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Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e >

Chapter 200: Caustic IngestionsNicole 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 challengesto exposure prevention and patient care include relative lack of childproof containers, easy and unregulatedaccess 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, o�en occupational or industrial contact exposures. The majority ofreported 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 di�icult 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 o�en lessconcentrated forms of industrial strength cleansers.

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TABLE 200-1

Common Caustic Compounds

Alkali Found in

Sodium hydroxide Industrial chemicals, drain openers, oven cleaners

Potassium

hydroxide

Drain openers, batteries

Calcium hydroxide Cement, hair relaxers, and 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

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

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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 tocause significant injuries at a pH <3 and alkalis at a pH >11. The physical properties of the productformulation (i.e., liquid, gel, granular, or solid) can influence the nature of the contact with the tissue.Following ingestion, solid or granular caustics o�en injure the oropharynx and proximal esophagus, whereasliquid alkali ingestions are characterized by more extensive esophageal and gastric injuries. TitraTable acid oralkaline 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 whitishexudates, 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 mucosalinjury, tissue remodeling occurs over roughly 2 months. In mild cases, normal esophageal function isrestored, but in severe cases, dense scar tissue forms, resulting in stricture formation. Esophageal stricturesare a source of significant morbidity and may require long-term treatments with dilations, stenting, orsurgery. Early phases of remodeling, particularly days 2 to 14, are associated with increased tissue friabilityand higher risk of perforation, both spontaneous and iatrogenic.

ALKALI INJURIES

Following caustic alkali exposures, the hydroxide ion easily penetrates tissues, causing immediate cellulardestruction via protein denaturation and lipid saponification. This is followed by thrombosis of localmicrovasculature that leads to further tissue necrosis. Alkali injuries induce a deep tissue injury calledliquefaction necrosis. Severe intentional alkali ingestion may cause deep penetration into surroundingtissues with resultant multisystem organ injuries, including esophageal injury, gastric perforation, andnecrosis of abdominal and mediastinal structures. Severe injuries to the pancreas, gallbladder, smallintestine, and mediastinum a�er intentional ingestion have been reported. Solid alkali ingestions, such assome lye preparations, have a greater potential for oropharyngeal and proximal esophageal tract injury andless for distal injury.

The most common household alkali is bleach, a 3% to 6% sodium hypochlorite solution with a pH ofapproximately 11. Household liquid bleach is minimally corrosive to the esophagus and rarely causessignificant 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 industrialstrength bleach containing much higher concentrations of sodium hypochlorite may result in gastric andesophageal necrosis. Bleach ingestion may cause emesis secondary to gastric irritation and/or pneumonitisa�er 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 anionspenetrate tissues, leading to cell death and eschar formation. This process is believed to limit continuedhydrogen 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 wereesophagus-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 tissuedestruction, strong acid ingestion results in high-grade gastric injuries (secondary to pylorospasm andpooling) and a higher mortality rate compared with strong alkali ingestions. Acid ingestion is sometimescomplicated 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 HydrofluoricAcid).

CLINICAL FEATURES

The cardinal features of caustic ingestion are a chemical burn to the oral mucosa,19 sometimes associatedwith chemical burns to the skin or eyes from splashes or dribbling (see chapters 217, Chemical Burns and241, Eye Emergencies). Pharyngeal burns from ingestion produce pain, odynophagia, drooling, and vocalhoarseness. Dyspnea may be caused by edema of the upper airway, aspiration of the caustic substance intothe 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 tothe anterior structures of the eye.

HISTORY

The key priority is rapid airway assessment and stabilization. Following that, obtain a directed history todetermine the type and amount of caustic ingested and the presence of coingestants. Determine if theingestion 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 chestare called "dribble burns" (Figure 200-2).

FIGURE 200-1.

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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 a�er pediatric unintentional ingestions

has been the focus of many studies.5,25-27,29,31,32 Although serious esophageal injury can occur in theabsence of oral burns, essentially all children with serious esophageal injuries (grade 2 or 3) a�er accidental

caustic ingestion have some initial sign or symptom, such as stridor, drooling, or vomiting.26,27,29 Pain aloneis an inconsistent predictor of severity of injury, and pain may be absent initially and early in the clinicalcourse.

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 viscousperforation. Consider mediastinitis in patients complaining of chest discomfort, and palpate the chest walland neck for signs of subcutaneous emphysema. Inspect the eyes for ocular burns and the skin for splashand dribble burns.

LABORATORY TESTING

For children who accidentally ingest common household alkalis (e.g., bleach) or acids (e.g., toilet bowlcleaner), the need for ancillary testing is only necessary in patients with signs or symptoms of significantinjury: drooling, respiratory distress, or vomiting. For an intentional ingestion, or one from a strong acid or

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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 causean anion gap acidosis based on lactate production due to direct tissue injury or shock. Strong acid ingestionsmay be associated with both severe anion gap (e.g., sulfuric acid) and nongap acidoses (e.g., hydrochloricacid). Obtain acetaminophen and salicylate levels to screen for potential coingestants in suicidal patients. AnECG is indicated following a hydrofluoric acid exposure to check for QT-interval prolongation fromhypocalcemia.

