VOL.

ii8.

No.

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CAUSTIC

DAMAGE
TRACT:

OF THE
ROENTGEN
E.

By

A.

GASTROINTESTINAL
FEATURES*

FRANKEN,

HE literature
and

on the

management

the gastrointestinal
with
the exception
scription

acute

effects

alkali,4

information

there

on

caustic

the

ingestion

In the

its

8 years

but,
de-

paucity

of

features

of
catishave
Medi-

elsewhere

and

because
course

of complications
of their
treatment.
a select

were

esophagus

for

of long-

3.

In

coagulation

and

a superficial

exerts

pyloric

its

maximum

region

pylorospasm

area.2
Alkali
teins to form
of fats.

The

of the

effect
stomach

on

result

involved

region.

and
age

esophagus
are
to the stomach

is a penetrating

The

From
Associate

the

Department
Professor

of Radiology,

Indiana

to

fibrous

contract,

and

the

inflam-

subsides.

Adhesions

areas

in the

to

seen

in the

superficial
only
may

CLINICAL

be

AND

of
4.
nation
may

Mouth
in
show

does
not
disease.8

and

Medical

of Radiology.

77

Center,

seen

ROENTGEN

are

of

in

the

acute

all layers
into

of the
the

pen-

FEATURES

PHASE

Pharynx.

Physical

examiingestion
absence

rule
out
Pharyngeal

of
Indianapolis,

in

significant
burns

that
they
probably

normal
Indiana.

the

involving

the
child
with
alkali
oral
burns,
but
their

significance
with
aspiration,

inhibition

of the

esophagus

ulcer

ACUTE

damoccurs

be-

lumen

are seen,
and stricture
forIn severe
burns
the mucosa
do not regenerate.

phase;
deep ulcers
involve
esophagus
and may
extend
esophageal
tissues.9

pre-

formation.

the

reaction

ulcers

stricture

mucosa

University

occurs
and
is
reac-

week

granulating

The

only
when
large
amounts
are
ingested.2
Hypochlorite
(bleach)
usually
results
in
only
superficial
mucosal
damage
to the
esophagus.
The quantity
of caustic
ingested
is pertit

begins

types:

pharynx,

usually
involved;
and small
bowel

death

fourth

necrosis

burn

mouth,

and

intestinal
tract
mation
begins.
and submucosa

with resultant
hold up in that
causes
precipitation
of proproteinates
and saponification

the

the

phases:9

inflammatory

the

secondary

to
3

coagulation,

and

third

matory

LOGY

produces

and

damage
into

Cellular

Cicatrization

tween

of caustic
damage
tract
are dependent
of the agent.
Acid

Plumr)

mouth

solutions.

by intense

the

tissue

complications.

The tYpe and location

to the gastrointestinal
on the chemical
nature

Liquid

the

tion in surrounding
tissues.
This
is seen
to 4 days after
ingestion.
2. Ulceration-granulation.
The
necrotic
mucosa
sloughs
at 3 to 5 days,
and repair
response
(fibroblastic
activity)
begins.
The
esophagus
is weakest
at this
time.

term
effects
of caustic
ingestion.
The purpose
of this
communication
is to
describe
the effects
of caustic
ingestion
in
the gastrointestinal
tract
with
particular
attention
to the
roentgenology
of late

PATHO

imporagent.9

divided

protein

accompanied

had

seldom

more
of the

corrosive
is

to

alkali

Of

in

dilute

necrosis.

secondary

referred

study

of

tract
Acute

I.

do

course

of

(e.g.,

burn

than

The

arising
in the
They,
therefore,

group

alkalis
a deeper

produce

intestinal

with

care

Concentrated

con-

complications.67

children

14

nent,
as small
amounts
produce
gastric
disease.
tance
is the concentration

of

of the gastrointestinal
tract
at the Indiana
University
All but
2 of
these
patients

acute

represent

roentgen

and

last

tic burns
been
seen
cal Center.

burns

of highly
is

INDIANA

nature

caustic

tract
is extensive,
of Martels
recent

of the

centrated

pathologic

of

M.D.f

JR.,

IXDIANAPOLIS,

are

esophageal
of clinical

are
associated
on the
basis

swallowing

reflexes

of

E. A. Franken,

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78

Jr.

MAY,

1973

i. Pharyngeal
burn from Drano
ingestion
5 weeks
previously.
(A) Lateral
neck roentgenogram.
The
retropharyngeal
space
is increased
secondary
to inflammation.
A narrow
esophageal
lumen
is filled with
air. The epiglottis
cannot
be visualized
on the roentgenogram
and at laryngoscopy
was noted
to be bound
to the posterior
surface
of the tongue
by adhesions.
(B) Barium
swallow
examination
on the same
patient
shows
barium
entering
both the esophagus
and trachea.

