Acute gastritis is a term covering a broad spectrum of entities that induce inflammatory changes in the gastric mucosa. Several different etiologies share the same general clinical presentation. However, they differ in their unique histologic characteristics. The inflammation may involve the entire stomach (eg, pangastritis) or a region of the stomach (eg, antral gastritis). Acute gastritis can be broken down into 2 categories: erosive (eg, superficial erosions, deep erosions, hemorrhagic erosions) and nonerosive (generally caused by Helicobacter pylori). See the images below.
No correlation exists between microscopic inflammation (histologic gastritis) and the presence of gastric symptoms (eg, abdominal pain, nausea, vomiting). In fact, most patients with histologic evidence of acute gastritis (inflammation) are asymptomatic. The diagnosis is usually obtained during endoscopy performed for other reasons. Acute gastritis may present with an array of symptoms, the most common being nondescript epigastric discomfort.
Other symptoms include nausea, vomiting, loss of appetite, belching, and bloating. Occasionally, acute abdominal pain can be a presenting symptom. This is the case in phlegmonous gastritis (gangrene of the stomach) where severe abdominal pain accompanied by nausea and vomiting of potentially purulent gastric contents can be the presenting symptoms. Fever, chills, and hiccups also may be present.
The diagnosis of acute gastritis may be suspected from the patient's history and can be confirmed histologically by biopsy specimens taken at endoscopy.
Epidemiologic studies reflect the widespread incidence of gastritis. In the United States, it accounts for approximately 1.8-2.1 million visits to doctors' offices each year. It is especially common in people older than 60 years.
See related CME at Evaluation of Acute Abdominal Pain Reviewed.
Acute gastritis has a number of causes, including certain drugs; alcohol; bile; ischemia; bacterial, viral, and fungal infections; acute stress (shock); radiation; allergy and food poisoning; and direct trauma. The common mechanism of injury is an imbalance between the aggressive and the defensive factors that maintain the integrity of the gastric lining (mucosa).
Acute erosive gastritis can result from an exposure to a variety of agents or factors. This is referred to as reactive gastritis. These agents/factors include nonsteroidal anti-inflammatory medications (NSAIDs), alcohol, cocaine, stress, radiation, bile reflux, and ischemia. The gastric mucosa exhibits hemorrhages, erosions, and ulcers. NSAIDs, such as aspirin, ibuprofen, and naproxen, are the most common agents associated with acute erosive gastritis. This results from both oral and systemic administration of these agents, either in therapeutic doses or in supratherapeutic doses.
Because of gravity, the inciting agents lie on the greater curvature of the stomach. This partly explains the development of acute gastritis distally on or near the greater curvature of the stomach in the case of orally administered NSAIDs. However, the major mechanism of injury is the reduction in prostaglandin synthesis. Prostaglandins are chemicals responsible for maintaining mechanisms that result in the protection of the mucosa from the injurious effects of the gastric acid. Long-term effects of such ingestions can include fibrosis and stricture formation.
Bacterial infection is another cause of acute gastritis. The corkscrew-shaped bacterium called H pylori is the most common cause of gastritis. Complications result from a chronic infection rather than from an acute infection. The prevalence of H pylori in otherwise healthy individuals varies depending on age, socioeconomic class, and country of origin. The infection is usually acquired in childhood. In the Western world, the number of people infected with H pylori increases with age.
Evidence of H pylori infection can be found in 20% of individuals younger than 40 years and in 50% of individuals older than 60 years. How the bacterium is transmitted is not entirely clear. Transmission is likely from person to person through the oral-fecal route or through the ingestion of contaminated water or food. This is why the prevalence is higher in lower socioeconomic classes and in developing countries. H pylori is associated with 60% of gastric ulcers and 80% of duodenal ulcers.
H pylori gastritis typically starts as an acute gastritis in the antrum, causing intense inflammation, and over time, it may extend to involve the entire gastric mucosa resulting in chronic gastritis.
The acute gastritis encountered with H pylori is usually asymptomatic. The bacterium imbeds itself in the mucous layer, a protective layer that coats the gastric mucosa. It protects itself from the acidity of the stomach through the production of large amounts of urease, an enzyme that catalyzes the breakdown of urea to the alkaline ammonia and carbon dioxide. The alkaline ammonia neutralizes the gastric acid in the immediate vicinity of the bacterium conferring protection.
H pylori also has flagella that enable it to move and help it to penetrate the mucous layer so that it comes into contact with gastric epithelial cells. It also has several adhesion molecules that help it to adhere to these cells. It produces inflammation by activating a number of toxins and enzymes that activate IL-8, which eventually attracts polymorphs and monocytes that cause acute gastritis.
Antigen-presenting cells activate lymphocytes and other mononuclear cells that lead to chronic superficial gastritis. The infection is established within a few weeks after the primary exposure to H pylori. It produces inflammation via the production of a number of toxins and enzymes. The intense inflammation can result in the loss of gastric glands responsible for the production of acid. This is referred to as atrophic gastritis. Consequently, gastric acid production drops. The virulence genotype of the microbe is an important determinant for the severity of the gastritis and the formation of intestinal metaplasia, the transformation of gastric epithelium. This transformation can lead to gastric cancer.
Reactive gastropathy is the second most common diagnosis made on gastric biopsy specimens after H pylori gastritis. This entity is believed to be secondary to bile reflux and was originally reported after partial gastrectomy (Billroth I or II). It is now considered to represent a nonspecific response to a variety of other gastric irritants.
Helicobacter heilmanii is a gram-negative, tightly spiraled, helical-shaped organism with 5-7 turns. The prevalence of H heilmanii is extremely low (0.25-1.5%). The source of H heilmanii infection is unclear, but animal contact is thought to be the means of transmission.
