Corrosive Bums of the Esophagus and Stomach:

Corrosive Bums of the Esophagus and Stomach: A Recommendation for an Aggressive Surgical Approach Aaron Estrera, M.D., Wayne Taylor, M.D., Lawrence J. Mills, M.D., and Melvin R. Platt, M.D. ABSTRACT During a six-year period ending in December, 980, 6 patients with a history or clinical evidence of corrosive ingestion were admitted into our institutions. The majority were adults who had attempted suicide. Strong alkali (lye), the most common corrosive agent involved, was ingested by more than half of the patients (39). The remaining 3 patients had ingested weak alkali or nonalkali corrosive agents. Of the 7 patients with severe esophagogastric bums (second- and third-degree), a 43.5% incidence overall, liquid lye was responsible in, including 7 of 8 patients with extensive full-thickness esophagogastric necrosis. In sharp contrast, only of the 3 patients who had ingested weak alkali or nonalkali corrosive agents had serious esophagogastric injury. In the first two years of this review, the management approach was the so-called standard one (esophagoscopy, steroids, antibiotics, and dilation) (Group ). The results were disappointing. In 5 of 9 patients with endoscopic findings of second-degree bums, stricture requiring dilation developed, and all 4 with extensive full-thickness esophagogastric necrosis died. In contrast, during the last four years, with the adoption of a more aggressive surgical approach, that is, early surgical intervention including the use of an intraluminal esophageal stent and radical resection as indicated, missed or delayed diagnosis of fullthickness esophagogastric necrosis with its prohibitive mortality was avoided and the complication of severe esophageal stricture was virtually eliminated (Group ). All 5 patients in this series who died (8% mortality) had extensive esophagogastric necrosis; 4 deaths resulted from injury caused by liquid lye ingestion. Delay in making the diagnosis, and thus delay in the management of transmural esophagogastric necrosis, is the single most important contributing factor to this significant mortality. Prior to 967, extensive, full-thickness esophagogastric injury caused by corrosive ingestion was a rare occurrence in the United States. Successful management of From the Department of Surgery, Division of Cardiothoracic Surgery, and the Department of Pathology, The University of Texas Health Science Center and Southwestern Medical School, and The Veterans Administration Medical Center, Dallas, TX. Accepted for publication May, 985. Address reprint requests to Dr. Estrera, Division of Cardiothoracic Surgery, The University of Texas Health Science Center, 533 Harry Hines Blvd, Dallas, TX 7535. such a catastrophic event was almost unheard of [l]. Reports on the subject of corrosive ingestion dealt mostly with the different methods of treatment, which were primarily directed toward the prevention of the complication of stricture formation [-4. This emphasis could be attributed mainly to the type of corrosive agent most frequently ingested. Lye, the traditional drain cleaner, the most commonly ingested corrosive agent, was then available only in solid form (granules, pellets, or powder). When ingested in these forms, lye tends to adhere to the mucosa of the oropharynx and proximal esophagus, and to inflict burns in patches or linear streaks rather than in a diffused, circumferential pattern. For this reason, among the estimated 0 to 5% of patients admitted to the hospital for corrosive ingestion injuries in whom stricture developed, the majority have proximal, localized stricture (, 5. Also, solid lye infrequently causes burns of the stomach on ingestion, since in this form it rarely reaches the stomach in sufficient quantity to do damage [6]. When liquid caustic agents were introduced into the commercial market of the United States in 967, more serious clinical problems were immediately apparent. Extensive esophagogastric necrosis and other serious complications, such as tracheoesophageal and esophagoaortic fistulas and nondilatable strictures, were reported with increasing regularity [7-3). Thus, liquid lye emerged quickly as a true public health hazard (9. Meanwhile, the so-called standard or conventional treatment for lye ingestion (esophagoscopy, steroids, antibiotics, dilation, and the watch, wait, and see attitude for possible full-thickness esophagogastric necrosis) remained the mainstay of the therapy. The overall results in the management of injury caused by this new form of corrosives have been unsatisfactory [7, 8. These observations and our own disappointing experience in the management of liquid lye ingestion have prompted us to revise our management concept toward a more aggressive approach. For a better perspective of this new approach, we reviewed and analyzed our experience with corrosive ingestion injuries during the six-year period from 975 through 980. Material and Methods The hospital records of all patients admitted to Parkland Memorial Hospital and the Veterans Administration Hospital in Dallas, TX, from January, 975, through December, 980, with a history of corrosive ingestion were reviewed. In each instance, attempts were made to identify the corrosive agent involved. In the first two years of 76 Ann Thorac Surg 4:76-83, Mar 986

