Ofcial reprint from UpToDate

www.uptodate.com 2016 UpToDate

Caustic esophageal injury in children

Author: Douglas S Fishman, MD
Section Editor: Craig Jensen, MD
Deputy Editor: Alison G Hoppin, MD

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through:Nov 2016.|This topic last updated:Nov 30, 2016.
INTRODUCTIONAccidental ingestion of caustic agents continuesot be a major concern for pediatric emergency
department clinicians. Caustic ingestions are seen most often in young children between one and three years of
age, and can cause severe acute injury and long-term complications, especially the de
velopment of esophageal
strictures [1-5].
The evaluation and management of a child with suspected ingestion of a caustic su
bstance is described here.
Caustic esophageal injury in adults is discussed separately. (See "Caustic esophageal injury in adults".)
EPIDEMIOLOGYThe National Poison Data System(NPDS) compiles data annually from a population of
approximately 300 million people served by the American Association of Poison Control Centers (AAPCC). In 2014,
2.1 million toxic exposures in humans were reported in the United States, of which 48 percent occurred in children
ve years or younger [6]. The most commonly ingested caustic substances wer
e household cleaning products
(particularly household bleach), which accounted for 11 per
cent of the toxic ingestions in young children [6]. Caustic
ingestion is most common in young children between one and three years of age [7], with boys accounting for 50 to
62 percent of cases [4,5].
Most ingestions by children are accidental and the amounts ingested tend ot be small. The opposite is the case in
adolescents and adults, in whom ingestion often is deliber
ate and related to attempted suicide [8,9]. In such cases,
the amount ingested may be large and the injury to the esophagus and stomach often severe [10]. Cases of alkali
ingestion as a result of child abuse have been reported [11,12].
TYPES OF CAUSTIC SUBSTANCESA substance is caustic if it is capable of burning or corr
oding organic tissue
by chemical action, typically due ot strong acid or alkaline properties.
Common caustic ingestions are of household cleaning products, including household bleach, oven and drain
cleaners, which are strong lyes that contain sodium and potassium hydroxides [1,7,13]. Other common cleaning
products include laundry and dishwasher detergents, and cleaning agents withsodium phosphate, sodium
carbonate, and ammonia 2
[ ,3,14]. Other caustic ingestions include cosmetic pr
oducts such as hair relaxer,
swimming pool products, and toilet bowl cleaners [6]. Alkaline agents are more commonly ingested compared with
acidic agents.
PATHOPHYSIOLOGY
Acid versus alkaliAlkalis and acids produce tissue injury by different mechanisms:
Alkali Alkaline agents tend to cause esophageal injury if the pH is above 11.5-12.5 [15,16], via liquefaction
necrosis [17]. This type of injury leads to early disintegration of the mucosa, allowing deep penetration and
even perforation [18,19]. Penetration into the esophageal wall by alkaline agents varies with the concentration
and the length of time the agent er mains in contact with the mucosa 2[ 0]. Experimentally, a 10 percent solution

of sodium hydroxide (lye) may require as long as one minute of contact o

t produce a deep burn, whereas a 30
percent sodium hydroxide can cause transmural esophageal necrosis within one second of contact [13]. In
animal experiments, even weakly concentrated alkaline agents (eg, 1.8 percent sodium hydroxide) can produce
supercial necrosis if left in contact with the mucosa for one hour20].
[
Acids Acids or corrosive agents tend to cause esophageal injury if the pH is less than 2, via coagulation
necrosis. As compared with alkali agents,esophageal injury from acids tend to be attenuated and perforation is
less common because the coagulum that forms on the mucosal sur
face may limit deeper penetration of the
caustic substance [18]. The alkaline pH and squamous epithelium of the esophagus also help limit the se
verity
of esophageal injury from acids. Despite these mitigating factors, 6 to 20 percent of acid ingestions result in
esophageal burns [4,19,21,22]. Upper airway injuries also are common with ingestion of acids 1
[ 8]. (See 'Airway
injury' below.)
Delayed injuryFollowing the initial necrosis (whether caused by alkali or acid), additional destruction tak
es place
over the rst week caused by inflammation and vascular thrombosis (table 1) [23,24]. By 10 days there is formation
of granulation tissue and weakening of the esophageal wall. During this early period, the esophagus is incr
easingly
vulnerable to perforation [7,25]. By three weeks, brogenesis and stricture formation are well under way, and
perforation is less likely.
RISKS OF SPECIFIC SUBSTANCESThe risk and severity of injury is affected by the corrosive properties of the
ingested substance (eg, the pH) (see'Acid versus alkali' above), but also by the amount, concentration, and physical
form of the agent (eg, solid or liquid), and the dur
ation of contact with the mucosa. The appr
oximate pH of various
cleaning products are shown in the gure (gure 1).
Esophageal injuryEsophageal burns account for most of the serious injuries and leadsotthe chronic
complications associated with ot xic ingestions, and have been reported in 18 to 46 percent of caustic ingestions in
children [7,21,26-30]. Injury to the lips, oropharynx, and upper airway also may occur.
The likelihood of esophageal injury depends in part on the substance ingested:
Standard liquid household detergents, phosphates, and bleaches have pHs ranging from 9 to 11, and rarely
cause serious injuries unless taken in large amounts [7,31]. However, concentrated forms of laundry or
dishwasher detergent are increasingly available and are much more likely to cause esophageal injury. In
particular, concentrated laundry detergent packaged into single-use packets ("capsules," "gel packs," or "pods")
has caused multiple cases of esophageal injur
y and airway compromise [32-35]. These products typically are
small and colorful, looking somewhat like candy. In 2012, the AAPCC issued asafety warning about this new
type of product [36].
Household bleaches are relatively common ingestions, but a
r rely cause esophageal burns. These are typically
composed of about 5 percent sodium hypochlorite and have a pH of approximately 11, which is below the pH
threshold of 11.5 to 12.5 that tends to cause esophageal injury [3,15,18]. When burns do occur with these
agents, they tend to be mild and do not require treatment [15,19,37]. Industrial strength bleaches or household
bleaches from other countries may be much more corrosive because of a higher concentration of sodium
hypochlorite [15].
Button batteries lodged in the esophagus can apidly
r
cause injury to the esophagus and critical surrounding
structures, in part due to leakage of alkaline material. This issue is discussed in a separ
ate topic review. (See
"Button and cylindrical battery ingestion".)
Cosmetic products such as hair relaxers are ingested commonly, but they appear to be rare causes of
esophageal injury [38,39]. In one review of 29 patients with hair er laxer ingestions who underwent upper
endoscopy, 6 patients (20 percent) had esophageal mucosal injury and 5 patients (17 percent) had gastric

