burns of the hypopharnyx is a contraindication to endoscopy. 3. A complete but careful examination of the esophagus and stomach must be attempted. 4. Endoscope can be safely advanced until a circumferential burn is seen. 5. Prudent to avoid endoscopy between days 515 as tissue softening increases the danger of perforation. 6. Risk of procedure related perforation is low.

though some authors state that endoscopy can be safely performed up to 96 hours post-ingestion.7 Wound softening begins after 2 to 3 days and lasts up to 2 weeks making endoscopy risky during this period. Endoscopy is usually avoided from 5 to 15 days after corrosive intake.7 Endoscopy should be performed as soon as possible because it serves a dual purpose. First, patients with no evidence of gastrointestinal injury can be discharged, provided there are no other complications. In fact, more than 50% of patients, with history of caustic ingestion, have no evidence of injury to the gastrointestinal tract.2 Secondly, patients with evidence of severe injury can be managed appropriately. Risk of Perforation Early reports advocated general anesthesia and endotracheal intubation prior to upper endoscopy because of the risk of perforation . However it was discovered that perforations were more likely to occur when rigid instruments were used and in children or uncooperative patients. The use of flexible endoscopy has made this procedure, in this situation, safer. No procedure related perforation occurred in series of 381 examinations reported in one study.7 Other authorities also concur with this finding.22 However the need for adequate sedation is emphasized. Endotracheal intubation is required only for patients in respiratory distress. Extent Every attempt must be made to assess the esophagus, stomach, and duodenum provided it can be done safely. Presence or absence of burns in the esophagus does not always imply extension of the same degree of injury to stomach. Therefore it is important to examine the stomach and the first part of duodenum, as well, in every patient. Generally accepted recommendations are that the endoscope should be advanced until a circumferential seconddegree burn or third degree burn is seen.4 Attempts to continue past this point may increase the risk of mechanical perforation. Endoscopic findings may be graded as shown in Table 2. In cases where endoscopy is terminated at the point of esophageal or gastric injury, the duodenum must then be evaluated by barium studies. Since severe duodenal injuries can involve the neighboring structures, double contrast CT scan should be performed in stable patients with endoscopic or radiologic evidence of significant duodenal abnormality to inspect those areas of gastrointestinal tract such as the colon, pancreas, and small bowel that are not routinely evaluated after caustic ingestion.23 Oral Intake Patient whose injuries are graded 1 and 2a are permitted oral intake and discharged within days with antacid therapy. In more severe cases of damage (grades 2 or 3), observation in an intensive care unit and nutritional support is required.

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Prevention of Strictures Stricture formation is the most important complication of corrosive damage to the esophagus. Attempts to prevent stricture formation include steroid use, stenting, use of indwelling nasogastric tube, and early dilatation. Steroids Although animal studies had shown that the use of steroids after alkali injury decreases the incidence of stricture formation, studies in humans have been inconclusive so far.2 A prospective study24 conducted in 60 children over an 18 year period concluded that there was no benefit from the use of corticosteroids. This study was severely limited by its small numbers. The results of a meta analysis25 in 361 subjects from a total of 13 studies produced more encouraging results. Strictures occurred in 40% of patients not receiving corticosteroids and antibiotics compared with 19% in the treated group. The difference was statistically significant. The usual recommended dose of steroids is methyl prednisolone 40 to 60 mg/ day intravenously. Steroids are usually given for at least 3 weeks.2 Most investigators would agree that since first degree burns of the esophagus rarely if ever cause strictures, corticosteroids are not necessary. It may be indicated in patients with third degree burns, which invariably cause strictures. However the use of corticosteroids continues to be a debatable issue. Antibiotics With regard to the use of antibiotics, the data is not very clear. Although in animals, antibiotics have shown to decrease infection in steroid treated esophageal burns, no controlled trials in humans are available.2 The consensus however appears to be that patients treated with steroids should be treated with antibiotics as well. A prophylactic antibiotic, in the absence of steroid therapy, is not advocated.26 Nasogastric Tube The insertion of nasogastric tube early in the course of the treatment has been suggested to ensure patency of the esophageal lumen2 but one needs to be cautious because a nasogastric tube itself can contribute to the development of long strictures and routine use is not warranted. Total Parenteral Nutrition Some investigators are of the opinion that total parental nutrition may prevent stricture formation, but the available data is not very convincing.2 Intraluminal Stent The insertion of specially designed silicone rubber stents may be helpful in preventing stricture formation after caustic ingestion according to some studies.27,28 Early Dilatation Early dilatation starting after injury results in a high incidence of perforation, and is not currently recommended.2

