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Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e > Chapter 200: Caustic Ingestions

Nicole C. Bouchard; Wallace A. Carter

INTRODUCTION AND EPIDEMIOLOGY

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.1,2,3,4 The challenges to exposure prevention and patient care include relative lack of childproof containers, easy and unregulated access to highly corrosive substances, cultural-specific propensities to ingest caustics in suicide attempts, sheer high volume of cases, delays to care in rural settings, malnutrition, financial resources of hospitals and families to provide the services needed, and poor follow-up.4 Alkaline ingestions predominate in the developed world,5 whereas acid ingestions are more common in developing countries.6

Caustic exposures tend to fall into three distinct groups: (1) intentional teen or adult ingestions with suicidal ideation7; (2) unintentional ingestions (the majority of which are by curious children in the toddler age group)8; and (3) other incidental, oen occupational or industrial contact exposures. The majority of reported exposures are unintentional or accidental, but although less frequent, 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 diicult to create encompassing recommendations or a consensus approach.4,9,10

Many chemicals used in industry have caustic potential (Table 200-1). Household caustics are oen less concentrated forms of industrial strength cleansers.

1/21 8/7/2018 TABLE 200-1 Common Caustic Compounds

Alkali Found in

Sodium hydroxide Industrial chemicals, drain openers, oven cleaners

Potassium Drain openers, batteries hydroxide

Calcium hydroxide Cement, hair relaxers, and perm products

Ammonium Hair relaxers and perm products, dermal peeling/exfoliation, toilet bowl cleaners, hydroxide glass cleaners, fertilizers

Lithium hydroxide Photographic developer, batteries

Sodium Detergents tripolyphosphate

Sodium hypochlorite

Acids

Sulfuric acid Automobile batteries, drain openers, explosives, fertilizer

Acetic acid Printing and photography, disinfectants, hair perm neutralizer

Hydrochloric acid Cleaning agents, metal cleaning, chemical production, swimming pool products

Hydrofluoric acids 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

2/21 8/7/2018 PATHOPHYSIOLOGY

The degree to which a caustic substance produces tissue injury is determined by a number of factors: pH, concentration, duration of contact, volume present, and titraTable acid or alkaline reserve. Acids tend to cause significant 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 the tissue. Following ingestion, solid or granular caustics oen injure the oropharynx and proximal esophagus, 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: 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 ulcerations and necrotic lesions. 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 dilations, stenting, or surgery. Early phases of remodeling, particularly days 2 to 14, 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 microvasculature that leads to further tissue necrosis. Alkali injuries induce 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 aer 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.11 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 aer aspiration. Pulmonary irritation related to chlorine gas production in the stomach or when mixed with

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other substances may also occur.12,13 A common reaction is the production of the highly irritating chloramine gas when bleach and ammonia household cleaners are combined.14

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.15,16,17 Despite relatively less tissue destruction, strong acid ingestion results in high-grade gastric injuries (secondary to pylorospasm and pooling) and a higher mortality rate compared with strong alkali ingestions. Acid ingestion is sometimes complicated by systemic absorption of acid with associated metabolic acidosis, hemolysis, and renal failure.18 Hydrofluoric acid is a unique ingestion discussed in chapter 217, Chemical Burns (see Hydrofluoric Acid).

CLINICAL FEATURES

The cardinal features of caustic ingestion are a chemical burn to the oral mucosa,19 sometimes associated with chemical burns to the skin or eyes from splashes or dribbling (see chapters 217, Chemical Burns and 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, particularly 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 and amount of caustic ingested and the presence of coingestants. Determine if the ingestion was intentional or unintentional.

PHYSICAL EXAMINATION

Look for signs of respiratory distress or circulatory shock. With ingestions, look for signs of pharyngeal injury (mucosal burns, drooling), respiratory injury (dysphonia, coughing, stridor, wheezing), and gastric injury (vomiting, epigastric tenderness) (Figure 200-1).5,19,20,21,22,23,24 Streaks of caustic burns on the face or chest are called "dribble burns" (Figure 200-2).

FIGURE 200-1.

4/21 8/7/2018 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.

