X-ray semiotics of inflammatory bowel diseases (nonspecific ulcerative colitis, Crohn's disease) in children. L iterativereview
Shaplov D.S. State Educational Institution of Further Professional Education "Russian Medical Academy of Postgraduate Education of Roszdrav", State Institution Russian Children's Clinical Hospital of Roszdrav
Inflammatory bowel diseases, modern concepts
One of the main problems of pediatrics is gastrointestinal diseases, given their prevalence, severity and frequent chronicity, leading to a decrease in the level of health and quality of life of the younger generation. Worldwide, there is a persistent increase in the incidence of chronic bowel diseases, the most severe and common of which are inflammatory bowel diseases (UC).
Constant growth The incidence of IBD among children and adults, the variety of clinical symptoms, extraintestinal manifestations and severe complications, the difficulties of diagnosis and differential diagnosis, the need for adequate treatment determine the relevance of an in-depth study of both the problem of IBD in general and individual clinical issues, diagnosis and treatment of CD and UC.
To date, the etiology of UC and CD is unknown. The mechanisms of the inflammatory process in the intestine, leading to disruption of the functional state of the organ, have not been fully studied; defense mechanisms and issues of mucosal repair (RM). Despite periodically arising doubts about the differences and similarities of these diseases, they are independent nosological units.
Crohn's disease(regional enteritis, granulomatous ileitis or colitis) – granulomatous inflammation of the digestive tract of unknown etiology with predominant localization in the terminal ileum; characterized by stenosis of the affected areas of the intestine, fistula formation and extraintestinal manifestations. Described by B.B. Crohn, L. Ginsberg, G.D. Oppenheimer in 1932. CD is considered a chronic transmural inflammation that can involve any part of the digestive tract from the oral cavity to the anal canal, combined with many extraintestinal manifestations.
CD is found in all regions of the world. Most often - in the northern regions of Europe and the USA, where newly detected cases are 0.7-14.6 per 100,000 population annually, in the southern regions of Europe - 3.6 per 100,000 population. According to various authors, the incidence in Northern Europe and the United States has somewhat stabilized in recent years, but continues to grow where CD was rare - in southern and central Europe, Asia, Africa, Latin America. The prevalence of CD in Russia as a whole has not been studied, but a study conducted in the Moscow region suggests that the incidence of CD in European Russia is approximately equal to that in Central Europe at 3.5 per 100,000 population. Two peaks of incidence are described - at the age of 15-35 years (20-29 years) and 60-79 years, but the disease can begin at any age. According to I.L. Khalifa et al., women are affected somewhat more often than men.
The etiology of CD is not completely known and at the moment it is proposed to consider the following factors, which, according to most authors, play a major role in the occurrence of the disease. With CD, there is a pronounced genetic predisposition, increased concordance in monozygotic twins. The risk of developing IBD in the first generation is about 10%. With early onset of CD, 30% of patients have a positive family history, according to V.G. Rumyantsev (2007). CD has a polygenic inheritance pattern with incomplete penetrance. Seven loci responsible for susceptibility to IBD were identified on chromosomes 1,3,6,12,14,16 and X. Changes in chromosomes 6 and 16 are more typical for CD. On the other hand, the value of genetic typing is low, since the mutation may be present in healthy individuals without phenotypic manifestations. The role of various microbial agents and viruses in the development of CD and the positive clinical effect of treatment with antibacterial drugs continues to be debated. More often than others, the role of Mycobacteriumparatuberculosis, measles virus and Listeria monocytogenes is discussed in the literature as a possible etiological factor in CD. Mycobacteria were often detected in intestinal tissues in CD, and a positive clinical effect was noted with the use of anti-tuberculosis drugs. The literature discusses the hygiene hypothesis, according to which - good hygiene– a risk factor for the development of IBD. Infection has been shown to play an important role in the development of a balanced immune response through the generation of regulatory T cells. It has been hypothesized that IBD is a genetically determined pathological reaction of the human body to its own intestinal microflora. The increase in the permeability of the intestinal barrier in patients with CD and their relatives is of great importance, however, to date, no clear data have been obtained on the differences in the composition of the mucous secretion covering the intestinal epithelium. Among environmental factors, the negative role of smoking, taking medications is discussed (in particular, non-steroidal anti-inflammatory drugs (NSAIDs) and oral contraceptives increase the risk of developing CD), poor nutrition with a high content of easily digestible carbohydrates, and a deficiency of polyunsaturated fatty acids.
Pathophysiology, as well as the etiology of CD, is currently being discussed at the level of individual factors possibly involved in the pathophysiological mechanisms of development of this disease. An integral part of the mechanism of inflammation and tissue damage in CD are immune disorders, both humoral and cell-mediated immunity. It was found that in the colonic mucus there is a significantly increased number of IgG-producing cells, and in the area of the basement membrane and vessels there are deposits of IgG and complement components C3, C4 and C9, which indicates the participation of immune complexes in the chronic inflammatory process in CD. CD is considered to be characterized by the detection of antibodies to Saccharomyces cerevisiae (ASCA). A decrease in the number of T cells expressing gdT cell receptors was recorded, with a preserved balance of CD4 and CD8-positive T cells. It has been shown that epithelial cells normally stimulate CD8 positive T cells, and in CD they preferentially stimulate CD4 positive T cells. In the healthy gut, epithelial cells are thought to induce and maintain suppressive tolerance, whereas in CD the same cells may enhance or maintain chronic inflammation. The role of various pro- and anti-inflammatory cytokines, namely interleukin-10, natural inhibitors of interleukin-1 and tumor necrosis factor (TNF)-alpha, in the pathogenesis of CD has been proven. A deficiency of immunomodulatory and anti-inflammatory activity in the intestine contributes to the development and chronicity of the disease. The influence of arachidonic acid metabolites on the development of inflammation has been shown. Endothelial cells of the vessels of the intestinal wall and platelets take part in maintaining the inflammatory reaction; there is damage to the nervous regulation of the organ. Inflammatory mediators in CD include free radicals and NO. Currently, there is evidence of multiple disturbances of adhesion molecules in patients with CD, which are responsible for the composition of circulating leukocytes in the inflamed intestinal wall.
Thus, genetic predisposition, the capabilities of the individual’s immune response, and the impact of exogenous factors in the presence of a number of endogenous disorders are realized in damage and chronic inflammation of the intestinal mucosa in CD.
Pathomorphology. In CD, any part of the gastrointestinal tract can be affected, however, most often the disease begins in the terminal ileum. The length of the lesion can vary from 3-4 cm to 1 m or more. The process begins in the submucosal layer and spreads to all layers of the intestinal wall. According to V.G. Rumyantseva (2007), focal damage to crypts by neutrophils with the formation of crypt abscesses is the earliest sign of SO damage in CD. Aphthae-like ulcerations are considered an early macroscopic sign of CD. Next, ulcerations appear over the lymphoid follicles, macrophages and other inflammatory cells penetrate and proliferate in the lamina propria, forming granulomas consisting of giant epithelioid cells. They can be found in the inflammatory infiltrate in all layers of the intestinal wall, lymph nodes and mesentery. Granulomas are a pathognomonic sign of CD. Found in resected material in 50% of cases. The lesion is transmural in nature. The predominance of the inflammatory process in the deep layers of the intestinal wall leads to severe ischemia and the development of deep ulcers-cracks with smooth edges oriented along and across the intestinal axis, which gives the ulcer a characteristic “cobblestone” appearance. Ulcers penetrate deeply into the muscle layer, reaching the subserous layer and can penetrate into the surrounding tissue, which leads to the formation of adhesions, infiltrates and fistulas in the most affected areas. As the process progresses, the intestinal wall thickens, the intestine narrows, and becomes rigid. CD is characterized by segmental lesions, with the affected areas clearly demarcated from healthy tissue.
The clinical picture of CD depends on the location of the lesion and the type of disease (fibro-obstructive, penetrating or fistulous). According to various authors, ileitis occurs in 30-45-60% of cases, ileocolitis - 30-55%, colitis - 15-25%. Other BC localizations ( oral cavity, esophagus, stomach, duodenum) are detected in 5-9-19% of patients. About a third of patients with CD have perianal manifestations. Regardless of the location of the process, common symptoms of CD are abdominal pain, diarrhea, fever and weight loss. The most common location of CD is ileitis and, accordingly, the most common clinical manifestations are abdominal pain (repeated episodes localized in the right lower quadrant) and diarrhea. The pain is most often moderate and cramping, precedes defecation and is relieved by it. The situation may develop into an appendicitis-like variant (with a palpable mass formation in the right iliac region, fever, leukocytosis). Diarrhea has a complex genesis, the contribution of which is impaired passage, excessive bacterial growth, syndrome of impaired absorption of nutrients, bile acids, and exudation. The low-symptomatic variant of CD is characterized by minimal manifestations, often extraintestinal symptoms - weakness, fever, retardation in physical development, anemia. Small intestinal localization of CD can manifest itself as malabsorption and exudative enteropathy syndromes with the development of the corresponding clinical picture (deficiency of vitamins B12, A, E, zinc, etc.). When the process is localized in the colon, the main complaints are cramping abdominal pain, diarrhea (mushy, watery stools up to 10 times a day), bleeding occurs only in a third of patients with lesions localized in the colon, and massive bleeding is recorded in only 1-2% of patients BK. Rise in temperature with chills and sweating indicate purulent complications. Loss of body weight can be quite significant (up to 10-20%), associated with the course of the underlying disease, anorexia, and conscious dietary restriction due to the frequent urge to defecate. Perianal manifestations may be the first and one of the most pronounced complaints, characterized by the development of fissures, fistulas and/or abscesses.
With the development of CD along the fibrous-obstructive path and cicatricial narrowing of the intestine, the nature of the pain changes, diarrhea is replaced by stool retention and bloating. Intestinal strictures are one of the most common complications of CD. With the penetrating-fistulous route, perforation of ulcers into the abdominal cavity is quite rare; they are usually covered, which is explained by the fact that the chronic transmural process in CD leads to the formation of adhesions and fusion of serous surfaces. It is the transmural process that leads to the development of various fistula tracts. They can be external, with exit holes on the skin, and internal, ending blindly in the loops of neighboring intestines or hollow organs, leading to the formation of intra-abdominal abscesses, psoas abscess, hydronephrosis; be asymptomatic or manifest with severe pain, fever, etc. One of the extremely rare complications for CD is toxic dilatation of the colon.
Extraintestinal manifestations may precede, accompany or occur regardless of the course of CD (V.G. Rumyantsev (2007)). It is proposed to divide them into three categories: colitis-related, consequences of pathophysiological disorders in the small intestine, and mixed.
Diagnosis of CD. In typical cases, the diagnosis of CD is established on the basis of complaints, anamnesis, clinical observation, X-ray, endoscopic examination, and biopsy data. Laboratory diagnostics is aimed at determining the degree of activity of the process and identifying complications. The range of possible studies and identified changes is quite wide; we allow ourselves to mention only the main ones. In addition to general clinical studies, to assess the degree of inflammatory reaction, anemia, etc., it is necessary to exclude infections, exocrine pancreatic insufficiency, and enteral insufficiency. The level is determined C-reactive protein, ANCA and ASCA, the cellular and humoral components of immunity are assessed. Endoscopy for CD allows you to assess the condition of the mucous membrane (spotted hyperemia, erosions, thickened folds, aphthae and longitudinal ulcers), identify the segmentation of the lesion, and the presence of strictures. It should be noted that clinical remission does not correlate with the endoscopic picture of the disease, therefore, repeated endoscopic examinations to assess the effectiveness of therapy are not recommended (V.G. Rumyantsev (2007)). According to indications, patients with CD undergo esophagogastroduodenoscopy and intestinoscopy. During endoscopic examinations, it is mandatory to take a biopsy of the examined areas. The information content of SB biopsy in CD is limited by its superficial nature. The diagnosis can be assumed by identifying a number of histological signs, namely, granuloma in the submucosa (detection frequency 10-25%), accumulation of histiocytes and lymphocytes (microgranulomas), intermittent nature of the lesion, when normal SO is adjacent to crypt abscesses. Despite the development of endoscopy, X-ray examination has not lost its importance in the verification of CD. It is carried out to determine the location, nature and severity of the lesion. Fluoroscopy (and graphy) of the gastrointestinal tract with barium, irrigoscopy (and graphy) are used. A detailed description of the X-ray semiotics of CD is given below. According to modern concepts, the main role in establishing the diagnosis of CD is played by the results of x-ray and histological studies. In the diagnosis of CD, ultrasound techniques are used, the results of which, according to the literature, correlate quite well with the results of irrigoscopy. The non-invasiveness, safety and effectiveness of ultrasound (ultrasound) is attractive, which allows for accurate diagnosis of abscesses and strictures in CD, assessment of changes in the echo structure of the intestine, thickening of its wall, which can be indicative of CD. Currently, active research work is being carried out to assess the norm and pathological changes in the intestine using ultrasound, and to develop diagnostic criteria for various diseases, including CD. The use of radioisotope methods for diagnosing CD, computed tomography, magnetic resonance imaging, despite their sufficient effectiveness, is limited on the one hand by the large radiation dose to the patient (with CT), on the other hand, by the need for expensive equipment available to a limited number of medical institutions.
Differential diagnosis of CD is carried out with acute appendicitis, diverticulitis, tumors of the cecum, metastatic lesions, pathology of the fallopian tubes and ovaries. If the small intestine is affected, the diagnostic range may include systemic vasculitis, ischemic ileitis, and radiation enteritis. It is necessary to exclude the course of tuberculosis, amoebiasis, yersineosis. Typically, CD is quite easy to separate from UC based on radiological, endoscopic and morphological characteristics.
Treatment. The diet of patients with CD should contain complete proteins, dairy products, fats containing medium- and short-chain fatty acids, while limiting foods containing gluten. Depending on the severity of the condition, parenteral nutrition may be necessary. Aminosalicylates are used as initial therapy for mild and moderate forms of CD. Metronidazole and ciprofloxacin are often used, which by eliminating increased bacterial growth help improve the effectiveness of treatment. In the absence of treatment effect, they usually switch to local hormones (budesonide, budenofalk). Enteral nutrition demonstrates similar efficacy to budesanide and is used for both induction and maintenance of remission. If treatment with aminosalicylates and budesonide is ineffective, treatment with systemic steroids is indicated. The use of glucocorticoids may lead to the development side effects that worsen the quality of life of patients (osteoporosis, hypertension, cosmetic defects). When hormonal resistance develops, immunosuppressants azathioprine (or 6-mercaptopurine), methoterxate or mycophenolate mofetil are introduced into therapy, used both for induction and maintenance of remission. Treatment of severe exacerbation of CD includes parenteral nutrition, correction of electrolyte abnormalities, antibacterial therapy, intravenous administration glucocorticoids with subsequent transfer to oral administration. If there is no effect after 2-4 weeks, hormonal resistance is determined, and cyclosporine or infliximab (Remicade), chimeric monoclonal antibodies to TNF, are introduced into therapy. The effectiveness of remission induction reaches 70%. An important aspect The treatment of CD is the therapy of perianal manifestations - ulcers, fissures and fistulas. In addition to basic therapy for the underlying disease, local treatment is also used, which, however, usually gives a short-term effect. With frequent recurrence of fistulas, surgical treatment is required. The treatment strategy for CD also depends on the nature of the complications. Surgical intervention may be required in the event of the development of massive bleeding, toxic dilatation, strictures with a clinical picture of intestinal obstruction, abscesses and fistulas of various locations. In case of refractory course of the disease, there may be a need for surgical treatment - the affected parts of the intestine are disconnected and their partial resection is carried out. Surgical treatment should be carried out as sparingly as possible, since 60-70% of patients develop relapse of the disease in the proximal area of the anastomosis. Among non-drug methods treatment of CD, a positive effect of the use of hyperbaric oxygenation has been described, leading to a decrease in inflammatory activity in the gastrointestinal tract.
A number of BC classifications have been proposed, each of which has its own advantages and disadvantages. The most commonly used classification is developed at the Congress of Gastroenterologists in Vienna in 1998, which includes three categories: age at which the diagnosis was made (before and over 40 years), localization (terminal ileitis, colon, ileocolon, upper gastrointestinal tract) and course of the disease. (no strictures and penetrations, strictures, penetration). Several indices of CD activity have also been proposed (Best, Harvey, Van Gies), which are rarely used in clinical practice due to their cumbersomeness and are used mainly in scientific research. Currently, CD is considered a precancerous disease; according to studies, the average duration of the disease until cancer diagnosis is 15 years. The statistical increase in the risk of colorectal cancer increases with the onset of the disease at a young age (before 30 years of age).
In childhood, the main points of the pathogenesis of CD, the clinical picture, and the examination program correspond to those in adult patients. Among the features of CD in childhood, it is necessary to mention retardation in growth, physical and sexual development, which are associated with the production of cytokines and chronic failure nutrition and require dietary correction, and sometimes parenteral nutrition. As a feature of the clinical picture, one can note the frequent development of perianal changes (up to 50% of children with CD). Treatment of CD in its principles and means used is practically no different from that in adult patients. An additional factor considered when deciding on surgical treatment may be (unlike adults) severe malabsorption, leading to retardation in physical development. It has been shown that 89% of children operated on for CD experience a pronounced growth acceleration in the first year.
Nonspecific ulcerative colitis. UC is a necrotizing inflammation of the colon of a nonspecific nature of unknown etiology, spreading from the anal canal in the proximal direction.
Most common among the population Northern Europe, North America and Australia. According to the literature, there are about 250 thousand patients with UC in the United States. The incidence of UC in Europe and America is 8-11.4-15 per 100 thousand population per year, the prevalence is about 80-120 people per 100 thousand population. The prevalence of UC in the Moscow region is 22.3 per 100 thousand population, the incidence is 1.7 per 100 thousand population. More extensive epidemiological studies have not been conducted in Russia. The disease can begin at any age, most often it is quite young people (30-40 years old), white, with a high level of education, living in cities.
UC has been known for about 150 years, but until now the etiology and pathogenesis of the disease is considered by most authors to be poorly understood. The multifactorial nature of etiology and pathogenesis is recognized, which develops in the presence of a certain combination of exogenous and endogenous factors. Genetic predisposition is considered to be the basis for the development of the disease. Approximately 10-20% of patients with UC have relatives with IBD; concordance for twin pairs is lower than for CD. Currently, about 5 genes (localized on chromosomes 2, 3, 6, 7 and 12) are described that are responsible for susceptibility to the disease, and some of them are also responsible for the development of CD. The genetic heterogeneity of UC and the possibility of various forms of the disease within one nosological unit have been proven.
Resolving factors may include the influence of infections, dietary errors, and food allergies. The literature discusses the role of various microorganisms and viruses in the pathogenesis of UC and the possibility of the existence of an as yet undiscovered pathogen. It is described that frequent infections affecting the gastrointestinal tract and upper respiratory tract contribute to the early onset of the disease. Increased permeability of the intestinal barrier is considered as one of the petogenetic mechanisms, along with genetically determined inferiority of the local immune response. According to S.V. Bellmera (2004) and co-authors, insufficiency of immune regulation leads to uncontrolled responses to various external agents, which in turn causes local tissue damage and the development of local inflammation. As confirmation of the autoimmune nature of UC, the detection of perinuclear antineutrophil antibodies (p-ANCA) in 70% of patients with UC is indicated.
According to the literature, T-cell activation plays a major role in inflammation in UC. According to some authors, the main defect of the immune system in UC is the depletion of suppressor functions, followed by dysfunction of macrophages and activation of T-effectors with cytotoxic properties towards colon antigens. Various cytokines (interleukins, tumor necrosis factor, interferon) have a significant impact on the nature of the disease, mediating immunological reactions. The role of interleukins 2, 4, 10 and interferon-gamma has been proven. An increase in the level of B-lymphocytes during exacerbation and a decrease in their level during remission of the disease, an increase in the level of IgG in the blood and IgG-producing cells in the colon are also described. Inflammation of the mucous membrane in UC is superficial and is characterized only by functional disorders of the epithelium. V.G. Rumyantsev (2007) sets out the concept of SO damage in UC as follows: under the influence of unusual stimulation or as a result of impaired control, a significant number of Toll receptors that recognize endotoxins and peptidoglycans appear on the surface of the epithelium. The signaling pathways activated by these receptors in the intestinal epithelium are intact, leading to the activation of nuclear transcription factor and the production of chemokines. They, in turn, attract leukocytes from the vascular bed, neutrophils migrate to the epithelium and cause its damage, overcome the intestinal barrier, entering the lumen and crypts, forming crypt abscesses. Damaged epithelial cells form neoepitopes that excite an autoimmune response. The death of the intestinal epithelium occurs both as a result of the action of neutrophils and as a result of the action of immune complexes.
Among external factors The role of stress factors, taking certain medications (NSAIDs, oral contraceptives), poor nutrition (abuse of easily digestible carbohydrates, deficiency of polyunsaturated fatty acids) is discussed. In general, at present, the hypothesis for the development of UC can be presented as follows: the genetic predisposition of the immune system, the activation of which occurs under the influence of a number of provoking factors, leads to the launch of autoimmune mechanisms with damage to the mucous membrane of the colon, the formation of chronic immune pathological process.