11G.

with
pharyngeal
amination
of
demonstrates
pharynx,
glottic

damage.3
the
neck
in
soft

edema
(Fig.

as
i,4

well
and

a result
of pharyngeal
tinue
for several
weeks

as

B).

B.

depth

aspiration

with

Aspiration

damage
as shown

as

maST conin Figure

2.

Esophageal

same
main

patient

stem

perforation

of the chest.
and axilla; and
show

bronchus.

extraluminal

in

corrosive

The superior
a left pleural
contrast

of the

mediastinitis

known.2

They

The
wall

Mediastinum.

esophageal

determines
if mediastinal
occur.
Clinically
the child
is toxic

shock.
Roentgenographic
geal
perforation
with
ing,

roentgenogram
mediastinum

and

of penetration

by the corrosive
involvement
will

iB.

FIG.

Esophagus

about
the
of supra-

tissue
swelling
or destruction

structures,

pneumonia

Roentgen
exthese
patients

include

and

may

signs
mediastinitis

of

and

in

esophaare well

mediastinal

pneumomediastinunl,

be

widenpleural

effu-

esophagitis
following
esophagoscopy.
(A) Posteroanterior
mediastinum
is widened;
air is present
in the left superior
effusion
is seen. (B and C) Gastrografin
esophagograms
in the
material

with

the

site

of perforation

in the

region

of the

left

Downloaded from www.ajronline.org by 190.236.99.184 on 09/10/15 from IP address 190.236.99.184. Copyright ARRS. For personal use only; all rights reserved

\OL.

uS,
No.

79

E. A. Franken,

8o

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sion.
with
firms

In doubtful
cases
an
water
soluble
contrast
esophageal
perforation

Several

patients

silown
roentgen
abnormalities
ingestion
astinitis
signs

without
clinical
or esophageal
include

lateral

of

absence

4-C).
Most
should
dition
time

of

tracilea.

of actual

the

Esophagoscopy

adnl

(2)

para-

the

of the
posterior

Presumably

extent

tile

3,

the

be

assessed

permits;
of ingestion.

of
when

i.e.,

within
There

esophageal
the

patients

a few days
is disagreement

material
In

injury

mucosal
mucosal

as

burns

phase

disthe
and

when

and

delayed

spiral

folds.9
Martel4
folds
and
linear

tients

who

trated

alkali.

have

ingested

encountered,

by

the

shows

including

material

con-

is

followed

mild

acute

evalua-

of the

The
are:
(i)
is high;

mucosa.

area

more

inspection

is terminated

inflamed

contrast

ities,

of

offers
direct

the status
of the entire
esophagus
be visualized.3
Some
advocate
liminarv
esophagogram
with
water

mediastinitis
tilat

contrast

so

that

copy.9

agree

i ttedly
i.e.,

1973

of choice.

not

in

(Fig.

or
procedure

esophagoscopy
perforation

examination

severely

of peniesophageal
roentgen
changes

autilorities340

esophagoscopy
is the

,.
Atonic
esophagus
JO days
after alkali
ingestion.
(A)
is dilated
and filled with air. The thick periesophageal
soft
by air in the esophagus
and right
lung. The left paraspinal
the same
patient
confirms
the dilatation.
The
trachea
is
(C) Eight
months
later the entire esophagus
is narrowed.

11G.

whether

esophagography

advantages
of
risk of esophageal

of mediThese
of

to

MAY,

specific
information;
of damage
of esophageal

mediastinal
after
caustic

days

deviation

the

have

evidence
perforation.

ical
inflammation
produces
these

tissue

institution

reflection,
thickening
soft
tissue,
and

indentation
cilem

tion

this

evidence
in the first

spinal
pleural
periesophageal

tile

at

esophagogram
material
con(Fig.
2, 1-C).

Jr.

may

a presoluble

esophagos-

esophagogram

in

abnormal-

minimal
passage

of

appearance

contrast

of

the

notes
edematous
ulcerations
in

pa-

highl\T

concen-

Anteroposterior
roentgenogram.
The esophagus
tissue
noted
to the right of the spine is outlined
line is widened.
(B) Lateral
esophagogram
on
displaced
anteriorly
by the dilated
esophagus.
A small
hiatus
hernia
is also present.

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\OL.
III,

No.
,

Caustic
Damage
of
Gastroir

E.

82

A.

Franken,

Jr.

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ti()n

MAY,

Other.

Laryngeal
edema
may produce

of caustic

tion.
Gastric
perforation
ingestion
of large
amounts
Acute
tracheoesophageal
fistulas

agoaortic

per
follow-up.

