Ulcerative colitis pathological anatomy. Nonspecific ulcerative colitis macropreparation. Loose stools give way to constipation

(Colitis ulcerosa)

Nonspecific ulcerative colitis is a disease characterized by a chronic inflammatory process, the development of hemorrhages, ulceration and pus formation in the rectum and colon.

Etiology has not been completely clarified. Infectious factors (diplostreptococcus, non-spore-bearing anaerobes, staphylococcus, Escherichia coli, Proteus, fungi, viruses), intestinal dysbiosis of any origin, effects on the mucous membrane of proteolytic enzymes (trypsin, lysozyme), nutritional factors (vitamin U deficiency), damage to the intramural nervous system play a role. apparatus, disturbance of local blood and lymph circulation, neuropsychic overstrain, endocrine disorders (adrenal cortex insufficiency, activation of the ovarian system), exogenous allergies, disruption of autoimmune processes, changes in the connective tissue of the colon wall (collagenosis type).

Pathogenesis. The above factors cause sensitization of the colon mucosa and the occurrence of the process of autoimmune aggression. Subsequently, the development of a reaction between the autoantigen (colon wall) and antibodies leads to new pathological changes in various parts of the colon. Favorable conditions are created for the activation of intestinal flora and the addition of a secondary infection. The pathological process in the colon has an inhibitory effect on the function of the adrenal cortex, causes fatty degeneration of the liver, increases the number of mast cells in the colon mucosa with the release of biologically active substances from them (serotonin, histamine, hyaluronic acid), which contributes to the progression of the disease.

Morphologically, deformation of the colon (shortening, narrowing of the lumen), swelling and hypermia of the mucous membrane, multiple erosions, ulcers of various sizes, petechial hemorrhages, “fringed” pseudopolyps are observed. The process is localized more often in the distal sections.

According to the clinical course, there is an acute form, a chronic recurrent form (which can be in the phase of exacerbation, subsiding exacerbation, remission), and a chronic continuous form. Depending on the prevalence, there can be a total or segmental lesion (left-sided, transverse-colic, right-sided). Based on the nature of the damage to the colon, a distinction is made between superficial and deep (when there are ulcers, pseudopolyposis, sclerosis of the intestinal wall). Complications may include local (massive bleeding, toxic dilatation, perforation, peritonitis, polyposis, cancer) and general (anemia, endogenous dystrophy, sepsis, arthritis, phlebitis, skin lesions).

Clinic. The disease can begin in different ways:

1. Like acute dysentery with frequent loose stools, an admixture of mucus and blood, tenesmus.

2. With intestinal bleeding with formed or mushy stools (hemorrhoid-like onset).

3. With general malaise, weakness, prolonged low-grade fever (flu-like onset).

Total damage to the colon is characterized by frequent (up to 20 or more times a day) loose stools with blood and pus, sometimes with mucus; cramping pain in the abdomen, often in the area of ​​the sigmoid and rectum, bloating.

On examination - sudden weight loss, dehydration, trophic disorders, swelling of the legs (hypoalbuminemic). The tongue is coated. The abdomen is swollen or retracted, a sharply spasmodic and painful sigmoid colon or other parts of the large intestine are palpated. Low-grade body temperature.

Right-sided segmental lesions of the colon are characterized by moderate diarrhea (3-7 times a day), often bowel-like stool consistency, and cramping pain in the right iliac region. Discharge of blood and pus with feces is rare. With left-sided segmental lesions of the colon, stool disturbance is often manifested by constipation or alternating constipation and diarrhea; weight loss is less pronounced.

From other organs, gastric achylia, liver degeneration, dystrophic changes in the pancreas, kidney damage (urolithiasis), and mental disorders are observed.

In the blood: often hypochromic anemia, a tendency towards leukopenia, a sharp shift in the leukocyte formula to the left, an increase in ESR, hypoalbuminemia, hypokalemia, a decrease in the plasma levels of vitamins PP, B1, B2, increased transaminase activity. A scatological examination reveals leukocytes, erythrocytes, epithelium, and unchanged muscle fibers. Increased levels of enterokinase and alkaline phosphatase in feces.

X-ray examination reveals the absence of haustrations, jagged contours of the intestine, spasms, thickening of the folds, restructuring of the mucosal relief, narrowing of the lumen, shortening of the intestine, multiple filling defects (pseudopolyps).

During sigmoidoscopy - hyperemia, granularity and swelling of the mucous membrane, minor erosions, cryptabscesses, ulcers, bleeding when touched, purulent exudate, pseudopolyps.

Differential diagnosis. From bacillary dysentery Nonspecific ulcerative colitis is distinguished by: a) special severity of the course; b) early numerous complications; c) negative multiple bacteriological results; d) lack of rapid effect from antibacterial therapy; e) unusual bleeding of the rectal mucosa during sigmoidoscopy; f) pronounced radiological changes.

From amoebiasis this disease is distinguished by: a) rapid development of the clinical picture; b) severe intoxication; c) disturbance of general condition, anemia, exhaustion; d) the nature of the stool (in the form of meat slop with copious purulent discharge); e) sigmoidoscopy data (in case of amebiasis - ulcers with undermined edges, an uneven greasy bottom and a belt of hyperemia around against the background of unchanged mucosa); f) the results of an X-ray examination (amoebiasis is characterized by intermittent lesions and the absence of pseudopolyps); g) negative results of stool examination for the presence of amoebas.

From balantidiasis this disease is distinguished by: a) endoscopic picture of the mucosa (with balantidiasis, large slit-like ulcers with jagged edges and white loose plaque, hemorrhages against the background of unchanged mucosa); b) microscopic examination of stool (absence of ciliates).

From ulcerative tuberculosis of the colon Nonspecific ulcerative colitis can be distinguished by: a) localization of the process (in tuberculosis the left parts of the colon are rarely affected); b) its nature (tuberculosis is characterized by a diffuse type of lesion - ulcers of various sizes with undermined edges and a curdled bottom, located at a considerable distance from each other, the mucous membrane between them is slightly changed, the semilunar folds are preserved); c) absence of tuberculous lesions of other organs.

Treatment.

I. Bed rest.

II. Diet No. 4 (limiting fiber, fat to 50-75 g per day, increasing protein to 150 g/day, vitamins).

III. Drug treatment:

a) antibacterial therapy: sulfasalazine 1.5-2.0 4 times a day until acute pain subsides, then 0.5 3-4 times a day for several months; salazopyridazine or salazodimethoxin 0.5 4 times a day for 3-4 weeks, subsequently 0.5 2-3 times a day for 2-3 weeks (stage I of treatment);

b) immunosuppressive therapy: corticosteroids in minimally effective doses (starting from 15 mg per day) for 1-1.5 months; immunosuppressants (azathioprine 0.05 2-3 times a day for 2-3 weeks).

Indications for stage II therapy, i.e. the inclusion of steroids during stage I therapy is: 1) lack of a clear positive effect from therapy without steroids for 3-4 weeks; 2) severe course of the disease, where watchful waiting is impossible; 3) anamnestic evidence that previous therapy without steroid hormones was ineffective; c) to combat intoxication and dehydration - parenteral administration of saline, isotonic solution of potassium chloride, glucose, plasma (up to 500-1000 ml), albumin (50 ml), blood transfusions, vitamins B, C, K, anabolic steroids;

d) normalization of intestinal motility - anticholinergics, antidiarrheal drugs (reasec, codeine, opium tincture);

e) normalization of the nervous system - sedatives;

f) local treatment - in the subacute period: hydrocortisone emulsion (50 mg in 100-300 ml of saline), prednisolone (30 mg in 50 ml of warm distilled water), enemas with protargol, collargol, dermatol, rivanol, silver nitrate, sage infusions , chamomile, rosehip, caratolin, Shostakovsky balm, sea buckthorn oil, tanalbin, soda.

IV. Surgery. Absolute indications: 1. Perforation of the colon (or its threat). 2. Diffuse pseudopolyposis. 3. Carcinomatous degeneration. 4. Abscesses and fistulas. 5. Irreversible changes in the intestine (stricture, etc.). 6. Massive intestinal bleeding.

Relative indications: 1. Segmental damage to the intestine. 2. Frequent exacerbations. 3. Insufficient effectiveness of conservative therapy. 4. Systemic lesions (erythema nodosum, arthritis, uveitis, iritis, hepatitis, etc.).

The course of the disease is wavy. Spontaneous remissions are possible.

Work ability examination. Most patients during the period of remission are able to work. In severe cases of the disease, transfer to disability is indicated.

The prognosis varies. Recovery is possible. In severe forms, mortality reaches 18-27%.

GUT DYSBACTERIOSIS

(Dysbacteriosis)

The human body is in constant interaction with the environment. Of the huge number of microorganisms that continuously enter the human digestive tract, only certain types of microbes have found favorable living conditions in it; in the process of long evolution, they became established in the intestine and constituted its obligate flora, which performs important physiological functions for the body.

Normal intestinal flora performs a protective function in the body, vitamin-forming, enzyme, and also stimulates the immunological resistance of the body. Individual factors, such as the nature of nutrition, season of the year, age, have some influence on the composition of the intestinal microflora, but these fluctuations are small, and the ability of a healthy body to self-regulate ensures the rapid restoration of the relative constancy of the biocenosis. There are certain criteria and standards for the quantitative and qualitative composition of microflora. A condition in which the composition of the microflora in different areas does not exceed these criteria is called eubiosis.

The microflora in the stomach and small intestine is extremely poor, while the thick section contains a huge number of microorganisms. It is estimated that in the human colon there are approximately 1.5 kg of microorganisms, and in 1 g of feces up to 250 billion. According to Coandi, a person excretes over 17 trillion microbes per day with feces and by weight they make up 1/3 of dry feces.

