- Email: [email protected]
Chemical Burns of the Esophagus
Symposium on Esophageal Surgery
Chemical Burns of the Esophagus
R. W. Postlethwait, M.D.*
Ingestion of caustic chemical substances results in a spectrum of injuries ranging from a minor epithelial burn to full thickness necrosis of the wall of the esophagus. The variation depends on the nature of the chemical, the amount swallowed, the concentration, and the duration of exposure.
INCIDENCE The majority of chemical injuries are due to accidental ingestion by children. At this medical center, approximately 80 per cent of the patients were five years old or younger, an age that conforms to other reported series. In adults, the chemical is usually swallowed with suicidal intent.· The exact frequency of chemical injuries cannot be determined, although Leape and his associates 16 state that in this country accidental ingestion of lye occurs in approximately 5000 children under five years of age each year. Most reported series record over 100 patients, although a few (for example, Cardona and Daly6 ) describe over 1000 patients. CAUSATIVE AGENT In the past, lye has been the agent most frequently ingested. In 4713 reported cases, 19 this was the agent in 60 per cent, with 5 per cent or less being bleach; sulfuric, hydrochloric, or nitric acid; ammonia; or iodine. In a more recent summary of 1850 cases, lye was the cause in 35.5 per cent, bleach 15.2 per cent, Lysol 10.2 per cent, iodine 8.2 per cent, ammonia 7.4 per cent, and the remainder miscellaneous. Biezins and Gaujen 4 reported from the Riga Hospital in the Soviet Union 1784 cases seen from 1923 through 1974. Of these 40.0 per cent were due to lye, 32.8 per cent acetic acid, 7.5 per cent ammonia, 5.2 per cent potassium permanganate, 3. 6 per cent sulfuric acid, 2. 0 per cent hydrochloric acid, and 8. 9 per cent *Professor of Surgery, Department of Surgery, Duke University Medical Center; Chief of Staff, Veterans Administration Medical Center, Durham, North Carolina
Surgical Clinics of North America-Yo!. 63, No. 4, August 1983
915
R. W. PosTLETHWAIT
916
miscellaneous. The frequency of lye burns decreased by about half in the last decade of their study. In recent years, highly concentrated drain cleaners of sodium or potassium hydroxide have been commercially produced in this country. Leape and his associates 16 have reported the concentration percentage of the more commonly used drain cleaners as follows: Liquid-Plumber 30.5, Drano 32.0, Plunge 25.0, Glamorene 25.0, Down the Drain 36.5, granular Drano 54.0, Mitee 98.0, and Rooto 71.0. The disastrous results of swallowing one of these materials will be noted below. Parenthetically, those currently on the shelves of the local supermarket are inadequately labeled. Ingestion of tablets used to test urine for sugar causes ulceration and frequently stricture. The tablets are not only strongly alkaline but produce heat during their hydration. Other unusual agents include tablets with a high concentration of potassium, ascorbic acid, chloral hydrate, and doxycycline. PATHOLOGY
As indicated previously, the severity of the pathologic damage will depend on the agent, the amount swallowed, the concentration, and the duration of exposure. Alkaline chemicals cause an edematous reaction with diffusion of the corrosive agent into the deeper layers of the wall of the esophagus. An acid will cause coagulation of the surface tissues, so that deep penetration is less likely to occur. For purposes of discussion, assuming a moderately severe alkalic injury through the submucosa involving the inner fibers of the muscularis propria, edema and cell necrosis with inflammation develop rapidly. At the edge of injury, polymorphonuclear leukocytes infiltrate and granulation tissue develops in this layer. Vessel thrombosis becomes apparent, and bacterial invasion occurs. After several days, the necrotic tissue is sloughed off. The acute inflammatory reaction begins to subside, and fibroblastic proliferation predominates during the second week, followed by deposition of collagen. At the same time in the same esophagus, various areas may show necrosis, ulceration, acute inflammation, granulation tissue, fibroblastic reaction, and collagen deposition. Ulceration may persist for months. As the acute inflammatory reaction decreases in each area, granulation tissue is formed by invasion of fibroblasts and capillaries, which is gradually replaced by mature fibrous tissue. With more extensive injury, the periesophageal tissues will be involved. The esophagus may eventually be replaced as a fibrous tube. The opportunity for stricture formation is readily apparent. Acutely, more severely injured areas may lead to perforation or formation of fistulas. Gryboski and his colleagues8 published one of the first descriptions of the consequences of ingesting one of the highly concentrated drain cleaners. These penetrate the tissues quickly, increasing the depth and extent of the severe injury. The entire esophagus may become necrotic; perforation and formation of fistulae are not unusual. In addition, the stomach is frequently involved with perforation or even total necrosis.