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DIAGNOSIS

Conflicting data exist on the reliability of presenting signs and symptoms to predict upper GI injuries.25,26,27,28,29 Intentional ingestions are associated with higher grades of GI tract injury, with or without clinically obvious signs.30 The incidence of serious GI injury aer pediatric unintentional ingestions has been the focus of many studies.5,25-27,29,31,32 Although serious esophageal injury can occur in the absence of oral burns, essentially all children with serious esophageal injuries (grade 2 or 3) aer accidental caustic ingestion have some initial sign or symptom, such as stridor, drooling, or vomiting.26,27,29 Pain alone is an inconsistent predictor of severity of injury, and pain may be absent initially and early in the clinical course.

Assess for hemodynamic instability. Causes of shock include GI bleeding, complications of GI perforation, volume depletion, and toxicity from coingestants. 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 accidentally ingest common household alkalis (e.g., bleach) or acids (e.g., toilet bowl cleaner), the need for ancillary testing is only necessary in patients with signs or symptoms of significant injury: drooling, respiratory distress, or vomiting. For an intentional ingestion, or one from a strong acid or

6/21 8/7/2018 alkali, laboratory evaluation should include a venous or arterial blood gas, electrolyte panel, hepatic profile, complete blood count, coagulation profile, 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). Obtain acetaminophen and salicylate levels to screen for potential coingestants in suicidal patients. 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. Thoracoabdominal CT scanning is useful to assess for esophageal injury aer ingestion of strong caustics or if intra-abdominal perforated viscus is suspected. Endoscopy is the gold standard for identifying the severity of esophageal injury. IV and oral contrast-enhanced CT scanning is an alternative when endoscopy is not readily available or during the postingestion time period when the risk of esophageal perforation by endoscopy is increased (see Endoscopy section).33 Because oral contrast can interfere with subsequent endoscopic visualization, it is best to discuss the need for oral contrast administration with the endoscopist prior to the CT study. Ultrasound can be used to evaluate and follow-up corrosive gastric injury if there is perforation or severe edema preventing endoscopy.34

ENDOSCOPY

Endoscopy is the gold standard for evaluating the location and severity of injury to the esophagus, stomach, and duodenum aer caustic ingestion. The controversy has been who needs endoscopy and when should it be done.28,29,32,35,36 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 not clear cut.28,29,32,35,36 Most children with serious caustic esophageal injury will be symptomatic,32 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.8,31,37 Early endoscopy is recommended aer 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 oropharyngeal burns.26,28,29,32,35,36,38

The general purpose of endoscopy is diagnosis.39–46 Early endoscopy permits grading of injuries, helps guide treatment, and predicts future morbidity (Table 200-2). Early endoscopy is safe and may decrease the time that patients will be without nutritional support. This is particularly important in children with low glycogen stores and in high-grade injuries, where caloric requirements will be high.

7/21 8/7/2018 TABLE 200-2 Correlation of Esophageal Injury Grade with Morbidity and Interventions

Grade 1 Endoscopic Esophageal Grade 2A Esophageal Injury Grade 2B and 3 Esophageal Injuries Injury Grade Injury

Future No risk of Strictures tend not to occur At risk for hemorrhage and perforation morbidity strictures (early), strictures (delayed), and or carcinoma (late) carcinoma

Nutritional Diet as If unable to tolerate PO, provide Initiate early percutaneous feeding support tolerated nutritional support via tube nasogastric, orogastric, or or percutaneous feeding tube Total parenteral nutrition or Total parenteral nutrition

General Supportive Admission recommended, Intensive care unit admission interventions care supportive care recommended; may require additional imaging or surgical exploration for gastric injuries

Tissue friability aer a caustic burn increases significantly at 24 to 48 hours aer injury and is maximal between days 5 and 14. Most experts agree that endoscopy should be performed early aer ingestion, ideally <12 hours and not >24 hours aer ingestion to avoid iatrogenic perforation.36,47 Traditionally, endoscopists have terminated their examination at the first sign of severe esophageal injury (grade 2B or 3). Experienced operators using smaller, flexible endoscopes with minimal insulation of air can decrease the incidence of perforation, permitting more distal visualization documenting all injuries to the esophagus, stomach, and duodenum.

TREATMENT

AIRWAY

The first priority is airway maintenance. Patients with respiratory distress may have significant oral, pharyngeal, and/or laryngotracheal injuries that require emergent airway management. If emergency airway management precedes patient decontamination, prevent exposure to the ED sta. Caustic airway injuries are

8/21 8/7/2018 diicult 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. Blind nasotracheal intubation is contraindicated due to the potential for exacerbating airway injuries. 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 diiculty later when secondary eects of injury, such as edema, complicate the situation. Cricothyrotomy may be needed if oropharyngeal edema, tissue friability, and bleeding make intubation diicult or impossible.