7-30

\Vith

Esophagus.

esophageal

strictures
cent

of
The

may

listula
been

with

corrosive.9
and

esoph-

reported)#{176}5

PHASE

current
are

alkali
location

aspiraobstruc-

occur
of

have
CHRONIC

4.

from
airway

1973

treatment,

encountered

burns
of

in

on long-term
caustic
stnic-

lic.
6. Esophageal
strictures
6 months
after
alkali
ingestion.
ihe higher
stricture
begins
at the level
ofT-2,
and has overhanging
margins
at its superior
aspect.
A small
diverticulum
is present
on
the
posterior

1-7

the

stricture

phageal
mucosal

surface
of the esophagus.
lrom
T-4 to
esophagus
is of normal
caliber.
A second
with
concentric
tapering
of
the
esolumen
is seen
l,elow
this.
The
normal
pattern
of the esophagus
is absent
in both

strictures.
peristaltic

geal

wave

motility

elevated
motor
gion.6
to

resting
incoordination
These

irritation

and
within

are

in these
esophageal
in

changes

have

secondary

destruction
the esophageal

of

).

(Fig.

seen

studies

Esopha-

patients

show

pressures
the
affected
been

to mucosal
Auerbachs
musculature.6

and
re-

attributed
injurys
plexus

7. Upper
gastrointestinal
examination
4 months
after
caustic
ingestion.
The
barium
in the esophagus
reflects
the severe
gastroesophageal
reflux
noted
at fluoroscopy.
The lucent
band
in the mid
esophagus
is the
result
of adhesions
between
granulating
surfaces
on the esophageal
mucosa.

FIG.

ii8,

VOL.

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tunes
tomic
occur

No.

is not
related
narrowing
in random

esophagus

spasm
of the

entire

strictures
The
by

are
severity
less

ofthe

than

esophagus
luminal

stricture
circumference

involves

well

folds
smooth,

wall

ture.
But
overhanging

the

lumen,

thus

esophageal
in that
\Vide

and

is that

does

not

severe

of a localized

esophagus

with

the
region
concentric
at

the

no

of the
tapering
margins

resembling

neoplasm

therefore
between

(Fig.
of

in

6).

tile

reflecting

They

stnic-

may
have
an
irregular

widening

be seen.
minimally

mu-

stricture,
of
the
of the

stricture
and

stricture

and

of

The

tissue
is seen,
area
(Fig.
8).
based
diverticuia

caustic
Adhesions

in-

circumference

obstruction.
roentgen
appearance

caustic

stricture
may
of esophagus

graded

partial

margins

severe

been

stricture

entire
thickness
and
esophageal
wall
as
tissues.
This
type

the

in

penfibrosis

tile

area

represent
affected

by

areas
the

(Fig.
in

6).
the

free to dilate
ulcerations

esophageal
wall occur
with healing
and
demonstrated
in
the
esophagognam
linear
lucent
bands
forming
pockets
contrast

material

(Fig.

7).

B.
quency

Gastroesophageal
of hiatus

geal reflux
esophagus
literature.22
series

mechanism

in

hernia

the

esophageal

definite

showed
definite

Junction.
The
and
gastroesopha-

hiatus

is similar

of neflux
esophagitis
producing
of the esophagus
with resultant

are
as
of

fre-

of the
in the
in

hernias

gastnoesophageal
hernia
(Fig 7; and

of production

of

lumen

following
caustic
injury
has not been appreciated
Four
of the 14 patients

developed

others
without

to

the
the

stricture
of

esophageal

In

total

peniesopilageal

narrowing
cosal
and

has

obstruction.

results
in
characteristic

of corrosive

seg-

Multiple

mildest

the

of

as

always
The

anaThey
tile

is ingested.7
from I cm.

(shelfstricture)

produce

of

esophagus.

The

al.5

of Gi

unpredictable

frequent.
ofstnicture

et

volves

the

on

when the caustic

stricture
varies

length

Fatti

Danlage

to the regions
of the
esophagus.
fashion
throughout

based

mental
Extent
the

Caustic

this
and

reflux
8).

The

to

that

shortening
hiatus
her-

E. A. Franken,

84

Jr.

mental

perforations

fnequent2

(Fig.

tieilts

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\Ir,

in

tracheal

this

F.

series

narrowing

proliferation
(Fig.

2,

of

of tile esophagus
4--C).
One
of tile
developed
progressive

as

result

of

are
pa-

chronic

periesopiiageal

scar

tissue

Infrequent

cases

have

to).
Carcino;iia.

9. Antral
fibrosis
secondary
to caustic
damage.
Ihe gastric
antrum
is narrow
arid rigid and normal
mucosal
folds arc absent.
The patient
ingested
a
toilet
bowl cleaner
containing
25 per cent
hvdrochloric
acid 4 months
previously.

