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1296 SECTION 15: Toxicology management. Administer oxygen to correct hypoxia. Inhaled β2-agonists may also be useful, especially in the setting of bronchospasm, but their role in the treatment of hydrocarbon pneumonitis has not been studied. Positive end-expiratory pressure or continuous positive-pressure airway ventilation may sometimes be required to maintain oxygenation, but may increase potential for further (barotrauma) injuries such as pneu mothorax or pneumatocele. In cases of severe pulmonary aspiration resulting in refractory hypoxemia, there are case reports of successful treatment with high-frequency jet ventilation or extracorporeal mem brane oxygenation. 35,36 Surfactant therapy has been used to treat acute lung injury from hydrocarbon aspiration.37-40 Treat hypotension with aggressive fluid resuscitation. Avoid administration of catecholamines such as dopamine, norepinephrine, and epinephrine. Catecholamines may cause dysrhythmias, especially after exposure to halogenated hydrocarbons and aromatic hydrocar bons. Hydrocarbon-induced dysrhythmias are generally seen shortly after the exposure, especially with inhalational use. Continuous cardiac monitoring should be initiated, and an ECG should be obtained. For hydrocarbon-induced ventricular dysrhythmias, class IA (procain amide) or class III (amiodarone, bretylium, and sotalol) antiarrhythmics should be avoided because of the risk of QT interval prolongation. 19 Propranolol, esmolol, and lidocaine have all been reported to successfully treat these ventricular dysrhythmias in case reports. 10,19,41 There is no indication for gastric lavage because risks of aspira tion far outweigh any theoretical benefits. 42 Activated charcoal is not recommended; it does not adsorb hydrocarbons well and poses a risk for vomiting and aspiration. In the rare case where a recent (<1 hour) exposure has occurred with a highly toxic hydrocarbon (e.g., aromatic or halogenated chemical) or in which a hydrocarbon has been combined with another highly toxic substance (e.g., pesticide), consultation with a poison center may result in recommendation for gastric lavage; even in these cases, benefit from gastric lavage is unproven. There is no clear evidence that corticosteroids are helpful in hydro carbon-induced pneumonitis. 13 One meta-analysis advocating lowdose steroids for acute lung injury and respiratory distress 43 has been criticized because the patients were not generally treated with current lung-protective ventilation strategies. 44 Antibiotics are not indicated unless there is clinical suspicion of superimposed bacterial pneumonitis. In summary, exogenous catecholamines (e.g., epinephrine), prophylactic antibiotics, and corticosteroids should be avoided. In dermal exposures, decontamination is preferably done at the scene or before entering the ED to avoid spreading fumes to patient treat ment areas. The patient needs to be fully undressed to prevent ongoing contamination from hydrocarbon-soaked clothes. Make sure staff wear protective gloves and aprons to prevent secondary exposure, especially to organophosphate-containing mixtures. Dermal decontamination with soap and cold water and eye decontamination with saline irrigation should be performed. DISPOSITION AND FOLLOW-UP If feasible, consult a medical toxicologist or regional poison control center for symptomatic hydrocarbon exposures and asymptomatic exposures to aromatic hydrocarbons or hydrocarbons with toxic addi tives.