Avoid laryngeal mask airways, combination tubes with pharyngeal and tracheal balloons, retrograde intubation, and bougies because these devices/techniques can increase tissue damage or cause perforation.

DECONTAMINATION, NEUTRALIZATION, AND DILUTION

The ED sta should take precautions to prevent ongoing injury to the patient and sta from continued caustic exposure. ED sta 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 re-expose patient and sta to the caustic agent.

Gastric decontamination with activated charcoal is contraindicated if a caustic is the only ingestion. Charcoal does not adhere well to most caustics and will impede visualization when endoscopy is performed. However, activated charcoal may be considered when coingestants pose a risk for severe systemic toxicity.48 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.49

In general, do not insert nasogastric tubes until aer 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 potential risk of gastric distension, vomiting, and perforation.50,51,52,53

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 currently no evidence of consistent benefit from systemic steroids, so steroids are not recommended as part of ED treatment.54,55,56,57,58,59,60

The ability of steroids to inhibit the inflammatory response led to the hypothesis that steroids may decrease stricture formation aer caustic ingestion, and animal models have suggested benefit. However, individual 9/21 8/7/2018

human trials and pooled meta-analysis have not shown benefit for injury,54,55,56,57,58,59,60 and steroids may increase the risk of infection, perforation, and hemorrhage.56

One criticism of pooled meta-analysis data is that the 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.59

There is no current evidence to support the ED administration of prophylactic antibiotics aer 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 treatment regimen.56,61 Because steroids have largely fallen out of favor, the need for antibiotics in the ED is rare.

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.62,63,64,65,66,67 Laparotomy is generally preferred over laparoscopic evaluation for posterior gastric visualization. The indications for emergency laparotomy 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 indications for surgical exploration.62

For grade 2B and 3 injuries without obvious perforation, recommendations include a period of esophageal rest,68 early gastrostomy for enteral feeding,38,69 and dilation therapy (in the first 3 weeks) with or without stenting.70,71,72,73 Once strictures form, they may be diicult to treat and require stenting and/or multiple balloon dilatations or bouginage.9 Controversy exists about the most appropriate treatment for esophageal stricture (i.e., long-term repetitive dilation therapy versus surgery).9,72,73,74

TREATMENT OF SYSTEMIC TOXICITY

Morbidity or death from alkali injuries usually results from the complications of direct tissue necrosis, but acid ingestions may result in additional systemic toxicity from absorption of the acid.18 Acid-base disorders (increased anion gap or normal anion gap acidosis depending on acid ingested), hemolysis, coagulopathy, and renal failure may result. In cases of systemic toxicity, traditional critical-care principles should be applied to optimize the patient's hemodynamics. Acute lung injury (noncardiogenic pulmonary edema) may follow caustic ingestions as a complication of local or systemic eects.

NUTRITIONAL SUPPORT

Nutritional support is oen necessary following a severe caustic injury to the esophagus or stomach. Support can be achieved by percutaneous (usually jejunostomy) feeding, nasoenteral feeding, or total parenteral nutrition.61,75 10/21 8/7/2018 EXPERIMENTAL THERAPIES

Animal experiments have found that drugs aecting collagen deposition, including interferon-α-2b, octreotide, β-aminopropionitrile, colchicine, N-acetylcysteine, and d-penicillamine,9,76 can prevent esophageal strictures aer caustic alkali ingestion. Pentoxifylline, a local inflammatory and microcirculation mediator, has experimental benefit. Mitomycin C, a fibroblast proliferation inhibitor, has been used topically on strictures with some success.9 Oral agents to coat and protect the GI tract from insult, including sucralfate, bismuth subsalicylate, and sodium polyacrylate, are beneficial in animal experiments. None of these agents have been evaluated in controlled human clinical trials, and no specific recommendation can be made 61 regarding their use. H2 blockers and proton pump inhibitors are oen used in the treatment protocol, but no evidence supports or refutes their use.

