Gastrointestinal Imaging • Original Research

Noh et al.
Esophagography and CT of Esophageal Carcinoma

Gastrointestinal Imaging
Original Research
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Corrosive-Induced Carcinoma of
Esophagus: Esophagographic and
CT Findings
Seung Yeon Noh1 OBJECTIVE. The purpose of this study was to evaluate the esophagographic and CT
Hyun Jin Kim findings of corrosive esophageal cancer.
Hyun Joo Lee MATERIALS AND METHODS. The records of all patients who presented with cor-
Seong Ho Park rosive esophageal strictures at one institution between June 1989 and April 2015 were retro-
Jong Seok Lee spectively identified. The search yielded the records of 15 patients with histopathologically
proven esophageal cancer. Esophagograms (13 patients) and chest CT images (14 patients)
Ah Young Kim
were interpreted independently by two reviewers. Esophagographic findings included the lo-
Hyun Kwon Ha cation of tumor, morphologic type, presence and length of mucosal irregularity, presence of
Noh SY, Kim HJ, Lee HJ, et al. asymmetric involvement, and presence of rigidity. CT findings included presence and type of
esophageal wall thickening, pattern of enhancement, presence of periesophageal infiltration,
and presence of hilar or mediastinal lymphadenopathy.
RESULTS. Esophagography showed that the tumor was involved with the stenotic portion
in 10 of the 13 patients (76.9%). The most common morphologic feature was a polypoid mass,
in 10 patients. In 12 patients (92.3%), mucosal irregularities were observed; the mean affect-
ed length was 4.92 cm. Asymmetric involvement and rigidity were observed in nine patients
(69.2%). On CT scans, eccentric wall thickening was observed in 10 of the 14 patients (71.4%),
homogeneous enhancement in nine (64.2%), and periesophageal infiltration in 11 (78.5%).
CONCLUSION. Esophagography commonly shows corrosive esophageal cancer as a
polypoid mass with long-segment mucosal irregularities at the stenotic portion, asymmetric
involvement, and rigidity. CT shows eccentric esophageal wall thickening with homogeneous
enhancement and periesophageal infiltration, which are suggestive of the development of ma-
lignancy in patients with corrosive esophageal strictures.

he development of esophageal

Keywords: caustic, corrosive, CT, esophageal
neoplasms, esophagography
DOI:10.2214/AJR.16.17138
Received July 25, 2016; accepted after revision
December 29, 2016.
1
All authors: Department of Radiology and Research
Institute of Radiology, Asan Medical Center, University
of Ulsan College of Medicine, 88 Olympic Ro, 43-Gil,
Songpa-gu, Seoul, 05505, Korea. Address correspon-
dence to H. J. Kim (leesoolbee@hanmail.net).
AJR 2017; 208:1237–1243
0361–803X/17/2086–1237
© American Roentgen Ray Society
T
cancer in patients with a history
of ingestion of a corrosive agent is
well known. Approximately
1–4% of all patients with esophageal cancer
have a history of caustic ingestion [1–4]. Esti-
mates of the prevalence of esophageal cancer
in patients with a history of ingestion of a cor-
rosive agent have ranged from 2% to 16% [5,
6]. Diagnosing corrosive esophageal cancer is
more difficult than diagnosing de novo esoph-
ageal cancer because of preexisting symptoms
of dysphagia. Furthermore, endoscopic evalu-
ation and surveillance have limited roles in
these cases because of severe esophageal lu-
minal narrowing. Hence, imaging diagnosis
has an important role in the evaluation of cor-
rosive esophageal cancer. In this study, we re-
view the esophagographic and CT findings of
corrosive esophageal cancer.
Materials and Methods
Patient Population
We conducted a retrospective search for the re-
cords of all patients who presented with corrosive
esophageal strictures at our institution between
June 1989 and April 2015. A total of 95 patients
were identified, 22 of whom had histopathologi-
cally proven esophageal cancer and were enrolled
in the analysis. Imaging findings were available for
15 of these 22 patients (esophagography, 13; chest
CT, 14). Our institutional review board waived the
requirement for informed patient consent because
of the retrospective nature of this study.
Review of Medical Records
One author reviewed the electronic medical re-
cords of the study patients to identify age, sex, type
of ingested corrosive agent, timing of ingestion, time
of detection of esophageal cancer, duration from in-
gestion to detection of esophageal cancer, preexist-

