View
13
Download
0
Category
Preview:
Citation preview
106: Caustics
Jessica A. Fulton
HISTORY AND EPIDEMIOLOGY
As early as 1927, legislation in the United States governing the packaging of lye- and acid-
containing products mandated that warning labels be placed on these products. In response to the
recognition that caustic exposures were more frequent in children, the Federal Hazardous
Substances Act and Poison Prevention Packaging Act were passed in 1970; these acts mandated
that all caustics with a concentration greater than 10% be sold in child resistant containers. By 1973,
the household concentration for child-resistant packaging was lowered to 2%. In addition, the
subsequent development of poison prevention education dramatically decreased the incidence of
unintentional caustic injuries in children in the United States. The positive impact of both regulatory
legislation and public health intervention is evident when observing the decreasing number of
significant exposures in the United States49 compared to the number of exposures in developing
nations that lack these policies.
In the United States, even though legislation limiting the concentration of caustics has existed since
the early 20th century, exposures to both acids and alkalis continue to be significant. Data collected
by the American Association of Poison Control Centers from 2007 through 2010 revealed 29,748
acid exposures and 13,800 alkali exposures. Of these, 4273 (14.4%) acid exposures and 2645
(19.2%) alkali exposures resulted in moderate to major outcomes and a total of 25 deaths occurred
(Chap. 136).
In children, exposures usually consist of household products and occur in an unsupervised setting.
In adults, exposures to household or industrial products may result from occupational exposure,
suicide attempts, and assaults. Exposure to caustics may occur via the dermal, ocular, respiratory,
and gastrointestinal routes.
Caustics cause diverse histologic and functional damage on contact with tissues depending on the
tissue and caustic involved. Table 106–1 lists common caustics and the commercial products that
contain them. Many are available for home use, in both solid and liquid forms, with variations in
viscosity, concentration, and pH.
TABLE 106–1. Sources of Common Caustics
View Large |
Favorite Table
Morbidity and mortality from exposures to caustics is a worldwide problem. One study from India that
described outcomes in patients with acid ingestions found that acute complications occurred in
39.1% of cases and death in 12.2%.106
Although less frequent, intentional exposures by adults are invariably more significant. One study
noted that while children comprised 39% of admissions for caustic ingestions, adults comprised 81%
of patients requiring treatment.36 The severity of a caustic injury may not be immediately evident in
patients who present shortly after exposure. Predicting which patients will require immediate
interventions to prevent morbidity and mortality requires the determination and evaluation of multiple
clinical and laboratory parameters. This chapter reviews the pathophysiology and approach to
patients with potentially serious exposures.
PATHOPHYSIOLOGY
A caustic is a xenobiotic that causes both functional and histologic damage on contact with tissue
surfaces. Although there are many ways to categorize caustics, they are most typically classified as
acids or alkalis. An acid is a proton donator and causes significant injury, generally at a pH below 3.
An alkali is a proton acceptor and causes significant injury, generally at a pH above 11. Chapter
12 contains a more detailed discussion of the chemistry of acids and bases. The extent of injury is
modulated by duration of contact; ability of the caustic to penetrate tissues; volume, pH, and
concentration; the presence or absence of food in the stomach; and a property known as titratable
acid/alkaline reserve(TAR). TAR quantifies the amount of neutralization needed to bring the pH of a
caustic to that of physiologic tissues. Neutralization of caustics takes place at the expense of the
tissues, resulting in the release of thermal energy, producing burns. Generally, as the TAR of a
caustic increases, so does the ability to produce tissue damage.5,40 Some xenobiotics, such as zinc
chloride and phenol, have a high TAR and are capable of producing severe burns even though their
pH is near physiologic.
Alkalis
Following exposure to an alkaline xenobiotic, dissociated hydroxide (OH–) ions penetrate tissue
surfaces, producing a histologic pattern of liquefactive necrosis (Figs. 106–1 and106–2). This
process includes protein dissolution, collagen destruction, fat saponification, cell membrane
emulsification, transmural thrombosis, and cell death.5 Animal studies following alkali exposure to the
eye39 demonstrate rapid formation of corneal epithelial defects with eventual deep penetration that
may lead to perforation. Similarly, animal studies of the esophagus demonstrate that erythema and
edema of the mucosa occur within seconds followed by an inflammatory reaction extending to the
submucosa and muscular layers. The alkali, such as sodium hydroxide (“liquid lye”), then continues
to penetrate until the OH– concentration is sufficiently neutralized by the tissues.5,53
FIGURE 106–1.
Photograph demonstrating burns to the lips and tongue of a 20 year-old man following ingestion of sodium
hydroxide. (Used with permission of The New York City Poison Center Toxicology Fellowship Program.)
View Full Size |
Favorite Figure | Download Slide (.ppt)
FIGURE 106–2.
Endoscopy images of a 20 year-old man following ingestion of sodium hydroxide. (A) Grade IIa noncircumferential
burn of the midesophagus. (B) Grade IIb circumferential burn of the distal esophagus. (Used with permission of The
New York City Poison Center Toxicology Fellowship Program.)
View Full Size |
Favorite Figure | Download Slide (.ppt)
Although federal regulations have lowered the maximal available household concentration of many
caustics, two industrial strength products seem to be readily available and therefore warrant special
mention: ammonium hydroxide and sodium hypochlorite. Ammonia (ammonium hydroxide) products
are weak bases—partially dissociated in water—that can cause significant esophageal burns,
depending on the concentration and volume ingested.36 Household ammonium hydroxide ranges in
concentration from 3% to 10%. Strictures have formed in patients who ingested 28%
solutions.72 Sodium hypochlorite is the major component in most industrial and household bleaches.
Severe injuries typically only occur in patients with large-volume ingestions of concentrated products
and most other patients do well with supportive care.13,36 A series of 393 patients with household
bleach ingestions demonstrated no stricture formation.52Likewise, a canine model found that
although vomiting was commonly associated with bleach ingestion, no esophageal lesions were
noted, and perforation occurred only following prolonged contact.52
Ingestion of button batteries were once considered a unique caustic exposure. Composed of metal
salts and a variety of alkaline xenobiotics, such as sodium and potassium hydroxide, leakage of
battery contents was a legitimate concern. In recent years, however, new techniques used in the
production of button batteries that effectively prevent leakage have shifted the concern following
their ingestion from caustic to foreign body exposure with the potential for electrical injury. For a
more in-depth review of the management of button battery ingestion, the reader is referred to the
previous editions of this text and one recent study that describes the electrical injuries that follow
ingestion of large-diameter lithium cells lodged in the esophagus for longer than 2 hours.54
Household detergents, such as laundry powders, laundry pods,89 and dishwasher detergents, contain
silicates, carbonates, and phosphates, and have the potential to induce caustic burns and strictures,
even when ingested unintentionally.14 Airway compromise also may occur,14,21,60 but the majority of
exposures result in only minor toxicity.
Cationic detergents include quinolinium compounds, pyridinium compounds, and quaternary
ammonium salts. These are frequently found in products for industrial use, as well as household
fabric softeners. A concentration greater than 7.5% can cause severe burns.58
Acids
In contrast to alkaline exposures, following exposure to an acid, hydrogen (H+) ions desiccate
epithelial cells, producing an eschar and resulting in a histologic pattern of coagulation necrosis. This
process leads to edema, erythema, mucosal sloughing, ulceration, and necrosis of tissues.
Dissociated anions of the acid (Cl–, SO42–, PO4
3–) also act as reducing agents, further injuring tissue.
Ophthalmic exposure to acids results in coagulative necrosis that tends to prevent further
penetration into deeper layers of the eye.
In most series, following an acid ingestion, both the gastric and esophageal mucosa are equally
affected.19,106 On occasion, the esophagus may be spared damage while severe injury is noted in the
stomach27,36 (Fig. 106–3). This result tends to be a rarer finding than concomitant injury to both
stomach and esophagus and is probably related to the rapid transit time of liquid acids through the
upper gastrointestinal tract. Skip lesions from acid ingestions may be a function of viscosity and
contact time.36 Additionally, acid-induced pylorospasm may lead to gastric outlet obstruction, antral
pooling, and perforation.19,105 A cat model of the effects of sulfuric acid on the esophagus revealed a
coagulative necrosis of the mucosa with whitish discoloration of the tissues and underlying smooth
muscle spasm.5 Other animal models demonstrate esophageal motility dysfunction and
shortening.92,93
FIGURE 106–3.