CHEMICAL BURNS OF THE ESOPHAGUS
917
EXPERIMENTAL STUDIES
Several interesting studies, which confirm the clinical observations, have been performed in animals. Only a few will be quoted. An excellent example is the work of Krey, 15 who investigated the concentration of sodium hydroxide required to produce caustic injury. He found that normal or 3.8 per cent sodium hydroxide with 10 sec contact caused necl\osis of the mucosa, submucosa, and some fibers of the inner muscle layer; 3 N or 10.7 per cent produced necrosis extending to the outer muscle layer; and 7 N or 22.5 per cent resulted in necrosis throughout the esophageal wall. Cleansing and washing powders have 8 to 50 per cent caustic soda as their chief ingredient, so the significance of these findings is apparent. Ashcraft and Padula2 confirmed in cats the severe injury caused by liquid drain cleaners. Lee and his associates 17 examined the effect of nonphosphate detergents on the feline esophagus and found that the injury similar to experimentally induced lye burns. The role of antibiotics and steroids in treatment has been examined, and an excellent, extensive study in dogs was that of Johnson. 13 He administered antibiotics and steroids in various combinations, both immediately and delayed after the injury, and given for various intervals. The esophagus was weakest after 10 to 12 days when collagenous connective tissue began to appear. Formation of strictures developed in the third or fourth week. Epithelization occurred as the inflammatory reaction subsided, which may be over a period of one to three months. He concluded that antibiotic medication should be started immediately to hasten the normal repair process by decreasing the infection and reducing the amount of scarring. Immediate steroid therapy is preferable but may be effective if started after four to six days. Steroids decrease the incidence and severity of strictures but do not prevent all formation of strictures. Haller and Bachman9 performed somewhat similar experiments in cats and reached about the same conclusions as those of Johnson. Steroids alone resulted in a number of deaths due to pneumonia. Perforation occurred after early dilatation in any of their groups of animals. The prevention of strictures was most likely after both a steroid and antibiotic; bougienage did not further decrease the incidence of stricture. Several experimental studies· have been reported on the use of Baminopropionitrile, which causes lathyrism because it inhibits intermolecular covalent cross-bonding in newly formed collagen. After animal studies of caustic burns, Butler and his associates 5 describe three major effects of the drug: (1) stenosis was as effectively prevented as with steroids and bougienage, (2) shortening of the esophagus occurred in the steroid-treated group but not those with lathyrism, and (3) the dogs with full thickness injury but no stricture had thinning of the wall in the involved area after treatment with B-aminopropionitrile. On the basis of their studies, they suggested that wound contraction is important in the pathogenesis of stricture. SYMPTOMS
The symptoms are related to the severity of the injury, which is directly related to the nature, amount and concentration of the agent. At
918
R. W. POSTLETHWAIT
times, this may readily be determined; for example, the adult patient may fairly accurately describe the amount and dilution of the corrosive. For children, the parents usually know what was swallowed but are much less likely to know the amount or the concentration. Frequently after ingestion of lye, the child will have been given vinegar or lemon juice. After the ingestion, moderate to severe pain begins in the lips, mouth, and pharynx, then in the neck and later in the chest. Salivation and, occasionally, vomiting occur. The subsequent symptoms depend on the severity of the burn. A slight burn will cause moderate pain on swallowing for several days, with few or no other symptoms. Intake may be limited to liquids, but healing is soon complete and a regular diet tolerated. In a more severe injury, the burns in the mouth and pharynx will cause persistent pain and limit oral intake. In addition, the esophageal burn causes both odynophagia and dysphagia. Infection is almost always superimposed on the injured esophagus, with resulting fever and tachycardia. Improvement is usually evident by the end of the first week; the pain decreases, and the child accepts oral feeding. In the esophagus, the necrotic tissue has been sloughed off, and the edema is less severe. Depending on the degree of injury, a soft or even a full diet may be tolerated during this period. Respiratory symptoms may be absent or develop slowly or rapidly. If the glottis and major respiratory passages have been injured by aspiration of the chemical agent, edema may acutely cause severe respiratory distress. A less severe burn or aspiration of oral pharyngeal secretions may result in more gradual development of less severe respiratory symptoms. Bronchitis and pneumonitis will add to the systemic manifestations. Involvement of all layers of the esophagus, usually including the periesophageal tissues, produces a severe injury, with the patient very rapidly becoming acutely ill. Severe pain, salivation, vomiting, and respiratory symptoms develop. Fever and tachycardia are prominent; shock may develop. The patient may die in this toxic state, but usually a complication such as sepsis and perforation occurs. Mediastinitis, empyema, tracheoesophageal fistula, overwhelming pneumonia, or sepsis may cause death of the patient. Bleeding may occur in a few patients, and unfortunately, several deaths have been caused by erosion into the aorta. In the injuries caused by the concentrated drain cleaners, the symptoms of involvement of the stomach may dominate. Perforation and necrosis of the stomach will of course result in severe abdominal pain and the manifestations of peritonitis. An important component of the symptomatology, to be emphasized under treatment, is the latent period that follows the acute phase of the moderate burns. After a week or so, swallowing may improve even to the point of the patient taking a full diet. With healing, formation of stricture occurs, and the symptoms of esophageal obstruction gradually develop. The length of the latent period is usually around two weeks but can extend for six weeks or even longer. Although the dysphagia usually develops gradually, acute obstruction may occur when a food bolus lodges above the stricture.
CHEMICAL BURNS OF THE EsOPHAGUS
919
The frequency of ulcerative esophagitis can be estimated from the report of Cardona and Daly. 6 The chemical swallowed, number of patients undergoing esophagoscopy, and per cent with ulcerative esophagitis are as follows: ammonia-88, 61 per cent; lye-203, 51 per cent; Clinitest tablets-18, 50 per cent; potassium permanganate-43, 16 per cent; Chlorox-212, 13 per cent; iodine-149, 7 per cent; and Lysol-188, 6 per cent. For the frequency of both ulcerative esophagitis and stricture, we have collected 2109 patients from ten reports 19 (since 1960); of these 28.9 per cent had ulcerative esophagitis. Of the latter group, 18.0 per cent developed stricture, which represents 5.2 per cent of the entire series. PHYSICAL EXAMINATION In the acute stage, the major findings may be limited to the lips, mouth, and pharynx; again, the extent will depend on the concentration of the agent and the length of contact. Mucosal damage appears as whitish, necrotic, edematous changes, which will later be replaced by ulceration as the slough separates. Unfortunately, the severity of changes in the oral cavity and pharynx may or may not correlate with the extent of the damage in the esophagus. The degree of pulmonary changes depends on the amount of aspiration; similarly, the abdominal findings will be related to the changes in the stomach. RADIOLOGIC STUDIES
-'-
Examination with the swallowing of contrast material is indicated except for the seriously ill patient, although the findings may be only atony or spasm. This, however, provides a baseline for the later examinations that must be obtained and, in addition, may occasionally demonstrate an unsuspected perforation. Films of the chest are required for determining the severity of pulmonary involvement and the possibility of mediastinitis. Several radiologists have described severe burns in patients who have swallowed liquid drain cleaner. Intramural retention of contrast material and gaseous dilatation of the esophagus due to air trapping are characteristic. In addition, blurred mucosal margins, linear streaking, and abnormal displacement of the pleural reflection may be seen. After the first or second week when the acute reaction has subsided, serial barium swallows will be necessary in order to identifY the development of stricture. The examination should be repeated at least as often as every-th'ree months when the depth of the caustic injury is unknown. After an extensive experience, Marchand 18 devised a classification of caustic strictures based on the radiologic findings and the early response to dilatation. The radiologic findings relate to the length of the stricture and the configuration and size of the lumen. The dilatation response essentially will identify the soft stricture easily dilated, the firm stricture requiring repeated dilatation, and the hard stricture difficult or impossible to dilate.
