Downloaded from www.ajronline.org by 119.96.90.141 on 10/30/15 from IP address 119.96.90.141. Copyright ARRS. For personal use only; all rights reserved
527
Phlegmonous
Gastritis
Mary Ann Turner,1 Dennis Stanley Phlegmonous
Michael
gastritis
C. Beachley,
is a rare
bacterial
and
infection
of the
gastric wall. The diagnosis should be strongly considered in any patient who has an acute abdomen by clinical examination and has radiographic findings of air in the gastric
wall,
thickened
radiographic dition has difficulty
folds,
and
rigidity
findings suggestive a very high mortality in making
gastric
diagnosis,
both
wall,
or
The conin part to
preoperatively
of this
The
patient
recovered
from
on the first postoperative wall grew alpha hemolytic and Proteus morgani.
As of 1 975 [1 ], 25 cases were documented literature. Our case reviews the diagnostic
and at surgery. in the American parameters
a correct
of the
of linitis plastica. rate that is due
inspection. Two frozen sections of the thickened gastric wall revealed phlegmonous gastnitis. Biopsy of the liven showed numerous microabscesses. The perforated gastric ulcer was ovensewn, the subdiaphragmatic abscess was drained, and a feeding jejunostomy tube was inserted. Cultures of the gastric wall taken at surgery grew Staphylococcus epidermidis, Enterobacter aerogenes, and Clostridium perfringens. surgery,
but
died
of a cardiac
day. Postmortem cultures streptococci, Enterobacter
arrest
of the gastric aerogenes,
disease. Discussion
Case
Report
C, T. , a 65-year-old black woman, was seen in the emergency room with a 3-4 day history of crampy midabdominal pain and 1 day of nausea and vomiting. Medical history included adult onset diabetes mellitus, organic heart disease with previous myocardial infarction, and several episodes of congestive heart failure requiring digoxin and furosemide. Vital signs on admission included an oral temperature of 35.6#{176}Cand a blood pressure of 1 40/75 mm Hg. Physical examination revealed a diffusely tender abdomen with guarding, but without rigidity or masses. Rectal examination was negative; the stool was positive for occult blood. Laboratory studies revealed blood urea nitrogen of 52 and a white blood cell count of 14,400/mm3 with a shift to the left. Blood urea nitrogen had decreased to 28 1 2 hours later after hydration, white blood cell count
had
increased
to 27,000/mm3,
and
temperature
had
risen
to
37.9#{176}C.Emergency superior mesentenic arteniography about 36 hr after admission to rule out mesentenic ischemia showed only diffuse atherosclerotic disease. Sonography showed cholelithiasis, and oral cholecystography did not visualize the gallbladder. Presumptive diagnosis of cholecystitis was made and the patient was started on antibiotics. Subsequent upper gastrointestinal series showed markedly thickened gastric mucosal folds with rigidity of the gastric wall (Fig. 1). Gastric cytology showed only a few squamous and inflammatory cells. The patient refused endoscopy. Surgery
on
hospital
day
1 4 revealed
an
infiltrative
process
in-
volving the entire stomach. There was a small ulceration high in the posterior gastric wall perforating into the diaphragm, with a localized left subphrenic abscess. There was a markedly thickened small bowel mesentery. The large bowel and gallbladder were normal to
Received November 3, 1 978; accepted 1 All authors: Department of Radiology,
Address reprint AJR
133:527-528,
requests
after revision April 1 7, 1979. Virginia Commonwealth University,
The history
patient with phlegmonous of heavy alcohol intake,
or upper
respiratory
peritoneal with most
signs. having
and
vomiting.
peritonitis ing this
infection, There a history
diagnosis. amylase
excluding
acute
elevated.
is
analysis
noncontributory. Preoperative
[2].
diagnosis
culture of the gastric abdominal film will
tritis the has
Medical
1979;
0361
-803x/79/1333-0527
$00.00;
© American
and
presence
is
cell
of
may
laboratory
be made
ominous
prognostic
be found
findings
by gastroscopy,
there
(emphysematous
are with
The plain ileus, but oc-
may
by gas, gas-
be air within
gastritis),
implication
in
is usu-
tract, if outlined If the phlegmonous
bacteria,
stomach
helpful
count
or achlorhydria
gastrointestinal series will show thickened cosal folds and may be accompanied dilatation or a rigid, thick-walled stomach ulating these when
The
].
which blood
Otherwise,
gastrointestinal gastric folds.
