Acute gastritis

Acute gastritis is a term that encompasses a wide range of entities that cause transient inflammatory changes in the gastric mucosa. Different etiologies (nonsteroidal antirheumatic drugs, alcohol, stress, etc.) share the same clinical picture, which is presented by varying degrees of epigastric discomfort, nausea, and vomiting, and in severe cases by mucosal erosion, ulceration, bleeding, hematemesis, melanoma, or, rarely, massive blood. Patients with histologically verified gastritis are mostly asymptomatic, and acute gastritis is characterized by infiltration of the antrum mucosa and corpus by polymorphonuclear cells. Inflammation can affect the entire stomach (e.g., pangastritis ) or part of the stomach (e.g., antral gastritis ).

Acute gastritis can be divided into two categories depending on the severity of mucosal damage: erosive ii non-erosive. The diagnosis of acute gastritis is usually established during endoscopic examination of the stomach for some other reason. Epidemiological studies show a wide incidence of gastritis, especially in people older than 60 years. Most acute gastritis forms are well tolerated and treated when the etiology is determined. The exception is phlegmonous 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, 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 gastric mucosa’s integrity.

Acute erosive gastritis  (acute hemorrhagic gastritis). It is the main and, certainly, the most impressive form of acute gastritis. Its occurrence can result from exposure to various agents such as nonsteroidal antirheumatic drugs (NSAIDs), alcohol, cocaine, stress, radiation, bile reflux, and ischemia, and is often called reactive gastritis. This term refers to bleeding from the gastric mucosa, which usually occurs in this form of gastritis, and a characteristic disruption of the mucosa’s integrity (erosion) with inflammatory changes and ulcerations. Gastric erosions and intermittent bleeding may be found diffusely within the gastric mucosa or localized in the stomach’s corpus or antrum. They are often linearly located at the apex of the gastric mucosa folds.

Nonsteroidal antirheumatic drugs (NSAIDs), such as aspirin, ibuprofen, or naproxen, are the most common agents associated with acute erosive gastritis. These drugs inhibit cyclooxygenase activity in the gastric mucosa. This reduces the synthesis and concentration of endogenous prostaglandins that play an important role in mucosal defense.

It has also been found that this form of gastritis occurs in more than 80-90% of severely ill, hospitalized patients. It most commonly affects patients hospitalized in internal medicine or surgical intensive care units which have suffered severe injuries, liver, kidney, and respiratory system failure, massive burns, severe sepsis infections, after major surgeries, or in a state of shock. Acute erosive gastritis, which occurs in these conditions, is usually called stress gastritis. Mucosal ischemia and acid in the gastric lumen are undoubtedly major factors in stress gastritis etiopathogenesis. Some of them are given specific names based on the place of occurrence and the clinical picture. For example:

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

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 are located in the deeper part of the mucus lining the gastric mucosa and between the mucus layer. The apical surface of the mucosal epithelial cells. H. pylori survive in the stomach’s acidic medium due to its ability to produce ammonia, which can erode the mucus barrier. The transmission of this bacterium from person to person takes place by fecal-oral route or by ingestion of contaminated food or water. The result of infection with this bacterium is more often chronic than acute gastritis.

Gastritis associated with infection H. pylori usually begins as acute gastritis in the antrum area, causing severe inflammation. Over time, it can spread to the entire gastric mucosa, ultimately resulting in chronic gastritis. H. pylori cause inflammation of the gastric mucosa by activating numerous toxins (cytotoxins) and enzymes (bacterial proteases, lipases) that activate IL-8, which attracts many polymorphonuclears and monocytes, which densely infiltrate the lamina propria of the mucosa and epithelial cells, which is the main histological feature of active chronic gastritis . The surface of the mucosa is usually intact, without erosions (non-erosive gastritis) or hemorrhagic lesions. If they do occur, the erosions are small and shallow. The mucosa’s endoscopic appearance is usually neat and does not follow the histological finding. The greater the mucosa’s infiltration with polymorphonuclear cells, the more severe the infection and the more likely it is to identify H. pylori. Proof of infection H. pylori you can find in 20% of the population under the age of 40 and 50% of the population over the age of 60.