AJR:208, June 2017 1237

 Noh et al.

ing symptoms, recent aggravation if any, newly devel-
oped or worsening symptoms, and pathologic results.
Imaging Techniques
All 15 patients with available imaging findings
underwent double-contrast or single-contrast esopha-
gography. Single-contrast studies were performed for
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fluoroscopy. Asymmetric involvement refers to
asymmetric luminal involvement. Esophageal can-
cer was divided into superficial or advanced esopha-
geal cancer on the basis of morphologic type on the
esophagogram. Superficial esophageal cancers are
classified as ulcerofungating, plaquelike, flat, or de-
pressed [7]. Elevated lesions with a height of more
Chest CT images were reviewed by two radi-
ologists who identified the presence and type of
esophageal wall thickening, pattern of enhance-
ment (homogeneous, heterogeneous), presence of
periesophageal infiltration, and presence of hilar
or mediastinal lymphadenopathy. Preoperative
clinical staging was performed retrospectively

patients with severe stenosis. A 220% weight/volume than 5 mm were classified as ulcerofungating, and with endoscopic ultrasound or chest CT.
barium suspension (Solotop Hd, Taejoon Pharm) was those with a height less than 5 mm as plaquelike.
used in all cases. Before imaging, all patients were Flat lesions had no definite elevation or depression. Statistical Analysis
asked about their degree of dysphagia, and the risk Depressed lesions were defined as having no definite Data were analyzed with SPSS software (ver-
of aspiration was evaluated. We also asked the pa- ulcerative component. Advanced esophageal can- sion 12.0a, IBM-SPSS).
tients whether they coughed when eating or drink- cers are classified as polypoid, infiltrative, varicoid,
ing or whether they had any history of aspiration or ulcerative [8]. Comparisons between previous Results
pneumonia. A patient was considered at high risk of esophagograms before and after the development of Twelve of the 15 patients (four men, 11
aspiration under the following conditions: evidence cancer were performed for patients for whom this in- women; mean age, 68 years; range, 47–87
of aspiration pneumonitis on chest radiograph, older formation was available. years) had ingested lye (i.e., caustic soda
age, or severe passage disturbance at real-time fluo-
roscopy. Esophagograms were obtained while the pa- TABLE 1:  Clinical and Pathologic Findings in the Study Cohort (n = 15)
tients, who were in a prone and slight left posterior Characteristic Result
oblique (LPO) position, swallowed the barium sus-
pension. Patients were then asked to change to an up- Age (y)
right LPO position and ingest the effervescent agent Mean 68
(Top Effervescent-G Gran, Taejoon Pharm). Double- Range 47–87
contrast esophagography was performed while pa-
Sex (no.)
tients again drank the barium suspension. In patients
with severe stenosis or at high risk of aspiration, only Men 4
a single-contrast study was undertaken with the pa- Women 11
tient in the upright LPO position. Type of ingested corrosive agent
CT images were obtained with one of six scan-
Lye 12 (80.0)
ners: Somatom Sensation 16 (Siemens Healthcare),
Somatom Plus (Siemens Healthcare), Somatom Glacial acetic acid 1
Definition Flash (Siemens Healthcare), Light- Hydrochloric acid 1
Speed QX/I (GE Healthcare), LightSpeed Ultra Sulfuric acid 1
(GE Healthcare), or HiSpeed (GE Healthcare). The
Time from ingestion to diagnosis (y)
imaging parameters included 120–140 kV and 100
effective mA with dose modulation. Image recon- Mean 42
struction was performed in both the axial and coro- Range 23–61
nal planes. For the standard algorithm, these recon- Preexisting dysphagia with recent aggravation 10
structions had 5-mm slice thickness with a 5-mm
New-onset symptom 5
interval and no gap. For the high-frequency algo-
rithm, 1-mm reconstruction with a 5-mm gap was Dysphagia 4
used. These scans were acquired 50 seconds after IV Cough 1
administration of 100 mL of iopromide (300 mg io- Pathologic type squamous cell carcinoma 15 (100)
dine/mL; Ultravist 300, Bayer Schering Pharma) de-
Initial treatment
livered at a rate of 2.5 mL/s through a power injector.
All images were uploaded to a PACS and viewed in Curative surgery 5 (33.3)
mediastinal (width, 350 HU; level, 35 HU) and lung Ivor-Lewis operation 3
(width, 1500 HU; level, 700 HU) windows. McKeown operation 2
Open biopsy with feeding jejunostomy 1
Image Interpretation
All esophagograms were reviewed by two radi- Chemotherapy or radiation therapy 3
ologists. These reviewers identified the following: No treatment (refusal) 6
location of tumor, morphologic type, presence and History of intervention before diagnosis of cancer 8 (53.3)
length of mucosal irregularity, presence of asym-
Balloon dilation only 5
metric involvement, presence of rigidity, and any
other ancillary findings. Rigidity refers to decreased Balloon dilation with stent placement 3
motility with a fixed appearance during real-time Note—Unless otherwise indicated, values are numbers of patients. Values in parentheses are percentages.

