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Large gastric ulcer presenting as gastric pneumatosis
  1. Michael Ladna1,
  2. John George2 and
  3. Christopher Forsmark2
  1. 1Department of Medicine, University of Florida College of Medicine, Gainesville, Florida, USA
  2. 2Division of Gastroenterology, Hepatology, and Nutrition, University of Florida, Gainesville, Florida, USA
  1. Correspondence to Dr Michael Ladna; michael.ladna{at}


A man presented with nausea, vomiting, abdominal pain and diarrhoea. Cross-sectional imaging of the abdomen and pelvis showed gastric pneumatosis. He was treated conservatively with broad-spectrum antibiotics, bowel rest, nasogastric tube placement for gastric decompression and intravenous proton pump inhibitor therapy. He developed an upper gastrointestinal bleed during hospitalisation and underwent an esophagogastroduodenoscopy (EGD) which revealed a large >50 mm cratered gastric ulcer. Initial biopsy was inconclusive for malignancy thus a repeat EGD was scheduled however prior to that procedure he returned to the emergency department with severe abdominal pain. CT of the abdomen and pelvis showed recurrence of gastric pneumatosis. Repeat EGD showed a 4 mm linear gastric ulcer and repeat biopsies showed gastric mucosa with moderate chronic inactive gastritis without any metaplasia, dysplasia, carcinoma or amyloid. He was once again treated successfully with conservative measures and discharged after short hospitalisation.

  • Endoscopy
  • Ulcer
  • GI bleeding
  • Stomach and duodenum

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Gastric pneumatosis which is defined as air in the stomach wall is an uncommon and ominous radiographic finding. It is not commonly associated with gastric ulcers. We present the case of an elderly male who was diagnosed with gastric pneumatosis in the setting of a large gastric ulcer which improved with conservative management. It should be noted that the majority of gastric pneumatosis cases can be managed with conservative therapy which includes bowel rest, gastric decompression via nasogastric (NG) tube placement, broad-spectrum intravenous antibiotics and proton pump inhibitor (PPI) therapy. It is important to identify the aetiology of gastric pneumatosis since gastric ischaemia secondary to volvulus is typically managed surgically.

Case presentation

A morbidly obese man in his 70s with a medical history of chronic obstructive pulmonary disease, atrial fibrillation on rivaroxaban s/p pulmonary vein isolation ablation in 2018, obstructive sleep apnoea, heart failure preserved ejection fraction due to light chain (AL) cardiac amyloidosis, hypertension, osteoarthritis and stage IV Merkel cell carcinoma in reported remission presented to the emergency department (ED) with 10 days of nausea, vomiting, abdominal pain and watery non-bloody diarrhoea (up to 10 BM per day). He denied the current use of tobacco or alcohol. He reported use of naproxen for chronic pain from osteoarthritis. He denied haematemesis, haematochezia or melena. He reported compliance with rivaroxaban despite vomiting.


Physical examination revealed epigastric abdominal tenderness without rigidity, rebound or guarding. Initial lab work showed a leucocytosis with a white cell count of 16.2×109 /L, stable normocytic anaemia with haemoglobin (hgb) of 12.4 g/L and lactic acid within norms at 1 mmol/L. A CT of the abdomen and pelvis revealed pneumatosis of the stomach which was distended with ingested contents and air (figure 1). There was no portal venous gas and no evidence of bowel obstruction or pneumoperitoneum.

Figure 1

CT abdomen and pelvis images of gastric pneumatosis axial plane and coronal plan on day of first admission.


