Caustic Injury to the Esophagus David A. Katzka, MD Address Gastroenterology Division, Hospital of University of Pennsylvania, 3400 Spruce Street, 3 Ravdin Building, Philadelphia, PA 19104, USA. Current Treatment Options in Gastroenterology 2001, 4:59–66 Current Science Inc. ISSN 1092-8472 Copyright © 2001 by Current Science Inc.
Opinion statement The potentially catastrophic presentation and lifelong complications that result from caustic ingestion make it one of the most challenging clinical situations in gastroenterology. Patients who present with a history of caustic ingestion, particularly with a strong alkali or acid, should undergo emergent endoscopy once stabilized to assess the degree of oropharyngeal, esophageal, and gastric damage regardless of presence or lack of symptoms. Once staged, patients with moderate to severe injury should be restricted from any oral intake, placed on intravenous fluids, and observed, provided there are no signs of perforation or transmural necrosis that require immediate esophagectomy. For those who will require lengthy periods without oral intake, feeding should be initiated through a jejunostomy tube (preferably) or through total parenteral nutrition. Patients that have survived the first several weeks of injury should be reassessed for esophageal stricture formation. Chronic strictures may require serial dilations initially to establish patency and in some patients, dilation will be needed chronically to maintain the adequate lumen diameter. More severe strictures may require esophagectomy or bypass with colon or small bowel interposition. Finally, although there is an increased incidence of esophageal carcinoma in these patients, regular endoscopic screening is not advocated.
Introduction Caustic ingestion secondary to either acid or alkali is unfortunately a common form of both accidental and intentional injury in the US population [1]. It is also one of the most devastating type injuries the esophagus can sustain. Typically, the ingestion of caustic substances causes immediate necrosis, commonly leading to transmural inflammation of the esophagus, often with gastric involvement. Furthermore, as demonstrated in animal studies [2] and shown through human ingestion [3], only small amounts of caustic are required for extensive injury. Extent of injury is determined by the type, concentration and quantity of corrosive agent ingested and the contact time between the corrosive and the esophageal mucosa [4]. Characteristically, the damage is rapid in onset, the degree of injury may be catastrophic, with immediate death common, particularly with alkali. If the patient survives a severe injury, often requiring weeks of hospitalization and total parenteral nutrition and sometimes surgery, complications may still last a lifetime in the form of stric-
ture formation, postoperative complications, and an increased incidence of esophageal carcinoma. To make matters worse, despite attempts by the government to control the presence of strong corrosives in our society, they still are readily available commercially for either accidental or intentional (ie, suicide) consumption (Tables 1– 4) [5]. Furthermore, in addition to the traditional caustics such as drain and toilet cleaners, new caustics are available in the form of hair relaxers and button batteries. To make matters more difficult, there are very few well-designed trials examining the effects of proposed specific therapies such as steroids and antibiotics on caustic esophageal injury [3,6,7•]. As a result, there is little convincing evidence that therapies other than good supportive care and surgery-specific therapies truly alter the course of the disease. Thus, a proposed treatment outline often is determined not by data but by personal experience and judgment of the physician, rather than by proven therapy with the ultimate correct
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Table 1. Ingested caustic agents and the injuries they produce Type of agent
Injury
Alkalis Acids Detergents Bleaches
Liquefaction necrosis of esophagus and stomach Coagulation necrosis of esophagus and stomach Mild esophageal injury Mild esophageal injury
Table 2. Common corrosive alkalis Examples of products
Major caustic ingredient(s)
Drano (liquid)* Drano Professional (liquid)* Drano Crystals* Lewis Red Devil Drain Opener† Dow oven cleaner‡ Clinitest tablets§ Efferdent Extra Strength tablets¶ Mr. Clean (liquid)** Top Job (liquid)** Lysol deodorizing cleanser† Hair relaxers
Sodium hydoxide (9.5%) Sodium hydoxide (32%) Sodium hydoxide (54%) Sodium hydoxide (96% to 100%) Sodium hydoxide (4%) Sodium hydoxide Sodium hydoxide (0.5% to 1.0%) Sodium carbonate Sodium carbonate/ammonia Ammonium chloride (2.7%) Sodium or calcium hydroxide Ammonium hydroxide Mercuric oxide (30.3%) Manganese oxide (17.6%) Silver oxide (30.3%)
Button batteries
