Etiopathogenetic therapy of acute viral etiology in children

In 1972, the Norwalk virus (norovirus) was discovered in Ohio, USA, as a causative agent of gastroenteritis in children. The role of rotavirus as an etiological factor of diarrhea was first established in animals in the 1950s. In 1973, rotavirus was detected in the coprofiltrate of children with gastroenteritis, and its role as an etiological factor was proven. In subsequent years, the etiological structure of viral diarrheas expanded significantly. It was established that human viral diarrheas can be caused by infectious agents such as astroviruses, sapoviruses, coronaviruses, toroviruses, adenoviruses (serotypes 31, 40, 41), Coxsackie A enteroviruses (serotypes 18, 20, 21, 22, 24), ECHO- and reoviruses, as well as influenza A virus (H5N1), bocaviruses, and others [1—5].

Rotaviruses are the cause of more than 125 million cases of childhood gastroenteritis and approximately 440,000 fatal outcomes annually. In the United States, up to 23 million cases of diseases caused by noroviruses are registered annually, with up to 300 fatal cases among them [6, 7, 8]. In Russia, the proportion of viral diarrheas in the overall structure of AII incidence in children ranges from 18—24% in the summer to 70—78% in the autumn-winter-spring period. In Moscow, group A rotaviruses (54.3%), noroviruses of the 2nd genotype (25.2%), and adenoviruses (13.2%) are the most common, while astroviruses (4.5%) are less frequent, and group C rotaviruses, noroviruses of the 1st genotype, and sapoviruses account for 1—1.2% of cases each [9—11].

Regardless of the etiological factor, viral enteritis and gastroenteritis proceed as osmotic-type diarrhea. The "trigger" mechanism of diarrhea and the infectious process is based on disaccharidase (primarily lactase) deficiency, which develops as a result of virus replication in the epithelial cells of the small intestine. As a result of enzymopathy, undigested carbohydrates (disaccharides) are not absorbed, accumulate in the intestinal lumen, and, having high osmotic activity, prevent water absorption from the intestine. Under the influence of microflora, disaccharides undergo fermentation, accompanied by the formation of a large amount of gas (fermentative dyspepsia - flatulence). Increased gas formation contributes to the appearance of pain syndrome and accelerated intestinal peristalsis - "watery" diarrhea. The severity and outcome of the disease depend on the presence and severity of toxemia and exsicosis (dehydration) (Fig. 1).

The diseases have a pronounced seasonal character (autumn-winter period), and predominantly affect young children. An acute onset is characteristic, with an increase in body temperature (up to 38—39°C) and repeated vomiting. Simultaneously or after a few hours, loose, copious, watery stools of yellow or yellow-green color appear, undigested, often foamy or explosive, up to 10—15 or more times a day. Abdominal pain is mainly associated with increased gas formation, has a cramping character, and is usually accompanied by rumbling in the abdomen. Pathological impurities in the stool (mucus, greens, blood) are absent, and the stools often have a sharp, sour smell.

Viral gastroenteritis is most often recorded in children aged 6 months to 3 years. It is at this age that the risk of infection and severe disease course with the development of severe dehydration and possible fatal outcome is highest.

Recently, along with the study of the etiological structure, features of clinical manifestations, and pathogenesis of viral diarrheas (Fig. 1), issues of strategy and tactics for complex therapy are being studied. Etiopathogenetic therapy is built mainly based on pathophysiological concepts of the mechanism of diarrhea and infectious process development (Fig. 2).