77 Estrera et al: Corrosive Burns of Esophagus and Stomach this review, as before, the therapeutic approach adopted was the conventional or standard one (Group ). Also, the watch, wait, and see attitude toward possible fullthickness esophagogastric necrosis and perforation was adhered to [, 4, 5. During the next four years, prompted by our dismal results in the previous years, particularly with patients who had ingested liquid lye, a new aggressive surgical approach was adopted (Group ). It entailed () early routine endoscopy, () immediate exploratory laparotomy for patients with at least a second-degree esophageal burn as evidenced by endoscopy, (3) intraluminal esophageal stenting for those with second-degree burn and those with third-degree burn not showing extensive full-thickness necrosis, and (4) immediate esophagogastric resection for those with extensive full-thickness necrosis. At first, this approach was limited to patients with a history of liquid lye ingestion; however, because of our excellent initial results, it was soon applied to all types of corrosive ingestion injuries. Most esophagoscopies were done within hours of ingestion, under general anesthesia, and with the rigid esophagoscope. Fiberoptic endoscopy has been used more recently. Concomitant panendoscopic examinations of the oropharynx and larynx were also performed in many patients. The endoscopic grading adopted for determining the depth and severity of burns is similar to that of thermal burns of the skin (Table ) [6]. Patients without esophageal injury or with only a first-degree burn underwent esophagoscopy in the usual manner. On the other hand, although attempts were made to visualize as much of the esophagus as possible in those with second- and third-degree burns, in the majority of patients, the instrument was not advanced beyond the area of the esophagus with the most severe circumferential injury. Barium esophagography was not a routine part of the initial evaluation for acute corrosive ingestion injuries, except for adult patients referred more than 4 hours after ingestion. However, for follow-up evaluation, it was performed the third week after injury and at inter- vals, as indicated. In children, it was done only when strongly indicated. More recently, gastric ph measurement is being added to our routine initial evaluation, particularly in cooperative adults. Patients without esophageal injury were discharged immediately. Those with first-degree burns were observed for 4 to 48 hours without any specific therapy. A few patients with first-degree esophageal burns, but with second-degree or third-degree oropharyngeal burns, were treated with the full course (3 to 4 weeks) of steroids and antibiotics. Those with second-degree or third-degree esophageal burns underwent exploratory laparotomy. At celiotomy, the intraluminal esophageal stent was inserted in those patients without gross evidence of extensive esophagogastric necrosis (Fig l). In all of these patients, a biopsy of the gastric wall was performed. If a question arose as to the viability of the stomach or esophagus, a "second-look" procedure was done within 36 hours. These patients were also given a full course of steroids and antibiotics, and the stent was left in place for at least days. After a satisfactory barium esophagogram, the stent was removed and esophagoscopy performed (Fig ). On the other hand, the presence of large, confluent patches or diffuse areas of black or grayish discoloration of the serosal surface of the stomach, with or without perforation or actual dissolution of the distal esophagus, was considered an indication for radical resection. These findings probably should be the only indications for this procedure in these patients (Fig 3). In some patients, the presence of burns to contiguous organs, such as the transverse colon, small bowel, pancreas, liver, and spleen, is obvious (Fig 4). Radical resection usually entails total esophagogastrectomy, cervical esophagostomy