[3].
which The
upper
or effaced muby either gastric very closely sim-
linitis plastica [4]. It is often impossible to distinguish two entities purely on a radiographic basis, except gas is present in the gastric wall. Clinical findings of
College
of Virginia,
MCV
to M. A. Turner.
September
[1
normal, White
can
to gas-forming
of the
a very
occur
fever,
predominance, pain, nausea,
contents, or radiographically. often show a nonspecific
the upper edematous
is due wall
usually
pancreatitis.
Hypochlorhydria
on a gastric
casionally will show
may
pain,
female epigastric
a
abdominal pain is very helpful in distinguishfrom linitis plastica, the primary radiologic
differential Serum ally
abdominal
is a slight of severe
Hematemesis
and disease
gastritis usually has a recent bout of ‘ ‘gastritis”
Roentgen
Ray
society
Station,
Box
728,
Richmond,
VA 23298.
Downloaded from www.ajronline.org by 119.96.90.141 on 10/30/15 from IP address 119.96.90.141. Copyright ARRS. For personal use only; all rights reserved
528
CASE
Fig.
1 -Prone
rigidity.
Mucosal
view folds
of barium-filled effaced
stomach
along
lesser
(A)
and
curvature,
supine
and
anteroposterior
markedly
thickened
AJR:133,
REPORTS
air-contrast along
view
greater
(B).
Virtually
B,
curvature.
identical
Triangular
outlines
September
of gastric
perforating
ulcer
wall
1979
secondary
projects
from
to
posterior
wall of fundus.
an
acute
inflammatory
process
with radiographic findings the correct diagnois. A number of
this
of factors
condition,
ingestion tion,
ulcer
abdomen
plastica
combined
should
suggest
seem
to predispose
the development
hypochlorhydria,
from
a more
alcoholism,
proximal
or carcinoma,
source
ingestion
of infec-
of caustic
mate-
rials, ingestion of foreign bodies, and previous gastric surgery [2]. Although the exact mechanism by which infection develops in the gastric wall has not been clearly defined, three pathways are proposed: (1 ) direct invasion by a violation of the gastric mucosa by sharp bones or vegetable substances;
(2)
as endocarditis; septic focus, of the gastric but when may
primarily
hematogenous
mucosa
invasive.
the submucosa
offending
organisms
mococci,
Staphylococci,
have
been
from
other
septic
foci
such
or (3) lymphatic spread from a contiguous most commonly cholecystitis [2]. The low pH fluid normally does not allow bacterial growth,
the gastric
become
reported
are
is damaged,
ingested
bacteria
The
suppurative
process
involves
and
muscularis.
hemolytic E.
[2].
Diagnosis gastritis simple
including
of bacteria
gastric
in the
of linitis
coli,
The
most
Clostridia,
common but
Streptococci,
and
the the
inspection
mistakenly
diverting
is difficult.
diagnosed
procedures
surgical treatment area with complete
and large review of
may
of choice resection
doses of 25 cases
systemic [1 ], the
Phlegmonous
as linitis be
plastica,
performed.
and
However,
includes wide of the involved
drainage gastric
antibiotics [5]. surgical mortality
treatment was 1 8%, whereas the medical 1 00%. The overall mortality was 67%.
In
of wall
a recent using this
mortality
was
REFERENCES 1
.
Miller
Al,
enterology
scess.
4.
5.
B,
Rogers
-238,
Cl, Kumpe A bizarre
452-459, 3.
Smith 68:231
2. Weinter
pneu-
Proteus
by surgical
is often
DA,
Diaconis
intramural
LL,
Schowengerdt gastnitis. Surg
Stephenson
SR Jr. Jasnebi
phlegmasia
of
J Surg
Phlegmonous
Gastro-
gastnitis.
JN:
location.
Am
Idiopathic
gastric
J Gastroenterol
ab64:
1975
Gonzalez physematous
Williams
Al:
1975
the
stomach.
BL, Beeby DI: Acute 60:498-500, 1973
C, Skinner
HH
Jr.
Lynch
P: Em-
Gynecol Obstet 1 1 6:79-87, 1963 H, Rhutigan R, Woodard ER: Acute Am
Surg
diffuse
36:225,
phlegmonous
1970
gastnitis.
