Pediatric inflammatory bowel disease
Introduction
Introduction to pediatric inflammatory bowel disease Inflammatory bowel disease (IBD) refers to a group of non-specific chronic gastrointestinal inflammatory diseases of unknown cause. Commonly referred to as non-specific ulcerative colitis (UC) and Crohn's disease (CD), but there are other types of IBD, such as uncolonized colitis, collagen and lymphocytic colitis. Ulcerative colitis, also known as non-specific ulcerative colitis, is a chronic diffuse inflammation that is confined to the colonic mucosa. It spreads continuously and symmetrically from the rectum to the proximal segment. The lesions are inflammation and ulceration. Crohn's disease can affect various parts of the gastrointestinal tract and is chronic granulomatous inflammation, which is most commonly affected by the end of the ileum and its adjacent colon. The lesions are mostly segmental and asymmetric, and the rectum is rarely involved. basic knowledge The proportion of children: the incidence rate of children is about 0.03% - 0.05% Susceptible people: children Mode of infection: non-infectious Complications: perianal abscess, blood in the stool, ascites, hypokalemia
Cause
Causes of pediatric inflammatory bowel disease
(1) Causes of the disease
So far, the etiology of inflammatory bowel disease, the pathogenesis is unknown, and it is believed that it is caused by the interaction of various factors, including genetics, infection, mental, environment, diet, mucosal local immune disorder and other factors. It is believed that the pathogenesis of IBD may be: These genetic determinants make susceptible individuals susceptible to disease, stimulating mucosa-associated lymphoid tissue under the action of infectious agents or intestinal antigens, causing up-regulated T cell responses, thereby activating networks of various cytokines and inflaming local tissues. And continue to enlarge and continue, causing damage to the intestinal wall and corresponding clinical manifestations.
(two) pathogenesis
Pathogenesis
(1) Genetic factors and environmental factors: There is a large amount of evidence that IBD has a certain genetic susceptibility. Epidemiological studies have found that the incidence of relatives of IBD patients is higher than that of the population, CD is 30 times higher, UC is 15 times higher, and monozygosis is reported. Among the 134 patients, 16% had secondary or immediate family members. The family aggregation phenomenon of IBD was related to heredity, but this inheritance did not conform to the simple del genetic law. The monozygotic twins of UC and CD were higher than the same rate. Double-oval twins, some IBD patients are often associated with genetic-related diseases and immune diseases with genetic susceptibility. IBD-related gene studies indicate that HLA-II genes are associated with IBD, and IBD is a multi-gene disease. IBD-related gene loci are located on multiple chromosomes, and UC and CD may or may not be in the same gene.
The occurrence of IBD is not only related to genetic factors, but also environmental factors. 100% of monozygotic twins are common genes. Actually, 100% of monozygotic twins are suffering from IBD, indicating that IBD has low gene permeability and environmental factors play a part. The incidence and prevalence of different geographical locations are significantly different. A survey of the incidence of Asian immigrants and their descendants showed an increase in IBD susceptibility after immigration, suggesting that IBD is not only related to genetic factors, but also affected by environmental factors.
(2) Immune factors: The autoimmune reaction process of inflammatory bowel disease has a common antigenicity between the protein of intestinal epithelial cells and the pathogen invading the intestinal wall. After repeated infection of the intestinal mucosa by the pathogen, it induces the production of autologous intestinal epithelial cells in vivo. Anti-killing antibodies, immune complexes, immune cells activated by immune lymphocytes, macrophages release a variety of cytokines and vasoactive substances, aggravating inflammatory response, intestinal mucosal lymphocytes have cytotoxic effects on intestinal epithelial cells, Therefore, in the inflammatory lesions, lymphocytes, plasma cells, mast cells increase, in addition to intestinal symptoms in addition to intestinal symptoms, a systemic disease, the use of corticosteroids and immunosuppressants to improve the condition, from clinical practical It is recognized that the pathogenesis of IBD is that some genetic factors make susceptible individuals susceptible to disease, stimulate mucosa-associated lymphoid tissue under the action of infectious agents or intracavitary antigens, causing up-regulated T cell responses, thereby activating each a network of cytokines that inflames local tissues and continuously enlarges and continues to cause damage to the intestinal wall And corresponding clinical manifestations.
(3) Infectious factors: For many years, the occurrence of IBD has been considered to be related to infectious factors. The infectious factor is the trigger factor, which initiated a series of intestinal mucosal immune responses and caused disease, paratuberculosis tuberculosis and measles virus infection. It is thought to be related to CD, and it has also been reported that Clostridium difficile exotoxin is associated with recurrence and activity of UC, but it has not been confirmed.