1238 AJR:208, June 2017

 Esophagography and CT of Esophageal Carcinoma

Fig. 1—49-year-old woman with history of sulfuric

acid ingestion 23 years previously.
A, Esophagogram shows ulcerofungating mass
(arrows) in mid esophagus involving stenotic portion
with extension to immediately proximal portion of
esophagus.
B, Esophagogram shows saccular luminal dilatation
(asterisk) proximal to stenotic portion of esophagus.
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A B

or NaOH), and three patients had ingested
strong acid (glacial acetic acid, hydrochloric
acid, and sulfuric acid). The mean duration
from ingestion to diagnosis of cancer was 42
years (range, 23–61 years).
All 15 patients had information avail-
able regarding symptoms. Ten patients had
preexisting dysphagia with recent aggra-
vation. The mean duration of aggravation
was 3.68 months. Five patients had new-on-
set symptoms: four had dysphagia, and one
had cough. The pathologic type was squa-
mous cell carcinoma in all 15 patients. Five
patients (33.3%) underwent curative surgery.
Three of these patients had pathologically di-
agnosed superficial esophageal cancers: two
were limited to the mucosa and one to the
submucosa. Five patients had a history of
balloon dilation, and three other patients had
undergone both balloon dilation and stent
placement before the diagnosis of esophageal
cancer (Table 1).
Among the 13 patients with available esoph-
agographic results, the tumor was found to in-
volve the stenotic portion (preexisting lye stric-
ture) of the esophagus in 10 (76.9%). In three
of these patients the tumor was limited to the
stenotic portion, whereas in seven patients the
tumor extended to a point just proximal to the
stenotic portion (53.8% of all esophagograph-
ic examinations) (Figs. 1A and 2B). Involve-
ment of tissue just proximal to the stenotic seg-
ment was seen in two patients and more than
1 cm proximal to the stenotic segment in one
patient. The most common morphologic fea-
ture was a polypoid mass (n = 10 [76.9%]) (Fig.
1A). Plaquelike lesions were observed in two
patients, and a depressed lesion was observed
in one patient. Superficial esophageal cancer
was diagnosed in three patients. An esophago-
gram was not available in one of these cases.
The esophagographic finding was plaquelike in

A B
Fig. 2—62-year-old woman with history of lye ingestion 40 years previously.
A, Esophagogram shows long-segment stenosis at distal esophagus and shallow depressed lesion with fold convergence (arrows) proximal to stenotic portion of
esophagus.
B, Patient underwent Ivor-Lewis operation. Photograph of gross specimen shows long-segment luminal stenosis with mural thickening at distal half of esophagus. Ill-
defined ulcerative mucosal lesion (arrows) measuring approximately 2.5 × 2 cm was found at proximal part of stenotic segment and is confined to mucosa. Remaining
esophageal and gastric mucosa was unremarkable.