Postmortem specimen from a man with an intentional ingestion of a mixture of phosphoric and hydrochloric acid that
was used as a brick cleaner. Note the relative sparing of the esophagus in contrast to full-thickness injury with
perforation of the stomach. (Used with permission of The New York City Poison Center Toxicology Fellowship
Program.)
View Full Size |
Favorite Figure | Download Slide (.ppt)
Chapters 98 and 107 contain a more detailed discussion of mercury and hydrofluoric acid,
respectively, each a unique caustic, and the management specific to their exposure.
Classification and Progression of Caustic Injury
Esophageal burns, secondary to both alkali and acid exposures, are classified based on endoscopic
visualization that employs a grading system similar to that used with burns of the skin. Grade I burns
are generally defined by hyperemia or edema of the mucosa without evidence of ulcer
formation.17,105 Grade II burns include submucosal lesions, ulcerations, and exudates. Some authors
further divide grade II lesions into grade IIa, noncircumferential lesions, and grade IIb, near-
circumferential injuries.13 Grade III burns are defined as deep ulcers and necrosis into the
periesophageal tissues (Table 106–2).26,30
TABLE 106–2. Evaluation of Caustic Injuries and Management
View Large |
Favorite Table
Human case reports, postmortem studies, histologic inspection of surgical specimens, and
experimental animal models reveal a consistent pattern of injury and repair following caustic
injury.86 As wound healing of gastrointestinal tract tissue occurs, neovascularization and fibroblast
proliferation take place, laying down new collagen and replacing the damaged tissue with
granulation tissue. A similar pattern of repair occurs following caustic injuries of the eye.
Burns of the esophagus may persist for up to 8 weeks as remodeling takes place and may be
followed by esophageal shortening. If the initial injury penetrates deeply enough, there is progressive
narrowing of the esophageal lumen. The dense scar formation presents clinically as a stricture.
Strictures can evolve over a period of weeks to months, leading to dysphagia and significant
nutritional deficits. Grade I burns carry no risk of stricture formation.17,105 Grade II circumferential
burns lead to stricture formation in approximately 75% of cases. Grade III burns invariably progress
to stricture formation and are also at a high risk of perforation.3,36
CLINICAL MANIFESTATIONS
The gastrointestinal tract, respiratory tract, eyes, and skin of a patient can be sites of caustic injury.
Caustics may produce severe pain on contact with any of these tissues. By far, the majority of long-
term morbidity and mortality from caustic exposure results from ingestion.
In general, patients who have ingested either alkalis or acids have similar initial presentations.
Depending on the type, amount, and formulation (solid vs. liquid) as well as the percent of tissue
exposed, ingestion may lead to the development of severe pain of the lips, mouth, throat, chest, or
abdomen. Oropharyngeal edema and burns may lead to drooling and rapid airway compromise.
Symptoms of esophageal involvement include dysphagia and odynophagia, whereas epigastric pain
and hematemesis may be symptoms of gastric involvement.
Respiratory tract damage may occur through direct inhalation or aspiration of vomitus, leading to the
clinical manifestations of hoarseness, stridor, and respiratory distress. Injury may result in epiglottitis,
laryngeal edema and ulceration, pneumonitis, and impaired gas exchange. Patients may also be
tachypneic or hyperpneic as a compensatory response to the metabolic acidosis, with elevated
lactate concentrations from necrotic tissue or hemodynamic compromise.
Predictors of Injury
Many attempts have been made to define a method for clinical identification of patients with grade II
or III esophageal injuries as these injuries typically progress to severe complications. Various
studies, mostly involving alkaline xenobiotics, examine the predictive value of stridor, oropharyngeal
burns, drooling, vomiting, and abdominal pain. A retrospective study of 378 children admitted for a
caustic injury found that signs or symptoms could not be used to predict significant esophageal
injury.26 However, one prospective study of 79 children evaluated for vomiting, drooling, and stridor
found that a combination of two or more of these signs were predictive of significant esophageal
injury as visualized on endoscopy.17 Another study found that drooling, buccal mucosal burns, and
white blood cell count were significant independent predictors of severe gastrointestinal tract injury
following acid ingestions.35 Studies evaluating the presence or absence of oropharyngeal burns as a
predictor of distal esophagogastric injury have repeatedly found this finding to be poorly
predictive.1,17,26,30,80,99 In one study esophageal injury was present 51.5% of the time in the absence of
oropharyngeal lesions, and 22.2% of these were second- and third-degree burns.80 A prospective
study of alkali ingestions in both adults and children found that stridor was 100% specific for
significant esophageal injury, but this was based on only three patients with this sign.30
Based on these findings, endoscopy, a standard diagnostic tool used in the management of caustic
ingestions, is recommended in all patients with intentional ingestions. Endoscopy should also be
performed in any patient with an unintentional ingestion in the presence of stridor and in any patient
with two or more of the following findings: pain, vomiting, and drooling.17,82 Children with unintentional
caustic ingestions who remain completely asymptomatic and tolerate liquids after a few hours of
observation probably require no further medical care.
The abdominal examination is likewise an unreliable indicator of the severity of injury. The presence
of abdominal pain suggests tissue injury, but the absence of pain or findings on abdominal
examination does not preclude life-threatening gastrointestinal damage.22,104Esophageal perforations
result in mediastinitis and are commonly associated with fever, dyspnea, chest pain, and
subcutaneous emphysema of the neck and chest. Although indicative of viscus perforation,
abdominal peritoneal signs are late findings.
In addition to the direct effects that occur with tissue contact, systemic absorption of acids may result
in damage to the spleen, liver, biliary tract, pancreas, and kidneys. This may also produce a
metabolic acidosis, hemolysis, and, ultimately, death.42
Significant complications can occur at various stages of wound recovery. Most importantly, these
include airway compromise, hemodynamic instability secondary to hemorrhage from vascular
erosion or septic shock, perforations of the gastrointestinal tract with the development of
mediastinitis or peritonitis, and other overwhelming infections from bacteria residing in the
oropharynx. A patient who survives acute injury with an acid or an alkali may also subsequently
develop stricture formation, gastric atony, decreased acid secretion, pseudodiverticula, and gastric
outlet obstruction.29,105
Other complications include dysmotility of the pharynx and esophagus,18 formation of aorto- and
trachea-esophageal fistulas, delayed massive hemorrhage from erosion into a great vessel, and
pulmonary thrombosis.9,36,70,91 Those patients surviving a few weeks after a grade II or III injury may
subsequently present with dysphagia and vomiting from stricture formation. Injury involving the entire
length of the esophagus as well as hematemesis and increased serum lactic dehydrogenase were
useful indicators for the development of strictures in one study.73 Strictures may also present with
esophageal motility disorders caused by impaired smooth muscle reactivity. The early assessment
and long-term prognosis may be better defined by manometric studies of the esophagus, which
provide precise information about the severity of the initial injury and aid in long-term prognosis.28
Long-term survivors of moderate and severe injury of the esophagus have a risk of esophageal
carcinoma that is estimated to be 1000 times higher than that of the general population and appears
to present with a latency of up to 40 years.4
DIAGNOSTIC TESTING
Laboratory
All patients with presumed serious caustic ingestion should have an evaluation of serum pH, blood
type and cross-match, complete blood count, coagulation parameters, electrolytes, and urinalysis.
Elevated prothrombin time (PT) and elevated partial thromboplastin time (PTT),104 as well as an
arterial pH lower than 7.22,11 are associated with severe caustic injury.
Absorption of nonionized acid from the stomach mucosa may result in acidemia. Following ingestion
of hydrochloric acid, hydrogen and chloride ions (both of which are accounted for in the
measurement of the anion gap) dissociate in the serum resulting in a hyperchloremic normal anion
gap metabolic acidosis. Other acids, such as sulfuric acid, result in an elevated anion gap metabolic
acidosis because the sulfate anion (SO42–) is not measured in the calculation of the anion gap.