Pathomorphology. The most pronounced changes are usually observed in the rectum. According to the literature, damage to the rectum and sigmoid colon is observed in 40-50% of patients, left parts - in 30-40%, total - in 20% of patients. With mild inflammation, the mucus is swollen, granular, and hyperemic. As the severity of the ulcer increases, it bleeds intensely, and ulcerations from pinpoint to ulcers appear. irregular shape with overhanging edges. As a result of excessive regeneration, pseudopolyps can form (with a long-term disease). SO has an atrophic appearance with a deformed vascular pattern. The intestine shortens and narrows.
Clinical picture. The main clinical symptoms of UC (during exacerbation) are rectal bleeding, abdominal pain, and stool upset. UC usually begins gradually, symptoms increase over weeks, sometimes months, but its acute development is also possible, as with infectious colitis. The severity of clinical symptoms depends on the extent and severity of the pathological process. Bleeding is the main symptom of UC; it is associated with an active necrotic process, large ulcerative defects of the colon, periodically over a long period. However, with mild UC (or in remission), there may be minimal or no blood in the stool. The second most common symptom is frequent loose stools, the frequency of stools, depending on the stage and characteristics of the course of UC, can be from 3-4 to 20 or more times a day with an admixture of blood, mucus and pus in varying quantities, false urges are possible, sometimes constant discharge associated with weakness of the anal sphincter. However, in 30-50% of patients (especially with distal forms of UC), even during an exacerbation, constipation with tenesmus and rectal bleeding may be observed. In any case, most often the urge to defecate in patients with UC occurs at night and in the morning, and can be provoked by every meal. Abdominal pain is quite common, but is not a constant symptom. Usually the pain is cramping in nature with a predominant localization in the left iliac region, intensifying before defecation and subsiding after it. In severe cases of UC, systemic manifestations of the disease develop - anorexia, weight loss, nausea, vomiting, protein-free edema, fever, anemia.
To date, there is no single generally accepted classification of UC. The proposed options usually depend on the localization of the process in the intestine, the clinical course and the severity of the process (the severity of the attack). UC always begins with damage to the mucous membrane of the rectum and spreads in the proximal direction. There are distal forms (proctitis and proctosigmoiditis (27-44%), left-sided (up to the middle of the transverse colon, about 40% of cases), subtotal and total colitis (20%), total colitis with retrograde ileitis (10-30% of cases). I. L. Khalif et al. true damage to the small intestine in UC. Three degrees of severity of exacerbation (attack) of UC were identified, proposed by Truelove and Witts (1995) and supplemented by M.H. Levitan, taking into account clinical and laboratory data. The active inflammatory process is accompanied by an increase in acute phase proteins of inflammation, platelets, ESR , neutrophilic leukocytosis is possible, sometimes with the appearance of young cells.There is a classification using indices of clinical and endoscopic activity of UC, proposed by Rachmilewitz in 1989. Currently, the assessment of the severity of UC according to Schroeder or the Mayo Clinic is often used, which determines the sum of points for each degree of activity UC taking into account stool frequency, rectal bleeding, endoscopic picture and clinical characteristics. By clinical course There are acute (fulminant) forms, chronic relapsing and chronic continuous course of the disease.
Complications. Complications of UC are divided into intestinal and extraintestinal. The most serious intestinal complications of the disease include bleeding, toxic dilation (about 5% of cases), and intestinal perforation. As the results of treatment of severe forms of UC improve, the problem of colon adenocarcinoma increasingly arises. The risk of mortality from colorectal cancer in patients with ulcerative colitis is 3 times higher than in the population, increases after 10 years of the disease, and is especially pronounced in those who become ill at an early age. According to the Mayo Clinic, after 10 years of UC, the risk of adenocarcinoma increases annually by 0.5-1%.
Among the extraintestinal complications of UC there are conditions associated with its activity (peripheral arthropathy, erythema nodosum, episcleritis, pyoderma gangrenosum, anterior uveitis) and not associated with it (sacroiliitis, ankylosing spondylitis and primary sclerosing cholangitis). A syndrome of impaired nutrition and absorption (5-10% of cases), manifested by weight loss, hypoalbuminemia, anemia, protein loss, and disorders of vitamin and mineral metabolism, can be considered as a complication in severe UC.
Diagnostics. The diagnosis of UC is established on the basis of anamnesis, characteristic clinical picture, microbiological examination of feces, X-ray, endoscopic and histological studies. Laboratory examination is carried out to identify signs of inflammation, anemia, immunological markers; its results depend on the degree of activity of the process. Microbiological examination of feces is necessary in primary patients in order to exclude infectious colitis in its endoscopic and sometimes clinical picture, similar to UC. Infections caused by Shigella spp., Salmonella spp., Campylobacter spp., Clostridium difficile and Yersinias pp. should be excluded first. Fibercolonoscopy reveals a polymorphism of macroscopic changes: increased bleeding of the mucus, absence of a vascular pattern, erosions, ulcers, inflammatory polyps, granularity of the mucus. Endoscopic changes in UC are usually divided into four degrees. Normal view SM with a deformed or unchanged vascular pattern is detected during remission of UC. With minimal activity, hyperemia and swelling of the mucous membrane with loss of pattern and granularity are visualized. The appearance of contact bleeding and minor ulcerations against this background indicates moderate activity. With severe activity, spontaneous bleeding, extensive ulcerations, and fibrous-purulent plaque occur. Microscopically, inflammation primarily involves CO. There is swelling of the lamina propria with dilated capillaries and extravasation of red blood cells. The inflammatory infiltrate consists of neutrophils, lymphocytes, plasma cells and macrophages. Crypt abscesses, crypt deformation, and gland depletion are visualized. According to V.G. Rumyantsev (2007) signs of chronicity make it possible to exclude infectious colitis with 80% accuracy. These include violations of the architectonics of the crypts, an increase in the intercryptal space, depletion of the glands, uneven surface of the crypt, basal lymphoid accumulations, chronic inflammatory infiltrate and often Paneth cell hyperplasia. In histological examination, three degrees of activity are most often followed. X-ray examination plays a significant role in the diagnosis of UC. Irrigoscopy is usually performed to reveal loss of haustration, shortening and narrowing of the colon. According to almost all authors, for adequate diagnosis it is necessary to use a combination of various techniques, especially fluoroscopic and endoscopic. Currently, promising results are demonstrated by ultrasound techniques for assessing the condition of the intestine in IBD. However, their use is in the development stage, the definition of norms and criteria for various diseases, and currently ultrasound cannot compete in the diagnosis of UC with the classical X-ray endoscopic diagnostic complex. Radioisotope research allows us to assess, first of all, the functional state of the intestine, its motor function. CT makes it possible to more accurately assess the thickness of the intestinal wall, determine the presence of abscesses, fistulas, etc., but is associated with a fairly large radiation dose.
Differential diagnosis of UC is usually carried out with infectious colitis, Crohn's disease, ischemic, drug-induced, radiation and microscopic colitis.
Treatment. The diet of a patient with ulcerative colitis should be complete and rational. The basic diet contains an increased amount of animal protein, vitamins, minerals, and a normal content of fats and carbohydrates. This involves culinary processing of foods; products with coarse fiber, milk, canned food, spicy and salty foods are excluded. According to indications, complete nutritional mixtures are used as additional or main nutrition, balanced in chemical composition, containing partially hydrolyzed protein, medium-chain or short-chain triglycerides and carbohydrates without lactose and ballast substances.
Basic drugs used in the treatment of ulcerative colitis include sulfasalazine and its analogues, systemic and local glucocorticoids, and immunosuppressants. Therapeutic tactics depend on the extent of the pathological process and the severity of the attack. The superficial nature of inflammation in UC allows one to successfully control the course of the disease using topical medications; their rectal administration is a mandatory element of therapy. Sulfasalazine has been used in therapy since 1942, both to induce remission and to maintain it. To overcome the side effects, 5-ASA formulations have been developed using pH-based release systems and time-dependent mechanisms. The high effectiveness of 5-ASA preparations for rectal use (suppositories, enemas) has been shown in the treatment of patients with distal lesions, since it is these forms that create a therapeutic concentration of 5-ASA in the mucus of the rectum and sigmoid colon. Glucocorticoids are effective in 70-90% of patients with active UC. Parenteral administration, oral administration, rectal administration in the form of enemas and suppositories are possible. The route of administration, dose, duration and treatment regimen depend on the activity of UC. They are used mainly to induce remission; they have low effectiveness as maintenance therapy. In recent years, new steroids have been developed - synthetic drugs that have comparable effectiveness and much fewer side effects. The best known of these is budesonide. If glucocorticoid monotherapy is insufficiently effective and/or hormone resistance, immunosuppressants are used. Azathioprine is most often used, and if it is intolerant, methotrexate is used, but the effectiveness of its use in UC is not as high as in CD. When treating a severe attack of UC, cyclosporine may be used. Recently, publications have appeared on the successful use of infliximab in hormone-resistant UC for induction and maintenance of remission. According to indications, symptomatic therapy is carried out (correction of metabolic and dysbiotic disorders, antibacterial therapy, pain relief, etc.).
Ulcerative colitis can be completely cured with surgery. According to statistics, about 5-10% of patients with ulcerative colitis undergo surgical treatment. Coloproctectomy, on the one hand, stops the clinical manifestations of UC, on the other hand, it reduces the patient’s quality of life due to the frequency of bowel movements, the possibility of stool and fecal incontinence, the risk of developing cholelithiasis and social restrictions. Indications for surgery include life-threatening complications, drug intolerance, hormonal dependence and resistance, and complications of therapy.
Features of UC in childhood. Children make up a fairly large group of patients with UC. According to Fergusona, the incidence rate of UC in children in Europe is 1.5-2 children per 100 thousand population per year. The disease is detected at any age, maximum – at the age of 10-19 years. Total colitis is diagnosed in 45–62% of children, left-sided – in 22-30%, distal – in 15-25%. It should be noted that distal colitis, which begins in childhood, has a high degree of spread in the proximal direction. Among the features of the clinical picture of UC in childhood are retardation in growth, physical and sexual development, loss of body weight, and a blurred clinical picture, leading to late diagnosis of the disease. Loose stools, as well as abdominal pain, are present in adult patients with UC. O.A. Kanshina proposed a classification of UC in children, taking into account the phase of the disease (exacerbation, remission), the extent of the lesion (segmental colitis, total colitis), form (mild, moderate, severe colitis) and the course of the disease (continuous or recurrent). Acute onset of UC is recorded more often among children than among adult patients: 30% of cases in children and 1.9%-12%, according to various sources, in adults. There is currently no consensus on assessing the severity of the attack and, accordingly, the frequency of various forms of the disease. So according to O.A. Kanshina, which includes in the assessment of severity the frequency of stool, the amount of blood in the stool, ESR, anemia, endoscopic activity, light form the most common in children - 50% of patients, the moderate-severe form of UC is about 25%, the severe form - 25%. According to other authors, a mild form of colitis occurs in approximately 40% of children, the remaining 60% are moderate to severe forms of the disease. Statistical differences in frequency were also revealed various options course of UC. Thus, the recurrent course in adult patients, according to various authors, is 67-95% of cases, in children 38-68.1%; a chronic continuous course is recorded in 12.7-30% of adult patients and in 5.2-7% of children with UC. Intestinal and extraintestinal complications occur in children as well as in adult patients, their frequency depends on both age and the extent of the lesion. In terms of diagnostics, it should be noted that the leading endoscopic signs of UC in children of all ages are contact bleeding and the absence of a vascular pattern. The main medications and treatment tactics are approximately the same as in adult patients. However, it has been described that in children under 11 years of age, sulfasalazine is effective in the treatment of both moderate and severe forms of UC, but age does not affect the effectiveness of prednisolone. Discussions continue in the literature regarding the use of glucocorticoids in children, both for the purpose of inducing remission and for its maintenance, discussion of the optimal doses of drugs of all groups used and the duration of treatment, the possibility of using local steroids and infliximab.
Thus, an analysis of modern literature shows that IBD (UC and CD) are one of the main problems of gastroenterology and pediatrics, taking into account the increasing incidence rate, “rejuvenation” of the pathology, the severity of the underlying disease and its complications. Uncertainties regarding the etiology, pathogenesis, and pathophysiology of IBD create the preconditions for problematic therapy and the absence of etiotropic drugs. The impact of a severe disabling chronic disease on the health and quality of life of the patient, the need for long-term expensive treatment, physical and social restrictions in the lives of patients, especially when the disease begins in childhood, make the issues of early diagnosis of IBD and differential diagnosis between UC and CD relevant. One of the significant methods of examining patients with IBD is radiological. Its non-invasiveness, effectiveness and reliability are attractive. Recently, the problems of IBD have been in the focus of attention of clinicians, while the main focus of diagnostic work is devoted to the development of new techniques, such as ultrasound, CT, and MRI. Considering, on the one hand, the evolution of IBD, the emergence of new effectively used drugs and treatment regimens, the success of treating severe forms of UC and CD, the achievement of remission in a larger number of patients and the possibility of long-term maintenance, and on the other hand, the emergence of new, more accurate x-ray devices with high resolution, it seems appropriate to evaluate the possibilities of X-ray examination for IBD in children.
X-ray diagnosis of gastrointestinal diseases, modern concepts.
The discovery of X-rays played a huge progressive role in the development of human society. Their importance is especially great in medicine, where the use of X-ray radiation has been and often remains practically indispensable in the diagnosis and treatment of many diseases.
The development of modern technologies has led to the creation of a large number of different diagnostic methods in various areas of medicine.
According to most authors, endoscopic examination of the gastrointestinal tract (GIT) has largely replaced traditional X-ray examination in identifying superficial, erosive and inflammatory changes in the mucous membrane (MU) of the digestive tract, especially as part of primary diagnosis.
In modern medicine, the statement of L.D. is increasingly relevant. Lindenbraten that “a medical diagnosis is a synthesis of all data - anamnestic, clinical, radiological, etc. - produced on the basis of systematized and generalized knowledge and personal experience already accumulated by science.” To determine treatment tactics, it is necessary to use data from all available examination methods. At the same time, it is very important to clearly understand what studies can with a high degree of probability confirm the diagnosis, what is the significance various methods radiodiagnosis in monitoring the course of the disease and, finally, what data can be used in determining treatment tactics. In this regard, X-ray methods still play a major role in the diagnosis of intestinal diseases.
According to many researchers, an X-ray examination of the small intestine should be carried out in all patients with intestinal diseases, which makes it possible to identify anomalies and malformations and assess the functional state of the intestine (tone, peristalsis, state of CO relief). X-ray changes are nonspecific and complement the clinical understanding of the severity of damage to the small intestine and the extent of changes. At the same time, survey radiographs provide only primary approximate information. To diagnose pathological processes in the intestines, it is necessary to carry out several types of contrast studies with a suspension of barium sulfate at varying degrees intestinal filling. Small filling makes it possible to study the relief of the intestinal mucosa; tight filling - its position, contours, shape, size, mobility. The study is usually carried out in the patient's polypositional position.
The X-ray examination technique is described in detail in relevant manuals, monographs, and dissertations.
The optimal method of X-ray diagnostics is currently considered to be a study using an enteroclyster according to Sellink. The most common modification is a two-phase study, in which methylcellulose is applied after the administration of a liquid barium suspension. The probe is installed through the nasal passages; it is recommended to advance the tip of the catheter along the lumen of the duodenum to the duodenal-jejunal flexure. The liquid contrast agent is administered using a pump, which allows you to regulate the rate of administration of the contrast agent and the pressure in the system. It is necessary to ensure continuity of the CV column and avoid excessive distension of the intestinal loops. When CV (500 m ml) reaches the terminal ileum, the introduction of a warm 0.5% methylcellulose solution (volume about 1-2 l) begins, which pushes the barium column forward, leads to stretching of the intestinal loops and increases the transparency of their contents, creating a double-contrast effect and allowing for a detailed assessment of the CO. The method increases the detection of tumors to 90%. To obtain double contrast, it is possible to use air, but this method is less tolerated by patients.
X-ray examination of the colon includes many different techniques. The main method is irrigoscopy, i.e. filling the colon with a contrast suspension through an enema. The method allows you to evaluate intramural, parietal, intraluminal formations in the intestine, small growths on the surface of the mucus. For this purpose, tight filling of the intestine with a barium suspension, studying the relief of the intestine after bowel movement, and additional research methods are used. These include, first of all, double contrast with filling the intestine with barium and air, taking special images (polygraphy, tomography, hard images), parietography with the introduction of air into the abdominal cavity. As a radiocontrast agent, it is preferable to choose high-density barium preparations, since they give good image contrast and fit tightly to the CO. An important point is the temperature of the barium suspension. The optimal option is considered to be a temperature of 36-37ºС, since HF cooled to 8-10ºС accelerates the motor activity of the gastrointestinal tract, and warmed to 45ºС slows it down.
A limited number of works are devoted to the X-ray diagnosis of gastrointestinal diseases in children. At the same time, it should be noted that most of them were written in the 50-80s of the last century. It is proposed to use the same techniques as in adult patients. It should be borne in mind that some of the proposed methods have limitations for use in childhood, for example, the Weintraub-Williams technique for fluoroscopy of the gastrointestinal tract (the use of ice water to stimulate the passage of electrolytic fluid through the small intestine) or the use of tannin for irrigoscopy. All authors indicate the need to examine the patient in a polypositional position using fluoroscopy and radiography.
X-ray anatomy of the small and large intestine is described in detail in many classical manuals, also mainly based on the results of examinations of adult patients.
Age-related features of the X-ray picture in children are described in a limited number of works. In general, according to most authors, the small intestine in a child, even a newborn, in general shape and location is not much different from the small intestine in an adult. The differences lie mainly in the macro and microscopic structure of CO and in physiological functions, especially in young children.
In children, X-ray examination of the colon using a contrast enema is carried out using the same method as in adult patients; double contrast with air is also used. Among the features, it should be noted that with tight filling in children in the descending and sigmoid colon, haustration is practically not determined. In newborns and children in the first months of life, even with light filling, the haustral pattern may not be determined. The haustra of the cecum in children are quite pronounced. In young children, the Bauginian valve is rarely identified as such, but very often its age-related insufficiency is detected. Features of childhood include the location of the splenic and hepatic flexures at the same level in newborns and children in the first month of life. The relief of the colonic mucosa is determined by two types of folds (pepper folds, intertwined with each other, and longitudinal ones).
Pathological processes in the gastrointestinal tract, accompanied by corresponding functional and morphological changes, cause the appearance of a radiological picture that differs from the norm by the presence of various radiological symptoms and their combinations, which is also described in detail in the literature. There are very few radiological symptoms characteristic of any one disease. Usually, with each disease, a number of signs are detected, the combination of which may be characteristic of a given pathological process.
According to the literature, X-ray examination still plays a huge role in diagnosing diseases of various parts of the gastrointestinal tract, clarifying the localization of the process and its complications, and determining treatment tactics. In our opinion, the virtual absence of work on x-ray examination, study, and x-ray diagnostics of the gastrointestinal tract, especially in childhood, over the past 20-30 years indicates an undeservedly low attention to the possibilities of x-ray diagnostics. The emergence of new X-ray machines that expand the capabilities for diagnosing more “subtle” changes in the relief and contour of the intestine, combined with increased knowledge about the pathogenesis and characteristics of the course of various diseases, opens up wide opportunities for X-ray diagnosis of gastrointestinal diseases, including in children.
X-ray diagnostics for inflammatory bowel diseases
Diagnosis of diseases from the IBD group (CD, UC) is a complex and multifaceted process. The diagnosis is established by a combination of clinical, endoscopic, morphological, radiological and laboratory data. “The inextricable continuity and connection of various research methods is obvious. After all, ultimately, they are all attached to one object - a person - and pursue a common goal. The undeniable strength of each diagnostic method lies in their close union and unconditional community, and not in opposing them to each other.” In choosing differentiated treatment tactics for chronic inflammatory bowel diseases, a decisive role is played by determining the prevalence of damage to the small and large intestines, disease activity, and the presence or absence of complications. At the same time, the role of x-ray examination is undeniable. Often, X-ray examination is carried out during dynamic observation and to assess the effectiveness of conservative and surgical treatment.
Despite the fact that the primary diagnosis of UC and CD is usually established on the basis of a clinical examination of the patient and endoscopy with targeted biopsy, the role of X-ray examination in recognizing this pathology is extremely important. This method allows you to: 1. determine the extent of the lesion; 2. clarify the diagnosis in cases where the data from endoscopic and histological studies are not convincing enough; 3. carry out differential diagnosis of UC with CD, diverticulum, ischemic colitis and other diseases of the colon; 4. identify signs of malignancy.
When diagnosing CD, an informative method is to conduct a fluoroscopic examination of the gastrointestinal tract with a contrast agent through the mouth (hereinafter referred to as “fluoroscopic examination of the gastrointestinal tract”), followed (after 7-8 days) by conducting a fluoroscopic examination of the colon using a contrast enema (hereinafter referred to as “irrigography or irrigoscopy").