920
R. W. PosTLETHWAIT
In addition to the stricture, shortening of the esophagus, hiatal hernia, and sphincter incompetence may develop. Reflux may then add further to the existing esophageal damage. In 32 patients with severe late complications, Imre and Koop 12 report 11 patients with hiatal hernia and ulcerative reflux esophagitis. When the ingested agent is acid, gastric injury may be more severe than that in the esophagus and may not be apparent until antral stenosis develops weeks or months later. In these patients, therefore, the follow-up barium x-ray studies should include examinations of the stomach.
ESOPHAGOSCOPY Most agree that esophagoscopy should be performed early after injury, although the recommended time ranges from a few hours to within the first week. A major advantage of early esophagoscopy is discovering those patients who have little or no burn; thus, needless treatment can be avoided. The endoscope is inserted only to the level of obvious severe injury to avoid perforation. Limitations include the inability of determining the depth of the burn and the lack of information obtained about the distal part if the upper portion of the esophagus is severely involved. After extensive experimental and clinical experience, Haller and his associates 10 propose that all patients except the extremely ill have esophagoscopy within 12 hours after admission. Though proof is not available, this appears to be the consensus in this country. COMPLICATIONS AND DEATHS Unfortunately, most authors reporting on large series do not list the complications. An exception is the paper by Strumboff, 21 but his report is of limited value because he does not state the number of his 1221 patients who developed complications. He stated only that complications were frequent. He listed the following as the percentages of those with complications: mediastinitis-20 per cent, esophageal perforation-15 per cent, gastric perforation-10 per cent, peritonitis-15 per cent, laryngeal edema-6 per cent, pneumonia-14 per cent, and fistula into the trachea or aorta (not separately stated)-20 per cent. We have collected series reported during the past 40 years totaling 2267 patients, showing a mortality of 13.6 per cent. Improvement, however, is evident. For example, BelinofP in 1941 reported 439 patients with a mortality of 36.9 per cent; in 1971 Cardona and Daly6 had a 2. 8 per cent mortality in 145 patients. The causes of death are indicated by the preceding list of complications. As might be anticipated, mortality after ingestion of a liquid drain cleaner is high. Ray and his colleagues 20 collected 11 cases operated upon early and found the mortality to be 45 per cent. We found reports totaling 17 patients with nine survivals after resection.
CHEMICAL BURNS OF THE EsOPHAGUS
921
Late Complications Formation of strictures and the development of reflux have been noted previously. The increased frequency of squamous cell carcinoma of the esophagus after caustic injury has been noted by several authors, although data are not available to determine the actual frequency. Kiviranta14 states the risk of carcinoma is increased a thousandfold in these patients. Appelqvist and Salmo 1 have reported the largest series: 63 or 2.6 per cent of the 2414 patients with carcinoma had a history of caustic ingestion. In our experience, u 12 or 1.4 per cent of 846 patients were in this category. In both series, resectability and survival were increased over the usual series of carcinoma of the esophagus.
EARLY TREATMENT Based on the extensive experience of authors such as Cardona and Daly6 and of Haller and his associates, 10 early treatment should include the following measures if the history and physical examination indicate the probability of esophageal injury: l. 2. 3. 4.
Nothing by mouth and appropriate intravenous fluids. Systemic antibiotics and steroids. Esophagoscopy within 12 hours. Chest films and, after endoscopy, barium swallow with cinefluorophotogra-
phy.
Obviously, treatment will be modified for each patient as required. The seriously ill patient may need tracheostomy and respiratory support as rapidly as possible. The questionably burned patient may have no indication for either antibiotics or steroids. A reasonably accurate estimate of the severity of the injury should be made within 24 hr or earlier, and further treatment provided accordingly. When no burn is found, the patient is discharged after care of mouth burns and returns for additional barium swallow examinations as indicated. With a caustic esophageal injury identified, the patient will remain in the hospital. After their experience with 285 children, Haller and his associates described the following plan of management. For acute injuries, the usual examinations, including chest films, are performed, and intravenous fluids started. Esophagoscopy is carried out within 12 hr, and cinefluoroscopy within 24 hr. If no burn is demonstrated during endoscopy, the patient is seen one month after discharge and followed for a year. When burns are identified during esophagoscopy, steroids and antibiotic therapy are started. Liquids and then a soft diet are given as tolerated. After three weeks, the cinefluoroscopy is repeated. If evidence of stricture is found, the steroids are stopped, and then dilatations started. If no stricture is present, the patient is seen monthly for one year, with repeat barium studies when indicated. Of their 235 patients, 69 had burns, but only eight developed strictures, all managed by dilatations. Nutrition must be maintained during the early recovery period, and the use of total parenteral nutrition has made this feasible. Some authors
922
R. W.
PosTLETHWAIT
feel strongly that a small plastic nasogastric tube should be passed, for aspiration at first, then for feeding, but partly to maintain a lumen. Gastrostomy may occasionally be considered. The extensive necrosis caused by liquid drain cleaners, which may involve both esophagus and stomach, may require early operation and resection of both. Ray and his associates in discussing these injuries suggest the high mortality is due to delayed or insufficient operation and a lack of appreciation of the severity of the injury.
TREATMENT OF STRICTURE A detailed description of all the methods of dilatation will not be attempted here, but because approximately 5 per cent of these patients with appreciable esophageal injury will develop a stricture, some note is justifiable. The Salzer method of very early and frequent bougienage, as far as can be determined, has been abandoned. Although excellent results were reported, it appears that most of these patients did not have endoscopy, so the number who would actually have required dilatation cannot be determined. The approach employed by Haller and his associates 10 appears to be logical. If formation of strictures becomes apparent, the steroid administration is reduced, and dilatations begun cautiously, keeping in mind the wall's weakness partly caused by the steroids. The stage of healing, particularly the disappearance of ulceration and the reepithelization, are important in determining the start of bougienage and may better be determined by repeated endoscopy. For a stricture of moderate degree, antegrade bougienage with the Maloney dilators may yield a satisfactory result. The usual principle of attaining size and then time interval is followed. The question of how long to persist in dilatations cannot be answered factually: some authors indicate continued dilatation for years; others suggest a satisfactory result should be obtained in 6 to 12 months. Certainly, the patient, his tolerance of the procedure, and the progress being made should all be considered. For the more extensive, firm strictures, other methods may have to be used. A string or wire guide over which metal olives can be passed for several treatments may gain enough lumen size to allow use of the Maloney dilators. In severe strictures, the safest course may be a gastrostomy with retrograde dilatation using the Tucker bougies.
