A 35-year-old immunocompromised male who was at 2-year status after simultaneous liver and kidney transplant presented to the emergency department with 1 week of nausea, vomiting, and epigastric pain and 1 day of coffee-grounds emesis. Both recipient and donor were known to be seropositive for the cytomegalovirus and the Epstein-Barr virus. The patient had a history of uncontrolled diabetes mellitus type 1 and was not compliant with his medications. He had also been taking immunosuppressants inconsistently for 1 month prior to the presentation due to financial constraints. He denied fever, chills, diarrhea, hematochezia, melena, or dysuria. He was an active smoker but denied alcohol and illicit drug use. The patient was hemodynamically stable on admission with a physical examination remarkable for scleral icterus, jaundice, and epigastric tenderness without rebound. Laboratory investigation showed a hemoglobin of 13 g/dL, white blood cell count of 15 × 109/L with left shift, a platelet count of 216 × 109/L, blood glucose of 773 mg/dL with an anion gap of 22 mEq/L, aspartate aminotransferase of 459 IU/L, alanine aminotransferase of 280 IU/L, total bilirubin of 24.7 mg/dL, alkaline phosphatase of 2570 IU/L, blood urea nitrogen of 67 mg/dL, and creatinine of 3.9 mg/dL. His blood B-hydroxybutyrate was positive. Computed tomographic (CT) scan of his abdomen revealed diffuse gastric wall thickening, gastric cardia pneumatosis, as well as air in the adjacent gastric vein, superior mesenteric vein, and main portal vein without intra-abdominal free air (Figure 1). Upper gastrointestinal endoscopy was performed and demonstrated esophagitis, portal hypertensive gastropathy, severely erythematous gastric mucosa with stigmata of recent bleeding, and dark red blood clots (Figure 2). Biopsies were taken for histology. The pathology of the gastric body biopsy is shown in Figure 3.
CT scan of the abdomen, showing diffuse gastric wall thickening and gastric cardia pneumatosis. Abbreviation: CT, computed tomographic.
Upper gastrointestinal endoscopy showing severely erythematous gastric body mucosa with stigmata of recent bleeding and dark red blood clots.
Hematoxylin and eosin stain of gastric biopsy specimen (original magnification, 400×).
What is your diagnosis?
Diagnosis: Emphysematous gastritis by Clostridium ventriculi infection.
The hematoxylin and eosin stain of the patient’s gastric biopsy specimen in Figure 5 demonstrated bacterial infiltrates with numerous Clostridium ventriculi.
Other organisms such as Escherichia coli, Streptococcus species, Enterobacter species, Clostridium species, and Pseudomonas aeruginosa are also known to cause emphysematous gastritis and should be considered as part of the differential diagnosis [1].
Emphysematous gastritis is a rare, lethal gastrointestinal emergency, especially in an immunocompromised patient, and traditionally has a mortality rate of approximately 60% or more [1]. It is generally caused by local gastric wall infection and invasion of gas-forming micro-organisms through a mucosal defect [1]. The diagnosis is by radiographic evaluation with CT scan that demonstrates gastric wall thickening and air within the gastric wall (Figure 4) [2]. The presence of gas in the portal vein is the most ominous sign that usually differentiates emphysematous gastritis from other noninfectious entities of gastric wall pneumatosis, such as gastric emphysema or traumatic injury of the gastric mucosa [2, 3].
CT scan of the abdomen, showing diffuse gastric wall thickening, gastric cardia pneumatosis, and adjacent gastric venous air (arrows). Abbreviation: CT, computed tomographic.
Hematoxylin and eosin stain of the gastric biopsy specimen, showing active gastritis with ulceration, necrosis, and bacterial infiltrate consistent with Clostridium ventriculi (arrow) (original magnification, 400×).
Clostridium ventriculi (previously known as Sarcina ventriculi) is a gram-positive, nonmotile, catalase-negative, spore-forming, anaerobic coccus that displays a classic cuboid-shaped tetrad or octet arrangement, which is a result of their cell division patterns occurring in at least 2 planes [4]. The organism is usually found in water and soil. It was postulated to have been ingested with soil particles in food. It can thrive in highly acidic environments like the gastric lumen and is capable of fermenting carbohydrates [4]. The clinical presentation of C. ventriculi infection ranges from asymptomatic, mild gastritis to rare, life-threatening severe complications including emphysematous gastritis and gastric perforation [5–8]. It was speculated that the local accumulation of acetaldehyde and ethanol formed from the fermentation process could induce mucosal injuries and could lead to lethal complications like emphysematous gastritis [4]. Within the past 40 years, 23 human cases have been reported, and it is postulated that delayed gastric emptying allows for organism growth [4, 9, 10].
No standard of treatment has been established for C. ventriculi emphysematous gastritis. Currently, therapeutic approaches have been based on clinical presentation and disease severity ranging from treatment with broad-spectrum antibiotics to surgical intervention [11, 12].
Our patient was treated with intravenous piperacillin-tazobactam and clindamycin. Clinically, the patient initially showed symptomatic improvement, and repeat endoscopy on day 5 showed clearance of the organisms. Unfortunately, he was also diagnosed with an acute rejection of his transplanted organs resulting from medication nonadherence. He suddenly deteriorated from profound metabolic acidosis and multisystem organ failure after 2 weeks of hospitalization. Despite aggressive medical management, the patient passed away.
Note
Potential conflicts of interest. The authors: No reported conflicts of interest. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest.