AJR:208, June 2017 1239

 Noh et al.
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A B C
Fig. 3—80-year-old woman with history of lye ingestion 40 years previously.
A, Esophagogram obtained before development of cancer shows smooth, tapered
segmental narrowing (arrowheads) in upper esophagus, suggesting benign
structure.
B, Esophagogram obtained after development of cancer shows long-segment mild
stricture (arrowheads) at mid to distal esophagus.
C, Double-contrast esophagogram shows ulcerofungating mass with mucosal
irregularity involving stenotic portion (arrows) with extension to proximal portion
of esophagus. Asymmetric involvement or rigidity was also noted in inferior portion
of mass.
D, Chest CT image shows eccentric esophageal wall thickening with
periesophageal infiltration (arrow) at mid esophagus.

one of the other two patients and depressed in
the other (Fig. 2A).
Mucosal irregularities were observed in 12
of the 13 patients (92.3%) with esophagograph-
ic results. The mean affected length was 4.92
cm (range, 5–10 cm). Asymmetric involve-
ment or rigidity was observed in nine patients
(69.2%) (Figs. 3B, 3C, and 4A). Ancillary find-
ings, such as mucosal dissection (n = 2), sac-
cular dilatation of the proximal lumen (n = 4)
(Fig. 1B), and ulcer (n  = 3) were also noted
(Table 2). Among the 15 study patients, previ-
ous esophagograms were available for five pa-
tients before the development of cancer, and
long-segment smooth luminal narrowing was
observed on these images. In addition, neither
mucosal irregularity nor masslike lesion was
evident on these esophagograms (Fig. 2A). Af-
ter the development of cancer, mucosal irregu-
larities and asymmetric involvement or rigid-
ity were observed in these five cases either at
the stenosis or proximal to the stenotic portion.
Among the 14 patients who had CT re-
sults available, eccentric wall thickening
was observed in 10 (71.4%) (Figs. 3C, 3D,
and 4B). Homogeneous enhancement of the
esophageal wall was observed in nine pa-
tients (69.2%), periesophageal infiltration in
11 (78.5%), and enlarged mediastinal or hi-
lar lymph nodes with a short-axis diameter
of more than 1 cm in two patients (14.3%).
In addition, two patients had no demonstrable
esophageal wall thickening or abnormally

1240 AJR:208, June 2017

 Esophagography and CT of Esophageal Carcinoma

enlarged lymph nodes. The results for the
other 12 patients are shown in Table 3.
Clinical staging was performed retrospec-
tively with endoscopic ultrasound or chest
CT according to the American Joint Com-
mittee on Cancer staging system, 7th edition.
Among the 15 patients, four patients (26.6%)
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The pathophysiologic mechanism of cor-
rosive esophageal cancer is not well known.
The epithelium overlying a cicatrix is known
to be vulnerable to neoplastic transformation,
especially if subjected to chemical, physical,
TABLE 2:  Esophagographic Findings (n = 13)
or thermal irritation for prolonged periods [9].
Previous reports [10, 11] have suggested that
esophageal food stasis is associated with local
chronic inflammatory responses in the esoph-
ageal mucosa and that these responses can