RESECTION OR BYPASS OPERATIONS The patient who has had emergency resection for esophageal necrosis will obviously require reconstruction as well as most of the patients who have had exclusion of the esophagus because of perforation or fistula. As with persistence with dilatations, the indications for operation are not uniformly accepted by all authors. A logical approach would be the
CHEMICAL BURNS OF THE ESOPHAGUS
923
indications stated by Daly and Cardona: 7 (1) complete stenosis with failure to establish a lumen, (2) marked irregularity and pocketing of the esophagus, (3) dilatation cannot be done without a severe periesophageal reaction or mediastinitis, (4) presence of a fistula, and (5) the lumen cannot be maintained above a 40 Fr bougie. As an addendum, they include those patients who are unable or unwilling to undergo the prolonged period of repeated dilatations. With or without resection of the esophagus, reconstruction has been accomplished using stomach, greater curvature tube, jejunum, or colon. We have collected a number of reports from the literature. 19 The stomach, usually after esophageal resection, was employed in 161 patients with a mortality of 14.3 per cent and good results in 87 per cent of the survivors. Jejunal substitution in 104 patients resulted in an 8.6 per cent mortality and 88 per cent good results. In 325 colon interpositions (mostly retrosternal), mortality was 4. 9 per cent, and good results were obtained in 92 per cent. The advantages and disadvantages of each are well known; the consensus currently appears to be that substernal colon interposition is the most satisfactory operation. Caustic injury and stricture sufficiently severe to require bypass will almost invariably involve the cervical portion of the esophagus, even when the lumen is not particularly decreased as seen by barium swallow. The caveat is that the anastomosis should be high in the cervical region, if not to the hypopharynx, if anastomotic stricture is to be avoided. After substernal colon interposition, most authors do not report resection of the esophagus; they believe that the increased postoperative mortality is greater than the possibility of developing carcinoma. Others disagree and remove the esophagus either through a thoracotomy or by blind dissection. Certainly, if the entire stomach is placed substernally and the esophagus isolated, the potential for the formation of cysts or abscesses is present.
SUMMARY The ingestion of caustic chemical agents, usually accidentally by children, produces a range of injury from minor mouth burns to necrosis of the esophagus and stomach. The type of agent, amount, concentration, and duration of exposure are the determining factors. The treatment of the average burn has been fairly well standardized, but the serious injuries require prompt recognition of complications and appropriate therapy.
REFERENCES l. Appleqvist, P., and Salmo, M.: Lye corrosion carcinoma of the esophagus. Cancer, 45:2655, 1980. 2. Ashcraft, K. W., and Padula, R. T.: The effect of dilute corrosives on the esophagus. Pediatrics, 53:226, 1974.
924
R. W.
PosTLETHWAIT
3. Belin off, S.: Can one prevent corrosive stricture of the esophagus (Kann man den Korrosionsstrikturen der Speiserohre vorbeugn). Wien. Med. Wochenschr., 91:275, 1941. 4. Biezins, A. P., and Gaujen, J. K.: Late results of chemical oesophageal burns in childhood. Prog. Pediatr. Surg., 10:19, 1977. 5. Butler, C., Madden, J. W., Davis, W. M., et al.: Morphologic aspects of experimental esophageal lye strictures. II. Effect of steroid hormones, bougienage, and induced lathyrism on acute lye burns. Surgery, 81:431, 1977. 6. Cardona, J. C., and Daly, J. F.: Current management of corrosive esophagitis-an evaluation of results in 239 cases. Ann. Otol., 80:521, 1971. 7. Daly, J. F., and Cardona, J. C.: Corrosive esophagitis. Am. J. Surg., 93:242, 1957. 8. Gryboski, W., Page, R., and Bush, B. F., Jr.: Management of total gastric necrosis following lye ingestion. Ann. Surg., 161:469, 1965. 9. Haller, J. A., Jr., and Bachman, K.: The comparative effect of current therapy on experimental caustic burns on the esophagus. Pediatrics, 34:236, 1964. 10. Haller, J. A., Jr., Andrews, H. G., White, J. J., eta!.: Pathology and management of acute corrosive burns of the esophagus: Results of treatment in 285 children. J. Pediatr. Surg., 6:578, 1971. ll. Hopkins, R. A., and Postlethwait, R. W.: Caustic burns and carcinoma of the esophagus. Ann. Surg., 194:146, 1981. 12. lmre, J., and Koop, M.: Arguments against long-term conservative treatment of oesophageal strictures due to corrosive burns. Thorax, 27:594, 1972. 13. Johnson, E. E.: A study of corrosive esophagitis. Laryngoscope, 73:1651, 1963. 14. Kiviranta, U. K.: Corrosion carcinoma of the esophagus; 381 cases of corrosion and 9 cases of corrosion carcinoma. Acta Otolaryngol., 42:89, 1952. 15. Krey, H.: On the treatment of corrosive lesions in the oesophagus; an experimental study. Acta Otolaryngol. (Suppl.), 102):1, 1952. 16. Leape, L. L., Ashcraft, K. W., Scarpelli, D. G., eta!.: Hazard to health-liquid lye. N. Engl. J. Med., 284:578, 1971. 17. Lee, J. F., Simonowitz, D., and Block, G. E.: Corrosive injury of the stomach and esophagus by nonphosphate detergents. Am. J. Surg., 123:652, 1972. 18. Marchand, P.: Caustic strictures of the oesophagus. Thorax, 10:171, 1955. 19. Postlethwait, R. W.: Surgery of the Esophagus. New York, Appleton-Century-Crofts, 1979. 20. Ray, E. S., and Morgan, D. L.: Cortisone therapy of lye burns of the esophagus. J. Pediatr., 49:394, 1956. 21. Strumboff, A. V.: Chemical burns of the oral cavity and esophagus. Arch. Otolaryngol., 52:419, 1950. Department of Surgery Duke University Medical Center Durham, NC 27710
Chemical Burns of the Esophagus
R. W. Postlethwait, M.D.*
Ingestion of caustic chemical substances results in a spectrum of injuries ranging from a minor epithelial burn to full thickness necrosis of the wall of the esophagus. The variation depends on the nature of the chemical, the amount swallowed, the concentration, and the duration of exposure.
