56-year-old woman with recently diagnosed pancreatic cancer presented with hematemesis and epigastric pain radiating to the back.
Prepared by Shabnam A. Fidvi, MBBS and Susan A. Klein, MD,
Department of Radiology, New York Medical College, Valhalla,
A 56-year-old woman with recently diagnosed pancreatic cancer
presented with hematemesis and epigastric pain radiating to the
back. She had completed 3 cycles of chemotherapy and radiation. A
contrast-enhanced CT scan 2 weeks prior had demonstrated a large
necrotic mass arising from the pancreatic body and tail, thrombosis
of the superior mesenteric vein, partial occlusion of the portal
vein, and a thickened stomach wall (figure 1). In addition, there
was intrahepatic biliary duct dilatation with a dilated,
thick-walled gallbladder and metastatic disease in the liver and
On the day of admission, she was afebrile, dehydrated and
tachycardic. Her abdomen was diffusely tender and guarded with
absent bowel sounds. Laboratory data included an elevated white
blood cell (WBC) count (42,000/mm
with 98% neutrophils), prolonged prothrombin time (22 sec), and
elevated liver enzymes. Serum amylase and lipase were normal.
An emergent contrast-enhanced CT scan showed the pancreatic mass
invading the posterior wall of the stomach (figure 2A). Numerous
air bubbles were present in the stomach wall, and the superior
mesenteric vein remained thrombosed (figure 2B). The celiac,
splenic, superior mesenteric, and inferior mesenteric arteries
enhanced normally. The common hepatic artery was patent but
diminished in caliber and appeared to arise from the superior
mesenteric artery. The left gastric artery could not be identified
definitively. There was gas within portal venous radicles (figure
3), but no free intraperitoneal air. Chest and abdominal x-rays
revealed no diagnostic abnormality.
A diagnosis of emphysematous gastritis was made and therapy with
broad-spectrum parenteral antibiotics and acid suppression was
initiated. At exploratory laparotomy, a fibrinous exudate covered
the anterior stomach wall. There was bluish discoloration with
thinning of the antrum anteriorly reflecting ischemia, but no
perforation was identified. The small and large intestines were
normal. Intraoperative endoscopy revealed diffuse ischemic changes
involving the gastric mucosa. Endoscopic biopsies were not obtained
because of the perceived risk of gastric perforation.
We believe that locally invasive pancreatic cancer caused
gastric infarction by a combination of arterial occlusion and
venous stasis. This, in the setting of increased gastric
intraluminal pressure from forceful vomiting, may have facilitated
bacterial invasion with the subsequent formation of intramural gas
and emphysematous gastritis. A review of the existing literature
revealed only three case reports describing vascular occlusion
precipitating gastric infarction as the cause of emphysematous
Three variations of gas within the stomach wall have been
described: interstitial gastric emphysema, cystic pneumatosis
(pneumatosis cystoides intestinalis), and emphysematous gastritis.
Interstitial gastric emphysema and cystic pneumatosis are
noninfectious in origin, whereas emphysematous gastritis is
associated with infection by gas-forming organisms. These three
variants can be differentiated on the basis of clinical and
Interstitial gastric emphysema is seen when air from an
extrinsic source enters the stomach wall and accumulates in the
submucosa, subserosa, or both. The formation of intramural air is
frequently preceded by gastric distension and vomiting. Gastric
outlet obstruction, pulmonary emphysema, and instrumentation of the
stomach are common contributing factors.
Based on the etiologic mechanism, interstitial gastric emphysema is
classified into three major categories: 1) obstructive, due to
raised intragastric pressure; 2) pulmonary, secondary to rupture of
bullae and dissection of air along the bronchopulmonary bundles to
the mediastinum and then to the retroperitoneum; and 3) traumatic,
from mucosal trauma secondary to endoscopic manipulation and air
Plain radiographs characteristically demonstrate a linear lucency
conforming to the contour of a thin-walled, distended stomach and
enveloping any intraluminal gas and fluid content. The clinical
course is most frequently benign with spontaneous resolution of
intramural air once the obstruction is relieved.
Cystic pneumatosis (pneumatosis cystoides intestinalis) refers
to the radiographic observation of multiple 1- to 2-mm gas-filled
cysts in the wall of the stomach and intestine of patients with
little or no gastrointestinal symptoms.
It has been suggested that cystic pneumatosis of the stomach should
be placed in the obstructive or pulmonary category of gastric
emphysema as there are no etiologic or prognostic differences.
Emphysematous gastritis occurs when there is diffuse
infiltration of the stomach wall by pathogenic gas-forming
bacteria. The stomach is normally resistant to bacterial invasion
as a result of its abundant blood supply, acid pH, and mucosal
barrier. An antecedent gastric mucosal injury allows gas-forming
organisms to gain access to deeper tissue layers. Usual
predisposing factors include ingestion of corrosive substances (~
37%), alcohol abuse (~ 22%), gastroenteritis (~ 15%), and recent
abdominal surgery (~ 15%).
Emphysematous gastritis has also been described in association with
and adenocarcinoma of the stomach.
There have been isolated reports of this condition occurring with
phytobezoar, leukemia, diabetes mellitus,
and following the ingestion of large amounts of carbonated
are the commonest etiologic agents.
The clinical presentation of emphysematous gastritis may closely
mimic acute perforation of an abdominal viscus with the explosive
onset of severe abdominal pain, nausea, vomiting, and diarrhea with
or without hematemesis. Vomiting of a necrotic cast of the stomach
due to dissection along the plane of the muscularis mucosae by the
invading organisms is considered pathognomonic.
The diagnostic features on plain radiographs are innumerable gas
bubbles that silhouette the stomach in a mottled fashion and remain
constant with positional change. Thickening of the rugal folds and
occasionally portal venous air are associated findings. An upper
gastrointestinal series confirms the extraluminal location of the
gas and may demonstrate a cobblestone appearance of the mucosa due
to submucosal blebs and irregular rugal thickening. Intramural
penetration of contrast medium may also be seen. Abdominal CT plays
an important role in the detection of small amounts of intramural
gas and in the demonstration of gastric wall thickening, which may
serve to differentiate emphysematous gastritis from gastric
Broad-spectrum antibiotics (with coverage against gram-negative
and anaerobic organisms), intravenous fluids, and nutritional
support form the mainstay of treatment. Gastric resection during
the acute phase of emphysematous gastritis is not advocated due to
poor healing of the infected tissue. The major indication for
emergent surgery is acute perforation.
The overall mortality for emphysematous gastritis is >60%.
Gastric strictures requiring surgical intervention have been
described in 21% of survivors. Gastric sinus tract formation is an