had stage I disease, one patient (6.7%) had

Finding No. of Patients
stage II disease, nine patients (60.0%) had
stage III disease, and one patient (6.7%) had Location of tumor
stage IV disease. The 5-year survival rate Both stenotic and just proximal to stenotic portion 7 (53.8)
was 33.3% (5/15) in the overall patient popu-
Stenotic portion only 3 (23.1)
lation but was 57.1% (4/7) among the treat-
ed patients. The 10-year survival rate was Just proximal to stenotic portion only 2 (15.4)
28.5% (4/14) overall and 57.1% (4/7) among Proximal to stenotic portion (> 1 cm) 1 (6.7)
the treated patients. Information regarding Morphologic type
10-year survival outcome was not available
Polypoid 10 (76.9)
for one patient.
Plaquelike 2 (15.4)
Discussion Depressed 1 (6.7)
In this study cohort, corrosive esophageal Mucosal irregularity 12 (92.3)
cancer was evident at esophagography as
Asymmetric involvement 9 (69.2)
an ulcerofungating mass with long-segment
mucosal irregularity involving the stenotic Rigidity 9 (69.2)
portion and asymmetric involvement or ri- Ancillary findings
gidity. CT showed eccentric esophageal wall Saccular dilatation of proximal lumen 4 (30.7)
thickening with homogeneous enhancement
Ulcer 3 (23.1)
and periesophageal infiltration suggestive of
a malignancy arising from a corrosive esoph- Mucosal dissection 2 (15.4)
ageal stricture. Note—Values in parentheses are percentages.

A B
Fig. 4—47-year-old man with history of lye ingestion 44 years previously.
A, Esophagogram shows ulcerofungating mass at stenotic portion and just proximal to stenotic portion of mid esophagus (arrows). Shouldering is evident in upper margin
of mass. Small ulcer is evident at midstenotic portion (arrowhead).
B, Chest CT image shows eccentric esophageal wall thickening with periesophageal infiltration (arrows) at mid esophagus.

