Background

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.

Acute gastritis with

superficial erosions.
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Mucosal erythema and

edema consistent with acute gastritis.
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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.
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 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
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 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 inchronic gastritis.
The acute gastritis encountered with H pyloriis 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 togastric 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, andEscherichia 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, on immunosuppression
medications, after transplants, and AIDS. Gastric involvement can be
localized or diffuse.
Fungal infections that cause gastritis includeCandida 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 withH pylori infection. [1] 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 andulcerative colitis.
Eosinophilic gastritis is often seen in conjunction with eosinophilic
gastroenteritisbut 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 pyloriinfections. An eosinophilic infiltrate is seen involving
the gastric wall or epithelium.
Etiology
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), Clostridiumspecies (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)
 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 decreased
blood supply to the stomach. This rare etiology is due to the rich blood
supply to the stomach.
 Direct trauma
Epidemiology
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. [2]
Gastritis affects all age groups. The incidence of H pylori infection
increases with age.
Prognosis
Gastritis generally clears spontaneously. With treatment, the mortality rate
of phlegmonous gastritis is 65%.
Mortality/morbidity
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
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
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, seeDigestive Disorders Center, as
well asGastritis. NEW