Br
527
Phlegmonous
Gastritis
Mary Ann Turner,1 Dennis Stanley Phlegmonous
Michael
gastritis
C. Beachley,
is a rare
bacterial
and
infection
of the
gastric wall. The diagnosis should be strongly considered in any patient who has an acute abdomen by clinical examination and has radiographic findings of air in the gastric
wall,
thickened
radiographic dition has difficulty
folds,
and
rigidity
findings suggestive a very high mortality in making
gastric
diagnosis,
both
wall,
or
The conin part to
preoperatively
of this
The
patient
recovered
from
on the first postoperative wall grew alpha hemolytic and Proteus morgani.
As of 1 975 [1 ], 25 cases were documented literature. Our case reviews the diagnostic
and at surgery. in the American parameters
a correct
of the
of linitis plastica. rate that is due
inspection. Two frozen sections of the thickened gastric wall revealed phlegmonous gastnitis. Biopsy of the liven showed numerous microabscesses. The perforated gastric ulcer was ovensewn, the subdiaphragmatic abscess was drained, and a feeding jejunostomy tube was inserted. Cultures of the gastric wall taken at surgery grew Staphylococcus epidermidis, Enterobacter aerogenes, and Clostridium perfringens. surgery,
but
died
of a cardiac
day. Postmortem cultures streptococci, Enterobacter
arrest
of the gastric aerogenes,
disease. Discussion
Case
Report
C, T. , a 65-year-old black woman, was seen in the emergency room with a 3-4 day history of crampy midabdominal pain and 1 day of nausea and vomiting. Medical history included adult onset diabetes mellitus, organic heart disease with previous myocardial infarction, and several episodes of congestive heart failure requiring digoxin and furosemide. Vital signs on admission included an oral temperature of 35.6#{176}Cand a blood pressure of 1 40/75 mm Hg. Physical examination revealed a diffusely tender abdomen with guarding, but without rigidity or masses. Rectal examination was negative; the stool was positive for occult blood. Laboratory studies revealed blood urea nitrogen of 52 and a white blood cell count of 14,400/mm3 with a shift to the left. Blood urea nitrogen had decreased to 28 1 2 hours later after hydration, white blood cell count
had
increased
to 27,000/mm3,
and
temperature
had
risen
to
37.9#{176}C.Emergency superior mesentenic arteniography about 36 hr after admission to rule out mesentenic ischemia showed only diffuse atherosclerotic disease. Sonography showed cholelithiasis, and oral cholecystography did not visualize the gallbladder. Presumptive diagnosis of cholecystitis was made and the patient was started on antibiotics. Subsequent upper gastrointestinal series showed markedly thickened gastric mucosal folds with rigidity of the gastric wall (Fig. 1). Gastric cytology showed only a few squamous and inflammatory cells. The patient refused endoscopy. Surgery
on
hospital
day
1 4 revealed
an
infiltrative
process
in-
volving the entire stomach. There was a small ulceration high in the posterior gastric wall perforating into the diaphragm, with a localized left subphrenic abscess. There was a markedly thickened small bowel mesentery. The large bowel and gallbladder were normal to
Received November 3, 1 978; accepted 1 All authors: Department of Radiology,
Address reprint AJR
133:527-528,
requests
after revision April 1 7, 1979. Virginia Commonwealth University,
The history
patient with phlegmonous of heavy alcohol intake,
or upper
respiratory
peritoneal with most
signs. having
and
vomiting.
peritonitis ing this
infection, There a history
diagnosis. amylase
excluding
acute
elevated.
is
analysis
noncontributory. Preoperative
[2].
diagnosis
culture of the gastric abdominal film will
tritis the has
Medical
1979;
0361
-803x/79/1333-0527
$00.00;
© American
and
presence
is
cell
of
may
laboratory
be made
ominous
prognostic
be found
findings
by gastroscopy,
there
(emphysematous
are with
The plain ileus, but oc-
may
by gas, gas-
be air within
gastritis),
implication
in
is usu-
tract, if outlined If the phlegmonous
bacteria,
stomach
helpful
count
or achlorhydria
gastrointestinal series will show thickened cosal folds and may be accompanied dilatation or a rigid, thick-walled stomach ulating these when
The
].
which blood
Otherwise,
gastrointestinal gastric folds.