AJR:208, June 2017 1241


TABLE 3:  Chest CT Findings (n = 12)
Finding No. of Patients
Symmetricity
Eccentric 10 (83.3)
Symmetric 2 (16.6)
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Enhancement pattern
Homogeneous 9 (75.0)
Heterogeneous 3 (25.0
Periesophageal infiltration 11 (91.6)
Mediastinal or hilar lymph nodes 2 (16.6)
Note—Values in parentheses are percentages.
Among the 14 patients with available chest CT
scans, two patients with no esophageal wall
thickening or enlarged mediastinal or hilar lymph
nodes were excluded from the analysis.
result in a predisposition to carcinoma. Re-
peated trauma by dilation causes recurrent ul-
ceration and epithelial healing, which can also
increase the risk of cancer [4]. In our study,
eight patients had a history of intervention,
such as balloon dilation or stent placement for
esophageal stricture, before the diagnosis of
esophageal cancer was made.
The mechanism of injury leading to corro-
sive esophageal cancer can differ depending
on whether the injury was caused by alkali or
acid. Alkalis are known to combine with tis-
sue proteins and cause liquefaction necrosis
and saponification with immediate severe in-
flammation. They also penetrate deeper into
tissues because of their higher viscosity and
longer contact time while passing through
the esophagus. The extent and degree of in-
juries caused by acids are less severe than
those caused by alkalis. This can be attrib-
uted to coagulation necrosis, which causes
a firm protective eschar that delays injury,
limits penetration, and increases the rate of
passage through the esophagus, thereby re-
ducing injury [1, 12]. In our study, strong al-
kalis were ingested by 12 patients and acids
by three patients.
Previous reports [1–4] have shown that
1–4% of patients with esophageal cancer
have a history of ingesting corrosive agents.
The risk of development of carcinoma of the
esophagus among patients with corrosive-
induced esophageal strictures is more than
1000 times that of persons without strictures
[1, 13]. In various published reports [2, 4, 9,
13–18], the interval between corrosive inges-
tion and development of carcinoma ranges
from 10 to 71 years. In our study, the mean
duration from ingestion to diagnosis of can-
cer was estimated at 42 years.
1242 AJR:208, June 2017
Noh et al.
Previous reports have suggested that most
corrosive carcinomas occur at the level of
the tracheal bifurcation, probably owing to
more severe injury at this site caused by ana-
tomic narrowing and stasis [1, 2, 14]. In our
study series, involvement of the stenotic por-
tion was observed in 10 patients (76.9%). The
explanation may be that the longer duration
of food stasis in the stenotic portion, with or
without extension to the tissue just proximal
to the stenotic portion, than in other areas
consequently causes cancer.
The prognosis of corrosive esophageal can-
cer is said to be better than that of de novo
esophageal cancer [1, 10, 11, 16]. Csíkos et al.
[16] reported that among 36 surgically treat-
ed patients with corrosive esophageal cancer,
45.6% were living after 5 years and 14.4% after
10 years. In our study population, the 5- and 10-
year survival rates among the treated patients
were 57.1% and 28.5%. This improved prog-
nosis is attributable to the fact that a carcino-
ma developing in a lye stricture is initially sur-
rounded by a rigid scar. This protects against
both local spread and nodal dissemination and
allows only intraluminal growth, which causes
early dysphagia through luminal obstruction.
Early dissemination is prevented in the same
way [11, 16]. In an earlier study by Ruol et al.
[11], patients with scar cancers had a higher re-
section rate (68% vs 56%) than patients with-
out a history of caustic injury, although this dif-
ference was not statistically significant. Those
authors also stated that the percentage of pa-
tients with an esophageal cancer limited to the
muscular layer was twice as high in the corro-
sive injury group as in other esophageal cancer
groups. In our study, five patients underwent a
curative operation. Three of these patients were
tumor-free at 5-year follow-up evaluation, one
patient had progression at the 7-month follow-
up evaluation after the initial diagnosis, and
one patient was lost to follow-up.
Superficial esophageal cancers, defined as
esophageal carcinomas with tumor invasion
limited to the submucosa regardless of me-
tastasis to the lymph nodes, account for 6.7%
of total esophageal cancers [7]. In our study
cohort, three patients had a pathologic diag-
nosis of superficial esophageal cancer. Two
of the cancers were limited to the mucosa,
and one to the submucosa.
Kochhar et al. [1] and Ruol et al. [11] sug-
gested that corrosive esophageal cancers have
a relatively good prognosis because of early
detection due to the obstructive symptoms
they cause and close follow-up; because the
stricture is surrounded by scar tissue, prevent-
ing early dissemination; and because of the
younger age of this patient population [1]. The
level of operability is also higher in corrosive
esophageal cancer than in de novo esopha-
geal cancer (40% vs 30%) [2, 9, 13, 19]. In our
study, five patients (33%) were able to undergo
surgery with curative intent, which is consis-
tent with previous data. These findings sug-
gest that once diagnosed, corrosive esopha-
geal cancers have a favorable prognosis.
However, the diagnosis of esophageal can-
cer in patients with a corrosive stricture is be-
lieved to be more difficult than in those with
de novo esophageal cancer. This is probably
due to preexisting symptoms of dysphagia in
these cases, the long interval from initial in-
gestion, and the limited role of endoscopy due
to luminal narrowing, which causes inacces-
sibility for standard endoscopic examinations
and biopsies [10]. Both clinicians and patients
have difficulty suspecting the development of
cancer. Even though patients may undergo im-
aging during regular follow-up, the detection
of cancer in patients with a corrosive stricture
can be more difficult for the radiologist than is
detection of de novo early esophageal cancer.
Close attention should therefore be paid to the
imaging findings in cases of corrosive esopha-
geal cancer. The imaging modality is thought
to play a major role in the detection of cor-
rosive esophageal cancer, especially in cases
with severe esophageal strictures.
This study had limitations. First, we in-
cluded only a small number of patients,
largely because corrosive esophageal can-
cer is a rare disease. Second, selection bias
cannot be completely excluded because the
study was retrospective.
Conclusion
The common esophagographic findings
of corrosive esophageal cancer are a polyp-
oid mass with long-segment mucosal irregu-
larities at the stenotic portion, asymmetric in-
volvement, and rigidity. The chest CT findings
suggestive of the development of malignancy
are corrosive esophageal stricture, eccentric
esophageal wall thickening with homogeneous
enhancement, and periesophageal infiltration.
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