Tuberculous gastritis

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

Phlegmonous gastritis

Phlegmonous gastritis is also a rare form of acute gastritis caused by several bacterial species, including streptococci, staphylococci, Proteus species, Clostridium species, and E. coli. This form of gastritis usually occurs in people who have a weakened immune system. It is also associated with recent high alcohol intake, concomitant upper respiratory tract infection, and AIDS. The very name of this form of gastritis, phlegmonous, means the diffuse spread of inflammation or within the connective tissue. As this inflammation involves spreading to deeper layers of the stomach (submucosa and muscular), it can lead to gangrene of the stomach 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 commonly found in immunocompromised individuals, including neoplasms, immunosuppression, transplantation, and AIDS.

Fungal gastritis

Fungal infections that cause gastritis are Candida albicans and histoplasmosis. The predisposition for this form of gastritis is immunosuppression. C. Albicans rarely affects the gastric mucosa, and when isolated in the stomach, it is most commonly found within a gastric ulcer or erosion. Disseminated histoplasmosis may involve the stomach. It is usually presented as clinically significant bleeding from a gastric ulcer or erosion on large gastric folds.

Parasitic gastritis

Parasitic infections are rarely the cause of gastritis. Anisakidosis is associated with the consumption of contaminated “sushi” food or contaminated raw fish; it is more common in the Far East than in our country. It is caused by the migrating larva Anisakis, which reaches humans by eating insufficiently processed fish, crabs, and mollusks. The host of the parasite are marine mammals, and the parasite migrates from the entrails to the meat of the fish after the fish dies, and therefore the fish, after being caught, needs to remove the entrails soon as possible.

Eosinophilic gastritis

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

Enteropathic erosive gastritis

Enteropathic erosive gastritis is a rare clinical entity involving multiple erosions of the unknown cause’s gastric mucosa. Erosions, which may be single or numerous, are usually found at the gastric fold tips but may be present in any part of the mucosa. A gastric biopsy is performed primarily to rule out other diseases such as gastric lymphoma, cancer, and Crohn’s disease.

Gastritis caused by corrosive agents

Corrosive agents such as acetic acid and NaOH – rock soda create severe pangastritis and diffuse peritonitis. If a small corrosive agent is ingested and the patient survives intoxication, the gastric mucosa will remain damaged and chronic gastritis will develop.

Pathology

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

With greater mucosal damage, erosions and damage develop, with concomitant bleeding. Erosion means loss of superficial epithelium, creating a mucosal defect limited to the lamina propria. It is accompanied by a pronounced neutrophilic infiltrate in the mucosa and a purulent exudate containing fibrin in the lumen.

Bleeding may occur and cause a dark puncture in the usually hyperemic mucosa. The bleeding and erosion competition is more described in the text as acute erosive hemorrhagic gastritis. Non-mucosal surfaces may be affected. If the erosions spread deeper, they can progress to ulcers.

Clinical picture

IN anamnesis  In patients with acute gastritis, we most often experience burning epigastric pain that begins suddenly and lasts for several days, occasionally accompanied by nausea and/or vomiting. The pain may worsen or decrease by eating. Appetite is weak, and there is an aversion to food. Patients with mild erosive gastritis are mostly asymptomatic, and in severe cases of acute gastritis, we also encounter mucosal erosions, ulcerations, bleeding, hematemesis, melena, or, rarely, massive blood loss. Often in the anamnesis, the patient states a previous injury to the gastric mucosa such as gastritis, peptic ulcer disease, endoscopic injuries after polypectomy, or injuries caused by previous surgery. Patients with acute gastritis also state the etiological reasons mentioned in the previous section where the etiology is discussed. As a common cause, the use of nonsteroidal antirheumatic drugs should be repeated.

Physical examination, the patient often has no pathological signs present. Sometimes we find dry and coated tongue, epigastric tension of the abdominal muscles, pain on the abdomen’s pressure, and fetor ex ore. Examination tends to show more pathological signs with the development of complications related to acute gastritis. Thus, in acute hemorrhagic gastritis, tachycardia, pallor, and hypotension occur with greater blood loss.

Complications

Complications of acute gastritis include:

  • bleeding from erosions or ulcers,
  • obstruction of the outlet of the stomach caused by edema and therefore an inadequate transfer of food from the stomach to the small intestine,
  • dehydration from vomiting,
  • renal failure as a consequence of dehydration.
Acute gastritis

Diagnosis

In the diagnosis of acute gastritis, laboratory tests are often prescribed, such as:

  • complete blood count analysis to assess anemia, which may be the result of gastrointestinal bleeding,
  • assessment of liver and kidney function,
  • assessment of bile and pancreatic function,
  • pregnancy test,
  • occult bleeding test.