*SC Johnson, Racine, WI †Reckitt & Benckiser, Wayne, NJ ‡ Dow Chemicals, Midland, MI §Bayer Corp., Diagnostic Division, Tarrytown, ¶Warner-Lambert, Morris Plains, NJ **
NY
Proctor & Gamble, Cincinatti, OH
treatment determined only by careful observation and expectant treatment of the patient. Given these marked limitations in treatment, attempts have been made to strategize therapeutic options. In general, treatment options are guided to some degree by the three specific phases of injury: acute, latent, and chronic. In the acute phase, which lasts up to one week, treatment is based on initial severity of disease as established by clinical criteria, a history of the type and amount of corrosive agents ingested, and emergent endoscopy (once patient is stable) to assess the degree and extent of mucosal injury. Although patients may complain of symptoms such as drooling, dysphagia, vomiting, or chest and abdominal pain, endoscopy is considered mandatory as it has been well shown that symptom severity is a poor indicator of the extent of esophageal injury and often underestimates the degree of damage [8–11]. Furthermore, the extent of oral injury does not reliably predict the presence or absence of esophageal involvement [12,13]. After endoscopy, patients with mild esophageal damage and little gastric
damage do not need further care. Patients with moderate to severe esophageal injury (extensive mucosal inflammation with suggestion of intramural or transmural necrosis) will need hospitalization and total parenteral nutrition. Patients also may need laryngeal and pharyngeal evaluation if they complain of stridor or wheezing or if extensive oropharyngeal and proximal esophageal injury is present at the time of endoscopy. As is discussed in this article, at this point there are not enough convincing data to uniformly support the use of systemic steroids and antibiotics for caustic burns [7•,14•], although some centers still use them routinely [15•]. Many physicians feel that antibiotics only should be used when infection is suspected. The most difficult decision in acute disease is whether to perform emergency esophagectomy with the intention of replacing the esophagus later with small bowel or colon. Some authors have proposed specific criteria for emergent surgery, such as type and quantity of caustic ingestant, presence of shock or disseminated intravascular coagulation, acidosis, need for hemodialysis, and degree of endoscopic injury [16]. Many others
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Table 3. Common corrosive detergents Examples of products
Major caustic ingredient(s)
Oxydol laundry detergent* Electrasol dishwasher detergent† Calgonite dishwasher detergent‡ Cascade dishwasher detergent* Comet cleanser* Clorox bleach§ Tilex Instant Mildew Remover§
Sodium tripolyphosphate Sodium tripolyphosphate Sodium phosphates Phosphates Trisodium phosphate Sodium hypochlorite Sodium hydroxide Sodium hypochlorite Hydrogen peroxide
Peroxide * Proctor & Gamble, Cincinatti, OH † Reckitt & Benckiser, Wayne, NJ ‡ Beecham Inc., Clifton, NJ §
Clorox, Oakland, CA
Table 4. Common corrosive acids Examples of products
Major caustic ingredients
SnoBol toilet bowl cleaner* Saniflush toilet bowl cleaner† Vanish toilet bowl cleaner‡ Battery acid
Hydrochloric acid (15%) Sodium bisulfate (75%) Sodium bisulfate (75%) Sulfuric acid (99.5%)
*Church & Dwight, Inc., Princeton, † Reckitt & Benckiser, Wayne, NJ ‡
NJ
SC Johnson, Racine, WI
advocate early surgery for all severe injuries, pointing to improvement in survival compared historically with supportive therapy alone [17•,18–20]. Certainly, signs of perforation, mediastinitis, peritonitis, or destabilization mandate surgery although patients admitted with fulminant disease with rapid progression rarely survive, even with surgical intervention. As a result, some patients may arrive to the hospital in such extremis that surgery is not indicated. Patients not judged severe enough to undergo emergent surgery should be made “nothing by mouth” and placed on total parenteral nutrition with aggressive fluid resuscitation. Recently, patients have had jejunostomy tubes inserted early in the course of their disease to avoid total parenteral nutrition, and in some patients a nasogastric tube may be placed for nutrition providing it is not contraindicated by the extent of esophageal and gastric injury. Some authors also advocate aggressive acid suppression to prevent superimposed reflux injury although there are no scientific trials to support this practice. Patients surviving the acute phase may enter a latent phase and then a chronic phase. The latent phase lasts 1 to 4 weeks, during which time the patient seems more stable. Nutritional support with nothing by mouth and close clinical monitoring is usually continued at this stage. Endoscopy is contraindicated during