DISEASE COMPLICATIONS

Short-term prognosis is worse with grade 3 GI injury, systemic complications, and age >65 years.47,77 Most long-term sequelae from caustic exposure are related to injuries to the GI tract. Acid ingestions may scar the pylorus and result in gastric outlet obstruction. Caustic alkali ingestions may result in esophageal strictures, which may result in dysphagia, odynophagia, and malnutrition. Persistent drooling, reluctance to eat, severe oropharyngeal burns, and persistent fever correlate with the development of esophageal stricture aer accidental caustic ingestion in children.78

Patients with grade 3 caustic injuries to the esophagus have about a 1000-times increased risk for squamous cell cancer of the esophagus that can occur decades aer the initial ingestion and resulting esophageal injury.79 Because cancer can develop if a portion of the esophagus remains aer reconstructive surgery for esophageal stricture, total removal of the esophagus is recommended.80

DISPOSITION AND FOLLOW-UP

Admit all patients with symptomatic caustic ingestions. Patients with grade 1 injuries can be discharged from hospital aer endoscopy, provided they can tolerate oral fluids and food. Grade 2A injuries warrant hospitalization to ensure that symptoms and injury do not progress. Grade 2B and 3 injuries are significant, require enteral or parenteral nutrition, and have an early risk for bleeding or perforation; admit to an intensive care unit.61 Organ perforation or extensive necrosis is an indication for surgery. Contact the regional poison control center for data collection purposes and assistance with management.

SPECIAL CONSIDERATIONS

LAUNDRY DETERGENT POD INGESTIONS

11/21 8/7/2018 detergent pods, also known as capsules, liquitabs, or sachets, have been available in Europe for over a decade and were introduced to the U.S. market in 2010.81,82 Each pod contains concentrated detergent within a dissolvable plastic membrane. An individual pod may have internal chambers that contain a remover and brightener separate from the detergent. Exposure to the concentrated preparation in these pods is more likely to produce symptoms than exposure to traditional products.83

Dermal or ocular exposure to the contents can produce irritation of the skin, conjunctiva, or cornea. Ingestion by young children can produce serious toxicity with profuse vomiting, respiratory distress, and neurologic depression.84 The etiology of these systemic symptoms is unknown. Caustic injury to the pharynx and esophagus can produce diiculty swallowing with drooling and aspiration during recovery.85 Treatment is supportive with airway protection and mechanical ventilation. In severe cases, ventilation may be required for days.

Acknowledgment: The authors wish to thank Dr. G. Richard Bruno for his contributions to this chapter in previous editions.

REFERENCES

1. Contini S, Scarpignato C, Rossi A, Strada G: Features and management of esophageal corrosive lesions in children in Sierra Leone: lessons learned from 175 consecutive patients. J Pediatr Surg 46: 1739, 2011. [PubMed: 21929983]

2. Ogunleye AO, Nwaorgu GB, Grandawa H: Corrosive oesophagitis in Nigeria: clinical spectrums and implications. Trop Doct 32: 78, 2002. [PubMed: 11933901]

3. Rodríguez MA, Meza Flores JL: [Clinical-epidemiological characteristics in caustics ingestion patients in the Hipólito Unanue National Hospital.] Rev Gastroenterol Peru 23: 115, 2003. [PubMed: 12853988]

4. Contini S, Swarray A, Scarpignato C: Oesophageal corrosive injuries in children: a forgotten social and health challenge in developing countries. Bull World Health Organ 87: 950, 2009. [PubMed: 20454486]

5. Riat F, Cheng A: Pediatric caustic ingestion: 50 consecutive cases and a review of the literature. Dis Esophagus 22: 89, 2009. [PubMed: 18847446]

6. Chibishev A, Pareska Z, Chibisheva V, Simonovska N: Clinical and epidemiological features of acute corrosive poisonings. Med Arh 66 (3 Suppl. 1): 11, 2012. 12/21 8/7/2018 [PubMed: 22937683]

7. Chibishev A, Pereska Z, Chibisheva V, Simonovska N: Corrosive poisonings in adults. Mater Sociomed 24: 125, 2012. [PubMed: 2 3678319]

8. Kay M, Wyllie R: Caustic ingestions in children. Curr Opin Pediatr 21: 651, 2009. [PubMed: 19543088]

9. Pace F, Antinori S, Repici A: What is new in esophageal injury (infection, drug-induced, caustic, stricture, perforation)? Curr Opin Gastroenterol 25: 372, 2009. [PubMed: 19530274]