or pharyngostomy and jejunostomy, and resection of adjacent involved organs. For reconstruction, substernal isoperistaltic colon interposition from the posterior pharynx to a Hunt-Lawrence jejunal pouch was preferred and was usually performed 6 to 8 weeks following injury. Extended follow-up of most patients was made possi- Table. Endoscopic Grading of Corrosive Burns of Esophagus and Stomacha Grade Pathological Condition Endoscopic Findings First degree Second degree Third degree Superficial involvement of mucosa Transmucosal involvement, with or without involvement of muscularis No extension into the periesophageal or perigastric tissue Full-thickness injuries with extension into periesophageal or perigastric tissues Mediastinal or intraperitoneal organs may be involved Mucosal hyperemia and edema (occasionally superficial mucosal desquamation) Sloughing of mucosa Hemorrhages, exudates, and ulceration, pseudomembrane formation and granulation tissue if examined late Sloughing of tissues with deep ulcerations Complete obliteration of esophageal lumen by massive edema; charring and eschar formation; full-thickness necrosis with perforation 'This grading system was adopted and modified from the classification of thermal injury of the skin 6.

78 The Annals of Thoracic Surgery Vol 4 No 3 March 986 \ Fig I. Technique of intraluminal esophageal stenting for corrosive esophagogastric inju y. Fig 3. Gross appearance of stomach and esophagus with extensive full-thickness necrosis after ingestion of liquid lye. Fig. Contrast esophagogram made after 3 weeks of therapy including use of intraluminal esophageal stent. Note the free passage of barium around the stent. A widely patent esophagus is also clearly demonstrated. Fig 4. Gross appearance of stomach with extensive full-thickness necrosis. Coagulation and thrombosis of blood vessels along the greater and lesser curvature of the stomach were grossly evident. The spleen was removed because of burn and thrombosis of splenic vessels.

79 Estrera et al: Corrosive Burns of Esophagus and Stomach ble by our clinic system. Since most adult patients had underlying psychiatric problems, they were also under psychiatric care. Results During this six-year period, 69 patients who had a history of corrosive ingestion were seen. Because of either the decision of the emergency room physician or the inability to obtain parental consent, 7 patients were discharged from the emergency room and were excluded from this review. Of the 6 patients in the study group, were children ranging in age from 4 months to 5 years, with most (8) less than 5 years of age. All but of these children had accidental ingestion; attempted suicide. In contrast, most corrosive ingestion among adults (patients older than 5 years) was an apparent suicide attempt (30; the ingestion was accidental in the other 0 adult patients). Overall, 7 of 6 patients had a serious esophagogastric injury of either a second-degree or third-degree burn (Table ). Although various corrosive agents were ingested, strong alkali (lye) was involved in more than half of the patients (Table 3), and in most (7 of 39), liquid lye was involved. Other corrosive agents consisted of mild alkalis (i.e., ammonia and bleaching agents), acids, and assorted caustic substances (e.g., soaps and detergents). The most common clinical presentation in our patients with corrosive esophageal injuries involved burns of the Table. Findings Based on Endoscopic Examination and Exploratory Laparotomy Findings No evidence of burns 4 First-degree burns 8 Second-degree burns Third-degree burns 0 Total 3 Table 3. Ingested Corrosive Agents Corrosive Agents Corrosive Agents Weak Alkalis, Others Lye (strong alkali) 39 Acid 4 Ammoniab 8 Bleaching agents, soaps, detergents, 8 and other chemicals (Clorox, Purex, Comet, Tide, Lysol) Miscellaneous (furniture polish, hair 3 dye, boiling coffee) Total 6 Alkalis (Lye) 7 6 3 3 39 No. of Patients This includes patients who ingested clinitest tablets, an anhydrous sodium hydroxide. qhis is a weak alkali. These are chlorinated alkalis. buccal mucosa and oropharynx (3 patients). Although there are documented cases of patients with severe esophageal burns without detectable oropharyngeal burns, in general, esophageal injury is unusual in the absence of this finding. In our series, patients with major esophagogastric injury were not seen with oropharyngeal burns, and both had ingested the tablet form of lye (clinitest). Chest pain and dysphagia were also common findings (8 patients). One distinctive feature we observed among patients with severe esophagogastric injury was profuse drooling of large amounts of mucus and