mucosal injury, but these injuries were limited to grade 1 (supercial) injuries 4[ 0]. Wart or callus removers
containing salicylic acid have caused esophageal injury and scarring in case reports; the colloid suspension is
viscous, which likely contributes to the injury by prolonging contact with the mucosa 41,42].
[
Common acid household products include toilet bowl cleaners, battery fluids, and muriatic (hydrochloric) acid
used in swimming pools 2
[ ,43]. Children living on farms may be at particularly high risk for incurring serious
burns because industrial-strength agents are more commonly used in this setting 44].
[
Solid caustic materials, which tend ot adhere to the mucosa, can produce deep burns of the oral cavity and
esophagus [19], but they are less likely to reach the stomach [45]. The immediate and severe pain produced by
these products may limit the amount ingested and thus lessen the extent of injur
y [16]. Powdered or granular
detergents tend to injure the upper airway; esophageal injury is less common but has been reported [16,35,46].
(See 'Airway injury' below.)
Gastric injuryThe incidence and severity of gastric lesions in caustic ingestion ha
ve not been described
extensively, in part because this type of injury is less common than esophageal injury. In addition, older reports may
have underestimated the presence of gastric injury because of the use of rigid endoscopes that frequently were not
advanced beyond the rst visible esophageal burn 37].
[ In a review in which flexible endoscopeswere used to
evaluate 156 children with caustic ingestion, 11 percent had both esophageal and gastric burns, and 9 per
cent had
gastric burns only [30].
Among patients with alkaline ingestions, gastric injur
y is most common in those who ingest relatively large volumes
(200 to 300 mL); in one series of such patients, gastric injur
y was seen in more than 80 percent [10]. Large
ingestions have resulted in gastric perforation, hemorrhage, and death from erosion into a bronchial vein [19].
Gastric injury often is most severe with acids, such as sulfuric acid, which trigger antr
al spasm, leading to pooling of
acid in the antrum, which may cause severe burns in the prepyloric area and result in pyloric obstruction [19]. In a
review of 98 children with ingestion of acid substances, 8 (8.2 per
cent) developed gastric outlet obstruction at a
mean of 27 days after ingestion, necessitating gastrojejunostomy [47]. In a smaller series of 20 patients with gastric
outlet obstruction, two also had esophageal strictur
es [48]. Duodenal erosions have been reported in occasional
cases [10]. (See 'Pyloric stenosis' below.)
Airway injuryUpper airway injuries are more common with ingestion of acids, perhaps elated
r
to their bad taste,
which tends to stimulate gagging, choking, and attemptsot spit out the ingested material 18].
[ Powdered or granular
detergents also tend to injure the upper airway, resulting in stridor and epiglottitis.
CLINICAL MANIFESTATIONSThe clinical features of caustic ingestions vary widely. Early signs and/or symptoms
may not correlate with the severity and extent of tissue injury, particularly in young children.
The following symptoms are common after a caustic ingestion:
Gastrointestinal tract injury
The most common symptom is dysphagia which can occur even with mild esophageal injury [4]. This
symptom may be caused by loss of esophageal motility during the acute phase of injur
y [49], similar to
what is seen in peptic esophagitis 50,51].
[
Esophageal dysmotility and prolonged esophageal transit time
may persist for several weeks following severe esophageal burns. Persistent dysphagia also may be
caused by brosis of deeper muscle layers, with or without stricture formation [49]. Fibrosis alone
produces a decrease in the amplitude of esophageal contractions and elevated basal pressure. (See
"Evaluation of dysphagia in children".)

