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TITLE: Chemical Burns of the Digestive Tract
SOURCE: Dept. of Otolaryngology, UTMB, Grand Rounds
DATE: December 8, 1993
RESIDENT PHYSICIAN: Robert Hoffman, MD
FACULTY: Francis B. Quinn, Jr. MD
DATABASE ADMINISTRATOR: Melinda McCracken, M.S.
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"This material was prepared by resident physicians in partial fulfillment
of educational requirements established for the Postgraduate Training
Program of the UTMB Department of Otolaryngology/Head and Neck Surgery
and was not intended for clinical use in its present form. It was
prepared for the purpose of stimulating group discussion in a conference
setting. No warranties, either express or implied, are made with respect
to its accuracy, completeness, or timeliness. The material does not
necessarily reflect the current or past opinions of members of the UTMB
faculty and should not be used for purposes of diagnosis or treatment
without consulting appropriate literature sources and informed professional
opinion."

History and Epidemiology:
With the industrialization of society, people were afforded access to a
variety of conveniently packaged acidic and cleaning agents. Availability,
lack of warning labels, adequate public awareness of the toxicity of these
materials led to an alarming number of severe pediatric esophageal injuries
caused by their ingestion. A typical cleaner in the early twentieth century
was sodium hydroxide, which is colorless and odorless. In the 1920s,
Chevalier Jackson and other otolaryngologists began lobbying for legislation
to control the sale of these substances. Legislation over the next several
decades culminated in the Poison Prevention Packaging Act and the Hazardous
Substance Act of the 1970s, which greatly reduced the caustic content of the
cleaners and improved quality of labeling and child-resistant packaging.
Despite these measures, digestive caustic injuries are still prevalent, with
an estimated 5000 cases occurring yearly in the United States. Caustic
injuries are caused overwhelmingly by alkaline substances, especially by
liquid drain cleaners. Small "button" alkaline batteries, Clinitest
tablets, bleaches, detergents, hydrochloric acid, sulfuric acid, and
concentrated ammonia also have caused aerodigestive injuries. Children have
the most frequent caustic injuries, caused mostly by accidental ingestions;
most adult aerodigestive caustic injuries can be credited to suicide
attempts. In the United States today, a variety of household agents remain
caustic enough to cause injury if ingested. Although highly concentrated
liquid is no longer sold for household use, the moderately concentrated
(<10%) liquid drain cleaners available today are still strong enough to
occasionally cause visceral perforation. More often, the patient who
ingests one of these moderately concentrated products recovers from the
acute injury, but later, strictures may develop. Currently available
crystalline drain cleaners may contain more than 50% sodium hydroxide and
can produce transmural injury if consumed in quantity. However, pain
usually limits the quantity swallowed so that perforation is uncommon. Most
household detergents are only mildly alkaline, but nonphosphate detergents
contain builders (often silicates and carbonates) that increase the pH.
Nonphosphate detergents produce severe experimental esophageal injuries, but
there are few reports of serious human esophageal injuries due to these
agents. Liquid automatic dishwashing detergents and liquid laundry
detergents may have a pH above 12, but the titratable base content is less
than that for sodium hydroxide. Although rare cases of serious injury due
to detergents have been reported, the scarcity of such reports suggests that
detergents cause serious injury only in special circumstances. Ammonia
solutions in excess of 4% concentration are caustic, but most household
ammonia products are of lower concentration. Liquid household bleaches
contain 5.25% or less sodium hypochlorite. Concentrations in this range
have only rarely been reported to cause serious injuries. Granular or
powdered household bleaches are more injurious, in part because they remain
in contact with the mucosa longer than liquid preparations and in part
because they are more concentrated. The primary morbidity in aerodigestive
caustic injuries results from injury to the esophagus. The mortality from
caustic esophageal burns has decreased over the last 100 years as the
management of their sequelae has improved. Earlier in this century chronic
esophageal strictures alone accounted for a mortality rate of more than 40%,
and management of the unvisualized esophageal burns usually centered on
crude supportive care. In this century, diagnostic imaging and endoscopy
provided a basis for the development of safe stricture dilatation and
esophageal reconstruction. Current mortality rates are between O% and 20%,
with most deaths caused by the most severe transmural burns.