Recently, a different opinion about the promotion of IBD by microorganisms is increasingly accepted. IBD, especially CD, is caused by an abnormal immune response against normal flora. Most animals do not develop colitis in a sterile environment, IBD. The patient's cellular and humoral immune responses to bacterial antigens are enhanced, bacterial retention is beneficial for IBD, and fecal bypass prevents CD recurrence; antibiotics and microecological preparations have therapeutic effects in some IBD patients. These studies indicate that IBD may be The normal flora is caused by a lack of immune tolerance.
(4) Others: Mental stress, anxiety and the surrounding environment can induce or aggravate the condition of children, and milk can also cause colon inflammation in some infants.
2. Pathological changes The pathological range of this disease is limited to 75% in the left colon and rectum, and the rectum is the most common, 10% can be inverted to the end of the ileum, generally not more than 20cm, the affected part of the diffuse lesions.
The colonic mucosa is hyperemia, edema, uneven particles, and the blood vessels are blurred. As the inflammation is aggravated, mucous membranes are diffuse, erosive and ulcerous, and there is exudate on the surface of the ulcer. There may be pseudopolyps or even mucosal bridge formation. A few patients may Intestinal stenosis, shortening, disappearance of intestinal folds, and lead tube signs.
Under the microscope, the colonic mucosa showed non-specific inflammatory changes. During the active period of the lesion, the mucosa changed significantly, the goblet cells decreased, the neutrophil infiltration in the glandular epithelium, the abscess was formed, and the lesions concentrated in the mucosa and submucosa. Erosion and ulcer formation, severe ulcers deep, can reach the serosa layer, even perforation, epithelial regeneration during ulcer repair, fibrous tissue hyperplasia and residual island-like mucosa constitute pseudopolyps, remission mucosal congestion, edema disappear, light gland The structure of the tube can be restored to normal, and the lesion may persist or repeatedly. The author may have fibrous tissue hyperplasia, lymphatic vessel dilatation, adenoid atrophy, and sometimes there are still false polyps, but there is no active inflammation.
Prevention
Pediatric inflammatory bowel disease prevention
The etiology of this disease is not very clear, it is relatively difficult to prevent, but infection factors, dietary allergies and mental factors can be taken to prevent it.
Any child with gastrointestinal tract disease, the problems that should be paid attention to in diet are similar, the principle of treatment, the principle of attention on diet is the same, such as eating less irritating things, smoke, alcohol, spicy sweet and sour things. Try to eat as little as possible, too oily, too greasy to eat less. For ulcerative colitis, there are some cold medicines. The so-called aspirin non-steroidal anti-inflammatory drugs should be especially careful, try not to eat because these The drug is likely to induce an increase in the condition.
Complication
Pediatric inflammatory bowel disease complications Complications, perianal abscess, blood ascites, hypokalemia
1. Toxic megacolon: one of the most serious complications of ulcerative colitis, the mortality rate is as high as 20% to 30%, and its incidence is about 3% to 5%, generally in the first 5 years of ulcerative colitis Occurred within the year, 25% to 40% occurred in the first episode, mostly in patients with severe and total colitis, using cholinergic receptor blockers, barium enema or colonoscopy and hypokalemia Can be induced, its pathophysiological changes are not very clear, pathology can be seen in the inflammation of the entire intestinal wall, due to inflammation and muscle and intermuscular nerves, the tension of the intestinal wall is reduced, peristalsis is weakened, intestinal gas accumulation, content deposition, The wall of the intestine is highly dilated, leading to the development of peritoneal inflammation, the release of bacterial decomposition products and toxins, resulting in symptoms of systemic poisoning.
The diagnostic points of toxic megacolon are as follows:
(1) Clinical and radiological examination: evidence of colonic expansion, colon width > 6 cm.
(2) the performance of systemic poisoning: including fever, tachycardia, peripheral white blood cells increased, anemia, etc.; the disease rapidly deteriorated, and even peritoneal inflammation and intestinal perforation.
(3) Others: There may also be ascites, mental symptoms, electrolyte imbalance, hypotension and hypoproteinemia.
Toxic megacolon can occur within a few hours or several days, so patients with severe ulcerative colitis should always pay attention to changes in abdominal signs, especially after the occurrence of toxic megacolon, The frequency and amount of stool may be reduced, which is mainly the result of siltation of intestinal contents, and does not mean that the condition is alleviated.
2. Gastrointestinal hemorrhage: Blood in the stool is one of the main symptoms of this disease. However, about 3% of patients with ulcerative colitis may develop intestinal bleeding, mostly severe cases, which occur more suddenly and even require blood transfusion. Most cases can not find a single fixed hemorrhagic lesion, but the result of general ulcer bleeding in the intestinal mucosa. It is noted that there may be hypoprothrombinemia in the case of massive hemorrhage, which may be one of the causes of major bleeding. Most cases are effective in conservative treatment. If there is low prothrombinemia, it should be positively corrected.