INCIDENCE The majority of chemical injuries are due to accidental ingestion by children. At this medical center, approximately 80 per cent of the patients were five years old or younger, an age that conforms to other reported series. In adults, the chemical is usually swallowed with suicidal intent.· The exact frequency of chemical injuries cannot be determined, although Leape and his associates 16 state that in this country accidental ingestion of lye occurs in approximately 5000 children under five years of age each year. Most reported series record over 100 patients, although a few (for example, Cardona and Daly6 ) describe over 1000 patients. CAUSATIVE AGENT In the past, lye has been the agent most frequently ingested. In 4713 reported cases, 19 this was the agent in 60 per cent, with 5 per cent or less being bleach; sulfuric, hydrochloric, or nitric acid; ammonia; or iodine. In a more recent summary of 1850 cases, lye was the cause in 35.5 per cent, bleach 15.2 per cent, Lysol 10.2 per cent, iodine 8.2 per cent, ammonia 7.4 per cent, and the remainder miscellaneous. Biezins and Gaujen 4 reported from the Riga Hospital in the Soviet Union 1784 cases seen from 1923 through 1974. Of these 40.0 per cent were due to lye, 32.8 per cent acetic acid, 7.5 per cent ammonia, 5.2 per cent potassium permanganate, 3. 6 per cent sulfuric acid, 2. 0 per cent hydrochloric acid, and 8. 9 per cent *Professor of Surgery, Department of Surgery, Duke University Medical Center; Chief of Staff, Veterans Administration Medical Center, Durham, North Carolina
Surgical Clinics of North America-Yo!. 63, No. 4, August 1983
915
R. W. PosTLETHWAIT
916
miscellaneous. The frequency of lye burns decreased by about half in the last decade of their study. In recent years, highly concentrated drain cleaners of sodium or potassium hydroxide have been commercially produced in this country. Leape and his associates 16 have reported the concentration percentage of the more commonly used drain cleaners as follows: Liquid-Plumber 30.5, Drano 32.0, Plunge 25.0, Glamorene 25.0, Down the Drain 36.5, granular Drano 54.0, Mitee 98.0, and Rooto 71.0. The disastrous results of swallowing one of these materials will be noted below. Parenthetically, those currently on the shelves of the local supermarket are inadequately labeled. Ingestion of tablets used to test urine for sugar causes ulceration and frequently stricture. The tablets are not only strongly alkaline but produce heat during their hydration. Other unusual agents include tablets with a high concentration of potassium, ascorbic acid, chloral hydrate, and doxycycline. PATHOLOGY
As indicated previously, the severity of the pathologic damage will depend on the agent, the amount swallowed, the concentration, and the duration of exposure. Alkaline chemicals cause an edematous reaction with diffusion of the corrosive agent into the deeper layers of the wall of the esophagus. An acid will cause coagulation of the surface tissues, so that deep penetration is less likely to occur. For purposes of discussion, assuming a moderately severe alkalic injury through the submucosa involving the inner fibers of the muscularis propria, edema and cell necrosis with inflammation develop rapidly. At the edge of injury, polymorphonuclear leukocytes infiltrate and granulation tissue develops in this layer. Vessel thrombosis becomes apparent, and bacterial invasion occurs. After several days, the necrotic tissue is sloughed off. The acute inflammatory reaction begins to subside, and fibroblastic proliferation predominates during the second week, followed by deposition of collagen. At the same time in the same esophagus, various areas may show necrosis, ulceration, acute inflammation, granulation tissue, fibroblastic reaction, and collagen deposition. Ulceration may persist for months. As the acute inflammatory reaction decreases in each area, granulation tissue is formed by invasion of fibroblasts and capillaries, which is gradually replaced by mature fibrous tissue. With more extensive injury, the periesophageal tissues will be involved. The esophagus may eventually be replaced as a fibrous tube. The opportunity for stricture formation is readily apparent. Acutely, more severely injured areas may lead to perforation or formation of fistulas. Gryboski and his colleagues8 published one of the first descriptions of the consequences of ingesting one of the highly concentrated drain cleaners. These penetrate the tissues quickly, increasing the depth and extent of the severe injury. The entire esophagus may become necrotic; perforation and formation of fistulae are not unusual. In addition, the stomach is frequently involved with perforation or even total necrosis.