Sucralfate Anecdotal reports suggest that the use of sucralfate may decrease stricture formation.29 Gastroesophageal Reflux Gastroesophageal reflux has a tendency to worsen the caustic insult to the esophagus probably accelerating stricture formation. Therefore patients with caustic ingestion should be screened periodically for GERD and treated aggressively.8 In fact it may not be a bad idea to maintain good acid control in all patients with caustic ingestion. Miscellaneous Agents Diverse agents such as heparin, epidermal growth factor (EGF), and caffeic acid phenethyl ester (CAPE) have been shown in animal studies to decrease the incidence of stricture formation but studies in humans are awaited.30,31 Treatment of Strictures Short strictures can be easily treated with endoscopic dilatation. Long strictures that are not amenable to endoscopic dilatation may require surgery. Retrograde dilation with Tuckers dilators may be attempted in severe strictures. Intralesional injection of steroids may decrease the frequency of dilation in these patients.32 In the past, patients with antral stenosis have required surgery, either pyloroplasty or gastroenterostomy. However, some cases may be successfully managed with endoscopic dilatation and this may be attempted prior to surgery. SURGERY Surgery has a role to play as an emergency measure and also later in delayed reconstruction. In the acute phase, it is clear that patients with evidence of perforation require immediate surgery. However, some patients who do not have peritoneal signs on admission go on to develop perforation, necrosis, and massive bleeding later on with disastrous results. Early surgical intervention may improve the outcome in this group of patients and certain clinical as well as endoscopic criteria may help in identifying this subset. Patients with shock, acidosis, and coagulation disorders and those who have ingested large amounts of corrosives, usually tend to have severe injury on laparotomy and early surgical intervention may prove beneficial to these patients.33 The finding of third degree burns on endoscopy also merits surgical exploration according to some surgeons.34 Zargar et al7 have suggested that prompt surgical resection may improve the mortality and morbidity in patients with grade 3b injuries. Patients with 3a lesions may not require emergency surgery. After recovery, surgery may be required to reconstruct the pharynx and esophagus and to treat any gastric outlet obstruction. REFERENCES
1. Litovitz TL, Swartz WK, White S, et al. 2000 Annual report of the American Association of Poison Control Centers. Am J Emerg Med. 2001;19:337395.