[3].
which The
upper
or effaced muby either gastric very closely sim-
linitis plastica [4]. It is often impossible to distinguish two entities purely on a radiographic basis, except gas is present in the gastric wall. Clinical findings of
College
of Virginia,
MCV
to M. A. Turner.
September
[1
normal, White
can
to gas-forming
of the
a very
occur
fever,
predominance, pain, nausea,
contents, or radiographically. often show a nonspecific
the upper edematous
is due wall
usually
pancreatitis.
Hypochlorhydria
on a gastric
casionally will show
may
pain,
female epigastric
a
abdominal pain is very helpful in distinguishfrom linitis plastica, the primary radiologic
differential Serum ally
abdominal
is a slight of severe
Hematemesis
and disease
gastritis usually has a recent bout of ‘ ‘gastritis”
Roentgen
Ray
society
Station,
Box
728,
Richmond,
VA 23298.
Downloaded from www.ajronline.org by 119.96.90.141 on 10/30/15 from IP address 119.96.90.141. Copyright ARRS. For personal use only; all rights reserved
528
CASE
Fig.
1 -Prone
rigidity.
Mucosal
view folds
of barium-filled effaced
stomach
along
lesser
(A)
and
curvature,
supine
and
anteroposterior
markedly
thickened
AJR:133,
REPORTS
air-contrast along
view
greater
(B).
Virtually
B,
curvature.
identical
Triangular
outlines
September
of gastric
perforating
ulcer
wall
1979
secondary
projects
from
to
posterior
wall of fundus.
an
acute
inflammatory
process
with radiographic findings the correct diagnois. A number of
this
of factors
condition,
ingestion tion,
ulcer
abdomen
plastica
combined
should
suggest
seem
to predispose
the development
hypochlorhydria,
from
a more
alcoholism,
proximal
or carcinoma,
source
ingestion
of infec-
of caustic
mate-
rials, ingestion of foreign bodies, and previous gastric surgery [2]. Although the exact mechanism by which infection develops in the gastric wall has not been clearly defined, three pathways are proposed: (1 ) direct invasion by a violation of the gastric mucosa by sharp bones or vegetable substances;
(2)
as endocarditis; septic focus, of the gastric but when may
primarily
hematogenous
mucosa
invasive.
the submucosa
offending
organisms
mococci,
Staphylococci,
have
been
from
other
septic
foci
such
or (3) lymphatic spread from a contiguous most commonly cholecystitis [2]. The low pH fluid normally does not allow bacterial growth,
the gastric
become
reported
are
is damaged,
ingested
bacteria
The
suppurative
process
involves
and
muscularis.
hemolytic E.
[2].
Diagnosis gastritis simple
including
of bacteria
gastric
in the
of linitis
coli,
The
most
Clostridia,
common but
Streptococci,
and
the the
inspection
mistakenly
diverting
is difficult.
diagnosed
procedures
surgical treatment area with complete
and large review of
may
of choice resection
doses of 25 cases
systemic [1 ], the
Phlegmonous
as linitis be
plastica,
performed.
and
However,
includes wide of the involved
drainage gastric
antibiotics [5]. surgical mortality
treatment was 1 8%, whereas the medical 1 00%. The overall mortality was 67%.
In
of wall
a recent using this
mortality
was
REFERENCES 1
.
Miller
Al,
enterology
scess.
4.
5.
B,
Rogers
-238,
Cl, Kumpe A bizarre
452-459, 3.
Smith 68:231
2. Weinter
pneu-
Proteus
by surgical
is often
DA,
Diaconis
intramural
LL,
Schowengerdt gastnitis. Surg
Stephenson
SR Jr. Jasnebi
phlegmasia
of
J Surg
Phlegmonous
Gastro-
gastnitis.
JN:
location.
Am
Idiopathic
gastric
J Gastroenterol
ab64:
1975
Gonzalez physematous
Williams
Al:
1975
the
stomach.
BL, Beeby DI: Acute 60:498-500, 1973
C, Skinner
HH
Jr.
Lynch
P: Em-
Gynecol Obstet 1 1 6:79-87, 1963 H, Rhutigan R, Woodard ER: Acute Am
Surg
diffuse
36:225,
phlegmonous
1970
gastnitis.
Br