 Patients may also present with drooling, retrosternal or abdominal pain, hematemesis. Deep esophageal
burns can be complicated by esophageal perforation, which can cause mediastinitis and the de
velopment
of a tracheoesophageal stula 1
[ 8].
Upper airway injury Symptoms suggesting upper airway injury include stridor, hoarseness, nasal flaring, and
retractions. Such symptoms suggest injury to the epiglottis, which can be severe, especially in children younger
than two years of age, and may require emergency intubation or tracheotomy [16,52]. Although symptoms of
upper airway injury usually begin rapidly after contact with caustic agents, ther
e may be a one- to two-hour
delay with ingestion of powdered agents [16]. Occasionally, the clinical presentation may mimic anaphylaxis,
leading to misdiagnosis if the history of caustic ingestion is not e
r vealed [53].
The presence or absence of any of the clinical features described above does not reliably predict ingestion or the
presence or severity of esophageal or gastric burns. In a single series of 378 caustic ingestions in childr
en, 12
percent had no symptoms but had severe esophageal burns, whereas 82 percent who were symptomatic at
presentation had minimal or no esophageal involvement [4]. The presence or absence of oral lesions also is a poor
predictor of esophageal injury. In a review of multiple case series o
t taling 489 children, 45 percent without oral
burns had esophageal burns, and 54 per
cent with oral burns had accompanying esophageal burns37].
[
INITIAL EVALUATIONDiagnostic evaluation and management of a patient with a known or suspected cau
stic
ingestion depends on whether the patient is sympt
omatic, tempered by the type of agent ingested.
History and examinationThe history should seek to establish the timing of the exposure, including whether it was
directly observed by a caretaker, and an estimation of the amount of the substance ingested. When possible, the
exact type and brand of substance ingested should be identied, and the pH measur
ed or determined from the
material safety data sheets or poison control center.
The physical examination includes apid
r
evaluation of mental status, vital signs, andpupils to evaluate for central
nervous system excitation or depression. The patient should be closely evaluated for respiratory compromise,
including the presence or absence of stridor, hoarseness, nasal flaring, e
r tractions, and wheezing. Drooling, food
refusal or complaints of dysphagia sugge
st oropharyngeal or esophageal injury. The lips and oropharynx should be
inspected for burns (picture 1). However, the presence or absence of oral burns is a poor predictor of esophageal
injury, as noted above.
Signs that suggest the possibility of esophageal per
foration include persistent severe retrosternal or back pain,
especially if fever is present suggesting mediastinitis. Localized severe abdominal tenderness, rebound, and rigidity
suggest the possibility of gastric perforation with peritonitis.
Other considerations that should be explored by the history and examination include:
The possibility of toxic effects in addition to the potential caustic injury, which depends on the nature of the
substance ingested. (See"Approach to the child with occult toxic exposure".)
The possibility that the ingestion was intentional (eg, suicide attempt or child abuse)
11].
[
The possibility of multiple ingestions in the same individual. This is mor
e likely for those in whom the exposure
was intentional (eg, adolescents or victims of child abuse).
ImagingA chest radiograph is appropriate in any patient with e
r spiratory symptoms. The goal is to evaluate for
other possible causes of the er spiratory symptoms (including foreign body or pneumonia), as well as for possible
complications of the caustic ingestion, such as esophageal or gastric per
foration. Signs of perforation include
pneumomediastinum mediastinal widening, subcutaneous emphysema in the neck, pleur
al effusions, hydrothorax,

hydropneumothorax, or subdiaphragmatic air. A chest radiograph generally is not necessary in asymptomatic

patients.
Radiologic contrast studies (upper gastrointestinal series) generally are not valuable in the initial stages of the
evaluation because they are unreliable in detecting acute injury or in predicting stricture formation [8,54]. Contrast
studies may be appropriate in the initial stages in selected patients in whom ther
e is a clinical suspicion of
esophageal perforation based on ndings from plain radiography or endoscopy [55]; in this case, only water-soluble
contrast should be used, rather than barium.
Computed tomography (CT) or magnetic resonance (MR) angiography is sometimes needed to evaluate patients for
the possibility of esophageal perforation with erosion into vascular structures, including an aortoesophageal stula.
A few cases of life-threatening or fatal hemorrhage have been reported, most of which were caused by button
battery ingestion and presented with a sentinel bleed (hematemesis or melena) up ot two weeks after removal of
the battery [56]. (See "Button and cylindrical battery ingestion", section on 'Esophageal impaction'.)
INITIAL MANAGEMENT
Stabilization and supportive careThe initial step in management of caustic ingestion is suppor
tive care and
close observation with an emphasis on preventing vomiting, choking, and aspiration (algorithm 1). The induction of
vomiting is contraindicated because vomiting may lead to additional esophageal injury if gastric contents come in
contact with the esophageal mucosa 37].
[ Similarly, attempts to dilute or neutralize the caustic agent, administration
of activated charcoal, or gastric lavage are not recommended.
The use of neutralizing agents is not recommended because of concern about additional damage om
fr heat
injury during the neutralization process [57].
The use of diluting agents, such as milk or water
, is not recommended because of safety considerations and
lack of efcacy. The safety concern is that ingestion of a large volume of a diluting agent can induce vomiting,
potentially leading to further complications. In the presence of acute airway swelling and obstruction, diluting
agents clearly are contraindicated [37]. In addition, the amount of milk or other fluids that would be necessar
y
to signicantly dilute a caustic agent is oo
t large to make such therapy practical.
Administration of activated charcoal generally is not recommended for children who have ingested acidic or
alkaline corrosives (eg, sodium or potassium hydroxide, or hydrochloric or sulfuric acid). This is because
charcoal will obstruct the view of the endoscopist and because these small, highly ioniz
ed chemicals are poorly
absorbed by charcoal. (See "Gastrointestinal decontamination of the poisoned patient", section on
'Contraindications'.)
Diagnostic evaluation and management depends on whether the patient is sympt
omatic, tempered by the type of
agent ingested.
Asymptomatic patientsPatients who are asymptomatic (no evidence of oral lesions, and no dysphagia, vomiting,
or other symptoms), should be observed for several hours to monitor fluid intake and overall status (algorithm 1)
[4,5,58]. The observation period is particularly important for children who may have ingested a powdered caustic
agent, for which the effects may be delayed by several hours after the ingestion. If the patient emains
r
asymptomatic with normal swallowingand if the suspected substance is known ot be of low causticity (eg,
household bleach), or if it is unclear from the history whether the patient ingested acaustic substance, then the
patient is at low risk for complications and endoscop
y usually is unnecessary [21,26,37,59,60]. By contrast,
endoscopy is appropriate for patients whoare suspected to have ingested a more caustic substance (eg, drain
cleaner) or substance of questionable causticity
, even if they are asymptomatic. This is because the presence or
absence of symptoms in young children is not a reliable predictor of injury [28,30].

