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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.

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 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.

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), 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)
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

Complications

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
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.

Diagnostic Considerations
Also consider the following in the differential diagnosis of patients with suspected
gastritis:
Hyperplastic gastropathy/Menetrier disease
Granulomatous gastropathy
Pregnancy
Differential Diagnoses
Acute Complications of Sarcoidosis
B-Cell Lymphoma
Cholecystitis
Crohn Disease
Gallstones (Cholelithiasis)
Gastric Cancer
Peptic Ulcer Disease
Viral Gastroenteritis
Imaging Studies
Four radiologic signs of acute gastritis are fairly consistent regardless of the
etiology. These signs include thick folds, inflammatory nodules, coarse area
gastrica, and erosions.
Thick folds are defined by a size greater than 5 mm in caliber. These folds
are measured on radiographs with the stomach moderately distended. If
thick folds are found in a patient who is symptomatic, H pylori is generally
involved.
Nodularity of the gastric mucosa (bumpy appearance) is a second sign of
acute or subacute gastritis. Its origin is uncertain. Nodules may represent
erosions that have epithelialized (healed) but still have the associated
edema. Compared with benign neoplastic polyps, gastritis-related nodules
are smaller, and their edges are less well defined. They taper onto the
adjacent mucosa, and they are seen most often in the distal stomach.
Nodules due to gastritis are referred to as inflammatory. They generally line
up on the folds of the gastric antrum and are a characteristic appearance of
gastritis.
Enlarged area gastrica are a sign of gastritis that is not strongly associated
with a specific cause. They usually are 1-3 mm in size. Enlargement of
these areas may reflect inflammatory swelling and is often associated with
gastritis. Because of the loss of the mucosal layer, the barium suspension
can more completely fill the intervening grooves.
Gastric erosions are noted to be one of the most specific signs of gastritis.
Erosions may be linear or serpiginous. They may be accompanied by
edema and may be seen on or near the greater curvature of the stomach. A
double-contrast examination usually is required to best reveal gastric
erosions.
Tomography scan and plain films of the abdomen can demonstrate
thickening of the gastric wall in the case of phlegmonous gastritis.
Double-contrast barium radiography can demonstrate the nematodes that
cause anisakidosis.

Other Tests
A number of H pylori tests are available. They are classified as either
nonendoscopy based or endoscopy based.
Three nonendoscopy-based H pylori tests are available.
The first test is the H pylori stool antigen test (HpSA). This test is
based on the detection of the H pylori antigen in the stool. It has
sensitivity and specificity of greater than 90%. It can be used for both
the diagnosis of H pylori and the confirmation of eradication after
therapy.
The second test is the urea breath test. It uses 13C- or 14C-labeled
urea taken orally. H pylori metabolizes the urea and liberates labeled
carbon dioxide that is exhaled. This, in turn, can be quantified in breath
samples. The sensitivity and specificity of the urea breath test is greater
than 90%. This is considered the noninvasive diagnostic method of
choice in situations where endoscopy is not indicated. It can also be
used to confirm eradication after therapy
The third test depends on the presence of antibodies to H pylori in
the serum. The major drawback to this test is that serologic assays may
remain positive for as long as 3 years after eradication of the bacteria.
Therefore, serologic assays are often unreliable to document
eradication of H pylori. This test can be used for the diagnosis of H
pylori, provided that the patient has not received any prior therapy for it.
Three endoscopy-based H pylori tests are available.
The first test is the rapid urease test (RUT). It is performed by placing
a gastric biopsy specimen, obtained at endoscopy, onto a gel- or
membrane-containing urea and a pH-sensitive indicator. If H pylori is
present, the bacterial urease hydrolyzes urea and changes the color of
the media. The sensitivity and specificity of this test is greater than
90%.
Another test is bacterial culture H pylori. It is highly specific but is not
widely used because of the degree of expertise required. It is used
when antibiotic susceptibilities are necessary.
Histologic detection of H pylori in the biopsy specimen is another
endoscopy-based test. Appropriate staining is achieved using such
stains as hematoxylin and eosin, Warthin-Starry, Giemsa, or Genta.
American Society for Gastrointestinal Endoscopy guidelines suggest
endoscopic evaluation for patients older than 50 years who have alarm
features such as weight loss and anemia. For patients younger than 50
years with no alarm features who are H pylori negative, endoscopic
evaluation may be considered. [4]
Mycobacterium tuberculosis may be diagnosed when acid-fast stain
detects the bacilli in a biopsy specimen.
Syphilis may be diagnosed when the organism is found in the gastric
mucosa. Endoscopic biopsy, silver impregnation, and fluorescent antibody
techniques also can be used.