Although alkalis are not absorbed systemically, necrosis of tissue may result in a metabolic acidosis
with an elevated lactate concentration.
A gastric pH greater than 7.30 correlated retrospectively with severe alkaline injury. The prospective
usefulness of this information is limited, as obtaining gastric secretions without direct visualization is
dangerous. One prospective study in children also found an increase in uric acid and decreases in
phosphate and alkaline phosphatase concentrations to be useful in predicting the presence of
esophageal injuries.75
Radiology
Chest and abdominal radiographs are useful in the initial stages of assessment to detect gross signs
of esophageal or gastric perforation. Signs of alimentary tract perforation that may be present on
plain radiographs include pneumomediastinum, pneumoperitoneum, and pleural effusion. However,
these studies have a limited sensitivity, and an absence of findings does not preclude
perforation.104 Free intraperitoneal air is best visualized on an upright chest radiograph. Occasionally,
free air may only be visible on the lateral view. In patients too ill to obtain an upright chest
radiograph, an abdominal radiograph obtained with the patient in a left-side-down position may
reveal free intraperitoneal air adjacent to the liver. Additionally, bedside ultrasound may be useful in
the diagnosis of free air and is based entirely on the lack of visualization of the usual intraperitoneal
structures.10,71Computed tomography (CT) scanning is considerably more sensitive than both
radiography and ultrasound for detecting viscus perforation and should be obtained in patients with
potentially serious caustic ingestions as soon as is feasible.23,101
A contrast esophagram is useful for defining the extent of esophageal injury (Fig. 106–4). Late after
the ingestion, it can detect stricture formation. In patients for whom there is a high suspicion for
esophageal perforation and in whom adequate visualization of the upper gastrointestinal tract by
endoscopy is not possible (grade IIb circumferential burns or grade III burns), an enteric contrast
study (esophagram and upper gastrointestinal series) can be obtained 24 hours after the
ingestion.81 Extravasation of contrast outside of the gastrointestinal tract is diagnostic of
perforation.105 Water-soluble contrast should be used when perforation is suspected as it is less
irritating than barium contrast agents to mediastinal and peritoneal tissues if extravasated. However,
barium contrast agents are more radiopaque than water-soluble agents and offer greater
radiographic detail. Consequently, some authors recommend barium swallow if the water-soluble
contrast study is nondiagnostic but demonstrates no leak.32,57,94 In addition, if there is risk of
aspiration, barium is preferred because water-soluble contrast material can cause a severe chemical
pneumonitis. Significant necrosis with impending perforation may be suspected on enteric contrast
studies when there is esophageal dilation, displacement of the pleural reflection, and widening of the
pleuroesophageal line. Enteric contrast studies may fail to detect perforation and therefore must be
interpreted within the context of the patient’s clinical status.9,15,34
FIGURE 106–4.
(A) Barium swallow several days after ingestion of liquid lye shows the esophagus to be atonic. There is poor coating
of the esophagus, suggesting edema and intramural penetration. Note that the initial evaluation immediately following
a caustic ingestion to assess the extent of injury is esophagoscopy, rather than a contrast esophagram. (B) Four
months later, a repeat barium esophagram shows a severe stricture below the middle third of the esophagus. The
barium barely passes the stricture, and the remainder of the esophagus is pencil thin. (Used with permission of Emil
J. Balthazar, MD, Professor of Radiology, New York University.)
View Full Size |
Favorite Figure | Download Slide (.ppt)
The role for CT scans in caustic ingestions has not been prospectively investigated. In the acute
stage, CT has great sensitivity at detecting extraluminal air in the mediastinum or peritoneal cavity
as a sign ofperforation. In addition, CT can visualize the esophagus and stomach distal to severe
caustic burns that cannot be safely seen using endoscopy or an esophagram. CT may therefore
replace enteric contrast radiography for detection of perforation within 24 hours of a caustic
ingestion. Additionally, one retrospective study suggests that CT grading of esophageal injuries may
be superior to endoscopy for prediction of the degree of esophageal damage and the development
of stricture formation. These results suggest a promising future role for this noninvasive study
following caustic ingestions.88 Other imaging modalities have been proposed for assessing
esophageal injury after ingestion of caustic substances, including technetium 99m-labeled sucralfate
swallow for the presence of injury66 and esophageal ultrasonography for determining the depth of
injury.69
Another use of radiographic imaging is to noninvasively follow the patient after initial evaluation and
stabilization. For example, contrast radiography is routinely used in the weeks or months following a
caustic ingestion to detect esophageal narrowing representing stricture formation.96 Chest CT may
also be useful to determine the response of strictures to dilation procedures.
Endoscopy
Endoscopy should be performed within 12 hours and generally not later than 24 hours postingestion.
Numerous case series demonstrate that the procedure is safe during this period. Early endoscopy
serves multiple purposes in that it allows patients with minimal or no evidence of gastrointestinal
injury to be discharged. It also offers a rapid means of obtaining diagnostic and prognostic
information while shortening the period of time that patients forego nutritional support, permitting
more precise treatment regimens.13,22,36,56,65,82,90,100,105 The use of endoscopic assessment from the
second or third day postingestion is discouraged and should be avoided between 5 days and 2
weeks postingestion; at this time, wound strength is least and the risk of perforation is greatest.
The choice of rigid versus flexible endoscopy is dependent on the comfort and experience of the
endoscopist. The flexible endoscope has a smaller diameter but may require gentle insufflation of air
to achieve or enhance visualization. A prospective evaluation of the role of fiberoptic endoscopy in
the management of caustic ingestions recommended the following guidelines: (a) direct visualization
of the esophagus prior to advancing the instrument, (b) minimal insufflation of air, (c) passage into
the stomach unless there is a severe (particularly circumferential) esophageal burn, and (d)
avoidance of retroversion or retroflexion of the instrument within the esophagus. Provided that the
patient is hemodynamically stable and endoscopy is indicated, every attempt should be made to
visualize the esophagus, stomach, and duodenum as soon as possible after a caustic
ingestion.105 The absence of burns in the esophagus does not imply that severe necrosis and
ulcerations do not exist in the stomach65,99,105 and duodenum. In the case of termination of endoscopy
because of grade IIb or grade III esophageal burns, barium studies,82 CT scan, or consideration of
surgical exploration should be undertaken to visualize remaining structures.
Endoscopy permits limited evaluation of gastrointestinal injury. For example, the endoscopist is able
to appreciate only the mucosal surface of tissues, not the serosal side. This is especially evident in
stomach ulcerations, which may appear black and necrotic from a true burn through the layers of the
stomach or from the effect of stomach acid on the blood exposed from a shallow lesion. As
mentioned above, in these cases, endoscopic ultrasonography during endoscopy may improve
assessment of injury depth.7,52 Often, however, only direct visualization of serosal and mucosal
tissues with laparoscopy or laparotomy allows for definitive evaluation.
Most cases of perforation clearly linked to endoscopy have occurred when the endoscope was
advanced through an esophagus with severe circumferential lesions—a violation of current
endoscopic standards.100 In addition, perforations are also more likely to occur when rigid instruments
are used in children or in uncooperative patients. Thus the use of the flexible endoscope and
adequate procedural sedation has decreased the complications from endoscopic evaluation.82 Some
authors advocate the presence of a surgeon during endoscopy to assist in the assessment for
potential surgical intervention.
MANAGEMENT
Acute Management
As in the case of any patient presenting with a toxicologic emergency, the health care provider must
adhere to universal precautions utilizing early decontamination as described in the following section.
Initial stabilization should include airway inspection and protection, basic resuscitation principles,
and decontamination. Examination of the oropharynx for signs of injury, drooling, and vomitus, as
well as careful auscultation of the neck and chest for stridor, may reveal signs of airway edema that
should prompt immediate airway protection. Careful and constant attention to signs and symptoms
of respiratory distress and airway edema, such as a change in voice, are essential and should
prompt early intubation as airway edema may rapidly progress over minutes to hours.