CHEMICAL BURNS OF THE ESOPHAGUS
917
EXPERIMENTAL STUDIES
Several interesting studies, which confirm the clinical observations, have been performed in animals. Only a few will be quoted. An excellent example is the work of Krey, 15 who investigated the concentration of sodium hydroxide required to produce caustic injury. He found that normal or 3.8 per cent sodium hydroxide with 10 sec contact caused necl\osis of the mucosa, submucosa, and some fibers of the inner muscle layer; 3 N or 10.7 per cent produced necrosis extending to the outer muscle layer; and 7 N or 22.5 per cent resulted in necrosis throughout the esophageal wall. Cleansing and washing powders have 8 to 50 per cent caustic soda as their chief ingredient, so the significance of these findings is apparent. Ashcraft and Padula2 confirmed in cats the severe injury caused by liquid drain cleaners. Lee and his associates 17 examined the effect of nonphosphate detergents on the feline esophagus and found that the injury similar to experimentally induced lye burns. The role of antibiotics and steroids in treatment has been examined, and an excellent, extensive study in dogs was that of Johnson. 13 He administered antibiotics and steroids in various combinations, both immediately and delayed after the injury, and given for various intervals. The esophagus was weakest after 10 to 12 days when collagenous connective tissue began to appear. Formation of strictures developed in the third or fourth week. Epithelization occurred as the inflammatory reaction subsided, which may be over a period of one to three months. He concluded that antibiotic medication should be started immediately to hasten the normal repair process by decreasing the infection and reducing the amount of scarring. Immediate steroid therapy is preferable but may be effective if started after four to six days. Steroids decrease the incidence and severity of strictures but do not prevent all formation of strictures. Haller and Bachman9 performed somewhat similar experiments in cats and reached about the same conclusions as those of Johnson. Steroids alone resulted in a number of deaths due to pneumonia. Perforation occurred after early dilatation in any of their groups of animals. The prevention of strictures was most likely after both a steroid and antibiotic; bougienage did not further decrease the incidence of stricture. Several experimental studies· have been reported on the use of Baminopropionitrile, which causes lathyrism because it inhibits intermolecular covalent cross-bonding in newly formed collagen. After animal studies of caustic burns, Butler and his associates 5 describe three major effects of the drug: (1) stenosis was as effectively prevented as with steroids and bougienage, (2) shortening of the esophagus occurred in the steroid-treated group but not those with lathyrism, and (3) the dogs with full thickness injury but no stricture had thinning of the wall in the involved area after treatment with B-aminopropionitrile. On the basis of their studies, they suggested that wound contraction is important in the pathogenesis of stricture. SYMPTOMS
The symptoms are related to the severity of the injury, which is directly related to the nature, amount and concentration of the agent. At
918
R. W. POSTLETHWAIT
times, this may readily be determined; for example, the adult patient may fairly accurately describe the amount and dilution of the corrosive. For children, the parents usually know what was swallowed but are much less likely to know the amount or the concentration. Frequently after ingestion of lye, the child will have been given vinegar or lemon juice. After the ingestion, moderate to severe pain begins in the lips, mouth, and pharynx, then in the neck and later in the chest. Salivation and, occasionally, vomiting occur. The subsequent symptoms depend on the severity of the burn. A slight burn will cause moderate pain on swallowing for several days, with few or no other symptoms. Intake may be limited to liquids, but healing is soon complete and a regular diet tolerated. In a more severe injury, the burns in the mouth and pharynx will cause persistent pain and limit oral intake. In addition, the esophageal burn causes both odynophagia and dysphagia. Infection is almost always superimposed on the injured esophagus, with resulting fever and tachycardia. Improvement is usually evident by the end of the first week; the pain decreases, and the child accepts oral feeding. In the esophagus, the necrotic tissue has been sloughed off, and the edema is less severe. Depending on the degree of injury, a soft or even a full diet may be tolerated during this period. Respiratory symptoms may be absent or develop slowly or rapidly. If the glottis and major respiratory passages have been injured by aspiration of the chemical agent, edema may acutely cause severe respiratory distress. A less severe burn or aspiration of oral pharyngeal secretions may result in more gradual development of less severe respiratory symptoms. Bronchitis and pneumonitis will add to the systemic manifestations. Involvement of all layers of the esophagus, usually including the periesophageal tissues, produces a severe injury, with the patient very rapidly becoming acutely ill. Severe pain, salivation, vomiting, and respiratory symptoms develop. Fever and tachycardia are prominent; shock may develop. The patient may die in this toxic state, but usually a complication such as sepsis and perforation occurs. Mediastinitis, empyema, tracheoesophageal fistula, overwhelming pneumonia, or sepsis may cause death of the patient. Bleeding may occur in a few patients, and unfortunately, several deaths have been caused by erosion into the aorta. In the injuries caused by the concentrated drain cleaners, the symptoms of involvement of the stomach may dominate. Perforation and necrosis of the stomach will of course result in severe abdominal pain and the manifestations of peritonitis. An important component of the symptomatology, to be emphasized under treatment, is the latent period that follows the acute phase of the moderate burns. After a week or so, swallowing may improve even to the point of the patient taking a full diet. With healing, formation of stricture occurs, and the symptoms of esophageal obstruction gradually develop. The length of the latent period is usually around two weeks but can extend for six weeks or even longer. Although the dysphagia usually develops gradually, acute obstruction may occur when a food bolus lodges above the stricture.
CHEMICAL BURNS OF THE EsOPHAGUS
919
The frequency of ulcerative esophagitis can be estimated from the report of Cardona and Daly. 6 The chemical swallowed, number of patients undergoing esophagoscopy, and per cent with ulcerative esophagitis are as follows: ammonia-88, 61 per cent; lye-203, 51 per cent; Clinitest tablets-18, 50 per cent; potassium permanganate-43, 16 per cent; Chlorox-212, 13 per cent; iodine-149, 7 per cent; and Lysol-188, 6 per cent. For the frequency of both ulcerative esophagitis and stricture, we have collected 2109 patients from ten reports 19 (since 1960); of these 28.9 per cent had ulcerative esophagitis. Of the latter group, 18.0 per cent developed stricture, which represents 5.2 per cent of the entire series. PHYSICAL EXAMINATION In the acute stage, the major findings may be limited to the lips, mouth, and pharynx; again, the extent will depend on the concentration of the agent and the length of contact. Mucosal damage appears as whitish, necrotic, edematous changes, which will later be replaced by ulceration as the slough separates. Unfortunately, the severity of changes in the oral cavity and pharynx may or may not correlate with the extent of the damage in the esophagus. The degree of pulmonary changes depends on the amount of aspiration; similarly, the abdominal findings will be related to the changes in the stomach. RADIOLOGIC STUDIES
-'-
Examination with the swallowing of contrast material is indicated except for the seriously ill patient, although the findings may be only atony or spasm. This, however, provides a baseline for the later examinations that must be obtained and, in addition, may occasionally demonstrate an unsuspected perforation. Films of the chest are required for determining the severity of pulmonary involvement and the possibility of mediastinitis. Several radiologists have described severe burns in patients who have swallowed liquid drain cleaner. Intramural retention of contrast material and gaseous dilatation of the esophagus due to air trapping are characteristic. In addition, blurred mucosal margins, linear streaking, and abnormal displacement of the pleural reflection may be seen. After the first or second week when the acute reaction has subsided, serial barium swallows will be necessary in order to identifY the development of stricture. The examination should be repeated at least as often as every-th'ree months when the depth of the caustic injury is unknown. After an extensive experience, Marchand 18 devised a classification of caustic strictures based on the radiologic findings and the early response to dilatation. The radiologic findings relate to the length of the stricture and the configuration and size of the lumen. The dilatation response essentially will identify the soft stricture easily dilated, the firm stricture requiring repeated dilatation, and the hard stricture difficult or impossible to dilate.