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2. Gumaste VV, Dave PB. Ingestion of corrosive substances by adults. Am J Gastroenterol. 1992;87:15. 3. Moore WR. Caustic Ingestions. Clin Pediatr. 1986;25:192. 4. Spiegel RJ, Sataloff RT. Caustic injuries of the Esophagus. In: Castell DO, Richter J, eds. The Esophagus. Philadelphia: Lippincott, Williams and Wilkins; 1999:557564. 5. Cox AJ, Eisenbeis JF. Ingestion of Caustic hair relaxer: Is endoscopy necessary? Laryngoscope. 1997;107:897902. 6. Zagar SA, Kochhar R, Nagar B, et al. Ingestion of corrosive acid. Gastroenterology. 1989;97:702707. 7. Zargar SA, Kuchhar R, Mehta S, et al. The role of fibroptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc. 1991;37:165169. 8. Mutaf O, Genc A, Herek O, et al. Gastroesophageal reflux: A determinant in the outcome of caustic esophageal burns. J Pediatr Surg. 1996;31:14941495. 9. Bautista A, Varela R, Villanueva A, et al. Motor function of the esophagus after caustic burn. Eur J Pediatr Surg. 1996;6:204207. 10. Nicosia JF, Thornton JP, Folk FA, et al. Surgical management of corrosive gastric injuries. Ann Surg. 1974;180:139143. 11. Dilwari JB, Sing S, Rao PN, et al. Corrosive acid ingestion in man: A clinical and endoscopic study. Gut. 1984;25:183187. 12. Gorman RL, Khin-Maung-Gyi MT, Klein-Schwartz W, et al. Initial symptoms as predictors of esophageal injury in alkaline corrosive ingestion. Am J Emerg Med. 1992;10:189194. 13. Gupta SK, Croffie JM, Fitzgerald JF. Is esophagogastroduodenoscopy necessary in all caustic ingestions? J Pediatr Gastroenterol Nutr. 2001;32:5053. 14. Christensen BT. Predictions of complications following unintentional caustic ingestion in children. Acta Pediatr. 1995;84:11771182. 15. Previtaria C, Guisti F, Gugliemi M. Predictive value of visible lesions in suspected caustic ingestion. Pediatr Emerg Care. 1990;6:176178. 16. Haller JA, Andrews HG, White JJ, et al. Pathophysiology and management of acute corrosive burns of the esophagus: results of treatment in 285 children. J Pediatr Surg. 1971;6:578584. 17. Hawkins DB, Demeter MJ, Barnett TE. Caustic ingestion: controversies in management. A review of 214 cases. Laryngoscope. 1980;90:98109. 18. McAuley CE, Steel DL, Webster MW. Late sequelae of gastric acid injury. Am J Surg. 1985;149:412415.

19. Skucas J. Contrast media. In: Gore R, Levine M, Laufer I, eds. Textbook of Gastrointestinal Radiology. Philadelphia: WB Saunders; 2000:214. 20. Harley EH, Collins MD. Liquid household bleach ingestion in children. Laryngoscope. 1997;107:122125. 21. Ahsan S, Haupert M. Absence of esophageal injury in pediatric patients after hair relaxer ingestion. Arch Otolaryngol Head Neck Surg. 1999;125:953955. 22. Rappert P, Preier L, Korab W, et al. Diagnostic and therapeutic management of esophageal and caustic burns in childhood. Eur J Pediatr Surg. 1993;3:202. 23. Guth AA, Pachter HL, Albanese C, et al. Combined duodenal and colonic necrosis and unusual sequalae of caustic ingestion. J Clin Gastroenterol. 1994;19: 303305. 24. Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Eng J Med. 1990;323:637 640. 25. Howel, Dalsey WC, Hartsell FW et al. Steroids for the treatment of corrosive esophageal injury. A statistical analysis of past studies. Am J Emerg Med. 1992; 10:421425. 26. Rao RB, Hoffman RS. Caustics and Batteries. In: Goldfrank LR, ed. Goldfranks Toxicologic Emergencies. Norwalk, CT: Appleton & Lange; 1998:13991428. 27. Berkovits RN, Bos CE, Wijburg FA, et al. Caustic injury of the esophagus. J Laryngol Otol. 1996;110:10411045. 28. De Peppo F, Zaccara A, DallOglio L, et al. Stenting for caustic strictures. J Pediatr Surg. 1998;33:5457. 29. Reddy AN, Budhraja M. Sucralfate therapy for lye-induced esophagitis. Am J Gastroenterol. 1988;83:7173. 30. Bingol-Kologlu M, Tanyel FC, Muftuoglu S, et al. The preventive effect of heparin on stricture formation after caustic esophageal burns. J Pediatr Surg. 1999;34:291294. 31. Koltuksuz U, Mutus HM, Kutlu R, et al. Effects of caffeic acid phenethyl ester and epidermal growth factor on the development of caustic esophageal stricture in rats. J Pediatr Surg. 2001;36:15041509. 32. Kochhar R, Ray JD, Shriram PV, et al. Intralesional steroids augment the effects of endoscopic dilation in corrosive esophageal strictures. Gastrointest Endosc. 1999;49:509513. 33. Wu MH, Lai WW. Surgical management of extensive corrosive injuries of the alimentary tract. Surg Gynecol Obstet. 1993;177:1216. 34. Andreoni B, Farina ML, Biffi R, et al. Esophageal perforation and caustic injury. Dis Esophagus. 1997;10:95.