Tuberculosis is a rare cause of gastritis, but an increasing number of cases have developed in patients who are immunocompromised. Gastritis caused by tuberculosis is generally associated with pulmonary or disseminated disease.
Secondary syphilis of the stomach is a rare cause of gastritis.
Phlegmonous gastritis is an uncommon form of gastritis caused by numerous bacterial agents, including streptococci, staphylococci, Proteus species, Clostridium species, and Escherichia coli. Phlegmonous gastritis usually occurs in individuals who are debilitated. It is associated with a recent large intake of alcohol, a concomitant upper respiratory tract infection, and AIDS. Phlegmonous means a diffuse spreading inflammation of or within the connective tissue. In the stomach, it implies infection of the deeper layers of the stomach (submucosa and muscularis). As a result, purulent bacterial infection may lead to gangrene.
Phlegmonous gastritis is rare. The clinical diagnosis is usually established in the operating room, as these patients present with an acute abdominal emergency requiring immediate surgical exploration. Without appropriate therapy, it can progress to peritonitis and death.
Viral infections can cause gastritis. Cytomegalovirus (CMV) is a common viral cause of gastritis. It is usually encountered in individuals who are immunocompromised, including those with cancer, immunosuppression, transplants, and AIDS. Gastric involvement can be localized or diffuse.
Fungal infections that cause gastritis include Candida albicans and histoplasmosis. Gastric phycomycosis is another rare lethal fungal infection. The common predisposing factor is immunosuppression. C albicans rarely involves the gastric mucosa. When isolated in the stomach, the most common locations tend to be within a gastric ulcer or an erosion bed. It is generally of little consequence. Disseminated histoplasmosis can involve the stomach. The usual presenting clinical feature is bleeding from gastric ulcers or erosions on giant gastric folds.
Parasitic infections are rare causes of gastritis. Anisakidosis is caused by a nematode that embeds itself in the gastric mucosa along the greater curvature. Anisakidosis is acquired by eating contaminated sushi and other types of contaminated raw fish. It often causes severe abdominal pain that subsides within a few days. This nematode infection is associated with gastric fold swelling, erosions, and ulcers.
Ulcero-hemorrhagic gastritis is most commonly seen in patients who are critically ill. Ulcero-hemorrhagic gastritis is believed to be secondary to ischemia related to hypotension and shock or to the release of vasoconstrictive substances, but the etiology is often unknown. The gastric mucosa reveals multiple petechiae, mostly in the fundus and body, or exhibits a diffusely hemorrhagic pattern. The gross pathology may resemble that of NSAID- or other ingestion-induced gastritis, except that the location of injury is different. This form of gastritis can be life-threatening if the patient experiences hemorrhaging and may even require emergency gastrectomy.
Inflammatory bowel disease and microscopic colitis appear to be inversely associated with H pylori infection.  Microscopic evidence of acute gastritis can be seen in patients with Crohn disease, though clinical manifestations are rare (occurring in only about 2-7% of patients with Crohn disease). Focally enhancing gastritis is now recognized as a condition seen in both Crohn disease and ulcerative colitis.
Eosinophilic gastritis is often seen in conjunction with eosinophilic gastroenteritis but can be associated with various disorders, including food allergies (eg, cow milk, soy protein), collagen vascular diseases, parasitic infections, gastric cancer, lymphoma, Crohn disease, vasculitis, drug allergies, and H pylori infections. An eosinophilic infiltrate is seen involving the gastric wall or epithelium.
Acute gastritis has a number of causes, including certain drugs; alcohol; bacterial, viral, and fungal infections; acute stress (shock); radiation; allergy and food poisoning; bile; ischemia; and direct trauma.
Note the following:
Drugs - NSAIDs, such as aspirin, ibuprofen, and naproxen; cocaine; iron; colchicine, when at toxic levels, as in patients with failing renal or hepatic function; kayexalate; chemotherapeutic agents, such as mitomycin C, 5-fluoro-2-deoxyuridine, and floxuridine
Potent alcoholic beverages, such as whisky, vodka, and gin
Bacterial infections - H pylori (most frequent), H heilmanii (rare), streptococci (rare), staphylococci (rare), Proteus species (rare), Clostridium species (rare), E coli (rare), tuberculosis (rare), secondary syphilis (rare)
Viral infections (eg, CMV)
Fungal infections - Candidiasis, histoplasmosis, phycomycosis
Parasitic infection (eg, anisakidosis)
Acute stress (shock)
Allergy and food poisoning
Bile: The reflux of bile (an alkaline medium is important for the activation of digestive enzymes in the small intestine) from the small intestine to the stomach can induce gastritis.
Ischemia: This term is used to refer to damage induced by decreased blood supply to the stomach. This rare etiology is due to the rich blood supply to the stomach.
Data from a national administrative database (2009-2011) revealed standardized estimated prevalence rates of 6.3 per 100,000 population for eosinophilic gastritis and 3.3 per 100,000 population for eosinophilic colitis; women were affected more often. 
Gastritis affects all age groups. The incidence of H pylori infection increases with age.
Gastritis generally clears spontaneously. With treatment, the mortality rate of phlegmonous gastritis is 65%.
The mortality/morbidity is dependent on the etiology of the gastritis. Generally, most cases of gastritis are treatable once the etiology is determined. The exception to this is phlegmonous gastritis, which has a mortality rate of 65%, even with treatment.
Complications of acute gastritis include the following:
Bleeding from an erosion or ulcer
Gastric outlet obstruction due to edema limiting the adequate transfer of food from the stomach to the small intestine
Dehydration from vomiting
Renal insufficiency as a result of dehydration
Explain the disease to the patient.
Encourage cessation of smoking and alcohol consumption, and warn patients of the potential effects of noxious drugs and chemical agents.
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