Acute gastritis is a term that encompasses a wide range of entities that cause transient inflammatory changes in the gastric mucosa. Different etiologies (non-steroidal antireumatics, alcohol, stress, etc.) share the same clinical picture presented by a variable degree of epigastric discomfort, nausea and vomiting, and in more severe cases mucosal erosion, ulcerations, bleeding, hematemesis, melene, or, rarely, and massive blood loss. Patients with histologically verified gastritis are mostly asymptomatic, and acute gastritis is characterized by infiltration of the mucous membrane of the antrum and corps polymorphonucleors. Inflammation can affect the entire stomach (e.g. pangastritis) or part of the stomach (e.g. anthropo-gastritis).

Acute gastritis can be divided into two categories depending on the severity of mucous membrane damage: erosiveand Non-erosive. Diagnosis of acute gastritis is usually established when the stomach is examined for some other reasons. Epidemiological studies show a wide incidence of gastritis, especially in people over 60 years of age. Most forms of acute gastritis are well tolerated and treated when etiology is determined. The exception is phlegmonosis gastritis with a mortality rate of as much as 65%, even with treatment.

Etiology and pathogenesis

The etiology of acute gastritis consists of certain types of drugs, alcohol, bile, ischemia, bacterial, viral and fungal infections, acute stress (shock), radiation, allergic reactions, food poisoning and direct trauma. A common mechanism of injury is an imbalance between aggressive and defensive factors that maintain the integrity of the gastric mucosa.

Acute erosion gastritis   (acute haemorrhagic gastritis). The main and, of course, most impressive form of acute gastritis. Its formation may be the result of exposure to various agents such as non-steroidal antireumatics (NSAIDs), alcohol, cocaine, stress, radiation, bile reflux and ischemia and is often called reactive gastritis. This term implies bleeding from the lining of the stomach, which usually occurs in this form of gastritis, and a characteristic interruption of the integrity of the mucous membrane (erosion) with inflammatory changes and ulceration. Stomach erosion and spotting bleeding can be found diffusely inside the gastric mucosa or localized in the corpus or antruma of the stomach. They are often linearly placed at the tip of the crease of the lining of the stomach.

Non-steroidal antireumatics (NSAIDs), such as aspirin, ibuprofen or naproxen, are the most common agents associated with acute erosive gastritis. These drugs inhibit the activity of cyclooxygenase in the lining of the stomach. This reduces the synthesis and concentration of endogenous prostaglandins which play an important role in the defense of the mucous membranes.

It has also been found that this form of gastritis occurs in more than 80-90% of severely ill, hospitalized patients. It most often affects patients hospitalized in internal or surgical intensive care units who have suffered serious injuries, liver, kidney and respiratory failure, massive burns, severe infections with sepsis, after major surgery or in a state of shock. Acute erosive gastritis, which occurs in these conditions is commonly referred to as stress gastritis. Ischemia mucous membranes and acids in the lumen of the stomach are undoubtedly the main factors of etiopatogenesis stress gastritis. Some of them were given specific names based on the place of appearance and the clinical picture. Like what:

  • Stress ulcers are in people in shock, sepsis or severe trauma
  • Curling ulcers   occur in the proximal duodenum after severe burns or trauma,
  • Cushing’s ulcers   are associated with an intracranial process and have a high propensity for perforation.

Acute gastritis associated with Helicobacter pylori

Acute gastritis associated with   Helicobacter pylori

  (active chronic gastritis). Helicobacter pylori,   spiral, gram-negative bacillus is the most common cause of gastritis. H. pylori   is located in the deeper part of the mucus that coats the lining of the stomach and between the mucus layer and the apical surface of the epithelial cells of the mucosa. H. pylori   survives in the acidic medium of the stomach thanks to the ability to create ammonia that can erod the musle barrier. The transmission of this bacteria from person to person takes place by feco-oral or ingestion of contaminated food or water. The result of infection with this bacterium is more common the onset of chronic than acute gastritis.

