INTRODUCTION

Emphysematous gastritis (EG) is a rare, lethal infection of the gastric wall mucosa by gas-producing bacteria with a mortality rate of 55%–80%.1–5 With radiologic imaging now more widely used, the diagnostic rate of EG has increased with its reported rate quadrupling after 20122; nonetheless, fewer than 120 cases have been reported in the literature.1–9 It has been proposed that gastric mucosal lesions (either ulcerative or ischemic) may serve as a nidus for penetration and mucosal breakdown vs hematogenous spread from a distant focus, with subsequent gas production.1–6 Typical organisms include Streptococci species, Escherichia coli, Clostridium spp, Klebsiella pneumoniae, and rarely Sarcina ventriculi.1,2,4,6–10 Gastric volvulus can compromise blood supply to the stomach and predispose to ischemia and EG. We present a rare case of EG associated with S. ventriculi, secondary to organo-axial volvulus of the stomach.

CASE REPORT

An 83-year-old woman with no pertinent medical history presented with nausea and sharp, constant abdominal pain which radiated to her back and several episodes of nonbloody vomiting for 2 days. On presentation, she was afebrile and hemodynamically stable. Physical examination was notable for a mildly distended abdomen with generalized tenderness. No guarding, rebound tenderness, or pulsatile mass was noted.

Laboratory test results were significant for a white blood cell count of 11.3 K/μL (reference range 4.0–10.5 K/μL). Computed tomography abdomen/pelvis without intravenous contrast revealed marked fluid and gaseous distention of stomach with air–fluid level, diffuse pneumatosis within gastric wall, and gastric volvulus (Figure 1). Imaging also showed diffuse, hepatic portal venous gas indicative of bowel ischemia (Figure 2). Iodinated contrast media/iohexol/ioxaglate sodium was not used because the patient had a severe allergy (anaphylaxis) to it.

Figure 1.:

Sagittal view of the computed tomography abdomen/pelvis showcasing the pylorus/duodenum (red arrow) superior to the gastroesophageal junction (blue arrow) indicative of organo-axial gastric volvulus.

Figure 2.:

Coronal view of the computed tomography abdomen/pelvis demonstrating a concentric ring of air around the stomach (red arrows) with diffuse, hepatoportal venous gas (blue arrows) indicating mucosal air infiltration.

Given her clinical presentation and imaging findings, the patient was taken emergently to the operating room. Diagnostic esophagogastroduodenoscopy revealed organo-axial volvulus which resolved on insufflation; however, the stomach mucosa was noted to have a diffusely pale gray appearance suggestive of gastric necrosis prompting exploratory laparotomy. On entering the abdomen, a rush of air was noted consistent with pneumoperitoneum suggesting bowel perforation. Evaluation of the stomach showed nonviable, diffuse, full-thickness necrosis, and total gastrectomy was performed as a lifesaving procedure.

Gastrectomy specimen histopathology showed ischemic and ulcerated mucosa with marked underlying submucosal edema. There were rare S. ventriculi bacterial forms on the mucosal surface. In addition, there were variably sized air spaces throughout the edematous submucosa confirming EG (Figure 3). Tissue sections from the site of gastric perforation showed numerous S. ventriculi (Figure 4).

Figure 3.:

(A, B) H&E stain of the gastrectomy specimen at 2×, 4× magnification, respectively. (C) Gram stain of the gastrectomy specimen demonstrating a gram-positive coccus bacterium in a cuboidal, tetrad formation (red arrows) consistent with Sarcina ventriculi, at 20× magnification. (D) H&E stain of the gastrectomy specimen showing basophilic staining of characteristic appearing Sarcina ventriculi (black arrow) at 20× magnification. H&E, hematoxylin and eosin.

Figure 4.:

(A) Gram stain and (B, C) hematoxylin and eosin stain of the gastrectomy specimen at the point of perforation showcasing Sarcina ventriculi at 20×, 4×, 20× magnification, respectively.

Thereafter the patient continued to decline clinically despite aggressive resuscitation with fluids, antibiotics, and vasopressors. Intraoperative findings on second look exploratory laparotomy demonstrated multiple areas of nonviable small bowel and colon (Figure 5). As extensive interventions and resuscitation would not subsequently achieve a meaningful quality of life, the family transitioned the patient to comfort care and she died shortly after palliative extubation.