10. Ekpe EE, Ette V: Morbidity and mortality of caustic ingestion in rural children: experience in a new cardiothoracic surgery unit in Nigeria. ISRN Pediatr 2012: 210632, 2012. [PubMed: 22778986]

11. Landau GD, Saunders WH: The eect of chlorine bleach on the esophagus. Arch Otolaryngol 80: 174, 1964. [PubM ed: 14160140]

12. Karnak I, Tanyel FC, Bukupamukcu N et al.: Pulmonary eects of household bleach ingestions in children. Clin Pediatr 35: 471, 1996. [PubMed: 8877246]

13. Turner A, Robinson P: Respiratory and gastrointestinal complications of caustic ingestion in children. Emerg Med J 22: 359, 2005. [PubMed: 15843706]

14. Tanen DA, Graeme KA, Raschke R: Severe lung injury aer exposure to chloramine gas from household cleaners. N Engl J Med 341: 848, 1999. [PubMed: 10490389]

15. Zargar SA, Kochhar R, Nagi B et al.: Ingestion of corrosive acids: spectrum of injury to the upper gastrointestinal tract and natural history. Gastroenterology 97: 702, 1989. [PubMed: 2753330]

16. Broor SL, Raju GS, Bose PP et al.: Long term results of endoscopic dilatation for corrosive oesophageal strictures. Gut 34: 1498, 1993. [PubMed: 8244131]

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17. Poley JW, Steyerberg EW, Kuipers EJ et al.: Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy. Gastrointest Endosc 60: 372, 2004. [PubMed: 15332026]

18. Cibisev A, Nikolova-Todorova Z, Bozinovska C et al.: Epidemiology of severe poisonings caused by ingestion of caustic substances. Prilozi 28: 171, 2007. [PubMed: 18356788]

19. Cowan D, Ho B, Sykes KJ, Wei JL: Pediatric oral burns: a ten-year review of patient characteristics, etiologies and treatment outcomes. Int J Pediatr Otorhinolaryngol 77: 1325, 2013. [PubMed: 23786788]

20. Havanond C: Clinical features of corrosive ingestion. J Med Assoc Thai 86: 918, 2003.

[PubMed: 14650703]

21. Doan Y, Erkan T, Cokura FC, Kutlu T: Caustic gastroesophageal lesions in childhood. Clin Pediatr (Phila) 45: 435, 2006. [PubMed: 1689 1276]

22. Tohda G, Sugawa C, Gayer C et al.: Clinical evaluation and management of caustic injury in the upper gastrointestinal tract in 95 adult patients in an urban medical center. Surg Endosc 22: 1119, 2008. [PubMed: 17965918]

23. Satar S, Topal M, Kozaci N: Ingestion of caustic substances by adults. Am J Ther 11: 258, 2004. [PubMed: 15266217]

24. Rafeey M, Shoaran M: Clinical characteristics and complications in oral caustic ingestion in children. Pak J Biol Sci 11: 2351, 2008. [PubMed: 19137870]

25. Gaudreault P, Parent M, McGuigan M et al.: Predictability of esophageal injury from signs and symptoms: a study of caustic ingestion in 378 children. Pediatrics 71: 767, 1983. [PubMed: 6835760]

26. Crain EF, Gershel JC, Mezey AP: Caustic ingestions—symptoms as predictors of esophageal injury. Am J Dis Child 138: 863, 1984. [PubMed: 6475876]

27. Gorman RL, Khin-Maung-Gyi MT, Klein-Schwartz W et al.: Initial symptoms as predictors of esophageal injury in alkaline corrosive ingestions. Am J Emerg Med 10: 189, 1992. [PubMed: 1586425]

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28. Gupta SK, Croie JM, Fitzgerald JF: Is esophagogastroduodenoscopy necessary in all caustic ingestions? J Pediatr Gastroenterol Nutr 32: 50, 2001. [PubMed: 11176325]

29. Celik B, Nadir A, Sahin E, Kaptanoglu M: Is esophagoscopy necessary for corrosive ingestion in adults? Dis Esophagus 22: 638, 2009. [PubMed: 19515187]

30. Ertekin C, Alimoglu O, Akyildiz H et al.: The results of caustic ingestions. Hepatogastroenterology 51: 1397, 2004. [PubMed: 15 362762]