saliva (3 patients). Vomiting or regurgitation or a combination of these soon after ingestion was also reported (9 patients). Two of these patients vomited bloody material containing casts and shreds of mucous membrane. Difficult breathing and stridor were evident in 5 patients. Two others had extreme stridor requiring emergency tracheostomy. Only patient was admitted with manifestation of an acute surgical abdomen. Of the corrosive agents ingested, strong alkali inflicted the most severe injuries, while weak alkali and nonalkali agents caused only minor injuries (see Table ). Twentysix of the 39 patients who ingested strong alkali had either a second-degree or third-degree esophagogastric burn, and liquid lye was responsible in an inordinate number of them (0 of 3 patients with second-degree and of 3 with third-degree burns), including 7 of 8 patients who had third-degree burns with extensive fullthickness esophagogastric necrosis. Measurements of gastric ph were made in 8 patients. Eight of 0 with serious esophagogastric alkali ingestion injuries had values greater than 7.8, 3 having values greater than 9. Among 8 patients with only minimal or first-degree burns, none had ph values greater than 6. Our overall results amplify the danger of liquid lye ingestion (Tables 4, 5). Of the 7 patients who sustained second- or third-degree esophagogastric burns, had ingested liquid lye. It was in the group with liquid lye injury that our results with conventional therapy were most disappointing (Group ). In 5 of 9 patients with second-degree burns, dense esophageal stricture requiring dilations subsequently developed, with patients having since undergone successful colon interposition. Even more distressing were the deaths of the 4 patients with extensive esophagogastric necrosis. In sharp contrast, with the more aggressive approach (Group ), stricture developed in none of the 4 patients with second-degree burns. Although stricture did develop in of 5 patients with third-degree, nonextensive, fullthickness injury, the stricture was very localized and pliable and was easily dilated; in fact, in patient, the stricture was in the proximal esophagus just above a low-lying misplaced stent. More importantly, with this aggressive approach, all 3 patients with extensive transmural necrosis survived, and all have undergone successful reconstructive procedures (Fig 5). Comment Of all the corrosive agents available today, lye is one of the most destructive to tissues on contact. Its cor-

80 The Annals of Thoracic Surgery Vol 4 No 3 March 986 Table 4. Overall Results with Conventional Therapy in Patients Ingesting Strong Alkali (Lye) Specific Form of No. of Treatment Alkali Endoscopic Findings Patients No. of Patients Outcome No. of Patients Solid Normal First-degree burns Second-degree burns Third-degree burns 0 Liquid Normal First-degree burns Second-degree burns 7 Third-degree burns 4 No specific therapy Short-term steroids, antibiotics Standard therapy... 0 No specific therapy Standard therapy Standard therapy 7 Delayed resection 3 Early nonradical resection... Sequelae Stricture requiring dilation Stricture requiring subsequent colon interposition Death Death 5 5 3 'Short-term therapy involved steroids and antibiotics during the short period of hospitalization. bstandard therapy involved steroids and antibiotics for at least 3 weeks and esophageal dilation, as indicated. Table 5. Overall Results with Aggressive Therapy in Patients Ingesting Strong Alkali (Lye) Endoscopic and Specific Form of Laparotomy No. of Treatment No. of No. of Alkali Findings Patients Patients Outcome Patients Solid Normal 3 First-degree burns Second-degree burns Third-degree burns No extensive full-thickness necrosis Extensive full-thickness necrosis No specific therapy 3 Short-term steroids, antibioticsb Standard therapy Intraluminal esophageal stent Intraluminal esophageal stent No specific therapy S e q u e a e Localized stricture requiring dilation Death 3 Liquid Normal First-degree burns Second-degree burns 3 Third-degree burns No extensive 4 full-thickness necrosis Extensive 3 full-thickness necrosis No specific therapy Standard therapy Intraluminal esophageal stent 3 Intraluminal esophageal stent 4 Early radical resection 3 Sequelae Laryngeal stricture requiring dilation Sequelae Localized stricture requiring dilation Sequelae Oral reconstructive procedure Laryngeal dilation Stricture of colopharyngeal anastomosis 3 3 'Short-term therapy involved steroids and antibiotics during the short period of hospitalization. bstandard therapy involved steroids and antibiotics for at least 3 weeks and esophageal dilation, as indicated.

