Prepared by Shabnam A. Fidvi, MBBS and Susan A. Klein, MD, Department of Radiology, New York Medical College, Valhalla, NY.

CASE SUMMARY

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 lungs.

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 ³ with 98% neutrophils), prolonged prothrombin time (22 sec), and elevated liver enzymes. Serum amylase and lipase were normal.

DIAGNOSIS

Emphysematous gastritis

IMAGING FINDINGS

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.

DISCUSSION

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 gastritis. ^1-3

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 roentgenologic characteristics. ⁴

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. ⁵ 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 insufflation. ⁶ 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. ⁴

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. ⁴ 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. ⁶

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%). ⁷ Emphysematous gastritis has also been described in association with gastrointestinal infarction, ³ acute pancreatitis, ^8,9 and adenocarcinoma of the stomach. ¹⁰ There have been isolated reports of this condition occurring with phytobezoar, leukemia, diabetes mellitus, ⁷ disseminated strongyloidiasis, ¹¹ gastric mucormycosis ¹² and following the ingestion of large amounts of carbonated beverages ¹³ Streptococcus species, Escherichia coli , Enterobacter species, Pseudomonas aeruginosa, and Clostridium perfringens are the commonest etiologic agents. ⁷ 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. ¹⁰ 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 emphysema. ¹⁴

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. ¹⁵ The overall mortality for emphysematous gastritis is >60%. ^7,12 Gastric strictures requiring surgical intervention have been described in 21% of survivors. Gastric sinus tract formation is an occasional complication. ⁷