Gastritis associated with infection H. pylori   usually as acute gastritis in the antrum area, causing severe inflammation, and over time it can spread to the entire lining of the stomach, which eventually results in chronic gastritis. H. pylori   causes inflammation of the gastric mucosa by activating numerous toxins (cytotoxins) and enzymes (bacterial proteases, lipase) that activate IL-8, which attracts a multitude of polymorphonuclears and monocytes, which densely infiltrate lamin’s mucous membrane propria and epithelium cells, which is the main histological characteristic of active chronic gastritis. The mucous membrane surface is usually acute, without erosion (non-erosive gastritis) or hemorrhagic lesions, and if they do, erosions are small and shallow. The endoscopic appearance of the mucous membrane is usually neat and does not follow histological findings. The greater the infiltration of the mucous membranes of polymorphophones, the more severe the infection is H. pylori. Evidence of infection H. pylori   can be found in 20% of the population under the age of 40 years and in 50% of the population over 60 years of age.

Tuberculosis gastritis

Tuberculosis is rarely a cause of gastritis, but an increasing number is recorded in immunocompromised patients and is associated with a pulmonary or disseminated form of the disease.

Phlegmonosis gastritis

Phlegmonosis gastritis is also a rare form of acute gastritis and is caused by a number of bacterial species, including streptococcal, staphylococcal, proteus species, Clostridium species and E. coli. This form of gastritis usually occurs in people who have a weakened immune system. It has also been linked to recent intake of large amounts of alcohol, accompanying upper respiratory tract infection and AIDS. The very name of this form of gastritis, phlegmonosis, means the diffuse spread of inflammation or inside connective tissue, and since this inflammation implies expansion into the deeper layers of the stomach (submucos and musularis), can lead to gangrene of the stomach wall and the spread of inflammation, resulting in a life-threatening condition, peritonitis.

Viral gastritis

Viral infections can cause gastritis. Cytomegalovirus (CMV) is a common cause of gastritis. It is usually met in individuals who are immunocompromised, including those with neoplasm, immunosuppression, transplantation, and AIDS.

Fungal gastritis

Fungal infections that cause gastritis are Candida albicans

  and histoplasmosis. The predisposition to this form of gastritis is immunosuppression. C. albicans   rarely affect the lining of the stomach, and when isolated in the stomach, it is most often found inside gastric ulcers or erosion. Disseminated histoplasmosis may include the stomach. It is usually presented as clinically significant gastric ulcer bleeding or erosion on large gastric folds.

Parasitic gastritis

Parasitic infections are rarely the cause of gastritis. Anisakidosis is associated with consuming contaminated “sushi” food or contaminated raw fish, more common in the Far East than with us. It is caused by the migrating larva of Anisakis, which reaches into man by eating under-processed fish, crustaceans and mollusks. The host parasite is a marine mammal, and the parasite migrates from the gut into the meat of the fish after the fish is caught, and after it is caught, the fish should be removed as soon as possible.

Eosinophilic gastritis

Eosinophilic gastritis is often associated with eosinophilic gastroenteritis, but may be associated with a variety of disorders, including food allergies (e.g. cow’s milk, soy protein), collagen vascular diseases, parasitic infections, stomach cancer, lymphoma,   Crohn’s disease, vasculitis, drug allergies and H. pylori   Infection. Eosinophilic infiltrates affect the gastric wall or epithelium.

Enteropathic erosive gastritis

Enteropathic erosive gastritis is a rare clinical entity involving multiple erosion of the lining of the stomach of an unknown agent. Erosions, which may be individual or numerous, are usually found in the tips of gastric folds but can be present in any part of the mucous membrane. A gastric biopsy is performed primarily to rule out other diseases such as stomach lymphoma, cancer and Chrono’s disease.

