Acute gastritis – first caused an inflammatory process that occurs with a primary lesion of the gastric mucosa (sometimes – the deeper layers of the gastric wall). Acute gastritis saw belching, nausea, vomiting, flatulence, diarrhea, severe pain, burning sensation and heaviness in the epigastric region. The diagnosis of acute gastritis is established by history (food, Epidemiological, allergic) data, the results of chemical and bacteriological examination of feces and vomit, x-ray of the stomach, gastroscopy. Depending on the type and severity of acute gastritis treatment may include gastric lavage, diet, antibiotics, oral rehydration, intravenous infusion therapy.
Gastritis is the most common pathology in gastroenterology. According to statistical data, the different forms of gastritis suffers every second adult world. In acute gastritis, inflammatory changes often affect the surface epithelium and the glandular apparatus of the stomach. Less inflammation spreads to the entire depth of the mucosa and even the muscular layer of the gastric wall. Insidious acute gastritis is at risk of erosion of the mucous, gastrointestinal bleeding, scarring in the stomach, septic complications, chronic gastritis.
Causes of acute gastritis
By the etiological mechanism of occurrence of isolated acute endogenous and exogenous gastritis.
The development of endogenous acute gastritis associated with an infection present in the body. The most common etiologic agent acts spiral bacterium Helicobacter pylori, which is diagnosed in 80% of patients with acute gastritis. Helicobacter secretes various toxins and enzymes (urease, etc.), Which under the influence of the gastric mucosa in inflammatory reactions develop. Helicobacter infection also contributes to the development of gastric ulcers.
Less common pathogens of endogenous acute gastritis are the streptococci, Proteus, Staphylococcus, E. coli, cytomegalovirus, agents of fungal infections (candidiasis, histoplasmosis, and others.) And others. Morphological plus functional prerequisites as the development of acute gastritis occur when influenza, scarlet fever, measles, diphtheria, viral hepatitis, pneumonia. In rare cases, secondary acute gastritis develops with disseminated tuberculosis, secondary syphilis.
Acute gastritis causes
Acute exogenous etiological factors of gastritis primarily nutritional agents act – thermal, mechanical, chemical. Irritation of the stomach lining too hot, sharp or rough foods can cause the development of acute gastritis. Adverse damaging effect on gastric mucosa has tobacco, alcohol, drinking strong coffee.
Among the exogenous causes of acute gastritis and often serve food poisoning caused by eating food contaminated with Salmonella, Shigella, Yersinia, Klebsiella. Also, irritation and damage to the stomach lining may be due to prolonged use of some pharmacological agents – salicylates, corticosteroids, bromides, iron preparations, sulfonamides, antibiotics. Acute gastritis may develop on the background radiation therapy for gastric cancer, deliberate or accidental ingestion of chemicals (acetic, nitric, hydrochloric, sulfuric, acid, mercuric chloride, ammonia, caustic soda, ethylene glycol, methanol, compounds iodine, arsenic, acetone, etc. and phosphorus.). At high concentrations, or the use of a significant amount of toxic substances may burn or perforation of the wall of the stomach and esophagus.
Acute allergic gastritis develops when you are hypersensitive to certain foods and usually accompanied by other allergic reactions – urticaria, angioedema, seizures, asthma and others.
Classification of acute gastritis
In acute gastritis in the gastric mucosa can develop various changes, depending on where the disease occurs in catarrhal (simple), fibrinous, necrotic (corrosive) or abscess (pus) forms.
In acute catarrhal gastritis in gastroscopy revealed thickening, congestion, swelling of the mucous membrane of the stomach contents of a large amount of mucus, sometimes – Small point superficial hemorrhage. In the case of multiple confluent erosions speak of acute erosive gastritis. For microscopic picture characteristic degeneration and desquamation of surface epithelium, serous exudation, the presence of diffuse infiltration, the intactness of the thick layers of the mucosa and gastric glands.
Pathological changes in acute gastritis are fibrinous necrotic changes in the mucosa, the formation of fibrinous-purulent exudate and fibrous film on the surface of the stomach. Depending on the depth of inflammation distinguish croupous (surface) and diphtheritic gastritis (dark) gastritis.
Acute necrotizing gastritis develops as a result of ingestion of aggressive substances (chemicals). If poisoning acids formed coagulation necrosis; in the case of poisoning with salts – liquefactive necrosis. It may be damaged not only the mucosal layer of the stomach but also to the entire thickness of the gastric wall with the formation of erosions and perforated ulcers.
In acute phlegmonous gastritis, inflammation is involved in all the layers of the stomach wall – mucosal, submucosal, muscular, dangerous. Purulent gastritis often occurs when ulcers, disintegrating tumors, stomach injuries. Macroscopic changes are characterized by thickening of the stomach wall due to mucosal and submucosal layers, massive fibrinous deposits. Against the background of an acute abscess may develop gastritis perigastric and peritonitis.