the latent phase because of the high risk of perforation, which also may occur “silently" [21•]. As a result, the extent and course of the disease often is monitored radiographically during this phase. The chronic phase is characterized by fibrosis with attending stricture formation often lasting a lifetime particularly after alkali ingestion and usually after high-grade injury as assessed by initial endoscopy [7•]. In some series, up to 55% of patients with severe injury sustain chronic stricture formation [17•]. Patients undergo serial dilations of varying frequency either endoscopically or by self-bougie depending on the degree of stricture formation. Altho ugh sati sfactory resu lts commonly are achieved, the relapse rate is expectantly high for patients with caustic strictures [22]. Organ interposition (either colon or small bowel) is another option but depends partly on the extent of luminal compromise, the failure of dilations and or occurrence of perforation and the involvement of areas proximal (eg, pharynx) and distal (stomach) that affect technical ease of the surgery. Finally, there are substantial retrospective data to suggest that the incidence of squamous cell carcinoma of the esophagus is significantly increased in the setting of lye ingestion [23,24•], although routine surveillance is not advocated at this time.
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Treatment Diet and lifestyle Acute phase (1 to 7 days) • It is recommended that oral intake should be avoided in patients with a history of acute caustic ingestion until they have been fully evaluated for the extent of esophagogastric damage. • As caustic ingestion past early childhood is associated most commonly with a suicidal intent, once such patients are stable they will need full psychiatric evaluation.
Total parenteral nutrition Total parenteral nutrition is indicated in patients with moderate injury where healing may be expected within 1 to 2 weeks. Contraindications Inability to gain central intravenous access, patient instability, coagulopathy, septicemia. Complications Line infection and septicemia.
Latent phase (1 to 4 weeks) • Patients with moderate to severe injury will continue with nothing by mouth. • Patients should continue on total parenteral nutrition if radiography suggests rapid healing and oral feedings may be attempted. If not, enteral feeding should be considered.
Enteral feeding via jejunostomy Enteral feeding is indicated in patients with moderate to severe injury requiring greater than 2 weeks of enteral therapy bypassing the esophagus and stomach. Contraindications Patient instability, coagulopathy. Complications Complications from the minor surgery involved placed either through laparotomy or through ultrasound guidance.
Chronic phase (more than 4 weeks) • Patients are instructed to take mostly a liquid diet with soft and more solid foods as tolerated. For patients with severe strictures, oral supplements initially may be used entirely.
Pharmacologic treatment • The overall aim of acute-phase pharmacologic treatment is to reduce inflammatory response to the caustic and prevent superinfection. • There are no pharmacologic treatments specifically useful in the latent or chronic phases.
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Proton pump inhibitors and H2-antagonists Aim: To reduce concomitant acid reflux injury during the acute phase of injury. Standard dosage Any of the proton pump inhibitors may be given at twice daily at standard dosages (omeprazole, 20 mg/d; lansoprazole, 30 mg/d; rabeprazole, 20 mg/d; pantoprazole, 40 mg/d) if enteral access is available. Patients without enteral access may receive continuously delivered intravenous H2-antagonists or proton pump inhibitors (once available). Contraindications Allergy to antisecretory agents. Main drug interactions Significant drug interactions with the agents are rare. Main side effects Rarely, thrombocytopenia with H2-antagonists. Special points There are no trials specifically evaluating the use of acid-suppressing therapy with proton pump inhibitors or H2-antagonists in caustic injury. The theory is to reduced concomitant acid reflux injury, particularly if the distal esophagus (ie, lower esophageal sphincter) has been injured. Because of the safety of these agents, their use is advocated until a trial specifically addresses this issue. Cost-effectiveness There are no data on cost-effectiveness.
Antibiotics Aim: To prevent superimposed infection. Standard dosage Broad spectrum antibiotics typically are used. There is no standard regimen suggested. Contraindications Clostridium difficile colitis, fungal infection, bacterial resistance. Main drug interactions Antibiotic-dependent. Main side effects Antibiotic-dependent; C. difficile colitis. Special points Some centers give broad-spectrum intravenous antibiotics to all patients but there are no controlled trials addressing supporting their use in all patients. Most centers give antibiotics only if there is evidence of infection. Cost-effectiveness There are no data available on cost-effectiveness.