Symptomatic patientsPatients with symptoms should be admitted to the hospital and closely monitored. Those
with signicant airway compromise (stridor or retractions) may require intensive care, endotracheal intubation,
and/or tracheostomy. All patients with symptoms also should be evaluated with upper endoscopy, to evaluate the
extent of the injury, unless endoscopy is contraindicated because of respiratory compromise (algorithm 1).
Endoscopic evaluationUpper endoscopy should be performed in all patients who are symptomatic, who have oral
burns, or are known to have ingested a substance with a high risk of esophageal injur
y. The endoscopy ideally
should be performed within 24 hours of the ingestion ot evaluate the extent of injury, predict prognosis, and guide
management [28,30,61,62]. While there is little data to determine the ideal timing of endoscopy, very early
endoscopy (eg, less than six hours after the ingestion) may not show the full extent of the injury, and endoscopy
after four days increases the risk of perforation [7,18,28,30,59,61]. Endoscopy is contraindicated in patientswho are
hemodynamically unstable, have severe respiratory distress or evidence of perforation on imaging (see'Imaging'
above), or exhibit severe oropharyngeal or glottic edema and necrosis.
If the endoscopy demonstrates signicant esophageal burns (grade 2A or higher (table 2)), we suggest follow-up
evaluation with barium contrast studies two to three weeks post ingestion, even if the patient is asymptomatic
(algorithm 1). Alternatively, it is reasonable to manage asymptomatic patients with close clinical follow-up and
perform a contrast study only if they develop symptoms suggestive of a stricture (see 'Stricture formation' below).
Collaboration with otolaryngology to evaluate the airway may be needed, dependingon the symptoms.
Flexible video endoscopes are typically used for this evaluation. Unless the esophageal burns are very severe
(raising concerns about perforation), it is important to pass the endoscope beyond the rst burn and into the
stomach, to fully evaluate the extent of injury (picture 2A-B) [7,10,28,30]. The endoscopist should specically
observe the vocal cords to evaluate for airway injury. Flexible endoscopy may be performed under conscious
(intravenous) sedation in many patients, but gener
al anesthesia should be used forthose with severe burns or with
upper airway signs or symptoms [14]. Rigid endoscopes are still used in somecenters, but because they are
associated with higher risks of perforation as compared with flexible endoscopes, they usually are not advanced
beyond the rst signicant esophageal burn, which limits their diagnostic utility30].
[
StagingA grading system for esophageal injury helps to predict clinical outcomes and guide management
(table 2). Grading should be documented in operative note to assist in follow-up assessments.
The most widely used grading system was developed based upon a study of 81 patients (primarily adults) with
corrosive ingestion, and is a modication of classication schemes used for cutane
ous burns [61]. This grading
scheme is widely used in adults, although ew
f studies have examined its validity.
Grade 0 Normal mucosa
Grade 1 (supercial) Mucosal edema and hyper
emia
Grade 2 (transmucosal) Friability, hemorrhages, erosions, blisters, whitish membranes, and supercial
ulcerations
Grade 2A No deep focal or circumferential ulcers
Grade 2B With deep focal or circumferential ulcers
Grade 3 Areas of multiple ulceration and areas of brown-black or greyish discoloration suggesting necrosis
Grade 3A Small scattered areas of focal necrosis
Grade 3B Extensive necrosis
Nasogastric tubeIn patients in whom endoscopy reveals extensive circumferential burns (grade 2B or 3 using the
system above), a nasogastric tube (NGT) should be placed under dir
ect visualization during the endoscopic