8 Estrera et al: Corrosive Burns of Esophagus and Stomach Fig 5. Microscopic appearance of stomach with extensive transmural necrosis. Stomach wall is a hyaline, homogeneous mass with no appreciable cellular details. rosiveness is based on its capacity to induce liquefaction necrosis, a process that leads to the dissolution of protein and collagen, the saponification of fats, the dehydration of tissues, and thrombosis of blood vessels. All these result in deeper tissue injuries and, at times, even injuries to contiguous organs. These effects also render surface irrigation ineffective in minimizing injury. On the other hand, acid, the other powerful corrosive agent, causes coagulation necrosis on tissue contact. The coagulum formed only hinders any further tissue penetration. Thus, from its actions, it is clear that alkali penetrates tissue more deeply and inflicts more tissue damage on contact than does acid. Several factors determine the degree of corrosive ingestion injury. The most obvious are the concentration and quantity of the ingested corrosive agent. Others, such as the state of the corrosive agent (solid or liquid), the amount of gastric content at the time of ingestion, the anatomical integrity of the esophagus and stomach, and the intent on the part of the victim must not be overlooked. Liquid corrosive, with its high viscosity and easy entry into the esophagus and stomach, inflicts more extensive and serious injury than does its solid counterpart (granule, pellet, and powder). Residual food in the stomach at the time of ingestion can act as a buffer and, therefore, should lessen the degree of injury. Surgical procedures that disrupt the normal esophagogastric anatomy can change the chemical milieu, surface volume, and emptying capacity of the stomach, thereby increasing the chances of a more serious injury after corrosive ingestion. The outcome for of our patients who had previous gastrectomy, and who both died, clearly proves this point. Finally, the victim s intent can also affect the severity of injury. We believe that the large number of suicide victims in this series played a major role in the rather high incidence (43.5%) of severe esophagogastric injury. Despite extensive clinical and animal laboratory studies on corrosive ingestion injuries, there is one aspect of the problem that is not yet fully understood-the expected intrinsic response of the esophagus and stomach to the ingested corrosive agent. It is predictable that strong alkali, on mixing with the gastric juice (a strong acid), initiates a powerful chemical reaction. The heat of hydration from the reaction contributes to the severity of injury and, more importantly, triggers the to-and-fro sloshing of the potent lye mixture from the stomach to the pharynx (the phenomenon of internal regurgitation), as demonstrated by Ritter and associates (0 in animal experiments. Although lasting only a few minutes, the sloshing of this highly potent mixture enhances injury to the esophagus and stomach, and provides the basis for the familiar warning, Do not induce vomiting, after ingestion of alkali. The spontaneous cessation of this process is probably reflected by a state of esophagogastric atony, a recognized radiographic manifestation of severe corrosive injury, clinically demonstrated by profound drooling of mucus or saliva [7]. The value of early endoscopy after corrosive ingestion is well known (, 5, 8. Not only does it confirm the diagnosis, but it also helps determine the degree of burn. Thus, endoscopy prevents unnecessary, long hospitalization and treatment of the uninjured patient and avoids the occasional missed diagnosis of severe esophageal injury in unsuspected cases [, 5. However, there is still no clinical, standardized system of interpreting endoscopic findings for corrosive ingestion injuries, and for this reason, data from various institutions are difficult to compare [, 3, 4, 8-0]. We have adopted a system of endoscopic