Gastritis is inflammation of the gastric mucosa and can be acute or chronic. Acute gastritis is most commonly associated with Helicobacter pylori infection, NSAID use, alcohol, stress, and caustic ingestion. Chronic gastritis can be atrophic (autoimmune/H. pylori associated) or non-atrophic type. On CT, mucosal thickening, target sign (enhancing mucosa + low-attenuation edematous submucosa + enhancing muscularis/serosa), wall edema, and surrounding fat infiltration are observed. Erosive/hemorrhagic gastritis may present with acute GI bleeding. Chronic atrophic gastritis carries risk of thin mucosa, gastric polyp formation, and intestinal metaplasia. Emphysematous gastritis (intramural gas in gastric wall) is rare but a high-mortality emergency. Corrosive gastritis develops after acid/alkali ingestion and carries perforation risk.
Age Range
20-80
Peak Age
45
Gender
Equal
Prevalence
Common
The pathophysiology of gastritis varies according to the underlying etiology. In H. pylori gastritis: bacteria disrupts the mucosal barrier, produces ammonia through urease enzyme to survive in acidic environment, and triggers mucosal inflammatory response — neutrophil and lymphocyte infiltration, cytokine release (IL-1, IL-6, TNF-alpha), mucosal damage and erosion develop. In NSAID gastritis: COX-1 inhibition reduces prostaglandin synthesis, mucosal blood flow and bicarbonate/mucin secretion are impaired, protection against acid damage is lost. In autoimmune gastritis: anti-parietal cell antibodies destroy parietal cells → achlorhydria → compensatory hypergastrinemia → ECL cell hyperplasia. The target sign on CT reflects the inflammatory process affecting different wall layers: mucosa enhances with hyperemia and congestion, submucosa shows low attenuation with edema (interstitial fluid accumulation), muscularis/serosa enhances with reactive hyperemia. In emphysematous gastritis, gas-producing organisms (Clostridium, E. coli) produce gas within the wall — appears as intramural gas collection on CT.
Three-layered stratification in gastric wall: enhancing mucosa + low-attenuation edematous submucosa + enhancing muscularis/serosa = target sign. This finding is a strong indicator of inflammatory etiology (gastritis, Crohn, infection) and distinguishes from malignant infiltration (which obliterates layers).
In the portal venous phase, gastritis is characterized by the target sign: inner mucosal layer shows intense enhancement (hyperemic/congested mucosa), middle submucosal layer remains low-attenuation (submucosal edema — interstitial fluid accumulation), outer muscularis/serosal layer enhances. Wall thickening may be diffuse (pangastritis) or focal (antral gastritis, fundal gastritis). In H. pylori gastritis, antrum-predominant involvement is typical; in autoimmune gastritis, fundus/body-predominant involvement.
Report Sentence
Diffuse/focal wall thickening is seen in the gastric ___ region with a target sign (enhancing mucosa + low-attenuation submucosa + enhancing muscularis/serosa); findings consistent with gastritis.
On CT, gastritis is characterized by diffuse gastric wall thickening (>5 mm distended, >10 mm collapsed) and perigastric fat infiltration. Wall thickening is symmetric and regular — does not form focal mass (unlike adenocarcinoma). Perigastric fat infiltration indicates transmural inflammation reaching the serosal surface. Perigastric fluid and reactive lymphadenopathy may accompany. If gastric distension is inadequate, wall thickening may appear exaggerated — adequate distension should be achieved with oral contrast or water.
Report Sentence
Diffuse gastric wall thickening (average ___ mm) and perigastric fat infiltration are seen; no focal mass finding, consistent with gastritis.
Emphysematous gastritis is a rare but life-threatening emergency characterized by intramural gas collection in the gastric wall. On CT, linear or bubbly gas density is seen throughout the gastric wall. Wall is thickened and edematous. Peritoneal fluid, portal venous gas, and pneumoperitoneum (perforation) may accompany. Mortality is 60-80%. Underlying causes: ischemia, infection (Clostridium, E. coli, Streptococcus), caustic ingestion, alcohol intoxication. Differentiation from gastric emphysema (benign intramural air — e.g., post-endoscopy) is important.