procedure. A NGT should not be inserted blindly because perforation or additional injury can occur while passing the
tube.
The NGT can provide a route for nutritional support during the healing phase and help maintain a lumen during
stricture formation. It also can serve as a guide for esophageal dilation 63].
[ There is no need to put the NGT to
suction, unless a patient has nausea, vomiting or concern for obstruction or perit
onitis. (See 'History and
examination' above.)
Gastrostomy tubeIn patients with severe extensive esophageal burns, consideration should be given to
placement of a gastrostomy during or shortly after the initial endoscopic evaluation. A gastrostomy can be used for
feeding and also for retrograde dilation of strictures. If retrograde dilation is anticipated, a string can be placed fr
om
the nose to the gastrostomy, which is used to guide the dilators. Unlike an NGT, which can be pulled out
inadvertently and may be impossible to replace, a string is less likely to be pulled out.
MedicationIt is common practice to give antibiotics prophylactically to selected patients with caustic esophageal
injury, but there are no clear standards or studies to guide patient selection. In our practice, we administer
antibiotics for patients with suspicion of per
foration on chest radiograph or endoscopy, and for those with grade 3
burns (endoscopic evidence of necrosis). We use a third-generation cephalosporin.
We do not recommend treatment with glucocorticoids for patients with caustic esophageal injuries, but ther
e is
ongoing study in this area. Although earlystudies in animals suggested that glucocor
ticoids prevented esophageal
scarring [17,64,65], studies in humans have shown no benet and possible harm. As an example, in arandomized
trial in children, administration of glucocorticoids had no effect on strictures, which developed in 20 to 38 percent of
documented esophageal burns, er gardless of treatment [28]. This is particularly true for patients with third-degree
burns, in whom stricture formation appears to be inevitable regardless of therapy. In addition, perforation is also
common in such patients, the presentation of which can be masked by glucocorticoids [19]. Similar conclusions
were reached by systematic reviews of patients with grade 2 or 3 burns [66,67]. Contrasting results were found in a
randomized trial of methylprednisolone (1 g/1.73 m2 for three days) versus placebo in 83 children with grade 2B
esophageal injuries [68]. Subjects in both groups were also treated with ceftriaxone and ranitidine. Rates of stricture
development were lower in the glucocorticoid-treated group (14.3 versus 45 percent, as assessed by radiography,
and 10.8 versus 30 percent as assessed by endoscopy). These ndings suggest a possible benet of a brief course
of high-dose corticosteroids in the subset of patients with deep focal or cir
cumferential ulcers (grade 2B). However,
because these ndings contrast with the results of several previous trials, additional research is needed to clarify
the role of glucocorticoids in patients with caustic esophageal injur
y. (See "Caustic esophageal injury in adults",
section on 'Esophageal strictures'.)
LATE COMPLICATIONSThe most common complication of caustic ingestion is strictur
e formation, which can
cause esophageal obstruction, presenting with dysphagia. Patients with severe gastric injury may develop pyloric
stenosis. Caustic ingestion also confers an increased risk for developing esophageal carcinoma, as described
below. Eosinophilic esophagitis developing after caustic ingestion has been describ
ed in a case report [69].
Stricture formation
Incidence and risk factorsStricture formation is the primary complication of caustic injury, occurring in 3 to 57
percent of ingestions with documented esophageal burns, and in virtually all patients with severe circumferential
burns (grade 2B or 3 in the scheme outlined above) [4,5,7,28]. More supercial or non-circumferential burns (grade 1
or 2A) are less likely to result in strictures [54], although one report found that half of the children with noncircumferential transmucosal burns (grade 2A) went on to develop esophageal stricture [70]. A few older reports
described patients with apparently normal endoscopic ndings who went on ot develop strictures [7], but it seems
likely that a burn was present but was missed because the endoscopy was performed with a rigid endoscope.

Clinical manifestations and diagnosisAll patients with signicant esophageal burns (gr
ade 2A or higher)
should be evaluated with a barium esophagogram to assess for stricture formation. The study should be performed
two to three weeks after the ingestion, orsooner if the patient develops dysphagia (difculty swallowing), which
suggests esophageal obstruction. Alternativ
e imaging such as water-soluble contrast agents should be used if a
perforation is suspected.
Most patients who develop a stricture will have obstructive symptoms within two months. In patients with the most
severe burns, there may be complete obstruction within three weeks [71]. At six weeks, the esophagram shows a
long constriction (image 1). Patients with severe strictures commonly have recurrent symptoms after two years,
despite repeated dilation.
DilationOnce a stricture is conrmed radiologically, esophageal dilation usually is er quired to maintain or
reestablish normal swallowing. Balloon di
lators under endoscopic control are our preferred approach; bougies also
may be used (picture 3). The endoscopic appearance of a stricture prior to dilation demonstrates an abrupt tapering
in the mucosa. This can be mild, with mucosal edema and er
ythema, or more pronounced, with friability, erosive
changes, whitish plaques, and brinous material. In mor
e severe cases there may be blistering or frank
necroinflammatory changes.
For patients who develop strictures, the optimal time for beginning dilation has not been established. Most
clinicians wait three to six weeks after theinitial injury before beginning dilation because there is some evidence
that performing earlier dilation will increase the risk of perforation [72-74]. However, two retrospective series in
children suggest that strictures were less likely to be recurrent if they were treated with early dilation (7 o
t 28 days
after the injury) versus later dilation (beginning 4 weeks or mor
e after the injury) [75,76].
A variety of dilators can be used, including balloon dilators, silicone or tungsten bougies, Malone
y antegrade
dilators, or Tucker dilators (used for retrograde dilation); some dilators can be passed over a string or guide wire.
Because caustic strictures appear to perforate easily, retrograde dilation has been considered the safest method,
although this method requires a gastrostomy and a string for guidance 63].
[ The risk of perforation probably
depends on many factors, including the cause of the stricture (perforation appears to be more common in caustic
strictures as compared with those due to esophageal atresia), interval of time since injury, length and diameter of
the stricture, total number of previous dilations, and operative technique (operator experience and selection of
maximal dilation) (see"Complications of endoscopic esophageal strictur
e dilation", section on 'Esophageal
perforation'). The techniques used for children are similar to those for adults, except that the maximal dilation of the
esophagus is smaller for a child. (See"Management of benign esophageal strictur
es".)
Balloon dilators under endoscopic control are commonly used in children and are our preferred approach [77-79]. In
theory, perforation should be less likely with balloon dilation because only adially
r
directed force is exerted, as
compared with use of a bougie, in which ht ere is also a longitudinal shearing force. The reported rates of
esophageal perforation for balloon dilation range from 1.6 to 13 percent per procedure [75,77,80-83], as compared
with 5.6 percent for bougienage [82]. Balloons come in a variety of sizes and lengths. The size of the balloon dilator
is selected using an estimate of the esophageal lumen diameter
. One group selects a balloon catheter with a
diameter equal to the interpeduncular distance of the child'
s thoracic spine, as measured on a pre-procedure
radiograph [82]. Dilation balloons are available as small as 2 mm (these are designed for biliary dilation), and these
can be used for the tightest strictures. For strictures narrower than 2 to 3 mm, dilation balloons with a wire guide
may prevent creating a "false-track" in which the balloon may pass through damaged tissue along the mucosal
surfaces rather than through the esophageal lumen.
The use of fluoroscopy varies widely among institutions. This technique may be of greatest benet for patients with
small diameter lumen or near-complete occlusion; in patients wher
e there is a high concern of perforation based on
endoscopic ndings; or in those with a prior hist
ory of perforation. Fluoroscopy can be used for any dilation
technique, and is used to identify the "waist" of the stricture (the area of narrowing relative to the non-dilated areas

