GASTROENTEROCOLITIS (gastroenterocolitis; grech, gaster a stomach + enteron a gut + kolon a colon + - itis) — an acute inflammatory disease of all went. - kish. a path with preferential defeat of thin or thick guts or their departments.
Distinguish G. infectious and noninfectious; carry also allergic to noninfectious.
Infectious G. can be a bacterial, virus, protozoan, fungal origin. Most often G. of a bacterial etiology meets (activators from group of salmonellas, and also conditionally pathogenic — colibacillus, proteas, etc.). The causal relationship of infectious G. is established with nek-ry viruses from Koksaki's group and ECHO (O. V. Baroyan, I. N. Gaylonskaya, 1962). The role of enteroviruses in infectious G.'s emergence is studied insufficiently.
Noninfectious, alimentary, G. arises hl. obr. as a result of disturbance of food. The allergic G. arising at the use of some foodstuff which is allergens is less often observed. Chemical poisons or medicines (derivatives salicylic to - you, Diuretinum, etc.) along with hron, damage of a stomach and guts can cause acute (medicamentous) G.
At infectious G. the pathogeny is defined by a type of the activator. The pathogenic agent always gets through a mouth. Reproduction and death of microbes ekzo-and endotoxins happen to education generally in intestines. Toxins make impact on a mucous membrane of a stomach and intestines and, getting into blood, cause the general intoxication of an organism. Special position is held by neurogenic exotoxins (see. Botulism , Dysentery ), the toxins breaking function of intestines, and first of all its epithelial cells (see. Cholera ), the toxins having necrotizing histologic effect (see. Amebiasis ). Some activators get into a mucous membrane of intestines, and from there into blood (see. Salmonelloses ).
In alimentary G.'s pathogeny paramount value has the acute disorder of digestive activity caused irrational (disturbance of a rhythm of food, an overeating, the use of very cold food, hot dishes, alcohol) or unilateral food (the excess use of the fatty products, carbohydrates especially rich with cellulose). In most cases alimentary G. arises at people with functional insufficiency of various links of the alimentary system (defects of the chewing device, insufficient secretory function of a stomach, pancreas and intestines, dyskinesia of intestines, frustration of a zhelchevydeleniye).
The allergic reaction to some food stuffs caused by both a food factor, and products of its splitting arises respectively soon after its use or in later terms.
The pathological anatomy
Pathological anatomy of noninfectious G. is characterized by inflammatory reaction of tissues of stomach and intestines (a hyperemia, hypostasis, the strengthened exudation, cellular infiltration, dystrophic changes of a superficial epithelium). Defeat went. - kish. a path can be generalized or localized. Preferential localization is caused etiol, a factor. Usually changes do not extend out of limits of a mucous membrane. Deeper layers are surprised at the long and complicated course of a disease.
At infectious G. development of dystrophic processes of parenchymatous bodies and emergence in them focal changes is observed (in case of bacteremia).
The clinical picture
the Clinical picture at all G. is characterized by the acute beginning and sudden development of the dispeptic phenomena. There are abdominal pains, diffuse or in a certain area, rumbling, a meteorism, an eructation, nausea and vomiting, lack of appetite. A chair the speeded-up liquid. Character of a chair depends on localization patol, process. At preferential defeat of small bowels plentiful allocation of the fecal mass of flavovirent color with impurity of slime, but without blood is marked. At microscopic examination the calla comes to light a syndrome of the broken digestion and absorption — a creatorrhea, a steatorrhea, etc. At preferential damage of a large intestine of kcal scantier, with a large amount of slime and it is frequent with impurity of blood, defecation more frequent, false desires become frequent, the koprologichesky research does not find the broken digestion and absorption. Disturbance of the main functions of intestines is characteristic: digesting, vsasyvatelny and motive. Excess allocation with an emetic and fecal mass of water and salts can lead to disturbance of water and electrolytic balance, dehydration and desalting of an organism (see. Water salt metabolism , Dehydration of an organism ). Quantitative ratios of microorganisms of intestines change, i.e. develops dysbacteriosis (see). At a palpation of a stomach the sites of a spazmirovanny large intestine alternating with the loops of guts stretched by a stake and gases are defined.
At infectious G., except the specified symptoms, symptoms of toxicosis appear. In the hard cases which are followed by sharp toxicosis the liver increases, easy yellowness of scleras is observed. At generalized forms of a disease with bacteremia the liver and a spleen are increased. The phenomena of acute vascular insufficiency can develop.
Noninfectious G. proceeds easier, than infectious. Clear symptoms of toxicosis are absent. Slime in Calais contains in small amounts, blood, as a rule, is not found.