Obligate, i.e. constant for the colon are anaerobes - B. Bifidum et Bacteroide and aerobes - Escherichia coli (Esherichia), Lactobacterium et Enterococcus.

The number of anaerobes is stable and averages 1-10 billion cells per 1 g of feces. They account for 95% of all intestinal flora. The number of aerobes is less constant and amounts to tens and hundreds of millions per 1 g of feces (on average 1-3 million).

The composition of the optional group is highly variable. This includes lactose-negative enterobacteria, staphylococci, Proteus, fungi, etc. Many of them stay there for a longer time, but normally do not exhibit a pathogenic effect.

Under certain conditions, all representatives of normal microflora, with the exception of bifidobacteria, have the ability to cause diseases.

The relationship between a macroorganism and its microflora is very great. Normal microflora influences the structure of the intestinal mucosa and its adsorption capacity. The presence of microflora doubles the process of renewal of the intestinal mucosa. The role of intestinal microorganisms in the metabolism of fatty acids, the metabolism of lipids, bile acids, bilirubin, water-salt metabolism and gas exchange is important. Microorganisms are also involved in many other enzymatic reactions. Microorganisms synthesize up to 9 different B vitamins: B1, B2, B6, B12, nicotinic, folic, pantothenic and other acids, vitamin K. Normal microflora plays an important role in creating immunity in the host. Its absence causes a weakening of both cellular and humoral factors of immunological defense. Normal microflora, due to the production of antibiotic compounds and pronounced antagonistic activity, protects the body from the introduction of pathogenic flora. Thus, bifidobacteria have an antagonistic effect on the development of putrefactive flora, and E. coli inhibits staphylococci, Proteus, Vibrio cholerae, etc. Thus, the activity of microflora is inextricably linked with important functions of the body. The macroorganism, in turn, regulates the composition of the microflora.

A stable violation of the species spectrum of the quantitative ratio and qualitative characteristics of microorganisms of the obligate and facultative groups is called dysbacteriosis. Those. Dysbacteriosis, in contrast to eubiosis, is understood as a violation of microbial balance in the intestine. Quantitative changes are manifested by the disappearance or sharp decrease in the number of bifidobacteria, a decrease or significant increase in the number of E. coli and enterococcus. Qualitative - the appearance of hemolytic and lactose-negative strains of Escherichia coli, pathogenic staphylococci and streptococci, Proteus, and Candida fungi.

G.T. Kuznetsova identifies the following stages of disturbance of biocenosis in the intestine: Stage I - reduction in the number or elimination of anaerobic microorganisms; Stage II - against the background of a decrease in the number of anaerobes, the colibacterial flora changes sharply, the number of atypical Escherichia (lactose-negative and hemolytic strains, as well as E. coli with reduced enzymatic properties) increases; Stage III - against the background of the two previous shifts, associations of hemolytic microorganisms are found in large numbers; Stage IV - the addition of abundant growth of bacteria of the genus Protea.

The reasons for microbial imbalance can be very different. For the regulation of intestinal microflora, the normal function of the digestive glands and the acidity of the stomach contents are crucial. With a decrease and absence of acid in the gastric contents, as well as with a weakening of the enzymatic systems of other digestive organs, a change in the bacterial flora occurs. As a result, the stomach and proximal small intestine can become colonized by various microorganisms. In addition, saprophytic microbes living in such conditions can acquire pathogenic properties. Reducing general resistance, vitamin and protein starvation are of great importance.

Over the past 20 years, drug-induced intestinal dysbiosis has become especially important. Disruption of the symbiotic balance in the intestinal microflora can occur under the influence of antibiotics and tuberculostatic drugs.

The development of dysbacteriosis depends on toxic and allergic factors, hereditary predisposition, the patient’s age, living and working conditions, nutrition, previous diseases, previous treatment, and the body’s immunological defense reactions.

Toxic damage to the intestine, as well as its sensitization, create favorable conditions for disruption of the eubiotic balance in the intestine. The spread of microbes into the proximal parts of the gastrointestinal tract is one of the factors that contribute to the maintenance of inflammatory processes in the mucous membrane, disruption of the motor and secretory functions of the intestine, which negatively affect the digestive processes and cause clinical manifestations of the disease.

With dysbacteriosis, not only cavity digestion suffers, but also parietal digestion. During the inflammatory process of the mucous membrane, the intensity of epithelial regeneration decreases, this leads to progressive atrophy of the mucosa, a decrease in the adsorption capacity of epithelial cells, parietal digestion is disrupted, which, in turn, leads to the accumulation of incompletely hydrolyzed products in the intestinal lumen, an increase in osmotic pressure, enteral syndrome - diarrhea, rumbling in the intestines, bloating. In parallel with this, colon dysfunction develops. In addition to the local and general effects of bacterial metabolic products and toxins, the ability of microorganisms to inactivate digestive enzymes coming from the proximal intestine is lost; they are excreted in large quantities with feces. The consequence of dysbacteriosis is a decrease in the intensity of endogenous bacterial synthesis of essential vitamins and their intestinal absorption, and metabolism is disrupted. Dysbacteriosis should be considered in terms of the development of sensitization and allergization of the diseased organism, which, in turn, can cause a protracted course of inflammatory diseases of the digestive tract.

A.F. Bilibin identifies the following forms of dysbacteriosis:

1. Compensated or latent dysbiosis, when the body does not respond to a violation of eubiosis.

2. Subcompensated dysbacteriosis, characterized by the appearance of a local inflammatory process.

According to the degree of severity: mild dysbiosis, in which there is a moderate imbalance in the ratio of E. coli and paraintestinal, and pronounced dysbiosis - E. coli makes up 50% of the intestinal group in the presence of Proteus, hemolytic colonies, and there is also a pronounced dysbiosis, characterized by a significant decrease in normal intestinal coli (less than 30%) or a predominance of staphylococcus, Proteus, fungi.

By type: staphylococcal, proteaceous, yeast, associated.

At mild dysbacteriosis body temperature is normal. The stool is mushy, 2-3 times with mucus, abdominal pain, the sigmoid colon may be spasmodic. The stool is restored within 20-40 days. No intoxication is observed. Sigmoidoscopy reveals a picture of severe catarrhal inflammation. There is normocytosis in the blood.

Medium-heavy. Low-grade fever, sometimes high, nausea, vomiting (more often with staphylococcal dysbacteriosis). Loose stools, 4-7 times with mucus and pus, abdominal pain, spasmodic sigmoid colon. Intoxication is moderate. Stool restoration - within 30-50 days. Sigmoidoscopy reveals a picture of catarrhal, hemorrhagic and ulcerative proctosigmoiditis. In the blood - leukocytosis, band shift, accelerated ESR.

Heavy. High temperature, chills (with staphylococcal dysbacteriosis). Loose stools 10-12 times or more, mucous-bloody, mixed with pus. There is tachycardia, a drop in blood pressure, and severe intoxication. Increased ESR, hypoproteinemia and hypocholesterolemia. In the urine - protein, red blood cells, white blood cells. With sigmoidoscopy - catarrhal, hemorrhagic, ulcerative and erosive proctosigmoiditis.

The duration of the disease is from 3 to 9 months or more. The disease can occur with bacteremia, and subsequently with the development of sepsis and septicopyemia, more often with staphylococcal dysbacteriosis.

Proteus dysbiosis is mainly a local lesion of the intestine. The course of the underlying disease, complicated by Proteus intestinal dysbiosis, is usually mild or moderate. Sepsis is rare. Much more often, generalization occurs with staphylococcal dysbiosis.

Candidiasis of the intestine is usually combined with other clinical manifestations of candidiasis (seeds, thrush, raspberry tongue).

Intestinal dysbiosis, which occurs as a result of the association of staphylococcus with other microbes, is especially severe.

Dysbacteriosis can be assumed in cases of persistent and difficult to treat chronic colitis, intestinal dysfunction in patients with chronic pancreatitis, long-term use of antibiotics for various diseases, but the final diagnosis is confirmed by bacteriological examination of stool.

The simplest qualitative research method. It allows us to identify qualitative changes in obligate and facultative flora. It is based on determining the percentage of microorganism colonies.

The method that meets the clinical requirements is a quantitative method with mandatory culture for bifidobacteria. It also makes it possible to detect a decrease or increase in the content of Escherichia coli, its hemolytic or lactose-negative strains, and the amount of staphylococcus and enterococcus. The method is based on the calculation of these microorganisms per 1 g of feces. This technique does not involve quantitative accounting of Proteus. Detection of Proteus in any quantity is a manifestation of intestinal dysbiosis.

The state of anaerobic flora (bifidobacteria) is determined by indicating the minimum dilution in which it is detected. Evidence of the presence of dysbacteriosis is the absence of growth of bifidobacteria at a dilution of 10 -7, a sharp decrease in the amount of E. coli (less than 1 million) with an average content of 300-400 million on Endo and Levin media and 800 million on blood agar, the appearance of hemolyzing E. coli , lactose-negative Escherichia more than 20 million/g, hemolyzing Staphylococcus and Proteus, Candida fungi, as well as in cases where the coccal flora makes up more than 25% of the amount of E. coli.

Treatment of dysbiosis is carried out in combination with the treatment of the underlying disease and the use of agents that directly affect the intestinal flora. Treatment should be differentiated taking into account the characteristics of the clinic. Main directions in treatment:

1. Increase the body's resistance.

2. Influence one or another opportunistic microbe that causes dysbacteriosis.

3. Contribute to the normalization of intestinal microflora. Eubiotics (drugs that selectively act on pathogenic flora and spare normal flora) include enteroseptol, intestopan, mexaform, and mexase.