proximal and distal to the stricture). Fluoroscopy also can demonstrate leaks or other procedure-related adverse
events.
Although esophageal dilation may be benecial initially, repeated dilations usually are needed. Only 33 to 48 percent
of patients with caustic strictures have long-term success with repeated dilations [5,28]. The remaining patients,
who often have long strictures, have increasing difculty in swallowing because of p
rogressive obstruction.
Other interventionsPreliminary data suggests thatmitomycin C, an inhibitor of broblast proliferation, helps to
prevent recurrent stricture formation in patients with severe caustic esophageal injury [84-88]. Mitomycin C is
applied topically to the strictured area of the esophagus at the end of a dilation ses
sion [89]. In a randomized trial in
40 patients with localized caustic esophageal strictures (<3 cm in length), treatment with mitomycin C was
associated with a reduced need for repeated dilation (3.85 versus 6.9 dilation sessions), and higher ates
r
of
complete resolution during the six-monthfollow-up period (80 versus 35 percent resolution), as compared with
placebo [87]. Similar results were seen in an international retrospective case series in which topical mitomycin C
was successful in eliminating or er ducing the need for repeated dilations in 82 percent of the patients [86].
Mitomycin C typically is used as a second- or thir
d-line agent, for strictures deemed resistant to repeated dilation or
steroid injections.
Esophageal stenting has been described in limited series for use in management ofefractory
r
caustic esophageal
strictures [90,91]. Stents have also been used in children after surgery for congenital strictures and esophageal
injury from batteries, with mixed success [90,92]. Most data is from studies of fully covered nitinol self-expanding
plastic in adults, but other nonmetal stents continueot be developed. The use of expandable uncovered metal
stents for benign esophageal strictures is not recommended because of a high incidence of complications and
difculty in removal. The use of biodegradable stents has been reported in adults with caustic ingestion, but has not
been studied in children [93]. (See "Management of benign esophageal strictur
es", section on 'Nonmetal stents'.)
Patients with progressive esophageal obstruction despite er peated dilation may ultimately require esophagectomy
with colon interposition, sometimes within two ears
y
following the ingestion 5[ ,28]. Although colon interposition can
be successful, many patients have persistent difculty swallowing. Complications focolon interposition surgery
include anastomotic strictures that may require periodic dilation and gastrocolic ulceration caused by reflux of
gastric contents into the neoesophagus [94,95].
CarcinomaEsophageal squamous cell carcinoma develops in approximately 2 percent of individuals with severe
caustic esophageal injury. Those who have had colonic interposition surgery face a risk of carcinoma in the
bypassed esophagus, with a e
r ported incidence of 2 to 8 percent [45]. As a result, some authors now recommend
resection of the esophagus at the time ofbypass with colon interposition.
In one study of 63 patients with lye ingestion, the mean latency period for de
velopment of esophageal cancer was
41 years with a range of 13 to 71 years [96]. For those who have had colonic interposition surgery, the time interval
between ingestion and the detection of tumor hasanged
r
from 16 to 42 years [45]. Based on these and other data,
the American Society for Gastrointestinal Endoscopy (ASGE) recommends beginning endoscopic surveillance 15 to
20 years after the caustic ingestion.
Any patient with a history of caustic ingestion and the late onset or worsening of dy
sphagia should be evaluated
promptly, and carcinoma should be suspected until proved otherwise. Since carcinomas tend to occur in strictured
areas, they are often resectable. (See "Caustic esophageal injury in adults", section on 'Esophageal squamous cell
carcinoma'.)
Pyloric stenosisPyloric stenosis can occur with both acids and alkalis and often is associated with esophageal
injury and strictures [22,97]. With severe injury to the stomach, gastric outlet obstruction may occur as early as 3

weeks or as late as 10 weeks 22,98].

