Benign gastric ulcer is a focal defect in the gastric mucosa extending beyond the muscularis mucosae, most commonly caused by Helicobacter pylori infection and non-steroidal anti-inflammatory drug (NSAID) use. Ulcers most frequently occur on the lesser curvature and near the angularis incisura. On imaging, CT demonstrates the ulcer crater, surrounding mucosal edema and thickening, and Hampton line (thin radiolucent line) indicating benign features. Endoscopy with biopsy is the gold standard for diagnosis. Complications include hemorrhage, perforation, penetration, and gastric outlet obstruction. PPI therapy and H. pylori eradication are primary treatment approaches.
Age Range
30-75
Peak Age
55
Gender
Male predominant
Prevalence
Common
Benign gastric ulcer develops when the balance between protective mechanisms of the gastric mucosa (mucus-bicarbonate barrier, mucosal blood flow, epithelial regeneration) and aggressive factors (acid, pepsin, H. pylori, NSAIDs) is disrupted. H. pylori directly damages the mucosal barrier through ammonia produced by urease enzyme and triggers inflammation. NSAIDs reduce prostaglandin synthesis through COX-1 inhibition, impairing mucosal blood flow and mucus secretion. The resulting mucosal damage extends beyond the muscularis mucosae into the submucosa or deeper layers — distinguishing it from erosion. On CT, the ulcer crater appears as a focal mural defect opening into the lumen. Surrounding reactive edema and inflammation cause mucosal thickening and increased enhancement. Chronic ulcers heal with fibrosis forming scar tissue — leading to wall retraction and deformity. In perforation, free air spreads into the peritoneal cavity and is detected as pneumoperitoneum on CT.
A thin radiolucent (low-density) line between the ulcer crater edge and surrounding thickened mucosa — representing the submucosal edema layer. This finding is a classic radiological sign of benign gastric ulcer and valuable in distinguishing from malignant ulcer. In malignant ulcers, the mucosal line is disrupted or irregular.
Focal ulcer crater in the gastric wall on portal venous phase — a mural defect opening into the lumen. Mucosal edema and symmetric thickening surrounds the crater. Adjacent mucosa is smooth-contoured with pronounced enhancement. The ulcer base may fill with contrast material. Hampton line (thin radiolucent line between crater edge and thickened mucosa) is difficult to see on CT but may be identified on thin-slice reformations.
Report Sentence
Focal mural defect consistent with an ulcer crater in the lesser curvature/angularis incisura region with symmetric surrounding mucosal edema/thickening is observed; benign gastric ulcer should be considered as the leading diagnosis.
Active contrast extravasation in the arterial phase in a bleeding ulcer — high-density contrast accumulation (>90 HU) within the lumen or ulcer crater. This finding indicates active arterial bleeding and requires emergent intervention. Sentinel clot sign — high-density clot (60-80 HU) around the ulcer or within the lumen is a sign of recent bleeding.
Report Sentence
Active contrast extravasation from the ulcer crater in the arterial phase consistent with active bleeding; emergent endoscopic or interventional management is recommended.
Free intraperitoneal air (pneumoperitoneum) on non-contrast CT in a perforated ulcer. Most commonly seen in the subdiaphragmatic region. Free fluid around the stomach and air accumulation at the anterior surface of the liver (perihepatic air) are typical. Stranding and streaky density increase in peritoneal fat planes indicate peritonitis.
Report Sentence
Free air (pneumoperitoneum) in the peritoneal cavity is detected, consistent with gastric ulcer perforation; emergent surgical consultation is recommended.
Hyperintense signal in the periulcer mucosa on T2-weighted images — reflecting edema and inflammation. The ulcer crater appears filled with fluid signal on T2. T2 hyperintensity in the surrounding gastric wall indicates submucosal edema. Preserved wall stratification supports benignity.
