1137

Acid Corrosive Esophagitis:

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Radiographic Findings

Carlos A. Muhletaler1 Thirty-nine esophagograms of 24 patients after ingestion of muriatic acid (27% HCI)
Amil J. Gerlock, Jr.1 in suicide attempts were reviewed. All esophagograms were obtained in the acute,

Ladis de Soto2 subacute, and chronic phases. In the acute and subacute phases, the radiographic
findings consisted of mucosal edema, submucosal edema or hemorrhage, ulcerations,
Susan A. Halter3
sloughing of the mucosa, atony, and dilatation. Strictures of the esophagus were
present in the chronic phase. These radiographic findings were not different from those
found in alkaline corrosive esophagitis. The severity of the corrosive esophagitis is
considered related to the concentration, amount, viscosity, and duration of contact
between the caustic agent and the esophageal mucosa.

The radiologic features of alkaline corrosive esophagitis have been well doc-
umented [1 -4]. Ihis is not true of the radiologic features of acid corrosive
esophagitis. Reports of ingested acid damaging the upper gastrointestinal tract
are few and are usually restricted to the abnormalities found in the stomach [3,
5-1 1 ]. This has resulted in the belief that acid corrosives ‘lick the esophagus ‘

and bite the pyloric antrum, while the alkaline

‘ ‘ corrosives ‘bite the esophagus ‘

and lick the pyloric This concept

‘ ‘ arose because alkalis have a destruc-
tive effect on the esophagus, but cause little destruction of the stomach. The
stomach is thought to be spared the destruction because the alkali is neutralized
by the highly acid gastric secretions. Acids have been reported to scar only the
esophagus, while causing severe injury to the stomach, especially the gastric
antrum [3, 5, 7, 8, 1 0-i 2]. Although these concepts are well supported, we have
encountered 24 patients with acid destructive lesions in both the esophagus and
the stomach. All resulted from suicide attempts with an ingested muriatic acid
solution (27% HCI). Muriatic acid is a commercially available household product
commonly used in Peru as a toilet bowl cleaner. We describe the radiologic

Received September 11 , 1 979; accepted after

features of acute, subacute, and chronic acid corrosive esophagitis as demon-
revision January 28, 1980. strated on the barium esophagograms in these patients.
I Department of Radiology and Radiological Sci-
ences, Vanderbilt University School of Medicine,
Nashville, TN 37232. Address reprint requests to Subjects and Methods
C. A. Muhletaler.
2 Departmento de Radiologia, Hospital Arzo- A total of 27 women aged 1 5-39 years was seen at Arzobispo Loayza Hospital (for
bispo Loayza, Lima, Peru. women 1 4 years and older) in Lima, Peru, from 1 963 to 1 974. All had a proven history of
muriatic acid ingestion (27% HCI). The exact amount of the swallowed acid was difficult to
3Department of Pathology, Vanderbilt Univer-
assess, although each patient had at least two big swallows of the acid solution. Chest and
sity School of Medicine, Nashville, TN 37232.
abdominal radiographs were taken in each patient before the barium studies were per-
AJR134:1137-1140, June1980
0361 -803X/80/1346-1 137 $00.00 formed. Endoscopy was not done in any patient within 3 weeks of acid ingestion. Steroids
© American Roentgen Ray Society were used as part of the treatment in all patients.
 1138 MUHLETALER El AL. AJR:134, June 1980

TABLE 1 : Radiographic Findings of 39 Esophagograms in Acid

Corrosive Esophagitis

Subacute Chronic Phase

Acute Phase
Radiographic Findings Phase 1 1 -20 21 or more
days
days days

Mucosal and submucosal

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edema or hemorrhage 7 9 ...

Ulcerations 7 9 ...

Sloughing of mucosa 7 . . . .

Atony 7 9 ..

Dilatation 2
Stenosis 9 21
Normal 1 . . 1
Total esophagograms per-
formed 8 9 22

A B
Fig. 2.-A, Esophagogram 4 days after acid ingestion. B, Closeup view.
Extensive mucosal and submucosal destruction.

A B
Fig. 1 -A, Esophagogram 2 days after acid ingestion. Sloughing of
mucosa. B, Close-up view of proximal esophagus. Mucosa sloughing (open
arrows) and contour irregularities of esophagus (arrow) due to mucosal and
submucosal edema.