Pathophysiology:
The depth of necrosis in experimental lye injury varies with the
concentration of the lye. After 10 seconds of exposure to 3.8% sodium
hydroxide, necrosis is largely confined to the mucosa and submucosa. With
10.7% and 16.9% solutions, the muscular layers are necrosed. Transmural
necrosis occurred after application of 22.5% sodium hydroxide. Experimental
lye injury of the esophagus may be divided into three phases. Lye causes
liquefaction necrosis, penetrating deeply into tissue. Destruction is
limited only when the destroyed tissue dilutes and neutralizes the alkali
sufficiently to render it harmless. The superficial epithelium is
destroyed, and necrosis may extend into the submucosa, the muscularis, or
even into periesophageal structures. The injured esophageal wall is invaded
by bacteria and polymorphonuclear leukocytes, and vascular thrombosis
occurs. Viewed grossly from the mucosal side, the injured tissue appears
red to cyanotic but does not immediately slough or ulcerate. Between the
second and fifth days, the vascular thrombosis and polymorphonuclear
response become more intense, and the superficial necrotic layers form a
cast and slough. Because of these delayed and evolving changes the depth of
early caustic lesions is often difficult to determine by gross inspection of
the mucosal surface. The second, or reparative, phase begins on about the
fifth day with the development of granulation tissue at the periphery of the
injury. Collagen deposition peaks during the second week but continues for
months. Mucosal re-epithelialization begins during this phase but may not
be complete for several weeks or even months. The third phase, scar
retraction, begins as early as the end of the second week. The recently
formed collagen contracts both circumferentially and longitudinally,
resulting in esophageal shortening and stricture formation. The collagen
fibers usually begin to contract 3 or 4 weeks after the initial insult, and
irregular formation of this collagen matrix enables adhesive bands to form.
Pseudodiverticula form between these adhesions as the contracting process
continues, and stricture formation continues in the esophageal lumen until a
dense fibrous scar replaces the submucosal and muscular layers. In general,
only circumferential burns lead to esophageal strictures severe enough to
cause clinically significant morbidity. In contrast to lye, strong acids
have often been said to cause severe gastric necrosis and stenosis, with
relative sparing of the esophagus. Acidic substances cause a coagulation
necrosis, which tends to limit extension into the muscular layer.
Commercially available liquid cleaning products contain hydrochloric and
sulfuric acids. The rapid transit of these acids through the esophagus,
coupled with the necrotic mucosal coagulum they produce, reduces their
contact with deeper submucosal and muscular esophageal layers, often sparing
the esophagus significant trauma. However, recent reports emphasize that
strong acids may cause serious esophageal and laryngeal injuries and that
liquid lye may cause gastric necrosis. The coagulum formed during the
coagulative necrosis induced by acid may limit the depth of penetration of
the acid; but gastric and esophageal perforations due to ingested acids have
been reported, so this distinction is of little clinical importance. The
distribution and severity of injury with acid or alkali depend as much on
the physical characteristics of the product (solid versus liquid,
volatility, titratable acid or base) as on the type os necrosis produced.
Clinitest tablets contain NaOH and should be regarded as equivalent to a
granular drain cleaner. Excessively long contact with bleaches containing
sodium hypochlorite has caused stricture formation in the laboratory
esophageal model but stricture formation from shorter contact has been
infrequent. Significant mucosal injuries from alkaline dishwashing
detergents are rare. Household ammonia can produce impressive esophageal
burns. The increasingly available disk-type alkaline battery contains KOH
or NaOH within the plastic seal that joins its cathode and anode.
Esophageal injury from an ingested battery may be caused by chemical leakage
or by an electrolytic phenomenon from a generated current. Esophageal
obstruction with these objects leads to an aggressive lytic process that
frequently results in esophageal perforation. A useful classification of
caustic lesions is borrowed from thermal burns. First-degree burns can be
characterized by mucosal edema and erythema with superficial mucosal slough.
Second-degree burns involve deeper tissue, with the necrotic process
extending into the muscular layer; exudate, ulceration, and loss of mucosa
are characteristic. In third-degree burns, the entire esophageal wall is
necrotic, with possible extension of the damage into the periesophageal
tissues.