920
R. W. PosTLETHWAIT
In addition to the stricture, shortening of the esophagus, hiatal hernia, and sphincter incompetence may develop. Reflux may then add further to the existing esophageal damage. In 32 patients with severe late complications, Imre and Koop 12 report 11 patients with hiatal hernia and ulcerative reflux esophagitis. When the ingested agent is acid, gastric injury may be more severe than that in the esophagus and may not be apparent until antral stenosis develops weeks or months later. In these patients, therefore, the follow-up barium x-ray studies should include examinations of the stomach.
ESOPHAGOSCOPY Most agree that esophagoscopy should be performed early after injury, although the recommended time ranges from a few hours to within the first week. A major advantage of early esophagoscopy is discovering those patients who have little or no burn; thus, needless treatment can be avoided. The endoscope is inserted only to the level of obvious severe injury to avoid perforation. Limitations include the inability of determining the depth of the burn and the lack of information obtained about the distal part if the upper portion of the esophagus is severely involved. After extensive experimental and clinical experience, Haller and his associates 10 propose that all patients except the extremely ill have esophagoscopy within 12 hours after admission. Though proof is not available, this appears to be the consensus in this country. COMPLICATIONS AND DEATHS Unfortunately, most authors reporting on large series do not list the complications. An exception is the paper by Strumboff, 21 but his report is of limited value because he does not state the number of his 1221 patients who developed complications. He stated only that complications were frequent. He listed the following as the percentages of those with complications: mediastinitis-20 per cent, esophageal perforation-15 per cent, gastric perforation-10 per cent, peritonitis-15 per cent, laryngeal edema-6 per cent, pneumonia-14 per cent, and fistula into the trachea or aorta (not separately stated)-20 per cent. We have collected series reported during the past 40 years totaling 2267 patients, showing a mortality of 13.6 per cent. Improvement, however, is evident. For example, BelinofP in 1941 reported 439 patients with a mortality of 36.9 per cent; in 1971 Cardona and Daly6 had a 2. 8 per cent mortality in 145 patients. The causes of death are indicated by the preceding list of complications. As might be anticipated, mortality after ingestion of a liquid drain cleaner is high. Ray and his colleagues 20 collected 11 cases operated upon early and found the mortality to be 45 per cent. We found reports totaling 17 patients with nine survivals after resection.
CHEMICAL BURNS OF THE EsOPHAGUS
921
Late Complications Formation of strictures and the development of reflux have been noted previously. The increased frequency of squamous cell carcinoma of the esophagus after caustic injury has been noted by several authors, although data are not available to determine the actual frequency. Kiviranta14 states the risk of carcinoma is increased a thousandfold in these patients. Appelqvist and Salmo 1 have reported the largest series: 63 or 2.6 per cent of the 2414 patients with carcinoma had a history of caustic ingestion. In our experience, u 12 or 1.4 per cent of 846 patients were in this category. In both series, resectability and survival were increased over the usual series of carcinoma of the esophagus.
EARLY TREATMENT Based on the extensive experience of authors such as Cardona and Daly6 and of Haller and his associates, 10 early treatment should include the following measures if the history and physical examination indicate the probability of esophageal injury: l. 2. 3. 4.
Nothing by mouth and appropriate intravenous fluids. Systemic antibiotics and steroids. Esophagoscopy within 12 hours. Chest films and, after endoscopy, barium swallow with cinefluorophotogra-
phy.
Obviously, treatment will be modified for each patient as required. The seriously ill patient may need tracheostomy and respiratory support as rapidly as possible. The questionably burned patient may have no indication for either antibiotics or steroids. A reasonably accurate estimate of the severity of the injury should be made within 24 hr or earlier, and further treatment provided accordingly. When no burn is found, the patient is discharged after care of mouth burns and returns for additional barium swallow examinations as indicated. With a caustic esophageal injury identified, the patient will remain in the hospital. After their experience with 285 children, Haller and his associates described the following plan of management. For acute injuries, the usual examinations, including chest films, are performed, and intravenous fluids started. Esophagoscopy is carried out within 12 hr, and cinefluoroscopy within 24 hr. If no burn is demonstrated during endoscopy, the patient is seen one month after discharge and followed for a year. When burns are identified during esophagoscopy, steroids and antibiotic therapy are started. Liquids and then a soft diet are given as tolerated. After three weeks, the cinefluoroscopy is repeated. If evidence of stricture is found, the steroids are stopped, and then dilatations started. If no stricture is present, the patient is seen monthly for one year, with repeat barium studies when indicated. Of their 235 patients, 69 had burns, but only eight developed strictures, all managed by dilatations. Nutrition must be maintained during the early recovery period, and the use of total parenteral nutrition has made this feasible. Some authors
922
R. W.
PosTLETHWAIT
feel strongly that a small plastic nasogastric tube should be passed, for aspiration at first, then for feeding, but partly to maintain a lumen. Gastrostomy may occasionally be considered. The extensive necrosis caused by liquid drain cleaners, which may involve both esophagus and stomach, may require early operation and resection of both. Ray and his associates in discussing these injuries suggest the high mortality is due to delayed or insufficient operation and a lack of appreciation of the severity of the injury.
TREATMENT OF STRICTURE A detailed description of all the methods of dilatation will not be attempted here, but because approximately 5 per cent of these patients with appreciable esophageal injury will develop a stricture, some note is justifiable. The Salzer method of very early and frequent bougienage, as far as can be determined, has been abandoned. Although excellent results were reported, it appears that most of these patients did not have endoscopy, so the number who would actually have required dilatation cannot be determined. The approach employed by Haller and his associates 10 appears to be logical. If formation of strictures becomes apparent, the steroid administration is reduced, and dilatations begun cautiously, keeping in mind the wall's weakness partly caused by the steroids. The stage of healing, particularly the disappearance of ulceration and the reepithelization, are important in determining the start of bougienage and may better be determined by repeated endoscopy. For a stricture of moderate degree, antegrade bougienage with the Maloney dilators may yield a satisfactory result. The usual principle of attaining size and then time interval is followed. The question of how long to persist in dilatations cannot be answered factually: some authors indicate continued dilatation for years; others suggest a satisfactory result should be obtained in 6 to 12 months. Certainly, the patient, his tolerance of the procedure, and the progress being made should all be considered. For the more extensive, firm strictures, other methods may have to be used. A string or wire guide over which metal olives can be passed for several treatments may gain enough lumen size to allow use of the Maloney dilators. In severe strictures, the safest course may be a gastrostomy with retrograde dilatation using the Tucker bougies.