Report Sentence
Diffuse intramural gas collection is seen in the gastric wall with wall thickening and edema; portal venous gas and peritoneal fluid are present — EMERGENCY findings consistent with emphysematous gastritis.
In erosive/hemorrhagic gastritis, active bleeding may be seen as intraluminal contrast extravasation on CT angiography. Focal high-attenuation (>90 HU) contrast accumulation within the gastric lumen in the arterial phase indicates the active bleeding focus. Expansion of contrast accumulation in the delayed phase confirms bleeding. Intraluminal blood clot (fresh blood: 50-70 HU) may be seen at erosion areas. Active bleeding at rate >0.5 mL/min can be detected on CT angiography.
Report Sentence
Intraluminal active contrast extravasation is seen in the gastric ___ region in the arterial phase (attenuation: ___ HU); contrast accumulation has expanded in the delayed phase — consistent with active bleeding.
On ultrasonography, gastritis is characterized by gastric wall thickening. Normal gastric wall shows 5-layer structure on US; in gastritis, layers are preserved but submucosal layer is prominently thickened due to edema — hypoechoic submucosal band is widened. Perigastric fluid collection may accompany. Transabdominal US is generally limited but may be useful in emergency evaluation.
Report Sentence
Gastric wall thickening is seen on transabdominal US with preserved layered structure and widened submucosal layer consistent with edema.
Criteria
NSAID, alcohol, stress-related acute mucosal erosion. Multiple superficial erosions on endoscopy.
Distinct Features
Mild wall thickening, increased mucosal enhancement on CT. Active bleeding possible. Rapid healing with cause removal.
Criteria
Glandular atrophy and intestinal metaplasia from prolonged inflammation. Autoimmune: fundus/body predominant. H. pylori: antrum predominant.
Distinct Features
Thin mucosa, gastric polyps on CT. Hypergastrinemia → NET risk in autoimmune type. Adenocarcinoma risk increased.
Criteria
Intramural gas in gastric wall + systemic sepsis signs. Gas-producing organisms. Mortality 60-80%.
Distinct Features
Linear/bubbly gas in gastric wall on CT, portal venous gas possible. Emergency surgery/IV antibiotics. Distinction from gastric emphysema: presence of systemic toxicity.
Distinguishing Feature
Adenocarcinoma focal, asymmetric wall thickening, obliterates wall layers; gastritis diffuse, symmetric, layers preserved with target sign.
Distinguishing Feature
Lymphoma marked wall thickening (>20 mm), layers may be disrupted; gastritis milder thickening, target sign. Splenomegaly and LAP may accompany lymphoma.
Distinguishing Feature
Gastric Crohn rare, usually antrum/pyloric region, skip lesions, small bowel involvement accompanies; isolated gastritis shows no skip lesions.
Distinguishing Feature
Ménétrier disease giant rugal folds, protein-losing enteropathy; gastritis regular wall thickening. Ménétrier giant folds in fundus/body.
Urgency
routineManagement
medicalBiopsy
Not NeededFollow-up
6-monthAcute gastritis usually resolves with conservative treatment (PPI, cause removal). H. pylori eradication therapy is applied in positive cases. Regular endoscopy follow-up is needed in chronic atrophic gastritis — due to adenocarcinoma and NET risk. Emphysematous gastritis requires emergency surgical consultation, IV broad-spectrum antibiotics, and intensive care. In corrosive gastritis, early endoscopy (24-48 hours) determines damage degree; emergency CT and surgical evaluation if perforation suspected.
Gastritis is usually treated with H. pylori eradication or proton pump inhibitors. Chronic gastritis is a risk factor for gastric cancer through intestinal metaplasia and dysplasia pathway. Endoscopy should be performed with persistent symptoms.