31. Kaya M, Ozdemir T, Sayan A, Ar?kan A: The relationship between clinical findings and esophageal injury severity in children with corrosive agent ingestion. Ulus Travma Acil Cerrahi Derg 16: 537, 2010. [PubMed: 21153948]

32. Betalli P, Falchetti D, Giuliani S et al.: Caustic ingestion in children: is endoscopy always indicated? The results of an Italian multicenter observational study. Gastrointest Endosc 68: 434, 2008. [PubMed: 18448103]

33. Ryu HH, Jeung KW, Lee BK et al.: Caustic injury: can CT grading system enable prediction of esophageal stricture? Clin Toxicol 48: 137, 2010. [PubMed: 20199130]

34. Aviram G, Kessler A, Reif S et al.: Corrosive gastritis: sonographic findings in the acute phase and follow- up. Pediatr Radiol 27: 805, 1997. [PubMed: 9323246]

35. Christesen HB: Prediction of complications following unintentional caustic ingestion in children. Is endoscopy always necessary? Acta Paediatr Scand 84: 1177, 1995. [PubMed: 8563232]

36. Lamireau T, Rebouissoux L, Delphine D et al.: Accidental caustic ingestion in children: is endoscopy always mandatory? J Pediatr Gastroenterol Nutr 33: 81, 2001. [PubMed: 11479413]

37. Elshabrawi M, A-Kader HH: Caustic ingestion in children. Expert Rev Gastroenterol Hepatol 5: 637, 2011. [PubMed: 21910581]

38. Karagiozoglou-Lampoudi T, Agakidis CH, Chryssostomidou S, Arvanitidis K, Tsepis K: Conservative management of caustic substance ingestion in a pediatric department setting, short-term and long-term

15/21 8/7/2018 outcome. Dis Esophagus 24: 86, 2011. [PubMed: 20659141]

39. Zargar SA, Kochhar R, Mehta SK: The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc 37: 165, 1991. [PubMed: 2032601]

40. Arévalo-Silva C, Eliashar R, Wohlgelernter J et al.: Ingestion of caustic substances: a 15-year experience. Laryngoscope 116: 1422, 2006. [PubMed: 16885747]

41. Gün F, Abbasolu L, Celik A, Salman ET: Early and late term management in caustic ingestion in children: a 16-year experience. Acta Chir Belg 107: 49, 2007. [PubMed: 17405598]

42. Mamede RC, De Mello Filho FV: Treatment of caustic ingestion: an analysis of 239 cases. Dis Esophagus 15: 210, 2002. [PubMed: 1244 4992]

43. Cheng HT, Cheng CL, Lin CH et al.: Caustic ingestion in adults: the role of endoscopic classification in predicting outcome. BMC Gastroenterol 8: 31, 2008. [PubMed: 18655708]

44. Rigo GP, Camellini L, Azzolini F et al.: What is the utility of selected clinical and endoscopic parameters in predicting the risk of death aer caustic ingestion? Endoscopy 34: 304, 2002. [PubMed: 11932786]

45. Temiz A, Oguzkurt P, Ezer SS, Ince E, Hicsonmez A: Predictability of outcome of caustic ingestion by esophagogastroduodenoscopy in children. World J Gastroenterol 18: 1098, 2012. [PubMed: 22416185]

46. Cabral C, Chirica M, de Chaisemartin C et al.: Caustic injuries of the upper digestive tract: a population observational study. Surg Endosc 26: 214, 2012. [PubMed: 21858575]

47. Cheng HT, Cheng CL, Lin CH et al.: Caustic ingestion in adults: the role of endoscopic classification in predicting outcome. BMC Gastroenterol 8: 31, 2008. [PubMed: 18655708]

48. Chyka PA, Seger D, Krenzelok EP, Vale JA: American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Position paper: single-dose activated charcoal. Clin

16/21 8/7/2018 Toxicol 43: 61, 2005. [PubMed: 15822758]

49. [No authors listed]: Position paper: ipecac syrup. J Toxicol Clin Toxicol 42: 133, 2004. Review. Erratum in: J Toxicol Clin Toxicol 42: 1000, 2004. [PubMed: 15214617]