Presentation, Diagnosis, and Emergency Treatment:
Patients presenting with caustic injuries of the upper digestive tract
display a wide variety of symptoms and physical findings. Accurate
correlation of these findings with the extent of injury would be useful in
developing a therapeutic plan, especially in the pediatric or uncooperative
patient. However, multiple studies have failed to show a consistent
relationship between symptoms and signs and the ability to predict
esophagogastric injury. Although lO% of the patients in several large
series have had significant esophageal injury without accompanying signs or
symptoms attributable to caustic ingestion, as many as 70% of patients in
other series have had oropharyngeal burns without associated esophageal
injury. In contrast indicators of severe injury, such as thoracoabdominal
pain or tachycardia with hypotension, can be correlated reliably with a
significant injury, as can progressive airway obstruction from supraglottic
and glottic edema. Although airway difficulties are not confined to one age
group, they are more frequent in children because of the smaller, more
easily compromised pediatric larynx. There are many important points to
remember when initially evaluating a patient. The absence of visible
lesions cannot exclude the occurrence of visceral burns. In the patients
showing cheeks, lips or oropharyngeal lesions, the risk of dangerous
visceral burns (second or third degree) is higher than in those with theses
lesions. Higher than first degree cheek, lip or oropharyngeal lesions
almost invariably are associated with dangerous visceral burns. Signs or
symptoms do not adequately predict the presence or the severity of visceral
lesions, even if spontaneous vomiting is associated with a high incidence of
second to third degree visceral burns. When individual signs or symptoms
are correlated with the severity of esophageal lesion, vomiting, followed by
dysphagia, excessive salivation, and abdominal pain are most frequently
associated with a second or third degree lesion. For every patient with
signs, symptoms, or a history of caustic ingestion, verification of the
ingested agent and assessment of the injury are paramount. The approximate
time and amount of ingestion and the pH and physical form of the caustic
material should be established. If the pH is not available from published
toxicology information, standard pH paper can be used on its liquid remains.
The initial physical examination of the patient suspected of having ingested
a caustic material should focus first on detection of the immediate
complications. Patients with oral mucosal burns and tongue edema should be
monitored closely for developing airway obstruction, which may be heralded
by dyspnea, hoarseness, and stridor. Fiberoptic laryngoscopy is a valuable
adjunct in the assessment of the larynx and hypopharynx for injury. Because
blind nasotracheal intubation may lead to obstructive bleeding and
esophageal or hypopharyngeal perforation, it should not be performed. In
the patient with rapid airway deterioration and poor visualization of the
larynx, safer procedures are emergency cricothyrotomy or tracheotomy. In
less critical cases, an intravenous bolus of dexamethasone (pediatric dose,
0.5 to 1.0 mg /kg; adult dose, 20 to 30 mg total dose) can help to maintain
airway patency. Dyspnea associated with rales and rhonchi suggests
pulmonary infiltrates from aspiration or mediastinitis. Chest and abdominal
radiographs should be obtained to rule out infiltrates, free air, and
widening of the mediastinum. Arterial blood gas measurements are helpful in
detecting hypoxia or acid-base derangements. Associated severe
thoracoabdominal pain, abdominal rigidity, and tenderness suggest esophageal
or gastric perforation. As in all patients suspected of having a severe
injury, large bore intravenous catheters for medications and fluid
resuscitation should be established. Admitting the patient into the
hospital for observation and further treatment is essential. The injury
associated with extremely alkaline substances is completed almost
immediately on mucosal contact. In contrast, the acute injury phase of
acidic injuries may be prolonged. Productive initial therapy should be
directed at preventing further injury, especially after acid ingestion.
Burns of the oral mucosa and lips can be cleansed with water; granules of
lye that are still visible transorally should be removed. The use of
emetics is condemned. Emetics extend the time that the caustic material is
in contact with the esophageal mucosa, and they increase the risk of
obstructing laryngeal injury and aspiration. Although blind nasogastric
intubation in the emergency room generally should be avoided, some
physicians have advocated its use in patients with acid injuries to
decompress the stomach and provide a means for gentle lavage with cold
water. Neutralization of the ingested substance through buffering should
never be attempted. It is impractical to give an acidic antidote (eg, acetic
acid) in sufficient strength or volume to buffer a strong alkali, and the
injury has usually been completed by the time the patient arrives at the
emergency room. The use of antacid buffers in acidic injuries poses
additional theoretic risks of thermal injury to the stomach and surrounding
viscera and the real risk of inducing vomiting, producing more injury to the
upper aerodigestive tract.