Among the bacterial ones - colibacterin, bifidumbacterin, bificol, lactobacterin, bactisuptil, etc.

Treatment begins with the prescription of eubiotics at a dose of 1-2 tablets 3 times a day for 7-14 days.

Staphylococcal and Proteus dysbacteriosis require the prescription of antibiotics in short courses - 5-7 days under the control of an antibiogram. For staphylococcal dysbacteriosis, erythromycin, oleandomycin, monomycin, sigmamycin, as well as staphylococcal toxoid and chlorophyllipt are prescribed. For Proteus - drugs of the furazolidone series (blacks); for fungal infections - levorin, nystatin 500,000 units 4 times a day for 10-12 days.

In the treatment of various forms of dysbacteriosis, sulfonamide drugs (sulgin, phthalazol, etazol) are widely used, 1 g 4-5 times for 5-7 days, repeating the course according to indications after 3-4 weeks. After antibacterial therapy, patients receive bacterial drugs for a long time.

At the first stage, when the anaerobic flora suffers, bifidumbacterin orally, 1 amp containing up to 10-50 million, 3 times a day 30-40 minutes before meals for 1.5-2 months. For associated forms - colibacterin 2-4 biodoses 4 times a day before meals, course of treatment - 4-6 weeks, in 1 amp. from 2 to 10 doses; bifikol - 1 bottle contains 300-400 million B. bifida + B. coli - 1 bottle 2 times a day. These drugs are well tolerated by patients, do not cause side effects and help normalize the intestinal microflora.

Special bacteriophages - Proteus 25-30 ml 2 times a day for 10-12 days; staphylococcal bacteriophage - 20-30 ml orally or in enemas for 5-7 days.

For chronic pancreatitis, liver cirrhosis, severe enteritis, enterocolitis, enzyme preparations are prescribed: pancreatin, panzinorm, polyzyme, festal. Due to the presence of vitamin deficiency in dysbacteriosis, treatment is supplemented with vitamin therapy (groups B, PP, C, K). The prescription of antihistamines is indicated, especially for clinical manifestations of allergies: diphenhydramine, diprazine, diazolin, tavegil.

Stimulating therapy: administration of antistaphylococcal plasma intravenously daily or every other day, 150-250 ml, 3-5 infusions. The administration of plasma is alternated with intramuscular injections of specific globulin, 3 doses every other day, from 5 to 10 injections, depending on the severity of the condition. With a relatively mild course of staphylococcal dysbacteriosis, which occurs with symptoms of bacteremia, you can use only g-globulin 1.5-3 ml IM 2-4 injections with an interval of 1-2 days.

If a violation in the immune status of the body is established, an imbalance is identified in the system of lipid peroxidation and antioxidant defense, tocopherol (vitamin E), which is a natural bioantioxidant, is prescribed - one capsule (0.1 a-tocopherol acetate) 3 times a day for four weeks. For patients with predominantly impaired cellular immunity, it is recommended to take sodium nucleinate at a dose of 0.8 once a day in two three-day courses with a three-day break. If humoral immunity is predominantly impaired (decreased levels of serum immunoglobulin A, increased immunoglobulin G and circulating immune complexes), prodigiosan is recommended: four injections per course of treatment with an interval of four days between them. The first two injections are 0.4 ml of a 0.005% solution, then 0.8 ml.

Rectal suppositories have proven effective in the treatment of dysbiosis; this is a complex immunoglobulin preparation (“CIP”), consisting of proteins and immunoglobulin fractions, 25% of which are immunoglobulin A. 5 suppositories are prescribed per course of treatment, one suppository is inserted into the rectum after stool or a cleansing enema at night every other day.

To prevent intestinal dysbiosis during antibiotic therapy, breaks between courses of antibiotics and periodic examination of stool for dysbiosis are necessary.

In patients with diseases of the gastrointestinal tract, stool must be examined for dysbacteriosis.

Early detection of dysbiosis (quantitative method) and timely treatment will help prevent serious complications.

CHRONIC PANCREATITIS

(Pancreatitis chronica)

The incidence of chronic pancreatitis has been steadily increasing in recent years in industrialized countries. The results of clinical observations show that the frequency of this disease ranges from 0.01 to 0.2%.

Etiology. Chronic pancreatitis is a polyetiological disease. The most common causes of its development are: alcoholism, diseases of the gallbladder and biliary tract, diseases of the duodenum, opisthorchiasis, allergies, hyperparathyroidism. In different countries, the frequency of one or another etiological factor in the development of chronic pancreatitis may be different.

The role of alcohol as a cause of the development of chronic pancreatitis is assessed by researchers ambiguously. While foreign authors consider alcohol to be the cause of the disease in 40-90% of cases, domestic researchers assign a more modest place to alcohol (5.4-9.0%). The mechanism of action of alcohol on the pancreas is not yet fully understood. According to some data, alcohol causes a direct toxic effect on the pancreatic parenchyma, increasing the viscosity and protein content of pancreatic secretions. At the same time, other authors believe that alcohol does not cause a direct cytotoxic effect on the secretory elements of the pancreas, but its effects are indirect. Indeed, numerous studies associate the adverse effects of alcohol with stimulation of the exocrine function of the pancreas, combined with retention of secretions in the ducts and an increase in intraductal pressure. In this case, an additional pathogenetic role is assigned to dietary violations.

Diseases of the gallbladder, biliary tract and liver as the cause of the development of chronic pancreatitis occur in 56.3% of cases. In addition, chronic pancreatitis occurs quite often (up to 25%) in people operated on for cholecystitis. The role of these diseases in the development of chronic pancreatitis is initially reduced to an increase in pressure in the pancreatic ducts, caused in some cases by microcholedocholithiasis, papillospasm, as well as biliary-pancreatic reflux, especially infected bile. In this case, the effect of pancreatic enzymes on bile leads to the formation of substances that cause bile toxicity. Experimental data with the introduction of infected bile into the pancreatic duct of dogs and the subsequent development of pancreatitis confirm the above pathogenetic mechanism.

A significant role in the development of chronic pancreatitis is also assigned to diseases of the duodenum, which is based on the classification of N.A. Zhukov distinguishes the “gastro-duodenal form” among the “combined forms” of chronic pancreatitis. In diseases of the duodenum (ulcer, duodenitis, diverticulitis), the main role in the mechanisms of development of chronic pancreatitis is given to the involvement of the sphincter of Oddi in the pathological process (inflammation, sclerosis of the large duodenal papilla, nipple polyposis, papillary diverticulitis, tumor), resulting in conditions for increased pressure in the duodenum. pancreatic ducts. With duodenal dyskinesia, especially with the development of duodeno-pancreatic and choledochal-pancreatic reflux, reflux of duodenal contents and bile into the pancreatic duct with an increase in intraductal pressure there can be observed. In addition, in recent years, in connection with the established role of the duodenum in the production of intestinal hormones involved in the regulation of the secretory function of the pancreas, attention has increasingly begun to be paid to their role in the development of chronic pancreatitis. The mechanism of these disorders comes down to the formation of antibodies to the duodenal mucosa and secretin in chronic duodenitis, followed by dysfunction of the pancreas.

Recently, science has received more and more evidence in favor of the viral etiology of development in some patients with chronic pancreatitis. Pancreatic viruses include Coxsackie B viruses and mumps viruses.

In addition, there are indications of the possibility of developing chronic pancreatitis in patients with hyperparathyroidism and lipid metabolism disorders. The issue of so-called “idiopathic pancreatitis”, the cause of which is unknown, is still unresolved. Meanwhile, such patients make up 20-30%.

So, the mechanism of the initial development of chronic pancreatitis is directly related to the etiological factor and is a trigger, which is followed by the inclusion of pathogenetic mechanisms in the pancreas itself, which ultimately shape the development of inflammatory processes in it.

Pathogenesis. The pathogenetic mechanism characterizing the processes occurring in the pancreas itself is represented by many links. The clinical and morphological picture of exacerbation of chronic pancreatitis, manifested by severe pain, release of pancreatic enzymes into the blood, edema and cellular infiltration of gland tissue, reflects the development of a typical inflammatory process in the organ. Moreover, the appearance of nucleic acid metabolism products in the urine during the same period indicates the destruction of the nuclear structures of the secretory elements in which the pancreas is so rich. All this indicates that in the pathogenesis of chronic pancreatitis, as well as acute pancreatitis, the triggering mechanism of the inflammatory process in the gland is the activation of intrapancreatic trypsin by enterokinase or infected bile thrown into the pancreatic duct. In this case, due to the activation of trypsin, a chain reaction occurs - A- and B-phospholipases are activated, converting bile lecetin into lysolycetin. The latter destroys the phospholipid layer of cell membranes, leading to coagulation necrosis.

A significant role in the pathogenesis of chronic pancreatitis is played by the kallikrein-kinin system of the pancreas, which is closely related to the proteolytic enzyme system of the organ. Thus, during the period of exacerbation of pancreatitis, there is an increased release of bradykinin from kininogen, an increase in the concentration of kallikrein in the blood, with a decrease in kallikreinogen, kallikrein inhibitor and alpha-2-macroglobulin in it.

Works in recent years increasingly point to the role of immunopathological processes in the pathogenesis of chronic pancreatitis, which is confirmed by the presence in the blood of patients of antibodies to the tissue and nuclear elements of the pancreas and an increase in the level of circulating immune complexes. Due to the fact that among patients with chronic pancreatitis there are people with and without changes immune to the pancreas, some researchers recommend differentiating immunopositive and immunonegative forms of chronic pancreatitis based on pathogenetic characteristics.