50. Penner GE: Acid ingestions—toxicology and treatment. Ann Emerg Med 9: 374, 1980. [PubMed: 7396252]

51. Homan CS, Maitra SR, Lane B et al.: Therapeutic eects of water and milk for acute injury of the esophagus. Ann Emerg Med 24: 14, 1994. [PubMed: 8010543]

52. Homan CS, Singer AJ, Henry MC et al.: Thermal eects of neutralization and water dilution for acute alkali exposures in canines. Acad Emerg Med 4: 27, 1997. [PubMed: 9110008]

53. Homan CS, Singer AJ, Thomajan C et al.: Thermal characteristics on neutralization therapy and water dilution for strong acid ingestion: an in-vivo canine model. Acad Emerg Med 5: 286, 1998. [PubMed: 9562189]

54. Anderson KD, Rouse T, Randolph JG: A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J Med 323: 637, 1990. [PubMed: 2200966]

55. Oakes DD: Reconsidering the diagnosis and treatment of patients following ingestion of liquid lye. J Clin Gastroenterol 21: 85, 1995. [PubMed: 8583091]

56. Karnak I, Tanyel FC, Büyükpamukçu N, Hiçsönmez A: Combined use of steroid, antibiotics and early bougienage against stricture formation following caustic esophageal burns. J Cardiovasc Surg (Torino) 40: 307, 1999. [PubMed: 1 0350123]

57. Howell JM, Dalsey WC, Hartsell FW et al.: Steroids for the treatment of corrosive esophageal injury: a statistical analysis of past studies. Am J Emerg Med 10: 421, 1992. [PubMed: 1642705]

58. Ulman I, Mutaf O: A critique of systemic steroids in the management of caustic esophageal burns in children. Eur J Pediatr Surg 8: 71, 1998. [PubMed: 9617603] 17/21 8/7/2018

59. Pelclová D, Navrátil T: Do corticosteroids prevent oesophageal stricture aer corrosive ingestion? Toxicol Rev 24: 125, 2005. [PubMed: 1618093 2]

60. Fulton JA, Homan RS: Steroids in second-degree caustic burns of the esophagus: a systematic pooled analysis of fiy years of human data: 1956–2006. Clin Tox 45: 402, 2007. [PubMed: 17486482]

61. Chibishev A, Pereska Z, Simonovska N, Chibisheva V, Glasnovic M, Chitkushev LT: Conservative therapeutic approach to corrosive poisonings in adults. J Gastrointest Surg 17: 1044, 2013. [PubMed: 23543337]

62. Wu MH, Lai WW: Surgical management of extensive corrosive injuries of the alimentary tract. Surg Gynecol Obstet 177: 12, 1995. [PubMed: 8322144]

63. Han Y, Cheng QS, Li XF, Wang XP: Surgical management of esophageal strictures aer caustic burns: a 30 years of experience. World J Gastroenterol 10: 2846, 2004. [PubMed: 15334683]

64. Keh SM, Onyekwelu N, McManus K, McGuigan J: Corrosive injury to upper gastrointestinal tract: still a major surgical dilemma. World J Gastroenterol 12: 5223, 2006. [PubMed: 16937538]

65. Zerbib P, Voisin B, Truant S et al.: The conservative management of severe caustic gastric injuries. Ann Surg 253: 684, 2011. [PubMed: 21475007]

66. Ceylan H, Ozokutan BH, Gündüz F, Gözen A: Gastric perforation aer corrosive ingestion. Pediatr Surg Int 27: 649, 2011. [PubMed: 2093647 7]

67. Robustelli U, Bellotti R, Scardi F et al.: Management of corrosive injuries of the upper gastrointestinal tract. Our experience in 58 patients. G Chir 32: 188, 2011. [PubMed: 21554849]

68. Chibisev A: Post-corrosive late complications in esophagus and stomach—role of the esophageal rest. Med Arh 64: 320, 2010. [PubMed: 21218746]

18/21 8/7/2018

69. Sánchez-Ramírez CA, Larrosa-Haro A, Vásquez Garibay EM, Larios-Arceo F: Caustic ingestion and oesophageal damage in children: clinical spectrum and feeding practices. J Paediatr Child Health 47: 378, 2011. [PubM ed: 21309879]

70. Doo EY, Shin JH, Kim JH, Song HY: Oesophageal strictures caused by the ingestion of corrosive agents: eectiveness of balloon dilatation in children. Clin Radiol 64: 265, 2009. [PubMed: 19185656]