Report Sentence
Hyperintense edema in the periulcer mucosa with preserved wall stratification on T2-weighted MRI, consistent with benign ulcer.
Focal gastric wall thickening with an echo-free or hypoechoic crater opening into the lumen on ultrasound. Hypoechoic thickening in the surrounding mucosa due to edema. Normal wall stratification is preserved. Air echogenicities or debris may be seen within the crater. Larger ulcers (>2 cm) are more easily identified on US.
Report Sentence
Focal gastric wall thickening with a crater opening into the lumen and hypoechoic thickening in the surrounding mucosa consistent with edema on ultrasound, consistent with benign gastric ulcer.
In a penetrating ulcer, delayed phase CT shows the ulcer crater extending beyond the gastric wall into an adjacent organ (pancreas, liver, omentum). Inflammatory thickening and fat stranding between the crater and adjacent organ are present. Unlike perforation, free air is not seen because penetration is organized and contained. Gastro-pancreatic penetration is most commonly seen with posterior wall ulcers.
Report Sentence
The ulcer crater is observed penetrating beyond the gastric wall into the adjacent ___, with inflammatory changes in surrounding tissues on delayed phase, consistent with penetrating ulcer.
Criteria
H. pylori-positive biopsy or non-invasive tests (urea breath test, antigen test). Chronic active gastritis in antral and body mucosa. Resolution with eradication therapy.
Distinct Features
Most common cause (60-70%). Antrum and lesser curvature predominance. Low recurrence rate after eradication (<5%). Risk of intestinal metaplasia and dysplasia in chronic cases.
Criteria
History of NSAID/aspirin use. Mucosal protection loss due to COX-1 inhibition. May present with multiple ulcers and erosions.
Distinct Features
Multiple erosions and ulcers in antrum and body. Less periulcer edema. Rapid healing with NSAID cessation and PPI. Coexistence with H. pylori increases ulcer risk.
Criteria
Critical illness (ICU, multiple organ failure, major burns, head trauma). Develops from mucosal ischemia and reperfusion injury.
Distinct Features
Fundus predominant (Curling ulcer — burns; Cushing ulcer — head trauma). Acute, superficial, multiple. Multiple shallow craters superimposed on mucosal edema on CT. Preventable with prophylactic PPI.
Distinguishing Feature
Malignant ulcer has irregular, ragged crater margins while benign ulcer has smooth, symmetric margins. In malignant ulcer, Carman meniscus sign (crater edge convex toward lumen), disruption of wall stratification, perigastric lymphadenopathy, and distant metastasis may be present.
Distinguishing Feature
In gastric lymphoma, ulceration accompanies diffuse wall thickening and may be multiple; benign ulcer is focal with normal thickness of surrounding wall. In lymphoma, the gastric wall may remain elastic and dilatable (aneurysmal dilation).
Distinguishing Feature
GIST ulceration develops over a submucosal mass and the mass component is prominent; benign ulcer has no mass component. GIST may show exophytic growth and heterogeneous enhancement is typical.
Distinguishing Feature
Gastritis shows diffuse mucosal thickening but no focal ulcer crater; benign ulcer has a focal crater defect. In erosive gastritis, multiple superficial mucosal defects may be seen but these do not extend beyond the muscularis mucosae.
Urgency
urgentManagement
medicalBiopsy
NeededFollow-up
3-monthAll gastric ulcers require endoscopic biopsy to rule out malignancy. PPI therapy (8 weeks) and H. pylori eradication are primary treatment. Follow-up endoscopy should confirm healing after treatment — non-healing ulcers require repeat biopsy for malignancy. Complicated ulcers (bleeding, perforation) require emergent intervention. Discontinuation of NSAID use or addition of gastroprotective agents is important.
Benign gastric ulcer heals with H. pylori eradication and PPI therapy. Complications include bleeding, perforation, and gastric outlet obstruction. Biopsy is mandatory for non-healing or suspicious ulcers to exclude malignancy.