soap and cold water and eye decontamination with saline irrigation should be performed. DISPOSITION AND FOLLOW-UP If feasible, consult a medical toxicologist or regional poison control center for symptomatic hydrocarbon exposures and asymptomatic exposures to aromatic hydrocarbons or hydrocarbons with toxic addi tives. In cases of inhalation or aspiration of nonhalogenated aliphatic hydrocarbons, asymptomatic patients may be discharged home after about 6 to 8 hours of observation with instructions to return if delayed symptoms develop. Further observation or hospitalization is required for patients who are symptomatic after hydrocarbon exposure. For pediatric hydrocar bon ingestions, the presence of wheezing, altered consciousness, or tachypnea within 2 hours predicts the need for further treatment. Hospitalization is also recommended for those who ingest hydrocar bons capable of producing delayed complications (e.g., halogenated hydrocarbons causing hepatic toxicity) or hydrocarbons with toxic additives (organophosphates and organic metal compounds). Patients with suicidal intent or with complications of solvent abuse need behavioral health evaluation. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Caustic Ingestions Nicholas J. Connors Wallace A. Carter INTRODUCTION Caustics are substances that cause both functional and histologic damage on contact with body surfaces. Many household and industrial chemicals have caustic potential. Caustics are broadly classified as alkalis (pH >7) or acids (pH <7). In developed nations, increased education and product regulation (especially of acids) have decreased morbidity and mortality from caustic exposures in both adults and children. However, in underdeveloped parts of the world, exposure to caustics remains a significant problem. 1-3 Alkaline ingestions predominate in the developed world,4 whereas acid ingestions are more common in developing countries.5 Caustic exposures tend to fall into three distinct groups: (1) inten tional adolescent or adult ingestions with suicidal ideation; (2) unin tentional ingestions (the majority of which are by curious children in the toddler age group); and (3) other incidental, often occupational or industrial contact exposures. The majority of reported exposures are unintentional or accidental, but intentional ingestions account for the majority of serious injuries. 1 The geographic variation in caustic ingestion circumstances, such as involved substances, intention, age of the patient, and extent of evaluation, make it important to base treatment decisions on each particular patient’s presentation. CHAPTER TABLE 199-4 Management of Hydrocarbon Exposures Airway and breathing Secure airway. Antidotes: Administer oxygen for carboxyhemoglobinemia and methylene blue for methemoglobinemia. Provide supplemental oxygen. Administer inhaled β 2-agonists. Ventilatory support: Provide positive end-expiratory pressure or continuous positive airway pressure as needed to achieve adequate oxygenation. Cardiac Circulation: Administer IV crystalloid fluid for initial volume resuscitation of hypotensive patients. Do not use catecholamines in cases of halogenated hydrocarbon exposure. Consider propranolol, esmolol, or lidocaine for ventricular dysrhythmias induced by halogenated hydrocarbon exposure. Consult the poison control center, toxicologist, and other appropriate specialists as needed. Decontamination Dermal: Remove hydrocarbon-soaked clothes, decontaminate skin with soap and water, and decontaminate eyes with saline irrigation. GI: Not indicated. See discussion below.

ed by halogenated hydrocarbon exposure. Consult the poison control center, toxicologist, and other appropriate specialists as needed. Decontamination Dermal: Remove hydrocarbon-soaked clothes, decontaminate skin with soap and water, and decontaminate eyes with saline irrigation. GI: Not indicated. See discussion below. Other Laboratory tests: Order CBC, basic metabolic panel, liver function tests (serum transaminase, bilirubin, albumin levels), prothrombin time, partial thromboplastin time, carboxyhemoglobin level, methemoglobin level, and/or radiologic studies as indicated (see text). Correct electrolyte abnormalities. Do not give steroids. Administer blood products as needed. Tintinalli_Sec15_p1187-1332.indd 1296 8/2/19 8:40 PM

, bilirubin, albumin levels), prothrombin time, partial thromboplastin time, carboxyhemoglobin level, methemoglobin level, and/or radiologic studies as indicated (see text). Correct electrolyte abnormalities. Do not give steroids. Administer blood products as needed. Tintinalli_Sec15_p1187-1332.indd 1296 8/2/19 8:40 PM CHAPTER 200: Caustic Ingestions 1297 a deep tissue injury called liquefaction necrosis. Severe intentional alkali ingestion may cause deep penetration into surrounding tissues with resultant multisystem organ injuries, including esophageal injury, gastric perforation, and necrosis of abdominal and mediastinal structures. Severe injuries to the pancreas, gallbladder, small intestine, and mediastinum after intentional ingestion have been reported. Solid alkali ingestions, such as some lye preparations, have a greater potential for oropharyngeal and proximal esophageal tract injury and less for distal injury. The most common household alkali is bleach, a 3% to 6% sodium hypochlorite solution with a pH of approximately 11. Household liquid bleach is minimally corrosive to the esophagus and rarely causes significant injury beyond grade 1 esophageal burns. Esophageal stricture was not observed as a complication of household bleach ingestion in a series involving almost 400 patients. 7 However, ingestion of industrial-strength bleach containing much higher concentrations of sodium hypochlorite may result in gastric and esophageal necrosis. Bleach ingestion may cause emesis secondary to gastric irritation and/or pneumonitis after aspiration. Pulmonary irritation related to chlorine gas production in the stomach or when mixed with other substances may also occur. 