X-ray examination for suspected IBD begins with a survey X-ray of the abdominal organs, which is especially important in cases of severe active UC, when colonoscopy and irrigoscopy are contraindicated. Plain radiographs may reveal thickening of the intestinal wall, shortening of the colon, lack of haustration, unevenness of the mucous membrane, increased intestinal diameter and toxic expansion of the colon (toxic megacolon), free gas under the dome of the diaphragm during perforation, and sometimes ulcers filled with gas in the form of spicules , as well as penetration of ulcers into the subserous layer. It should be noted that the described symptoms can only be detected in severe cases of diseases from the IBD group.
X-ray methods retain a leading role in the diagnosis of diseases of the small intestine, providing, among other things, the opportunity to examine areas of the intestine that are inaccessible during endoscopic examinations. The recently used video capsule endoscopy, due to the need for expensive equipment and consumables (capsules), is available to a few medical institutions and has limitations of the method (examination of parts of the intestine only in the direction of the video camera).
To diagnose damage to the small intestine, an X-ray of the gastrointestinal tract with a barium suspension is performed, while delayed images when the CV of the large intestine is reached allow one to assess its functional state. To assess structural changes in the colon, irrigoscopy is used, studying the relief after emptying and introducing air into it for the purpose of double contrast. In this case, it is necessary to fill the distal part of the ileum with a contrast suspension simultaneously with the colon.
Before fluoroscopy, no special preparation is required, except for following dietary recommendations and conducting the study on an empty stomach. X-ray examination of the stomach and small intestine is carried out in the absence of clinical symptoms of intestinal obstruction.
Irrigoscopy and irrigography help to establish the presence of an inflammatory process, determine its extent and the nature of functional disorders. The possibility of various complications arising from UC requires justified prescription and careful implementation of a retrograde radiopaque diagnostic procedure. Acute toxic dilatation of the intestine and the presence of free gas in the abdominal cavity are contraindications for irrigoscopy. Irrigoscopy is usually performed after acute symptoms have subsided and the patient’s condition has improved (to prevent the development of toxic megacolon).
It should be emphasized that if UC is suspected, irrigoscopy, like colonoscopy, should be carried out with great caution, since the studies themselves, and sometimes preparation for them, can have a negative impact on the patient’s condition and even provoke an exacerbation of the disease. The preparation of each patient for the study should be discussed between the radiologist and the clinician. It is possible to replace standard preparation with enemas and laxatives, a special liquid diet prescribed 2 days before barium enema. In mild forms of UC with stool frequency no more than 3 times a day and during the period of remission, preparation for the study can be standard (2 enemas and castor oil). If the frequency of bowel movements is more than 4-5 times a day, preparation is limited to one enema; for profuse diarrhea, preparation is not carried out at all. It is proposed to use an aqueous suspension of barium sulfate in a ratio of 1:5 or 1:6 as a contrast agent.
Almost all authors discussing the use of X-ray examination in IBD indicate that in both CD and UC, fairly unambiguous symptoms can be identified only in advanced, advanced variants of the disease. At the initial stages, radiological signs are not very specific, often scattered and ambiguous. However, the development of X-ray technology, in particular the emergence of digital equipment, expands the possibilities of X-ray diagnosis of IBD at the initial stages of the disease.
Once again, it is necessary to point out that only a few studies have been devoted to the X-ray diagnosis of IBD in children, assessing mainly the developed variants of the course of the disease, accompanied by pronounced changes in the X-ray picture, similar to that in adult patients.
X-ray diagnosis of Crohn's disease
According to modern concepts, the diagnosis of CD requires radiological confirmation. Since CD can damage any part of the gastrointestinal tract, it requires both a fluoroscopic examination of the gastrointestinal tract with a contrast agent through the mouth, and a fluoroscopic examination of the colon using a contrast enema. The main radiological signs of the disease vary depending on the phase of the process. The initial purpose of an X-ray examination for suspected CD is to establish the location, nature and severity of the lesion. Irrigoscopy is preferable to colonoscopy, because less invasive and produces images that can be used for comparison in subsequent studies. It is also preferred over endoscopy in the evaluation of rigidity, submucosal edema, pseudodiverticula, and fistulas.
The main localization of lesions in CD is the terminal ileum (in all patients) and the colon. According to G. Adler (2001), approximately 55% of patients have a combined lesion of the ileum and colon, in 15% of cases - only the colon (mainly its right parts), and in approximately 30% of cases, changes are limited only to the small intestine.
X-ray symptoms of CD in adult patients with intestinal damage are described quite well and are similar in different localizations of the process. The main characteristic features of this variant of the disease are segmental lesions involving individual segments of both the large and small intestine; the presence of unaltered sections of the intestine between the affected segments, while the border between the affected and unaltered areas of the intestine is clearly visible; wavy or uneven bowel contour; deep longitudinal ulcers (“depot” of contrast agent), alternating with bulging of edematous lymphoid tissue in the intestinal wall (“oval filling defects”), forming a “cobblestone pavement” relief; pseudodiverticula, which are deep ulcers penetrating into the tissue (the “brush” symptom); segmental narrowing of the affected areas (single or multiple), resulting from fibrous changes in the intestinal wall (“cord symptom”).
Irrigoscopy reveals not only damage to the colon, but also signs of ileitis - uneven relief and narrowing of the lumen of the ileum. The study allows us to record a string of narrowed sections of the intestine, characteristic of granulomatous enteritis, separated by normal segments. In early cases the diagnosis is more difficult, but by double contrast with a barium enema or during routine barium sulfate advancement, superficial aphthae and linear ulcers can be seen.
Morphological and radiological data in CD correlate well with each other; the stage of the disease can be characterized by the changes detected during enteroclyster. The classification of radiographic changes remains a matter of debate, as do many other aspects of CD, although there are no striking differences between the proposed classifications.
Some authors propose to distinguish three morphological stages of Crohn's disease based on X-ray data, based on the classification proposed by Herlinger H. and Maglinte D (1989). At stage I (early changes), thickening and straightening of folds due to submucosal edema, the presence of multiple small superficial ulcers with a diameter of 0.1-0.2 cm, surrounded by an inflammatory shaft, are detected. The intestinal wall remains elastic. At stage II (intermediate changes) – the presence of nodular relief, ulcerations, rigidity of the mesenteric edge and bulging of the opposite edge like pseudodiverticula. The intestinal wall is significantly thickened, the width of the intestinal lumen is within normal limits. Nodular defects less than 1 cm in diameter are usually of equal size and result from a combination of submucosal edema with mucosal atrophy and scarring. At stage III (pronounced changes), an ulcerative-nodular relief of the mucous membrane is diagnosed (the “cobblestone pavement” symptom), the presence of rough slit-like ulcerations with spasm and a formed narrowing of the lumen in the form of a cord. The distance between the loops is increased, the walls are thickened and rigid.
Other sources distinguish three phases of the process: prestenotic, transitional and stenotic. In the early prestenotic stage, radiological diagnosis is difficult; functional disorders are determined in the form of increased haustration with a gradual weakening of the evacuation ability of the intestine, as well as alternation of altered areas of the mucosa with normal ones and some rigidity of the affected areas. Early signs of the prestenotic phase are straightening, smoothing, thickening of folds in the area of the ileocecal valve (Bauhinian valve) or other affected area. There is a violation of the location of the loops, their moving apart. The intestinal lumen and its contour acquire an irregular shape, sometimes without a clear restructuring of the CO relief. The relief of the mucous membrane is changed, the folds are randomly located, wide, and rigid. Swelling of the mucous membrane looks like expansion and smoothing of valve formations in the intestine. Aphthous ulcers are defined as small patches of retained barium surrounded by a halo of edematous mucosa. The described changes in the early stage of development of the disease are the result of an inflammatory process developing in the mucous membrane and submucosal layer. Because ulcerations progress, they can merge to form large exposed areas of mucosa, having the appearance of a “cobblestone street”. In the transitional stage, scarring of ulcerations and regeneration of the atrophically altered mucous membrane occurs. As the disease progresses, radiological signs become more pronounced: narrowing of the lumen of the ileum, straightening of the walls and smoothing of the contours at the affected area, a sharp restructuring of the relief of the mucous membrane: from significant thickening in the form of a “cobblestone pavement” to its complete disappearance or the formation of diverticula. Inflammation ultimately leads to fibrosis and the characteristic “string” symptom. False sacculation occurs as a result of asymmetrical shortening of the intestine, which is characteristic of the mesenteric edge of the small intestine. Loops of intestine may be “forced” to be positioned or pressed apart from one another due to induration of the mesentery and enlargement of the lymph nodes. In the stenotic phase with further development fibrous tissue and intestinal stenosis, the intestinal loop becomes rigid, its diameter is from 1 to 2 cm, the length of the affected area can be different, from 7-8 to 30 cm. Sometimes there is an expansion of the proximal intestine, which depends on the duration of the stenosis. Subsequently, as the intestinal section becomes stenotic, suprastenotic expansions occur, while the shape and angle of the transition of the ileum to the cecum changes, and the intestinal walls become rigid.
In the large intestine, as in the small intestine, one or more of its sections may be affected. In these cases, alternation of sharply narrowed and normal sections of the intestine is visible. In narrowed, rigid areas of the intestine, the contrast suspension and introduced air do not contribute to the straightening of the intestine; it remains sharply narrowed and rigid. The symptom of insufficiently complete emptying of the intestine after defecation is considered very characteristic, while the affected fragment of the intestine, when filled tightly and after emptying, has almost the same lumen width. Difficulties arise when large areas of the small intestine are affected in the prestenotic phase. In this case, the clinical picture is similar to severe enteritis, and the presence of fluid in the intestinal loops and pronounced functional changes do not allow us to identify the relief of the mucous membrane. When the process is localized in the ileum and duodenum, the x-ray picture may have a number of features. Persistent deformation and narrowing of the descending duodenum is revealed. Its contours are straightened and low-elastic. The small intestine is deformed and narrowed in the distal segment of the ileum for 25-30 cm, has rigid contours and individual polyp-like protrusions on the relief of the mucous membrane. Thus, with CD, the radiological signs are uneven narrowing of the affected part of the intestine, alternating with areas of expansion and more or less normal segments, i.e. changes are intermittent. The relief of the mucous membrane acquires a granular, polypoid character; the contours of the intestine become uneven and unclear. When the process spreads to the cecum, it becomes deformed and wrinkles.
Descriptions of the X-ray picture of CD localized in the stomach are rare and contradictory. In some cases, the X-ray picture of gastric CD is difficult to distinguish from a malignant tumor of the antrum. CD of the duodenum is rare, in 1.5-2% of cases and is often combined with damage to the stomach, can be combined with ileitis or develop in isolation. In the duodenum, scattered ulcers and fistulas are rarely formed, spasm is often observed, which complicates early diagnosis. One of the variants of CD is jeunitis with a characteristic alternation of multiple affected areas with unchanged ones. Changes in CO are similar to those with lesions of the ileum. During the stenotic phase, pronounced suprastenotic dilatations develop, in which dilated areas of the jejunum resemble the colon. Ulcers, perforations and their consequences are less common.
One of the tasks of an x-ray examination is to identify complications of the underlying disease. Fistulas originate from transmural ulcers, passing through the entire thickness of the intestine and penetrating into adjacent structures. These can be simple isolated passages or a “star-shaped” complex spreading in various directions, retroperitoneal abscesses with the formation of fistulas, eccentric involvement of the intestinal wall in the pathological process. In 5-30% of patients, entero-intestinal, vesico-intestinal, enterovaginal or enterocutaneous fistulas are formed. Abscesses that arise after perforation are also found. In approximately 20% of patients with advanced stages of the disease, strictures occur, often accompanied by clinical symptoms of stenosis. According to a number of authors, in the stage of stenosis with the development of adhesions and fistulas, the use of CT and ultrasound is informative, which, however, are inferior to radiography in assessing early injuries of the mucous membrane.
In the classic book by I.L. Tager and M.A. Filippkina (1974) CD in children is considered mainly as terminal ileitis. For diagnosis, irrigoscopy is used, during which it is recommended to achieve colonic reflux in order to assess the condition of the ileum. The main radiological symptoms are described as the identification of a marginal filling defect along the medial contour of the cecum, which usually has a semicircular shape and corresponds to the location of the bauginian valve, which is explained by hyperplasia of the lymphatic apparatus of the valve and its edema. When assessing the terminal ileum, its narrowing and uneven contour, local soreness of the mobile intestine are revealed. The relief is altered by rounded filling defects caused by hyperplastic lymph nodes and Peyer's patches. In contrast to the normal relief, these defects are usually larger and more numerous; there are practically no longitudinal folds between them, characteristic of a normally functioning terminal ileum.
Almost all modern works on the issue of CD in children are clinical, where data obtained from X-ray examination are presented as one of the research methods. In this case, the material presented is mainly descriptive in nature. So E.I. Aliyev and V.G. Rumyantsev, as the main radiological sign of CD in children, indicates the segmentation of the lesion with a clear boundary between the changed and unchanged areas. Among other signs, the authors identify “aphthous ulcerations” - small, deep ulcerative defects, clearly visible with double contrast. As in adult patients, the progression of the process leads to the development of changes that are radiographically manifested by the “cobblestone pavement” symptom; strictures and fistulas are diagnosed (in 6-9% of patients). In acute cases of CD O.V. Vodilova (2004) did not reveal radiological signs of damage to the terminal ileum in 33% of children.
X-ray diagnosis of nonspecific ulcerative colitis
The first publications on the X-ray diagnosis of UC appeared in 1912, but to date there is no consensus on the X-ray semiotics of this disease. The main method of X-ray diagnosis of UC is irrigoscopy.
X-ray signs of UC are diverse and polymorphic. Irrigoscopy allows you to confirm the diagnosis based on a number of characteristic symptoms. However, according to almost all authors, the characteristic radiological symptom complex of UC can be observed only in patients with gross changes in the wall of the colon with an active (severe) and, as a rule, quite long-lasting disease with a frequency of 72-95%. At the same time, it should be noted that UC occurs without any specific pattern or sequence of development of the picture. It is possible to detect pronounced radiological changes with a short history and quiet course of the disease. And with a long-term active process, sometimes the most thorough X-ray examination does not reveal significant changes, even in the presence of damage to all layers of the intestinal wall, including muscle, cryptitis and crypt abscesses. The frequency of the X-ray negative form of UC, when there are no changes on X-ray examination or macroscopic specimens, but are detected only by histological examination of the intestinal wall, is, according to various sources, from 2.7% to 53%. Currently, a contrast study of the colon for the purpose of primary diagnosis is not indicated.
A thorough examination of all parts of the intestine is necessary, both during tight filling and after emptying. It is important to evaluate the location, thickness of the folds of the mucous membrane, and the nature of their surface in each small area. It is currently believed that inflammation in this disease begins in the rectum, spreading proximally until total colitis. Sometimes the appendix and distal ileum may be involved. Most authors believe that without damage to the rectum there is no UC. However, according to some authors, changes in the rectum are observed in only half of patients with colitis.
Variants of radiological segmental UC are also described with a frequency of 6.4% to 10.4%, in which one or more individual segments of the colon may be affected, which in this case are separated by areas of intact intestine. The location of the lesions most often coincides with the location of the sphincter zones of the colon. The radiomyotic characteristics of the affected areas coincide with those of common lesions, developing in a limited area of the intestine. Currently, this variant of the disease is distinguished conditionally, since histological examination reveals total damage to the colon in almost all of these patients.
With UC in the early stage, radiological changes are minimal and are manifested only by jagged contour of the colon and symptoms of functional disorders (spasms, accelerated filling of the colon, urge followed by rapid emptying).
The earliest sign of UC, detected with double contrast, is fine granularity of the mucosa; due to pronounced swelling, the surface of the mucous membrane becomes uneven and resembles sandpaper. The mucosal line becomes uneven, the contours of the intestine become jagged. As it progresses, the mucosa thickens, takes on a wavy appearance, with clearly visible superficial ulcerations. Deep ulcers give the impression that the mucous membrane is “pocked with nails.” Ulcerative niches can take the form of flat depressions surrounded by an infiltrative shaft, or small pointed protrusions on the contour of the intestine (a “brush” or “hedgehog” symptom). Irregularity of haustrations appears, haustrations become asymmetrical, deformed, and as the pathological process deepens, they disappear altogether. Changes in haustration are associated with both functional disorders and local violations vagosympathetic innervation, excessive increase in tone, infiltration and fibrosis of the submucosal layer, that is, with processes leading to a decrease in the plasticity of the intestinal wall. Straightening of the intestine develops, narrowing of the intestinal lumen and its shortening, alternation of pseudopolyps, islands of normal mucosa between the ulcers, which gives the intestine the appearance of a “drainpipe”.
To the radiological symptoms of UC in the early stage N.U. Schniger (1989) refers to the symptom of the “marginal barium strip” or “dotted line”, which is explained by the “sticking” of the barium suspension to the inflammatory changes in CO in ulcerative colitis.
After emptying, the X-ray picture is represented by thickened folds changing direction to longitudinal (“combed relief”). With the progression of the pathological process, the folds of the mucus become intermittent and pad-shaped due to sudden swelling, creating a picture of a rough cellular pattern similar to pseudopolyposis. In places of erosions and ulcers, accumulations of barium suspension are possible, causing the general spottiness of the relief (fine mesh, marbling). Irregular mosaic relief of the intestine as a result of its ulceration and edema is considered one of the characteristic signs of UC. The ulcerated mucous membrane of the colon is revealed on photographs in the form of characteristic jagged contours or well-defined craters.
Among the most significant radiological signs of UC are the accelerated (lightning-fast) filling of the altered, “irritated” area of the colon with barium suspension, often accompanied by pain, and its accelerated evacuation.
An important symptom is the presence or absence of haustrations, changes in the intestinal lumen, the extent and persistence of its narrowing. According to various authors, jagged contours of the intestine with its tight filling is a specific symptom of UC, although the interpretation of this symptom is different. Some authors believe that small protrusions are a reflection of the ulcers themselves, in the form of “niches” overlooking the contour of the intestine. Others believe that these fine serrations reflect the accumulation of barium between thickened folds.
It should be emphasized that there is no parallelism between the clinical and radiological picture of UC. X-ray semiotics and the severity of radiological symptoms of UC depend on the stage of the disease, the depth and nature of morphological changes and the duration of the disease. It has been described that during the period of remission of UC, partial or complete reversibility of radiological signs of the disease may occur.
In the initial stage of the disease, the x-ray picture is poor and is manifested mainly by “functional” disorders nonspecific to UC, often of a spastic nature. At the next stage of the disease, when endoscopic examination reveals certain changes in the relief of the mucous membrane (small ulcers, changes in the surface of the folds), and morphological studies reveal changes in all layers of the intestinal wall, the x-ray picture becomes more definite. The colon, when filled tightly, can be shortened, the intestinal lumen is narrowed due to the smoothness of the haustra. These symptoms are caused by spastic contractions of the muscle fibers of the submucosal layer. The intestinal contour becomes finely jagged due to densely located ulcerative niches or the flow of barium sulfate suspension between thickened and rigid folds of the mucous membrane. The relief of the intestinal mucosa after emptying has a fine mesh, “marble” appearance. The morphological basis of these changes are flat ulcerations on the surface of the folds of the mucous membrane, accumulation of mucus, blood and pus.
Ulcerations are better identified when double contrast is used, revealing multiple superficial ulcers located close to each other and poorly demarcated from the surrounding mucosa. According to V.B. Antonovich, the most reliable symptom of ulcers is the niche symptom. As the disease progresses, radiographs reveal large, irregularly shaped ulcerations, which also do not have sharply defined boundaries. Further destruction of the mucous membrane, submucosal and muscular layers leads to the formation of a fringed intestinal contour. The appearance of a double contour of the colon on radiographs is explained by the penetration of a suspension of barium sulfate under the serosa and indicates a perforated condition. It has been suggested that a double circuit can also be observed when a suspension of barium sulfate penetrates not into the subserosal space, but under the fibrous film or under a layer of mucus covering the inner surface of the intestine. It is possible that the double circuit of the intestine is due to the lack of full contact with the walls of the affected area due to excessive secretion of altered mucous blood and mucus.
In all stages of UC, pseudopolyposis states may be observed radiologically in 10-20% of patients. Their disappearance after successful therapy has also been described. Radiologically, pseudopolyps are small in size (up to 1 cm), sit on a wide base, most often they are located nearby, and they can often be connected into a single chain. Pseudopolyps are visualized as marginal or central filling defects, and after emptying - as a honeycomb, looped relief pattern (picture of a “granite pavement”, “turtle shell”). When the intestines are inflated with air, they may smooth out or shrink. Opinions about their radiological substrate vary widely. According to some authors, the picture of pseudopolyposis can be given by islands of inflammation on the surface of the mucous membrane and the reparative process at the site of former ulcerations against the background of newly emerging destruction of the mucous membrane. According to others, pseudopolyps are nodules of granulation tissue lacking epithelium. Perhaps they are islands of hyperplastic mucous membrane of various sizes and shapes, located between areas of ulceration. This combination of ulcerations and pseudopolyposis growths is radiologically difficult to distinguish from the cobblestone pattern in Crohn's disease.