interpretation based on a similar system used in thermal burns of the skin (see Table ) (6,. It should be noted, however, that without laparotomy, distinguishing a third-degree burn without extensive transmural necrosis from one with extensive fullthickness necrosis is very difficult. In fact, based on the results of endoscopy, 3 of 8 patients in this series with extensive esophagogastric necrosis were thought to have deep second-degree esophageal burns. This mistake has disastrous consequences. Despite the adoption of the standard therapy, the management of corrosive injuries of the esophagus and stomach remains controversial (7-0, 8, 9,. To date, there is still no unanimity on the choice of ther-

8 The Annals of Thoracic Surgery Vol 4 No 3 March 986 apy-further proof of dissatisfaction with the results of all the various therapeutic techniques [, 3. These different therapeutic techniques have evolved for one purpose only, the prevention of stricture formation. Death from corrosive ingestion was only a minor consideration. With this justifiable concern over the complication of stricture formation, there was also a prevailing notion among physicians that all forms of lye damaged tissue to the same degree. It was this attitude that contributed greatly to our own early disappointing experience with patients who had ingested liquid lye. The danger of liquid lye cannot be underestimated [9, lo]. Its destructive capability was most dramatically demonstrated by Leape and associates [9] in their report of a -year-old girl who sustained severe, extensive esophageal injury after merely licking the cap of a container of Liquid-plumr and by Habener [4] in correspondence about a -year-old boy in whom esophageal stricture developed after he took a dose of cough syrup from an unwashed spoon that had been dropped into a wash basin containing water and Liquid-plumr. Furthermore, in their report on tracheoesophageal fistulas complicating caustic ingestion, Burrington and Raffensperger [ll] found that 5 of their 6 patients had ingested a liquid lye preparation. Our experience has proved the same and has revealed even more disturbing facts. First, liquid lye is the most frequently ingested form of corrosive. Undoubtedly, its popularity and easy availability are the main reasons. Second, liquid lye caused most of the deaths associated with corrosive ingestion. It should be emphasized, however, that ingestion of other types of corrosive agents must not be taken lightly. If mixed or dissolved in liquids before ingestion, granular lye, with its high concentration (some approaching loo%), can have far more damaging effects than do commercial liquid lye preparations. Although, in general, ingestion of nonalkali or weak alkali causes only minor injuries, research has shown that such agents can cause more serious damage [5]. Our experience with acid ingestion has been very limited. Acid, for the most part, causes a less penetrating injury than does alkali and is more damaging to the stomach [6, 8. Insufficient experience with extensive esophagogastric corrosive injuries hinders firm generalizations about its natural history [6]. Some investigators [5] claimed that early laparotomy must be avoided among patients with corrosive ingestion injuries, even in the presence of signs of peritoneal irritation, on the premise that they do not prove actual perforation. The same investigators also stated that the extent of resection, as based on the appearance of healthy and gangrenous tissue, is difficult to determine at this time. Others [7] suggested that black discoloration of the gastric wall, as noted through a fiberoptic endoscope, indicates full-thickness necrosis. Our experience and the experiences of others [7, 8) have shown otherwise. Strict reliance on endoscopic and clinical findings and on the watch, wait, and see attitude for possible extensive full-thickness esophagogastric ne- crosis in patients with corrosive ingestion injuries