Depending on the area involved in the inflammatory process, distinguish focal (localized) and diffuse (widespread) acute gastritis. Focal forms of acute gastritis according to the affected part of the stomach, in turn, are subdivided into funding, antral.
Symptoms of acute gastritis
Manifestations of acute gastritis usually occur after 6-12 hours after exposure to the etiological factor. The most expressed diarrheal disorders: loss of appetite, discomfort, and heaviness in the epigastric pain, moderate pain, an unpleasant taste in the mouth, belching, nausea, vomiting eaten food with mucus and bile. When food infections, frequent stools, flatulence, increased body temperature. Repeated vomiting and diarrhea with acute gastroenteritis may cause dehydration, which manifested by weakness, dizziness, headache.
In acute allergic gastritis but signs of dyspepsia, joined the symptoms of dermatitis – a rash, erythema, pruritus, angioedema, etc. In acute. Erosive gastritis may experience vomiting blood or melena, indicating gastric bleeding. For acute gastritis, an abscess characterized by high fever, chills, vomiting with an admixture of pus, severe cramping pain in the upper abdomen.
The Severe condition develops in acute corrosive gastritis, caused by the use of active chemicals. In patients remarked, not bringing relief vomiting; in vomit, message contains mucus, blood, pieces of the mucosa of the digestive tract. On the lips and in the mouth of the patient determined by the following chemical burns; by ingestion of poisons into the larynx occurs laryngospasm and asphyxia. Overall condition exacerbated by shock events: hypotension, tachycardia, paleness of skin, shallow breathing.
Clinical manifestations of acute gastritis should distinguish from a peptic ulcer, pancreatitis, cholecystitis, myocardial infarction, occlusion of mesenteric vessels, acute appendicitis and others.
Diagnosis of acute gastritis
In explaining the circumstances of the disease are paying attention to the food, drug history, comorbidities. Objective status in acute gastritis characterized by pallor and dry skin, painful epigastric palpation. On examination, the oral tongue coated with a grayish bloom is determined by halitosis.
In severe cases, acute gastritis marked oliguria; in the study of general urinalysis detected albuminuria, urate. Changes in the peripheral blood include mild leukocytosis, increased erythrocyte count, and hemoglobin; for bleeding – anemia. To identify possible signs of bleeding investigated stool for occult blood.
Advanced Biochemical analysis of blood in acute gastritis allows identifying violations of the liver, biliary system, pancreas, and kidneys. To evaluate the functional state of the gastrointestinal tract study conducted a program to detect pathogens – bacteriological seeding feces. To detect H. pylori, infection is performed breathing test for helicobacter, the definition of H. Pylori in blood and stool by ELISA, PCR diagnosis.
In some cases, acute gastritis is a gastroscopy, which is determined with the help of hyperemia, swelling of the mucous, the presence of erosions, intramucosal hemorrhages, sometimes – signs of stomach bleeding.
X-ray of the stomach in acute gastritis reveals coarse folds and modularity mucosal erosion, increasing gastric fields.
Treatment of acute gastritis
The basic principles of treatment of acute gastritis are the elimination of the causes of the disease and prevention of complications. In acute gastritis in the first 12-24 hours of fasting is shown, then assigned a light diet. When food or chemical poisoning, gastric lavage performed. Need refusal to take a stomach irritant drugs, smoking, and alcohol.
Of the medicines in acute gastritis appointed blockers H 2 histamine receptors, having antisecretory action (ranitidine, cimetidine, famotidine), proton pump inhibitors (omeprazole and its analogs), antacid (Maalox, Aluminium phosphate gel, Gustav) gastroprotective. In acute gastritis, specific etiology were under treatment (H. pylori, antifungal, anti-tuberculosis therapy).
For pain relief in acute gastritis applied atropine, platifillin, papaverine; vomiting showed appointment prokinetics – Cerucalum, raglan, Motilium. In marked dehydration, infusion therapy is performed with salt solutions.
Treatment of acute gastritis abscess surgically performed: in this case shows gastrotomy, drainage of purulent focus; in some cases – gastric resection or gastrectomy.
Prediction and prevention of acute gastritis
This Acute gastritis with timely and correct treatment is usually complete recovery in 3-4 days. Prognostically unfavorable for corrosively of acute gastritis: the patient may die of shock, perforation of the stomach and peritonitis. Exodus chemical gastrointestinal burns may be the stricture of the esophagus, stomach, scar deformity, which may require implementation of esophagopathy, imposing gastrostomy and others. Interventions.
Also notes the grave prognosis in acute phlegmonous gastritis, which does not exclude the development of gastric perforation, peritonitis, empyema, mediastinitis, liver abscess, subphrenic abscess, sepsis.
Prevention of acute gastritis requires the exclusion of nutritional reasons of refusal from alcohol and tobacco, careful use of drugs, adequate treatment of endogenous infections.