Allergic G. arises suddenly, proceeds violently, with temperature reaction, quite often in combination with other allergic manifestations. Positive skin tests with allergen and Prausnitts's reaction — Kyustnera are characteristic (see. Prausnittsa-Kyustnera reaction ). The quantity of eosinophils in blood increases.
the Diagnosis is made on the basis epidemiol, the anamnesis, clinical symptomatology, results of tool inspection, data serol, blood analyses, bacterial. researches calla and emetic masses. At suspicion on the virus nature of a disease are carried out corresponding virusol. researches. If necessary carry out allergol. inspection.
Found at rektoromanoskopiya (see) changes of a mucous membrane of sigmoid and direct guts differ in a big variety that is connected with localization patol, process. At dominance of enteritis the diffusion catarral changes which were more expressed in proximal department, occasionally with dot hemorrhages come to light. At dominance of colitis the picture from moderately expressed catarral to a fibrinous inflammation in combination with focal changes of a mucous membrane as hemorrhages, erosion and ulcers can be observed.
At differential diagnosis it is necessary to consider that G. is frequent display of acute intestinal infectious diseases. However at some infections, napr, at tuberculosis, also secondary specific damage of a digestive tract is possible. G.'s symptoms can accompany also a number of acute conditions of an abdominal cavity (appendicitis, cholecystitis, pancreatitis etc.) that can conduct to diagnostic mistakes.
Both in the acute period of G., and in the period of reconvalescence is shown decrease in functional loads on bodies of the alimentary system, in particular on intestines; it is reached by a diet and a sparing diet. It is necessary to eat food 4 — 5 times a day in a warm look in the small portions. In 1 — the 2nd day of a disease food of the patient, as a rule, is sharply limited: mucous rice or oat soups, beef-infusion weak broth, liquid porridges on water with butter, fruit and berry kissels or jelly, white crackers. Drink (unsweetened tea with a lemon, alkaline still mineral waters, broth of bilberry, a dogrose) is not limited. At the expressed intoxication recommend only drink (to 2 l) within 1 — 2 days. With 3 — the 4th day at improvement of a condition of the patient transfer to a diet No. 4 (see. Clinical nutrition ), and in 7 — 10 days — gradually on usual food.
The gastric juice, fermental drugs contributing to normalization of digestion and absorption are shown. For recovery of a homeostasis, disturbance to-rogo is generally connected with loss of significant amounts of water and salts, administration of solutions of salts in the large volumes corresponding to losses is required. Usually dehydration at G. has isotonic extracellular character. For the purpose of a regidratation use of solutions trisol, kvartasol and Ringera is more proved.
Make drop intravenous injection of isotonic solutions of salts and glucose for desintoxication (to 2 — 3 l), Haemodesum (100 — 250 ml), a blood plasma or its substitutes (100 — 200 ml), a hydrocortisone (125 mg) or Prednisolonum (30 mg). At suspicion on availability of bacterial toxins do a gastric lavage. Use drugs of a tetracycline row, ampicillin and levomycetinum, and also derivatives of nitrofuran (furasolidone) and 8 oxyquinolines (Enteroseptolum, 5-HOK). Use of the knitting, enveloping and adsorbing means is shown.
The importance, especially at allergic G., has use of antihistaminic and antiallergic drugs (Suprastinum, Pipolphenum, Dimedrol, Stugeronum). At dysbacteriosis appoint biol, the drugs promoting recovery of normal flora of intestines (kolibakterin, bifidumbacterium, bifikol).
the Acute period of infectious G. is short, the disease usually comes to an end with recovery. The complete recovery of function of intestines occurs in 3 — 6 weeks after subsiding of the acute phenomena and depends on weight of the postponed disease. Acute G. of an alimentary etiology comes to an end with recovery in 5 — 7 days at the correct dietotherapy. In some cases (if G.'s disease was preceded by functional insufficiency of a stomach or intestines, a disease of bodies of the alimentary system, including helminthoses) after the postponed acute infectious G. can develop hron, gastritis, hron, a coloenteritis.
Prevention: balanced diet, observance dignity. - a gigabyte. conditions at preparation and storage of food, observance of rules of personal hygiene.
Bibliography: Baroyan O. V. igaylonsky I. N. Intestinal viruses and diseases caused by them, M., 1962; B to an e-spinning top. And. N. I iyekisenina. Chronic enterita and colitis, M., 1975, bibliogr.; Ghukasyan A. G. Diseases of intestines, M., 1964; Menshikov F. K. Diseases of intestines, M., 1962; The Multivolume guide to internal diseases, under the editorship of E. M. Tareeva, t. 4, M., 1965; Tashevt., etc. Stomach diseases, intestines and a peritoneum, the lane with bolg., Sofia, 1964; The differential diagnosis of diarrhea, ed. by S. M. Mellinkoff, N. Y. a. o., 1964; Grady G. F. a. To eu s with h G. T. Pathogenesis of bacterial diarrheas, New Engl. J. Med., v. 285, p. 831, 891, 1971, bibliogr.; Phillips S. F. Diarrhea a current view of the pathophysiology, Gastroenterology, v. 63, p. 495, 1972.
E. A. Beyul; V. P. Mashilov (inf.).