Procedures
Endoscopy may reveal a thickened, edematous, nonpliable wall with
erosions and reddened gastric folds. The edema can be severe resulting in
gastric outlet obstruction. Ulcers and frank bleeding might be present.
The nematodes that cause anisakidosis can be seen on endoscopy.
Endoscopy can be used to help diagnose gastric syphilis and tuberculosis.
A meta-analysis has shown that for individuals who undergo endoscopy for
dyspepsia, the most common finding is erosive esophagitis (though
prevalence was lower when the Rome criteria were used to define
dyspepsia) followed by peptic ulcers. [5]

Histologic Findings
Histologic examination of a biopsy specimen can help in establishing the
etiologic agent of gastritis.
H heilmanii is better diagnosed on smears using Giemsa or Warthin-Starry
silver stains than by gastric biopsy specimens via observation of distinct
morphology. A culture of H heilmanii has not been established yet, and the
diagnosis of this bacterial infection is based on morphological identification
by histologic examination and tissue smear cytology.
As mentioned earlier, H pylori can be found by histologic staining of a
gastric mucosal biopsy specimen. It has a sensitivity and specificity of
greater than 90%.
The main histologic feature of CMV infection is cytomegalic cells with
intranuclear inclusions. Viral cultures, immunocytochemistry, and in situ
hybridization can further aid in establishing the diagnosis.
The main histologic feature of C albicans infection is yeast forms in a
biopsy specimen.
The main histologic feature of tuberculosis is necrotizing granulomas.
The main histologic feature of histoplasmosis is presence of nonnecrotizing
granulomas containing the organisms. The diagnosis of histoplasmosis
requires a positive culture result from the gastric mucosal biopsy specimen.
In ulcero-hemorrhagic gastritis, the epithelium appears eroded with edema
and hemorrhage with typically little inflammation. In severe cases, the
lumen of the stomach may be coated with fibropurulent exudates and the
lamina propria may be replaced by eosinophilic hyaline material.

TREATMENT

Approach Considerations
Surgical intervention is not necessary, except in the case of phlegmonous
gastritis. With this entity, surgical intervention with resection of the affected
area may be the most effective form of treatment.
Consult a gastroenterologist in complicated cases.

Medical Care
Administer medical therapy as needed, depending on the cause and the
pathological findings.
No specific therapy exists for acute gastritis, except for cases caused by H
pylori. The American College of Gastroenterology guidelines suggest that
the current evidence does not support the notion that treating H
pylori worsens gastroesophageal reflux disease (GERD). For patients who
need eradication of H pylori, this should not be a concern. [6] In patients with
persistent H pylori infection despite appropriate initial treatment,
combination therapy with a a proton pump inhibitor (PPI), levofloxacin, and
amoxicillin for 10 days appears to be more effective and better tolerated
than a PPI, bismuth, tetracycline, and metronidazole. However this has not
been validated in the US literature. [6, 7, 8, 9]
Administer fluids and electrolytes as required, particularly if the patient is
vomiting.
Discontinue the use of drugs known to cause gastritis (eg, NSAIDs,
alcohol). A long-term prospective study found that patients with arthritis who
were older than 65 years and regularly took low-dose aspirin were at an
increased risk for dyspepsia severe enough to necessitate the
discontinuation of NSAIDs. [10] This suggests that better management of
NSAID use should be discussed with older patients in order to reduce
NSAID-associated upper GI events.
There has been a growing concern in recent years regarding the interaction
between PPIs and clopidogrel. A decrease in the antiplatelet activity of
clopidogrel with a possible increase in adverse cardiac events is
postulated. Pharmacokinetically it has been shown that omeprazole and
lansoprazole interact significantly with clopidogrel, and that omeprazole,
rabeprazole, and esomeprazole interact with prasugrel. Pantoprazole has
been shown to have the least interaction and thus, pantoprazole with low
CYP2C19-inhibiting properties appears to be the safest PPI to be used with
clopidogrel until more concrete evidence is available. [6,11]

