Monday 10 January 2005
Acute gastritis (accompanied by acute mucosal injury) results from many disorders with multifactorial etiologiesand diverse histologic patterns.
The clinical symptoms, endoscopic ﬁndings, and histologic features rarely correlate with one another due to the non-speciﬁcity of the symptoms, the diverse etiologies,and the diffuseness (or focality) of the process.
Acute gastritis appears hemorrhagic, nonhemorrhagic, erosive,or non-erosive.
The use of the term "acute gastritis" without qualifiers is discouraged because of the persisting confusion between "acute" and "active".
Although only rarely encountered in routine biopsy specimens, two principal categories of acute gastritis are recognized:
(a) acute hemorrhagic or erosive gastritis usually related to acute chemical or irritant injury;
(b) acute Helicobacter gastritis.
A third variety, "acute phlegmonous" or "suppurative gastritis", is a rare and almost invariably fatal condition because of its association with septicemia. Most cases are recognized only at autopsy.
A wide range of substances has been implicated in causing acute damage to the gastric mucosa including:
alcohol, aspirin, cortisone, phenylbutazone, and a number of other NSAIDs
shock after major trauma or surgery, sepsis, burns, and hypothermia.
Acute hemorrhagic or erosive gastritis is common, therefore, in patients in intensive care units.
Alcohol and NSAID-associated hemorrhagic gastritis and stress-related acute (hemorrhagic) gastritis initially involve all segments of the stomach; later, antral lesions predominate and duodenal lesions may also develop.
Histologically, abnormalities are usually found only in areas immediately adjacent to the lesions.
In these areas, the findings are similar whether the underlying cause is hypoperfusion, NSAIDs, or alcohol.
In the subepithelial zone, there is diffuse edema of the lamina propria, capillary congestion, and variable degrees of interstitial hemorrhage.
Erosions can be sparse or even not demonstrable, as they are often repaired with considerable rapidity, leaving thin, regenerative epithelium as the only evidence of their occurrence.
Inflammation is slight or absent, usually consisting of no more than a few neutrophils.
Endoscopically normal areas are also histologically normal, and if inflammation is present, it is often caused by H. pylori infection.
In fact, because inflammation is typically sparse or absent, gastropathy is appropriate as a substitute for gastritis, and the former term is favored by some authors.
The acute phase of Helicobacter infection is rarely encountered in gastric biopsy specimens because the initial illness has trivial symptomatology and goes unnoticed by the patient.
Thus, in most cases, the presence of an acute phase is inferred from serological findings.
Biopsy specimens reveal marked degenerative changes in the surface epithelium, including mucus depletion, cellular exfoliation, and syncytial regenerative changes.
Neutrophil polymorphonuclear infiltration into foveolar and surface epithelium is conspicuous, and one can find “pit abscesses” and adherent polymorph exudate on the surface.
There appears to be relatively equal involvement of antrum and body.
The numbers of organisms present can be extremely variable.
In the few documented cases of accidental H. pylori infection, the corpus element quickly subsides, but the antral element persists.
- Phlegmonous gastritis is an acute suppurative condition of the stomach in which pyogenic organisms gain access to the submucosa and spread diffusely throughout the organ.
- The submucosa is thickened by pus formation and edema, which may go on to form a mural abscess, but the mucosa remains intact.
- It is difficult to diagnose in biopsy specimens because the polymorph exudation is centered in the submucosa.
- acute alcoholism
- corrosive agents
- acute allergic gastritis
- renal insufficiency (uremia)
- severe burns
- major surgery
- multiorgan failure
- portal hypertension
- congestive heart failure
- respiratory failure
- increased intracranial pressure