8,9 A common reaction is the production of the highly irritating chloramine gas when bleach and ammonia household cleaners are combined.10  ACIDS Injuries by strong acids produce coagulation necrosis. Dissociated hydrogen ions and their associated anions penetrate tissues, leading to cell death and eschar formation. This process is believed to limit continued hydrogen ion penetration and protect against deeper injury. When ingested acids settle in the stomach, gastric necrosis, perforation, and hemorrhage may result. Although it was previously thought that acids were esophagus sparing with most tissue injury concentrated in the stomach, endoscopy following an acid ingestion finds a similar incidence of gastric and esophageal injury. 11-13 Acid ingestion may be complicated by systemic absorption of acid with associated metabolic acidosis, hemolysis, and renal failure. 14 Hydrofluoric acid is a unique ingestion discussed in Chapter 218, “Chemical Burns” (see “Hydrofluoric Acid”). CLINICAL FEATURES The cardinal features of caustic ingestion are a chemical burn to the GI mucosa, 15 sometimes associated with chemical burns to the skin or eyes from splashes or dribbling (see Chapter 217, “Thermal Burns, ” and Chapter 241, “Eye Emergencies”). Pharyngeal burns from ingestion produce pain, odynophagia, drooling, and vocal hoarseness. Dyspnea may be caused by edema of the upper airway, aspiration of the caustic substance into the tracheobronchial tree, or inhalation of fumes, par ticularly acids. Esophageal burns produce dysphagia, odynophagia, and chest pain. Ocular burns are painful, reduce visual acuity, and produce visible damage to the anterior structures of the eye.  HISTORY The key priority is rapid airway assessment and stabilization. Following that, obtain a directed history to determine the type, amount, and timing of the ingested caustic and the presence of co-ingestants. Deter mine if the ingestion was intentional or unintentional.  PHYSICAL EXAMINATION Look for signs of respiratory distress or circulatory shock.

y assessment and stabilization. Following that, obtain a directed history to determine the type, amount, and timing of the ingested caustic and the presence of co-ingestants. Deter mine if the ingestion was intentional or unintentional.  PHYSICAL EXAMINATION Look for signs of respiratory distress or circulatory shock. With inges tions, look for signs of oropharyngeal injury (mucosal burns, drooling), respiratory injury (dysphonia, coughing, stridor, wheezing), and gastric injury (vomiting, epigastric tenderness) ( Figure 200-1). 4,15-20 Streaks of caustic burns on the face or chest are called “dribble burns” (Figure 200-2). DIAGNOSIS Conflicting data exist on the reliability of presenting signs and symp toms to predict upper GI injuries.21-25 Intentional ingestions are associated with higher grades of GI tract injury, with or without clinically obvious signs. 26 The incidence of serious GI injury after pediatric TABLE 200-1 Common Caustic Compounds Compound Found In Alkalis Sodium hydroxide Industrial chemicals, drain openers, oven cleaners Potassium hydroxide Drain openers, batteries Calcium hydroxide Cement, hair relaxers, perm products Ammonium hydroxide Hair relaxers and perm products, dermal peeling/ exfoliation, toilet bowl cleaners, glass cleaners, fertilizers Lithium hydroxide Photographic developer, batteries Sodium tripolyphosphate Detergents Sodium hypochlorite Bleach Acids Sulfuric acid Automobile batteries, drain openers, explosives, fertilizer Acetic acid Printing and photography, disinfectants, hair perm neutralizer, pickling solution Hydrochloric acid Cleaning agents, metal cleaning, chemical production, swimming pool products Hydrofluoric acid Rust remover, petroleum industry, glass and microchip etching, jewelry cleaners Formic acid Model glue, leather and textile manufacturing, tissue preservation Chromic acid Metal plating, photography Nitric acid Fertilizer, engraving, electroplating Phosphoric acid Rust proofing, metal cleaners, disinfectants Many chemicals used in industry have caustic potential (Table 200-1). Household caustics are often less concentrated forms of industrialstrength cleansers. PATHOPHYSIOLOGY The degree to which a caustic substance produces tissue injury is deter mined by a number of factors: pH, concentration, duration of contact, volume, and titratable acid or alkaline reserve. Acids tend to cause sig nificant injuries at a pH <3 and alkalis at a pH >11. The physical properties of the product formulation (i.e., liquid, gel, granular, or solid) can influence the nature of the contact with tissue. Following ingestion, solid or granular caustics often injure the oropharynx and proximal esopha gus, whereas liquid alkali ingestions are characterized by more extensive esophageal and gastric injuries. Titratable acid or alkaline reserve refers to the amount of acid or base required to neutralize the agent; the greater this value, the greater is the potential for tissue injury. Esophageal mucosal burns from caustic ingestions are classified by a visual endoscopic grading system, which correlates with risk of future complications: Grade 1 burns involve tissue edema and hyperemia; grade 2 burns include ulcerations, blisters, and whitish exudates, which are subdivided into grade 2A (noncircumferential) and 2B (deeper or circumferential) lesions; and grade 3 burns are defined by deep ulcer ations and necrotic lesions. 6 Following the initial mucosal injury, tissue remodeling occurs over roughly 2 months. In mild cases, normal esophageal function is restored, but in severe cases, dense scar tissue forms, resulting in stricture formation. Esophageal strictures are a source of significant morbidity and may require long-term treatments with dila tions, stenting, or surgery.