Since hypercoagulation phenomena are observed in chronic pancreatitis, microcirculation disorders in the pancreas with subsequent activation of proteolytic intrapancreatic enzymes play a certain role in the mechanisms of development of chronic pancreatitis.

Recently, a significant role in the pathogenesis of the disease has been assigned to the activation of lipid peroxidation processes in the membranes of pancreatic cells. As a result, the permeability of cell membranes increases, facilitating the release of lysosomal enzymes into the surrounding tissue of the organ with the additional generation of tissue elements.

Genetic factors also play a certain role. Thus, in patients with chronic pancreatitis, the frequency of detection of antigens of the HLA system A1, B8, B27, Cwl is increased and the frequency of antigens A2, Cw4 is reduced, which suggests the existence of genetically determined forms of the disease.

Clinic and diagnostics. In chronic pancreatitis, the most common complaints of patients are indications of pain in the epigastric region or left hypochondrium. The pain is often girdling in nature or radiates under the left shoulder blade, the left half of the lumbar region, or adjacent regions of the left half of the chest. However, it should be borne in mind that along with the above localization of pain, the latter can be in the right hypochondrium, due to exacerbation of cholecystitis, and in the upper half of the abdomen, associated with exacerbation of duodenitis or chronic colitis. The nature of pain for pancreatitis does not have any features different from other gastroenterological diseases. However, more often it is dull, pressing, difficult to relieve with antispasmodics, and deprives the patient of sleep.

In addition to pain, chronic pancreatitis is also characterized by dyspeptic disorders (decreased appetite, nausea, sometimes vomiting, bloating, impaired intestinal function), which become most pronounced during the period of exacerbation of the disease. The highest frequency and duration of dyspeptic disorders is observed in long-term patients with pancreatitis, which occurs with frequent relapses. The cause of the development of dyspeptic disorders in chronic pancreatitis is exocrine pancreatic insufficiency, which causes impaired digestion and absorption in the intestine, and also leads to the development of intestinal dysbiosis and impaired intestinal motor function.

It is important for the diagnosis of chronic pancreatitis to indicate to patients weight loss, sometimes quite significant. The main reasons for weight loss are considered to be disturbances in the processes of digestion and absorption and excessively strict adherence to the diet by patients.

Symptoms such as jaundice, hypoglycemic manifestations, glucosuria, fever are rare in chronic pancreatitis.

Of the methods of physical examination of patients necessary to diagnose the disease, special attention should be paid to palpation of the pancreas. If it can be palpated, then the severe pain that occurs during palpation acquires diagnostic significance. The latter is often so intense that patients involuntarily begin to cry. The gland itself, depending on the degree of morphological (sclerotic) changes, can be palpated in the form of varying degrees of density of a transversely located cord. This diagnostic technique can also be valuable if the gland itself is not palpable, but the patient notes pain in the area where it is located. In some cases, this technique is most effective when the patient is standing with the torso quickly tilted in the direction of the palpated arm.

Other methods of physical examination described in textbooks, due to their low diagnostic value, have not justified themselves in practice.

Since chronic pancreatitis has a pathogenetic connection with a number of gastroenterological diseases, indicating to the patient that he has opisthorchiasis, cholelithiasis, duodenal ulcer, cholecystectomy, and allergic diseases can have diagnostic value. An essential point in diagnosing a disease may be identifying the cause of its exacerbation. Pancreatitis is characterized by its exacerbation after eating fatty foods, overeating, drinking alcohol, and exacerbation of cholecystitis.

Due to the fact that the clinical manifestations of chronic pancreatitis are in many ways similar to the symptoms of other diseases of the digestive system, there is a need to carry out a wide range of differential diagnostic techniques to exclude other gastroenterological diseases. Among them, the following require exclusion first of all: cholelithiasis, cholecystitis, opisthorchiasis, peptic ulcer of the stomach and duodenum, cancer of the digestive organs, erosive gastritis and duodenitis, enterocolitis, etc. This necessity obliges the doctor to use a whole range of additional research methods: x-ray, endoscopic , ultrasound, in some cases computed tomography, etc.

However, even the identification of one or more of the listed diseases does not completely exclude their combination with chronic pancreatitis. Therefore, a necessary condition for its diagnosis is not only the exclusion of other diseases of the digestive system, but also confirmation of pancreatitis by functional and instrumental research methods.

Diagnostic tests for chronic pancreatitis. All diagnostic tests, according to the purpose of their use, should be divided into 2 groups: those capable of identifying the activity of the inflammatory process in the pancreas (exacerbation of pancreatitis) and those reflecting the morphological and functional changes in the organ that have arisen in the pancreas as a result of chronic inflammation.

Diagnostic tests to detect exacerbation of chronic pancreatitis are based on the determination of pancreatic enzymes and a number of biochemical ingredients in the blood and urine, the level of which increases there due to inflammatory damage to the secretory elements of the pancreas. These include the determination of diastase in the urine, trypsin in the blood, and products of nucleic acid metabolism in the urine that appear in it as a result of the destruction of the acinar structures of the gland rich in nuclear substance.

In addition, our studies give reason to recommend for the diagnosis of exacerbation of chronic pancreatitis the study of lipid peroxidation processes (Schiff bases and diene conjugates). Their content in the blood increases during exacerbation of the disease, reflecting the activation of lipid peroxidation processes. The resulting damage to the cell membranes of the secretory elements of the pancreas causes an increase in their permeability and promotes an increased release of pancreatic enzymes into the blood.

Determination of the level of circulating immune complexes in the blood can be used as a diagnostic test for exacerbation of the disease. Their increased formation during exacerbation of pancreatitis is associated with pronounced destructive processes in the pancreas and the release of tissue antigenic structures into the blood, in response to which antibodies are formed and circulating immune complexes are formed.

Indicators of the level of trypsin in the blood, Schiff bases, diene conjugates, and circulating immune complexes can also be used to monitor the effectiveness of treatment. At the same time, according to the transition of exacerbation of the disease into remission, the levels of indicators decrease.

Methods for studying the pancreas that can reveal its structural and functional changes include ultrasound, X-ray, endoscopic research methods, as well as a significant number of functional research methods based on assessing the enzyme-forming function of the pancreas after its stimulation.

Thus, the method of ultrasound examination of the pancreas allows, according to our data, to detect changes in the organ in the structure of its echo density in 60% of patients with chronic pancreatitis.

The X-ray method also quite often reveals valuable indirect symptoms indicating chronic pancreatitis, such as deformation of the stomach with the formation of a bend and depression along the posterior wall of the body and the greater curvature of the gastric outlet, enlargement of the duodenal ring or calcification of the gland. With relaxation duodenography, it is possible to detect expansion of the duodenal ring, depression along the entire contour of the descending part of the duodenum and the “backstage” symptom due to uneven pressure on the intestinal walls of the enlarged head of the pancreas.

Gastroduodenoscopy has received a positive assessment as a method that helps diagnose chronic pancreatitis. With its help, it is possible to identify changes in the contours of the stomach and duodenum due to an enlargement of the pancreas, the presence of papillitis, lymphangiectasis in the descending part of the duodenum, etc.

Among the functional methods of studying the pancreas, the simplest, although not always indisputable, is the assessment of the coprogram by the presence of steatorrhea and creatorrhoea. The latter reflect the development of exocrine pancreatic insufficiency due to disruption of the processes of digestion and absorption.

In the practice of non-specialized therapeutic departments, the proserine test, proposed in 1961 by N.A., has become widespread. Zhukov. Its essence lies in a fractional study of urine for the content of diastase after stimulation of the secretory function of the pancreas with proserin. The nature of the curves provides an assessment of functional pancreatic insufficiency.

The most common functional methods used when examining patients with chronic pancreatitis are fractional tests of pancreatic enzymes in the duodenal contents after stimulation of the pancreas. These are the secretin-pancreozymine test, the gland stimulation test with olive oil, the method of Lund and others is close to them. However, their disadvantage is that, due to their complexity, they are available only to specialized gastroenterological departments.

In the diagnosis of chronic pancreatitis, methods for studying the intrasecretory function of the pancreas can also be used: determination of sugar in the urine and TSH. However, their information content is small.

Principles of treatment.

Diet. In case of severe exacerbation, fast for 1-2 days. Subsequently, slimy soups from cereals, steam soufflé from boiled meat, crackers from white bread. Subsequently, stale wheat bread, vegetable and cereal soups, lean varieties of beef, fish and chicken - boiled and steamed, low-fat fresh cottage cheese, cheese, boiled vegetables, baked apples are allowed. Meals are taken at least 5 times during the day. During the period of exacerbation of the disease, it is also advisable to include in the diet foods that have properties that inhibit proteolytic enzymes (egg whites, oatmeal, potatoes).

Painkillers. Prescribed: antispasmodics (no-spa, papaverine), H2-histamine receptor blockers (cimetidine, ranitidine), ganglioblockers (gangleron, quateron), analgesics (baralgin, promedol), anticholinergics (atropine, metacin, gastrocepin).

Pathogenetic therapy. To inhibit the activity of proteolytic pancreatic enzymes, including lysosomal ones, it is necessary to use anti-enzyme drugs (protease inhibitors) - conrical 10-15 thousand units per day intravenously, trasylol 50 thousand units per day intravenously, gordox 100 thousand units per day intravenously, in courses of up to 10 days. Pentoxyl and methyluracil also have trypsin-inhibiting properties.

Due to the participation of lipid peroxidation processes in the mechanisms of exacerbation of chronic pancreatitis, it is necessary to prescribe antioxidants (a-tocopherol acetate 100 mg intramuscularly, course 10 days); Essentiale as a stabilizer of cell membranes, 2 capsules 2 times a day orally, course 14 days.