Medication Summary
Specific treatment is dependent on the etiology of gastritis.
According to the Centers for Disease Control and Prevention (CDC), the
treatment of tuberculosis consists of a 2-month course of daily isoniazid,
rifampin, and pyrazinamide, followed by 4 months of daily isoniazid along
with rifampin. See Tuberculosis.
Medical management generally is ineffective in treating phlegmonous
gastritis. No effective antiviral therapy exists for the treatment of human
cytomegalovirus (HCMV) infection, though 2 agents (ie, ganciclovir,
foscarnet) have been shown to be virostatic. See Cytomegalovirus.
The treatment of C albicans includes a variety of agents, including nystatin,
oral clotrimazole, itraconazole, fluconazole, amphotericin B, and
ketoconazole. See Candidiasis.
The treatment of disseminated histoplasmosis includes a variety of agents,
including amphotericin B, itraconazole, and fluconazole. They have all been
determined to be effective. See Histoplasmosis.
No drugs are available to treat anisakidosis. Endoscopic removal may be
necessary.
Antacids
Class Summary

Used for general prophylaxis. Antacids containing aluminum and


magnesium can help relieve symptoms of gastritis by neutralizing gastric
acids. These agents are inexpensive and safe.
Aluminum and magnesium hydroxide, magnesia and alumina oral suspension (Rulox)

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Dosage Forms & Strengths

aluminum hydroxide/magnesium hydroxide/simethicone


liquid
(200mg/200mg/20mg)/5mL
(400mg/400mg/40mg)/5mL
suspension
(225mg/200mg/25mg)/5mL
tablet, chewable
200mg/200mg/25mg (Gelusil)
MORE...
Dyspepsia, Abdominal Bloating

10-20 mL PO q4-6hr taken 1 hour before or 3 hours after meals, OR


Chew 2-4 tablets q4-6hr; not to exceed 12 tablets/24 h

Drug combination that neutralizes gastric acidity and increases pH of the


stomach and duodenal bulb. Aluminum ions inhibit smooth-muscle
contraction and inhibit gastric emptying. Magnesium/aluminum antacid
mixtures are used to avoid bowel function changes.
H2 blockers
Class Summary

This class includes drugs whose mechanism of action is competitive


inhibition of histamine at the histamine 2 (H2) receptor. Histamine plays an
important role in gastric acid secretion, thereby making H2 blockers
effective suppressors of basal gastric acid output and acid output
stimulated by food and the neurological system. There are different drugs
with different potencies and half-lives (eg, cimetidine, ranitidine, famotidine,
nizatidine). Cimetidine will be discussed below as a representative of this
class of drugs.
Cimetidine (Tagamet)

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Dosage Forms & Strengths

injectable solution
150mg/mL
oral solution
300mg/5mL
tablet
200mg
300mg
400mg (Rx)
600mg (Rx)
800mg (Rx)
MORE...
Benign Gastric Ulcer

800 mg PO qHS OR
400 mg PO q12hr OR
300 mg PO q6hr
Duodenal Ulcer

800 mg PO qHS OR
400 mg PO q12hr OR
300 mg PO q6hr
Erosive Gastroesophageal Reflux Disease

800 mg PO q12hr OR
400 mg PO q6hr
Heartburn

Over the counter only


To relieve symptoms: 200 mg PO up to q12hr
To prevent symptoms: 200 mg PO with glass of water right before or any
time up to 30 minutes before eating food or drinking beverages that cause
heartburn
Pathological Hypersecretory Conditions

300 mg PO q6hr with meals and HS


Renal Impairment

CrCl<30 mL/min
300 mg IV/IO q12hr
Prevention of upper GI bleeding: 25 mg/hour continuous IV infusion
Other Indications & Uses