If airway involvement is significant enough to warrant intubation, it is best to mobilize a team of the
most skilled physicians early in case of unforeseen complications. A delay in prophylactic airway
protection may make subsequent attempts at intubation or bag-valve-mask ventilation difficult or
impossible. Direct visual inspection of the vocal cords with a fiberoptic laryngoscope may also reveal
signs of impending airway compromise. Patients necessitating intubation are best served by direct
visualization of the airway either via direct laryngoscopy or fiberoptic endoscopy, as perforation of
edematous tissues of the pharynx and larynx is a grave complication that may occur during blind
nasotracheal intubation attempts. Neuromuscular blockers should be avoided for induction of
intubation as airway edema and bleeding may distort the anatomy limiting the ability to successfully
ventilate via bag-valve-mask should intubation be unsuccessful.
Nonsurgical airway placement is recommended whenever possible as both cricothyrotomy and
tracheostomy may interfere with the surgical field if esophageal repair is required.104Some patients
with significant ingestions, however, may require emergent surgical airway intervention. The decision
to perform a surgical airway is dependent on the status of the patient, the ability to orotracheally or
nasotracheally intubate via a fiberoptic endoscope, and the comfort of the physician performing the
procedure.
Following control of the airway, large-bore intravenous access should be secured and volume
resuscitation initiated. Although not studied, most clinicians agree that patients with signs of caustic-
induced airway edema benefit from dexamethasone 10 mg (intravenous) in adults and 0.6 mg/kg up
to a total dose of 10 mg in children. Both acid and alkali ingestions cause “third spacing” of
intravascular fluid to the interstitial space, which can result in hypotension. Empiric rehydration with
clinical assessment of central venous pressures should be used to guide individual fluid
requirements. Serial physical examinations and constant monitoring of the vital signs and urine
output may provide information on the severity of the exposure and the progression in clinical status.
Decontamination, Dilution, and Neutralization
Decontamination should begin with careful, copious irrigation of the patient’s skin and eyes when
indicated to remove any residual caustic and to prevent contamination of other patients, staff, and
equipment.
Gastrointestinal decontamination is usually limited in patients with a caustic ingestion. Induced
emesis is contraindicated, as it may cause reintroduction of the caustic to the upper gastrointestinal
tract and airway. Activated charcoal is also contraindicated, as it will interfere with tissue evaluation
by endoscopy and preclude a subsequent management plan. Additionally, most caustics are not
adsorbed to activated charcoal.
Exceptions, such as cationic detergents, that do bind well to activated charcoal57 have not been
evaluated with a large series. For this reason, therapy with activated charcoal following any caustic
ingestion cannot be recommended. Gastric emptying via cautious placement of a narrow nasogastric
tube with gentle suction may be attempted to remove the remaining acid in the stomach only in
patients with large, life-threatening, intentional ingestions of acid who present within 30 minutes.
Although this technique has never been studied and carries the risk of perforation, the outcome for
this particular group of patients with massive exposure is often grave, and options for treatment are
limited. Therefore, preventing absorption of some portion of the ingested acid may have potential
benefit in reducing systemic toxicity. Although the procedure has the potential to induce injury, a risk-
to-benefit analysis favors gastric emptying following a presumed lethal ingestion.
In contrast, gastric emptying should be avoided with alkaline and unknown caustic ingestions as
blind passage of a nasogastric tube carries the risk of perforation of damaged tissues, a risk that
outweighs the benefit.
Exceptions to the general rules of gastrointestinal decontamination of caustics exist in the
management of zinc chloride (ZnCl2) and mercuric chloride (HgCl2).49,95 Both are caustics with severe
systemic toxicity.12,62,63,79 Ingestion of these xenobiotics causes life-threatening illness from cationic
metal exposure. The local caustic effects, though of great concern, are less consequential than the
manifestations of systemic absorption. Therefore, prevention of systemic absorption should be
addressed primarily, followed by the direct assessment and management of the local effects of these
xenobiotics. Initial management to prevent systemic absorption includes aggressive decontamination
with gentle nasogastric tube aspiration and administration of activated charcoal. In vitro data exist to
suggest adequate activated charcoal adsorption of Hg2+.2
The use of dilutional therapy has been examined using in vitro, ex vivo, and in vivo models in an
attempt to assess its efficacy in caustic ingestions. An early in vitro model demonstrated a dramatic
increase in temperature when either water or milk was added to a lye containing crystal drain opener
(NaOH).87 Another in vitro model found less consequential increases in temperature despite large
volumes of diluent. Results of both studies suggested that dilutional therapy was of limited
benefit.61 Dilutional therapy was also attended by an increase in temperature in an ex vivo study of
harvested rat esophagi that examined the histopathologic effects of saline dilution after an alkali
injury. Additionally, the usefulness of dilution appeared to be inversely related to the length of time
from exposure, with minimal efficacy when delay to initiation was as short as 30 minutes.42,43 In
contrast, an in vivo canine model of alkaline injury demonstrated that water dilution did not cause an
increase in either temperature or intraluminal pressures.45
The extrapolation of these variable results to humans with caustic ingestions is limited and suggests
that histologic damage can only be attenuated by milk or water when administered within the first
seconds to minutes following ingestion.5,42, 43, 44, and 45,53 For solid, as opposed to liquid, substances (eg,
crystal lye), there may be some value for delayed dilutional therapy, as tissue contact time is
increased with solids and their concentration is usually 100% over a small surface area. Milk may be
the best diluent to attenuate the heat generated by a caustic.
Caution should be used in advising patients or family members about the use of diluents. A child
who refuses to swallow or take oral liquids should never be forced to do so. In general, dilutional
therapy should be limited to the first few minutes after ingestion in patients who have no airway
compromise; are not complaining of significant pharyngeal, chest, or abdominal pain; are not
vomiting; and are alert. Dilutional therapy should be avoided in patients with nausea, drooling,
stridor, or abdominal distension as it may stimulate vomiting and result in reintroduction of the
caustic into the upper gastrointestinal tract.87
Attempts at neutralization of ingested caustics should likewise be avoided. This technique has the
potential to worsen tissue damage by forming gas and generating an exothermic reaction. In vitro
and ex vivo models demonstrate that neutralization of caustics generates heat, requires a large
volume to attain physiologic pH, and may have limited usefulness in preventing histologic damage if
delayed beyond the first several minutes following caustic exposure.41,87 In one in vivo canine model,
orange juice was used to neutralize sodium hydroxide–induced gastric injury and demonstrated no
change in temperature or intraluminal pressure.45 Despite this study, neutralization is not
recommended; there are no other data demonstrating that clinical outcome is improved.
Surgical Management
The decision to perform surgery in patients with caustic ingestions is obvious in the presence of
either endoscopic or diagnostic imaging evidence of perforation,104 severe abdominal rigidity, or
persistent hypotension. Hypotension is a grave finding and often indicates perforation or significant
blood loss. Additionally, elevated PT and PTT,104 as well as acidemia,11 are correlated with severe
caustic injury.
Many patients will not have an obvious indication for surgical intervention despite impending
perforation, necrosis, sepsis, or delayed hemorrhage. Although more challenging to diagnose, all
these sequelae are potentially avoidable if surgery is performed early74 as morbidity and mortality
increase in patients whose surgery is delayed.22,47,85 For this reason, some surgeons advocate
surgery for all patients with grades II and III esophageal burns identified on endoscopy.22,65 This
aggressive approach allows for direct inspection of serosal surfaces and an opportunity for early
surgical repair.
Multiple studies have attempted to codify the signs and symptoms necessary or sufficient to rapidly
identify patients who would benefit from surgery but who lack clear clinical indications. Several
retrospective and prospective series of caustic ingestions found that patients with large ingestions
(>150 mL), shock, acidemia, or coagulation disorders tended to have severe findings on surgical
exploration. These studies also reinforce that the abdominal examination was frequently unreliable in
predicting the need for surgery.104,106 It should be noted, again, that patients with severe acid injuries
may lack abdominal pain, abdominal tenderness, and have positive findings on diagnostic
imaging.19,106 One author used a stepwise approach of bronchoscopy, endoscopy, and abdominal
ultrasonography to provide additional information regarding extent of injury prior to surgery.