IMAGING

Obtain a chest radiograph in patients with chest pain, dyspnea, or vomiting to check for peritoneal andmediastinal air. Thoracoabdominal CT scanning is useful to assess for esophageal injury a�er ingestion ofstrong caustics or if intra-abdominal perforated viscus is suspected. Endoscopy is the gold standard foridentifying the severity of esophageal injury. IV and oral contrast-enhanced CT scanning is an alternativewhen 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 withsubsequent endoscopic visualization, it is best to discuss the need for oral contrast administration with theendoscopist 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 a�er 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 becauseingestions 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 clinicalfindings 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 a�er unintentional caustic ingestions in adults andchildren 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 guidetreatment, and predicts future morbidity (Table 200-2). Early endoscopy is safe and may decrease the timethat patients will be without nutritional support. This is particularly important in children with low glycogenstores and in high-grade injuries, where caloric requirements will be high.

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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 and 3 Esophageal Injuries

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 support via

nasogastric, orogastric, or

percutaneous feeding tube

or

Total parenteral nutrition

Initiate early percutaneous feeding

tube

or

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

Tissue friability a�er a caustic burn increases significantly at 24 to 48 hours a�er injury and is maximalbetween days 5 and 14. Most experts agree that endoscopy should be performed early a�er ingestion, ideally

<12 hours and not >24 hours a�er ingestion to avoid iatrogenic perforation.36,47 Traditionally, endoscopistshave terminated their examination at the first sign of severe esophageal injury (grade 2B or 3). Experiencedoperators using smaller, flexible endoscopes with minimal insu�lation of air can decrease the incidence ofperforation, permitting more distal visualization documenting all injuries to the esophagus, stomach, andduodenum.

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 airwaymanagement precedes patient decontamination, prevent exposure to the ED sta�. Caustic airway injuries are

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di�icult airways. Ideally, patients with potential airway injuries should have fiberoptic evaluation of theairway before intubation to determine the extent of the damage, but this may not always be possible. Blindnasotracheal intubation is contraindicated due to the potential for exacerbating airway injuries. Oralintubation with direct visualization is the first choice for definitive airway management. For potential airwaycompromise, establish a secure endotracheal airway early rather than risk greater di�iculty later whensecondary e�ects of injury, such as edema, complicate the situation. Cricothyrotomy may be needed iforopharyngeal edema, tissue friability, and bleeding make intubation di�icult or impossible.

Avoid laryngeal mask airways, combination tubes with pharyngeal and tracheal balloons, retrogradeintubation, 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 continuedcaustic 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 andsoap (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. Charcoaldoes 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 Ipecacsyrup 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 a�er endoscopic evaluation. With high-grade esophagealburns, 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, aswell as metabolic disarray from acid-base derangements, can lead to shock. Central venous access may berequired 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 decreasestricture formation a�er caustic ingestion, and animal models have suggested benefit. However, individual

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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 betweengrade 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 a�er causticingestions 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 Becausesteroids 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 evaluationfor 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, respiratorydistress, 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 di�icult 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 appliedto optimize the patient's hemodynamics. Acute lung injury (noncardiogenic pulmonary edema) may followcaustic ingestions as a complication of local or systemic e�ects.

NUTRITIONAL SUPPORT

Nutritional support is o�en necessary following a severe caustic injury to the esophagus or stomach. Supportcan be achieved by percutaneous (usually jejunostomy) feeding, nasoenteral feeding, or total parenteral

nutrition.61,75

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EXPERIMENTAL THERAPIES

Animal experiments have found that drugs a�ecting collagen deposition, including interferon-α-2b,

octreotide, β-aminopropionitrile, colchicine, N-acetylcysteine, and d-penicillamine,9,76 can prevent

esophageal strictures a�er caustic alkali ingestion. Pentoxifylline, a local inflammatory and microcirculationmediator, 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 agentshave been evaluated in controlled human clinical trials, and no specific recommendation can be made

regarding their use. H2 blockers and proton pump inhibitors are o�en used in the treatment protocol,61 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 Mostlong-term sequelae from caustic exposure are related to injuries to the GI tract. Acid ingestions may scar thepylorus 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, severeoropharyngeal burns, and persistent fever correlate with the development of esophageal stricture a�er

accidental caustic ingestion in children.78

Patients with grade 3 caustic injuries to the esophagus have about a 1000-times increased risk for squamouscell cancer of the esophagus that can occur decades a�er the initial ingestion and resulting esophageal

injury.79 Because cancer can develop if a portion of the esophagus remains a�er 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 fromhospital a�er endoscopy, provided they can tolerate oral fluids and food. Grade 2A injuries warranthospitalization 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 theregional poison control center for data collection purposes and assistance with management.

SPECIAL CONSIDERATIONS

LAUNDRY DETERGENT POD INGESTIONS

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1. 

2. 

3. 

4. 

5. 

6. 

Laundry 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 concentrateddetergent within a dissolvable plastic membrane. An individual pod may have internal chambers thatcontain a stain remover and brightener separate from the detergent. Exposure to the concentratedpreparation in these pods is more likely to produce symptoms than exposure to traditional laundry detergent

products.83

Dermal or ocular exposure to the contents can produce irritation of the skin, conjunctiva, or cornea. Ingestionby 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 di�iculty swallowing with drooling and aspiration during recovery.85 Treatment issupportive with airway protection and mechanical ventilation. In severe cases, ventilation may be requiredfor days.

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

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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

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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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