In severe UC, the mucous membrane is completely destroyed. On radiographs taken after emptying, its relief is completely absent. On the walls of the intestine, only isolated blots of barium suspension are visible, lingering on fibrous films or lumps of mucus. At this stage of the ulcerative process, the entire intestinal wall is affected, including the muscular layer. The walls of the affected areas become thickened and rigid, which leads to shortening of the intestine and displacement (smoothing) of its natural curves. The large intestine in the affected areas takes on the appearance of a “hose”.
This causes the intestine to shorten and narrow. The contrast suspension easily fills the intestine and is easily removed from it, however, when filled tightly, the intestine looks like a tape or cast. The undulation and cyclical nature of the course of UC lead to the fact that a clearly defined picture cannot always be seen. Most often, fresh ulcerations and areas of proliferation, scars at the site of former ulcers and fresh inflammatory swelling of the mucous membrane are simultaneously present in the intestine. This creates a “variegated” picture and requires careful differential diagnosis, taking into account data from other research methods. A narrowing of the lumen may be detected due to swelling of the submucosal layer and hypertrophy of the muscular layer, expansion of the presacral space.
The terminal ileum should also be examined. Often it is not changed. But in patients with total damage to the colon, ulceration of the mucous membrane or expansion of the lumen of this section is often detected, in contrast to the narrowing characteristic of CD. According to various authors, in 10-50% of cases, inflammatory changes in UC spread to the terminal ileum - the so-called “reflux ileitis” (“retrograde ileitis”) occurs, although it is believed that regurgitation of the contents of the colon does not play a significant role in the occurrence of ileitis in this disease. In this case, in the affected part of the ileum, the disappearance of normal folding is observed, the mucous membrane takes on an uneven “granular” appearance and resembles that of the colon. The length of the affected area usually does not exceed 20 cm.
The classification of UC involves dividing it by localization. The latter is correctly established in 94.5% during X-ray examination. According to N.U. Schniger (1989) damage to the rectum only is detected in 2% of patients, proctosigmoiditis - in 20.5% of cases, left-sided - in 18.9%, with damage to the distal parts - 6.1%, total colitis - in 47.5%, regional – in 4% of cases.
Among the signs of total colitis, one should indicate a symptom of free movement: with semi-tight filling of the transverse section of the colon, the barium suspension is displaced into the ascending and descending sections of the colon. When the patient is moved from the back to the stomach, the radiopaque substance returns to the transverse intestine.
A serious complication of UC is intestinal perforation with the formation of fistulas and abscesses, both intraperitoneal and retroperitoneal. When conducting a standard x-ray examination, these complications are rarely detected; if suspected, it is necessary to conduct a study with a very liquid barium suspension or other contrast agents. As already mentioned, a survey x-ray of the abdominal cavity of a patient with severe ulcerative colitis can reveal the so-called toxic dilatation of the colon. In this case, the intestinal lumen can reach 20 cm in diameter, the intestinal wall becomes thinner, and the haustra disappear. Additional shadows are revealed (against the background of gases) caused by thickening of CO folds. Sometimes, against the background of a pathologically distended intestine, gas-filled ulcers in the form of spicules or mottling of the wall are visible, signs of their penetration into the subserous layer (in the form of a thin strip of gas in the intestinal wall). When ulcers perforate, free gas is detected in the abdominal cavity or in the retroperitoneal tissue. Most often, the colon is dilated (52.4%), less often transverse and descending (19%), left flexure (14.2%), total dilatation is observed in 9.5% of cases. It is believed that the basis of toxic dilatation of the colon is acute inflammation its muscle layer, paralysis of the intestinal wall. Among the complications of UC, intramural pneumatosis intestinalis has been described. It is possible to develop colonic strictures ranging from 5 to 10 cm in length. In the process of effective treatment, positive x-ray dynamics are observed. During the period of remission in patients with mild and moderate forms of ulcerative colitis, radiographs of the colon may be normal.
Based on observation of 60 children with UC I.L. Tager and M.A. Filippkin (1974) indicate the possibility of developing the disease in children of any age with a maximum frequency of 6-7 years. The authors especially emphasize the presence of X-ray positive and X-ray negative variants of the disease and the lack of strict parallelism between the data of X-ray examination, the clinical picture and endoscopic examination of the intestine. In mild forms of the disease and in remission, expansion of the intestine or its individual sections is possible, which may be explained by a decrease in tone and loss of contractility. In severe cases, the intestine is usually shortened and reduced in size due to the development of organic lesions, indicating deep damage to the intestinal wall. Very often there are signs of spastic colitis. A characteristic symptom is intestinal rigidity, leading to the development of the UC sign described by S.A. Ginzburg (1965): if the filling is not tight enough in the position of the patient on the back, the CV is not retained in the transverse colon and overflows into the descending and ascending colon, the transverse colon remains empty. If the patient is turned onto his stomach, the CV will flow into the transverse colon, freeing the descending and ascending ones. As in adult patients, one of the early symptoms is a change in the haustral pattern, primarily in the transverse colon, in the form of a decrease in their height, unevenness in their location and size, up to complete disappearance. With successful treatment, the haustral pattern can be restored. In this area, due to pronounced spastic contractions, the development of a radiological symptom described as a “bundle of sausages” may develop. Another important symptom UC – jagged contour. Both ulcerative defects and haustral deformation, uneven edema of the mucous membrane, and pseudopolyps may be involved in the formation of this sign. With multiple exposures to the contour of densely located ulcerative niches, a “spicule” pattern is created, however, a similar picture can also be created by the entry of CV into the Luberkühn glands or innominate recesses. Edema of the mucous membrane leads to the disappearance of the clear course of folds, changes in their direction, and the formation of filling defects. The latter may be caused by pseudopolyps. Most often, changes are recorded in the sigmoid colon. In advanced cases, there is no CO relief over a long distance at all, there is no haustration, and the intestine takes on a “hose-like” appearance.
Over the past 30 years, there have been virtually no other studies on the X-ray semiotics of UC in children. In a few pediatric (clinical) works there is a description of the X-ray picture of this disease. So N.E. Shchigoleva et al (2002) point out the dependence of the frequency of detection of radiological signs of UC on the age of patients. According to the authors, in children over 15 years of age they were detected in 93% of cases, while in other age groups - in no more than half of the cases. As in adult patients in the initial stages of the disease, irrigoscopy is not very informative and is contraindicated in cases of severe exacerbation. If toxic dilatation is suspected, a plain radiography of the abdominal cavity is necessary, which reveals the characteristic signs of this complication of UC. The main objectives of an X-ray examination are to identify the extent and degree of damage to the colon and conduct a differential diagnosis with CD. In severe and moderately severe colitis, the intestine is devoid of haustra, narrowed, its contours are jagged, the folds of the mucous membrane are either absent or have a longitudinal course (“combed relief”).
X-ray differential diagnosis of nonspecific ulcerative colitis and Crohn's disease
The nature of the spread of the process: with CD it is intermittent, eccentric, spreading in the distal direction, while with UC it is consistent, concentric, spreading in the proximal direction.
Localization also has its own characteristics. In CD, the terminal ileum and right parts of the colon are almost always affected; the rectum is not affected in most cases. With UC, the rectum and left parts of the colon are almost always changed, while the terminal part of the ileum is often intact. WELL. Schniger indicates the expansion of the affected part of the ileum in UC and vice versa, its narrowing in CD.
Segmented lesions and intermittent fields are characteristic of CD, while UC is characterized by continuous changes. As a rule, CD is characterized by the presence of a fairly sharp boundary between the affected and healthy areas of the intestine.
Ulcers of various localizations can occur in both CD and UC. In UC they are often irregular in shape, superficial and scattered. In CD - in the form of spicules, “nail heads”.
The cobblestone sign and pseudodiverticula are pathognomonic radiological symptoms of CD and do not occur in UC. The X-ray picture of UC is often supplemented by pseudopolyps of irregular shape in all altered sections, which is not typical for CD. Although G. Adler describes both pseudopolyposis and pseudodiverticula as symptoms characteristic of CD.
Strictures, fistulas, and peri-intestinal abscesses are detected much more often in CD than in UC.
Acute dilatation of the intestine is an extremely rare complication of CD, in contrast to UC, in which intestinal perforation often develops.
Thus, most of the works are devoted to the X-ray picture of advanced, long-term diseases from the group of IBD in adult patients. Currently, there is practically no data on the X-ray semiotics of this pathology in childhood. Early radiological symptoms of CD and UC remain poorly understood. It should be noted that in recent years there have been quite a few publications devoted to the X-ray diagnosis of gastrointestinal diseases, which is probably due to the opinion that it is insufficiently effective compared to endoscopic and other research methods. However, the availability, low cost, fairly high information content and uniqueness of the obtained X-ray data make it useful, and sometimes necessary, to carry it out as part of the diagnosis of IBD.
– 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; UC is 30% more common in them. 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 and collapse due to a significant fall 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 nonspecific 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 (vascular inflammation) , 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 proper 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 chronic inflammation intestines, it is recommended to increase the protein content in the 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 - derivatives of 5-aminosalicylic acid (sulfasalazine, mesalazine) and corticosteroids - are used as anti-inflammatory drugs for this pathology. hormonal drugs. 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 ineffective diet and conservative therapy, development of complications (massive bleeding, perforation of the colon, if there is a suspicion of a malignant neoplasm, 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
(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) violation 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 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.
In the stomach and thin section The intestinal microflora is extremely scarce, while its 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 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 especially great importance acquires medicinal intestinal dysbiosis. 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 severity. 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 dysbiosis, 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 and do not cause side effects and contribute to the normalization of 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 is established in immune status body, an identified imbalance in the system of lipid peroxidation and antioxidant protection is prescribed tocopherol (vitamin E), which is a natural bioantioxidant - 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. Most common reasons 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 direct toxic effect on the pancreatic parenchyma, increasing the viscosity and protein content of pancreatic secretion. 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 viral etiology 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 nuclear structures secretory elements, which the pancreas is so rich in. 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, chain reaction- A- and B-phospholipases are activated, converting bile lecithin 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.
In the works recent years The role of immunopathological processes in the pathogenesis of chronic pancreatitis is increasingly being pointed out, 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.
From methods physical examination patients needed to make a diagnosis of the disease should be given Special attention 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, peptic ulcer duodenum, cholecystectomy, allergic diseases may 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 taking fatty foods, overeating, drinking alcohol, 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 first to be excluded are: 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 back wall body and 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. This is a secretin-pancreozymine test, a gland stimulation test. 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 of their 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.
Ph.D. I.N. Shchetinina
Synonyms: severe ulcerative nonspecific colitis, ulcerative colitis, severe ulcerative colitis, severe nonspecific colitis, idiopathic ulcerative colitis, chronic hemorrhagic colitis, chronic purulent colitis, thromboulcerous colitis, parietal colitis, hemorrhagic-ulcerative rectocolitis, muco-hemorrhagic proctocolitis.
The most accepted and most correct name for the disease as an independent nosoological unit and to some extent reflecting the pathogenetic essence of the disease should be considered the name “ulcerative nonspecific colitis” or, if we take into account the potential severity inherent in this disease, “severe ulcerative nonspecific colitis.”
Ulcerative nonspecific colitis- a severe disease of unknown etiology, characterized by hemorrhagic-ulcerative inflammation of the large intestine with a tendency towards a chronic relapsing course, the presence of intoxication, often fever, endocrine metabolic and functional disorders of many organs and systems, as well as changes in the reactivity of the macroorganism.
Story [show]
The first mentions of the disease date back to the end of the last and the beginning of this century. Thus, Wilks and Mohan, then Allchin and Whise (1883) drew the attention of clinicians to a peculiar lesion of the large intestine, which occupies a special place among the numerous and varied lesions of the intestine. True, at that time there was no talk of a definite distinction between ulcerative nonspecific colitis and other diseases, for example bacillary dysentery or amoebiasis.
In 1903, Boas differentiated this disease from chronic dysentery.
The name ulcerative nonspecific colitis was given by A. S. Kazachenko in 1914, who described the bacteriological and some clinical manifestations of this disease.
In the further study of the disease in our country, the work of clinicians - I. A. Kassirsky, I. P. Bush - had a certain significance; A. G. Alekseeva, G. I. Terekhova and others.
The intensity of studying ulcerative colitis in various countries has paralleled the increase in its incidence. The largest number of studies and works in foreign countries dates back to the post-war period, starting from 1945-1950. In the Soviet Union, a relatively rare ulcerative nonspecific colitis in the last 5-6 years has been intensely attracting the attention of a number of clinical specialists, pathophysiologists, microbiologists, radiologists, pathomorphologists, also due to a slight increase in incidence in our country.
In Europe and America, the incidence of ulcerative nonspecific colitis, according to various authors (Mosbech, Rath, etc.), ranges from 4.5-5 to 10-15 per 10,000 patients in various hospitals. Moreover, in the countries of America, the incidence is approximately 10 times higher than in European countries.
It is apparently not yet possible to name the percentage of incidence of ulcerative nonspecific colitis in the Soviet Union due to its much lower prevalence, on the one hand, and also partly due to the lack of knowledge of this disease and its incomplete registration, on the other. The latter can be explained by insufficient familiarity practitioners a wide network with manifestations of the disease, since the increase in the incidence of ulcerative nonspecific colitis in our country compared to foreign countries occurred much later (only in the last 4-5 years) and did not reach the same extent as in European countries and especially America.
Detailed clinical descriptions of ulcerative colitis with development clinical features courses, complications abroad made by Bacon, Kirsner, Kuhn, Reiffersheid, Bargen, Bocus.
In our country, the works of A.F. Bilibin, E.M. Tareev, N.V. Davydovsky, S.M. Ryss are of great importance for deciphering the essence of the disease and its patterns. In recent years, the work of V.K. Karnaukhov, I.F. Lorie, S.I. Ratner and others has been devoted to the study of the clinical forms of the disease, the characteristics of the course and outcomes.
Much attention is paid to the study of metabolic disorders and biochemical changes in ulcerative colitis (M. E. Turchins, Ya. A. Makarevich, etc.). Pathogenetic treatment methods are being actively developed (A.F. Bilibin, S.I. Ratner, S.M. Ryss, Ya.A. Makarevich, I.N. Shchetinina, Kirsner, Watkinson, Kuhn, etc.), methods and techniques are being improved surgical treatment (A. A. Busalov and I. Yu. Yudin, A. A. Vasilyev, A. N. Ryzhikh and Zh. M. Yukhvidova). Important works regarding the virological, bacteriological study and the significance of superinfection in ulcerative colitis are the works of V. N. Krasnogolovets, S. I. Ratner, B. Ya. Padalka, Weinstein, Schneierson, Gailock, Syverton and others.
Thanks to in-depth, comprehensive studies by these authors and many others, the study of ulcerative colitis has advanced significantly.
The nosological independence of the disease became indisputable (A.F. Bilibin, E.M. Tareev, S.M. Ryss, Kirsner, Bacon, etc.).
A number of clinical classifications have been created that have practical value (A.F. Bilibin and I.N. Shchetinina, S.M. Ryss, V.K. Gerasimov, V.K. Karnaukhov, Khun, Reifferscheid).
X-ray diagnostic methods have been developed that are of great importance in this disease (S. A. Ginzburg, Cattan et al., etc.).
The ongoing study of ulcerative nonspecific colitis improves methods of recognition, treatment, helps decipher the disease in etiopathogenetic terms, which is extremely important for the treatment, and possibly for the prevention of this serious disease.
Etiology and pathogenesis
Despite the significant interest that has been shown over the past 10-15 years in the study of ulcerative colitis, many issues of etiology and pathogenesis remain incompletely deciphered and controversial.
None of the described microorganisms (protozoa or viruses) is given a special role in ulcerative colitis. However, the participation of microflora in the etiology and pathogenesis of ulcerative colitis certainly occurs, since damage by the inflammatory process occurs in an organ rich in diverse microflora, such as the large intestine. A variety of intestinal flora, especially such as staphylococci, Proteus, yeast-like fungi, due to the often developing intestinal dysbiosis in ulcerative nonspecific colitis secondarily, especially in seriously ill patients, can lead to manifestations of severe superinfection as a complication.
On the other hand, intestinal dysbiosis, resulting from any reason, for example, long-term use of antibiotics, can lead to clinical manifestations of superinfection and the development of enterocolitis (staphylococcal, proteus, fungal). Dysbacteriosis enterocolitis, causing chronic inflammation of tissues, changing the biochemistry and pH of the environment, can cause the occurrence of ulcerative colitis, thus playing the role of a primary factor and causing local damage to the mucous and submucosal layers.
In the etiology and pathogenesis of ulcerative colitis, a large role belongs to endogenous factors with processes of sensitization, autosensitization and, apparently, systemic lesions.
The etiology and pathogenesis of ulcerative nonspecific colitis in this regard is to some extent close to diseases such as the group of collagenoses, streptococcal and staphylococcal infections, and allergic diseases.
The etiology and pathogenesis of ulcerative colitis, closely intertwined with each other, like no other disease, should be considered in close connection.
Regarding the etiology and pathogenesis of ulcerative colitis, there are a number of theories in the literature that consider the disease from various aspects. Thus, supporters of the infectious or viral theory consider various microbes or viruses to be the causative agents of ulcerative colitis (A.N. Ryzhikh and Zh.M. Yukhvidova, Buil and J. Bargen, Hurst, Maskie, Felsen).
B.Ya. Padalka, based on his own observations and studies conducted with co-authors, came to the conclusion that the symptom complex of ulcerative nonspecific colitis in some cases may be caused by microbes of the Proteus group. The enzyme theory considers the cause of ulcerative nonspecific colitis in damage to the integumentary epithelium as a result of autolysis by enzymes of the gastrointestinal tract of the mucous membrane, devoid of protective mucus.
Proponents of the nutritional and vitamin theory explain the occurrence of ulcerative colitis by nutritional deficiency, the allergenic properties of certain animal products or vitamin deficiency, especially vitamin A, folic acid, nicotinic acid, as well as B vitamins. For hypersensitivity to food products and especially Truelove, Varro, Jung, Csernai, Szarvas indicate milk. Disruption of intestinal enzymatic processes in animal experiments due to changes in the nature of nutrition is noted by S. Ya. Mikhlin. Folic and nicotine deficiency in the experiment leads to morphological changes in the intestinal mucosa with ulcerations. Clinically, deficiency of folic and nicotinic acids in animals is manifested by profuse bloody diarrhea and exicosis.
Neurogenic and psychogenic theories of the pathogenesis of nonspecific colitis emphasize the role of damage to the autonomic nervous system and imbalance of autonomic innervation. Engel believes that a “mental state” (depression, asthenia) is a necessary condition for the development of ulcerative colitis, when the body’s defenses are lost. Kuhn also recognizes the importance of mental characteristics of the individual in the causes of the development of ulcerative colitis. Proponents of this theory attach great importance to neuropsychic factors and conflict situations, mental and physical trauma in the occurrence of ulcerative colitis or its relapses. I.F. Lorie considers ulcerative nonspecific colitis as a special form of corticovisceral neurosis.
In the pathogenesis of nonspecific ulcerative colitis, a number of authors quite rightly attach importance, along with other aspects, to endocrine disorders, in particular dysfunction of the adrenal glands (S. M. Ryss, M. E. Turchins, etc.). The observations of these authors show the phenomena of hypocortism and a decrease in the reserve capacity of the adrenal cortex under ACTH load.
Among other theories of pathogenesis, one can mention theories of blockage of the lymphatic vessels of the mesentery, similar to blockage of the lymphatic ducts in regional ileitis.
The most noteworthy and most widespread at present is the theory of allergy, which explains the cause of ulcerative colitis in the processes of sensitization and autoimmunization (Kirsner, Kuhn). The importance of autoimmune processes with the production of autoantibodies is indicated by S.E. Makievskaya and I.S. Atserova and others.
If we approach the etiology of ulcerative nonspecific colitis in a simplified manner and look for the cause among certain microbes or viruses, or in understanding the essence of this disease we see only enzymatic, endocrine or other selective lesions, then the general patterns of development with extreme variability and diversity of clinical forms will remain undeciphered. The uniqueness in ulcerative nonspecific colitis, as in other diseases, is also determined by individual characteristics - the degree of inflammatory reactions, adaptation processes, changes in the body's reactivity, characteristics of nervous activity and endocrine correlations (I. P. Pavlov, A. F. Bilibin, I. V. Davydovsky, A. D. Speransky, E. I. Tareev).
Our observations, as well as observations of other authors (V.K. Karnaukhov, M.V. Lorie, S.L. Erez and employees, Kuhn, Varro, Law and employees, etc.) revealed the importance of various unfavorable factors in the development of ulcerative colitis impacts: mental stress, physical trauma, unsystematic and uncontrolled treatment with antibiotics and chemotherapeutic agents, hormonal changes and endogenous intoxications (for example, during pregnancy), excessive solar radiation and, possibly, others.
Analyzing the features of ulcerative nonspecific colitis, one should emphasize the damaging nature of the injury, when the inflammatory and generally protective reaction, due to its redundancy, follows the type of hyperergic inflammation and sometimes completely reproduces the phenomenon of Arthus, Schwartzman and Auer with necrosis, destruction of the mucous, submucous membranes and even muscle layers over a large area of the large intestine. In such patients, the disease is characterized by acuteness, severity, and a “fulminant” course.