Steroids Aim: To reduce the inflammatory response of the caustic injury. Prednisolone, 2 mg/kg intravenously. Infectious complications from esophageal injury. None. Immunosuppression and hyperglycemia. Several centers still administer steroids to all patients with severe caustic injury but most do not. There is only one randomized controlled study on this treatment that shows no benefit of steroids. Most of the basis for this therapy is derived from animal data. Cost/cost-effectiveness Low cost; there are no data on cost-effectiveness. Standard dosage Contraindications Main drug interactions Main side effects Special points
Endoscopic therapy Acute phase (1 to 7 days) Flexible esophagoscopy and gastroscopy • The aims of endoscopy are to assess the severity of injury, to assess the extent of injury, and to predict prognosis and guide treatment during the acute phase. All patients with a history of acute caustic ingestion will need upper endoscopy regardless of symptoms or physical examination.
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Chronic phase (more than 4 weeks) Stricture dilation
Standard procedure
Contraindications Complications Special points
Cost-effectiveness
Aims: To reevaluate extent of disease and to perform stricture dilation to enable adequate oral intake. Endoscopy may be performed with a standard or pediatric endoscope depending on the luminal diameter identified on radiography. Savary dilators are preferred, passed over a guidewire under fluoroscopic guidance for complicated strictures. Severe oropharyngeal involvement or high esophageal stricture making esophageal intubation difficult. Significant chance of perforation. Patients with strictures may require several dilations initially, usually at weekly intervals, and then stabilize for long periods of time. Other patients may require a chronic course of dilation. Some motivated patients may learn self-bougie technique but there is risk of perforation to this in unskilled hands. There is no evidence as of yet that endoscopic screening for carcinoma in these patients is worthwhile. Requires large expense and time but only other alternative is surgery.
Surgery Acute phase (1 to 7 days) Esophagectomy
Standard procedure Contraindications Complications Special points
Cost/cost-effectiveness
Aims: To prevent death from esophageal perforation or transmural necrosis and sepsis, and to avoid risk of impending perforation or transmural necrosis if presence of high-grade injury. Esophagectomy with probable gastrectomy with cervical esophagostomy and closure or the proximal duodenum. Severe patient instability suggesting that death is imminent, evidence of extensive abdominal injury in addition to esophageal injury. Very high morbidity and mortality rate. There is great debate on when surgery is indicated. Some authorities advocate surgery only for patients with clear evidence of perforation or transmural necrosis, whereas others recommend surgery for all patients with severe injury. If patients survive, they ultimately will need interposition with either small bowel or colon, which is also an extensive surgery and has long-term morbidity. Still, surgery may be the only chance for survival for many of these patients, particularly with alkali injury. There are high short- and long-term expenses.
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Chronic phase (more than 4 weeks) Esophagogastrectomy Aim: To resect esophagus and establish oral route of alimentation. Standard procedure Esophagogastrectomy with either small or large bowel interposition. Contraindications High operative risk, diseased small bowel or colon unsuitable for interposition. Complications High morbidity and mortality with often persistent dysphagia from and stasis within the interposed bowel. Dumping syndrome common as a result of the gastrectomy. Special points This is very difficult surgery that should be performed only by expert hands. Patients may still have a very compromised lifestyle following surgery, but most are able to eat adequately after surgery. It should not be used as a prophylactic measure to prevent esophageal carcinoma in patients with lye strictures, as advocated by some authors. Cost/cost-effectiveness Expensive.
References and Recommended Reading Recently published papers of particular interest have been highlighted as: • Of importance •• Of major importance 1.