is too dangerous. Benignity of the physical findings, despite the presence of a life-threatening abdominal process, is not an unusual observation in corrosive ingestion injuries [8, 3, 6. Of the 8 patients with extensive fullthickness esophagogastric necrosis in this series, only had signs of an acute surgical abdomen on admission to the emergency room. Three other patients, all of whom died, were observed for several days before they manifested signs of abdominal catastrophe. We have not experienced the difficulty of determining the extent and degree of esophagogastric injury at the time of celiotomy. Large areas of full-thickness necrosis were clearly evident on the serosal surface of the distal esophagus and stomach on inspection (see Figs 3,4). We fully concur with Kirsh and associates [6], particularly with liquid lye injury, that extensive full-thickness necrosis of the stomach and distal esophagus also implies a similar injury to the remaining esophagus, and in this situation, a compromised resection, as we performed in of our patients, can lead to serious complications and even death. The finding of black discoloration of the gastric wall at endoscopy did not indicate full-thickness necrosis in all of our patients. Two patients with this finding, confirmed by direct intragastric inspection at celiotomy, were successfully managed with an intraluminal stent. It is clear from our experience that in the presence of endoscopic findings of at least a seconddegree burn of the esophagus, stomach, or both, exploratory laparotomy is crucial. The risks of this procedure are much less than the danger of missing the diagnosis of extensive full-thickness necrosis. Furthermore, we think that laparotomy is invaluable for the safe conduct of the intraluminal stenting procedure. Based on this experience, we consider ourselves justified in using intraluminal stenting for the treatment of second-degree and some third-degree esophagogastric corrosive injuries and reserving resection of the stomach and esophagus for those with third-degree, extensive full-thickness necrosis. We are optimistic this therapeutic approach might yet prove to be the treatment of choice for many of the unfortunate victims of corrosive ingestion. The pathophysiology, technique, and rationale of stenting have been thoroughly discussed previously [, 8, 9. The effectiveness of esophageal stenting is best demonstrated during endoscopy at the time of stent removal: the esophagus in which a stent has been inserted will look almost completely normal, while the oropharyngeal area that has not been so treated will still look intensely inflammed and granulating. This technique is basically an extension of the idea proposed by Salzer [, 30 of "immediate and continued prophylactic bougienage." The same physiological principle has found application in plastic and reconstructive surgery. In burn victims, plastic and burn surgeons have now successfully minimized cutaneous scar formations and contractures by applying constant pressure with splints to burned areas [3]. In conclusion, the responsibility for the care and man-

83 Estrera et al: Corrosive Burns of Esophagus and Stomach agement of patients with caustic injuries must be shared by multiple disciplines, with primary responsibility resting on the thoracic or pediatric surgeon. Because associated severe oropharyngeal and laryngeal injuries are common, the ear,nose, and throat surgeon has a critical role. The gastroenterologist, radiologist, and psychiatrist are all important in the total care of such patients. Liquid lye is a major public health hazard; we fully agree with Leape and colleagues [9] that the best solution to the problems of corrosive ingestion is their prevention. We are indebted to our colleagues who have made a strong stand in the fight to prevent this needless injury. This plea for prevention must continue. For the unfortunate who sustain serious corrosive injury either by their own