Gastritis induced by corrosive agents

Corrosive agents such as acetic acid and NaOH – stone soda create severe complications – pangastritis and diffuse peritonitis. If a small amount of corrosive agent is entered and the patient survives intoxication, the lining of the stomach will remain damaged and chronic gastritis occurs.

Pathology

Pathohistologically, mild acute gastritis can be difficult to identify, since only mild oedema is present in the lamina propria, with mild vascular congestion. The surface epithelium is intact, although some neutrophils may be present scattered between epithelial cells or in the mucous glands. In contrast, chronic disease is characterized by an abundance of lymphocytes. The presence of neutrophils above the basal membrane in direct contact with epithelial cells is abnormal in all parts of the gastrointestinal tract and indicates active inflammation. This term is preferred instead of acute inflammation, since it has been shown above that active inflammation may be present in both acute and chronic diseases.

With greater mucous membrane damage, erosion and damage develop, with concomitant bleeding. Erosion means loss of the surface epithelium, creating a mucous membrane defect limited to the lamin propria. It was accompanied by a pronounced neutrophil infiltrator in the mucous membrane and a purulent exudate containing fibrin in the lumen.

Bleeding may occur and cause a dark puncture in the usually hyperemic mucosa. Competition of bleeding and erosion is more in the text already described as acute erosive hemorrhagic gastritis. May not be affected by mucous membranes. If erosion spreads deeper, they can spread into ulcers.

Clinical picture

in the history   patients with acute gastritis are most often encountered with burning epigastric pain that starts abruptly and lasts for several days, occasionally accompanied by nausea and/or vomiting, and the pain may be exacerbated or reduced by eating. The appetite is weak and there is an abomination to the food. Patients with mild erosive gastritis are mainly asymptomatic, and in severe cases of acute gastritis we also encounter mucous membrane erosion, ulcerations, bleeding, haematemesis, melene, or, rarely, and massive blood loss. Often in a history of the patient’s previous injury to the lining of the stomach such as gastritis, peptic ulcer disease, endoscopic injuries after polypektomy or injuries caused by previous surgery. Patients with acute gastritis also cite the etiological reasons mentioned in the previous section where etiology is discussed, and as a common cause it is necessary to repeat the use of non-steroidal antireumatics.

Physical examination   the patient often do not present any pathological signs, and sometimes we find dry and coated tongue, epigastric tension of the abdominal muscles, abdominal pressure pain and fetor ex ore. The review tends to show more pathological signs with the development of complications related to acute gastritis. Thus, for example, in acute hemorrhagic gastritis tachycardia, pallor and hypotension occur with greater blood loss.

Complications

In the complications of acute gastritis include:

  • bleeding from erosion or ulcers,
  • obstruction of the exuding part of the stomach caused by oedema and therefore inadequate transfer of food from the stomach to the small intestine,
  • dehydration from vomiting,
  • renal insufficiency as a result of dehydration.
Acute gastritis

Diagnosis

Laboratory tests such as:

  • analysis of complete blood counts to evaluate anaemia, which may be the result of gastrointestinal bleeding,
  • assessment of liver and kidney function,
  • assessment of bile and pancreatic function,
  • pregnancy test,
  • occult haemorrhage test.

Radiological

  there are four characteristic signs for acute gastritis regardless of etiology, which are thick gastric folds, inflammatory nodes in the mucous membrane, erosion and rough aree gastricae.

Thick gastric folds (folds thick of 5 mm) in patients who are symptomatic suggest infection H. pylori. Enlarged arena gastricae are not strictly related to a specific cause, they are usually 1-3 mm large and due to the loss of the mucous membrane of the barium porridge can fully fill them. Erosions are one of the most specific signs of gastritis, can be flat or curved, can be accompanied by swelling and can be seen at or near a large corner of the stomach, and are best displayed by the application of double contrast (barium porridge and air).

A number of tests to prove H.pylori are available. There are three neendoscopic and three endoscopic tests.

