Pediatric inflammatory bowel disease

　　1. Etiology

　　To date, the etiology and pathogenesis of inflammatory bowel disease are unclear. It is generally believed to be caused by the interaction of multiple factors, including genetics, infection, mental health, environment, diet, and mucosal local immune disorders. Currently, it is believed that the pathogenesis of IBD may be: certain genetic determinants make susceptible individuals more prone to disease, and under the action of infectious factors or intestinal lumen antigens, stimulate mucosal-associated lymphoid tissue, causing an upregulated T cell response, thereby activating various cytokine networks, causing local tissue inflammation, and continuously amplifying and persisting, leading to intestinal wall injury and corresponding clinical manifestations.

　　2. Pathogenesis

　　1. Pathogenesis

　　(1) Genetic and environmental factors: There is a large body of evidence indicating that IBD has a certain genetic susceptibility. Epidemiological studies have found that the incidence rate of IBD in relatives of patients is higher than in the general population, with CD being 30 times higher and UC 15 times higher. Among the 134 monozygotic twin cases reported, 16% had first or second-degree relatives with IBD. The familial aggregation of IBD suggests a genetic component. However, this genetic pattern does not conform to simple Mendelian inheritance. The concordance rate of UC and CD in monozygotic twins is higher than in dizygotic twins. Some IBD patients often have associated diseases related to genetic genes and immune diseases with genetic susceptibility. Research on IBD-related genes shows that HLA-Ⅱ class genes are associated with IBD, and IBD is a polygenic disease. The IBD-related gene loci are located on multiple chromosomes, and UC and CD can be in the same gene or not in the same gene.

　　The occurrence of IBD is not only related to genetic factors, but also involves environmental factors. Monozygotic twins share 100% of the same genes, yet not all monozygotic twins develop IBD, indicating a low genetic penetrance of IBD and the partial role of environmental factors. There are significant differences in incidence and prevalence rates of IBD in different geographical locations. A survey of the incidence of IBD in Asian immigrants and their descendants showed an increased susceptibility to IBD after immigration, suggesting that IBD is not only related to genetic factors but also influenced by environmental factors.

　　(2) Immune Factors: The autoimmune reaction process in inflammatory bowel disease involves the protein of intestinal epithelial cells and the pathogenic organisms invading the intestinal wall having common antigenicity. After repeated infections of the intestinal mucosa by pathogens, antibodies, immune complexes, activated immune cells, and macrophages releasing various cytokines and vasoactive substances are induced in the body, which activate the immune cells and increase the inflammation. Lymphocytes, plasma cells, and mast cells increase in the mucosal lesions. Clinically, in addition to intestinal symptoms, there are extra-intestinal manifestations, indicating a systemic disease. The use of adrenal cortical hormones and immunosuppressants improves the condition. The clinically practical and widely recognized pathogenesis of IBD is that certain genetic factors make susceptible individuals prone to disease, and under the action of infection factors or intraluminal antigens, the mucosal-associated lymphoid tissue is stimulated, leading to an upregulated T cell response, thereby activating a network of various cytokines, causing local tissue inflammation, and continuously amplifying and continuously causing damage to the intestinal wall and the corresponding clinical manifestations.

　　(3) Infection Factors: For many years, it has been believed that the occurrence of IBD is related to infection factors, which act as 'trigger factors', initiating a series of intestinal mucosal immune reactions leading to disease. Paratuberculosis-like bacteria and measles virus infections are considered to be associated with CD, and there are also reports that Clostridium difficile toxin is associated with the recurrence and activity of UC, but none have been confirmed.

　　Recently, a different view regarding the role of microorganisms in the occurrence of IBD is increasingly accepted. IBD, especially CD, is caused by an abnormal immune response against the normal flora. Most animals do not develop colitis in a sterile environment, and the cellular and humoral immune responses of IBD patients against bacterial antigens are enhanced, bacterial retention is conducive to the occurrence of IBD, and fecal diversion prevents CD recurrence; antibiotics and probiotics have a therapeutic effect on some IBD patients, and these studies all indicate that IBD may be due to a lack of immune tolerance to the normal flora.

　　(4) Others: Stress, anxiety, and the surrounding environment can induce or exacerbate a child's condition, and milk can also cause some infants to develop colonic inflammation.

　　2. Pathological Changes

　　The lesion range of this disease is limited to the left half of the colon and rectum in 75% of cases, and the rectum is the most common, with 10% extending to the distal ileum, generally not exceeding a range of 20cm. The involved areas develop diffuse lesions.