3. Colon perforation: mostly occurs on the basis of toxic megacolon, occasionally also in moderately severe patients, the incidence rate is about 1.8%, perforation occurs in the left colon, can be multiple sites perforation, clinical It is characterized by severe abdominal pain. The body has signs of diffuse peritonitis such as diffuse abdominal tenderness, rebound tenderness and muscle tension. It should be noted that the use of hormone therapy often masks the clinical manifestations of perforation, and the mortality rate is as high as 50%.
4. Colonic stenosis: Ulcerative colitis with colonic stenosis is rare, about 1/3 of which occurs in the first 5 years of the disease, most of which occur between 5 and 25 years, and the most common sites are in the rectum and sigmoid colon, others Part of the colon can also occur, usually in the 2 ~ 3cm intestine segment of the stenosis, severe obstruction can occur, histological examination showed that the mucosal muscle layer of the diseased atrophy and thickening, should be noted in the colon stenosis should be distinguished from cancer.
5. Carcinogenesis: The incidence of cancerous ulcerative colitis is significantly higher than that of the general population. Western countries report that the rectal cancer rate is about 5%. It is generally believed that the risk of cancer increases with the prolongation of the disease. It has been reported that The annual cancer rate of patients with the disease for more than 10 years is 0.5% to 1%. The risk of canceration is 15% after lifetime follow-up. For young patients, the cancer rate is higher. Under 21 years old, the diagnosis is ulcerative colitis. The cancer rate of patients in the 20 years after the onset of morbidity is 9% to 20%. The cancerous rate of the lesions involving the whole colon is higher. The tissue type of colonic mucosa is adenocarcinoma, which occurs in the flat or slightly elevated mucosa. Carcinogenesis occurs at multiple points, and all parts of the colon can occur. In Europe and the United States, this disease is considered as precancerous lesions, while in China, most patients with mild ulcerative colitis have a relatively low cancer rate, which has been reported to be 0.8%-1.1. %.
6. Perianal abscess and fistula: Occasionally, but rare.
Symptom
Symptoms of inflammatory bowel disease in children Common symptoms Weak abdominal pain Anorexia anaesthesia diarrhea grows slowly and then loses weight and dehydrates blood in the stool
In addition to the common gastrointestinal manifestations, clinical signs and symptoms of children with IBD often have obvious extraintestinal manifestations, such as arthritis, growth retardation, weight loss, malnutrition, anemia, anorexia nervosa, etc., especially growth retardation is growth The most unique symptoms of a child are often present in infancy.
1. Ulcerative colitis Most UC onset is concealed, or mild diarrhea, blood in the stool, only see fecal occult blood, about 30% of children with obvious symptoms, more acute onset, more common infants, diarrhea up to 10 to 30 times / d, bloody stool or mucus bloody stool, pus and bloody stools, infringe the rectum, there is urgency and heavy, sputum abdominal pain often occurs before the stool, it occurs, relieves after the stool, the left lower abdomen is obvious, may have muscle tension or touch the hard tubular colon.
Systemic symptoms include fever, fatigue, anemia; severe cases of dehydration, electrolyte imbalance, acid-base balance disorders, weight loss, growth retardation is also the earliest clinical manifestations of pediatric UC, may have extraintestinal manifestations such as arthritis, joints Pain, iridocyclitis, liver enlargement, etc.
Ulcerative colitis can be typed as follows:
(1) Degree: According to clinical manifestations, it is divided into mild, moderate, severe and extremely severe.
1 Mild: patients with diarrhea 4 times / d or less, blood in the stool is light or no, no fever, pulse speed, anemia, normal blood sedimentation.
2 Moderate: Between moderate and severe.
3 severe: diarrhea 6 times / d or more, obvious mucus bloody stool, body temperature above 37.5 °, pulse speed, hemoglobin <100g / L, ESR> 30mm / h.
4 Extremely severe: If the blood is on the basis of the severe index more than 10 times a day, the plasma protein <30g / L, with severe poisoning or consumption is extremely severe.
(2) Classification: According to the clinical process, it is divided into initial hairstyle, acute fulminant, chronic relapsing, chronic persistent, initial gestation refers to the first episode of no previous history, fulminant symptoms with severe systemic toxicity symptoms, may be associated with toxicity Colonic dilatation, intestinal perforation, sepsis and other complications, in addition to fulminant hair, each type has different degrees of classification and mutual transformation.
(3) range of lesions: divided into proctitis, straight-sigmoid colitis, left colitis, right colitis, regional colitis, total colitis.
(4) Degree of disease activity: divided into active period and remission period.
Pediatric total colitis accounts for about 62%. Common complications are intestinal bleeding, intestinal stenosis, intestinal perforation, sepsis and toxic megacolon.