Respiratory distress, ascites, pleural fluid, and a serum pH less than 7.2 were used as indications for
surgery.104 A history of a large-volume caustic ingestion (between 40 and 200 mL) should also
prompt consideration of early surgical intervention as delay is associated with increased
mortality.19,104
Surgical intervention may include laparotomy for tissue visualization, resection, and repair of
perforations. Laparoscopy may also be used, although it may not allow inspection of the posterior
aspect of the stomach.
Subacute Management
The extent of tissue injury dictates the subsequent management and disposition of patients with
caustic ingestions.
Grade I Esophageal Injuries.
Patients with isolated grade I injuries of the esophagus do not develop strictures and are not at
increased risk of carcinoma. Their diet can be resumed as tolerated. No further therapy is required.
These patients can be discharged from the emergency department as long as they are able to eat
and drink and their psychiatric status is stable.
Grade IIa Esophageal Injuries.
If endoscopy reveals grade IIa lesions of the esophagus and sparing of the stomach, a soft diet can
be resumed as tolerated or a nasogastric tube can be passed under direct visualization. If oral intake
is contraindicated because of the risk of perforation, feeding via gastrostomy, jejunostomy, or total
parenteral nutrition should be instituted as rapidly as possible. Providing interim enteral support is
imperative as metabolic demands are increased in any patient with a significant burn.
Grades IIb and III Esophageal Injuries.
Patients with grades IIb and III lesions must be followed for the complications of perforation,
infection, and stricture development. Strictures are a debilitating complication of both acid and alkali
ingestions that can evolve over a period of weeks or months. Strictures form as a result of the
natural process by which the body repairs injured tissue through the production of collagen with
resultant scar formation. Although corticosteroid therapy is theorized to arrest the process of
inflammatory repair and potentially prevent stricture formation, there is some evidence that grade III
burns, in particular, will progress to stricture formation regardless of therapy.3,36,100 In addition to
stricture formation, patients with grade III burns are also at high risk for other complications,
including fistula formation, infection, and perforation with associated mediastinitis and peritonitis. The
use of corticosteroids in the management of grade III burns may mask infection and make the
friable, necrotic esophageal tissue more prone to perforation.78 For these reasons, corticosteroid
therapy is not a recommended therapy for grade III esophageal burns. When required in these
patients for other indications such as caustic-induced airway inflammation, short-term corticosteroids
should be administered.
Currently, some controversy exists regarding the use of corticosteroid therapy in the management of
grade IIb circumferential esophageal burns. A meta-analysis of studies completed from 1956 to
1991, with a total of 361 patients, evaluated the efficacy of corticosteroid therapy and found that in
patients with grades II and III esophageal burns, strictures formed in 19% of the corticosteroid-
treated group and in 41% of the untreated group.46 The usefulness of the results of this study,
however, are limited as no distinction was made between grades II and III burns. Another meta-
analysis of studies from 1991 to 2003, with a total of 211 patients, was unable to find a benefit in
treating patients with corticosteroids with grades II and III esophageal burns.78 However, no
distinction was made between grades II and III burns. A systematic pooled analysis of studies from
1956 to 2006, with a total of 328 patients, attempted to reevaluate the usefulness of corticosteroid
therapy in grade II esophageal burns. Although methodologically limited, this study found no benefit
in treating patients with steroids with grade II esophageal burns. A major limitation to the clinical
usefulness of this study is that no distinction was made between grades IIa and IIb burns.24 In
addition, a multitude of case series also failed to clearly differentiate between grades IIa, IIb, and III
lesions, making clinical application of their results difficult.3,15,68,100
Two prospective studies attempted to evaluate the efficacy of corticosteroid therapy for caustic
injuries to the esophagus. Both these studies failed to show a benefit of corticosteroid therapy, and
one even suggested harm.2,3,49 It is imperative that the clinician understands that neither study clearly
differentiates between grades IIb and III lesions.
Adequate human data demonstrating the efficacy of corticosteroids with or without antibiotics in the
treatment of grade IIb circumferential lesions have yet to be generated. Because of the inherent risks
involved in this therapy and the paucity of data supporting their use, corticosteroid therapy in the
management of grade IIb esophageal burns can no longer be routinely recommended.
No major outcome studies have investigated the use of antibiotics alone as prophylactic treatment
for stricture prevention, but most clinicians would agree that it is probably best to reserve antibiotics
for an identified source of infection.
A variety of other management strategies have been used in an attempt to prevent strictures and
esophageal obstruction. In both animal models84 and in human case series,38,67,83 intraluminal stents
and nasogastric tubes67 made of silicone rubber tubing can successfully maintain the patency of the
esophageal lumen. For nutritional support, the stents are usually attached to a feeding tube secured
in the nasopharynx through which the patient can receive feedings without interfering with
esophageal repair. These tubes are left in place for 3 weeks83,84 and are often used with concomitant
corticosteroid and antibiotic therapy. In animal models, the use of a stent for 3 weeks is superior in
maintaining esophageal patency when compared to corticosteroids and antibiotics alone.84
Potential disadvantages of esophageal stents include mechanical trauma at the site and increased
reflux, both of which may inhibit healing.93 A feline model of esophageal exposure to sodium
hydroxide used stents but reported deaths from aspiration and mediastinitis.84 One series of 251
humans exposed to caustics who were managed with silicone rubber stents found that the
procedure was successful in preventing stricture formation.8
Additionally, a plethora of animal models have attempted to identify therapies that attenuate
oxidative damage, inhibit synthesis, or stimulate breakdown of collagen and thereby prevent stricture
formation. β-Amino propionitrile,59 penicillamine,27 N-acetylcysteine,55 halofuginone,31,77 vitamin E,
sphingosylphosphorylcholine, colchicine, erythropoietin,6 mitomycin C,98 ozone,33 fibroblast growth
factor,76 5-fluorouracil,20ibuprofen,37 and retinoic acid16 are some of these xenobiotics. As none of
these treatments have been adequately studied in humans, they cannot currently be recommended
in the routine management of caustic ingestions.
Chronic Treatment of Strictures
Commonly, the management of esophageal strictures includes early endoscopic dilation, for which a
variety of types of dilators are available. Contrast CT can be used to determine maximal esophageal
wall thickness, which can then be used to predict response, as well as the number of sessions
required to achieve adequate dilation. Multiple dilations are often necessary. In one study, patients
with a maximal esophageal wall thickness of 9 mm or greater required more than seven sessions to
achieve adequate dilation. This was significantly higher than in patients with a lesser maximal wall
thickness. Measurement of maximal wall thickness may be also be useful in determining long-term
follow-up, type of nutritional support, and the potential need for surgical repair as an alternative to
dilations. It may also provide an indication for those who should undergo dilation under fluoroscopy
to limit the risk of perforation.
The risk of perforation from esophageal dilation is decreased if the initial procedure is delayed
beyond 4 weeks postingestion, when healing, remodeling, and potential stricture formation in the
esophagus have already taken place. Several series report perforation secondary to esophageal
dilation.36,81,100 Following perforation, patients may complain of dyspnea or chest pain with associated
subcutaneous emphysema or pneumomediastinum. Diagnostic imaging may identify the perforation
and provide information for emergent surgical repair if the diagnosis is unclear.
Patients with stricture formation require long-term endoscopic follow-up for the presence of
neoplastic changes of the esophagus that may occur with a delay of several decades.6
Management of Ophthalmic Exposures
Ophthalmic exposures frequently occur from splash injuries and malicious events as well as from the
alkaline byproducts of sodium azide released in automobile air bag deployment and rupture.102 The
mainstay of therapy for these patients is immediate irrigation of the eye for a minimum of 15 minutes
with 0.9% sodium chloride, lactated Ringer solution, or tap water, if it is the only therapy immediately
available. Several liters of irrigation fluid are recommended. The normal pH of ophthalmic secretions
is approximately 6.5 to 7.6. This can be tested colorimetrically by using a urine dipstick, which can
test a range of pH from 5 to 9.64 Litmus paper can be used in the same fashion. Another useful option
in acid exposures is Nitrazine paper, which changes color from yellow to dark blue at a pH above
6.5.25 These different test strips can be applied to the ophthalmic secretions to test the baseline pH
and followed with intermittent evaluations after 15 minutes of lavage to determine the adequacy of
irrigation. If these xenobiotics are not readily available, irrigation should not be delayed, as the depth
of penetration of the caustic agent will determine outcome. Anterior chamber irrigation may be
required and should be performed emergently by an ophthalmologist. A thorough eye examination
should be completed, and follow-up should be arranged. Chapter 25 contains a more detailed
description of the evaluation and management of toxicologic emergencies of the eye.
