Abstract
Emphysematous gastritis is a rare disease characterised by air in the wall of the stomach due to gas-forming microorganisms. This is a highly lethal entity for which only prompt diagnosis and treatment can avoid mortality. Different factors have been described that disrupt the integrity of the mucosa such as corrosive ingestion, alcohol abuse, recent abdominal surgery or cancer. We report a case of emphysematous gastritis in a 92-year-old woman who presented to the emergency department with abdominal pain, nausea and vomiting. Inflammatory markers were elevated and abdominal X-rays showed intramural gastric air, confirmed by CT scan. The patient received intravenous fluids, nutritional support and broad-spectrum antibiotic with resolution of gastric wall emphysema. However, the diagnosis of poorly cohesive gastric adenocarcinoma was made and the patient was referred to palliative care. This case highlights the importance of prompt recognition of this lethal entity that represents a rare and aggressive presentation of gastric cancer.
Keywords: gas/free gas, stomach and duodenum
Background
Emphysematous gastritis, first described by Frankael in 1889,1 represents a rare condition characterised by the presence of gas in the stomach wall secondary to infection by gas-producing organisms.2 3 It is frequently associated with systemic toxicity and shock.2 4 Early recognition and treatment are vital since it carries a mortality rate of 60%.5
This report describes a case of emphysematous gastritis associated with adenocarcinoma of the stomach with fatal outcome. Besides being an infrequent presentation of gastric cancer, our case highlights the importance of early recognition of emphysematous gastritis to prevent significant morbidity and mortality.
Case presentation
A 92-year-old woman with history of hypertension and severe dementia (WHO performance status 4) presented to the emergency department with a few-days history of diffuse abdominal pain, nausea and vomiting. Haematemesis and haematochezia were denied by her family.
At presentation, she was afebrile and normotensive with generalised abdominal tenderness without guarding or rebound tenderness.
Investigations
Her blood tests showed haemoglobin 118 g/L (normal range (NR) 130–170 g/L), leucocytosis (white blood cell count 16 500/µL (NR 4–10 000/µL)) with 84% of neutrophils (NR 40%–80%), platelets 206 000/µL (NR 150 000–400 000/µL), creatinine 0.63 mg/dL (NR 0.7–1.2 mg/dL), urea 62 mg/dL (NR 13–43 mg/dL), C reactive protein 8.7 mg/dL (NR <0.5 mg/dL). Aspartate transaminase, alanine transaminase, bilirubin and lipase were within normal values.
Abdominal radiograph revealed marked gastric distension and air within gastric wall. Abdominal CT scan confirmed the presence of intramural gas along the entire gastric wall extension (figures 1 and 2).
Figure 1.
Abdominal radiograph shows marked gastric distention with a smooth lucent line along the wall of the stomach consistent with emphysematous gastritis.
Figure 2.

Coronal CT image of the abdomen confirms diffuse intramural air in the stomach.
Localised hyperaemia of the gastric mucosa was unveiled by upper endoscopy and biopsies showed poorly cohesive gastric adenocarcinoma.
Treatment
Intravenous fluids, meropenem and esomeprazole were started for the presumed diagnosis of emphysematous gastritis. Blood cultures were persistently negative.
Clinical improvement was noted after 1 week of meropenem which she maintained for 17 days. A CT of abdomen was obtained 2 weeks later and showed resolution of intramural air (figure 3). Due to pronounced gastric stasis, oral feeding was not possible, and the patient started total parenteral nutrition.
Figure 3.

CT image showing resolution of gastric emphysema.
Outcome and follow-up
In face of patient’s age, comorbidities and cancer diagnosis, a conservative management was decided and she was referred to receive palliative care. The patient was maintained on broad-spectrum antibiotics (as previously stated) and total parental nutrition with gradual clinical improvement. Oral feeding was never possible, neither with nasojejunal tube or pyloric prothesis, due to cancer-induced gastroparesis. The patient developed acute pancreatitis—which was possibly related with lipid enriched parenteral nutrition—and died.