, tissue remodeling occurs over roughly 2 months. In mild cases, normal esophageal function is restored, but in severe cases, dense scar tissue forms, resulting in stricture formation. Esophageal strictures are a source of significant morbidity and may require long-term treatments with dila tions, stenting, or surgery. Early phases of remodeling, particularly days 2 to 14 after exposure, are associated with increased tissue friability and higher risk of perforation, both spontaneous and iatrogenic.  ALKALI INJURIES Following caustic alkali exposures, the hydroxide ion easily penetrates tissues, causing immediate cellular destruction via protein denaturation and lipid saponification. This is followed by thrombosis of local micro vasculature that leads to further tissue necrosis. Alkali injuries induce Tintinalli_Sec15_p1187-1332.indd 1297 8/2/19 8:40 PM

i exposures, the hydroxide ion easily penetrates tissues, causing immediate cellular destruction via protein denaturation and lipid saponification. This is followed by thrombosis of local micro vasculature that leads to further tissue necrosis. Alkali injuries induce Tintinalli_Sec15_p1187-1332.indd 1297 8/2/19 8:40 PM 1298 SECTION 15: Toxicology FIGURE 200-1. Acid ingestion. A. Moderate intraoral burns on buccal mucosa and tongue. B. Lingual burns. FIGURE 200-2. Acid ingestion. Dermal dribble burns on upper chest. unintentional ingestions has been the focus of many studies. 4,21-23,25,27,28 Although serious esophageal injury can occur in the absence of oral burns, essentially all children with serious esophageal injuries (grade 2 or 3) after accidental caustic ingestion have some initial signs of injury, such as stridor, drooling, or vomiting. 22,23,25 Pain alone is an inconsistent predictor of severity of injury. Assess for hemodynamic instability. Causes of shock include GI bleeding, complications of GI perforation, volume depletion, and tox icity from co-ingestants. Examine for peritoneal signs due to hollow viscous perforation. Consider mediastinitis in patients complaining of chest discomfort, and palpate the chest wall and neck for signs of subcutaneous emphysema. Inspect the eyes for ocular burns and the skin for splash and dribble burns.  LABORATORY TESTING For children who unintentionally ingest common household alkalis (e.g., bleach) or acids (e.g., toilet bowl cleaner), the need for ancil lary testing is only necessary in those with signs or symptoms of sig nificant injury (e.g., drooling, respiratory distress, or vomiting). For an intentional ingestion or ingestion of a strong acid or alkali, laboratory evaluation should include a venous or arterial blood gas, electrolyte panel, hepatic profile, complete blood count, lactate, and blood type and screen. Caustic ingestions can cause an anion gap acidosis based on lactate production due to direct tissue injury or shock. Strong acid ingestions may be associated with both severe anion gap (e.g., sulfuric acid) and nongap acidoses (e.g., hydrochloric acid). In suicidal patients, obtain acetaminophen and salicylate levels to screen for potential coingestants. An ECG is indicated following a hydrofluoric acid exposure to check for QT interval prolongation from hypocalcemia.  IMAGING Obtain a chest radiograph in patients with chest pain, dyspnea, or vomiting to check for peritoneal and mediastinal air. In 2015, the World Society of Emergency Surgery consensus conference recommended the use of IV contrasted thoracoabdominal CT scans in caustic ingestion management. 29 Although endoscopy has been the traditional gold stan dard for grading esophageal injury and predicting stricture rates, recent evidence suggests CT scans outperform endoscopy in the prediction of stricture and the need for surgical esophageal reconstruction due to the greater ability to determine the depth of injury, 30,31 although conflicting results are noted and some authors see CT as a useful adjunct to endos copy but not a replacement.32 US can be used to evaluate and follow up corrosive gastric injury if there is perforation or severe edema prevent ing endoscopy.33  ENDOSCOPY Endoscopy is the traditional gold standard for evaluating the loca tion and severity of injury to the esophagus, stomach, and duodenum after caustic ingestion. The controversy has been who needs endoscopy and when should it be performed. 24,25,28,34,35 Regardless of symptoms, patients with intentional caustic ingestions should undergo early endoscopy because ingestions with suicidal intent carry the highest risk of clinically important injury. In unintentional ingestions, particularly by children, the decision to perform endoscopy is less clear cut.