2. The symptoms of Crohn's disease depend on the location of the lesion and the degree of inflammation. Abdominal pain is the most common complaint of CD, usually located in the umbilical cord, often occurs at mealtimes or after meals, causing the child to be unwilling to eat and anorexia, only Abdominal pain at the end of the ileum is located in the right lower abdomen. Diarrhea is common in 90% of children. It can be caused by many factors, such as large intestinal mucosal dysfunction, bile salt absorption disorder, bacterial overgrowth, inflammatory protein loss, etc., diarrhea occurs in After the meal with abdominal pain, the colon is affected by blood in the stool, the small intestine is affected by watery stools, electrolytes need to be monitored at the same time, CD blood is less common than UC, CD in the upper digestive tract is less common, but also endoscopic and histological examination confirmed stomach ten Digestive lesions are often difficult to distinguish from other diseases such as gastroesophageal reflux, Helicobacter pylori infection, and peptic ulcer.
Some children may have different degrees of perianal lesions such as: anal fistula, anal abscess, anal fissure, etc. These lesions may be early manifestations of CD, often masking gastrointestinal symptoms and causing misdiagnosis.
Weight loss and growth retardation are the most common and most prominent symptoms of CD. No matter whether it is diffuse lesions of the small intestine or individual lesions of the colon, it can show weight loss and growth retardation, and can be earlier than gastrointestinal symptoms for several years. For height and bone age are lower than normal standards, children with persistent growth retardation are highly suspected of IBD. The growth hormone levels in children with IBD are normal. The reason for growth retardation is due to malabsorption, protein loss, and insufficient calorie intake. Increased protein breakdown, multivitamins, trace element deficiency, etc., growth retardation is often accompanied by sexual developmental delay, leading to malnutrition (Table 1):
Parenteral manifestations include joint pain, arthritis, nodular erythema, clubbing, sclerosing cholangitis, and chronic active hepatitis.
Common complications of CD are intestinal obstruction, gastrointestinal bleeding, fistula (intraperitoneal, perianal), abdominal abscess and intestinal perforation.
Crohn's disease can be classified according to the following conditions:
(1) Lesion range: According to the extent of the lesion, diffuse enteritis, ileal end, ileal colon, colon, rectal anus, lesion range reference image and endoscopic results were determined.
(2) Degree: According to clinical severity, it is light, medium and severe, but the division is not as clear as UC.
No systemic symptoms, abdominal tenderness, mass and obstruction were mild. Significant systemic symptoms such as high fever, weight loss with severe abdominal pain, tenderness, vomiting and diarrhea, painful mass or intestinal obstruction are severe. It is moderate between the two.
The CD Activity Index (CDAI) correctly estimates the condition and evaluates the efficacy.
Examine
Examination of pediatric inflammatory bowel disease
The purpose of laboratory tests for inflammatory bowel disease is to:
1 Exclude infectious colitis.
2 to understand the activity of the disease, suggesting that the disease is relieved or early prediction of recurrence.
3 Guide the development of treatment plans, evaluate the efficacy, and predict the outcome.
4 understand the impact of ulcerative colitis on other organ function.
5 provides an objective basis for the differential diagnosis of the disease and other diseases. However, in the diagnosis of ulcerative colitis and the assessment of the condition, the laboratory indicators are not specific and can only be used as part of the comprehensive analysis of the disease.
Hematological examination
(1) Hemoglobin and plasma protein: light or normal or only mildly decreased, moderate or severe, mild or moderately decreased, even severe anemia and low protein edema, Hb decline can be attributed to chronic inflammatory bleeding and Loss of protein, lack of iron or other hematopoietic substances or malabsorption, especially ileal lesions of Crohn's disease are prone to vitamin and mineral absorption disorders and bone marrow hematopoietic inhibition associated with chronic inflammation, in addition, although patients with normal renal function, erythropoietin Insufficient secretion also plays an important role in the formation of anemia of inflammatory bowel disease.
(2) white blood cell count: most patients with normal, moderate, severe patients may have a slight increase, a small number of critically ill patients can be as high as 30 × 109 / L, sometimes with neutrophil increased, in severe cases can appear neutral particles The nucleus moves to the left and has poisonous particles. The increase of white blood cell count in ulcerative colitis may be related to inflammatory activity. Systemic application of glucocorticoids can also increase granulocytes. In addition, the use of immunosuppressive agents during treatment may reduce lymphocyte count.
(3) platelet count: in patients with ulcerative colitis and Crohn's disease, platelet count can be increased, relatively light, medium ulcerative colitis, platelet count of severe patients is more than 400 × 109 / L more common, but this The indicators are not widely used in the diagnosis of inflammatory bowel disease.
2. Fecal examination
(1) routine examination of feces: the naked eye is the most common paste-like mucus pus and blood, the severe cases of fecal matter is very small, a small number of patients with bloody stools, accompanied by a small amount of mucus or no mucus, microscopic examination showed a lot of red blood cells, pus cells, Eosinophils are also seen, and a large number of multinucleated macrophages are commonly found in fecal smears during acute attacks.