It is difficult to understand the pathogenetic essence of acute forms of ulcerative colitis without manifestation of the hyperergic nature of inflammation. As an illustration of the damaging nature of the lesion and necrosis of the mucous and submucosal layers over a large area, a photograph of a macroscopic specimen of the large intestine of a patient we observed with an acute form of ulcerative nonspecific colitis of a very severe fulminant course is given. The duration of the disease is 2 months. Perforation of 2 ulcers of the transverse colon, diffuse purulent peritonitis (Fig. 34).
Extensive fields of necrosis of the mucous and submucosal membranes, and in some places of the muscle layers, are visible. The mucous membrane was preserved in the form of separate rare islands (dark spots).
Hyperergic reactions characteristic of ulcerative colitis indicate a change in the body's reactivity.
Changes in reactivity, sensitization, allergic processes develop to a certain extent not only in severe, but also in moderate and mild cases of ulcerative nonspecific colitis (own observations, V.K. Karnaukhov, S.E. Matsievskaya and I.S. Atserova, Kirsner, Koffeer et al., Good and Condie, etc.).
Confirmation that sensitization and allergic reactions occur in ulcerative nonspecific colitis is the combination of ulcerative colitis with allergic diseases, such as bronchial asthma, stated by many authors. allergic conjunctivitis, combination with erythema nodosum, joint damage. Drug intolerance, eczema, and allergic rhinitis are often observed. An increase in eosinophils with simultaneous lymphocytosis, characteristic of diseases with altered reactivity, is often observed in ulcerative colitis.
Allergic reactions not only develop during ulcerative colitis and thus play a role in pathogenesis, but also precede the development of ulcerative colitis, and in our opinion, partially determine it. This is evidenced by the work of a morphological profile, which speaks of early primary vascular damage, occurring even before pronounced inflammatory reactions, as well as the nature of the inflammation itself with the proliferation of plasmacytic cells, edema, eosinophilia and abundant infiltration of lymphocytic cells (T.F. Kogoi, Kirsner, Lumb and etc.) (Fig. 35).
In some patients, it is clearly possible to detect the development of ulcerative nonspecific colitis as a result of long-term massive treatment with antibiotics with allergic reactions to them and superinfection.
Many authors, whom we join (I. Polsak, Vo Vokurka, and M. Skalova, E. S. Makievskaya and I. S. Atserova, Par, Bernier, Kirsner, Koffeer et al.), believe that sensitization (change in reactivity towards hyperergy) in ulcerative colitis is associated with autoimmune processes. Autoantibodies to colon tissue can be detected in the blood of patients with ulcerative colitis. The presence of autoantibodies in the blood of patients, the increase in their titer during relapses and the gradual disappearance after colectomy confirm the importance of autoimmunization in ulcerative colitis. The circulation of autoantibodies in the blood is also known in other diseases, in which autoimmunization and conflict situations play a role ( hemolytic anemia, systemic collagenosis, acute nephritis, myocardial infarction and some others). It was in the light of autoimmune processes that the recurrent and progressive nature of collagenosis and the significance of para-allergies in this process became clear.
Severe ulcerative colitis is also characterized by a recurrent and often progressive nature of the lesion.
Ulcerative nonspecific colitis, like many autoimmune diseases, is characterized by an increase in globulin fractions in the blood serum, especially γ-globulins. An increase in globulins has been noted by many authors both in active phases and during remissions.
A necessary condition for tissue to acquire antigenic properties and cause autoimmune processes with the production of autoantibodies is tissue damage, similar to what happens with myocardial infarction or glomerulonephritis. Damage to colon tissue is possible during various diseases with inflammation of colon tissue. Of these diseases, chronic dysentery should be mentioned first of all, which is also characterized by allergic processes, dystrophic changes, and dysbacteriosis. That is why it is impossible not to dwell on the significance of dysentery or other lesions of the large intestine, especially chronic ones, as in the first link with the subsequent development of the process and deeper sensitization of tissues, deepening during dysbacteriosis, changes in pH, disturbances in vitamin metabolism, and enzyme disorders.
The development of ulcerative nonspecific colitis among patients who have had dysentery is indicated by S.L. Erez et al., L.G. Ghukasyan et al. In addition, apparently, various intestinal dysfunctions with enzyme or motor disorders and various types of dyspepsia (hepatic, gastrogenic, fermentative), gastric ulcer, amoebiasis, etc., have a certain significance in the development of the symptom complex of ulcerative nonspecific colitis.
The above observations do not indicate an etiological connection between ulcerative nonspecific colitis and a dysenteric pathogen, but indicate a pathogenetic cause of ulcerative nonspecific colitis in some patients with dysenteric lesions. A.F. Bilibin, highlighting ulcerative nonspecific colitis as a nosological form, emphasized the possibility of such a connection and conditionality (IV form of chronic dysentery with severe vasculitis and neurodystrophic lesions).
Secondary flora in ulcerative nonspecific colitis at certain stages, due to the development of severe dysbiosis, can not only cause vitamin and enzymatic changes, not only support the inflammatory process, altered pH, but also occupy the leading pathogenetic link and even cause death as a result of the development of sepsis, septicopyemia, septic endocarditis. However, dysbacteriosis cannot be considered the cause of ulcerative colitis in all cases. Among our even seriously ill patients with acute and chronic forms of ulcerative nonspecific colitis, intestinal dysbiosis was registered only as the disease progressed in some of these patients after 1-2 months, and sometimes more, from the onset of the disease.
According to the observations of V.N. Krasnogolovets, intestinal dysbiosis does not develop in all patients with mild and moderate ulcerative colitis at the onset of the disease, while the classic onset of ulcerative nonspecific colitis is precisely the gradual development of the disease, when only an admixture of blood appears in the stool without mucus and pus, increased bowel movements and disturbances in the patient's condition. Rectoscopic changes in such patients in these initial phases do not show an inflammatory process; a decrease in resistance, fragility of blood vessels, bleeding, and edema are detected.
Analyzing the main features and conditions of ulcerative nonspecific colitis, which characterize the occurrence and course of ulcerative nonspecific colitis, the scheme of etiological and pathogenetic development, in our opinion, can be imagined as a chain of links with complex cause-and-effect processes, often closing in the form of a circle due to interdependence chain reactions.
Scheme of the main links of the pathogenetic chain
- Local damage to the mucous and submucosal lining of the large intestine with sensitization, neurodystrophic changes with vascular damage during dysentery, dysbacteriosis, protozoal colitis and other diseases of the gastrointestinal tract.
- Dysbacteriosis - enzyme and vitamin disorders, increased tissue sensitization, inflammatory reactions.
- Allergic reactions, hyperergic nature of inflammation with destruction and destruction of the mucous and submucosal layers.
- Intoxication as a result of absorption of toxic substances and autointoxication as a result of necrotic processes.
- Various metabolic and functional disorders of internal organs and systems. Endocrine-vegetative disorders of the regulatory functions of the central and autonomic nervous system. Dystrophic processes.
- Autoimmune processes as a result of qualitative changes in the tissues of the large intestine due to necrotic processes. Autosensitization. Disadaptation.
- Remissions are a result of the protective-adaptive mechanisms of the macroorganism and the pronounced compensatory capabilities of the gastrointestinal tract.
Desensitization. Restoring physiological balance (Fig. 36).
The recurrent nature of ulcerative nonspecific colitis with persistent and sometimes long-term remissions of 5-10-20 years (own observations, Carlson et al., Kirsner, Kiefer) indicates the possibility of stopping the development of ulcerative nonspecific colitis, and therefore the promise of therapeutic and conservative treatment methods that are gradually replenished and corrected in parallel with the study of pathogenesis and features of clinical manifestations.
Pathological anatomy
Pathoanatomical changes in ulcerative colitis, due to high mortality, have been studied quite widely using sectional material. In addition, studies were conducted using intravital biopsies of the large intestine, as well as surgical specimens during total or partial colectomies.
Morphological changes in ulcerative colitis affect primarily the large intestine, sometimes part of it (segmental damage), sometimes all parts (total damage). In most cases, even severe ones, the lesion does not extend above the ileocecal valve. However, often in cases of chronic persistent course, the lesion can spread to the terminal ileum.
Inflammatory changes of a limited or diffuse nature are expressed by a necrotic-ulcerative process, acute or more often chronic.
Despite the significant amount of work carried out on the morphological profile, there is currently no consensus on the interpretation of the morphological changes that develop with ulcerative colitis in the large intestine, as well as their pathogenetic significance. Some authors (Warren, Sommers) consider “cryptitis,” i.e., purulent inflammation of the liberkühn glands, to be the initial manifestations of the disease. However, the position of primary purulent “cryptitis” is denied by many authors. According to Levine et al., the primary lesion in the development of ulcerative colitis is damage to the basement membranes of the intestinal epithelium. This damage causes the penetration of various microorganisms into the thickness of the intestinal wall and the development of an inflammatory process in it, followed by ulceration. However, this view is also disputed by researchers.
Most authors believe that the early and even primary lesion in ulcerative colitis is vascular damage. The defeat is expressed in circulatory disorders, hyperemia, capillary ectasia and hemorrhages in the intestinal wall. The mechanism of these circulatory disorders is unclear, but may be associated with neurovascular disorders or a consequence of sensitization of colon tissue with a subsequent hyperergic inflammatory response, which is characterized by early vascular damage (Goldgraber, Kirsner, Gallar Mones, Gallart Esquerdo, Delarue, Busson) .
Lumb, along with the inflammatory process in the liberkühn glands, also attaches great importance to vascular changes, which are always sharply expressed in cases of acute severe course. A common finding in ulcerative colitis is desquamation of the endothelium, thrombosis of blood vessels that contribute to ulceration. A number of authors describe vascular damage in the form of vasculitis and even vasculitis such as nodose periarteritis (T. F. Kogoi and others).
Of interest is the point of view expressed by some authors that ulcerative nonspecific colitis is based on sensitization of the tissues of the large intestine due to various external allergens or due to autoallergy, since it helps to decipher some aspects of the pathogenesis, in particular the phenomena of hyperergy, especially pronounced in acute forms with rapid manifestations of the disease and high mortality. These authors (T.V. Kogoi, Goldgraber, Kirsner) see confirmation of the allergic nature of the disease not only in early vascular damage, but also in the nature of the cellular reaction with infiltration of eosinophils, plasma cells, and lymphocytes.
Regarding the nature of the morphological changes in the large intestine during ulcerative colitis, there are also views that are less common and so far unproven, namely, that in the development of the lesion the main role belongs to the factor of congenital inferiority of the regeneration of the thick epithelium. The nature of morphological changes was studied, in addition to the use of sectional and biopsy material, also experimentally on animals. The difficulty of this kind of research for morphological work and for elucidating pathogenesis lies in the lack of an experimental model. However, in experiments on animals (monkeys, dogs, rabbits), a significant frequency of vascular lesions with a hyperergic nature of inflammation of the tissues of the large intestine was established.
Based on our own clinical and morphological observations in collaboration with T.F. Koga and I.Yu. Yudin, we showed that in acute, subacute forms of ulcerative nonspecific colitis, as well as in acute (the morphological part of the work was carried out at the Department of Pathological Anatomy II Moscow Medical Institute named after N. I. Pirogov T. F. Kogoy, head of the department - full member of the USSR Academy of Medical Sciences Prof. I. V. Davydovsky) in severe relapses of chronic forms, the colon is macroscopically swollen, hyperemic, easily torn, multiple ones are found on the mucous membrane erosions and ulcers with uneven edges and bottom. There is a tendency of ulcers and erosions to merge with each other into extensive erosive and ulcerative surfaces, covering the entire surface of the intestine. In some patients, the mucous membrane was preserved only in the form of separate islands (“destructive pseudopolyps”).
Histological examination of this material revealed that the inflammation is necrotic-ulcerative in nature with the lesion spreading to the submucosal layer inclusive, and in some cases spreading to deeper layers. In the development of perforations, not only the spread of the necrotic process of the mucous membrane deep into the intestinal wall is important, but also focal changes in the muscle layer in the form of myomalacia and hemorrhages.
Extremely characteristic of ulcerative colitis, in our opinion, are lesions of the vessels of the submucosal layer and collagen tissue in the form of fibrinoid necrosis, found in most cases. These changes indicate a hyperergic tissue reaction, characteristic of diseases with altered reactivity. In some cases, productive endovasculitis is found.
In addition to the described changes, abundant infiltration, especially of the submucosal layer, with plasma cells, eosinophils and lymphoid cells is characteristic. T.F. Kogoy did not find cryptitis, or cryptoabscesses as they are called, in the acute progressive course of the disease, which, apparently, is explained by necrosis and death of the mucous membrane almost throughout its entire length. On the contrary, in chronic forms, cryptabscesses are often found. In cases of the formation of granulation tissue during an acute course with reparative phenomena, purulent infiltration took place, apparently as a manifestation of the activation of secondary flora and the inflammatory process.
It should be noted that more or less pronounced reparation also occurs in acute severe ulcerative colitis, which indicates the possibility of a favorable course and reverse development even in this severe form of ulcerative nonspecific colitis. However, the restoration is incomplete. The surface of the intestine in such cases is granulation tissue without full epithelialization with pseudopolyposis.
In the chronic course of the disease, the large intestine becomes deformed, sharply shortens, thickens and becomes rigid. Diffuse or segmental narrowing of the lumen is often observed. The described opinions depend on the fibrous and sclerotic processes of the submucosal layer, and sometimes the muscular one. The degree of deformation is related to the depth of the ulcerative process during active manifestations. In cases of chronic forms, the formation of multiple pseudopolyps, less often true adenomatous or mixed ones, is also often observed.
Findings of cancerous degeneration in ulcerative colitis based on observations are quite rare. However, malignancy is possible. The range of percentage of malignancy described by various authors is quite wide and to a certain extent depends on the duration of the disease. In the chronic form, vascular damage also occurs; characterized by sclerosis vascular wall. Acute vasculitis is rare. Changes in the type of periarteritis nodosa are possible. As with acute form, in chronic forms, perivascular infiltrates are found in all layers, as well as abundant infiltration of the mucous and submucous membranes with eosinophils, plasma cells and lymphocytes. Sometimes Roussel's bodies, a kind of giant cell granulomas, consisting of epithelioid cells with single Langhans-type cells, are found. The presence of such granulomas is described by various authors and is even classified as a special form of lesion - granulomatous colitis. Granulomas also form in regional lymph nodes.
Lesions in ulcerative nonspecific colitis of any form are also found in the intramural nervous apparatus of the intestinal wall with its deep destruction. When the terminal segment of the ileum is involved in the process, changes similar to processes in the large intestine develop.
Pathoanatomical changes in ulcerative colitis from other internal organs and systems, in addition to the intestines, have been less studied. Dystrophic changes in parenchymal organs and myocardium are described. Liver damage is common. By studying changes in the liver using puncture biopsy, it was possible to show that severe fatty degeneration of liver cells, a mesenchymal reaction, and edema are developing. Detectable infiltrates consist of mononuclear cells - lymphocytes, histiocytes. Focal necrosis may be found. Similar changes (M. T. Sinelnikova and M. E. Turchins) occur in cases of severe acute forms (“fast-flowing forms”), Ya. A. Makarevich also notes similar changes in the liver in his studies. Fibrosis and cirrhotic changes in ulcerative colitis, according to these authors, are uncharacteristic.
In patients with superinfection, especially in cases of accession staphylococcal infection, it is possible to detect various secondary purulent foci in the lung tissue, liver, brain, and develop acute or subacute septic lesions of the valvular apparatus of the heart.
Clinic
Clinical manifestations of ulcerative colitis are very diverse and extremely variable. Beginning gradually, in most cases the disease then develops differently both in terms of severity and duration, with peculiar clinical manifestations in each individual patient, depending on the individual characteristics of the macroorganism and environmental conditions.
Various authors (clinicians and pathologists) have proposed a number of classifications. However, there is still no single generally accepted clinical classification. The classifications of V.K. Karnaukhov, V.K. Gerasimov are certainly interesting and have practical significance, and among the classifications of foreign authors - the classifications of Reifferscheid, Kirsner. According to the classification of V.K. Gerasimov, the following clinical forms are distinguished: 1) acute fulminant, 2) acute, 3) chronic.
- A. Chronic relapsing form: a) relapse stage (without general reactions of the body, with a moderate general reaction of the body); b) remission stage.
- B. Chronic continuous form.
- Localization (prevalence of the process).
- Total damage to the colon: a) with damage to the ileum; b) without damage to the ileum.
- Segmental lesions of the large intestine: a) right-sided - cecum and ascending colon; b) transverse - transverse colon; c) left-sided - descending, sigmoid colon, rectum.
- The degree of damage to the mucous membrane of the rectum and S-shaped intestine (sigmoidoscopy picture):
1st degree - swelling, hyperemia, bleeding, slight soreness, granularity, single petechiae, erosion;
2nd degree - everything is the same as in I degree, only to a more pronounced degree, as well as multiple petechiae and erosions, single large ulcers;
3rd degree - everything is the same as in the first two degrees, and extensive ulcerative surfaces;
4th degree - mixed (1st, 2nd, 3rd degrees). - Complications.
- Local: 1) pseudopolyps, 2) polyposis, 3) narrowing of the intestinal lumen, 4) secondary infection, 5) perforation, 6) intestinal bleeding, 7) pericolitis, 8) fistulas.
- General: 1) arthritis, 2) phlebitis, 3) colon cancer, 4) hepatitis and fatty liver, 5) endogenous dystrophy, 6) skin lesions, 7) septicemia, 8) endocarditis, 9) nephritis.
Below is a classification of clinical forms of ulcerative nonspecific colitis, developed on the basis of the characteristics of the clinical manifestations of ulcerative nonspecific colitis by A.F. Bilibin and I.N. Shchetinina (Table 8 [show] ).
| Table 8. Classification of ulcerative colitis | |||||
| Form | Heaviness | Clinical signs | Localization of colitis | Complications | Exodus |
| I acute | Heavy, including lightning fast | Acute onset, high temperature, severe intoxication, frequent mucous-purulent-bloody stools. RRS - significant changes. Stomach ache | More often total, less often left-sided | Common: perforation, bleeding. Dysbacteriosis. Toxic Megacolon. Pseudopolyposis |
Mortality 40-50%. Transition to chronic form |
| Moderate | Acute onset, fever, loose, frequent mucous-bloody stools. RRS - pronounced changes. Stomach ache | More often left-sided or segmental, less often - total | Perforation and bleeding are less common. Local. Dysbacteriosis | ||
| Lightweight | Acute onset, symptoms of enterocolitis, mucous-bloody stool. RRS - typical changes, but often not ulcerative lesions | Most often left-sided or segmental | Local | Transition to chronic form. Remissions | |
| II subacute | The same options as for the acute form | The onset is gradual, then the rapid development of the disease with symptoms of acute forms and often severe course. RRS - pronounced changes | Rapidly progressive left-sided. Total | The same as in the acute form | The same as in the acute form of severe and moderate severity |
| III chronic 1) Recurrent |
Heavy | Recurrent nature of the course, periods of remission. Relapses with symptoms of acute severe forms. Possibility of developing acute relapses of fulminant course | Left-sided or total, rarely segmental | Perforation, bleeding pseudopolyposis. Dysbacteriosis. Local | High mortality in acute relapses and long-term (over 10 years) course. Unstable and incomplete remissions |
| Moderate | Longer remissions, less relapse severity, RRS normalizes during remissions | Left-sided, slowly progressive segmental | Local. Bleeding, pseudopolyposis | Relapses. Remissions | |
| Lightweight | Muco-bloody or purulent-bloody impurities in the stool. RRS pathological during exacerbation | Most often segmental. Sigmoid and/or rectum | Local | Relapses. Persistent and long-term remissions | |
| 2) Continuous | More often severe, less often moderate | Persistent, long-term course, absence of remissions. Liquid, mucous-purulent-bloody stool. RRS - pronounced changes when localized on the left | Total. Left-handed or right-handed | The same as for chronic recurrent forms of severe and moderate severity | The same as in the chronic recurrent form of severe and moderate severity |
| Note. Abbreviation RRS - sigmoidoscopy. | |||||
In the above classification, in addition to the acute and chronic forms described by most authors, we have identified a peculiar form of subacute course, initially reminiscent of chronic forms, but rapidly progressing with the spread of the lesion to the entire large intestine and increasing severity within 2-4 months from the onset of the disease. type of acute lightning forms. The above classification is constructed highlighting the form of the course, severity, clinical signs, localization of the process, possible complications and outcomes of the disease.
Each of the forms - acute, subacute and chronic - has its own characteristic clinical and some pathogenetic features, the significance of which is necessary for timely recognition and treatment.