d. 24,25,28,34,35 Regardless of symptoms, patients with intentional caustic ingestions should undergo early endoscopy because ingestions with suicidal intent carry the highest risk of clinically important injury. In unintentional ingestions, particularly by children, the decision to perform endoscopy is less clear cut. 24,25,28,34,35 Most children with serious caustic esophageal injury will be symptomatic, 28 and although there is a correlation between clinical findings and corrosive severity, lack of symptoms is judged by some authors not to be an adequate predictor of no injury. 27,36,37 Early endoscopy is recommended after unintentional caustic ingestions in adults and children with signs or symptoms of serious injury such as stridor or significant oropharyngeal burns and/or vomiting, drooling, or food refusal, with or without oropha ryngeal burns. 22,24,25,28,34,35,37 The primary purpose of endoscopy is diagnosis, 6,38-40 with high accu racy for grade 3 injuries and less so for grade 2 damage when compared to biopsy. 41 Early endoscopy permits grading of injuries, helps guide treatment, and predicts future morbidity ( Table 200-2). Early endoscopy is safe, improves clinical course, and reduces costs of admission. 42 Tintinalli_Sec15_p1187-1332.indd 1298 8/2/19 8:40 PM

injuries and less so for grade 2 damage when compared to biopsy. 41 Early endoscopy permits grading of injuries, helps guide treatment, and predicts future morbidity ( Table 200-2). Early endoscopy is safe, improves clinical course, and reduces costs of admission. 42 Tintinalli_Sec15_p1187-1332.indd 1298 8/2/19 8:40 PM CHAPTER 200: Caustic Ingestions 1299 An additional benefit of endoscopy is endoscopic guidance of an oro gastric or nasogastric tube past injured areas of esophagus or stomach to allow enteral feeding while healing occurs. 43 This is particularly impor tant in children with low glycogen stores or with high-grade injuries, in whom caloric requirements will be high. Tissue friability after a caustic burn increases significantly at 24 to 48 hours after injury and is maximal between days 5 and 14, although endoscopy has been performed safely 5 days after exposure. 44 Experts recommend that endoscopy should be performed early after inges tion, within 12 to 24 hours from the time of ingestion, to avoid iat rogenic perforation.43,45-47 Traditionally, endoscopists have terminated their examination at the first sign of severe esophageal injury (grade 2B or 3). Experienced operators using modern, smaller, and flexible endo scopes with minimal insufflation of air can usually obtain more distal visualization documenting all injuries to the esophagus, stomach, and duodenum, an important point in pediatric acid ingestions where gastric and duodenal burns are common. TREATMENT  AIRWAY The first priority is airway protection. Patients with respiratory dis tress may have significant oral, pharyngeal, and/or laryngotracheal injuries that require emergent airway management. Respiratory injuries from caustic ingestion can cause significant morbidity and mortality, especially in elderly patients. 49 Approach caustic ingestions as difficult airways. Ideally, patients with potential airway injuries should have fiberoptic evaluation of the airway before intubation to determine the extent of the damage, but this may not always be possible. Oral intubation with direct visualization is the first choice for definitive airway management. For potential airway compromise, establish a secure endotracheal airway early rather than risk greater dif ficulty later when secondary effects of injury, such as edema, complicate the situation. Cricothyrotomy may be needed if oropharyngeal edema, tissue friability, and bleeding make intubation difficult or impossible. Blind nasotracheal intubation is contraindicated due to the potential for exacerbating airway injuries. If possible, avoid laryngeal mask airways, combination tubes with pharyngeal and tracheal balloons, retrograde intubation, and bougies because these devices and techniques can increase tissue damage or cause perforation.  DECONTAMINATION, NEUTRALIZATION, AND DILUTION The ED staff should take precautions to prevent ongoing injury to the patient and staff from continued caustic exposure. ED staff involved should wear protective gowns, gloves, and masks with face shields. Standard decontamination, with removal of soiled or soaked clothing and copious irrigation with towels and soap (as needed), is adequate in most cases. Vomiting may reexpose the patient and staff to the caustic agent. Gastric decontamination with activated charcoal is contraindi cated if a caustic is the only ingestion. Charcoal does not adhere well to most caustics and will impede visualization when endoscopy is per formed. Ipecac syrup is contraindicated , because vomiting will result in repeat exposure of the airway and GI mucosa to the caustic agent and could precipitate perforation. In general, do not insert nasogastric tubes until after endoscopic evaluation.