PUD (treatment, maintenance), gastric ulcer treatment, GI bleeding


prevention in critically ill patients, hypersecretory conditions (e.g., Zollinger-
Ellison)

Inhibits histamine at H2 receptors of gastric parietal cells, which results in


reduced gastric acid secretion, gastric volume, and hydrogen
concentration.
Proton pump inhibitors
Class Summary

Proton pump inhibitors are potent inhibitors of the proton (acid) pump (ie,
the enzyme H+,K+-ATPase), located in the apical secretory membrane of
the gastric acid secretory cells (parietal cell). Proton pump inhibitors can
completely inhibit acid secretion and have a long duration of action. They
are the most effective gastric acid blockers. Omeprazole will be discussed
as a representative of this class of drugs.
Omeprazole (Prilosec)

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Decreases gastric acid secretion by inhibiting the parietal cell H+/K+-
ATPase pump.
Antibiotics
Class Summary

Bacterial infections also can cause gastritis. The most common causative
organism is H pylori. A number of therapeutic regimens are effective
against H pylori. Single antimicrobial agents generally are not
recommended because of the potential development of resistance.
Dual therapy includes a proton pump inhibitor plus amoxicillin (no longer
recommended because eradication rates are only 30-80%) or a proton
pump inhibitor plus clarithromycin (eradication rate of roughly 71%). Adding
a second antimicrobial agent is recommended for successful eradication.
Triple regimens are preferred in clinical practice. One drug is a proton
pump inhibitor or a bismuth-based drug, the second drug is clarithromycin,
and the third drug is amoxicillin or metronidazole. Quadruple therapy
regimens (ie, 2 antibiotics, bismuth, antisecretory agent) generally are
effective; however, because more drugs are prescribed and taken,
increased adverse effects and decreased patient compliance can occur.
This regimen is used in the event that triple therapy fails.
The decision as to which medications to use is based on the following 4
criteria: (1) the different toxicities of the various medications, (2) the relative
costs of each medication and regimen, (3) the emergence of antimicrobial-
resistant bacteria, and (4) the level of patient compliance.
Amoxicillin (Amoxil, Trimox)

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Interferes with synthesis of cell wall mucopeptides during active
multiplication, resulting in bactericidal activity against susceptible bacteria.
Tetracycline (Sumycin)

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Inhibits bacterial protein synthesis by binding with 30S and possibly 50S
ribosomal subunit(s).
Metronidazole (Flagyl)

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Imidazole ring-based antibiotic active against various anaerobic bacteria
and protozoa.
Clarithromycin (Biaxin)

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Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA
from ribosomes and causing arrest of RNA-dependent protein synthesis.
Antidiarrheal agents
Class Summary

Used in combination with antibiotics and proton pump inhibitors/H2


receptor antagonists to eradicate H pylori.
Bismuth subsalicylate (Bismatrol, Pepto-Bismol)

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Dosage Forms & Strengths

tablet, chewable
262mg
525mg
caplet
262mg
oral suspension
262mg/15mL
525mg/15mL
MORE...
Diarrhea, Gas, Upset Stomach, Indigestion, Heartburn, Nausea

2 tablets (262 mg/tab) or 30 mL (regular strength) PO q-1hr PRN;


maximum daily dose: 8 regular-strength doses or 4 extra-strength doses
Traveler's Diarrhea

Prophylaxis
2 tablets (262 mg/tab) q6hr for up to 3 weeks
Helicobacter Pylori

525 mg (2 regular-strength tablets or 1 extra-strength tablet) + 250 mg


metronidazole + 500 mg tetracycline PO q6hr for 14 days, plus an H2
antagonist (Helidac Therapy pack)
Dosing Modifications

Renal impairment: Overdose may cause nephrotoxicity


Administration

Drink plenty of clear fluids to prevent dehydration caused by diarrhea


Do not use for >2 days
Helidac Therapy pack: Bismuth subsalicylate tablets should be chewed and
swallowed; if a dose is missed, double doses should not be taken

Drug combination that treats active duodenal ulcer associated with H pylori.