Assessment of Injury:
After the initial examination and stabilization of a patient
with caustic ingestion, an accurate assessment of the esophageal
and gastric injury is vital. If the injury is left untreated,
severe, debilitating esophageal strictures can lead to chronic
malnutrition and dehydration, potentially ending in death.
Failure to intervene in esophageal or gastric perforations
results in peritonitis, mediastinitis, and death. Therefore,
proper characterization of the type and extent of injury provides
the otolaryngologist with the information needed to guide care
and avoid significant morbidity and catastrophic complications.

Radiology:
Radiographic techniques using water soluble contrast media for studying
acute injuries have sometimes been inaccurate in showing clinically
significant esophageal injury, with 30% to 90% false-negative rates
reported. These conflicting findings highlight the value of direct
endoscopic visualization of the esophagus and stomach as a secure method of
establishing the degree of injury. However, severe esophageal injury has
been predicted by the radiographic demonstration of atony and poor
distensibility as early as the day of injury. Initial findings included
esophageal dilatation with atony, poor distensibility of the esophagus, and
localized esophageal narrowing. Barium swallows should first be used at
three weeks when stricture formation may first start. It should then be
performed periodically to reevaluate for strictures and whenever new
dysphagia is reported by the patient.

Endoscopy:
Several days after a caustic esophageal injury, any necrotic mucosa,
submucosa, and muscularis will have sloughed. The resulting ulcerated
portion of the esophageal wall is prone to perforation by a nasogastric tube
or esophagoscope. Many early investigators advocated limiting endoscopy to
patients with mild to moderate oral burns and systemic symptoms and advised
against using it in patients suspected of having severe burns. Some
investigators studying pediatric injuries advocated endoscopy 2 weeks after
injury, but only in patients suspected of having sustained significant
burns. However, because of the inaccuracy of predicting the degree of
injury from signs and symptoms, most investigators now recommend
esophagoscopy as soon as possible after ingestion. Only if endoscopy is not
possible should water soluble contrast radiologic studies be the initial
method of study. Endoscopy can be performed safely at any time, provided
the patient is stable and there is no evidence of perforation. Endoscopy
should be performed as soon as possible, because it serves a dual purpose.
First, patients with no evidence of gastrointestinal injury may be
discharged home, provided there are no other complications. Second,
patients with evidence of severe injury may be managed appropriately. The
next question involves the extent of endoscopic examination. Some authors
suggest that the endoscope should not be passed beyond the first burn site.
However, recent studies have shown that flexible fiberoptic evaluation of
the entire esophagus and stomach can be safely performed. The importance of
complete examination was recently illustrated by Thompson. He reported on
nine patients who presented simultaneously following ingestion of a highly
concentrated alkali solution. Each had endoscopy which stopped at the at
the first circumferential burn visualized. However, because of progressing
symptoms, three of the patients required repeat endoscopy and laparotomy
because severe full thickness burns were noted past the first
circumferential burn. The goal of the endoscopist is to document the site
and the extent of burns in the upper aerodigestive tract. Discoloration
from blood, the ingested agent, or burned and necrotic tissue can obscure
the deeper layers of the esophagus and make it difficult to differentiate
between second-degree and third-degree burns. Although any portions of the