In case of high levels of circulating immune complexes in the blood and severe disease, it is advisable to perform plasmapheresis and prescribe delagil as a medication.

Due to the tendency to hypercoagulation, the use of heparin and hypoaggregants (trental, chimes, aspirin) is indicated.

Replacement therapy. In connection with the development of exocrine pancreatic insufficiency, the following drugs are recommended: festal, pancreatin, panzinorm, digistal and other enzyme-containing drugs. The disappearance of creatorrhoea and steatorrhea is an indicator of the effectiveness of the use of enzyme preparations.

Means of reparative action. During the transition phase of the disease into remission, anabolic steroids are indicated (retabolil 1 ml IM once every 7 days). In addition, solcoseryl and oxyferriscorbone can be used for reparative purposes.

Physiotherapy. Inductothermy, UHF, is indicated when the disease goes into remission.

Therapy of diseases pathogenetically associated with chronic pancreatitis. In case of exacerbation of cholecystitis, gastric and duodenal ulcers, duodenitis, chronic colitis and opisthorchiasis, a complex of therapeutic measures is provided, developed for these diseases,

Spa treatment. During the period of remission, treatment is indicated in Essentuki, Truskavets, Zheleznovodsk, Jermuk, Morshin, Dorokhov.

Related information.

Nonspecific ulcerative colitis(synonyms: idiopathic ulcerative colitis, ulcerative proctocolitis) is a chronic relapsing disease based on inflammation of the colon with suppuration, ulceration, hemorrhage and outcome in sclerotic deformation of the wall. This is a fairly common disease that occurs more often in young women.

Etiology and pathogenesis. Local allergies, which are apparently caused by intestinal microflora, are certainly important in the occurrence of this disease. The allergic nature of colitis is supported by its combination with urticaria, eczema, bronchial asthma, rheumatic diseases, and Hashimoto's goiter. In the pathogenesis of the disease, autoimmunization is of great importance. This is confirmed by the discovery of autoantibodies in ulcerative colitis that are fixed in the epithelium of the intestinal mucosa, the nature of the cellular infiltrate of the mucous membrane, which reflects a delayed-type hypersensitivity reaction. The chronic course of the disease and the imperfection of reparative processes are apparently associated not only with autoaggression, but also with trophic disorders due to the pronounced destruction of the intramural nervous apparatus of the intestine.

Pathological anatomy. The process usually begins in the rectum and gradually spreads to the cecum. Therefore, there are both relatively isolated lesions of the rectum and sigmoid or rectum, sigmoid and transverse colon, and total damage to the entire colon. Morphological changes depend on the nature of the disease - acute or chronic.

Acute form corresponds to an acute progressive course and exacerbation of chronic forms. In these cases, the wall of the colon is swollen, hyperemic, with multiple erosions and superficial ulcers of irregular shape, which merge and form large areas of ulceration. The islands of mucous membrane preserved in these areas resemble polyps ( fringed pseudopolyps). Ulcers can penetrate into the submucosal and muscular layers, where fibrinoid necrosis of collagen fibers, foci of myomalacia and karyorrhexis, and extensive intramural hemorrhages are noted. At the bottom of the ulcer, both in the zone of necrosis and along their periphery, vessels with fibrinoid necrosis and arrosion of the walls are visible. Perforation of the intestinal wall in the area of ​​the ulcer and intestinal bleeding often occur. Such deep ulcers form pockets with necrotic masses, which are rejected, the intestinal wall becomes thinner, and the lumen becomes very wide ( toxic dilatation). Individual ulcers undergo granulation, and granulation tissue grows in excess in the area of ​​the ulcer and forms polypoid outgrowths - granulomatous pseudopolyps. The intestinal wall, especially the mucous membrane, is abundantly infiltrated with lymphocytes, plasma cells, and eosinophils. During the period of exacerbation, the infiltrate is dominated by neutrophils, which accumulate in the crypts, where they form crypt abscesses.

For chronic form characterized by a sharp deformation of the intestine, which becomes much shorter; There is a sharp thickening and compaction of the intestinal wall, as well as diffuse or segmental narrowing of its lumen. Reparative-sclerotic processes prevail over inflammatory-necrotic ones. Granulation and scarring of ulcers occur, but their epithelization is usually incomplete, which is associated with the formation of extensive scar fields and chronic inflammation. The manifestation of perverse reparation is multiple pseudopolyps and not only as a result of excessive proliferation of granulation tissue (granulomatous pseudopolyps), but also reparative regeneration of the epithelium around areas of sclerosis ( adenomatous pseudopolyps). Productive endovasculitis, wall sclerosis, and obliteration of the lumen are noted in the vessels; fibrinoid vascular necrosis is rare. Inflammation is predominantly productive in nature and is expressed in infiltration of the intestinal wall with lymphocytes, histiocytes, and plasma cells. Productive inflammation is combined with crypt abscesses.

Complications Nonspecific ulcerative colitis can be local and general. TO local include intestinal bleeding, wall perforation and peritonitis, stenosis of the lumen and intestinal polyposis, cancer development, general- anemia, amyloidosis, exhaustion, sepsis.

Crohn's disease- a chronic recurrent disease of the gastrointestinal tract, characterized by nonspecific granulomatosis and necrosis.

Etiology and pathogenesis. The cause of Crohn's disease is not known. Suggestions have been made about the role of infection, genetic factors, hereditary predisposition of the intestine to respond to various influences with a stereotypical granulomatous reaction, and autoimmunization. Among the pathogenetic theories, in addition to the autoimmune one, the so-called lymphatic one is widespread, according to which primary changes develop in the lymph nodes of the mesentery and lymphoid follicles of the intestinal wall and lead to “lymphatic edema” of the submucosal layer, resulting in destruction and granulomatosis of the intestinal wall.

Pathological anatomy. Most often, changes are found in the terminal segment of the ileum, in the rectum (especially in the anus) and appendix; other localizations are rare. Affected the entire thickness of the intestinal wall, which becomes sharply thickened and swollen. The mucous membrane is lumpy, reminiscent of a “cobblestone street,” which is associated with alternating long, narrow and deep ulcers, which are located in parallel rows along the length of the intestine, with areas of normal mucous membrane. There are also deep slit ulcers, located not along the length, but along the diameter of the intestine. The serous membrane is often covered with adhesions and multiple whitish nodules, which are similar to tuberculosis. The intestinal lumen is narrowed, and fistula tracts form in the thickness of the wall. The mesentery is thickened and sclerotic. Regional lymph nodes are hyperplastic and white-pink in section.

The most characteristic microscopic feature is nonspecific granulomatosis, which covers all layers of the intestinal wall. Granulomas have a sarcoid-like structure and consist of epithelioid and giant cells of the Pirogov-Langhans type. Edema and diffuse infiltration of lymphocytes, histiocytes, and plasma cells are also considered characteristic submucosal layer, hyperplasia of its lymphoid elements, formation of slit-like ulcers. These changes are often accompanied by abscesses in the thickness of the wall, sclerosis and hyalinosis as a result of the evolution of diffuse infiltrate cells and granulomas. With a long course, a sharp cicatricial deformation of the wall occurs.

Complication in Crohn's disease there is perforation of the intestinal wall with the formation of fistulous tracts, and therefore purulent or fecal peritonitis develops. There are frequent stenoses of various parts of the intestine, but more often the ileum, with symptoms of intestinal obstruction. Crohn's disease is considered a precancer of the intestine.

Dysbacteriosis- represents a state of microbial imbalance on or within the body. Dysbiosis most often occurs in the digestive tract or on the skin, but can also occur on any exposed surface or mucous membrane - such as the vagina, lungs, mouth, nose, sinuses, ears, nails or eyes. Dysbiosis is associated with various diseases, such as inflammatory bowel disorder, since intestinal inflammation can cause an imbalance of the intestinal microflora, or chronic fatigue syndrome. At the same time, dysbiosis itself is not a disease, but can sometimes be its consequence.

Stage I Dysbacteriosis is characterized by a moderate decrease in the number of obligate bacteria in the intestinal cavity. Pathogenic microflora, as a rule, is slightly developed, and there are no signs of intestinal dysfunction (symptoms of the disease).

Stage II Dysbacteriosis is characterized by a critical decrease in the number of bifidobacteria and lactobacilli of the intestine (obligate flora). At the same time, there is a rapid development of the population of pathogenic bacteria. If dysbiosis is caused by a disease, then, in addition to dysbiosis, it may exhibit other symptoms, for example, diarrhea, abdominal pain, and flatulence.

Stage III Dysbacteriosis is characterized by the influence of pathogens. This stage of dysbiosis can also be one of the symptoms of any disease, other symptoms of which may be inflammatory damage to the intestinal walls, persistent chronic diarrhea. Sometimes dysbiosis at this stage can manifest itself in children with diseases that cause developmental delays.

IV stage Dysbacteriosis is a stage at which obligate intestinal flora is present in very small quantities. The majority of microbes are conditionally pathogenic and pathogenic bacteria and fungi. This stage of dysbacteriosis can occur with general exhaustion of the body, anemia, and vitamin deficiency.

– diffuse ulcerative-inflammatory damage to the mucous membrane of the large intestine, accompanied by the development of severe local and systemic complications. The clinic of nonspecific ulcerative colitis is characterized by cramping abdominal pain, diarrhea mixed with blood, intestinal bleeding, and extraintestinal manifestations. Ulcerative colitis is diagnosed based on the results of colonoscopy, irrigoscopy, CT, and endoscopic biopsy. Treatment of ulcerative colitis can be conservative (diet, physiotherapy, medications) and surgical (resection of the affected area of ​​the colon).