RESECTION OR BYPASS OPERATIONS The patient who has had emergency resection for esophageal necrosis will obviously require reconstruction as well as most of the patients who have had exclusion of the esophagus because of perforation or fistula. As with persistence with dilatations, the indications for operation are not uniformly accepted by all authors. A logical approach would be the
CHEMICAL BURNS OF THE ESOPHAGUS
923
indications stated by Daly and Cardona: 7 (1) complete stenosis with failure to establish a lumen, (2) marked irregularity and pocketing of the esophagus, (3) dilatation cannot be done without a severe periesophageal reaction or mediastinitis, (4) presence of a fistula, and (5) the lumen cannot be maintained above a 40 Fr bougie. As an addendum, they include those patients who are unable or unwilling to undergo the prolonged period of repeated dilatations. With or without resection of the esophagus, reconstruction has been accomplished using stomach, greater curvature tube, jejunum, or colon. We have collected a number of reports from the literature. 19 The stomach, usually after esophageal resection, was employed in 161 patients with a mortality of 14.3 per cent and good results in 87 per cent of the survivors. Jejunal substitution in 104 patients resulted in an 8.6 per cent mortality and 88 per cent good results. In 325 colon interpositions (mostly retrosternal), mortality was 4. 9 per cent, and good results were obtained in 92 per cent. The advantages and disadvantages of each are well known; the consensus currently appears to be that substernal colon interposition is the most satisfactory operation. Caustic injury and stricture sufficiently severe to require bypass will almost invariably involve the cervical portion of the esophagus, even when the lumen is not particularly decreased as seen by barium swallow. The caveat is that the anastomosis should be high in the cervical region, if not to the hypopharynx, if anastomotic stricture is to be avoided. After substernal colon interposition, most authors do not report resection of the esophagus; they believe that the increased postoperative mortality is greater than the possibility of developing carcinoma. Others disagree and remove the esophagus either through a thoracotomy or by blind dissection. Certainly, if the entire stomach is placed substernally and the esophagus isolated, the potential for the formation of cysts or abscesses is present.
SUMMARY The ingestion of caustic chemical agents, usually accidentally by children, produces a range of injury from minor mouth burns to necrosis of the esophagus and stomach. The type of agent, amount, concentration, and duration of exposure are the determining factors. The treatment of the average burn has been fairly well standardized, but the serious injuries require prompt recognition of complications and appropriate therapy.
REFERENCES l. Appleqvist, P., and Salmo, M.: Lye corrosion carcinoma of the esophagus. Cancer, 45:2655, 1980. 2. Ashcraft, K. W., and Padula, R. T.: The effect of dilute corrosives on the esophagus. Pediatrics, 53:226, 1974.
924
R. W.
PosTLETHWAIT
3. Belin off, S.: Can one prevent corrosive stricture of the esophagus (Kann man den Korrosionsstrikturen der Speiserohre vorbeugn). Wien. Med. Wochenschr., 91:275, 1941. 4. Biezins, A. P., and Gaujen, J. K.: Late results of chemical oesophageal burns in childhood. Prog. Pediatr. Surg., 10:19, 1977. 5. Butler, C., Madden, J. W., Davis, W. M., et al.: Morphologic aspects of experimental esophageal lye strictures. II. Effect of steroid hormones, bougienage, and induced lathyrism on acute lye burns. Surgery, 81:431, 1977. 6. Cardona, J. C., and Daly, J. F.: Current management of corrosive esophagitis-an evaluation of results in 239 cases. Ann. Otol., 80:521, 1971. 7. Daly, J. F., and Cardona, J. C.: Corrosive esophagitis. Am. J. Surg., 93:242, 1957. 8. Gryboski, W., Page, R., and Bush, B. F., Jr.: Management of total gastric necrosis following lye ingestion. Ann. Surg., 161:469, 1965. 9. Haller, J. A., Jr., and Bachman, K.: The comparative effect of current therapy on experimental caustic burns on the esophagus. Pediatrics, 34:236, 1964. 10. Haller, J. A., Jr., Andrews, H. G., White, J. J., eta!.: Pathology and management of acute corrosive burns of the esophagus: Results of treatment in 285 children. J. Pediatr. Surg., 6:578, 1971. ll. Hopkins, R. A., and Postlethwait, R. W.: Caustic burns and carcinoma of the esophagus. Ann. Surg., 194:146, 1981. 12. lmre, J., and Koop, M.: Arguments against long-term conservative treatment of oesophageal strictures due to corrosive burns. Thorax, 27:594, 1972. 13. Johnson, E. E.: A study of corrosive esophagitis. Laryngoscope, 73:1651, 1963. 14. Kiviranta, U. K.: Corrosion carcinoma of the esophagus; 381 cases of corrosion and 9 cases of corrosion carcinoma. Acta Otolaryngol., 42:89, 1952. 15. Krey, H.: On the treatment of corrosive lesions in the oesophagus; an experimental study. Acta Otolaryngol. (Suppl.), 102):1, 1952. 16. Leape, L. L., Ashcraft, K. W., Scarpelli, D. G., eta!.: Hazard to health-liquid lye. N. Engl. J. Med., 284:578, 1971. 17. Lee, J. F., Simonowitz, D., and Block, G. E.: Corrosive injury of the stomach and esophagus by nonphosphate detergents. Am. J. Surg., 123:652, 1972. 18. Marchand, P.: Caustic strictures of the oesophagus. Thorax, 10:171, 1955. 19. Postlethwait, R. W.: Surgery of the Esophagus. New York, Appleton-Century-Crofts, 1979. 20. Ray, E. S., and Morgan, D. L.: Cortisone therapy of lye burns of the esophagus. J. Pediatr., 49:394, 1956. 21. Strumboff, A. V.: Chemical burns of the oral cavity and esophagus. Arch. Otolaryngol., 52:419, 1950. Department of Surgery Duke University Medical Center Durham, NC 27710