Acute Gastritis Workup

Updated: Jun 13, 2019
  • Author: Mohammad Wehbi, MD; Chief Editor: BS Anand, MD  more...
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Workup

Laboratory Studies

A number of laboratory tests are usually ordered, including the following:

  • Complete blood cell (CBC) count to assess for anemia, as acute gastritis can cause gastrointestinal bleeding [4]

  • Liver and kidney function tests

  • Gallbladder and pancreatic function tests

  • Pregnancy test

  • Stool for blood

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Imaging Studies

Four radiologic signs of acute gastritis are fairly consistent regardless of the etiology. These signs include thick folds, inflammatory nodules, coarse area gastrica, and erosions.

Thick folds are defined by a size greater than 5 mm in caliber. These folds are measured on radiographs with the stomach moderately distended. If thick folds are found in a patient who is symptomatic, H pylori is generally involved.

Nodularity of the gastric mucosa (bumpy appearance) is a second sign of acute or subacute gastritis. Its origin is uncertain. Nodules may represent erosions that have epithelialized (healed) but still have the associated edema. Compared with benign neoplastic polyps, gastritis-related nodules are smaller, and their edges are less well defined. They taper onto the adjacent mucosa, and they are seen most often in the distal stomach. Nodules due to gastritis are referred to as inflammatory. They generally line up on the folds of the gastric antrum and are a characteristic appearance of gastritis.

Enlarged area gastrica are a sign of gastritis that is not strongly associated with a specific cause. Area gastrica are small polygonal areas, 1-3 mm in diameter, separated by linear depressions on the surface of the mucous membrane of the stomach; they contain the gastric pits. Enlargement of these areas may reflect inflammatory swelling and is often associated with gastritis. Because of the loss of the mucosal layer, the barium suspension can more completely fill the intervening grooves.

Gastric erosions are noted to be one of the most specific signs of gastritis. Erosions may be linear or serpiginous. They may be accompanied by edema and may be seen on or near the greater curvature of the stomach. A double-contrast examination usually is required to best reveal gastric erosions.

Tomography scan and plain films of the abdomen can demonstrate thickening of the gastric wall in the case of phlegmonous gastritis.

Double-contrast barium radiography can demonstrate the nematodes that cause anisakidosis.

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Other Tests

A number of H pylori tests are available. They are classified as either nonendoscopy based or endoscopy based.

Three nonendoscopy-based H pylori tests are available, as follows:

  • The first test is the H pylori stool antigen test (HpSA). This test is based on the detection of the H pylori antigen in the stool. It has sensitivity and specificity of greater than 90%. It can be used for both the diagnosis of H pylori and the confirmation of eradication after therapy.

  • The second test is the urea breath test. It uses 13C- or 14C-labeled urea taken orally. H pylori metabolizes the urea and liberates labeled carbon dioxide that is exhaled. This, in turn, can be quantified in breath samples. The sensitivity and specificity of the urea breath test is greater than 90%. This is considered the noninvasive diagnostic method of choice in situations where endoscopy is not indicated. It can also be used to confirm eradication after therapy

  • The third test depends on the presence of antibodies to H pylori in the serum. The major drawback to this test is that serologic assays may remain positive for as long as 3 years after eradication of the bacteria. Therefore, serologic assays are often unreliable to document eradication of H pylori. This test can be used for the diagnosis of H pylori, provided that the patient has not received any prior therapy for it.

Three endoscopy-based H pylori tests are available, as follows:

  • The first test is the rapid urease test (RUT). It is performed by placing a gastric biopsy specimen, obtained at endoscopy, onto a gel- or membrane-containing urea and a pH-sensitive indicator. If H pylori is present, the bacterial urease hydrolyzes urea and changes the color of the media. The sensitivity and specificity of this test is greater than 90%.

  • Another test is bacterial culture of H pylori. It is highly specific but is not widely used because of the degree of expertise required. It is used when antibiotic susceptibilities are necessary.

