Gastritis

Helicobacter pylori infection may cause both acute and chronic gastritis.[3]

Acute gastritis involves temporary sudden-onset inflammation of the stomach lining. It may be due to surgery, stress to the gastric mucosa, burns, sepsis, drugs, or infections. When the infection is not effectively cleared, it may result into chronic gastritis.[3] Chronic gastritis primarily results from childhood H pylori infection.[24]

Chronic gastritis may start with a non-atrophic morphology (stomach lining inflammation with no tissue loss) and progress to an atrophic morphology (stomach lining thinning and loss of glands due to prolonged inflammation). A permanent acid-free stomach may be seen with atrophic gastritis in the most extreme cases.[24] Eradication of H pylori before progression to the atrophic stage may be beneficial.[25]

Acute erosive gastritis may be caused by chronic non-steroidal anti-inflammatory drug (NSAID) or alcohol use/misuse.[2][26] Factors that have been identified as placing patients at increased risk for NSAID-related gastrointestinal (GI) complications include prior history of a GI event (peptic ulcer, haemorrhage), age >60 years, high dosage of NSAIDs, and concurrent use of corticosteroids or anticoagulants.[27][28]

Erosive gastritis may also be due to reflux of bile salts into the stomach as a result of compromised pyloric function (e.g., following gastric surgery).[4][5][6][7]

Critically ill patients are at risk of developing stress-induced GI bleeding.[8] The main risk factors associated with clinically important haemorrhage are mechanical ventilation for >48 hours and coagulopathy (platelet count <50 × 10⁹/L [<50 × 10³/microlitre], partial thromboplastin time >2 times the upper limit of the normal range, international normalised ratio >1.5).[8]

Autoimmune-mediated atrophic gastritis is associated with the development of antibodies to the gastric parietal cells (present in about 90% of patients).[2][9][29] Autoimmune disorders associated with increased risk of autoimmune gastritis include thyroid disease, idiopathic adrenocortical insufficiency, vitiligo, type 1 diabetes mellitus, and hypoparathyroidism. North European or Scandinavian ancestry is a recognised risk factor for autoimmune gastritis.[9][20]

Phlegmonous gastritis is an uncommon form of acute gastritis caused by Staphylococcus aureus, streptococci, Escherichia coli, Enterobacter, other gram-negative bacteria, and Clostridium welchii.[10][11][12][13]

Emphysematous gastritis is a rare infection of the stomach wall caused by gas-producing organisms such as C welchii.[10][11][12][13] Risk factors for emphysematous gastritis include gastric surgery, corticosteroid use, use of NSAIDs, ingestion of corrosive agents, stress, diabetes mellitus, immunodeficiency, high alcohol consumption, malnutrition, and renal failure.[30]

There are a variety of processes that are characterised by acute and chronic inflammation and disruption of the gastric mucosal protective layer:

H pylori infection induces a severe inflammatory response with gastric mucin degradation and increased mucosal permeability, followed by gastric epithelial cytotoxicity.[2][3]
NSAIDs and alcohol decrease gastric mucosal blood flow with loss of the mucosal protective barrier.[2] NSAIDs inhibit prostaglandin production, whereas alcohol promotes depletion of sulfhydryl compounds in gastric mucosa.[26]
In autoimmune atrophic gastritis, antiparietal cell antibodies stimulate a chronic inflammatory, mononuclear, and lymphocytic infiltrate involving the oxyntic mucosa, leading to the loss of parietal and chief cells in the gastric corpus.[2][29][31][32]
The high concentration of hydrochloric acid normally present in gastric fluid prevents the growth of bacteria in the stomach and small intestine. Gastric atrophy and acid blocking drugs raise gastric pH and disrupt the acid barrier to bacterial overgrowth. Under rare circumstances, damage to the gastric mucosa (e.g., gastric ulcer or carcinoma, ingestion of caustic materials, ingestion of foreign bodies) may allow ingested bacteria to become invasive, resulting in phlegmonous gastritis.[33] In phlegmonous gastritis, the suppurative process primarily involves the submucosa and muscularis layers of the gastric wall.[33]

Aetiological classification

A variety of classification systems describe the causes of gastritis and their associated histological features. Classifications that are in use include the updated Sydney system and the operative link on gastritis assessment (OLGA).[14][15] In clinical practice, an aetiological classification often provides a basis for therapy. Aetiologies responsible for the development of gastritis include:

H pylori infection
Chemical substances
- NSAIDs or alcohol
- Bile reflux
Autoimmune-related
Mucosal ischaemia
Bacterial invasion of the gastric wall

Kyoto classification

The Kyoto classification score for gastritis can be used to determine the risk of H pylori as well as gastric cancer. A score of 2 or greater represents a greater risk of H pylori infection, while a score of 4 or greater represents a higher risk for gastric cancer. Classification is broken down below:[16]

Mucosal atrophy (0 none - CO-CI per Kimura Takemoto classification, 1 mild - CII-CII, 2 severe - OI-OIII)
Intestinal metaplasia (0 none - none present, 1 mild - in the antrum, 2 severe - to the corpus)
Enlarged folds (0 negative - width of gastric fold less than 5 mm, 1 positive - width of gastric fold 5 mm or greater)
Nodularity (0 negative - none, 1 positive - small nodules in antrum present)
Diffuse redness (0 none - none, 1 mild - collecting venules with mild translucency in the body, 2 severe - collecting venules with severe translucency in the body)

Your Organisational Guidance

Pathophysiology

Classification

Aetiological classification

Kyoto classification