[
Surgical bypass may be necessary, but endoscopic balloon dilation also has
been used successfully in case er ports [99,100].
SUMMARY AND RECOMMENDATIONS
Esophageal burns account for most of the serious injuries and chr
onic complications of caustic ingestion.
Injury to the lips, oropharynx, and upper airway also may occur. (See 'Esophageal injury' above and 'Acid versus
alkali' above.)
The most common causes of caustic esophageal burns ar
e alkaline household cleaning products, such as
oven and drain cleaners, strong lyes that contain sodium and potassium hy
droxides, and concentrated
laundry detergents and cleaning agents with sodium phosphate, sodium carbonate, and ammonia.
Esophageal burns are rare with household bleaches (sodium hypochlorite) becausethese typically have a
pH of approximately 11, which is below the pH threshold of 11.5 to 12.5 that tends to cause esophageal
injury.
Some caustic ingestions are caused by acid household products including toilet bowl cleaners, battery
fluids, and muriatic (hydrochloric) acid used in swimming pools. Esophageal injur
y from acids may be
attenuated compared with alkalis, and perforation of the esophagus is less common. Nonetheless, 6ot 20
percent of acid ingestions result in esophageal burns. Acids or corrosive agents tend to cause esophageal
injury if the pH is less than 2.
Following the initial necrosis, additional destruction takes place over the rst week (table 1). The risk for
esophageal perforation peaks at this stage. (See'Delayed injury' above.)
The most common symptom of caustic ingestion is dysphagia, which can occur ven
e without severe
esophageal injury. Patients may also present with drooling, retrosternal or abdominal pain, hematemesis, and
features suggesting upper airway injury. The presence or absence of any of the clinical eatures
f
described
above does not reliably predict ingestion or the presence or severity of esophageal or gastric burns. (See
'Clinical manifestations' above.)
The initial steps in management of caustic ingestion is suppor
tive care and close observation, with an
emphasis on preventing vomiting, choking, and aspiration. The induction of vomiting is contraindicated
because vomiting may lead to additional esophageal injury if gastric contents comein contact with the
esophageal mucosa. Similarly,attempts to dilute or neutralize the caustic agent, administration of activated
charcoal, or gastric lavage are not recommended. (See'Initial management'above.)
We suggest against using glucocorticoids in children with caustic esophageal injuries (Grade 2C). A
preponderance of evidence suggests thatthese agents do not help protect against the development of
esophageal strictures and may be harmful. Additional research is needed to determine whether glucocorticoids
may be benecial for selected patients. (See'Medication' above.)
Upper endoscopy should be performed for most patients with a denite history of caustic ingestion, even if
asymptomatic; endoscopy should always be performed in patients with symptoms or oral lesions (algorithm 1).
The endoscopy ideally should be performed within 24 hours of the ingestion, ot evaluate and stage the
esophageal injury (table 2). (See 'Endoscopic evaluation' above.)
Endoscopy is generally unnecessary in patients with a questionable history of ingestion, no evidence of oral
lesions, no dysphagia, vomiting, or other symptoms, and who remain asymptomatic and continue to swallow
normally during several hours of observation. Patients who have ingested household bleaches rarely have
signicant tissue injury and, therefore, rarely require endoscopy. (See 'Initial management'above.)

 All patients with signicant esophageal burns (eg, gr

ade 2A and higher) noted on endoscopy, or those with
persistent dysphagia, should be evaluated with barium contrast studies two to three weeks post ingestion to
assess for stricture formation. (See'Stricture formation' above.)
Stricture formation is the primary complication of caustic injury. Most patients who develop strictures present
with obstructive symptoms within two months. The presence of a stricture is conrmed with radiographic
contrast studies. If strictures develop, esophageal dilation is performed to maintain or reestablish normal
swallowing. In our practice, we generally use balloon dilators, accessing the esophagus either through the
anterograde (peroral) or retrograde (via a gastrostomy) route. (See 'Stricture formation' above.)
ACKNOWLEDGMENTThe editorial staff at UpToDate would like to acknowledge George D Ferry, MD, who
contributed to an earlier version of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
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Topic 5862 Version 17.0

GRAPHICS
Timing of tissue damage and e
r pair after caustic injury of the esophagus
Injury

Time

Acute injur y

Day 0

Inflammation, v ascular thrombosis

1 to 7 days

Granulation tissue

10 to 21 days

Fibrosis/stricture

3 weeks

Graphic 68864 V ersion 2.0

Approximate pH of selected cleaning products and other substances

NOTE:
All pH v alues ar e appr oximates
Solvents do not ha ve a pH because the y do not ioniz e in aqueous solution
pH does not measur e the corr osiveness of an ac id (ie, hy drochloric acid with a pH of 1 is
stronger than phosphoric acid with a pH of 1)
* Hair relaxers may be made with ly e (pH typically 12 t o 14), or without ly e (pH typically 9 t o 11).
Adapted with permission fr om: Unisource Canada, Inc. pH Scale. A vailable at:
https://www.unisource.ca/tools-and-resources/calculators/facility-supplies/ph-scale (accessed on
October 10, 2016).
Graphic 110162 V ersion 1.0

Supercial burns to the lips and oropharynx after caustic ingestion

Photographs showing supercial burns t o the lips and or ophar ynx in a child after
ingestion of a caustic substance.
Courtesy of Cour tesy of Glenn Isaacson, MD , FAAP.
Graphic 93916 V ersion 2.0

Evaluation of a patient with suspected ingestion of caustic substances

UGI: upper gastr ointestinal; NG: nasogastric.