From neendoscopic tests, insulation is made  H. pylori  

antigen (HpSA) from the stool, urea breath test and antibody test on the H.pylori   in serum. Endoscopic fast urease test (RUT), bacterial culture H.pylori   and histological evidence by biopsy of the sample taken.

Endoscopy   is of great importance in the diagnosis of acute gastritis, especially the erosive form. Erosive gastritis should be suspected in patients with blood tests in the stools and blood tests in the stomach aspirate. Diagnosis is best placed with an endoscopy that detects bleeding, congestion, fragility and mucous membrane erosion, and in some cases superficial or deep ulcers, usually in the fundus or corpus of the stomach.

Histological treatment with biopsy of the taken material is also of great assistance in the etiological classification of gastritis. The sensitivity and specificity of this search in diagnostics H. pylori   is above 90%.

In   the differential diagnosis   of such patients, we must be:

  • Cholecystitis
  • Cholelithiasis
  • Appendicitis
  • Crohn’s disease
  • Stomach cancer
  • Viral gastroenteritis
  • B-type lymphoma
  • gastric ulcer
  • Sarcoidosis

Treatment

The use of appropriate acute gastritis therapy, if necessary, should be based on the cause and pathological findings.

There is no specific therapy for acute gastritis, other than cases of H. pylori, which uses modern combination therapy: a combination of two antibiotics against H. pylori   with a medicine that blocks acid secretion or with a protection (e.g. azithromycin + amoxicillin + omeprazole. It relieves symptoms, kills its causative agent and prevents recurrence. Verification of the effect of medicinal products on H. pylori   endoscopic search or breath-shing 4 weeks after therapy. Antidiaroics (bismuth compounds) are used in case of the onset of diarrhea, which occurs as a side effect of triple therapy.

Drugs that neutralize stomach acid (antacids) or other drugs that reduce stomach acid secretion will usually eliminate symptoms and improve the course of the disease.

Antacids are used for prophylaxis, contain aluminium and magnesium and can ease symptoms of gastritis by neutralising stomach acid. These drugs are cheap and safe.

On the market are two groups of preparations for reduced gastric acidity: H2-antagonists (ranitidine, cimetidine, famotidine) and proton pump inhibitors (omeprazole, pantoprazole, lansoprazole). H2-antagonists by competitive inhibition act on H2 receptors of gastric parietal cells, and since histamine plays a major role in gastric acid secretion, so the result of their action is a decrease in basal secretion of gastric acid and a decrease in the volume of stomach acid excreted on food and nervous system stimulation. Proton pump inhibitors are potent proton pump inhibitors (i.e. enzyme H+, K +-ATPaze), located on the apical secretory membrane of the performed cells (parietal cells). Proton pump inhibitors can completely prevent acid secretion and have a long-lasting effect. They are the most effective gastric acid blockers.

Drugs that can cause gastritis, too, should be stopped, especially alcohol and NSAIDs. Also stop smoking.
In therapy can serve gastric lavage with lukewarm water via nazo – gastric probe, then chamomile is given during one to three days to suppress disgust and to regain appetite. After calming the problems, it is switched to lighter food.

Apply fluids and electrolytes if necessary, especially if the patient vomits. In severe forms, bleeding is treated with fluid IV and, if necessary, transfusions.

Surgical intervention is not required, except in the case of phlegmoous gastritis or massive bleeding. In phlegmonose gastritis, surgical intervention with resection of the affected area is the most effective form of treatment, since the drugs are not effective in this form of the disease. In case of massive bleeding should try endoscopic haemostasis, with surgical intervention (total gastrectomy) as a deviation.

Prevention

Prevention may reduce the frequency of acute stress gastritis. However, it benefits the most high-risk patients in ICU (severe burns, sepsis, shock, CNS trauma, polytrauma, etc.). By default, H2-blockers intravenous and antacids per axis are given in intensive care units to increase intragastric pH above 4.0. Early enteral therapy also reduces the occurrence of bleeding.

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