SUMMARY
Initial management of all patients with caustic exposures begins with universal precautions in
an effort to prevent further contamination of staff, other patients, and equipment.
In patients with caustic ingestions, airway assessment and stabilization are of primary
importance. Airway edema is the only indication for initiation of corticosteroid therapy.
There is no routine recommendation for induced emesis, lavage, activated charcoal,
neutralization, or dilutional therapy.
Significant caustic injury should be suspected in all patients with intentional ingestions and in
patients with unintentional ingestions presenting with stridor; vomiting; drooling; and pain in
the oropharynx, chest, or abdomen.
All patients with suspected significant ingestions should undergo endoscopy or CT
emergently so that effective treatment strategies may be initiated expeditiously.
Surgeons should be involved in the initial assessment of all patients with suspected
significant ingestions and those who have an acute abdomen or hypotension so that any
surgical intervention deemed necessary may be performed promptly.
Acknowledgments
Robert S. Hoffman, MD, and Rama B. Rao, MD, contributed to this chapter in previous editions.
References
1.
Alford BR, Harris HH: Chemical burns of the mouth, pharynx and esophagus. Ann Otol Rhinol
Laryngol. 1959;68:122–128.
CrossRef [PubMed: 13627948]
2.
Andersen AH: Experimental studies on the pharmacology of activated charcoal.III. Adsorption of
gastrointestinal contents. Acta Pharmacol. 1948;4:275–284.
CrossRef
3.
Anderson KD, Rouse TM, Randolph JG: A controlled trial of corticosteroids in children with
corrosive injury of the esophagus. N Engl J Med. 1990;323:637–640.
CrossRef [PubMed: 2200966]
4.
Appelqvist P, Salmo M: Lye corrosion carcinoma of the esophagus: a review of63
cases. Cancer. 1980;45:2655–2658.
CrossRef [PubMed: 7378999]
5.
Ashcraft KW, Padula RT: The effect of dilute corrosives on the
esophagus. Pediatrics.1974;53:226–232. [PubMed: 4812007]
6.
Bakan V, Garipardic M, Okumus M et al.: The protective effect of erythropoietin on the acute
phase of corrosive esophageal burns in a rat model. Pediatr Surg Int.2010;26:195–201.
CrossRef [PubMed: 19760200]
7.
Bernhardt J, Ptok H, Wilhelm L, Ludwig K: Caustic acid burn of the upper gastrointestinal tract:
first use of endosonography to evaluate the severity of the injury.Surg
Endosc. 2002;16:1004. [PubMed: 12163973]
8.
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. 1996;110:1041–
1045.
CrossRef [PubMed: 8944879]
9.
Borja AR, Ransdell HT, Thomas TV, Johnson W: Lye injuries of the esophagus: analysis of ninety
cases of lye ingestion. J Thorac Cardiovasc Surg. 1969;57:533–538. [PubMed: 5774631]
10.
Chen SC, Weng HP, Chen WJ et al.: Selective use of ultrasonography for the detection of
pneumoperitoneum. Acad Emerg Med. 2002;9:643–645.
CrossRef [PubMed: 12045083]
11.
Cheng YJ, Kao EL: Arterial blood gas analysis in acute caustic ingestion injuries.Surg
Today. 2003;33:483–485. [PubMed: 14506990]
12.
Chobanian SJ: Accidental ingestion of liquid zinc chloride: local and systemic effects.Ann Emerg
Med. 1981;10:91–93.
CrossRef [PubMed: 6784611]
13.
Christensen BT: Prediction of complications following unintentional caustic ingestion in children. Is
endoscopy always necessary? Acta Paediatr. 1995;84:1177–1182.
CrossRef [PubMed: 8563232]
14.
Clausen JO, Nielsen TL, Fogh A: Admission to Danish hospitals after suspected ingestion of
corrosives. Dan Med Bull. 1994;41:234–237. [PubMed: 8039438]
15.
Cleveland WW, Thornton N, Chesney JG, Lawson RB: The effect of prednisone in the prevention
of esophageal stricture following the ingestion of lye. South Med J.1958;51:861–864.
CrossRef [PubMed: 13556202]
16.
Corduk N, Koltuksuz U, Calli-Demirkan N et al.: Effects of retinoic acid and zinc on the treatment
of caustic esophageal burns. Pediatr Surg Int. 2010;26:619–624.
CrossRef [PubMed: 20204651]
17.
Crain EF, Gershel JC, Mezey AP: Caustic ingestions—symptoms as predictors of esophageal
injury. Am J Dis Child. 1984;138:863–865.
CrossRef [PubMed: 6475876]
18.
Dantas RO, Mamede RCM: Esophageal motility in patients with esophageal caustic injury. Am J
Gastroenterol. 1996;91:1157–1161. [PubMed: 8651163]
19.
Dilawari JB, Singh S, Rao PN, Anand BS: Corrosive acid ingestion in man—a clinical and
endoscopic study. Gut. 1984;25:183–187.
CrossRef [PubMed: 6693046]
20.
Duman L, Buyukyavuz BI, Altuntas I et al.: The efficacy of single-dose 5-fluorouracil therapy in
experimental caustic esophageal burn. J Pediatr Surg. 2011;46:1893–1897.
CrossRef [PubMed: 22008323]
21.
Einhorn A, Horton L, Altieri M et al.: Serious respiratory consequences of detergent ingestions in
children. Pediatrics. 1989;84:472–474. [PubMed: 2671913]
22.
Estera A, Taylor W, Mills LJ: Corrosive burns of the esophagus and stomach: a recommendation
for an aggressive surgical approach. Ann Thorac Surg.1986;41:276–283.
CrossRef [PubMed: 3954499]
23.
Fadoo F, Ruiz DE, Dawn SK et al.: Helical CT esophagography for the evaluation of suspected
esophageal perforation or rupture. AJR Am J Roentgenol. 2004;182:1177–1179.
CrossRef [PubMed: 15100114]
24.
Fulton JA, Hoffman RS: Steroids in second degree caustic burns of the esophagus: a systematic
pooled analysis of fifty years of human data: 1956-2006. Clin Toxicol (Phila). 2007;45:402–408.
CrossRef [PubMed: 17486482]
25.
Garite TJ, Spellacy WN: Premature rupture of membranes. In: Scott JR, DiSaia PJ,
Hammond CB, Spellacy WN, ed. Danforth’s Obstetrics and Gynecology. 7th ed. Philadelphia:
Lippincott; 1994:30.
26.
Gaudreault P, Parent M, McGuigan MA et al.: Predictability of esophageal injury from signs and
symptoms: a study of caustic ingestion in 378 children. Pediatrics.1983;71:767–770. [PubMed:
6835760]
27.
Gehanno P, Geudon C: Inhibition of experimental esophageal lye strictures bypenicillamine. Arch
Otolaryngol. 1981;107:145–147.
CrossRef [PubMed: 7469901]
28.
Genc A, Mutaf O: Esophageal motility changes in acute and late periods of caustic esophageal
burns and their relation to prognosis in children. J Pediatr Surg.2002;37:1526–1528.
CrossRef [PubMed: 12407532]
29.
Gillis DA, Higgins G, Kennedy R: Gastric damage from ingested acid in children. J Pediatr
Surg. 1985;20:494–496.
CrossRef [PubMed: 4057013]
30.
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.1992;10:189–194.
CrossRef [PubMed: 1586425]
31.
Gunel E, Caglayan F, Caglayan O et al.: Effect of antioxidant therapy on collagen synthesis in
corrosive esophageal burns. Pediatr Surg Int. 2002;18:24–27.
CrossRef [PubMed: 11793058]
32.
Gupta S, Levine MS, Rubesin SE et al.: Usefulness of barium studies for differentiating benign
and malignant strictures of the esophagus. AJR Am J Roentgenol. 2003;180:737–744.