esophageal wall may be burned, the areas with the greatest anatomical
narrowing are those most prone to injury: the cricopharyngeus, the aortic
arch and left main stem bronchus compression sites, and the distal esophagus
at the esophagogastric junction. Solid-form alkalis and alkaline batteries
tend to lodge in these areas, which accounts for their sometimes severe,
localized injuries. The endoscopist should be aware of the possibility of
subsequent tracheoesophageal fistula formation at the upper esophageal and
midesophageal narrowings. Tracheoscopy should be undertaken in any patient
with a third degree anterior burn in the esophageal wall to determine
whether the posterior tracheal wall is susceptible to perforation. The
traditional dictum for endoscopic evaluation of esophageal injury was to
avoid passing the esophagoscope beyond any area of second-degree or
third-degree circumferential burn. In recent years, successful total
esophagogastric endoscopy despite proximal esophageal injury become
increasingly common. Although the risk of perforating a weakened esophageal
wall can be exacerbated by the surrounding edema and discoloration that make
identification of the lumen difficult, flexible and rigid endoscopes can be
used safely for full-length examination of the esophagus if care is taken
and there is a lumen. The flexible model is needed for adequate
visualization of esophagogastric junction, the stomach, and beyond. With
either type of esophagoscope, extreme care should be used to avoid further
injury, and the procedure should be formed only by an experienced
endoscopist. The accurate estimation of injury by endoscopy is determined
by examiner's experience. In the patient believed to have a transmural
injury of the esophagus with widespread necrosis, emergency esophagectomy is
recommended to avoid lethal complications. Avoidance of thoracotomy,
coupled with rapid diagnosis and treatment, has markedly decreased
mortality. As with the esophagus, any truly necrotic stomach and
surrounding viscera should be resected as soon as possible. If the
viability of abdominal viscera is questionable, second-look procedures are
reasonable before definitive resection.

Treatment:
After injury in a salvageable esophagus is confirmed, therapy depends
on the depth and location of the injury. First degree burns and
superficial, noncircumferential second degree burns require no treatment
other than observation for swallowing difficulties and infection. Extensive
circumferential second-degree and nonperforating third degree esophageal
burns are at great risk for stricture development. Therapy of these lesions
has varied over the years and remains somewhat controversial.

Steroids:
Patients in whom endoscopy demonstrates near-circumferential esophageal
burns are at risk for strictures, which may appear at any time after the
second week. Since the 1950s, corticosteroids have been the mainstay of
prophylaxis against stricture formation for most physicians. The rationale
for the use of steroids is provided in several animal studies showing that
steroid administration begun soon after experimental lye injury and
continued for at least 6 to 8 weeks reduced the incidence of stricture
formation. Anderson et al recently reported the results of a controlled
intervention trial involving 60 children with documented esophageal injury
from lye or acid. In this unblinded study, the children were randomized to
receive either prednisolone or no prophylactic therapy. Ampicillin was also
administered to those receiving steroids. Steroids were continued at full
dose for 3 weeks, then use was tapered over 2 to 3 weeks. They found no
benefit from steroid administration. However, only 21 children had burn
significant enough to produce a stricture. Of these 21 children, 20 formed
strictures. With 11 of the children in the control group and 10 in the
steroid group, no significant difference was found.

