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A woman in her 80s with a history of diabetes mellitus (DM) was admitted with acute myocardial infarction. She had been treated with oral hypoglycaemic agents including teneligliptin and voglibose at another hospital; however, her DM was not controlled well. Laboratory tests on admission revealed an elevated serum glucose level of 373 mg/dL and haemoglobin A1c level of 9.2%. An ECG showed ST-segment elevation in leads V1–V4. Since her Killip classification was class IV, she was intubated with sedation. Coronary angiography revealed significant stenosis of the mid left anterior descending artery, and she subsequently received stent implantation. Her condition became stable after these treatments; however, she still required tube feeding after the withdrawal of intubation because of her poor swallowing function. At 2 weeks after the admission, she vomited several times after the administration of tube feeding. After 2 days, she suddenly experienced epigastric pain, in addition to vomiting. Her vital signs were a heart rate of 110 beats/min and a blood pressure of 118/72 mm Hg. A physical examination showed abdominal distension and epigastric abdominal tenderness without rebound tenderness or guarding. Laboratory findings showed white blood cells of 10 100 /µL, C reactive protein level of 1.00 mg/dL and elevated levels of liver enzymes (aspartate aminotransferase of 222 U/L and alanine aminotransferase of 198 U/L) with normal levels of renal function and electrolytes. Chest radiograph (figure 1) and enhanced abdominal CT revealed air in the gastric wall with gastric tube and hepatic portal venous gas (figure 2A,B). No air was detected in other intestinal tracts, and no obvious impairment of arterial flow was noted. As her vital signs were stable without malfunction of other organs, she did not undergo surgery but received conservative treatments with antibiotics and intravenous nutrition. The blood culture was positive for Bacteroides uniformis. A follow-up CT scan performed 2 days later revealed the disappearance of hepatic portal venous gas (figure 2C). She was diagnosed with emphysematous gastritis and received antibiotic therapy for 2 weeks, and her condition finally remained stable.
Chest radiograph showing air in the gastric wall (arrows).
(A and B) Enhanced abdominal CT revealing air in the gastric wall with gastric tube and hepatic portal venous gas. (C) Follow-up CT scan performed 2 days later showing the disappearance of hepatic portal venous gas.
Emphysematous gastritis was first reported by Fraenkel in 1889, and it is relatively rare disease caused by gas-producing bacteria with the high mortality rate of 55.3%.1 2
Emphysematous gastritis can be confused with gastric emphysema, which is also identified by accumulation of gas within the stomach wall, but gastric emphysema is a relatively benign condition that occurs when air enters the gastric wall usually following trauma to the gastric mucosa. A distinguishing factor between these is that with gastric emphysema there is no associated infection as well as patients not presenting with acute abdomen and having an excellent prognosis even with no treatment.3 The risk factors for emphysematous gastritis include gastric surgery, corticosteroid uses, non-steroidal anti-inflammatory drug uses, ingestion of corrosive agents, stress, DM, immunodeficiency, high alcohol consumption, malnutrition and renal failure, whereas gastric emphysema results from air penetrating the wall from non-infectious aetiologies, such as raised intragastric pressures, trauma including gastric wall injury with nasogastric tube, malignancy, inflammation and ischaemia.4 Diagrammatic explanations of the mechanism of emphysematous gastritis are shown in figure 3. Although the exact pathophysiology of emphysematous gastritis remains unclear, it is thought that pre-existing gastric ulcers or ischaemic lesions provide the nidus for bacterial infection, overgrowth and penetration into the gastric wall. The organisms produce gas after the penetration, and finally emphysematous gastritis develops. The differentiation between emphysematous gastritis and gastric emphysema can be challenging but is important as clinical outcomes are totally different and indication for surgical treatment can vary.5 Recent studies reported on the successful conservative treatments including fluid resuscitation, broad-spectrum antibiotics, bowel rest, fluid hydration and total parenteral nutrition. Surgical removal of the ischaemic gastric area by total gastrectomy or partial gastrectomy may be considered for patients with evidence of transmural ischemia, peritonitis or haemodynamic instability despite appropriate resuscitation.6
Diagrammatic explanations of the mechanism of emphysematous gastritis.
Gupta listed the treatment and the outcome of 57 case reports published from 1980 to 2018.7 Therefore, we searched PubMed for English articles published from 2019 to June 2022, and 40 cases of emphysematous gastritis were found (table 1).5 8–43
Literature review of emphysematous gastritis published from 2019 to June 2022
The median age of the population was 62 years (IQR, 52–78 years of age), of which 20 (50%) were male and 20 were female. Surgical treatments were selected in 13 of the 40 cases (32.5％), whereas conservative treatments were selected in 27 cases (67.5％). Of note, organisms were identified in only the half of the cases. Isolated organisms included Sarcina ventriculi (n=5), mucormycosis (n=3), Klebsiella pneumoniae (n=2), Escherichia coli (n=2) and so on. Overall, 12 out of 40 cases died; however, of 20 cases that identified the causative organisms, 11 cases (55％) died, and the mortality rate was almost the same as the previous report.2
In our case, emphysematous gastritis occurred in the setting of pre-existing DM, acute stress for myocardial infarction and use of nasogastric tube. Our case was notable in that appropriate and prompt conservative treatments prevented fatal outcome and led to disappearance of hepatic portal venous gas, and this was the first reported case of emphysematous gastritis associated with Bacteroides uniformis infection.
In conclusion, physicians should institute prompt treatment including fluid resuscitation, broad-spectrum antibiotics and bowel rest if the patient is suspected of emphysematous gastritis.
Learning points
Emphysematous gastritis can be confused with gastric emphysema, which is also identified by gas accumulation within the stomach wall.
Emphysematous gastritis is associated with infection with poor prognosis, while gastric emphysema is a benign condition occurring when air enters the gastric wall following trauma to the gastric mucosa.
Physicians should institute prompt treatment including fluid resuscitation, broad-spectrum antibiotics and bowel rest if the patient is suspected of emphysematous gastritis.
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Footnotes
Contributors RO contributed to patient management, conception and design of case report; acquisition, analysis and interpretation of data; and drafting the article. RI, YK and KA contributed to patient management, conception and design of case report. YK contributed to interpretation of data and revising the article critically. All authors gave final approval of the article and have agreed to be accountable for all aspects of the work.
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.
Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.