CrossRef [PubMed: 12591686]
33.
Guven A, Gundogdu G, Sadir S et al.: The efficacy of ozone therapy in experimental caustic
esophageal burn. J Pediatr Surg. 2008;43:1679–1684.
CrossRef [PubMed: 18779006]
34.
Haller JA, Andrews HG, White JJ et al.: Pathophysiology and management of acute corrosive
burns of the esophagus: results of treatment in 285 children. J Pediatr Surg.1971;6:578–583.
CrossRef [PubMed: 5126277]
35.
Havanond C, Havanond P: Initial signs and symptoms as prognostic indicators as severe
gastrointestinal tract injury due to corrosive injury. J Emerg Med.2007;33(4):349–353.
CrossRef [PubMed: 17976790]
36.
Hawkins DB, Demeter MJ, Barnett TE: Caustic ingestion: controversies in management. A review
of 214 cases. Laryngoscope. 1980;90:98–109.
CrossRef [PubMed: 7356772]
37.
Herek O, Karabul M, Yenisey C, Erkus M: Protective effects of ibuprofen against caustic
esophageal burn injury in rats. Pediatr Surg Int. 2010;26:721–727.
CrossRef [PubMed: 20480167]
38.
Hill JL, Norberg HP, Smith MD et al.: Clinical technique and success of the esophageal stent to
prevent corrosive strictures. J Pediatr Surg. 1976;11: 443–450.
CrossRef [PubMed: 957069]
39.
Hirst LW, Summers PM, Griffiths et al.: Controlled trial of hyperbaric oxygen treatment for alkali
corneal burn in the rabbit. Clin Exp Ophthalmol. 2004;32:67–70.
CrossRef
40.
Hoffman RS, Howland MA, Kamerow HN, Goldfrank LR: Comparison of titratable acid/alkaline
reserves and pH in potentially caustic household products. J Toxicol ClinToxicol. 1989;27:241–261.
CrossRef [PubMed: 2600988]
41.
Homan CS, Maitra SR, Lane BP et al.: Effective treatment for acute alkali injury to the esophagus
using weak acid neutralization therapy: an ex vivo study. Acad EmergMed. 1995;2:952–958.
CrossRef [PubMed: 8536120]
42.
Homan CS, Maitra SR, Lane BP et al.: Histopathologic evaluation the therapeutic efficacy of water
and milk dilution for esophageal acid injury. Acad Emerg Med.1995;2:587–591.
CrossRef [PubMed: 8521203]
43.
Homan CS, Maitra SR, Lane BP et al.: Therapeutic effects of water and milk for acute alkali injury
of the esophagus. Ann Emerg Med. 1994;24:14–19.
CrossRef [PubMed: 8010543]
44.
Homan CS, Maitra SR, Lane BP, Geller ER: Effective treatment of acute alkali injury of the rat
esophagus with early saline dilution therapy. Ann Emerg Med. 1993;22:178–182.
CrossRef [PubMed: 8427427]
45.
Homan CS, Singer AJ, Henry MC, Thode HC: Thermal effects of neutralization therapy and water
dilution for acute alkali exposure in canines. Acad Emerg Med.1997;4:27–32.
CrossRef [PubMed: 9110008]
46.
Howell JM, Dalsey WC, Hartsell FW, Butzin CA: Steroids for the treatment of corrosive
esophageal injury: a statistical analysis of past studies. Am J Emerg Med.1992;10:421–425.
CrossRef [PubMed: 1642705]
47.
Hwang TL, Shen-Chen SM, Chen MF: Nonthoracotomy esophagectomy for corrosive esophagitis
with gastric perforation. Surg Gynecol Obstet. 1987;164:537–540. [PubMed: 3589908]
48.
Iino M, O’Donnell CJ, Burke MP: Post-mortem CT findings following intentional ingestion of
mercuric chloride. Leg Med (Tokyo). 2009;11:136–138.
CrossRef [PubMed: 19195921]
49.
Jovic-Stosic J, Todorovic V, Doder R: Steroid treatment of corrosive injury. J ToxicolClin
Toxicol. 2004;42:417–418.
50.
Kamijo Y, Kondo I, Soma K et al.: Alkaline esophagitis evaluated by endoscopic ultrasound. J
Toxicol Clin Toxicol. 2001;39:623–625.
CrossRef [PubMed: 11762671]
51.
Landau GD, Saunders WH: The effect of chlorine bleach on the
esophagus. ArchOtolaryngol. 1964;80:174–176.
CrossRef [PubMed: 14160140]
52.
Leape LL, Ashcraft KW, Scarpelli DG, Holder TM: Hazard to health—liquid lye. N Engl J
Med. 1971;284:578–581.
CrossRef [PubMed: 5100891]
53.
Litovitz T, Whitaker N, Clark L, White NC, Marsolek M: Emerging battery-ingestion hazard: clinical
implications. Pediatrics. 2010;125:1168–1177.
CrossRef [PubMed: 20498173]
54.
Liu A, Richardson M, Robertson WO: Effects of N-acetylcysteine on caustic burns.Vet Hum
Toxicol. 1985;28:316.
55.
Lowe JE, Graham DY, Boisaubin EV, Lanza FL: Corrosive injury to the stomach: the natural
history and role of fiberoptic endoscopy. Am J Surg. 1979;137:803–806.
CrossRef [PubMed: 453476]
56.
Luedtke P, Levine MS, Rubesin SE et al.: Radiologic diagnosis of benign esophageal strictures: a
pattern approach. Radiographics. 2003;23:897–909.
CrossRef [PubMed: 12853664]
57.
Mack RB: Decant the wine, prune back your long-term hopes. N C Med J.1987;48:593–
595. [PubMed: 3480430]
58.
Madden JW, Davis WM, Butler C, Peacock EE: Experimental esophageal lye burns II: correcting
established strictures with betaaminopropionitrile and bougienage. AnnSurg. 1973;178:277–284.
CrossRef [PubMed: 4729752]
59.
Mandarikan BA: Ingestion of dishwasher detergent by children. Br J Clin Pract.1990;44:35–
36. [PubMed: 2317439]
60.
Maull KI, Osmand AP, Maull CD: Liquid caustic ingestions: an in vitro study of the effects of buffer,
neutralization, and dilution. Ann Emerg Med. 1985;14:1160–1162.
CrossRef [PubMed: 4061986]
61.
McKinney PE: Zinc chloride ingestion in a child—exocrine pancreatic insufficiency.Ann Emerg
Med. 1995;25:562. [PubMed: 7710173]
62.
McKinney PE, Brent J, Kulig K: Acute zinc chloride ingestion in a child—local and systemic
effects. Ann Emerg Med. 1994;23:1383–1387.
CrossRef [PubMed: 7515217]
63.
McNeely MDD: Urinalysis. In: Sonnenwirth AC, Jarret L, ed. Gradwohl’s Clinical Laboratory
Methods and Diagnosis. St. Louis: Mosby; 1980:483.
64.
Meredith W, Kon ND, Thompson JN: Management of injuries from liquid lye ingestion. J
Trauma. 1988;28:1173–1180.
CrossRef [PubMed: 3411641]
65.
Millar AJ, Numanoglu A, Mann M et al.: Detection of caustic oesophageal injury with technetium
99m-labelled sucralfate. J Pediatr Surg. 2001;36:262–265.
CrossRef [PubMed: 11172412]
66.
Mills LJ, Estrera AS, Platt MR: Avoidance of esophageal stricture following severe caustic burns by
the use of an intraluminal stent. Ann Thorac Surg. 1979;28:63–65.
CrossRef
67.
Mitani M, Hirata K, Fukuda M, Kaneko M: Endoscopic ultrasonography in corrosive injury of the
upper gastrointestinal tract by hydrochloric acid. J Clin Ultrasound.1996;24:40–42.
CrossRef [PubMed: 8655667]
68.
Mozingo DW, Smith AA, McManus WF et al.: Chemical burns. J Trauma.1988;28:642–647.
CrossRef [PubMed: 3367407]
69.
Mutaf O, Avanoglu A, Ozok G: Management of tracheoesophageal fistula as a complication of
esophageal dilatations in caustic esophageal burns. J Pediatr Surg.1995;30:823–826.