Medical Therapy:
Lathyrogenic agents that reduce collagen cross-bonding have been used to
decrease esophageal strictures. Lathyrogens such as b-aminopropionitrile,
acetylcysteine, and penicillamine have decreased the formation of laryngeal
strictures from alkali injury. Although systemic toxicity has been a
limiting factor in the clinical use of these agents, continued work with
better tolerated drugs (eg, penicillamine) may prove useful. Protection of
the injured esophageal wall from the possible, effects of gastric acid may
prove to be extremely important in decreasing granulation tissue and
subsequent scar formation. Sucrafate therapy for lye and acid burns has
shown promise in the healing of esophageal ulcers without stricture
formation. As with steroid therapy, success with this regimen may be
greatest in the patient with midrange second-degree burns. The sucralfate
must be given orally as a liquid slurry of its tablet form, which may limit
its use in the more severe injuries. Future clinical and laboratory studies
with liquid antacids, H2-blockers, and omeprazole may yield other important
forms of therapy.

Mechanical Therapy:
The simplest mechanical method for maintaining a lumen is to place a
nasogastric tube at the time of initial endoscopy after confirming
third-degree or circumferential second-degree burns. As with steroid
therapy, the clinical value of this approach has varied. Some investigators
question its efficacy and place greater significance on pharmacologic
therapy to avoid strictures. However in a 1985 study, only 2 of 32 patients
with deep circumferential burns treated solely with nasogastric intubation
for 6 weeks showed stricture development within 6 months after injury; there
was also no stricture formation in patients with noncircumferential injuries
who were treated without stenting. A second article in 1989 studied 11
patients with deep and circular burns. These patients also had a
nasogastric tube placed at initial endoscopy. Only one of these patients
developed a mild stenosis. In second-degree and nonperforating third-degree
esophageal injuries, stricture formation should be suspected in any patient
who has persistent dysphagia from the time of injury or who redevelops
swallowing difficulties after a relatively asymptomatic period. This
quiescent period may last from 2 to 6 weeks or longer, depending on the
individual injury and the success of the initial therapy. In some patients,
dysphagia develops slowly as the stricture forms; in other patients, a
stricture may not be detected until it blocks the passage of a food bolus.
It is worthwhile to obtain barium contrast studies routinely 3 to 4 weeks
after injury, even in patients who are asymptomatic (or sooner if dysphagia
develops). Because strictures may develop slowly, periodic repeat
esophagograms over the course of a year are useful for any patient with a
severe esophageal burn. After radiologic evidence of stricture formation
has been obtained, serial dilatations should begin as soon as possible. The
frequency and technique of bougienage depends on the length and number of
strictures. Mild, localized strictures can be treated antegradely through
an esophagoscope using filiform dilators; cooperative patients may tolerate
periodic swallowing of mercury-filled dilators. Multiple strictures are
probably most safely treated with the retrograde method popularized by
Tucker in the 1920s. In Tucker's method, a swallowed string exiting from a
gastrostomy acts as a guide for a special retrograde dilator. The dilator
is attached to the string and pulled through the stomach and esophagus by
the other end, which exits the mouth. This procedure allows serial
increases in dilators while a safe position for each dilator in the
esophageal lumen is maintained. Perforation is the greatest risk, and rapid
increases in dilator size should be avoided. The frequency of dilatations
should vary with the patient's symptoms and progress. Steroid injections
into dilated strictures have been useful in isolated, well-defined stricture
bands. However, to avoid puncturing the aorta and adjacent left main stem
bronchus, great caution should be exercised when injecting strictures in the
middle third of the esophagus.