o most caustics and will impede visualization when endoscopy is per formed. Ipecac syrup is contraindicated , because vomiting will result in repeat exposure of the airway and GI mucosa to the caustic agent and could precipitate perforation. In general, do not insert nasogastric tubes until after endoscopic evaluation. With high-grade esophageal burns, feeding tubes may be inserted under endoscopic guidance if clinically indicated. Dilution and neutralization therapy are not recommended in the prehospital setting or ED because there is no proven human benefit and because of the potential risk of gastric distention, vomiting, and perforation. 51-54  FLUID RESUSCITATION Establish large-bore IV access and resuscitate with crystalloids. Coingestants, bleeding, and third spacing, as well as metabolic disarray from acid-base derangements, can lead to shock. Central venous access may be required for monitoring of resuscitation.  SYSTEMIC STEROIDS AND PROPHYLACTIC ANTIBIOTICS There is controversy concerning the benefit of systemic steroids in caustic ingestions. 55-63 The ability of steroids to inhibit the inflammatory response led to the hypothesis that steroids may decrease stricture for mation after caustic ingestion, and animal models have suggested benefit. One prospective human trial found statistically significant protection against the development of stricture formation in grade 2B lesions, and corticosteroids are recommended by some international treatment guidelines. 45,63 A subsequent pooled meta-analysis has not shown benefit for injury, and steroids may increase the risk of infection, perforation, and hemorrhage. 62 Use has been discouraged by other experts. 29,57 One criticism of pooled meta-analysis data is that some individual studies did not clearly distinguish between grade 1 and 2A lesions, which do not typically lead to strictures, and grade 2B and 3 injuries, which might theoretically benefit from steroids. There is no current evidence to support the ED administration of prophylactic antibiotics after caustic ingestions in humans. However, in protocols in which steroids are used or in grade 2B or 3 injury, addition of penicillin or another antibiotic that covers oral flora has been part of the treatment regimen. 57,64  SURGERY AND ESOPHAGEAL STENTING AND DILATION Major ingestions of caustic agents may result in perforation of the GI tract or extensive tissue necrosis requiring emergency surgery. 65-70 Laparotomy is generally preferred over laparoscopic evaluation for posterior gastric visualization. The indications for emergency surgery include esophageal perforation, peritoneal signs, or free intraperitoneal air. Large-volume ingestions (>150 mL), signs of shock, respiratory distress, persistent lactic acidosis, ascites, and pleural fluid may be other indica tions for surgical exploration. For grade 2B and 3 injuries without obvious perforation, recom mendations include a period of esophageal rest, 71 early gastrostomy for enteral feeding,37,72 and dilation therapy (in the first 3 weeks) with or without stenting.73-76 Once strictures form, they may be difficult to treat and require stenting and/or multiple balloon dilatations or bouginage.77 Controversy exists about the most appropriate treatment for esophageal stricture (i.e., long-term repetitive dilation therapy versus surgery).

n the first 3 weeks) with or without stenting.73-76 Once strictures form, they may be difficult to treat and require stenting and/or multiple balloon dilatations or bouginage.77 Controversy exists about the most appropriate treatment for esophageal stricture (i.e., long-term repetitive dilation therapy versus surgery). 75-78 TABLE 200-2 Correlation of Esophageal Injury Grade With Morbidity and Interventions Endoscopic Injury Grade Grade 1 Esophageal Injury Grade 2A Esophageal Injury Grade 2B or 3 Esophageal Injury Future morbidity No risk of strictures or carcinoma Strictures tend not to occur At risk for hemorrhage and perforation (early), strictures (delayed), and carcinoma (late) Nutritional support Diet as tolerated If unable to tolerate PO, provide nutritional sup port via nasogastric, orogastric, or percutaneous feeding tube Total parenteral nutrition Initiate early percutaneous feeding tube Total parenteral nutrition General interventions Supportive care Admission recommended, supportive care Intensive care unit admission recommended; may require additional imaging or surgical exploration for gastric injuries Tintinalli_Sec15_p1187-1332.indd 1299 8/2/19 8:40 PM