  • Histologic detection of H pylori in the biopsy specimen is another endoscopy-based test. Appropriate staining is achieved using such stains as hematoxylin and eosin, Warthin-Starry, Giemsa, or Genta.

American Society for Gastrointestinal Endoscopy guidelines suggest endoscopic evaluation for patients older than 50 years who have alarm features such as weight loss and anemia. For patients younger than 50 years with no alarm features who are H pylori negative, endoscopic evaluation may be considered. [5]

Mycobacterium tuberculosis may be diagnosed when acid-fast stain detects the bacilli in a biopsy specimen.

Syphilis may be diagnosed when the organism is found in the gastric mucosa. Endoscopic biopsy, silver impregnation, and fluorescent antibody techniques also can be used.

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Procedures

Endoscopy may reveal a thickened, edematous, nonpliable wall with erosions and reddened gastric folds. The edema can be severe resulting in gastric outlet obstruction. Ulcers and frank bleeding might be present.

The nematodes that cause anisakidosis can be seen on endoscopy.

Endoscopy can be used to help diagnose gastric syphilis and tuberculosis.

A meta-analysis has shown that for individuals who undergo endoscopy for dyspepsia, the most common finding is erosive esophagitis (though prevalence was lower when the Rome criteria were used to define dyspepsia) followed by peptic ulcers. [6]

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Histologic Findings

Histologic examination of a biopsy specimen can help in establishing the etiologic agent of gastritis.

H heilmanii is better diagnosed on smears using Giemsa or Warthin-Starry silver stains than by gastric biopsy specimens via observation of a distinct morphology. A culture of H heilmanii has not been established yet, and the diagnosis of this bacterial infection is based on morphological identification by histologic examination and tissue smear cytology.

As mentioned earlier, H pylori can be found by histologic staining of a gastric mucosal biopsy specimen. It has a sensitivity and specificity of greater than 90%.

The main histologic feature of CMV infection is cytomegalic cells with intranuclear inclusions. Viral cultures, immunocytochemistry, and in situ hybridization can further aid in establishing the diagnosis.

The main histologic feature of C albicans infection is yeast forms in a biopsy specimen.

The main histologic feature of tuberculosis is necrotizing granulomas.

The main histologic feature of histoplasmosis is the presence of nonnecrotizing granulomas containing the organisms. The diagnosis of histoplasmosis requires a positive culture result from the gastric mucosal biopsy specimen.

In ulcero-hemorrhagic gastritis, the epithelium appears eroded with edema and hemorrhage with typically little inflammation. In severe cases, the lumen of the stomach may be coated with fibropurulent exudates and the lamina propria may be replaced by eosinophilic hyaline material.

In iron-induced gastritis, erosions, foveolar hyperplasia, or even hyperplastic-type polyps can be detected. Iron has been associated with infarctlike necrosis given its corrosive properties. Iron stains can highlight the golden brown pigment in tissue samples, but these are often easily visible. Of note, such findings should be differentiated from glandular siderosis seen in systemic iron overload or hemochromatosis.

Histologic features of chemotherapy-induced gastritis may include atypical epithelial cells with bizarre features at the base of the glands, limited mitoses, and pleomorphic nuclei. These characteristics may make it difficult to differentiate from an adenocarcinoma.

The findings at histology of radiation-induced gastritis include nuclear karyorrhexis (destructive fragmentation of the nucleus of a dying cell) and cytoplasmic eosinophilia of the gastric pit epithelium during the first 10 days following treatment, followed by mucosal edema, congestion, submucosal collagen bundle swelling, fibrin deposition, and telangiectasia. If extensive, hemorrhage and ulceration may be evident.

In eosinophilic gastritis, a prominent eosinophilic infiltrate is present in the gastric wall or epithelium. Distribution can be patchy, so multiple biopsy specimens should be obtained during endoscopy.

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