Etiology and predisposing factors
The causes of inflammation are divided into external and internal.
Exogenous (primary) triggers include:
- Infectious agents, including the bacterium Helicobacter pylori.
- Alimentary factors (e.g., food allergens).
- Inake of aggressive medications.
- Exposure to caustic chemicals (provokes a specific and extremely severe form — corrosive gastritis).
Secondary gastritis develops against the background of a general decrease in immune status and a drop in mucosal resistance to pathogens. Focal purulent infections, sepsis, acute renal failure, acute and chronic infectious processes, as well as radiation injuries, contribute to this.
There are also background factors that increase the risk of the disease: constitutional characteristics of the organism, burdened heredity, past illnesses, as well as physical overwork and nervous system exhaustion due to a banal lack of rest.
Pathogenesis and clinical presentation
The mechanism of disease development starts with the irritation of the mucous membrane by the etiological factor. This leads to a disruption of normal digestive processes and hyperactivation of gastric juice enzymes, which only aggravates local tissue damage.
Symptomatology always develops acutely:
- Initial manifestations: general malaise, loss of appetite (anorexia); anxiety is pronounced in young children.
- Dyspeptic syndrome: nausea appears, giving way to repeated vomiting. Diarrhea may join at later stages.
- Pain syndrome: localized predominantly in the epigastric and umbilical regions. The pain is distending, diffuse, or cramping in character.
- Systemic manifestations: as the disease progresses, symptoms of intoxication and dehydration increase.
Diagnostics and differential diagnosis
The diagnosis is established primarily based on the clinical presentation. The main criteria are a characteristic anamnesis, acute onset of the disease, and the mandatory absence of «acute abdomen» symptoms.
Instrumental diagnostics in the form of endoscopy (EGD) is not routinely used and is prescribed only according to strict individual indications (depending on anamnesis, past biopsies, and the persistence of remission).
Special attention is paid to differential diagnosis. It is extremely important to exclude acute surgical pathology and exacerbation of peptic ulcer disease. Differentiation is especially critical if the patient experiences severe pain, pronounced intoxication, or if a full anamnesis cannot be taken.
Complex treatment
Therapy should be comprehensive and stepwise.
1. Emergency measures and regimen In the first hours, it is advisable to perform gastric lavage. During the first day, rehydration is carried out: warm fractional drinking in small portions is prescribed. Glucose-electrolyte solutions (dextrose + electrolytes), a combination of 0.9% sodium chloride solution with 5% dextrose, or low-mineralized water are used.
2. Diet therapy This is the basis of treatment. It is based on maximal mechanical, chemical, and thermal sparing of the mucous membrane. Return to the regular diet is carried out by the 5th–7th day.
3. Drug support (syndromic)
- Pain relief: myotropic antispasmodics (drotaverine, papaverine) and anticholinergics (platyphyllin, belladonna preparations, hyoscine butylbromide).
- Mucosal protection: non-absorbable antacids (aluminum phosphate, algeldrate + magnesium hydroxide).
- Detoxification: enterosorbents in a 7–14 day course (hydrolytic lignin, polymethylsiloxane polyhydrate, dioctahedral smectite).
- Antiemetics: prokinetics (domperidone, metoclopramide).
- Etiotropic therapy: antibiotics (aminoglycosides, co-trimoxazole) — strictly in case of a toxicoinfectious process.
4. Physiotherapy and sanatorium treatment To restore motility, sinusoidal modulated current (SMT) phoresis with prokinetics on the epigastrium is used; to correct autonomic status, electrosleep and decimeter-wave therapy on the collar zone are used. During remission, treatment in specialized sanatoriums (Caucasian Mineral Waters, Leningrad Oblast) is indicated. Surgical correction is resorted to extremely rarely, in case of treatment resistance and a drop in quality of life.
Prognosis, complications, and follow-up (dispensary observation)
In pediatric practice, the outcome of acute gastritis is predominantly favorable, with the disease ending in complete recovery. The exception is gastritis associated with Helicobacter pylori, which naturally transforms into a chronic form.
Specific complications include erosive and ulcerative bleeding (and subsequent post-hemorrhagic anemia) and the formation of esophageal strictures. The presence of Barrett's esophagus requires strict oncological vigilance due to the risk of developing adenocarcinoma or squamous cell carcinoma.
Dispensary observation is carried out by a pediatrician and a gastroenterologist (examinations at least 2 times a year). If there is a risk of extraesophageal manifestations, a dentist, ENT specialist, cardiologist, and pulmonologist are involved.
The rule of the three «S»s of diet therapy: for rapid mucosal recovery, it is necessary to provide thermal, mechanical, and chemical sparing.
Class and exam questions
Does acute gastritis always end in complete recovery?
In most cases, yes. However, if the inflammation is caused by the bacterium Helicobacter pylori, the process naturally transitions into a chronic form.
Is mandatory EGD required?
No, there are no rigid standards for the frequency of endoscopy in acute gastritis. The study is prescribed strictly individually according to indications.
When can a child return to normal nutrition?
With proper adherence to the treatment regimen and diet therapy, a return to the regular diet is usually achieved by the 5th–7th day of the disease.
What else to study on this topic
- Mechanisms of corrosive gastritis formation
- Esophageal strictures and post-hemorrhagic anemia
- Extraesophageal manifestations of gastroesophageal reflux
- Barrett's esophagus: pathogenesis and malignancy risks
- Acute renal failure and sepsis as causes of secondary gastritis
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