Nonspecific ulcerative colitis is a type of chronic inflammatory disease of the large intestine of unknown etiology. Characterized by a tendency to ulcerate the mucous membrane. The disease occurs cyclically, with exacerbations followed by remissions. The most characteristic clinical signs are diarrhea streaked with blood and spasmodic abdominal pain. Long-term nonspecific ulcerative colitis increases the risk of malignant tumors in the large intestine.

The incidence of nonspecific ulcerative colitis is about 50-80 cases per 100 thousand population. At the same time, 3-15 new cases of the disease are detected annually for every 100 thousand inhabitants. Women are more prone to developing this pathology than men; in them, UC occurs 30% more often. Nonspecific ulcerative colitis is characterized by primary detection in two age groups: young people (15-25 years old) and older people (55-65 years old). But besides this, the disease can occur at any other age. Unlike Crohn's disease, ulcerative colitis affects only the mucous membrane of the large colon and rectum.

Causes of development of nonspecific ulcerative colitis

Currently, the etiology of ulcerative colitis is unknown. According to researchers, immune and genetically determined factors may play a role in the pathogenesis of this disease. One theory for the occurrence of ulcerative colitis suggests that the cause may be viruses or bacteria that activate the immune system, or autoimmune disorders (sensitization of the immune system against one's own cells).

In addition, it has been noted that ulcerative colitis is more common in people whose close relatives suffer from this disease. Currently, genes have also been identified that may likely be responsible for hereditary predisposition to ulcerative colitis.

Classification of nonspecific ulcerative colitis

Ulcerative colitis is distinguished by localization and extent of the process. Left-sided colitis is characterized by damage to the descending colon and sigmoid colon, proctitis is manifested by inflammation in the rectum, and with total colitis the entire large intestine is affected.

Symptoms of nonspecific ulcerative colitis

As a rule, the course of nonspecific ulcerative colitis is wavy, periods of remission are replaced by exacerbations. At the time of exacerbation, ulcerative colitis manifests itself with various symptoms depending on the localization of the inflammatory process in the intestine and the intensity of the pathological process.

If the rectum is predominantly affected (ulcerative proctitis), bleeding from the anus, painful tenesmus, and pain in the lower abdomen may occur. Sometimes bleeding is the only clinical manifestation of proctitis.

In left-sided ulcerative colitis, when the descending colon is affected, diarrhea usually occurs, and the stool contains blood. Abdominal pain can be quite pronounced, cramping, mainly on the left side and (with sigmoiditis) in the left iliac region. Decreased appetite, prolonged diarrhea and indigestion often lead to weight loss.

Total colitis is manifested by intense abdominal pain, constant profuse diarrhea, and severe bleeding. Total ulcerative colitis is a life-threatening condition, as it threatens the development of dehydration, collapse due to a significant drop in blood pressure, hemorrhagic and orthostatic shock.

Particularly dangerous is the fulminant form of ulcerative colitis, which is fraught with the development of severe complications, including rupture of the colon wall. One of the common complications in this course of the disease is toxic enlargement of the large intestine (megacolon). It is assumed that the occurrence of this condition is associated with the blockade of intestinal smooth muscle receptors by excess nitric oxide, which causes a total relaxation of the muscle layer of the large intestine.

In 10-20% of cases, patients with ulcerative colitis have extraintestinal manifestations: dermatological pathologies (pyoderma gangrenosum, erythema nodosum), stomatitis, inflammatory eye diseases (iritis, iridocyclitis, uveitis, scleritis and episcleritis), joint diseases (arthritis, sacroiliitis, spondylitis ), lesions of the biliary system (sclerosing cholangitis), osteomalacia (softening of bones) and osteoporosis, vasculitis (inflammation of blood vessels), myositis and glomerulonephritis.

Diagnosis of nonspecific ulcerative colitis

The main diagnostic method for detecting ulcerative colitis is colonoscopy, which allows a detailed examination of the lumen of the large intestine and its internal walls. Irrigoscopy and X-ray examination with barium can detect ulcerative defects of the walls, changes in the size of the intestine (megacolon), impaired peristalsis, and narrowing of the lumen. An effective method for visualizing the intestine is computed tomography.

In addition, a coprogram, a test for occult blood, and bacteriological culture are performed. A blood test for ulcerative colitis shows a picture of nonspecific inflammation. Biochemical indicators can signal the presence of concomitant pathologies, digestive disorders, functional disorders in the functioning of organs and systems. During a colonoscopy, a biopsy of the altered area of ​​the colon wall is usually performed for histological examination.

Treatment of ulcerative colitis

Since the causes of nonspecific ulcerative colitis are not fully understood, the goals of therapy for this disease are to reduce the intensity of the inflammatory process, subside clinical symptoms and prevent exacerbations and complications. With timely correct treatment and strict adherence to the doctor’s recommendations, it is possible to achieve stable remission and improve the patient’s quality of life.

Ulcerative colitis is treated with therapeutic and surgical methods, depending on the course of the disease and the patient’s condition. One of the important elements of symptomatic treatment of nonspecific ulcerative colitis is dietary nutrition.

In severe cases of the disease at the height of clinical manifestations, the proctologist may recommend a complete refusal to eat, limiting yourself to drinking water. Most often, during an exacerbation, patients lose their appetite and tolerate the ban quite easily. If necessary, parenteral nutrition is prescribed. Sometimes patients are transferred to parenteral nutrition in order to more quickly alleviate the condition of severe colitis. Eating is resumed immediately after appetite is restored.

Diet recommendations for ulcerative colitis are aimed at stopping diarrhea and reducing irritation of the intestinal mucosa by food components. Products containing dietary fiber, fiber, spicy and sour foods, alcoholic beverages, and roughage are removed from the diet. In addition, patients suffering from chronic intestinal inflammation are recommended to increase the protein content in their diet (at the rate of 1.5-2 grams per kilogram of body per day).

Drug therapy for ulcerative colitis includes anti-inflammatory drugs, immunosuppressants (azathioprine, methotrexate, cyclosporine, mercaptopurine) and anticytokines (infliximab). In addition, symptomatic medications are prescribed: antidiarrheals, painkillers, iron supplements for signs of anemia.

Non-steroidal anti-inflammatory drugs - 5-aminosalicylic acid derivatives (sulfasalazine, mesalazine) and corticosteroid hormonal drugs are used as anti-inflammatory drugs for this pathology. Corticosteroid drugs are used during periods of severe exacerbation in cases of severe and moderate severity (or if 5-aminosalicylates are ineffective) and are not prescribed for more than a few months.

Corticosteroid hormones are prescribed to children with extreme caution. Anti-inflammatory hormone therapy can cause a number of severe side effects: arterial hypertension, glucoseemia, osteoporosis, etc. Physiotherapeutic methods of treatment for ulcerative colitis can include diadynamic therapy, SMT, interference therapy, etc.

Indications for surgical treatment are the ineffectiveness of diet and conservative therapy, the development of complications (massive bleeding, perforation of the colon, if a malignant neoplasm is suspected, etc.). Resection of the large intestine followed by the creation of an ileorectal anastomosis (connection of the free end of the ileum to the anal canal) is the most common surgical technique for treating ulcerative colitis. In some cases, a section of the affected intestine limited within healthy tissues is removed (segmental resection).

Complications of nonspecific ulcerative colitis

A fairly common and serious complication of ulcerative colitis is toxic megacolon - expansion of the colon as a result of paralysis of the muscles of the intestinal wall in the affected area. With toxic megacolon, intense pain and bloating in the abdomen, increased body temperature, and weakness are noted.

In addition, ulcerative colitis can be complicated by massive intestinal bleeding, intestinal rupture, narrowing of the colon lumen, dehydration as a result of large fluid loss with diarrhea and colon cancer.

Prevention and prognosis of nonspecific ulcerative colitis

There is currently no specific prevention of UC, since the causes of this disease are not completely clear. Preventative measures for the occurrence of relapses of exacerbation are compliance with the doctor’s lifestyle instructions (nutrition recommendations similar to those for Crohn’s disease, reducing the number of stressful situations and physical overexertion, psychotherapy) and regular medical supervision. Sanatorium-resort treatment has a good effect in terms of stabilizing the condition.

With a mild course without complications, the prognosis is favorable. About 80% of patients taking 5-acetylsalicylates as maintenance therapy do not report relapses or complications of the disease throughout the year. In patients with ulcerative colitis, relapses occur once every five years, in 4% there are no exacerbations for 15 years. Surgical treatment is resorted to in 20% of cases. The probability of developing a malignant tumor in patients with ulcerative colitis ranges from 3-10% of cases.

And we also have

Nonspecific ulcerative colitis is a disease of the gastrointestinal tract, namely the colon, in which an inflammatory process occurs. As a result of pathogenic inflammation, necrosis and ulcers form in some areas of the intestine. But since this is a chronic disease, it tends to progress.

The inflammation does not affect the small intestine, but partially affects only some areas of the large intestine. First, the disease manifests itself in the sigmoid or rectum, then during inflammation it spreads to other nearby areas.

Can ulcerative colitis be cured?

This issue is becoming increasingly relevant against the backdrop of an increasing number of patients with this diagnosis. Chronic diseases, as a rule, cannot be completely cured. Nonspecific ulcerative colitis refers specifically to this type, but this does not boil down to the fact that you need to refuse treatment and let everything take its course.

This gastrointestinal disorder can be controlled if you seek medical help in a timely manner. The specialist, in turn, will carry out diagnostic measures, collect test results, and based on them will be able to draw up a treatment plan. It will help significantly alleviate the patient's condition. This must be done immediately, since this disease has periods of exacerbation.