- Chronic forms [show]
Most often (in 85-90% of cases, according to some authors, and in 50-60%, according to others), ulcerative colitis begins gradually. The first and often the only manifestation of the disease in such cases of gradual onset is the admixture of blood in the formed stool. The well-being and condition of patients for some time (sometimes for a long time - months and even years) may not be disturbed, appetite is also preserved, and there may be no abdominal pain. The gradual onset of the disease is considered by most authors to be classic for ulcerative colitis. The lesion, as a rule, in chronic forms with a gradual onset begins with the rectum and sigmoid colon. Patients seeking medical advice and help are most often interpreted as having hemorrhoids. This erroneous diagnosis is made due to the presence of scarlet blood in the formed stool - a symptom characteristic of hemorrhoids, as well as due to the frequent tendency to constipation in patients with ulcerative nonspecific colitis during this period.
Repeated visits from patients with similar complaints usually force the doctor to assume the possibility of a malignant neoplasm of the large intestine, especially if by this time the patients begin to experience weakness, abdominal pain with intestinal dysfunction in the form of short-term diarrhea, weight loss, and weakness. Appetite is gradually impaired, weight loss increases, and loose stools appear more and more often.
Chronic forms of ulcerative colitis are characterized by exacerbations or relapses. Relapses are replaced by remissions. During the period of remission, all clinical manifestations of the disease may disappear, but weakness and loss of ability to work often persist for a long time.
During an exacerbation of chronic forms of a recurrent course, the well-being of patients is significantly disturbed, severe weakness is noted, there may be abdominal pain, and tenesmus is possible. The stool is liquid, frequent, with impurities not only of blood, but also of mucus or pus. Body temperature is usually normal or subfebrile. However, during periods of relapse with severe exacerbation, there may be an increase in temperature to high numbers, which characterizes the severity of the process or is associated with the activation of secondary intestinal flora and the development of various purulent complications.
Chronic relapsing forms in clinical picture due to periodic exacerbations resemble the clinical picture of chronic dysentery. However, the similarity is very distant.
From the very beginning of ulcerative colitis, changes detected during sigmoidoscopy are extremely characteristic. Early damage to the vessels of the mucous and submucosal layers in ulcerative nonspecific colitis explains the appearance of blood in the early period of the disease as the first symptom. The same early primary lesion of the vessels of the large intestine characterizes the picture of sigmoidoscopy in the early phases of the disease. The fragility of blood vessels and the appearance of bleeding of the mucous membrane when touched with a rectoscope should be considered characteristic. Bleeding can be expressed to a moderate degree, but often the bleeding is diffuse in the form of drops on the walls or a strip of blood that stretches behind the rectoscope when it is removed. Following a decrease in the resistance of the mucous membrane and bleeding, swelling of the mucous membrane, erosive and ulcerative lesions appear as a result of vascular damage and incipient tissue inflammation. These changes are characteristic of later periods of the disease. Mucopurulent-bloody effusion on the walls of the rectum and sigmoid colon is also often found in the later period of the disease, especially in patients with the addition of secondary flora in the form of secondary dysbacteriosis and superinfections. In these same cases, dense fibrinous films or widespread purulent folliculitis can be detected. Erosive and ulcerative lesions can be extensive up to the destruction of the mucous membrane over a significant extent, then the mucous membrane has the appearance of “chopped meat”. Individual ulcers can be of varying depth and size. The mucous membrane between individual ulcers or erosions is always changed, hyperemic, edematous with areas of old and fresh hemorrhages.
Since in ulcerative nonspecific colitis the lesion most often begins in the rectum and sigmoid colon, sigmoidoscopy reveals characteristic changes in almost 100% of cases (95%, according to our observations).
The peculiarities of damage to the mucous membrane in ulcerative nonspecific colitis should also include dynamics, which are characterized by persistence and long-term persistence of mucosal bleeding, even in patients with beginning remission and normalization of stool. Reduced resistance of the mucous membrane and fragility of blood vessels are often detected during periods of remission for a long time (months or years). Clinically, in these patients, with clear stool, the appearance of blood may occasionally be noted. Such patients should be under constant medical supervision due to the possibility of relapse.
In cases where the lesion is localized in some other segment of the colon, and not in the sigmoid or rectum, with clinical and anamnestic manifestations typical of ulcerative nonspecific colitis, a sigmoidoscopy examination does not reveal pathology. Segmental lesions that do not involve the rectum or sigmoid colon are rare in ulcerative colitis, but are possible, which the clinician must remember.
The duration of chronic forms of ulcerative colitis can be different - from 1-2 to 6-10-20 years or more.
Clinical manifestations of severity also vary. The prognosis is especially unfavorable in chronic forms with a progressive nature of the lesion, i.e. when each exacerbation, relapse of the disease, is accompanied by the involvement of more and more new parts of the large intestine in the process. The lesion can spread to all parts of the large intestine and rectum (“total colitis”). The progression of the process is usually accompanied by severe clinical manifestations during exacerbations.
In these cases, each subsequent relapse is more severe than the previous one, and remissions are short-term and often incomplete.
The recurrent nature of the course and the progression of the process indicate active manifestations of the disease. On the contrary, the absence of relapses or progression of existing manifestations of the lesion indicates compensation, more or less long-term remission in some and recovery in others. Most clinicians point out that the increasing severity of relapses of the disease, short-term and incomplete remissions are unfavorable with regard to severe complications and the overall prognosis of the disease. With these same forms, a higher mortality rate is also observed. The longer the course of the chronic form, the higher the mortality rate: from 4% in the first 3 years of the disease to 10-20-40% or more during 10-25 years of the disease (Dick, Kuhn, etc.). The longer the remission, the more complete the compensation during it, the more favorable the prognosis for the patient.
The duration of remission with a favorable course can vary - from 1-3 to 5-10 years or even more. Under our supervision there was a patient whose remission lasted about 20 years and was complete. The possibility of long-term full remissions is indicated by Garleson et al., Kirsner et al., Kiefer et al.
A fairly constant symptom, in addition to those described above, with ulcerative nonspecific colitis is the patient’s complaint of severe intestinal flatulence, rumbling, increased urge to defecate, increased number of bowel movements even in the absence of diarrhea. The appearance of these symptoms during remission is often associated with a violation of the functional activity of the gastrointestinal tract, the development various types dyspepsia and often precedes a relapse of the disease.
A type of clinical manifestation of severe chronic forms of ulcerative colitis is the continuous course of the disease without remissions with only a temporary weakening of symptoms. This course, as a rule, indicates significant severity and prevalence of the lesion. The course is especially persistent in cases where the process spreads to the small intestine. These patients have a malabsorption in the small intestine, a violation of many types of metabolism (protein, fat, water, carbohydrate, mineral) with a sharp depletion of the patients.
Acute relapses of a fulminant course occur most severely with high mortality in both chronic recurrent and chronic continuous forms of ulcerative nonspecific colitis.
Clinical manifestations during a severe acute relapse resemble the symptoms of acute forms of the disease: high (up to 39-40°) often remitting temperature, severe intoxication, abdominal pain, innumerable loose mucous-bloody-purulent stools.
An acute relapse of a severe course can develop after complete remission and apparent recovery, be the first, second or third, and occur several months or several years after the first manifestations of the disease. As a rule, relapses of the acute course are accompanied by total damage to the large intestine with pronounced destructive processes of inflammation, destruction of the mucous and submucosal layer and the formation of pseudopolyps (Fig. 37, 38).
In Fig. Figure 39 shows the temperature curve of a patient with an acute relapse of a severe course in a chronic form.
- Acute and subacute forms of ulcerative colitis [show]
These forms are characterized by severe hemorrhagic-ulcerative inflammation of the large intestine with sharp destructive changes in the mucous membrane and especially the submucosal membrane, and the formation of pseudopolyps. The extremely acute and rapid development of the disease, often with total damage to the large intestine, is accompanied by severe intoxication, high fever, damage to the cardiovascular system, significant changes in protein metabolism, an increase in leukocytosis, band shift and high ROE. The stool is frequent, sometimes without counting, liquid, mucous or purulent-bloody.
The high mortality rate in these forms (up to 30-50%) is explained by the frequency of severe complications - intestinal perforation, toxic expansion of the large intestine, the development of sepsis, septicopyemia and dystrophy, occurring by the end of the 1st or 2nd month from the onset of the disease, and sometimes and during the first 2-3 weeks.
Deaths from sudden intoxication and collapse during even the first days of illness have been described. Along with a severe course in patients with acute and subacute forms, the disease can also occur in a moderate form.
It can be assumed that acute forms are more common than they are described in the literature and recorded, due to the difficulty of diagnosing the initial period.
The acute onset of ulcerative nonspecific colitis, in addition to patients with acute forms, is also observed in chronic forms. In 39% of patients with chronic forms we observed, the disease had an acute phase, that is, it began as an acute form with subsequent transition to chronic.
The severity of the initial period varies, but it can be noted that the more acute and longer the initial period, the more severe and more frequent the disease returns subsequently and the more widespread the damage.
When assessing the severity of the course, in addition to clinical tests, serious prognostic biochemical changes should be taken into account - a simultaneous increase in α 1 - and α 2 -globulin fractions, an increase in blood transaminases, as well as an increase in leukocytosis, a sharp band shift and acceleration of ROE.
X-ray examination of the large intestine also influences the severity of the prognosis, but it is relatively contraindicated in acute manifestations of ulcerative colitis. In such cases, you should resort to a simple plain film of the abdominal cavity. The detection of toxic expansion of the large intestine seriously aggravates the prognosis, as it often precedes perforation.
With ulcerative nonspecific colitis, in addition to the intestines, there is frequent involvement of many organs and systems in the process - the liver, pancreas, the motor and secretory activity of the stomach and small intestine changes, the processes of absorption, assimilation, the processes of synthesis and assimilation of vitamins are disrupted. With ulcerative nonspecific colitis, many types of metabolism are disrupted, especially in severe cases (protein, water, electrolyte metabolism, etc.).
Liver. With ulcerative colitis, secondary hepatitis often develops. The liver (20-50%) is enlarged, compacted, and in severe cases, a change in its functional state occurs. Disturbances are observed in the pigment function of the liver (increased urobilin content in the urine, sometimes increased bilirubin in the blood). The most consistent reduction in blood cholesterol is to 110-115 and even to 65-70 mg% using the Engelhardt-Smirnova method.
In severe cases, a change in the colloidal reactions of the blood is observed - thymol, sublimate, formol, and the Takata-Ara reaction. We have found an increase in blood transaminases in patients with severe ulcerative colitis, mainly oxaloacetic colitis, and this increase often precedes a relapse or severe complication (intestinal bleeding, perforation), and is observed during an exacerbation.
M. E. Turchins found similar changes in blood transaminases in ulcerative colitis.
There is some controversy regarding changes in the protein formula of the blood in patients with ulcerative colitis. However, as analysis shows, depending on the form, period and severity of the disease, changes in the protein formula of the blood are constant and very characteristic.
Total protein decreases in acute forms or during severe relapses. During the period of remission, the amount of total blood protein approaches normal. The stronger the intoxication, the more pronounced the changes in the clinic, the more the total blood protein is reduced. Albumin also decreases more in cases of acute, subacute and exacerbations of chronic forms. On the part of globulin subfractions, during the period of acute phenomena and exacerbations, an increase in α 1 - and α 2 -globulins is noted.
During the period of remission, there is a gradual decrease in α 1 - and α 2 -globulins.
In patients with ulcerative colitis, γ-globulins increase. During the period of remission, a decrease in γ-globulins is not observed, in contrast to α 1 - and α 2 -globulins. M.E. Turchins found an increase in lipoproteins, glycoproteins, serum alkaline phosphatase, and copper oxidase in ulcerative colitis.
In addition to protein metabolism, dramatic changes are observed in water and electrolyte metabolism. Loss of fluid from tissues during ulcerative colitis often leads to a sharp decrease in potassium and calcium salts. The amount of potassium salts is especially reduced in seriously ill patients.
Spleen in ulcerative colitis increases in patients with secondary hepatitis, as well as in cases of severe disease with septic and septicopyemic manifestations of secondary infection.
The cardiovascular system. The changes are expressed in dystrophic disorders of the myocardium (myodystrophy). Clinically, muffled heart sounds, tachycardia, and decreased blood pressure are noted. The pulse rate in patients with high fever and severe intoxication can reach 120-140 beats per minute. Tachycardia is also partly associated with severe electrolyte disturbances and loss of potassium salts.
With severe intoxication in patients with acute manifestations of the disease, a decrease in blood pressure can be catastrophic with the development of collapse.
Blood and hematopoietic organs. On the red blood side, in severe cases of any form of ulcerative colitis, a drop in hemoglobin is observed with a simultaneous decrease in the number of red blood cells.
Anemia develops as a result of repeated prolonged intestinal bleeding in the chronic course of the disease or occurs suddenly as a result of massive intestinal bleeding. Reduction of hemoglobin to 10-8 g% or less.
Platelets, bleeding time, and clotting are generally unaffected. The number of reticulocytes usually increases, especially with the development of secondary anemia. On the white blood side, leukocytosis increases in patients with severe all forms of the disease with acute manifestations. The number of leukocytes is 10,000-12,000-14,000. An increase in leukocytes to 20,000-40,000 is possible. We observed 2 patients with an acute fulminant course of relapse and the development of “toxic megacolon”, when the increase in leukocytosis reached 45,000. In the formula, a band shift with the appearance of youthful forms. The shift is more pronounced in seriously ill patients and can reach 40-60%.
An increase in blood eosinophils should be considered frequent. ROE at the onset of the disease and for a long time in cases of benign course remains normal or slightly accelerated. In severe cases with acute manifestations of the disease, high fever, signs of intoxication and pronounced changes in the intestines, ROE sometimes reaches 40-60 and even 70 mm per hour. In terms of prognosis, accelerated ROE, like a sharp band shift, is a bad indicator. High ROE is often observed in patients with superinfection.
Nervous system. Many authors describe mental changes in patients with ulcerative colitis. Seriously ill patients, as a rule, develop astheno-vegetative disorders. All patients are characterized by weakness, headaches, and decreased ability to work. Among the factors contributing to the detection of the disease or the onset of relapse, various mental traumas and conflict situations are justifiably named. Patients are irritable, and symptoms of withdrawal into illness are frequent.
Complications [show]
Complications of ulcerative colitis can be divided into local and general. To the most severe local complications include intestinal perforation and intestinal bleeding. Perforations occur as a result of deep inflammatory and necrotic processes affecting all layers of the intestinal wall. Intestinal bleeding is also a serious complication. Minor intestinal bleeding - the main symptom of the disease - is associated with damage to small vessels. These bleedings usually do not lead to anemia for a long time in a benign course of the disease. Large massive bleeding associated with disruption of the walls of large vessels during a deep ulcerative process is a serious complication, sometimes requiring immediate surgical intervention to perform an ileostomy or subtotal colectomy. Massive intestinal bleeding more often occurs in patients with acute and subacute forms of severe disease or with the development of acute severe relapse of chronic forms. Intestinal perforations also often occur during acute manifestations of the disease in severe cases. Often there are multiple perforations, which greatly worsens the prognosis. Surgery is the only way to possibly cure the patient in these cases. However, the mortality rate during surgical interventions in cases of perforation and peritonitis is very high. The prognosis is better when surgical treatment is performed early in the presence of signs of preperforation. The picture of perforation and pre-perforation in ulcerative colitis does not repeat the typical picture of an acute abdomen characteristic of gastric ulcer, duodenal ulcer or appendicitis. The course of peritonitis is masked in many cases by severe intoxication, severe abdominal pain, often long preceding perforation, and ongoing diarrhea with mucopurulent-bloody discharge.
Often, even with developing peritonitis, there is no contraction of the abdominal muscles. On the contrary, from the very beginning, even in conditions of preperforation, abdominal distension is characteristic. Particularly indicative for recognizing the preperforative state is the detection of toxic expansion of the large intestine - “toxic colon” or “toxic megacolon”. Toxic expansion of the large intestine is a severe complication of ulcerative colitis, since in 40-60% of cases it ends in death due to the onset of multiple perforations of the large intestine or as a result of severe intoxication with collapse of the patient. The occurrence of toxic expansion of the large intestine is associated, according to some authors, with phlegmonous inflammation of all layers of the large intestine, severe hypokalemia, the onset of intestinal paresis and its expansion in the most affected area (more often toxic expansion is observed in the transverse colon). "Toxic megacolon" is observed in patients with the most severe fulminant (acute or subacute) form of ulcerative colitis; This complication may also develop during acute relapse of severe chronic forms. X-ray examination helps diagnose this complication. A simple survey of the abdominal cavity with the patient lying on his back without the introduction of a contrast agent reveals dilation of the large intestine. Irrigoscopy with barium injection is contraindicated in such patients, as it increases the percentage of perforations.
Other local complications include pararectal fistulas, colon polyposis, intestinal pseudopolyposis, malignant transformation into cancer, narrowing of the intestine, and atrophy of the mucous membrane.
To general complications include: secondary anemia, exhaustion of the patient, dystrophy. The degree of these complications may vary depending on the severity of the course, metabolic disorders, functional changes in various organs and systems.
A frequent complication is intestinal dysbiosis with superinfection.
The most severe of these complications are: superinfection of staphylococcal etiology with the possibility of developing staphylococcal sepsis, septicopyemia, and septic endocarditis. Intestinal dysbiosis requires the use of special agents in treatment, depending on the nature of the complication.
It is also necessary to use surgical intervention in cases of purulent foci that are accessible for surgical treatment.
Other common complications include damage to the joints, eyes, development of erythema nodosum and periarteritis nodosa. A frequent complication is the development of an asthenic state and progression into illness.
Forecast. Mortality is high - from 3-4% during the first 3-4 years of the disease (mostly mortality in the first years is associated with acute and subacute forms - 30-40-50 and even 60%) to 10-20-40% within 10- 20-30 years of illness (local and general complications, acute relapses of chronic forms). Mortality is reduced with timely surgical treatment in patients who have indications for this treatment. In every, even mild case of the development of ulcerative nonspecific colitis, the prognosis should be considered serious due to the tendency of the disease to have a chronic relapsing course and the possibility of acute manifestations.
However, with dispensary observation of patients, careful comprehensive treatment during acute manifestations of the disease, with a correct assessment of indications for surgical intervention, even in cases of severe or prolonged course of ulcerative nonspecific colitis, one can count on long-term remissions (5-10-20 years), practically turning into complete recovery.
Diagnosis
Issued on the basis of:
- History [show]
In each individual case, if ulcerative nonspecific colitis is suspected, it is necessary to carefully collect an anamnesis from the patient describing the symptoms of the initial period of the disease, as well as an epidemiological anamnesis to determine the possibility of contact with patients with dysentery, the patient’s stay in places with a higher incidence of dysentery or protozoal colitis. A disease characterized by the release of blood in formed stool, the gradual development of the disease with increasing weakness, periodic exacerbations with the appearance of diarrhea, when there is mucus, blood, pus in the stool, suspicious for ulcerative nonspecific colitis. The persistence of the course, the lack of effect from antibacterial therapy, intestinal bleeding that occurs periodically are characteristic of this disease, and the identification of these symptoms makes the diagnosis of ulcerative nonspecific colitis more reliable.
- Sigmoidoscopy [show]
The basic and often even decisive symptom for diagnosis is a sigmoidoscopy examination.
Detection of diffuse bleeding of the mucous membrane, its swelling, fragility of blood vessels, and in a later period the detection of erosions or ulcers are characteristic of ulcerative nonspecific colitis. Also characteristic is a long-term lack of normalization of the mucous membrane and a decrease in its resistance, even in patients with clinical recovery.
- Irrigoscopy [show]
Irrigoscopic examination by introducing barium through an enema into the large intestine provides great assistance in diagnosis. The percentage of negative results of irrigoscopy, according to various authors, is 30-40. Great importance should be attached to subtle changes that can only be detected on radiographs. When examining our patients together with radiologist S.A. Ginzburg, characteristic radiological changes were found in 72% of patients. The group of patients (28%) with X-ray negative data was characterized, as a rule, mild form diseases with localization of the process in the distal segment of the colon (sigmoid and rectum).
Irrigoscopy is relatively contraindicated in patients with acute manifestations of the disease with severe intoxication and is absolutely contraindicated in cases of preperforation. In patients with severe lesions, irrigoscopic examination reveals rigidity of the intestinal wall, hypermatility, shortening of the colon, smoothing of the hepatic and splenic flexures. The contours of the large intestine are often finely or roughly jagged and lack haustra. In the presence of pseudopolyps, multiple defects are noted. According to S.A. Ginzburg and other authors, the severity and extent of pseudopolyposis can be established only with double air contrast of the intestine. Radiographs after bowel movement in acute forms usually reveal a disturbance in the relief - a sharp thickening of the folds, their random arrangement. In patients with chronic forms, the relief is often granular or represented by 2-3 longitudinal rough folds.
At differential diagnosis ulcerative colitis, the following diseases must be taken into account.
- Dysentery [show]
In acute dysentery, the severity of clinical manifestations is noted - fever, intoxication, abdominal pain, tenesmus and frequent bowel movements in the first days of the disease with a gradual subsidence of these symptoms after a few days, especially in cases of the use of broad-spectrum antibiotics or sulfonamides, which are highly effective in dysentery and ineffective with ulcerative nonspecific colitis.