Bulletin of the National Clearing House for Poison Control Centers, vol. 25, no. 6. Rockville, MD: National Clearing House for Poison Control Centers; 1981:1–75. 2. Leape L, Ashcraft KW, Scarpelli DG, Holder TM: Hazard to health—liquid lye. N Engl J Med 1971, 284:578–581. 3. Butler C, Madden JW, Davis WM, Peacock EE: Morphologic aspects of experimental esophageal lye strictures. II. Effect of steroid hormones, bougienage, and induced lathyrism on acute lye burns. Surgery 1977, 81:337–341. 4. Goldman LP, Weigert JM: Corrosive substance ingestion: a review. Am J Gastroenterol 1984, 79:85–90. 5. Katzka DA: Caustic injury to the upper gastrointestinal tract. In Clinical Practice of Gastroenterology, vol 1. Edited by Brandt L. Philadelphia: Current Medicine, Inc; 1999:96–104. 6. Webb WR, Koutras P, Ecker RR, et al.: An evaluation of steroids and antibiotics in caustic burns of the esophagus. Ann Thorac Surg 1970, 9:95–102. 7.• Anderson KD, Rouse TM, Randolph JG: A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J Med 1990, 323:637–640. The only controlled randomized trial examining the effects of corticosteroids on survival and stricture formation after caustic ingestion. 8. Gaudrealut P, Parent M, McGuigan MA, et al.: Predictability of esophageal injury from signs and symptoms: a study of caustic ingestion in 378 children. Pediatrics 1983, 71:767–770. 9. Crain EF, Gershel JC, Mezey AP: Caustic ingestions. Symptoms as predictors of esophageal injury. Am J Dis Child 1984, 139:863–865. 10. Cello JP, Fogel RP, Boland CR: Liquid caustic ingestion. Spectrum of injury. Arch Intern Med 1980, 140:501–504.
11.
Bautista Casanovas A, Estevez Martinez E, Varela Cives R, et al.: A retrospective analysis of ingestion of caustic substances by children. Ten-year statistics in Galacia. Eur J Pediatr 1997, 156:410–414. 12. DiCostanzo J, Moirclerc M, Jouglard J, et al.: New therapeutic approach to corrosive burns of the upper gastrointestinal tract. Gut 1980, 21:370–375. 13. Symbas PN, Vlasis SE, Hatcher CR Jr: Esophagitis secondary to ingestion of caustic material. Ann Thorac Surg 1983, 36:73–77. 14.• Karnak J, Tanyel FC, Buyukpamukcu N, Hicsonmez A: Combined use of steroid, antibiotics and early bougienage against stricture formation following caustic esophageal burns. J Cardiovasc Surg 1999, 40:307–310. An uncontrolled trial, but recent experience with the disease. 15.• Broto J, Asensio M, Jorro CS, et al.: Conservative treatment of caustic esophageal injuries in children: 20 years of experience. Pediatric Surg Int 1999, 323–325. A recent retrospective study with relatively large patient population for this problem. 16. Brun JG, Celerier M, Koskas F, Dubost C: Blunt esophageal stripping: an emergency procedure for caustic ingestion. Br J Surg 1984, 71:698–700. 17.• Estrera A, Taylor W, Mills LU, Platt MR: Corrosive burns of the esophagus and stomach: a recommendation for an aggressive surgical approach. Ann Thorac Surg 1986, 41:276–283. A small number of patients, but points out both the benefits and pitfalls of early surgical intervention. 18. Lai K-H, Huang B-S, Huang M-H, et al.: Emergency surgical intervention for severe corrosive injuries of the upper digestive tract. Chin Med J 1995, 56:40–46.
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Andreoni B, Farina ML, Biffi R, Crosta C: Esophageal perforation and caustic injury: emergency management of caustic ingestion. Dis Esoph 1997, 10:95–100. 20. Cattan P, Munoz-Bongrand N, Berney T, et al.: Extensive abdominal surgery after caustic ingestion. Ann Surg 2000, 231:519–523. 21.• Zargar SA, Kochhar R, Nagi B, et al.: Ingestion of strong corrosive alkalis: spectrum of injury to the upper gastrointestinal tract and natural history. Am J Gastroenterol 1992, 87:337–341. A nice review.
22.
Broor SL, Bose PP, Lahoti D, et al.: Long term results of endoscopic dilatation for corrosive esophageal strictures. Gut 1993, 34:1498–1501. 23. Csikos M, Horvath O, Petri A, et al.: Late malignant transformation of chronic corrosive esophageal strictures. Langenbecks Arch Chir 1985, 365:231–238. 24.• Appelqvist P, Salmo M: Lye corrosion carcinoma of the esophagus. Cancer 1980, 45:2655–2658. The largest retrospective series associating squamous cell carcinoma of the esophagus with a prior history of lye ingestion.