Discussion
Emphysematous gastritis is a rare and life-threatening entity characterised by phlegmonous gastric inflammation. Local infection is caused by gas-producing bacteria that penetrate the gastric wall trough a mucosal defect or by haematogenous dissemination from a distant focus.4 6 Different factors have been described that disrupt mucosal integrity: alcohol abuse, diabetes, abdominal surgery, gastric infarction and treatment with corticosteroids and cytotoxins, ingestion of non-steroidal anti-inflammatory drugs and corrosive substances.3 4 6 As in our patient, malignancy, namely, adenocarcinoma was previously reported in one case by Smith.7 No causative organisms are found in the majority of cases.2 The bacteria most frequently isolated are streptococci, Escherichia coli, Enterobacter species, Pseudomonas aeruginosa and Clostridium perfringens. Other less frequent agents include Staphylococcus aureus and Candida species.5 6
Emphysematous gastritis should be distinguished from gastric emphysema, a relative benign situation, in which air dissects through the gastric wall usually following trauma to the gastric mucosa.5 8 It has been related to conditions that elevate intragastric pressure like air insufflation during endoscopy or obstruction (mechanical or not).3
The classical clinical presentation includes acute abdominal pain, nausea, vomiting and fever, all with a fulminant course. A more subtle presentation has been described, generally in association with confounding factors such as diabetes, steroids use and renal failure.2 Passage of necrotic tissue with emesis or in the nasogastric aspirate has been stated as a pathognomonic sign but it was not found in our patient.3 4 9 The rather benign presentation of this report may be attributed to patient’s age and severe dementia.
The CT scan is the imaging test of choice and a definitive diagnosis of emphysematous gastritis can be made when there is demonstration of intramural gas throughout the stomach.10 Plain abdominal radiograph can also be used as the initial imaging study. General characteristics of emphysematous gastritis include a distended stomach outlined with linear gas shadows in the gastric wall.8 The presence of portal venous gas is a poor prognostic marker indicative of gastric ischaemia, a situation with mortality rates as high of 75%.4 5
The mortality of emphysematous gastritis is high without prompt initiation of broad-spectrum antibiotics (covering anaerobes and Gram-negative bacilli), intravenous hydration and appropriate nutrition along with proton-pump inhibitors which are the cornerstone of treatment. Unless there is evidence of ischaemia or perforation, surgery is not indicated during acute infection due to friability of the mucosa and high risk of anastomotic leak.2 6 In a review by Watson, surgical intervention did not confer statistically significant benefit on mortality even when following in the previously stated indications.2 Development of strictures occur in up to 25% of patients and represent a late indication for surgery.
In summary, we report the second case of emphysematous gastritis associated with gastric cancer. Emphysematous gastritis is a rare but lethal entity of gastric wall inflammation and systemic toxicity associated with high mortality rates. Given that mortality is high, early recognition of this entity is crucial, so that appropriate diagnostic testing and therapies can be attempted, to limit morbidity and mortality.
Learning points.
Emphysematous gastritis is a rare infection characterised by the presence of gas bubbles in the stomach wall.
The risk of mortality is high without early interventions, so early recognition and treatment are crucial.
Broad-spectrum antibiotics and resuscitation are the cornerstone of treatment, with surgery being reserved for complications.
Acknowledgments
The authors would like to express their deepest appreciation to Dr Isabel Madruga, Dr João Lopes Delgado and Dr Rita Ivo for all valuable inputs that were necessary to complete this case report.
Footnotes
Contributors: MRF contributed to the planning, conduct and reporting of the work described in the article. AM, MC and IMV contributed to conduct the work described in the article.
Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests: None declared.
Patient consent for publication: Next of kin consent obtained.
Provenance and peer review: Not commissioned; externally peer reviewed.
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