CrossRef [PubMed: 7666316]
70.
Nirapathpongporn S et al.: Pneumoperitoneum detected by
ultrasound. Radiology.1984;150(3):831–832.
CrossRef [PubMed: 6695086]
71.
Norton RA: Esophageal and antral strictures due to ingestion of household ammonia—report of two
cases. N Engl Med. 1960;262:10–12.
CrossRef
72.
Nunes AC, Romaozinho JM, Pontes JM et al.: Risk factors for stricture development after caustic
ingestion. Hepatogastroenterology. 2002;49:1563–1566. [PubMed: 12397736]
73.
Ochi K, Ohashi T, Sato S et al.: Surgical treatment for caustic ingestion injury of the pharynx,
larynx, and esophagus. Acta Otolaryngol Suppl. 1996;522:116–119. [PubMed: 8740824]
74.
Otcu S, Karnak I, Tanyel FC et al.: Biochemical indicators of caustic ingestion and/or
accompanying esophageal injury in children. Turk J Pediatr. 2003;45:21–25. [PubMed: 12718366]
75.
Okata Y, Hisamatsu C, Nishijima E, Okita Y: Topical application of basic fibroblast growth factor
reduces esophageal stricture and esophageal neural damage after sodium hydroxide-induced
esophagitis in rats. Pediatr Surg Int. 2012;28:43–49.
CrossRef [PubMed: 22009209]
76.
Ozcelik MF, Pekmezci S, Saribeyoglu et al.: The effect of halofuginone, a specific inhibitor of
collagen type 1 synthesis, in the prevention of esophageal strictures related to caustic injury. Am J
Surg. 2004;187:257–260.
CrossRef [PubMed: 14769315]
77.
Pelclova D, Navratil T: Corrosive ingestion: the evidence base. Are steroids still indicated in
second- and third-degree corrosive burns of the oesophagus? J Toxicol Clin Toxicol. 2004;42:414–
416.
78.
Potter JL: Acute zinc chloride ingestion in a young child. Ann Emerg Med.1981;10:267–269.
CrossRef [PubMed: 6784612]
79.
Previterra C, Guisti F, Guglielmi M: Predictive value of visible lesions (cheeks, lips, oropharynx) in
suspected caustic ingestion: may endoscopy reasonably be omitted in completely negative pediatric
patients? Pediatr Emerg Care. 1990;6:176–178.
CrossRef [PubMed: 2216918]
80.
Ragheb MI, Ramadan AA, Khalia MA: Management of corrosive
esophagitis.Surgery. 1976;79:494–498. [PubMed: 1265656]
81.
Ramasamy K, Gumaste VV: Corrosive ingestion in adults. J Clin Gastroenterol.2003;37:119–124.
CrossRef [PubMed: 12869880]
82.
Reyes HM, Hill JL: Modification of the experimental stent technique for esophageal burns. J Surg
Res. 1976;20:65–70.
CrossRef [PubMed: 1256046]
83.
Reyes HM, Lin CY, Schlunk FF, Repogle RL: Experimental treatment of corrosive esophageal
burns. J Pediatr Surg. 1974;9:317–327.
CrossRef [PubMed: 4843986]
84.
Ribet ME: Esophagogastrectomy for acid injury. Ann Thorac Surg. 1992;53:738–742.
CrossRef [PubMed: 1554296]
85.
Ritter FN, Newman DE: A clinical and experimental study of corrosive burns of the stomach. Ann
Otol Rhinol Laryngol. 1968;77:830–842.
CrossRef [PubMed: 5680934]
86.
Rumack BH, Burrington JD: Caustic ingestions: a rational look at diluents. Clin
Toxicol. 1977;11:27–34.
CrossRef [PubMed: 577479]
87.
Ryu H, Jeung K, Lee B et al.: Caustic injury: can CT grading system enable prediction of
esophageal stricture? Clin Toxicol (Phila). 2010;48:137–142.
CrossRef [PubMed: 20199130]
88.
Scharman EJ: Liquid “laundry pods” : a missed global toxicosurveillance opportunity.Clin Toxicol
(Phila). 2012;50:725–726.
CrossRef [PubMed: 22845559]
89.
Schild JA: Caustic ingestion in adult patients. Laryngoscope. 1985;95:1199–1201.
CrossRef [PubMed: 4046703]
90.
Scott JC, Jones B, Eisele DW, Ravich WJ: Caustic ingestion injuries of the upper aerodigestive
tract. Laryngoscope. 1992;102:1–8. [PubMed: 1731151]
91.
Shirazi S, Schulze-Delrieu K, Custer-Hagen T et al.: Motility changes in opossum esophagus from
experimental esophagitis. Dig Dis Sci. 1989;34:1668–1676.
CrossRef [PubMed: 2582979]
92.
Sinar DR, Fletcher JR, Cordova CC et al.: Acute acid-induced esophagitis impairs esophageal
peristalsis in baboons. Gastroenterology. 1981;80:1286.
93.
Swanson JO, Levine MS, Redfern RO, Rubesin SE: Usefulness of high-density barium for
detection of leaks after esophagogastrectomy, total gastrectomy, and totallaryngectomy. AJR Am J
Roentgenol. 2003;181:415–420.
CrossRef [PubMed: 12876019]
94.
Tayyem R, Siddiqui T, Musbahi K, Ali A: Gastric stricture following zinc chloride ingestion. Clin
Toxicol (Phila). 2009;47:689–690.
CrossRef [PubMed: 19640233]
95.
Thompson JN: Corrosive esophageal injuries I: a study of nine cases of concurrent accidental
caustic ingestions. Laryngoscope. 1987;97:1060–1066. [PubMed: 3306232]
96.
Tugay M, Utkan T, Utkan Z: Effects of caustic lye injury to the esophageal smooth muscle
reactivity: in vitro study. J Surg Res. 2003;113:128–132.
CrossRef [PubMed: 12943821]
97.
Turkyilmaz Z, Sonmez K, Karabulut R et al.: Mitomycin C decreases the rate of stricture formation
in caustic esophageal burns in rats. Surgery. 2009;145:219–225.
CrossRef [PubMed: 19167978]
98.
Viscomi GJ, Beekhuis GJ, Whitten CF: An evaluation of early esophagoscopy and corticosteroid
therapy in the management of corrosive injury of the esophagus. J Pediatr. 1961;59:356–360.
CrossRef [PubMed: 13781585]
99.
Webb WR, Koutras P, Ecker RR, Sugg WL: An evaluation of steroids and antibiotics in caustic
burns of the esophagus. Ann Thorac Surg. 1970;9:95–101.
CrossRef [PubMed: 5410979]
100.
White CS, Templeton PA, Attar S: Esophageal perforation: CT findings. AJR Am
JRoentgenol. 1993;160:767–770.
CrossRef [PubMed: 8456662]
101.
White JE, McClafferty K, Orfon RB et al.: Ocular alkali burn associated with automobile air-bag
activation. CMAJ. 1995;153:933–934. [PubMed: 7553495]
102.
Woodring JH, Heiser MJ: Detection of pneumoperitoneum on chest radiographs: comparison of
upright lateral and posteroanterior projections. AJR Am J Roentgenol.1995;165:45–47.
CrossRef [PubMed: 7785629]
103.
Wu MH, Lai WW: Surgical management of extensive corrosive injuries of the alimentary tract. Surg
Gynecol Obstet. 1993;177:12–16. [PubMed: 8322144]
104.
Zargar SA, Kochlar R, Mehta S, Mehta SK: The role of fiberoptic endoscopy in the management
of corrosive ingestion and modified endoscopic classification of burns.Gastrointest
Endosc. 1991;37:165–169.
CrossRef [PubMed: 2032601]
105.
Zargar SA, Kochlar R, Nagi B et al.: Ingestion of corrosive acids: spectrum of injury to upper
gastrointestinal tract and natural history. Gastroenterology. 1989;97:702–707. [PubMed: 2753330]
106.
Zwischenberger JB, Savage C, Bidani A: Surgical aspects of esophageal disease: perforation and
caustic injury. Am J Respir Crit Care Med. 2002;165:1037–1040.
Recommended