acute gastritis – emedicine – 12 jan 2011

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Acute Gastritis Emedicine 12 jan 2011

Background

Acute gastritis is a term covering a broad spectrum of entities that induce inflammatory changes in the gastric mucosa.

The 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).

Acute gastritis with superficial erosions.

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 maypresent 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 approximately1.8-2.1 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 the 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 asaspirin, ibuprofen, and naproxen, are the most common agents associated with acute erosive gastritis. This results from

oral or 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.
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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.

Bacterial infection is another cause of acute gastritis. The corkscrew-shaped bacterium called H pyloriis the most

common cause of gastritis. Complications result from a chronic infection rather than from an acute infection. The

prevalence ofH pyloriin 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 ofH pyloriinfection 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 pyloriis associated with 60% of

gastriculcersand80%ofduodenalulcers.

H pylorigastritis 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 conferringprotection.

H pylorialso 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 adhesions 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 asatrophic gastritis. Consequently, gastric acid productiondrops. 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 pylorigastritis.

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 heilmaniiis a gram-negative, tightly spiraled, helical-shaped organism with 5-7 turns. The prevalence ofH

heilmaniiis extremely low (0.25-1.5%). The source ofH heilmaniiinfection 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 because of 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 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 progresses to peritonitis and death.

Viral infections can cause gastritis. Cytomegalovirus (CMV) is a common viral cause of gastritis. It is usually encountered
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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.

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 bothCrohn diseaseandulcerative colitis.

Eosinophilic gastritis is often seen in conjunction witheosinophilic 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.

Epidemiology

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.

Sex

No sexual predilection exists.

Age

Gastritis affects all age groups. The incidence ofH pyloriinfection increases with age.

History

Gnawing or burning epigastric distress, occasionally accompanied by nausea and/or vomiting. The pain

may improve or worsen with eating.

Previous mucosal injury (eg, gastritis, peptic ulcer disease, endoscopic injury caused by polypectomy,

injury caused by any surgery)

History of eating raw fish

Exposure to potentially noxious drugs or chemical agents. This includes corticosteroids or other

prescription medications that can cause gastritis.

Routine use of aspirin or NSAIDs, especially at high doses

Physical

The physical examination findings are often normal with occasional mild epigastric tenderness. The examination tends

to exhibit more abnormalities as the patient develops complications in relation to gastritis.
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Causes

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.

Drugs - NSAIDs, such as aspirin, ibuprofen, and naproxen; cocaine; iron; colchicine, when at toxic levels, as in patientswith 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), Proteusspecies (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 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 etiologyis due to the rich blood supply to the stomach.

Direct trauma

Differentials

Cholecystitis

Cholelithiasis

Crohn Disease

Gastric Cancer

Gastroenteritis, Viral

Lymphoma, B-Cell

Peptic Ulcer Disease

Sarcoidosis

Laboratory Studies

A number of laboratory tests are usually ordered.

CBC count to assess for anemia, as acute gastritis can cause gastrointestinal bleeding

Liver and kidney function tests

Gallbladder and pancreatic function tests

Pregnancy test

Stool for blood

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 pyloriis 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
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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 ofH pyloritests are available. They are classified as either nonendoscopy based or endoscopy based.

Three nonendoscopy-based H pyloritests are available.

The first test is the H pyloristool antigen test (HpSA). This test is based on the detection of the H pyloriantigen in thestool. It has sensitivity and specificity of greater than 90%. It can be used for both the diagnosis ofH pyloriand

the confirmation of eradication after therapy.

The second test is an urea breath test. It uses 13C- or 14C-labeled urea taken orally. H pylorimetabolizes the urea andliberates labeled carbon dioxide that is exhaled. This, in turn, can be quantified in breath samples. Thesensitivity 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 pyloriin the serum. The major drawback to this test is thatserologic assays may remain positive for as long as 3 years after eradication of the bacteria. Therefore, serologic

assays are often unreliable to document eradication ofH pylori. This test can be used for the diagnosis ofH

pylori, provided that the patient has not received any prior therapy for it.

Three endoscopy-based H pyloritests are available.