Radiologically there are four characteristic signs of acute gastritis regardless of etiology, and these are thick gastric folds, inflammatory nodules in the mucosa, erosions, and rough area gastrique.

Thick gastric folds (folds thicker than 5 mm) in symptomatic patients suggest infection H. pylori. Enlarged area gastrique is not strictly related to a specific cause. They are usually 1-3 mm in size. Due to the mucous membrane’s loss, barium porridge can fill them. Erosions are one of the most specific signs of gastritis. They may be flat or curved, may be accompanied by swelling, be seen at or near the large curvature of the stomach, and are best-displayed double-contrast (barium porridge and air).

Numerous tests to detect H.pylori are available. There are three non-endoscopic and three endoscopic tests.

Isolation is done from non-endoscopic tests H. pylori stool antigen (PSA), urea exhalation test, and antibody test on H.pylori  in serum. An endoscopic rapid urease test (RUT), a bacterial culture, is performed H.pylori  and histological evidence of a biopsy sample.

Endoscopy is of great importance in diagnosing acute gastritis, especially erosive form. Erosive gastritis should be suspected in patients with blood in the stool and blood in the gastric aspirate. The diagnosis is best made by endoscopy, which reveals bleeding, congestion, fragility, and erosions of the mucosa, and in some cases superficial or deep ulcers, usually in the fundus or corpus of the stomach.

Histological processing of biopsy material is also of great help in gastritis’s etiological classification. This test’s sensitivity and specificity in diagnostics H. pylori are above 90%.

IN  differential diagnosis, such patients must be on our minds:

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

Treatment

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

There is no specific therapy for acute gastritis, except in cases caused by H. pylori, which uses modern combination therapy: a combination of two antibiotics against H. pylori with a drug that blocks acid secretion or with a protective agent (e.g., azithromycin + amoxicillin + omeprazole. It alleviates symptoms, kills its cause, and prevents recurrence. Checking the effect of drugs on H. pylori is performed by endoscopic examination or breath examination 4 weeks after therapy. Antidiarrheals (bismuth compounds) are used in diarrhea, which occurs as a side effect of triple therapy.

Medicines that neutralize stomach acid (antacids) or other medicines that reduce the secretion of stomach acid will usually eliminate the symptoms and improve the disease’s course.

Antacids are used for prophylaxis, contain aluminum and magnesium, and relieve gastritis symptoms by neutralizing stomach acid. These drugs are cheap and safe.

There are two groups of preparations for reducing gastric acidity on the market: H2-antagonists (ranitidine, cimetidine, famotidine) and proton pump inhibitors (omeprazole, pantoprazole, lansoprazole). H2-antagonists act by competitive inhibition on H2 receptors of gastric parietal cells. As histamine plays a major role in gastric acid secretion, its effect is to reduce basal gastric acid secretion and reduce gastric acid volume secreted by food and nervous system stimulation. Proton pump inhibitors are potent inhibitors of the proton pump (i.e., the enzyme H +, K + -ATPase), located on the apical secretory membrane of stem cells (parietal cells). Proton pump inhibitors can completely prevent acid secretion and have a long action. They are the most effective stomach acid blockers.

Medications that can cause gastritis should be stopped, especially alcohol and NSAIDs. Also, quit smoking.
In therapy, gastric lavage with lukewarm water through a nasogastric tube can be used; then chamomile is given for one to three days to suppress nausea and restore appetite. After the symptoms have subsided, they switch to lighter foods.

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

Surgical intervention is not required, except in phlegmonous gastritis or massive bleeding. In phlegmonous gastritis, surgical intervention with resection of the affected area is the most effective treatment, as drugs are not effective in this form of the disease. In massive bleeding, endoscopic hemostasis should be attempted, with surgical intervention (total gastrectomy) as a regression.

Prevention

Prevention can reduce the incidence of acute stress gastritis. However, it is most beneficial to high-risk patients in ICU (severe burns, sepsis, shock, CNS trauma, polytrauma, etc.). H2-blockers are given intravenously and antacids per os as standard in intensive care units to raise the intragastric pH above 4.0. Early enteral therapy also reduces the incidence of bleeding.
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