If you completely ignore your condition over a long period of time, then exacerbations may occur, even leading to death. The correct treatment technology and dietary nutrition will help prevent repeated attacks along with outbreaks of relapses. Therefore, if everything is done correctly, the course of treatment is followed exactly, the person’s quality of life is preserved without significant deterioration. But with all this, persistent remission can make itself felt for many years.

Symptoms

Before moving on to describing the symptoms, each patient should know that they, first of all, depend on the location of the inflammatory process and its intensity. And conditionally they are divided into intestinal and extraintestinal symptoms. Now we will consider them in as much detail as possible so that no one has any questions. But it is worth keeping in mind that this material is primarily given for information, so that a person knows what is happening in his body and what signs are characteristic of his condition.

Intestinal symptoms

Diarrhea

Mucus and bloody clots may be present in the stool. If there is pus in the stool, it has a rather specific smell. It is not at all necessary that they will be observed during every act of defecation; it can be between breaks. The frequency of bowel movements is up to twenty times a day. A patient can lose about three hundred milliliters of blood per day. If the disease occurs in a milder form, bowel movements occur twice a day - in the morning and late evening.

Pain syndromes

The pain depends on the intensity, but in nature it can be sharp or weak. In some cases, it is not possible to get rid of pain attacks with the help of medications. This already indicates that an exacerbation has begun.

The pain is usually localized in the left side of the abdominal cavity or in the iliac region. They get worse before bowel movement, but go away after bowel movement and the condition stabilizes a little. Also, pain can bother a person after eating, and it can be relieved with the help of painkillers. But any medication should be taken only after consultation with a medical professional.

High temperature, signs of intoxication

The temperature in this case does not rise to subfebrile numbers on the thermometer.

General signs of intoxication:

• exhaustion;
• dizziness;
• depression;
• change of mood. This manifests itself in the form of irritability and tearfulness;
• decreased appetite. Against this background, a decrease in body weight occurs. This condition can lead to anorexia.

These signs manifest themselves if the disease is severe.

Tenesmus (false defecation positions)

If the intestines are empty, there has already been an urge to go to the toilet, and pus or mucus may be released. In addition, fecal incontinence is a pronounced symptom of flatulence.

Loose stools give way to constipation

This sign indicates that progressive inflammation has begun in the mucous membrane that lines the large intestine.

It is very important to know that ulcerative colitis can evolve in different ways. It depends on the period from which treatment was started, immediately after receiving a conclusion about the state of health, or no measures were taken. Sometimes ulcerative colitis can develop rapidly. This form is called fulminant. It will be discussed a little further in the text, and you can learn more about it in your doctor’s office.

Extraintestinal symptoms

Erythema, necrosis

With increased circulation in the blood of pathogenic microbes and immanent complexes to combat them, the appearance of erythema nodosum and pyoderma gangrene is possible. These are subcutaneous nodules that are easily detected by palpation. There may also be focal dermatitis, pustular and urticarial rashes.

Oropharynx lesion

Occurs in ten percent of patients. This manifests itself due to the spread of aphthae after remission is observed. In parallel with this, ulcerative stomatitis, glossitis, and gingivitis develop in the mouth.

Eye disease

This phenomenon is observed extremely rarely. According to statistics, chorioditis, conjunctivitis, keratitis, neuritis, anophthalmos are observed in less than eight percent. With timely treatment and seeking medical help, everything goes away without a trace. In advanced cases, of course, relapses can occur. Such outbreaks are controlled by specialists in hospital settings. These measures are not feasible at home.

Joint damage

The precursors of ulcerative colitis are arthritis, spondylitis, sacroiliitis. Damage to joint tissue is also possible. More often than other internal organs, the lungs are affected.

Endocrine system disorders

Very rarely, patients complain of glomerulonephritis, vasculitis, osteoporosis. Against the background of endocrine system disorders, malfunctions of the biliary tract and liver function occur.

In practice, the development of hemolytic anemia and autoimmune thyroiditis is not uncommon.

Nonspecific ulcerative colitis, signs

In order not to confuse the initial symptoms with other similar gastrointestinal diseases, you need to know what signs are characteristic of colitis.

The disease can develop in several scenarios:

1. Loose stools. After some time, mucus and bloody discharge can be found in the stool.
2. Anal bleeding. It may become exposed immediately after the manifestation of inflammation. In this case, the stool will not be liquid, but more formed.
3. Simultaneous occurrence of the first 2 signs.

The disease begins to progress with diarrhea, which is caused by the development of extensive inflammation in the colon. Against this background, it is no longer in a state to adsorb water and sodium. Blood appears because ulcers form on the mucous membrane, forming loose connective tissue penetrated by the vascular network. Symptoms may subside, but then increase in severity again.

In addition to loose stools, the initial symptoms may be: fever and pain, with a predominant localization in the left side. The patient may experience pain in the joints, since soft tissues are affected at an accelerated rate of development of the disease.

So, four signs with which you can independently identify nonspecific ulcerative colitis. These are diarrhea with blood, abdominal discomfort, high fever, pain and aches in the joints and muscles.

Causes of the disease

The etiological question still remains open to study the reasons that contribute to the development of ulcerative colitis.

Today there are known risk factors that have a provoking effect on the development of inflammation:

1. Genetic predisposition. The risk that a loved one will suffer from ulcerative colitis increases if similar diagnoses have already been identified in the family.
2. Infectious nature of the disease. The intestinal tract is an organ that contains multiple beneficial and pathogenic microorganisms. In most cases, it is the latter that begin to provoke inflammation.
3. Autoimmune mechanisms. Ulcerative colitis is associated with seasonal exacerbations. It can be treated with hormonal drugs. Scientists, after conducting several studies, have proven that the more severe the inflammatory process in the intestines, the more complicated the changes in immunity become.
4. Violation of the daily diet. A person should eat five times a day, in small portions. The menu should be varied, including fresh fruits and vegetables. By the way, this is useful not only for people who are already sick, but also for completely healthy people.
5. Constant stress, depression and other traumatic factors. But since there are situations in life that simply cannot be controlled, the best option would be to consult a psychologist. He, in turn, will listen to the reasons that contribute to the outburst of negative emotions and prescribe the appropriate medicine. These can be soothing decoctions, infusions, or tablets.

Experts come to a unanimous conclusion that ulcerative colitis can appear due to the influence of many factors. But the main role goes to intestinal pathogenic bacteria.

Types of Ulcerative Colitis

In medicine, there are several forms of this disease, which are divided only by location and intensity.

Depending on the location, it can be:

• Left-handed. Symptoms: bloody diarrhea, pain on the left side, loss of appetite. The latter leads to the development of dystrophy. This form is distinguished by the fact that it mainly affects the colon;
• Total. Symptoms include persistent pain, bloody diarrhea, dehydration, decreased blood pressure, and hemorrhagic shock. This form is considered the most life-threatening for the patient. If there is a delay in treatment, irreversible consequences may appear in the form of complications;
• Distal. Symptoms: sharp pain in the left iliac region, mucus and blood in the stool, flatulence, constipation. It is characterized mainly by inflammation in the sigmoid and rectum simultaneously.

In addition, it can be “Pancolitis” (inflammation of the entire rectum) and “Proctitis”.

Depending on the degree of development, it tends to be chronic continuous, acute (fulminant) or chronic recurrent colitis.

Diagnostics

The diagnosis is made not at home, but in a special laboratory. To do this you will need to submit:

1. General blood analysis. It can be used to determine the number of leukocytes and signs of anemia.
2. Blood chemistry. Indicates the number of immunoglobulins, the content of albumin, magnesium and calcium.
3. Immunological blood test. Using this, specialists are able to identify cytoplasmic antibodies.

Endoscopy, colonoscopy and rectoscopy indicate the presence of swelling, hyperemia, bleeding in the intestinal lumen. If this study is carried out during a period of remission, atrophy of the intestinal mucosa is observed.

In addition, scientists are developing new types of surveys. One of these is capsule. In some cases, it can replace conoscopy. This procedure does not cause discomfort and is not painful. However, imaging is poorer than rectal examination.

Treatment

Therapy is carried out using symptomatic methods, because it is not possible to influence the source of inflammation with medication. The main goal of the specialist is to relieve inflammation, prevent complications and establish a state of stable remission.

Conservative methods of combating the disease

Diet food

It is necessary to adhere to a diet when the disease is acute. The patient completely limits himself to food and tries to drink more clean water. When the acute form is cured, you can switch to protein foods - eggs, cottage cheese, low-fat meat/fish products. Consumption of various porridges and berry compotes is also beneficial. In especially severe cases, the patient is transferred to artificial feeding.

Other treatments:

• taking vitamins;
• taking anti-inflammatory drugs;
• taking corticosteroids and hormonal drugs. You should first consult your doctor;
• taking symptomatic and antibacterial medications.

In addition, physiotherapeutic methods are used to influence the disease. Current treatment, interference therapy and some others have been found to be particularly effective.

Surgery is necessary for profuse bleeding, perforation of the intestinal wall, accumulation of pus, and the presence of toxic megacolon.

In the absence of complete statistical data, one cannot help but see that the number of patients suffering from nonspecific ulcerative colitis (UC) and Crohn's disease (CD) of various localizations, including granulomatous colitis, has now significantly increased. Now patients with this pathology constitute a permanent and stable contingent in gastroenterological and coloproctological departments.

Despite the increased diagnostic capabilities, it can take years from the first clinical manifestations of UC and CD to a firmly established diagnosis. Thus, G. Adler (2001) gives as an example the case histories of two patients with Crohn's disease and ulcerative colitis, in whom the correct diagnosis of the disease could only be determined after 4 years and 10 years, respectively. At the same time, in the first patient the disease began and lasted for a long time under the guise of gonarthritis, and in the second the picture of stenosing cholangitis had already developed. The title of this section in the monograph of the indicated author is symbolic - “The Long Path to Diagnosis.”