The first test is the rapid urease test (RUT). It is performed by placing a gastric biopsy specimen, obtained onendoscopy, onto a gel- or membrane-containing urea and a pH-sensitive indicator. IfH pyloriis present, thebacterial urease hydrolyzes urea and changes the color of the media. The sensitivity and specificity of this test is

greater than 90%.

Another test is a bacterial culture H pylori. It is highly specific but is not widely used because of the degree ofexpertise required. It is used when antibiotic susceptibilities are necessary.

Histologic detection ofH pyloriin the biopsy specimen is another endoscopy-based test. Appropriate staining isachieved using such stains as hematoxylin and eosin, Warthin-Starry, Giemsa, or Genta.

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.[1]

Histologic Findings

Histologic examination of a biopsy specimen can help in establishing the etiologic agent of gastritis.


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H heilmaniiis better diagnosed on smears using Giemsa or Warthin-Starry silver stains than by gastric biopsy specimens

via observation of distinct morphology. A culture ofH heilmaniihas 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 pylorican 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 ofC 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 nonnecrotizing granulomas containing the organisms. The diagnosis of

histoplasmosis requires a positive culture result from a 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.

In iron-induced gastritis, erosions, foveolar hyperplasia, or even hyperplastic-type polyps can be detected. Iron has been

associated with infarctlike necrosis given its corrosive properties. Iron stains can highlight the golden brown pigments in

tissue samples, but these are often easily visible. Of note, such findings should be differentiated from glandular siderosis

seen in systemic iron overload orhemochromatosis.

Histologic features of chemotherapy-induced gastritis may include atypical epithelial cells with bizarre features at the

base of the glands, limited mitoses, and pleomorphic nuclei. These characteristics may make it difficult to differentiate

from an adenocarcinoma.

The histology of radiation-induced gastritis include nuclear karyorrhexis and cytoplasmic eosinophilia of the gastric pit

epithelium in the first 10 days following treatment, followed by mucosal edema, congestion, submucosal collagen

bundle swelling, fibrin deposition, and telangiectasia. If extensive, hemorrhage and ulceration may be evident.

In eosinophilic gastritis, a prominent eosinophilic infiltrate is present in the gastric wall or epithelium. Distribution can

be patchy, so multiple biopsy specimens should be obtained during endoscopy.

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.

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.[2] This suggests that better management of

NSAID use should be discussed with older patients in order to reduce NSAID-associated upper GI events.

Surgical Care

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.

Consultations

Consult a gastroenterologist in complicated cases.

Medication Summary

Specific treatment is dependent on the etiology of gastritis.
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According to the Centers for Disease Control and Prevention (CDC), the treatment of tuberculosis consists of a 2-month

period of daily isoniazid, rifampin, and pyrazinamide, followed by 4 months of daily isoniazid along with rifampin.

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.

The treatment ofC albicans includes a variety of agents, including nystatin, oral clotrimazole, itraconazole, fluconazole,

amphotericin B, and ketoconazole.

The treatment of disseminated histoplasmosis includes a variety of agents, including amphotericin B, itraconazole, and

fluconazole. They have all been determined to be effective.

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)

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. When used alone, they are

frequently used as antisecretory drugs in H pyloritherapy regimens. 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)

Inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume,

and hydrogen concentrations.

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)

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

Antibiotics

Class SummaryBacterial 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.
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Dual therapy includes a proton pump inhibitor plus amoxicillin (no longer recommended because eradication rates are

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 of 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)

Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against

susceptible bacteria.

Tetracycline (Sumycin)

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

Metronidazole (Flagyl)

Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa.

Clarithromycin (Biaxin)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes and causing RNA-

dependent protein synthesis to arrest.

Antidiarrheal agentsClass Summary

Used in combination with antibiotics and proton pump inhibitors/H2 receptor antagonists to eradicate H pylori.

Bismuth subsalicylate (Bismatrol, Pepto-Bismol)

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

Complications

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 dehydrationPrognosis

Gastritis generally clears spontaneously. With treatment, the mortality rate of phlegmonous gastritis is 64%.Patient Education

Explain the disease to the patient.

Encourage cessation of smoking and alcohol consumption.Warn patients of the potential effects of noxious drugs and chemical agents.
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acute gastritis – emedicine – 12 jan 2011

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