Acute Gastritis

Updated: Jul 12, 2020
  • Author: Sarah El-Nakeep, MD; Chief Editor: BS Anand, MD  more...
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Overview

Background

Acute gastritis is a term that encompasses 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 divided into two categories: erosive (eg, superficial erosions, deep erosions, hemorrhagic erosions) and nonerosive (generally caused by Helicobacter pylori). See the images below.

Acute gastritis. Acute gastritis with superficial Acute gastritis. Acute gastritis with superficial erosions.
Acute gastritis. Mucosal erythema and edema consis Acute gastritis. Mucosal erythema and edema consistent with acute gastritis.

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, as in cases of phlegmonous gastritis (gangrene of the stomach) in which 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.

See related CME at Evaluation of Acute Abdominal Pain Reviewed.

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Pathophysiology

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 exposure to a variety of agents or factors. This is referred to as reactive gastritis. These agents/factors include nonsteroidal anti-inflammatory drugs (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 or 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 over 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 the mechanisms that result in the protection of the mucosa from the injurious effects of 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 H pylori is the most common cause of gastritis, and complications result from a chronic infection rather than from an acute infection. The prevalence of H pylori in otherwise healthy individuals varies depending on the patient's 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, but 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 those of 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. H pylori 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, thereby 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 the gastric epithelial cells. It also has several adhesion molecules that help it to adhere to these cells. H pylori produces inflammation by activating a number of toxins and enzymes that activate interleukin (IL)-8, which eventually attracts polymorphs and monocytes that cause acute gastritis.

Antigen-presenting cells (APCs) 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 that are 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 acquired immunodeficiency syndrome (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, phlegmonous gastritis can progress to peritonitis and death.

Acute necrotizing hemorrhagic gastritis (a rare variant of phlegmenous gastritis) is mostly related to bacterial infection, which could progress to gastric gangrene. More recently, it has also been associated with new chemotherapeutic drugs, such as multi-antityrosine kinase (midostaurin) which is used in acute myloid leukemia. Necrotizing gastritis cases are severe and may mandate emergency gastrectomy. [1]

Cytomegalovirus (CMV) rarely causes gastritis; its prevalence among CMV patients is unknown. [2]  CMV gastritis is usually, but not always, encountered in individuals who are immunocompromised, including those with cancer, on immunosuppression medications, after transplants, and AIDS. Yamamoto and Sakai described a case of gastritis due to concurrent infection with Epstein-Barr virus (EBV) and CMV in an immunocompetent adult. [3] Gastric involvement can be localized or diffuse. CMV gastritis is essentially diagnosed by gastroscopy and biopsy because viral load and immunoglobulin (Ig) M level could be misleading. [2]

Acute gastritis has been noted in patients receiving immune-checkpoint inhibitors for cancer immunotherapy, such as pembrolizumab. Histology shows lymphocytic infiltration, mostly of the CD8+ type along with CD3+. Treatment depends mainly on a short course of corticosteroids for lympholysis. Stopping immunotherapy is mandatory only when there is a risk of gastric perforation. The condition may be discovered accidentally during follow-up positron emission tomography (PET) computed tomography (CT) scanning, because patients could be asymptomatic despite having acute gastritis. Diagnosis occurs only after exclusion of other possible causes (eg, NSAID, CMV, etc). [4]

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.

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Etiology

As noted earlier, the causes of acute gastritis include the following:

  • Drugs: Nonsteroidal anti-inflammatory drugs (NSAIDs) (eg, aspirin, ibuprofen, and naproxen); cocaine; iron; colchicine (when at toxic levels, as in patients with failing renal or hepatic function); kayexalate; chemotherapeutic agents (eg, mitomycin C, 5-fluoro-2-deoxyuridine, floxuridine, tyrosine kinase inhibitors such as midostaurin, [1]  and cancer immunotherapeutic agents, such as pembrolizumab). [4]

  • 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, cytomegalovirus)

  • Fungal infections: Candidiasis, histoplasmosis, phycomycosis

  • Parasitic infection (eg, anisakidosis)

  • Acute stress (shock)

  • Radiation

  • 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 a decreased blood supply to the stomach. This rare etiology is due to the rich blood supply to the stomach.

  • Direct trauma

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Epidemiology

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.

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. [5]

Gastritis affects all age groups; however, this condition is especially common in people older than 60 years. The incidence of H pylori infection increases with age.

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Prognosis

Gastritis generally clears spontaneously. With treatment, the mortality rate of phlegmonous gastritis is 65%.

Morbidity/mortality

Morbidity/mortality 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 of 65%, even with treatment.

Complications

Complications of acute gastritis include the following:

  • Bleeding from an erosion or ulcer

  • Gastric outlet obstruction due to edema limiting an adequate transfer of food from the stomach to the small intestine

  • Dehydration from vomiting

  • Renal insufficiency as a result of dehydration

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Patient Education

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.

For patient education resources, see Digestive Disorders Center, as well as Gastritis.

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