On the other hand, ulcerative colitis with the full range of its standard manifestations can arise suddenly and after a short period of time end in tragedy or drama (acute fulminant, or fulminant, form).

At the beginning of March 2003 Patient M., 16 years old, was admitted to the Hospital Surgery Clinic (CHC) in extremely serious condition. She became acutely ill about two weeks ago (abdominal pain, frequent loose stools with blood). For three days she hid what happened from her parents. She was hospitalized in the infectious diseases hospital, from where a week later she was transferred to the surgical department with suspicion of acute appendicitis. Three days later, with a diagnosis of UC, she ended up in a specialized gastroenterology department. Due to the ineffectiveness of complex conservative treatment, including hormone therapy, and the resulting complication (toxic megacolon), she was operated on at the KHC. A colectomy with Brooke ileostomy was performed. Due to the extremely difficult general condition, it was decided to refrain from removing the rectum. Sudden death the next day (cardiac and respiratory arrest).

The body's resources are not unlimited. “And since nature has lost its strength, goodbye, science! We must dig a grave,” J. Chaucer correctly noted back in the 14th century.

Patient K., 34 years old, was admitted to the KGC on January 19, 2004. The general condition is extremely serious. Anemia (Er-1.45x10 12/l, Hb-39g/l, Leu-3.3xl0 9A, Ht-15.4%), hypoproteinemia (38.3g/l), protein-free edema in the lower extremities, ascites. I noticed bowel disorder since June 2003, and obvious signs of UC since November of the same year. Consistently consulted and examined in five medical institutions in Samara. Fibercolonoscopy (FCS) was performed only up to the left flexure of the colon (01/20/04): due to a sharp narrowing of the lumen, the endoscope could not be extended further. The entire surface of the examined intestine is covered with ulcers, a mass of polyps of inflammatory origin (pseudopolyps). There are minimal changes in the rectum. Operation 01/28/04 - colectomy with the formation of an ileostomy according to Brooke. During surgery, it was discovered that the pathological process involved the cecum and all parts of the colon. Toxic megacolon. Intensive postoperative therapy was effective. The sutures were removed on the 13-14th day. The laparotomy wound healed by primary intention. The patient was discharged under the supervision of a surgeon and gastroenterologist at his place of residence. In the future, a reconstructive operation is not excluded - the creation of an ileorectal anastomosis.

Thus, UC can be extremely aggressive, and loss of time (delay in laparotomy) most often results in failure. Some surgeons were able to understand this back in the middle of the last century. For example, G.Crile and C.Y.Thomas (1951) stated: “The safest and fastest way to cure a patient with ulcerative colitis is a one-stage colectomy with ileostomy. Patients tolerate even extensive operations well, provided that the disease is eliminated. the patient is in a hopeless condition, the more urgent are the indications for simultaneous subtotal colectomy and ileostomy.”

Leading coloproctologists in our country now adhere to this point of view (G.I. Vorobyov et al., 1999). In case of UC, even during the period of remission of the disease, ileo- or colostomy cannot be considered the operation of choice. Here is one of the observations.

Patient D., 31 years old, disabled person of the second group. Hospitalized at KGH in August 1992. Diagnosis: UC, total lesion, severe course; cecostoma; end ileostomy. General weakness is expressed. Weight loss (height - 175 cm, weight 52 kg). Blood and mucus are constantly released from the cecostoma and rectum. Anemia, hypo- and dysproteinemia.

Ill since 1979. Standard conservative treatment using small doses of prednisolone. In connection with the intensification of the process in December 1989. a cecostoma was formed. Two weeks later, due to the increasing deterioration of the general condition, a Brooke ileostomy was performed. These operations did not have any positive effect on the course of the underlying disease. Chyme loss through an ileostomy is up to 1.5-2.0 l/day.

In November 1992, the patient underwent a subtotal colectomy at the KGH with the formation of a single-barreled sigmostoma. During the operation, a disconnected part of the ileum about 20 cm long was found. When the colon was mobilized to a distance of about 1.5-2 cm from the ileocecal valve (ICV), the cecum was cut off. Its section adjacent to the ICC has been demucosed. Proximal to the ileostomy, the ileum is incised transversely. The entire ileocecal section is sewn here in an isoperistaltic position.

In March 1994, a reconstructive operation was performed with the mobilization of the ileo- and sigmostoma and the creation of an anastomosis between them. Consulted in December 1997. The patient does not adhere to a diet. The frequency of stools is 2-3 times a day. Body weight - 67 kg. Continues to work as an engineer. The inflammatory process in the rectum periodically worsens, but there is no rectal bleeding. Conservative treatment appears to be effective.

In emergency surgery for UC, it is difficult to decide on a one-stage coloproctectomy (CPE) - an operation that is undoubtedly more traumatic than a colectomy (CE). But since in a significant proportion of patients the inflammatory process is initially more pronounced in the rectum, after previously performed CE, and in the end, it is necessary to resort to proctectomy. Only this final operation can relieve the patient of the underlying disease and its complications.

Here are our observations.

Patient K., 32 years old (case history No. 6260/617), became acutely ill in February 1990: due to mental stress, heavy rectal bleeding occurred. Diagnosed with UC. She was treated conservatively. At the beginning of October, she was urgently transferred from the gastroenterology department to the intensive care unit of one of the city hospitals in Samara. Due to toxic dilatation of the colon, a right-sided double-barrel transversostomy was created. A week later, severe bleeding was discovered from the leading end of the transversostomy. A typical subtotal CE was performed with removal of about 12 cm of the ileum, formation of an end ileostomy and suturing of a tightly protected area of ​​the sigmoid colon. The postoperative period was complicated by intestinal obstruction and an abdominal abscess, for which laparotomy was performed twice.

By February 1991, the issue of choosing tactics in treating the patient was being decided again: bleeding from the rectum resumed with the same force. She was transferred to KGH, where in March she underwent proctectomy and an ileoanal anastomosis was formed. Unfortunately, due to the formation of a pararectal fistula in the perineum, the reduced ileum had to be removed and a 180° inverted (antiperistaltic) Brooke ileostomy was created. The patient's last consultation was in December 1999: her general condition was quite satisfactory, her body weight increased by 23 kg and became the same as before the disease. Stool no more than twice a day, fairly formed. Sometimes it is necessary to empty the reservoir formed at the junction of iso- and antiperistalsis with a rubber catheter. Group 1 disabled person. Works at home as a seamstress.

No less dramatic is the fate of patient K., 41 years old, who was once again hospitalized at KGH on January 12, 2004. Having fallen ill with UC in 1999, she successively, over the course of 5 years, underwent 7 different operations on the colon and perineum. In this patient, the underlying disease was combined with its extraintestinal manifestations, primarily polyarthritis (at the level of the knee and elbow joints) and gangrenous pyoderma (on the upper and lower extremities, in the perineum and buttocks) with the formation of large and deep, accompanied by excruciating pain, completely ulcers that cannot be treated.

Only the last operation on February 20, 2004 - CPE with the formation of an ileostomy according to Brooke - radically changed the situation for the better: pain in the joints stopped, numerous ulcers on the skin began to intensively epithelialize.

In some patients, neither the medical history, nor clinical symptoms, nor endoscopic and radiological data, nor intraoperative diagnostics, including examination of a removed macroscopic specimen, nor even histological examination allow one to accurately differentiate UC and CD. This is a rare variant of the so-called indeterminate colitis (indeterminate colitis by English-speaking authors), which later, for unknown reasons, can transform into UC or CD (Isbister W.H., Hubler M., 1998; Swan N.C. et al., 1998 ).

Of course, in most cases, histological examination of the removed macroscopic specimen (colon or entire colon) is decisive in the final determination of the true nature of the pathology.

Thus, patient S., 44 years old), disabled group 1, operated on 02.02.04. (subtotal proximal CPE) there were, although not all, signs of CD: a cobblestone pattern throughout the entire colon and, most importantly, rectovaginal and pararectal fistulas. However, histological examination revealed only multiple superficial ulcers and a mass of pseudopolyps, in the absence of accumulations of lymphoid elements (granulomas) and Pirogov-Langhans cells.

Advances in the conservative treatment of patients with chronic inflammatory processes in the colon are obvious. Paradoxically, this is probably one of the main reasons that in some patients the indications for surgical intervention are determined late. This may lead to performing emergency mutilation operations when complications have already developed. The prevalence of the disease in the terminal ileum, the severe general condition of the patient (anemia, hypoproteinemia, water-electrolyte disorders) do not allow either preserving the ICC, or creating a renervoir with ileoanal anastomosis, or even resorting to an inverted ileostomy due to the high risk of failure of the interintestinal anastomosis.

If complex therapy for UC and CD is ineffective, intensive preoperative preparation should not be long: if the pathological focus persists, one cannot hope for improvement and normalization, for example, of many blood parameters - red blood cells, hemoglobin, hematocrit, total protein, etc. Resuscitation measures should continue in full during and after surgery.

In our opinion, the joint work of gastroenterologists and coloproctologists can become a factor that will allow timely determination of indications for surgical intervention in patients with UC and CD and, consequently, the use of surgical methods for correcting postcolectomy or postcoloproctectomy syndrome.

Almost 200 years ago C.L. Dumas (1807) believed that the clinician must "anticipate the beneficial and harmful events that occur during the course of treatment... determine with precision when to act and when to wait; to choose carefully between the numerous methods of treatment offering all the advantages and disadvantages , choosing the one whose application gives the maximum speed, the best agreement, the greatest confidence in success; use experience, take advantage of the opportunity; correlate all the chances, calculate all the chances...". The relevance of these requirements is beyond doubt in our time.