11G.

of

caustic

strictures.

dominant

symptom

secondar

to

antacid

In

is

is seen
alkali

was

per

tiates
an intense
tion of the agent

the

most

patient
Brain

of

with
ini-

with

antral

reten-

area

causing

there.
The
renarrow,
non-

loss
of a
resembling
caustic
ingestion

of
reliable

evidence
The

may

mediastinitis,

needing
abscesses

but

patients
material

normal

witil

tissues

grade

gastric

burns,

carcipro-

thus

entiation
(Fig.
9).
D. Mediasthium.
esophageal

the

acid

pviorospasm

distensible
antrum
mucosal
pattern,
noma.
A histor

low

cent
Corrosive

for

fibrosis
be

be
and

benefit.

of

chemical
effects
fibrosis
produces

maximum

vides

of

of

in the

lwe-

to
refi ox,

characteristic

in 4-10
ingestion.2

sultant

the

thought

Narrowing

Stomath.

antrum

patient

gastroesophageal

treatment

C.

W1S

differ-

of

pen-

associated

with

particularly

in tile

periodic
dilatations.52#{176}
as a complication
of this

process
have
been
reported.8
perforation
of the esophagus
quent
acute
mediastinitis
months
after
the acute
illness,

Spontaneous

with
may
and

subseoccur

instru-

10. Esophagogram
15 months
after
alkali
ingestion. There
is a stricture
of the lower
cervical
and
upper
thoracic
esophagus.
Below
this
there
is
discrete
narrowing
of the
tracheal
air column.
Chronic
inflammation
of
the periesophageal
soft
tissue
is evident
by the wide separation
of the
trachea
and esophagus.
Extrinsic
compression
of
the trachea
was confirmed
at bronchoscopy.

11G.

VOL.

uS,

been

No.

Caustic

reported

caustic

of

burns

Damage

carcinoma

mans

years

of Gastrointestinal

arising
after

in

initial

in-

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jurv.
TR

EATM

ENl

A detailed
discussion
ciples
of caustic
injury
of this article.
Antibiotics
terial

invasion

duce
vocated

inflammation
during

for

and

treatment

ture

of treatment
is beyond
the
to decrease
corticostenoids

and
acute

the
and/or

is begun

at

prinscope
bacto

fibrosis
phase.

stenosi

of

stric-

caustica.
Radiol.
med.
(Milan)
877-885.
8. HARDING,
J. C. Caustic
burns
ofesophagus:
tenyear analysis.
Am. 7. Surg.,
1956, z, 742-748.
9. JOHNSON,
E. E. Study
of corrosive
esophagitis.
Laryngoscope,
i 963, 73, 1 6g i- i 696.
10. KINNMAN,
J. E. G., LEE, B. C., and SHIN, H. I.
Management
of severe
lye
corrosions
of
oesophagus.
7. Laryng.
& Oto/.,
1969,
83,

I 2.

of

gastrointestinal

tion.

Acute

with

corrosive

are

changes

agents

and

the

hiatus

gastric

antrum;

hernia;
and

Department
of Radiology
indiana
University
Medical
iioo West Michigan
Street

Indianapolis,

Indiana

agents.
15.

esopha-

the

i6.

mediastinitis.
17.

Center
i8.

46202

2.

3.
4.
5.

6.
7.

J. M. Treatment

of caustic
alkali poisonTreatment, 1971,
8, 6i-6i8.
CHAS5IN,
J. L., and SLATTERY,
L. R. Jejunal
stricture
due to ingestion
of ammonia:
report
of case complicated
by severe
potassium
deficiency.
7.A.M.A.,
1953,
152,
134-136.
DAFOE,
C. S., and Ross,
C. A. Acute
corrosive
oesophagitis.
Thorax,
1969, 24, 291-294.
EGAN,
R. S. Corrosive
esophagitis-review
of
therapy.
Northwest
Med.,
1969,
68, 1007-1009.
FATTI,
L., MARCHAND,
P., and CRAWSHAW,
G. R.
Treatment
of caustic
strictures
of esophagus.
Surg.,
Gynec.
& Obst.,
1965,
102,
195-206.
FOGEL,
M. Inflammatory
strictures
of oesophagus. Radio/. c/in. et bio/., 1964,
33, 190-197.
FRACAS5O,
E., and GURIAN,
G. Aspetti
radiologici
delle
alterationi
periesofagee
nelle
ing.

757-765.
caustic
soda
injuries
African
M. 7., 1955.

1964,

Acute
South

&

91,

of
29,

Radiologic
secondary

to

features
of esophagoextremely
caustic

don

between

W.

esophagus,

G.

aorta,

and
sive

trachea
as complication
of acute
corroesophagitis:
report
of case. Am. Surgeon,
1969, 35, 450-454.
MOODY,
F. G., and GARRETT,
J. M. Esophageal
achalasia
following
lye ingestion.
Ann.
Surg.,
1969,
/70,
775-784.
PALMER,
E. D. The Esophagus
and Its Diseases.
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