71. Hosseini SM, Sabet B, Falahi S, Zarenezhad M: Our experience with caustic oesophageal burn in South of Iran. Afri J Paed Surg 8: 306, 2011. [PubMed: 22248896]

72. Broor SL, Kumar A, Chari ST et al.: Corrosive oesophageal strictures following acid ingestion: clinical profile and results of endoscopic dilatation. J Gastroenterol Hepatol 4: 55, 1989. [PubMed: 2490943]

73. Atabek C, Surer I, Demirbag S et al.: Increasing tendency in caustic esophageal burns and long-term polytetrafluorethylene stenting in severe cases: 10 years experience. J Pediatr Surg 42: 636, 2007. [PubMed: 17448758]

74. Berkovits RN, Bos CE, Wijburg FA, Holzki J: Caustic injury of the oesophagus: sixteen years experience, and introduction of a new model oesophageal stent. J Laryngol Otol 110: 1041, 1996. [PubMed: 8944879]

75. Kochhar R, Poornachandra KS, Puri P et al.: Comparative evaluation of nasoenteral feeding and jejunostomy feeding in acute corrosive injury: a retrospective analysis. Gastrointest Endosc 70: 874, 2009. [PubMed: 19573868]

76. Kaygusuz I, Celik O, Ozkaya OO et al.: Eects of interferon-alpha-2b and octreotide on healing of esophageal corrosive burns. Laryngoscope 111: 1999, 2001. [PubMed: 11801986]

77. Chang JM, Liu NJ, Pai BC et al.: The role of age in predicting the outcome of caustic ingestion in adults: a retrospective analysis. BMC Gastroenterol 11: 72, 2011. [PubMed: 21672200]

78. Uygun I, Aydogdu B, Okur MH et al.: Clinico-epidemiological study of caustic substance ingestion accidents in children in Anatolia: the DROOL score as a new prognostic tool. Acta Chir Belg 112: 346, 2012. [PubMed: 23175922]

19/21 8/7/2018

79. Zhang X, Wang M, Han H, Xu Y, Shi Z, Ma G: Corrosive induced carcinoma of esophagus aer 58 years. Ann Thorac Surg 94: 2103, 2012. [PubMed: 23176921]

80. Okonta KE, Tettey M, Abubakar U: In patients with corrosive oesophageal stricture for surgery, is oesophagectomy rather than bypass necessary to reduce the risk of oesophageal malignancy? Interact Cardiovasc Thorac Surg 15: 713, 2012. [PubMed: 22821650]

81. Centers for Disease Control and Prevention (CDC): Health hazards associated with laundry detergent pods–United States, May-June 2012. MMWR Morb Mortal Wkly Rep 61: 825, 2012. [PubMed: 23076090]

82. Fraser L, Wynne D, Clement WA, Davidson M, Kubba H: Liquid detergent capsule ingestion in children: an increasing trend. Arch Dis Child 97: 1007, 2012. [PubMed: 22956626]

83. Forrester MB: Comparison of pediatric exposures to concentrated “pack” and traditional laundry detergents. Pediatr Emerg Care 29: 482, 2013. [PubMed: 23528511]

84. Beuhler MC, Gala PK, Wolfe HA, Meaney PA, Henretig FM: Laundry detergent “pod” ingestions: a case series and discussion of recent literature. Pediatr Emerg Care 29: 743, 2013. [PubMed: 23736069]

85. Schneir AB, Rentmeester L, Clark RF, Cantrell FL: Toxicity following laundry detergent pod ingestion. Pediatr Emerg Care 29: 741, 2013. [PubMed: 23736068]

USEFUL WEB RESOURCES

Agency for Toxic Substances & Disease Registry—http://www.atsdr.cdc.gov/index.html

American Association of Poison Control Centers (AAPC)—http://www.aapcc.org/DNN

American Academy of Clinical Toxicology (AACT)—http://www.clintox.org/index.cfm

Asia Pacific Association of Medical Toxicology (APAMT)—http://www.asiatox.org

European Association of Poisons Centres and Clinical Toxicologists (EAPCCT)—http://www.eapcct.org 20/21 8/7/2018

South Asian Clinical Toxicology Research Collaboration (SACTRC)—http://www.sactrc.org

TOXBASE: The primary clinical toxicology database of the National Poisons Information Service— http://www.toxbase.org

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