(2) Pathogen examination: The purpose of the pathogen examination of inflammatory bowel disease is to exclude infectious colitis, which is an important step in the diagnosis of this disease. The contents of the pathogen examination include:
1 Bacterial culture: It should be repeated and repeated examinations. If it is satisfied with clinical diagnosis, it must be done more than 3 times in succession. If scientific research cases are selected, it should be more than 6 times in succession.
2 dissolved tissue amoebic trophozoites: take fresh feces, especially bloody mucus, repeated examinations (same bacterial culture).
3 fecal collection of eggs: to retain all the feces each time, to do egg collection and hatching, should be carried out several times in a row (same bacterial culture), can exclude chronic schistosomiasis and other parasitic infections.
4 virological examination: In the acute attack of this disease, as far as possible, use electron microscopy or immunoelectron microscopy to find virus particles in the feces, or immunological methods to find virus-specific antigens to rule out opportunistic infections.
3. ESR (ESR) examination: ESR in patients with inflammatory bowel disease generally increased, ESR generally reflects disease activity, foreign reports, patients with remission period, the average ESR is 18mm / h, mild activity is 43 mm / h, moderate activity 62mm / h, severe activity 83mm / h.
ESR changes reflect changes in the concentration of certain proteins in the serum during the active period of the disease. When certain protein concentrations in the serum, especially r-globulin, fibrinogen and Y-globulin, and hematocrit change, ESR will Changes, due to the long half-life of serum proteins associated with ESR, if the clinical symptoms improve quickly, ESR often declines several days after the clinical symptoms are relieved, therefore, ESR can not reflect the patient's condition changes in time.
4. Monitoring of serum acute phase reaction protein: Inflammatory bowel disease active period, especially in critically ill patients, acute phase reaction may occur, acute phase reaction is stress reaction, which is the body's various infections or injuries, including inflammatory bowel disease. a basic reaction involving many immune and inflammatory processes, as well as functional changes in many organs, often accompanied by abnormal serum protein content in the liver, such as a1-acid glycoprotein, C-reactive protein, A1-antitrypsin, fibrinogen, a2-macroglobulin and complement C3, etc. These serum proteins are called acute phase response proteins or acute phase proteins, and their serum levels are monitored. It has certain value for understanding the severity of the disease activity and evaluation.
C-reactive protein (CRP) is a non-specific acute phase response protein. Its important advantage as a laboratory indicator of inflammatory bowel disease is its ability to respond rapidly to inflammation and regression. Its concentration can vary up to 1000 times. The serum CRP content can reflect the disease activity, the extent and severity of the disease. Sharma et al found that 29 patients with inflammatory bowel disease had CRP <10g/ml during remission, while patients with moderate and severe CRP had significantly higher CRP than normal (P). <0.05, P<0.001); dynamic observation showed that with the remission of the disease, the CRP content gradually decreased until normal. When CRP>40g/ml, the patient had poor response to medical treatment, such as CRP>70g/ml during treatment, often Severe or medical treatment failure, suggesting that patients with surgically removed diseased bowel, but CRP is less sensitive in the diagnosis of inflammatory bowel disease than Crohn's disease.
CRP itself selectively attaches to the cell membrane and binds to free DNA. The half-life of CRP in the blood circulation is short, only l9h. Therefore, after the inflammation is relieved, the serum content will fall rapidly, interleukin-1, leukocyte Cytokines such as cytokines-6, tumor necrosis factor a and metastatic growth factor p can promote the synthesis of CRP by hepatocytes.
5. Immunological examination: Patients with inflammatory bowel disease have changes in humoral immunity and cellular immune function. Therefore, they are often classified as autoimmune diseases. The immunological examination of this disease is helpful to understand the mechanism of the disease. And to determine the activity of the disease, can be used as an auxiliary indicator for the diagnosis of this disease.
(1) Humoral immunity: In the active period of ulcerative colitis, serum IgG, IgA, IgM can be elevated, especially elevated serum IgA reflects the recovery of intestinal mucosal immune system.
(2) Cellular immunity: The pathogenesis of Crohn's disease is dominated by mid-cell immunity, and the ratio of helper T cells/suppressor T cells (Th/Ts) in the peripheral blood of the disease active period is increased, and the disease is relieved, Th/ The Ts gradually decreased, and the dynamic monitoring of the change in Th/Ts ratio was valuable for estimating the activity and efficacy of patients with Crohn's disease.