Follow Up:
The late development of hiatal hernia, reflux esophagitis, and peptic
stricture 25 to 69 years after injury makes esophagectomy and reconstruction
a reasonable alternative to long-term stricture dilatation. It has been
theorized that contracting fibrosis pulls the esophagogastric junction
superiorly, with subsequent esophagitis from gastroesophageal reflux. The
traditional dilatation of preexisting and resulting distal strictures may
only worsen the situation. In a large series of esophageal carcinomas, a 1%
to 4% incidence of caustic ingestion was found in the clinical histories.
Although the exact degree of increased risk for carcinoma is unknown, it has
been estimated to be 1000-fold. Fortunately, because these carcinomas
typically develop in scar tissue, their tendency for local invasion is
lower, and potential cure with resection is higher. For this reason alone,
long-term follow-up of patients with esophageal stricture seems warranted,
regardless of their symptoms. Any patient who develops dysphagia years
after a caustic injury should undergo radiologic evaluation and
esophagoscopy, if indicated.
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BIBLIOGRAPHY

1. Anderson KD, Rouse TM, Randolph JG. A controlled trial of
corticosteroids in children with corrosive injury of the esophagus. N Engl J
Med 1990;323:637-40.

2. Chen YM, Ott DJ, Thompson JN, Gelfand DW. Progressive roentgenographic
appearance of caustic esophagitis. South Med J 1988;81:724-728.

3. Ferguson MK, Migliore M, Staszak VM, Little AG. Early evaluation and
therapy for caustic esophageal injury. Am J Surg 1989;157:116-120.

4. Gaudreault P, Parent M, McGuigan MA, Chicoine L, Lovejoy FH.
Predictability of esophageal injury from signs and symptoms: A study of
caustic ingestion in 378 children. Pediatrics 1983;71:767-770.

5. Gorman RL, Khin-Maung-Gyi MT, Klein-Schwartz W, Oderda GM, Benson B,
Litovitz T, McCormick M, McElwee N, Spiller H, Krenzelok E. Initial symptoms
as predictors of esophageal injury in alkaline corrosive ingestions. Am J
Emerg Med 1992;10:189-194.

6. Gumaste VV, Dave, PB. Ingestion of corrosive substances by adults. Am J
Gastroenterol 1992;87:1-5.

7. Gundogdu HZ, Tanyel FC, Buyukpamukcu N, Hicsonmez A. Conservative
treatment of caustic esophageal strictures in children. J Pediatr Surg
1992;27:767-770.

8. Holinger LD, Tucker GF. Trauma. In Otolaryngology-Head and Neck Surgery.
Ed Cummings, Charles. : Mosby-year Book, St. Louis, MO 1993.

9. Kikendall JW. Caustic ingestion injuries. Gastroenterol Clin North Am
1991;20:847-857.

10. Previtera C, Giusti 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.

11. Riding KH, Bluestone CD. Burns and acquired strictures of the esophagus.
In Pediatric Otolaryngology. Ed. Bluestone, Charles. W.B. Saunders,
Philadelphia, PA, 1990.

12. Seiden AM. Esophageal disorders. In Otolaryngology. Edited by Paparella
MM and Shumrick DA. 3rd ed. 1991 WB Saunders Company

12. Sugawa C, Lucas CE. Caustic injury of the upper gastrointestinal tract
in adults: A clinical and endoscopic study. Surgery 1989;106:802-807.

13. Thompson JN. Corrosive esophageal injuries I. A study of nine cases of
concurrent accidental caustic ingestion. Laryngoscope 1987;97:1060-1068.

14. Thompson JN, Browne JD. Caustic Ingestion and foreign bodies in the
aerodigestive tract. In Head and Neck Surgery - Otolaryngology. Ed. Bailey,
Byron. J.B. Lippincott Co. Philadelphia, PA 1993.

15. Wijburg FA, Beuders MM, Heymans HS, Bartelsman JF, Jager FC.
Nasogastric intubation as sole treatment of caustic esophageal lesions. Ann
Otol Rhinol Laryngol 1985;94:337-341.

16. Wijburg FA, Heymans HSA, Urbanus NAM. Caustic esophageal lesions in
childhood: Prevention of stricture formation. J Pediatr Surg
1989;24:171-173.
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