In contrast to ulcerative nonspecific colitis, with dysentery, the admixture of blood in the stool is combined from the first days of the disease with an admixture of mucus or pus, while with ulcerative nonspecific colitis, even in acute forms in patients with high fever at the onset of the disease, only an admixture of blood is characteristic. Stool in the form of rectal spitting is also not typical for ulcerative colitis. The urge is often imperative, tenesmus is possible, however false urges on defecation, characteristic of dysentery, in ulcerative colitis, as a rule, is not observed.
When differentiating from chronic dysentery, the persistence of the course, the duration of blood impurities in ulcerative nonspecific colitis during an exacerbation in liquid feces, and in the beginning of remission - in formed feces, are taken into account.
In the acute form of ulcerative colitis, in contrast to dysentery, increasing leukocytosis, neutrophilia, a pronounced shift to the left and acceleration of ROE are characteristic. Often, sigmoidoscopy and irrigoscopy play a decisive role in the differential diagnosis of these diseases. With dysentery there is no diffuse bleeding, contact bleeding, extensive erosive and ulcerative fields. The process is characterized by rapid dynamics during antibacterial treatment. Irrigoscopy for dysentery, both acute and chronic, does not reveal changes characteristic of ulcerative colitis. Bacteriological and serological examination methods for dysentery provide some assistance.
- Amoebiasis [show]
Amebiasis is the most difficult section of the differential diagnosis due to the great similarity of clinical pictures. The chronic relapsing nature of the disease, gradual onset, lack of effect from the use of antibacterial treatment, eosinophilia in the blood and feces bring these two diseases closer together. A carefully collected epidemiological history, detection of histological amoeba in the stool during amebiasis, and a positive effect of anti-amoeba treatment help. A sigmoidoscopy examination reveals ulcers with deep, undermined edges against the background of an unchanged mucous membrane, without bleeding during amoebiasis.
- Polyposis [show]
Sigmoidoscopy and irrigoscopic examination of the large intestine resolves the issue of diagnosis.
- Sarcomatosis and colon cancer [show]
The age of the patient is taken into account (ulcerative nonspecific colitis often begins at a young age). Remissions are not typical for cancer and sarcoma. Irrigoscopy and rectoscopy are a decisive factor when discussing these diagnoses. A biopsy of areas suspicious for blastomatosis is used.
- Intestinal reticulosis and blood diseases [show]
Acute forms of severe fulminant course with high fever and general severe condition of patients with frequent mucous-bloody stools have similar features in their course. In addition to sigmoidoscopy and irrigoscopic examination, diagnostic aid is provided by the study of sternum punctures and peripheral blood tests.
- Intestinal tuberculosis [show]
In some cases, one should keep in mind the need for a differential diagnosis of ulcerative colitis and intestinal tuberculosis. A medical history indicating previous tuberculosis of the lungs or other organs is very important. Stool tests for tuberculosis should be done, and sigmoidoscopy and irrigoscopic examination of the large intestine should be performed.
Treatment
There are currently no specific treatments for ulcerative colitis.
Treatment of patients with ulcerative nonspecific colitis should be based on a pathogenetic principle, be comprehensive and include means of combating intoxication, reducing allergic, inflammatory and destructive processes, means regulating the state of the nervous and endocrine systems, metabolic, metabolic and vitamin disorders of the body.
Absence specific treatment With this severe disease with a tendency towards a chronic relapsing course, further development and improvement of treatment methods is extremely important. The relevance of such an improvement is undoubted, since to date the mortality rate remains high, especially in patients with acute manifestations of the disease (acute and subacute forms, acute relapses of chronic forms) due to severe surgical complications - intestinal perforations, profuse intestinal bleeding, as well as associated with severe intoxication.
The currently developed system of measures for the treatment of patients with ulcerative colitis includes conservative (therapeutic) and surgical methods.
The promise of various conservative treatment methods is indicated by V.K. Karnaukhov, S.M. Ryss and V.K. Gerasimov, S.I. Ratner, Kirsner, Kiefer, Watkinson and others. Observations of the clinic led by prof. A.F. Bilibin are also given the right to talk about efficiency conservative treatment with ulcerative colitis in most patients, with proper consideration of indications for surgical intervention. The reversibility of ulcerative colitis, delayed development of the process and long-term (5-10-20 or more years) remissions are described by many authors. Kirsner observed patients with ulcerative colitis with complete cure. The author notes the possibility of not only clinical recovery, but also complete normalization of the X-ray picture even in cases of severe lesions.
Long-term remissions turning into recovery in ulcerative nonspecific colitis apparently occur much more often than we observed, since due to the difficulty of diagnosis, patients with moderate and especially mild forms may be partially missed and the disease is not diagnosed in them.
When constructing a treatment plan and choosing methods, as shown by the study of the clinical features of ulcerative nonspecific colitis, it is necessary to take into account the form, phase and severity of the disease, as well as individual characteristics the patient with an assessment of the degree of allergic manifestations, concomitant diseases, the functional state of various organs and systems, the depth of intestinal dysbiosis.
All patients during an exacerbation, especially in cases of acute manifestations, must be provided with inpatient treatment for the entire time until signs of remission appear (from 1-2 to 3-6 and sometimes more than months). Only hospitalization can provide patients with an appropriate regimen, proper dietary treatment and complex pathogenetic therapy.
Therapeutic measures are divided into:
- impact on intoxication [show]
Means that reduce the effects of intoxication include intravenous and subcutaneous infusions of glucose, saline, administration of plasma and blood, and protein fluids. Steroid hormones have a pronounced antitoxic effect in ulcerative colitis. In addition to the antitoxic effect, corticosteroids in patients with ulcerative colitis have, which is extremely important, anti-inflammatory and antiallergic effects. Among the justifications for steroid therapy, the phenomena of adrenal insufficiency should also be taken into account in ulcerative colitis.
Corticosteroids (cortisone, prednisone, prednisolone, and ACTH) have been used to treat patients with ulcerative colitis for more than 10 years. A positive effect is noted by most authors (Truelove, Watkinson, V.K. Karnaukhov, S.M. Ryss and V.K. Gerasimov, Ya.A. Makarevich, I.N. Shchetinina, etc.). However, while recognizing the expediency, and in some cases the necessity, of using steroid therapy, most authors do not consider steroid treatment to be able to prevent relapses of the disease. The use of steroid therapy in patients with ulcerative colitis requires certain caution due to the possibility of deepening necrotic processes, as well as activation of secondary flora. In addition, general contraindications to the use of corticosteroids should be taken into account, as with any other disease.
Changes in reactivity with pronounced allergic reactions, sensitization, an inflammatory process with a hyperergic nature of inflammation and significant intoxication phenomena are especially pronounced in acute, subacute forms, acute relapses of severe chronic forms. Therefore, the use of steroid drugs should be considered indicated specifically for such forms. Treatment must be strictly individualized; It is difficult to recommend any regimens, but some rules must be followed: 1) the lack of effect of steroid therapy for 8-10 days in case of ulcerative nonspecific colitis is an indication for its discontinuation; 2) any deterioration during treatment with corticosteroids (increased abdominal pain, increased intestinal bleeding, activation of secondary flora) requires their withdrawal.
The duration of drug administration, described by various authors, ranges from 8-10 to 21-30 days, rarely more. Some authors considered it advisable to continue administering small doses as anti-relapse treatment, but the expected results were not obtained.
Comparison of corticosteroids in terms of effectiveness showed top scores in patients receiving prednisolone or cortisone rather than prednisone or ACTH. There are indications that triamsinolone is less effective for ulcerative colitis than prednisolone and cortisone.
As for the second newest steroid drug - dexamethasone, then, according to our observations, it has a pronounced therapeutic effect and is well tolerated by patients.
Commonly used daily dose cortisone averages 100 mg, prednisolone - 30-40 mg, dexamethasone - 3-4.5 mg.
The daily dose when administered orally is given in 4 doses. Hydrocortisone for enemas is prescribed in the amount of 60-100 mg, prednisolone - 20-40 mg daily, at least 10-14 enemas per course of treatment.
Steroid drugs are discontinued according to generally accepted rules with a gradual reduction in doses every 4-5 days.
Some authors, for example Glyn et al., theoretically consider it advisable to prescribe large doses of corticosteroids to patients with ulcerative colitis. Herlinger used initial doses of prednisolone of 40-50 mg per day with good effect and without side effects, believing that doses of prednisolone below 25 mg could even lead to a worsening of the condition.
- impact on the reactivity of the macroorganism [show]
The means of influencing the reactivity of the macroorganism in ulcerative nonspecific colitis include: blood products, protein liquids. Hematotransfusions have a stimulating effect on the body. In addition, they increase blood clotting, which is important for repeated intestinal bleeding. Blood transfusion and especially red blood cell transfusion for ulcerative nonspecific colitis is also replacement therapy. Usually 100-250 ml of blood or red blood cells in a blood replacement solution are prescribed per transfusion at 3-7 day intervals.
Corticosteroids, the use of which in ulcerative colitis is described above, are also powerful means of influencing the body's reactivity.
Influences aimed at increasing nonspecific protective factors include diet therapy, protective and restorative regimen, and psychotherapy.
Diet therapy and vitamin therapy occupy an important place in the organization of treatment of patients with ulcerative colitis. Food must be well mechanically and thermally processed, well fortified, and contain a sufficient amount of liquid. A predominantly protein diet is prescribed, the amount of carbohydrates is limited.
Observations by A.F. Bilibin showed the need to completely exclude all dairy products from the diet, except butter, as well as raw apples and tomatoes.
When choosing a diet, individual intolerance to certain products of plant or animal origin is taken into account. More often we observe intolerance to foods that enhance fermentation (potatoes, grapes, cabbage). Alcoholic drinks are prohibited. Some patients, apparently, need to limit or completely eliminate gluten from food (Knapp, Gruschwitz).
It is recommended to eat 4-5 meals a day with 3-4 meals of fish and meat dishes, eggs, and black caviar. Meat dishes should be prepared from lean varieties of beef and chicken. Cod fish or lean river fish (pike perch, bream, pike, perch, etc.) are recommended. Recommended are water porridges with butter, broths, vegetable soups, egg white omelettes, black coffee, tea, jam, dry biscuits, fruit - black currant juice, lemons. Oranges, tangerines, and pomegranates should be limited.
Often, especially during remissions, the patient is allowed herring, jellied fish and meat dishes.
It is important that the food is varied and has good taste due to the need for long-term adherence (years) to the diet, even in patients with stable remission. Crackers, white and gray bread are allowed. During acute manifestations of the disease, the diet should be more limited, and the food should be more easily digestible, better heat-treated and pureed. The number of meals can be increased to 5-6 times a day.
Since dairy products are completely excluded and vegetables and fruits are somewhat limited, it is recommended to introduce additional vitamins of the B complex (B 1, B 2, B 6, B 12), C, PP, folic and nicotinic acid. The prescription of vitamins should be a course and be systematically repeated. During exacerbations, it is also advisable to prescribe vitamins such as rutin and vitamin K (in cases of bleeding). If you have severe flatulence, you can drink alkaline mineral waters (such as Borjomi). In case of constipation, more vegetables are introduced into the diet.
- desensitizing treatment [show]
Desensitizing agents, in addition to corticosteroids, for the treatment of patients with ulcerative nonspecific colitis include antihistamines- diphenhydramine, pipolfen, as well as suprastin, bellaspon. You can also use aspirin, calcium chloride, novocaine.
- the use of anti-inflammatory drugs, especially topical ones [show]
The use of anti-inflammatory drugs, especially local ones, is necessary in most patients with ulcerative colitis. These include: the Hungarian drug enteroseptol, which received a good rating, according to our observations, especially in patients with ulcerative colitis, complicated by intestinal dysbiosis, or in cases of combination with protozoal colitis, dysentery.
Recommended doses: 1-2 tablets 3-4 times (1 tablet contains 0.25 g of iodine-chloroxyquinoline-salicylic acid) for 7-10 days. With rare exceptions, the drug is well tolerated. Enteroseptol courses can be repeated after 1-2 weeks according to indications.
Watkinson, Truelove, and others describe a good anti-inflammatory effect from the use of salazopyrine, especially when combining salazopyrine with corticosteroids. There is also a positive effect of poorly absorbed sulfonamide drugs (Moertol, Vargen, etc.), as well as long-acting drugs - sulfapyridazine (Kinex), madribon, etc. The duration of use of the latter is from 2-4 weeks to several months and even more than a year in maintenance doses (0.5 g every 2-3 days).
Therapeutic enemas have a local anti-inflammatory effect. It is possible to use enteroseptol and the silver salt of norsulfazole in the form of a 1% solution for this purpose. A number of authors give a positive assessment of therapeutic enemas of hydrocortisone and prednisolone (S. M. Ryss, Truelove, Watkinson, own observations, etc.).
- antibacterial therapy with the aim of targeting the secondary flora in cases of dysbacteriosis and superinfections [show]
The prescription of antibiotics for ulcerative nonspecific colitis should be strictly limited to indications, since intestinal dysbiosis, which often develops during the course of the disease or even precedes its development, can deepen under the influence of antibiotics, especially broad-spectrum ones, which aggravates the course of the disease. Intensification of allergic reactions as a result of antibiotic therapy is equally undesirable.
Broad-spectrum antibiotics may be prescribed in short courses during steroid treatment.
The prescription of targeted drugs depending on the nature of dysbacteriosis is more justified. In this case, the sensitivity of the isolated microbes (for example, staphylococcus) should be taken into account and, depending on this, one or another drug or a combination of them should be used. For staphylococcal superinfections, it is rational to prescribe erythromycin, sigmamycin, monomycin and some other drugs. In case of complications with Proteus dysbacteriosis, antibacterial drugs should also be used depending on the sensitivity of the isolated Proteus. The effect against proteus dysbacteriosis is provided by drugs of the nitrofuran series - furazolidone, furagin (produced by the Institute of Organic Synthesis of the Academy of Sciences of the Latvian SSR) in doses of 0.1 g 3-4 times a day, from 6 to 10 days per course.
The use of colibacterin (Peretz dry colibacterin) for the treatment of patients with ulcerative nonspecific colitis deserves a separate description due to its great value. The positive effect of treatment with this drug was noted by most authors (S.I. Ratner et al., A.N. Ryzhikh et al., V.N. Krasnogolovets and P.I. Sakharov’s own observations). A particularly high therapeutic assessment of colibacterin is given in the works of S.I. Ratner et al. and A.N. Ryzhikh et al. Recommended doses: 1 dose 2-3 times a day cases of lung and moderate course and 4-6-10 doses - in cases of moderate and severe disease. Duration of use with a gradual reduction of the drug to 3-2-1 dose per day for 2-4 months, for some patients 6-8 months or more.
According to our observations, the prescription of colibacterin should be carried out for patients with ulcerative nonspecific colitis according to indications and specifically in cases of intestinal dysbiosis. In a number of patients, it is rational to prescribe treatment with colibacterin after courses of targeted antibiotic therapy for follow-up treatment and restoration of intestinal flora.
Colibacterin should be included in the complex of pathogenetic therapy as a means of influencing one of the most important pathogenetic links of ulcerative colitis. Restoration of normal intestinal microflora with a decrease in inflammatory processes, normalization of vitamin synthesis, and restoration of the pH of the environment plays a large role in the healing processes of ulcerative nonspecific colitis.
- impact on other individual links in the pathogenetic chain [show]
The impact on other individual links in the pathogenetic chain should be aimed at restoring disturbances in the functioning of internal organs and systems, as well as treating complications, metabolic disorders - protein, salt, water. This includes transfusions of blood, protein fluids, saline solutions, especially potassium salts.
For disorders of cardiovascular activity, camphor, cordiamine, caffeine, corglycone, and ephedrine are prescribed. In cases of collapse, massive cardiovascular therapy is required using, in addition to the above mentioned drugs, adrenaline, norepinephrine, mesatone, etc.
Massive intestinal bleeding requires complete rest, blood and red blood cell transfusions, vitamin K administration, and calcium chloride infusions.
Surgical treatment
The need for surgical treatment for severe forms of ulcerative colitis was reported back in 1913 by the Russian surgeon A.S. Kazachenko. Over the past years, surgical treatment of patients with ulcerative colitis has been constantly discussed both in foreign and Soviet literature. At the same time, types of interventions are being improved and indications are being developed.
Some authors give extremely broad indications for surgery. Most authors consider it necessary to use surgical treatment in 15-25% of cases for ulcerative nonspecific colitis. Surgical treatment should be carried out by patients in the absence of effect from conservative treatment methods.
Among the indications for surgical intervention are:
- absolute readings [show]
Absolute indications include intestinal perforation, massive intestinal bleeding, malignant degeneration, intestinal polyposis. Absolute indications include a severe acute course of the disease with severe intoxication, high fever, and lack of effect from complex therapeutic treatment carried out for 2-4 weeks.
It is also necessary to operate on patients when the process of chronic forms progresses and anemia and exhaustion increase.
Indications for mandatory surgical treatment are and local complications from the intestines - fistulas, strictures.
In our opinion, the development of toxic expansion of the large intestine should also be considered an absolute indication. This issue is controversial in the literature. Some authors consider toxic expansion of the large intestine to be a preperforative condition and therefore surgical intervention is necessary.
Others suggest postponing surgery if possible due to the general serious condition of the patient. We observed the development of toxic expansion of the large intestine in 4 patients; In 3 of them, intestinal perforation occurred with severe diffuse peritonitis.
- relative readings [show]
Relative indications include a long, persistent course of the disease with disruption of the patient’s general condition and the occurrence of frequent exacerbations.
Some authors believe that when ulcerative colitis lasts for more than 3-4 years, especially with severe exacerbations, one should seriously think about surgical intervention. The indication for it is pseudopolyposis that occurs during the course of the disease.
Most often, for the surgical treatment of patients with ulcerative colitis, the method of staged removal of the large intestine is used, sometimes with removal of the rectum (subtotal or total colectomy). In this case, the unnatural anus of the ileum is temporarily or permanently exposed to the abdominal wall.
Simply switching off the colon with an ileostomy does not eliminate the process.
After subtotal colectomy, persistent long-term treatment (on average 6-12 months) in some patients leads to healing and makes it possible to eliminate the unnatural anus (I. Yu. Yudin). However, healing may not occur. In such patients, it is necessary to remove the rectum and sigmoid colon and lower the ileum into the anus, creating an artificial ampoule with the imposition of a wide enteroanastomosis (A. N. Ryzhikh and Zh. M. Yukhvidova). A. A. Vasiliev considers it possible to perform colectomy in a number of patients with simultaneous application of ileorectal anastomosis and temporary ileostomy.
The gradual removal of the large intestine with the imposition of an ileostomy as the first stage of the operation in almost all patients extremely quickly leads to an improvement in general condition, weight gain (within 1-3 months, patients on average gain 10 and even 15 kg of weight), equalization of metabolism, especially protein and electrolyte Such an improvement in general condition may be necessary in seriously ill patients to perform a more complex operation - colectomy and the next stages of the operation.
The question of the need for surgical treatment should be decided by the therapist at the patient’s bedside together with the surgeon.
Methods of surgical treatment, as well as methods of conservative pathogenetic treatment, require further development and improvement. The current successes in the study of ulcerative colitis are constantly evolving thanks to in-depth study of the disease in a number of leading clinics in our country, as well as abroad.
LITERATURE [show]
- Bilibin A.F., Shchetinina I.N. Doctor, case, 1963, 5, 99.
- Bilibin A.F., Sakharov P.I., Vorotyntseva N.V. Treatment of dysentery. M., 1959.
- Busalov A. A., Yudin I. Yu., Ginzburg S. A. Klin, med., 1963, 3, 41.
- Vasilyev A. A. Surgical treatment of nonspecific ulcerative colitis. Diss. doc. M., 1964.
- Gerasimov V.K. Conservative therapy of nonspecific ulcerative colitis. In the book: Current issues of gastroenterology, 1964, 79, 175.
- Davydovsky I.V. Problems of causality in medicine. M., 1962.
- Karnaukhov V.K. Nonspecific ulcerative colitis. M., 1963.
- Kogoy T. G. Arch. pathol., 1963, 9, 47.
- Krasnogolovets V. N. Dysbacteriosis in patients intestinal diseases treated with antibiotics. Abstracts of reports of the scientific conference "Physiology and pathology of the intestine". M., 1962, 112.
- Makievskaya S. E., Atserova I. S. Clinical, immunological and virological studies in nonspecific ulcerative colitis. Abstracts of reports of the scientific conference "Physiology and pathology of the intestine". M., 1962, 122.
- Mikhlin S. Ya. Study of enzymatic processes in the intestines during nutritional disorders and some diseases. Diss. doc. M., 1963.
- Padalka B. Ya., Karmanova E. E., Chernomordik A. B., Lukach I. G., Bass T. M. Doctor, case, 1963, 10, 99.
- Polchak I., Vakurka V., Skalova M. Sov. Med., 1960, 10, 68.
- Ratner S. I., Fain O. I., Mashilov V. V., Mitrofanova V. G., Khudyakova G. K., Vilshanskaya F. L. Klin, med., 1963, 41, 2, 109.
- Ryzhikh A.N., Yukhvidova Zh.M. Expert. hir., 1961, 2, 36.