6. Coagulation function test: In addition to changes in platelet count during the active period of ulcerative colitis, there may be some changes in clotting factors. In acute fulminant cases, vitamin K deficiency can cause a decrease in prothrombin (factor II). And mild to moderate reduction of factor VII and factor X, resulting in prolonged prothrombin time (PT). In a wide range of lesions, factors V, VIII and plasma fibrinogen (factor I) increased, but During the stagnation activity, the local blood supply is in a hypercoagulable state. Due to the inflammatory stimuli, the number of platelets in the blood increases, and the adhesion increases, which promotes the aggregation of the platelets, and the blood cells adhere to them, forming a strong thrombus in the blood vessels on the surface of the mucosa. This is one of the theoretical basis for the clinical use of anticoagulant therapy.
7. Liver function test: Inflammatory bowel disease combined with liver damage, serum alanine aminotransferase, alkaline phosphatase, bilirubin and sulphonium bromide test can be abnormal, especially worthy of attention for patients with ulcerative colitis In the detection of protein metabolism, serum albumin (albumin, A) decreased, globulin (G) increased, albumin to globulin ratio (A / G) decreased; serum protein electrophoresis showed white Protein is reduced, a2 and Y-globulin can be increased, a2 globulin is increased in severe cases, Y-globulin is low, and serum albumin is decreased during active period of ulcerative colitis, which is related to protein loss and malnutrition in intestinal inflammation. Some authors pointed out that there is a good negative correlation between serum albumin content and intestinal protein loss. The increase of globulin is related to the increase of acute phase reaction protein. The abnormal protein metabolism of ulcerative colitis reflects the disease activity to some extent. Sex, severity of disease, extent of disease and course of disease.
8. Electrolyte and acid-base balance check: Patients with ulcerative colitis have normal blood electrolytes and acid-base balance examination. Patients with severe diarrhea may have hypokalemia, hyponatremia and metabolic acidosis. People with frequent vomiting may have hypokalemia. , low blood chlorine, low blood sodium and metabolic alkalosis.
9. Skin test: The phytohemagglutinin skin test and the tuberculin skin test were inferior.
10. X-ray examination: Barium enema and barium meal is one of the important means to diagnose IBD, especially the double contrast of gas sputum can show small lesions of mucous membrane and improve the diagnosis rate.
(1) UC: early manifestations can be normal or only the mucosal folds are coarse, the edge of the intestine is blurred, and the mucosa of the severe cases is brush-like, serrated, visible ulcers, pseudopolyps, colonic bags disappear, intestinal duct stiffness, shortened tubular, intestinal The cavity is narrow.
(2) CD: early or normal mucosal irregular thickening, disorder, thickening, typical typical cases in the late stage can be seen ulcers, fissures, fistulas, paving stone-like reticular changes, intermittent intestinal stenosis with adjacent intestinal dilatation or lesions There is a normal intestinal segment between the intestines, which is a leaping distribution.
11. Endoscopy: Pediatric fiber colonoscopy can be delivered to the ileocecal area, the whole colon can be observed, the location, extent and extent of the lesion can be determined, and tissue biopsy can be taken at multiple sites to improve the diagnosis rate.
(1) UC: lesions from the rectum, diffuse distribution, mucosal congestion and edema, rough granular, increased fragility, easy bleeding, ulcer size, shallow, purulent or purulent exudate, chronic inflammation For mucosal hyperplasia, pseudopolyps, stenosis, lesions develop continuously from the distal end of the colon to the proximal end, or to the entire colon.
(2) CD: mucosal congestion and edema, not easy to bleed, ulcers round, oval or linear fissures longitudinal distribution, called "aphthous ulcer", or paving stone-like changes, inflammatory polyps, intestinal stenosis, lesion jumping Distribution, lesions adjacent to normal tissue, perianal fissure, fistula.
12. Histopathological changes
(1) UC: What is seen is different from the disease activity and remission. The active mucosa is inflammatory, the crypt is deformed, lymphocytes, multinucleated cells, plasma cells infiltrate into the lamina propria, goblet cells are reduced, crypt abscess formation, abscess Ulceration forms an ulcer, and the intestinal epithelial hyperplasia occurs during the remission period, and the glandular epithelium shrinks.
(2) CD: segmental whole wall inflammation, the main histological features have two points: First, the fissure ulcer can reach the abdominal wall serosa, and the second is non-caseous necrotizing granuloma, containing multinucleated giant cells and epithelioid cells, the number Less, scattered, and less complete.
Diagnosis
Diagnosis and diagnosis of pediatric inflammatory bowel disease
diagnosis
Diagnosis should be performed in conjunction with clinical presentation, laboratory tests, X-ray, endoscopy, and histological examination.
According to the typical symptoms, repeated examination of feces to eliminate pathogen infection, and adequate antibiotic treatment, should be highly suspected, can be based on colonoscopy or X-ray examination, but must be carefully combined with clinical and autoimmune diseases to confirm the diagnosis .