* A substance is caustic if it is capable of burning or corr oding organic tissue b y chemical action, typically due t o strong acid or alkaline
properties. Common caustic ingestions ar e of household cleaning pr oducts, including laundr y or dishwasher deter gents, household bleach,
drain cleaners, t oilet bowl or o ven cleaners, hair r elaxer, and swimming pool pr oducts.
If signicant r espiratory symptoms are present, we suggest consultation with a specialist (eg, ear-nose-thr oat [ENT]) to evaluate the air way.
If grade 2B burn is pr esent (deep focal or cir cumferential ulcers), consider placing an NG tube. F or a description of gr ading, refer to text of
topic on caustic esophageal injur y in children.
Antibiotics ar e given prophylactically t o selected pat ients with se vere caustic esophageal injur y, but there are no standards to guide patient

selection. In our pr actice, we administer antibiotics t o patients with gr ade 3 burns (endoscopic e vidence of necr osis), and to those with
suspicion of per foration on chest x-r ay or endoscop y. We do not recommend tr eatment with glucocor ticoids for patients with caustic
esophageal injuries.
Modied with permission fr om: Ferry GD. Caustic Inge stion. In: Pediatric Gastr ointestinal Disease: P athphysiology, Diagnosis, Management.
Wyllie R, Hyams JS (Eds), WB Saunders, Philadelphia 1 993. Copyright 1993 Else vier.
Graphic 70113 V ersion 5.0

Grading of esophageal burns from caustic injury

Injury

Findings

Grade 0

Normal mucosa

Grade 1
(supercial)

Mucosal edema and hyper emia

Grade 2
(transmucosal)

Friability, hemorrhages, er osions, blisters, whitish membr anes, and supercial ulcer ations

Grade 2A

No deep focal or cir cumferential ulcers

Grade 2B

Deep focal or cir cumferential ulcers

Grade 3

Areas of multiple ulcer ation and areas of brown-black or greyish discoloration suggesting necr osis

Grade 3A

Small scatter ed areas of focal necr osis

Grade 3B

Extensiv e necrosis

This scheme for gr ading of esophageal burns was described b y Zargar and colleagues in 1991. In a study of 81 patients (primarily
adults) with corr osive esophageal burns, this sch eme helped t o predict complications. Early major complications occurr ed only in
patients with gr ade 3 injur y. Late complications including esophageal strictur es wer e limited t o patients with gr ade 2B or 3
injuries.
Reference: Zargar SA, Kochhar R, Mehta S, Mehta SK. The r ole of beroptic endoscop y in the management of corr osive ingestion and modied
endoscopic classication of burns. Gastr ointest Endosc 1991; 37:165.
Graphic 77228 V ersion 2.0

Esophageal burns after caustic ingestion

Endoscop y in a child one da y after ingestion of a caustic substance r eveals moder ate esophagea l
burns (gr ade 2A and 2B).
Courtesy of Glenn Isaacson, MD , FAAP.
Graphic 93918 V ersion 1.0

Alkali injury to the esophagus

Endoscopic appear ance of caustic esophageal injur y 24 hours after intentional ingestion
of batter y fluid (alkali) A: Pr oximal esophagus with supercial ulcers, bleeding and
exudates (gr ade 2A) B: Distal esophagus with cir cumef erential ulcers and exudates
(grade 2B) C: Gastric antrum with extensiv e necr osis and ulcer ation (gr ade 3B) D:
Duodenum with mucosal edema and hyper emia (gr ade 1).
Courtesy of George Triadalopoulos, MD .
Graphic 62223 V ersion 2.0

Esophageal stricture after caustic ingestion

Left panel shows an esophageal strictur e six weeks after ly e ingestion. A gastr ostomy
with retrograde string placement was per formed with multiple dilatations b y string
bougie. The patient was able t o eat normally for two to three weeks after each dilatation,
but required monthly dilatation. Right panel shows the strictur e after two y ears and
multiple dilatations. A colonic r eplacement was per formed shor tly after the last study .
Courtesy of George D Ferry, MD.
Graphic 74287 V ersion 2.0

Caustic strictures of the esophagus

This 17-y ear-old patient pr esented with r ecurrent dysphagia after ingesting an unknown
quantity of pine oil solv ent and sodium hy droxide six weeks prior . Endoscopic e valuation
noted multiple strictur es and edema. Inital dir ect lar yngoscop y one da y after
ingestionhad beenunr emarkable.
Courtesy of Karen Murray, MD.
Graphic 53496 V ersion 2.0

Contributor Disclosures
Douglas S Fishman, MDNothing to disclose Craig Jensen, MD Speaker's Bureau: Mead Johnson Nutrition
[pediatric nutrition (pediatric formulas)]. Consultant/Advisor
y Boards: Mead Johnson Nutrition [pediatric nutrition
(pediatric formulas)].Alison G Hoppin, MDNothing to disclose
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