Figure 5.:

(A, B) Intraoperative small bowel and (C) anterior transverse colon noted to have patchy areas of full thickness ischemia near perforation (black arrows), with poor perfusion, hyperemia, associated mucosal thickening, and serosal petechiae (blue arrows).

DISCUSSION

EG is a potentially fatal condition associated with gas-producing bacterial infection of the gastric wall. Despite aggressive clinical management, EG has abysmal morbidity and mortality outcomes.1–4 Clinical presentation of EG is nonspecific; however, patients typically present in an acutely ill manner with signs/symptoms of acute abdomen (eg, nausea/vomiting, abdominal pain), fever, hemodynamic instability, and/or shock. Laboratory analysis may reveal elevated white blood cell count and elevated lactate.2–5

Abdominal imaging is crucial in diagnosing EG. Computed tomography of the abdomen with contrast is the study of choice due to its higher sensitivity relative to single view radiographs. Key imaging features include gastric distention, gastric mucosal wall/fold thickening in the setting of edema, and infiltrating gas within the wall—especially within the fundus and/or greater curvature.2–5 Changes in body position do not affect these features.3 Portal venous gas (PVG) can also be present and is a negative prognostic marker as EG mortality exceeds 75% when simultaneously present.2,4

Microorganisms may be seen on histology, and its presence supports EG as the ongoing/underlying pathologic process.3,5 One such organism, S. ventriculi, is an anaerobic, nonmotile, gas-producing, gram-positive coccus that characteristically appears as a cuboidal, tetrad formation with basophilic staining.2,4,6,7,10 Favorable growth conditions of this bacterium are categorized into those associated with gastric outlet obstruction (eg, pyloric stenosis) or delayed gastric emptying (eg, gastroparesis) as these sequelae allocate additional time for bacterial overgrowth/penetration. S. ventriculi grows at a pH of 1; thus, the acidity of the stomach acts as a catalyst for growth rather than a deterrent.4,6 Many predisposing conditions of EG result in outlet obstruction vs delayed emptying, demonstrating overlap between the 2.1,2,4

No formal diagnostic criteria for EG exists as it remains a rare condition. Conflicting literature exists on this subject as some have suggested that imaging findings alone are satisfactory,2 while others deem factors such as clinical presentation, elevated inflammatory markers, evidence of bacterial infection, and a high index of suspicion contribute to making the diagnosis of EG.2,3,5

No established management guidelines for EG exist; however, surgical intervention has been the mainstay of treatment—particularly if PVG is present. Recently, a conservative approach (eg, bowel rest, fluid resuscitation, empiric antibiotics, endoscopy with biopsy) has been used due to poor postsurgical outcomes and minimal difference in overall prognosis.1–5,7 While no longer first line, surgical intervention is still warranted in severe cases of EG which refers to those who fail conservative therapy and possess red-flag signs (eg, peritonitis, perforation, hemodynamic instability, ischemia).1–5 Nevertheless, EG mortality remains a challenge as recent literature reports a rate of 55%–61% up to 80%, with higher levels of mortality seen when either PVG or S. ventriculi is involved.2–4,7

Gastric ischemia secondary to organo-axial volvulus leading to EG represents an extremely rare clinical scenario. Moreover, the association of S. ventriculi in our case was an intriguing finding also. Whether the presence of S. ventriculi is incidental or accelerates the process of ischemia remains a question of debate.4,6,7,10 As the volvulus resolved with insufflation during esophagogastroduodenoscopy, this implies that the ongoing ischemic damage was promoted by S. ventriculi and was not only due to mechanical aspects. More case reports and studies pertaining to this rare clinical entity are needed to help with early diagnosis and perhaps guide management.

DISCLOSURES

Author contributions: J. Rozenberg reviewed charts, drafted, and edited the article, and is the article guarantor. A. Mir reviewed charts, drafted, and edited the article. K. Mönkemüller reviewed charts and edited the article. D. Grider provided the pathology images, and edited the article. B. Collier supervised the project and edited the article.

Financial disclosure: None to report.

Informed consent was obtained for this case report.

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