The complete diagnosis of the disease should include the type of clinical, severity, extent of the lesion and stage of the lesion.
Differential diagnosis
Due to the lack of specific diagnostic criteria for UC, it is difficult for CD to obtain the results of pathological histology that can be diagnosed - non-case-like granuloma, which is currently difficult to diagnose for IBD.
1. Diagnosis and differential diagnosis of ulcerative colitis: Ulcerative colitis is a chronic diffuse inflammation confined to the colonic mucosa. It spreads continuously from the rectum to the proximal segment, and is symmetrically distributed. The lesions are inflammation and ulcer.
The clinical manifestations are characterized by bloody diarrhea, alternating episodes and remissions. Diarrhea can also be manifested as mucus, which can be associated with abdominal pain, urgency, vomiting, anorexia, often with obvious growth retardation, anemia, fever, hypoproteinemia and other systemic manifestations. Arthritis, iridocyclitis, hepatosplenomegaly and other gastrointestinal manifestations.
Colonoscopy and mucosal biopsy are the key to diagnosis. The lesions start from the rectum and are diffusely distributed. Under colonoscopy, the mucosal vascular texture is blurred, disordered, congested, edematous, fragile, hemorrhagic, and purulent. Attachment of the object; obvious lesions are still visible in the diffuse majority of erosion, ulcers. Chronic lesions can be seen in shallow colon pockets, pseudopolyp formation and mucosal bridge formation. Histological findings vary with lesion activity and remission. UC lesions mainly involve mucosa and submucosa. Mucosal muscularis is only in fulminant UC. Involved, acute inflammatory cell infiltration of epithelial and crypt in active period, especially epithelial neutrophil infiltration, cryptitis, crypt abscess formation; chronic crypt structure change, early crypt epithelial hyperplasia, late crypt size Irregular, abnormal orientation, disordered glandular arrangement, distorted bifurcation, decreased mucus secretion, altered cytoplasmic basophilic, chronic inflammatory cell infiltration of the lamina propria, such as the discovery of inflammatory activity and chronic syndrome comprehensive diagnostic value.
Ulcerative colitis is distinguished from the following diseases:
(1) Infectious enteritis: Many infectious enteritis such as Salmonella, Shigella, Escherichia coli, Yersinia, Amoeba and Clostridium difficile are caused by acute onset mucus Pus and blood, bloody stools, colonoscopy and histological changes, such as mucosal vascular texture blur, disorder, congestion, edema, brittleness, bleeding, erosion, ulceration, acute or chronic inflammatory cell infiltration, similar to early or atypical UC Therefore, UC should be differentiated from the above diseases.
1 general bacterial enteritis: the main difference between UC and most bacterial enteritis is the duration of symptoms, UC-induced bloody stools, mucus pus and blood often lasts for weeks to months, while bloody diarrhea of bacterial enteritis is shorter, by sandmen Enteritis caused by bacteria, Shigella, Campylobacter infection Although the symptoms are similar to UC, bloody stools can be relieved after 3 to 5 days, Yersinia enteritis symptoms last for 14 to 17 days, bacterial enteritis stool culture Positive, another important difference between UC and infectious enteritis is pathological changes. UC often has changes in crypt structure, irregular distortion and bifurcation, reduced number, lack of mucus secretion and crypt expansion.
2 refractory Clostridium enteritis: also known as pseudomembranous colitis, diarrhea can last from several weeks to several months, but the child has a history of taking antibiotics before the onset of the disease, water is more common, blood is rare, in the stool There may be pseudo-membranes of different sizes. Under the colonoscopy, a typical round or oval yellow pseudomembrane is attached to the intestinal wall to help distinguish it from UC. If necessary, the determination of Clostridium difficile (CD) toxin is performed. .
3 dissolved tissue amoebic enteritis: symptoms lasted for several weeks to several months, the stool is dark red jam-like, heavy can be whole blood, colonoscopy showed focal, hemorrhagic ulcer, central opening subsidence, flask-like, lesion The mucosa is normal, and UC is diffusely altered. Those with conditions should be tested for amoeba serology.
(2) ischemic colitis: the age of onset is large, mostly for the elderly. Colonoscopy is mainly characterized by edema, erythema and ulcer formation. The lesions are mainly colonic spleen, descending colon and sigmoid colon, and the rectum is rarely affected.
(3) Radioactive colitis: a complication that occurs after pelvic or abdominal radiation therapy, involving the rectum, the sigmoid colon is more common, and the damage of the radiation to the intestinal tract is mainly to inhibit epithelial mitosis and cause submucosal arteriolar occlusive inflammation and Endometritis causes ischemic changes in the intestinal wall, diarrhea occurs after radiotherapy, mostly mucus and bloody stools, diffuse congestive edema of the affected intestines can be seen under colonoscopy, and there are erythema and granule-like changes, brittle, erosive, ulcer; late The mucus is pale, the submucosal blood vessels are abnormally dilated, the intestinal tract is narrow, and the intestinal wall is thickened. The pathological changes of the colon are inflammatory cell infiltration and submucosal vasculitis or telangiectasia.