He was made strict nothing by mouth (NPO) to ensure bowel rest and NG tube was placed to suction for gastric decompression. He was started on broad-spectrum intravenous antibiotics with piperacillin-tazobactam and vancomycin, and intravenous PPI therapy. Acute care surgery was consulted and recommended continuation of conservative therapeutic measures without the need for any emergent surgical intervention. The patient had a high risk for intraoperative and postoperative complications due to advanced age, morbid obesity and underlying comorbidities. As such surgical intervention would be pursued as a last resort. This was explained to the patient who was in agreement with the treatment plan. Gastrointestinal (GI) PCR and Clostridium difficile toxin PCR were negative during infectious workup for diarrhoea. A repeat CT of the abdomen and pelvis done 3 days into the hospitalisation showed significant interval improvement in the gastric pneumatosis. Blood cultures did not yield any growth. He completed a total of 5 days of vancomycin and 9 days of piperacillin-tazobactam. On day 4 of hospitalisation, he developed an acute blood loss anaemia (hgb dropped from 12.2 g/dL to 10.5 g/dL and then 8.7 g/dL over a period of 3 days) from an upper GI bleed which was first noticed due to NG tube suctioning gross blood. Transfusion of packed red cells was not required. Rivaroxaban was held and gastroenterology was consulted. An esophagogastroduodenoscopy (EGD) was done the following day which revealed a large amount of fresh red as well as clotted blood throughout the entire stomach with around 700 mL being suctioned out and revealed a single large >50 mm non-obstructing oozing cratered gastric ulcer of significant severity with an adherent clot in the gastric body (figure 2). The lesion was concerning for malignancy. Several areas were successfully injected with 6 mL of a 0.1 mg/mL solution of epinephrine for haemostasis prior to clot removal. After clot removal, several areas with visible vessels were exposed with slow oozing. Haemostasis was achieved via a combination of coagulation using bipolar probe followed by deployment of two haemostatic clips and then multiple haemostatic sprays. There was no bleeding at the conclusion of the procedure. Biopsies were taken with cold forceps for histology. Pathology showed rare synaptophysin and cytokeratin positive cells in fibroinflammatory and necrotic debris. There were no Helicobacter pylori organisms and no viral cytopathic effects with negative herpes simplex virus and cytomegalovirus immunostains. There was a focus of AE1/E3 and synaptophysin-positive cells on immunostain not present on deeper H&E stain. Metastatic carcinoma was unable to be excluded with this biopsy. The NG tube was removed and his diet was successfully progressed. He was hospitalised for a total of 10 days and discharged to a rehab facility with a plan for repeat EGD in the outpatient setting 2 weeks after discharge. His rivaroxaban was not restarted on discharge.

Figure 2

Esophagogastroduodenoscopy images showing the large >50 mm gastric ulcer.

Outcome and follow-up

He presented to the emergency room 2 weeks later prior to outpatient EGD with severe epigastric abdominal pain. CT of the abdomen and pelvis showed recurrence of gastric pneumatosis. Acute care surgery was consulted and once again did not recommend any emergent surgical intervention but rather conservative management due to advanced age, morbid obesity and numerous underlying comorbidities placing him at high risk for intraoperative and postoperative complications. He was made NPO for bowel rest along with placement of NG tube for decompression and started on broad spectrum intravenous antibiotics as well as intravenous PPI. A CT angiography of the chest revealed provoked bilateral pulmonary embolisms and thus therapeutic heparin infusion was started. Gastroenterology was consulted and a repeat EGD was done inpatient which showed one non-bleeding linear gastric ulcer with no stigmata of recent bleeding on the lesser curvature of the stomach. The lesion was 4 mm at the largest dimension. There was also diffuse severely erythematous and edematous mucosa without bleeding in the body and fundus of the stomach. Biopsies were taken with cold forceps. Pathology showed fragments of gastric mucosa with moderate chronic inactive gastritis without any metaplasia, dysplasia, carcinoma or amyloid. Another EGD was done 5 days later which had a large amount of food In the stomach despite being NPO since midnight concerning for gastroparesis. It showed a non-bleeding gastric ulcer that was once again biopsied and once again showed gastric mucosa with moderate chronic inactive gastritis, reactive changes, stromal oedema and negative for any evidence of malignancy or amyloid. H. pylori was negative on both biopsy specimens. He was hospitalised for a total of 12 days and did not have a recurrence of an upper GI bleed during this time despite the initiation of therapeutic anticoagulation thus was discharged with instructions to resume his rivaroxaban.


Gastric pneumatosis is defined as air in the stomach wall. It is an uncommon and ominous radiographic finding which can be seen in X-ray and cross-sectional imaging. Gastric pneumatosis can be seen in potentially fatal pathologies such as emphysematous gastritis or gastric ischaemia and benign pathologies such as gastric emphysema. There are numerous entities associated with gastric pneumatosis. These include gastric outlet obstruction whether from malignancy, pyloric or duodenal stenosis, or volvulus,1 intractable nausea and vomiting from any cause such gastroparesis2 or chemoradiation in setting of cholangiocarcinoma,3 penetrating gastric ulcer4 and gastric ischaemia which has been documented in case reports associated with disseminated intravascular coagulation,5 severe mesenteric ischaemia,6 as a complication of endoscopic submucosal dissection for early gastric cancer7 and following intra-arterial infusion of vasopressin into the left gastric artery.8 There have also been case reports describing gastric pneumatosis associated with desmoid tumour.9 The most common presenting symptoms of gastric pneumatosis are abdominal pain, GI bleeding and acute toxic metabolic encephalopathy. CT imaging may also show evidence of portal vein air.10