- Ryss S. M., Gerasimov V. K. Some basic issues of the problem of nonspecific ulcerative colitis. Abstracts of reports of the scientific conference "Physiology and pathology of the intestine". M., 1962, 143.
- Tareev E. M. Sov. Med., 1958, 9, 15.
- Shchetinina I. N. Clinical forms of severe ulcerative colitis. Abstracts of reports of the scientific conference "Physiology and pathology of the intestine". M., 1962, 152.
- Erez S. L., Ryklina L. G., Bondarev A. S. Kaz. honey. zhurn., 1962, 1, 19.
- Bacon N. Ulcerative Colitis, 1958.
- Carlson R., Fristedt B., Philipson J. Acta. med. scand., 1962, 172, 6, 647.
- Cattan R., Bucaille M. et Carasso R. La rectocolite hemorragique et purulente (Ulcerative Colitis), 1959, Paris.
- Engel G. Gastroenterology, 1961,40,2,2,313.
- Herbinger W. Med. Klin., 1963, 28, 1149.
- Kirsner J. Gastroenterology, 1961, 40, 2, 2, 287, 307.
- Knapp A., Gruschwitz E. Unsere Erfahrungen bei der Diagnose und Behandlung der einheimschen eines Falles mit Antikorper-mangelsyndrome. Dtsch. Gesundh-Wes, 1963, 24, G.D.R., 1033.
- Kuhn H. Internist., 1961, 2, 9, 536.
- Lumb G. Gastroenterology, 1961, 40, 2, 2, 290.
- Par M., Bernier J., Lambeing A., Terris G. Arch. Mai. Appar. die., 1962, 51, 10, 1161.
- Reifferscheid M. Internist., 1961, 2, 9. 545.
- Roth J., Valdes-Dapena A., Stein G. and Boskus H. Gastroenterology, 1959, 37, 3, 239.
- Truelove S. Brit. med. J., 1961, 5220, 154.
- Truelove S., Watkinson G., Draper G. Brit. med. J., 1962, 53, 21, 1708.
- Watkinson G. Medical Management of Ulcerative. Brit. med. J., 1961, 5220, 147.
Nonspecific ulcerative colitis (UC) is a disease of unknown etiology, characterized by the development of a necrotizing inflammatory process of the mucous membrane of the large intestine with the formation of ulcers, hemorrhage and pus.
Etiology and pathogenesis
The etiology of UC is unknown. Presumable etiological factors are infection (viruses, bacteria), poor nutrition (diet low in dietary fiber). By many, the latter factor is considered as predisposing to the development of the disease.
Main pathogenetic factors are:
Intestinal dysbiosis is a disruption of the normal composition of microflora in the large intestine, which has a local toxic and allergenic effect, and also contributes to the development of non-immune inflammation of the colon;
Violation of neurohumoral regulation of intestinal function due to dysfunction of the autonomic and gastrointestinal endocrine systems;
Significant increase in the permeability of the colon mucosa for protein molecules and bacterial antigens;
Damage to the intestinal wall and the formation of autoantigens, followed by the formation of autoantibodies to the intestinal wall. Antigens of some strains of E. coli induce the synthesis of antibodies to colon tissue;
The formation of immune complexes localized in the wall of the colon, with the development of immune inflammation in it;
Development of extraintestinal manifestations of the disease due to multifaceted autoimmune pathology.
The etiopathogenesis of UC is presented in Fig. 13.
Pathomorphology
With UC, a pronounced inflammatory process develops in the mucous membrane of the colon. Progressive destruction of the epithelium and fusion of inflammatory infiltrates cause the development of ulcers of the mucous membrane.
In 70-80% of patients, a characteristic sign of UC develops - microabscesses of the colon crypts. In the chronic course, dysplasia of the intestinal epithelium and fibrosis of the intestinal wall are noted.
Most often, with UC, the distal parts of the colon and rectum are affected, and the latter is involved in
pathological process in almost 100% of cases. Pancolitis develops in 25% of patients.
Classification
The classification of nonspecific ulcerative colitis is given in table. 25.
Table 25.Classification of ulcerative colitis
(V. D. Fedorov, M. X. Levitan, 1982; Yu. V. Baltaitis et al., 1986; G. A. Grigorieva, 1996)
Military activity* Presence of burning (according to the given complication)
endoscopy
Lightning fast
Chronic
relapses
Chronic
continuous
Total colitis with or without retrograde ileitis
Left-handed
Distal colitis (proctosigmoiditis,
Minimum
Moderate
Expressed
System
Clinical picture
The incidence (primary incidence) is
Genetic influences, increased familial predisposition
Dietary factor? Food allergens, dietary fiber deficiency
Infections?
Bacteria,
surrounding
Immunological I defect? I
Dysregulation, ______ to
pathological ^4 immunotolerance I
Chronic inflammation of the colon mucosa I
Rice. 13. Etiopathogenesis of nonspecific ulcerative colitis (Ra1k, 1998).
4-10 diseases per 100,000 inhabitants per year, incidence (number of patients) - 40-117 patients per 100,000 population. In most patients, the disease is first diagnosed at the age of 15-30 years.
The main symptoms of UC are the following.
1. Diarrhea with blood, mucus and pus. With a pronounced clinical picture of the disease, frequent loose stools mixed with blood, mucus, and pus are characteristic. Stool up to 20 times a day, and in severe cases up to 30-40, mainly at night and in the morning. In many patients, the amount of blood in the stool is quite significant, sometimes defecation occurs almost pure blood. The amount of blood lost by patients during the day can range from 100 to 300 ml. Stool contains large amounts of pus and may have a foul odor.
The onset of the disease may vary depending on the time of appearance of blood in the stool; The following options are possible:
First, diarrhea appears, and after a few days there is mucus and blood;
The disease immediately begins with rectal bleeding, and the stool may be formed or mushy;
At the same time, diarrhea and rectal bleeding begin, while patients experience other symptoms of the disease (abdominal pain, intoxication).
Diarrhea and bleeding are considered the main clinical manifestations of UC. Diarrhea is caused by extensive inflammatory damage to the colon mucosa and a sharp decrease in its ability to reabsorb water and sodium. Bleeding is a consequence of ulceration of the colon mucosa and the development of loose connective tissue with a richly developed vascular network.
2. Abdominal pain. A constant symptom of UC. The pain is cramping in nature and is localized mainly in the projection of parts of the large intestine, most often in the sigmoid, transverse colon, rectum, less often in the cecum, in the periumbilical region. Usually the pain intensifies before defecation and calms down or weakens after stool. The pain may increase after eating.
It should be noted that extremely severe pain and symptoms of peritonitis are not typical for UC, since the inflammatory process in this disease is limited to the mucous membrane and submucosal layer. With a complicated course of UC, the inflammatory process spreads to the deep layers of the intestinal wall (see below).
3. Abdominal pain on palpation. A characteristic sign of UC. On palpation, clearly defined pain is detected in the area of the sigmoid, transverse colon and cecum. The more pronounced the inflammatory process in the large intestine, the more significant the pain when palpating its parts. Symptoms of peritoneal irritation and muscle tension are usually not observed in an uncomplicated course of the disease, but in severe cases the appearance of resistant muscles in the anterior abdominal wall is possible.
4. Intoxication syndrome. Characteristic for severe UC and acute fulminant forms of the disease. Intoxication syndrome is manifested by severe weakness, adynamia, increased body temperature (often to high levels), weight loss, decreased or even complete absence of appetite, nausea, depression, severe emotional lability, tearfulness, and irritability.
5. Syndrome of systemic manifestations. Systemic manifestations of UC are characteristic of severe disease and in some cases occur in moderate forms. Typical systemic manifestations include:
Polyarthritis - usually affects the ankle, knee, interphalangeal joints, the intensity of pain and the degree of restriction of movement in the joints are usually small. With the onset of remission, articular changes completely disappear, deformations and dysfunction of the joints do not develop. Some patients develop transient spondyloarthritis and sacroiliitis. Sacroiliitis occurs more often and is more severe with more extensive and severe lesions of the large intestine. Symptoms of sacroiliitis may precede clinical manifestations of UC by many years;
Erythema nodosum - develops in 2-3% of patients, manifests itself in multiple nodes, most often on the extensor surface of the leg. The skin over the nodes has a purple-violet color, then becomes greenish, yellowish and then acquires a normal color;
Skin damage - possible development of gangrenous pyoderma (in severe septic disease); skin ulcerations; focal dermatitis; postulous and urticarial rashes. Gangrenous pyoderma is especially difficult;
Eye lesions - noted in 1.5-3.5% of patients, the development of iritis, iridocyclitis, uveitis, episcleritis, keratitis and even panophthalmitis is typical;
Lesions of the liver and extrahepatic bile ducts are of great importance for assessing the course of the disease, treatment tactics and prognosis. The following forms are observed in UC:
liver damage: fatty degeneration, portal fibrosis, chronic active hepatitis, liver cirrhosis. According to Yu. V. Baltaitis et al. (1986), liver lesions practically do not change under the influence of conservative therapy for UC, but in severe forms they progress and lead to the development of liver cirrhosis. After colectomy, changes in the liver regress. A typical lesion of the extrahepatic bile ducts is sclerosing cholangitis (see the corresponding chapter); /
Damage to the mucous membrane of the mouth is characterized by the development of aphthous stomatitis, glossitis, gingivitis, occurring with very severe pain; possible ulcerative stomatitis;
Nephrotic syndrome is a rare complication of UC. Its symptoms are described in Chap. "Nephrotic syndrome";
Autoimmune thyroiditis (its symptoms are described in the corresponding chapter);
Autoimmune hemolytic anemia.
The development of the syndrome of systemic manifestations is caused by autoimmune disorders and reflects the activity and severity of the pathological process in ulcerative colitis.
6. Dystrophic syndrome. The development of dystrophic syndrome is characteristic of the chronic form, as well as the acute course of UC. Dystrophic syndrome is manifested by significant weight loss, pale and dry skin, hypovitaminosis, hair loss, and changes in nails.
Clinical forms of the course
Most gastroenterologists distinguish the following forms of UC: acute (including fulminant) and chronic (recurrent, continuous).
Acute course
The acute form of the disease is characterized by the rapid development of the clinical picture, the severity of general and local manifestations, early development complications, involving the entire colon in the pathological process. The acute course of ulcerative colitis is characterized by severe diarrhea and significant intestinal bleeding. With severe diarrhea, discharge from the rectum contains almost no feces; blood, mucus, pus, and tissue detritus are released from the rectum every 15-20 minutes. Severe exhaustion develops (weight loss can reach 40-50%). Patients are adynamic, pale, and symptoms of intoxication are pronounced (dry skin and oral mucosa; tachycardia; increased body temperature; lack of appetite; nausea). On palpation of the abdomen, severe pain in parts of the large intestine is noted. The acute course of the disease is characterized by
complications (toxic dilatation of the colon, perforation, peritonitis - see below).
The fulminant form is the most severe form of UC and usually requires surgical treatment. It is characterized by a sudden onset, rapid development of the clinical picture (sometimes within several days or 1-2 weeks). In the fulminant form, severe diarrhea, significant intestinal bleeding, high body temperature, severe intoxication are observed, and life-threatening complications often develop. In the fulminant form of UC, there is total damage to the colon and rapid development of systemic manifestations of the disease.
Chronic forms
The chronic continuous form is diagnosed if, 6 months after the initial manifestations, there is no remission of the process (Yu. V. Baltaitis et al., 1986). With this form of exacerbation, exacerbations often follow each other, remissions are very unstable, short-term, systemic manifestations of the disease quickly form, and complications often develop.
The chronic relapsing form is the most common and is characterized by remissions lasting 3-6 months or more, followed by exacerbations of varying severity.
Severity
In UC, the severity of the disease is determined by the degree of involvement of parts of the large intestine in the pathological process. Proctosigmoiditis is the most common (70% of patients), isolated lesions of the rectum are recorded in 5% of patients, total colitis - in 16% of patients.
In table 26 presents the severity of UC.
Complications
1. Perforation of the colon. One of the most severe complications of UC, observed in 19% of patients with severe disease. Ulcers of the colon can perforate; multiple perforations of an overstretched and thinned colon are also possible against the background of its toxic dilatation.
Perforations occur in the free abdominal cavity and can be covered.
The main symptoms of colon perforation are:
The appearance of sudden sharp pain in the abdomen;
The appearance of local or widespread muscle tension in the anterior abdominal wall;
A sharp deterioration in the patient’s condition and worsening symptoms of intoxication;
Detection of free gas in the abdominal cavity during plain fluoroscopy of the abdominal cavity;
The appearance or intensification of tachycardia;
The presence of toxic granularity of neutrophils;
Severe leukocytosis.
Peritonitis can develop without perforation due to extravasation of intestinal contents through the thinned wall of the colon. The diagnosis of colon perforation and peritonitis can be clarified using laparoscopy.
2. Toxic dilatation of the colon. A very serious complication, characterized by excessive expansion. The development of this complication is facilitated by narrowing of the distal sections of the colon, involvement in the pathological process of the neuromuscular apparatus of the intestinal wall, smooth muscle cells of the intestine, loss of muscle tone, toxemia, ulceration of the intestinal mucosa.
Glucocorticoids, anticholinergics, and laxatives can also contribute to the development of this complication.
The main symptoms of toxic colon dilatation are:
Increased abdominal pain;
Increasing symptoms of intoxication, lethargy of patients, confusion;
Increase in body temperature to 38-39°C;
Decreased tone of the anterior abdominal wall and palpation
palpation (palpate carefully!) of a sharply dilated large intestine; ^
Weakening or disappearance of peristaltic bowel sounds;
Detection of distended areas of the colon during plain radiography of the abdominal cavity.
Toxic dilatation of the large intestine has a poor prognosis. The mortality rate for this complication is 28-32%.
3. Intestinal bleeding. The admixture of blood in the stool with UC is a constant manifestation of this disease. Intestinal bleeding as a complication of UC should be discussed when blood clots are released from the rectum. The source of bleeding is:
Vasculitis on the bottom and edges of ulcers; these vasculitis are accompanied by fibrinoid necrosis of the vessel wall;
Table 26. Severity of ulcerative colitis
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The clinical picture of severe bleeding is similar to that described in Chapter. "Complications of peptic ulcer disease."
4. Strictures of the colon. This complication develops when UC lasts for more than 5 years. Stictures develop over a small area of the intestinal wall, affecting an area 2-3 cm long. Clinically, they manifest themselves as intestinal obstruction of varying degrees of severity. In the diagnosis of this complication, irrigoscopy and fibrocolonoscopy play an important role.
5. Inflammatory polyps. This complication of UC develops in 35-38% of patients. In the diagnosis of inflammatory polyps, irrigoscopy plays an important role, which reveals multiple filling defects of the correct shape along the colon. The diagnosis is verified using colonoscopy and biopsy, followed by histological examination of biopsy samples.
6. Colon cancer. Currently, there is a point of view that UC is a precancerous disease. G. A. Grigorieva (1996) indicates that the greatest risk of developing colon cancer is in patients with total and subtotal forms of ulcerative colitis with a disease duration of at least 7 years, as well as patients with left-sided localization of the process in the colon and a disease duration of more than 15 years. The symptoms of colon cancer are described in Chapter. “Chronic non-ulcerative colitis” (section “Differential diagnosis”). The basis of diagnosis is colonoscopy with targeted multiple biopsy of the colon mucosa.
Laboratory and instrumental data
1. UAC. UC is characterized by the development of anemia of varying severity. With massive intestinal bleeding, acute posthemorrhagic anemia. With constant slight blood loss in chronic flow2y*-zabozh?’-
In this case, chronic iron deficiency anemia develops. Some patients develop autoimmune hemolytic anemia, caused by the appearance of autoantibodies to red blood cells. In the analysis of peripheral blood, reticulocytosis appears. The acute course and exacerbation of the chronic form of UC is characterized by the development of leukocytosis and a significant increase in ESR.
2. OAM. In severe cases of the disease and its systemic manifestations, proteinuria and microhematuria are detected.
3. LHC: the content of total protein and albumin decreases, an increase in the content of a2- and γ-globulins is possible; in case of liver damage, hyperbilirubinemia and an increase in the activity of alanine aminotransferase are observed; with the development of sclerosing cholangitis - γ-glutamyl transpeptidase; with the development
This type of jelly deficiency anemia is characterized by a decrease in iron content. .
4. Scatological analysis. The degree of the inflammatory-destructive process in the mucous membrane of the large intestine is reflected in the severity of changes in the coprocytogram. UC is characterized by detection in stool when microscopic examination a large number of leukocytes, erythrocytes, large accumulations of intestinal epithelial cells. The reaction to soluble protein in feces (Tribulet reaction) is strongly positive.
Bacteriological examination of stool reveals dysbacteriosis:
The appearance of Proteus microorganisms, hemolyzing Escherichia, staphylococci, fungi of the genus Capella;
The appearance of a large number of strains of Escherichia coli with weakly expressed enzymatic properties, lactonegative enterobacteria.
Macroscopic examination of stool reveals characteristic changes - pasty or liquid stool, blood, large amounts of mucus, pus.
5. Endoscopic examination (sigmoidoscopy, colonoscopy) and histological examination of biopsy samples of the colon lining.
P. Ya. Grigoriev and A. V. Vdovenko (1998) describe endoscopic changes depending on the severity of chronic UC as follows.
Mild severity:
Diffuse hyperemia of the mucous membrane;
Lack of vascular pattern;
Single superficial ulcers;
Localization of the pathological process is mainly in the rectum.
Medium form:
“granular” mucous membrane of the large intestine;
Mild contact bleeding;
Multiple non-confluent superficial ulcers of irregular shape, covered with mucus, fibrin, pus;
Localization of the pathological process is predominantly in the left parts of the colon.
Severe form:
Severe necrotizing inflammation of the colon mucosa;
Severe purulent exudation;
Spontaneous hemorrhages;
Microabscesses;
Pseudopolyps;
The pathological process affects almost all parts of the large intestine.
Colonoscopy also reveals rigidity of the intestinal wall and narrowing of the colon.
Histological examination of biopsy specimens reveals the presence of inflammatory infiltrates only within the mucous membrane and submucosal layer. In the early stage and period of exacerbation of ulcerative colitis, lymphocytes predominate in the inflammatory infiltrate; in the long-term course, plasma cells and eosinophils predominate. In the area of the bottom of the ulcers, granulation tissue and fibrin are found.
6. X-ray examination of the colon (irrigoscopy). UC is characterized by swelling, changes in the relief (graininess) of the colon mucosa, pseudopolyposis, lack of haustration, rigidity, narrowing, shortening and thickening of the intestine; ulcerative defects. Granularity of the mucous membrane is considered an early radiological sign of UC. Due to swelling, the surface of the mucous membrane becomes uneven.
In the case of toxic dilatation of the colon, irrigoscopy is not performed due to the risk of perforation. In this situation, a plain radiography of the abdominal cavity is recommended, and it is often possible to see distended segments of the colon.
Differential diagnosis
1. Dysentery. At the beginning of its development, UC has common features with bacterial dysentery: acute onset, diarrhea with blood, abdominal pain, fever, intoxication, and sometimes polyarthralgia. The most important role in diagnosing dysentery is played by bacteriological examination of stool - inoculation of fresh feces on differential nutrient media (shigella isolation is possible after 48-72 hours). There are express methods for determining Shigella in feces (using fluorescent microscopy and the carbon agglomeration reaction), which allows one to draw a conclusion about the presence of the dysentery pathogen within 2-3 hours.
2. Amoebiasis. The similarity between UC and amoebiasis lies in the presence of diarrhea mixed with mucus and blood, increased body temperature, and symptoms of intoxication. The characteristic distinguishing signs of amoebiasis are the following:
Stool in the form of “raspberry jelly” (due to blood in the stool);
Accumulation of glassy mucus in the stool in the form of “frog poop”;
Detection of tissue and histolytic form of amoeba in feces; stool should be examined no later than 10-15 minutes after defecation);
A typical sigmoidoscopy picture: against the background of a slightly changed mucous membrane of the colon, areas of hyperemia, ulcers of various sizes with undermined edges, filled with cheesy necrotic masses are revealed; there is a large amount of mucus mixed with blood on the wall and in the lumen of the colon;
Detection of Ep1achoeba Lido1y1ya in biopsy material (in necrotic masses surrounding ulcers of the mucous membrane).
3. Granulomatous colitis (Crohn's disease of the colon) - see chap. "Crohn's disease"),
4. Ischemic colitis - see the corresponding chapter.
5. Pseudomembranous colitis - see the corresponding chapter.
Examination program
1. General analysis of blood and urine.
2. Scatological analysis: coprocytogram, bacteriological analysis, stool examination for dysentery and protozoal infection (amoebiasis, balantidiasis).
4. Endoscopic examination: sigmoidoscopy (for distal forms of the disease), fibrocolonoscopy (preferable) with a biopsy of the colon mucosa.
5. Plain radiography of the abdominal cavity: only in severe forms of the disease to identify signs of toxic dilatation of the colon.
6. Irrigoscopy: performed after the acute manifestations of the disease have subsided if it is impossible to perform a colonoscopy (in the absence of suspicion of toxic dilatation of the colon).