A total of 39 esophagograms was performed in this group of 27

patients. The esophagograms were reviewed to determine the type
and incidence of the lesions found in the esophagus following the
ingestion of the acid. Because these esophagograms were obtained
at various intervals after the acid ingestion, it was also possible to
determine when the lesions would be expected to occur in the
esophagus. This was evaluated by dividing the time at which the
esophagograms were obtained after the acid ingestion into three
phases. The esophagograms obtained in the first 1 0 days after the
acid ingestion were considered in the acute phase, while those
obtained within 1 1 -20 days were considered in the subacute phase
Fig. 3.-A, Esophagogram 7 days after acid ingestion. B, Close-up view
of the esophageal injury. Esophagograms obtained 21 days or later
of upper third of esophagus. Mucosal sloughing outlined by intramural barium
after the ingestion of the acid were considered in the chronic phase. (open arrows), and barium in lumen of esophagus. Aspirated barium is
The esophagograms were reviewed for evidence of: mucosal and presented.
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A B C
Fig. 6.-Esophagograms of three different patients. A, 1 month after acid
ingestion. Single stricture of upper thoracic esophagus. B, 2 months after
acid ingestion. Two strictures (arrows). C, 4 months after acid ingestion.
Multiple strictures resulting in filiform esophagus.

4 5
One esophagogram was normal, while seven showed areas
Fig. 4.-Esophagogram 1 3 days
acid ingestion. after of stenosis. Fourteen of the esophagograms in this group
Short narrowed segment in midesophagus (white arrow)
and long narrowed segment in distal esophagus (arrows) were obtained a minimum of 30 days after acid ingestion. A
were rigid on fluoroscopy. Serration of esophageal mar- single area of stenosis was present in 1 3 esophagograms;
gins is due to ulcerations and submucosal edema.
nine of these were located in the upper thoracic esophagus
Fig. 5.-Esophagogram 23 days after acid ingestion.
Two stenotic areas (arrows). (fig. 6A). Multiple esophageal stenoses were seen in eight
of the esophagograms (figs. 66 and 6C).
submucosal edema or hemorrhage, ulcerations, sloughing of the
mucosa, presence or absence of peristalsis, dilatation, narrowing
or stenosis, and perforation. Discussion

Accidental or suicidal ingestion of acids is infrequently

Results reported [1 0-1 3], although acids are the most common type
of ingested caustic agent in several countries in the Middle
Acute Phase East, Europe, and Latin America [2, 6-8, 1 0]. Most of these
Esophagograms were obtained in eight of 1 1 patients reports deal with the late sequelae of the acid caustic injury,
seen in the acute phase. One was normal, while seven and only in few instances are the acute esophageal mucosal
showed mucosal and submucosal edema, ulcerations, lesions described [2, 1 0]. Esophageal strictures associated
sloughing of the mucosa, atony, and in two patients esoph- with acid ingestion occur in 6.5%-50% of the patients [2,
ageal dilatation (table 1 (figs. 1 -3). The other three patients
) 3, 5, 6, 1 2, 1 4]. Unfortunately, the concentration and
underwent emergency laparotomy due to the presence of amount of the ingested acid has been rarely mentioned. In
free peritoneal air or emphysematous gastritis. i wo of these our series, seven of eight esophagograms obtained 2-8
patients died shortly after the surgical procedure. days after acid ingestion showed evidence of mucosal and
intramural injuries. Esophageal lesions also occurred in the
other three patients who underwent emergency laparotomy
Subacute Phase for severe necrotizing lesions of the stomach.
Nineesophagograms were obtained in this group within The edema and ulcerations of the esophageal mucosa
1 1 -1 6 days after the acid ingestion. All esophagograms were noted as a blurring or as irregularities of the esopha-
showed areas of narrowing, mucosal ulcerations, submu- geal margins (figs. 1 A and 1 B). The submucosal edema
cosal edema, and atony (table 1 and fig. 4). and/or hemorrhage was seen as a scalloping and
straightening of the esophageal contours (fig. 1 A). Deep
ulcerations appeared as linear, streak, or plaquelike collec-
Chronic Phase
tions of contrast material in the esophageal wall. Martel [1]
This group comprised 22 esophagograms. Eight were described thin linear defects as representing elevated par-
obtained 20-30 days after the ingestion of the acid (fig. 5). tially sloughed mucosa, with intramural dissection of con-
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A B
Fig. 7.-Sections from esophagus 2 days after injury. Necrosis and acute inflammation of mucosa along with perivascular inflammation and edema of
submucosa. A, x200; B, x250.

esophageal injuries, probably more often than is reported in

trast material (fig. 1 A). He also noted that contrast intramur-
ally beneath the sloughing mucosa remained there for sev- the literature.
eral hours. The esophageal atony, with or without significant
ACKNOWLEDGMENT
dilatation, is probably an indication of the severe muscular
injury or inflammation [1 2, 1 5, 1 6]. Significant
, dilatation of We thank Linda Naylor for assistance in manuscript preparation.
the esophagus in the acute phase of the caustic injury has
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