A retrospective study of all patients with gastric pneumatosis from 2010 to 2020 from four tertiary care centres identified a total of 58 patients. Fifty-two (90%) had portal venous gas and 17 (29%) had evidence of bowel ischaemia. The 30-day mortality was 31% with abdominal guarding, haemodynamic instability, arterial lactate >2 mmol/L and absence of gastric dilatation being predictors of mortality.11 Another retrospective study of 24 patients showed a mortality of 21% with patients who died having significantly higher median serum lactate and creatinine levels. Coexistent small bowl pneumatosis (80% vs 0%; p<0.001) and colonic pneumatosis (40% vs 0%; p=0.04) were significantly more common in patients who died.12

Known risk factors for gastric ischaemia include advanced age, smoking, atherosclerosis, hyperlipidaemia, diabetes mellitus, hypertension and portal hypertension.13 Ageing and diabetes decrease gastric motility and delay gastric emptying which leads to gastric distention which then results in increased intragastric pressure.14 This mechanism has been shown to decrease gastric blood flow in animal models.15 Smoking increases acid and pepsin secretion and levels of oxygen-free radicals as well as decreasing prostaglandin synthesis, gastric blood flow and mucus secretion.16 Portal hypertension decreases gastric blood flow due to vascular congestion.13

Management options for gastric pneumatosis are divided into surgical and conservative. Conservative approaches involve gastric acid suppression with PPIs, broad-spectrum antibiotics, NG tube decompression, fluid resuscitation and total parenteral nutrition.10 Intervention can be surgical via gastric resection or with interventional radiology (IR). For example, in the latter case, if the aetiology is hepatic artery ostial stenosis, then a stent can be placed with IR.10 Surgical intervention is recommended for gastric perforation and gangrenous or necrotising gastritis that does not respond to conservative management or ischaemia secondary to gastric volvulus.17

Our patient had amyloidosis which raised concerns for gastric amyloidosis. This condition has been reported to mimic gastric ulcers with a case report even describing a large gastric ulcer concerning for malignancy just as in our patient, however there were light chain (AL) amyloid deposits on congo red staining. Gastric ulcers with pneumatosis intestinalis of the small bowel were reported in another case report of gastric amyloidosis.18 Amyloid deposits tend to be greatest in the small intestine with common symptoms being diarrhoea or constipation and steatorrhoea.19 Our patient had no evidence of amyloid on careful inspection of all biopsy specimens from multiple endoscopies.

Whenever a large gastric ulcer is encountered malignancy must be ruled out initially. Gastric pneumatosis associated with a gastric ulcer is a rare complication with only a few case reports in the current literature.4 20 The cause of gastric pneumatosis in our patient was likely gastric emphysema due to intractable nausea and vomiting with a significant breakdown in the stomach lining from a large penetrating gastric ulcer facilitating the entry of air into the stomach lining. There may have also been a component of global gastric ischaemia due to our patient having multiple risk factors which included advanced age and hypertension. The stomach was distended with ingested contents and air suggesting a potential component of gastric outlet obstruction and gastroparesis which may further contributed to development of gastric pneumatosis.

Learning points

  • Gastric ulcers can present with gastric pneumatosis.

  • Gastric malignancy must be ruled out for large suspicious appearing gastric ulcers.

  • Gastric pneumatosis is typically treated with conservative measures via bowel rest, gastric decompression, broad-spectrum antibiotics and proton pump inhibitor.

  • The aetiology of gastric pneumatosis must be correctly identified since gastric ischaemia due to volvulus requires emergent surgical intervention.

  • Clinicians should be aware of the rare entity of gastric amyloidosis which can present with both gastric ulcers and pneumatosis intestinalis.

Ethics statements

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  • Contributors ML wrote and edited the manuscript. Edits provided by JG and CF. ML, JG and CF were responsible for drafting of the text, sourcing and editing of clinical images, investigation results, drawing original diagrams and algorithms, and critical revision for important intellectual content.

  • 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.