2. Diagnosis and differential diagnosis of Crohn's disease
(1) CD disease: Crohn's disease (CD) is an unexplained cause that can affect chronic granulomatous inflammation in various parts of the gastrointestinal tract. The end of the ileum is extremely adjacent to the colon, and the lesions are mostly segmental. Symmetrical distribution, the rectum is rarely involved.
1 diagnosis: clinical manifestations of chronic onset, repeated abdominal pain, diarrhea, may be associated with abdominal mass, intestinal fistula and anal lesions, as well as fever, anemia, weight loss, developmental delay, arthritis, iridocyclitis, liver disease and other systemic mergers Syndrome, comprehensive clinical manifestations, imaging, endoscopy and histological examination, using exclusion diagnosis.
Imaging examination is very important for diagnosis. Small bowel sputum angiography and (or) barium enema can be seen multiple, segmental inflammation with stenosis, cobblestone-like changes, fissure ulcers, fistula or pseudopolyposis, B-ultrasound, CT, MRI Shows thickening of the abdominal wall or pelvic abscess in the intestinal wall.
The earliest seen under endoscopy, the most obvious is the small and well-defined mucus ulcer, called "Aphtha" ulcer, often multifocal distribution, the lesions are separated by normal mucosa, also visible segmental, asymmetric Sexual mucosal inflammation, longitudinal ulcers, cobblestone-like changes, sinusoidal stenosis and intestinal wall stiffness.
The main histological features are twofold: one is the perforation of inflammation, the formation of lymphoid aggregates around the lymph and small blood vessels, these lymphatic accumulation changes can be distributed to any part of the intestinal wall; the second is the formation of non-case-like granuloma, a small number , scattered distribution, the composition is not complete.
2 Exclude related diseases: to exclude acute appendicitis, intestinal tuberculosis, other chronic infectious enteritis (such as Yersinia enteritis), intestinal lymphoma, ulcerative colitis and other diseases.
(2) Identification with appendicitis: CDs in ileocecal areas are often confused with acute appendicitis. Appendicitis often has acute onset, severe abdominal pain with muscle tension, and CD often has a history of diarrhea before the onset of the disease.
(3) Identification with intestinal tuberculosis: Intestinal tuberculosis and CD are very similar in clinical manifestations and pathology. The most common part of intestinal tuberculosis is ileocecal area. If the child has tuberculosis at the same time, the diagnosis of intestinal tuberculosis is not difficult, but the intestine Tuberculosis can occur without tuberculosis. If there is germline tuberculosis or tuberculosis with other organs, the activity of adenylate deaminase (ADA) in the blood is increased, and intestinal tuberculosis is considered. The intestinal wall lesions of intestinal tuberculosis can be examined by biopsy. There is caseous necrosis, submucosal atresia, such as intestinal fistula, intestinal wall or organ abscess, perianal intestinal lesions, active blood in the stool, intestinal perforation and other complications or recurrence after resection, etc., should consider CD, pathological living tissue Examination of visible sarcoidosis-like granuloma, fissure ulcer, lymphocyte aggregation, but no cheese-like necrosis, it is important not to misdiagnose intestinal tuberculosis as CD, because the application of hormones will make intestinal tuberculosis worse, it is recommended to identify first For anti-tuberculosis treatment, surgical indications are performed by surgical indications. In addition to pathological examination of the resected intestinal segments, multiple mesenteric lymph nodes should be taken for pathological examination.
(4) Identification with small intestinal lymphoma: Some symptoms of small intestinal lymphoma are similar to CD, such as fever, weight loss, diarrhea, abdominal pain, etc., imaging examination is helpful for differential diagnosis, intestinal lymphoma is mostly diffuse intestinal wall Sexual involvement is accompanied by intestinal wall shadows, while CD lesions are often confined to the ileum, which is characterized by ulceration of the intestinal wall and narrowing of the intestinal lumen.
3. The clinical manifestations of ulcerative colitis and Crohn's disease are different. UC is mainly bloody stool. CD children rarely see bloody stools, mainly chronic abdominal pain, sometimes in the ileocecal area can touch a pain, soft inflammatory mass, CD often combined with intestinal fistula.
The other major difference between the two is the location of the disease. UC often starts from the rectum and extends to the proximal segment and involves a part of the colon. The lesion is continuous, often involving only the colon, while CD can affect the entire gastrointestinal tract. In any part of the tract, the most common lesions are the ileum and proximal colon, the lesions are segmental, and the mucus between the lesions is normal.
Endoscopic findings and histopathological examinations have their own characteristics.