design or unwillingly, the best chance for an acceptable morbidity and improved survival is through adoption of this aggressive approach, including the technique of intraluminal esophageal stenting. References. Gryboski W, Page R, Rus BF: Management of total gastric necrosis following lye ingestion. Ann Surg 6:469, 965. Cardona JC, Daly JF: Management of corrosive esophagitis: analysis of treatment, methods and results. NY State J Med 4:307, 964 3. Owens H: Chemical burns of the esophagus. Arch Otolaryngol 60:48, 954 4. Rosenberg H, Kunderman PV, Vroman L, Woolten S: Prevention of experimental lye strictures of the esophagus by Cortone. Arch Surg 63:47, 95 5. Tucker JA, Yarington CT: The treatment of caustic ingestion. Otolaryngol Clin North Am :343, 979 6. Gray HK, Holmes CL: Pyloric stenosis caused by ingestion of corrosive substances: report of a case. Surg Clin North Am 8:0, 948 7. Gago 0, Ritter FN, Martel W, et al: Aggressive surgical treatment for caustic injury of the esophagus and stomach. Ann Thorac Surg 3:43, 97 8. Ray JF, Myers WO, Lawton BR, et al: The natural history of liquid lye ingestion. Arch Surg 09:436, 974 9. Leape L, Ashcraft KW, Scrapilli DG, et al: Hazard to health-liquid lye. N Engl J Med 84:478, 97 0. Ritter FN, Gago 0, Kirsh MM, et al: The rationale of emergency esophagogastrectomy in the treatment of liquid caustic burns of the esophagus and stomach. Ann Otol Rhino Laryngol80:53, 97. Burrington JD, Raffensperger JG: Surgical management of tracheoesophageal fistula complicating caustic ingestion. Surgery 84:39, 978. Nicosia JF, Thornton JP, Folk FA, Saletta JD: Surgical man- agement of corrosive gastric injuries. Ann Surg 80:39, 974 3. Allen RE, Thoshinsky MJ, Stallone RJ, Hunt TK: Corrosive injuries of the stomach. Arch Surg 00:409, 970 4. Hawkins DB, Demeter MJ, Barnett TE: Caustic ingestion: controversies in managements. Laryngoscope 9098, 980 5. Steigman F, Dolehide RA: Corrosive (acid) gastritis. N Engl J Med 5498, 956 6. Artz CP, Yarborough DR: Burns. In Sabiston DC (ed): Textbook of Surgery, 0th edition. Philadelphia, Saunders, 97, p 7 7. Martel W: Radiographic features of esophagogastritis secondary to extremely caustic agents. Diagn Radio 03:3, 97 8. Haller JA Jr, Andrews HC, White JJ, et al: Pathophysiology and management of acute corrosive burns of the esophagus: results of treatment in 85 children. J Pediatr Surg 6:578, 97 9. Webb WR, Koutras P, Ecker RR, Sugg WL: An evaluation of steroids and antibiotics in caustic burns of the esophagus. Ann Thorac Surg 9:95, 970 0. Meager LE, Yarington CT Jr: Emergency management of esophageal bums: a review for the primary care physician. Nebr Med J 59:64, 970. Mills LJ, Estrera AS, Platt MR: Avoidance of esophageal stricture following severe caustic burns by the use of an intraluminal stent. Ann Thorac Surg 8:60, 979. Salzer H: Early treatment of corrosive esophagitis. Wien Klin Wochenschr 33:307, 90 3. Middlekamp JN, Ferguson TB, Roper CL, Hoffman FD: Management and problems of caustic burns in children. J Thorac Cardiovasc Surg 57:34, 969 4. Habener SA: Letter to the Editor. N Engl J Med 84:43, 97 5. Lee JF, Simonowitz D, Block GE: Corrosive injury of the stomach and esophagus by nonphosphate detergents. Am J Surg 3:65, 97 6. Kirsh MM, Peterson A, Brown JW, et al: Treatment of caustic injuries of the esophagus. Ann Surg 88:675, 978 7. Chung RSK, DenBesten L: Fiberoptic endoscopy in treatment of corrosive injury of the stomach. Arch Surg 0:75, 975 8. Fell SC, Denize A, Becker MH, Hunvitt ES: The effect of intraluminal splinting in the prevention of caustic stricture of the esophagus. J Thorac Cardiovasc Surg 5:675, 966 9. Reyes HM, Hill JL: Experimental treatment of corrosive esophageal burns. J Pediatr Surg 9:37, 974 30. Bokay J: Salzer s treatment of lye poisoning. Wien Klin Wochenschr 378, 94 3. Larson DL, Abston S, Evans EB, et al: Techniques for decreasing scar formation and contractures in the burned patient. J Trauma :807, 97