　　The colon mucosa seen by the naked eye shows congestion, edema, and irregular granules, with blurred blood vessel courses. With the aggravation of inflammation, there is diffuse hemorrhage of the mucosa, erosion, and the formation of ulcers. The ulcer surface may have exudates attached, and there may be pseudopolyps or mucosal bridges. A few patients may develop intestinal stricture, shortening, and the disappearance of intestinal villi, presenting as a lead pipe sign.

　　Microscopic examination shows non-specific inflammatory changes in the colonic mucosa. During the active phase of the lesion, mucosal changes are significant, goblet cells are reduced, neutrophils infiltrate between the glandular epithelium, and cystic abscesses form. The lesion is concentrated in the mucosa and submucosa, with widespread erosion and the formation of ulcers. In severe cases, the ulcers are deep and large, reaching the serosa, and even perforating. During the healing of ulcers, epithelial regeneration, fibrous tissue proliferation, and residual islet mucosa form pseudopolyps. During the remission period, mucosal congestion and edema disappear, and in mild cases, the glandular duct structure can return to normal. In cases with persistent or recurrent lesions, fibrous tissue proliferation, lymphatic dilation, and glandular atrophy may occur. Sometimes, although pseudopolyps may still exist, there is no active inflammation.

　　1. Gastrointestinal Hemorrhage

　　Blood in the stool is one of the main symptoms of the disease, but about 3% of patients with ulcerative colitis can experience massive intestinal bleeding, which is mostly in severe cases. It occurs suddenly and may require blood transfusion for rescue. Most of these cases do not have a single fixed bleeding focus but are the result of widespread ulceration and bleeding of the intestinal mucosa. Some have noted that in cases with massive bleeding, there may be hypoproteinemia, which may also be one of the causes of massive bleeding. Most cases respond well to conservative treatment. If there is hypoproteinemia, it should be actively corrected.

　　2. Colonic Perforation

　　It often occurs on the basis of toxic megacolon. Occasionally, it also occurs in patients with moderate to severe conditions, with an incidence rate of about 1.8%. Perforation mostly occurs in the left half of the colon and can be multiple perforations. Clinical manifestations include severe abdominal pain, diffuse abdominal tenderness, rebound pain, and muscle tension, indicating diffuse peritonitis. It should be noted that the use of corticosteroids often masks the clinical manifestations of perforation. The mortality rate is as high as 50%.

　　3. Colonic Stricture

　　The occurrence of colonic stricture in ulcerative colitis is relatively rare. About one-third of cases occur in the first 5 years of the disease, and the rest mostly occur between 5 and 25 years. The common sites are the rectum and sigmoid colon, and other parts of the colon can also be affected. Strictures usually appear in 2 to 3 cm segments of the intestine, and severe cases can lead to obstruction. Histological examination shows atrophy and thickening of the mucosal muscle layer in the affected intestinal segment. When colonic stricture occurs, attention should be paid to distinguish it from cancer.

　　4. Cancer

　　The incidence of cancer in ulcerative colitis is significantly higher than that in the general population. In Western countries, the concurrent incidence of colorectal cancer is about 5%, and it is generally believed that the risk of cancer increases with the progression of the disease. Reports indicate that the annual cancer incidence rate in patients with the disease for more than 10 years is 0.5% to 1%, and the risk of cancer is 15% when followed up for life. For young patients, the cancer incidence rate is even higher; for patients diagnosed with ulcerative colitis under the age of 21, the cancer incidence rate within 20 years of onset is 9% to 20%. The cancer rate is higher in patients with lesions involving the entire colon. The tissue type of colonic mucosal cancer is adenocarcinoma, which often occurs in flat or slightly elevated mucosal sites and can appear in multiple locations. Cancer can occur in any part of the colon. In Western countries, this disease is considered a precancerous lesion, while in China, most patients with mild ulcerative colitis have a relatively lower cancer rate, with reports ranging from 0.8% to 1.1%.

　　5. Perianal abscess and fistula

　　Occasionally occur, but rare.

　　1. Ulcerative colitis

　　Most UC cases have an insidious onset or mild diarrhea, hematochezia, only occult blood in stool, about 30% of children have obvious symptoms, onset is acute, mostly seen in infants and young children, diarrhea can reach 10-30 times a day,呈血便或黏液血便,脓血便, those involving the rectum have tenesmus, spastic abdominal pain often occurs before or during defecation, and relieves after defecation, significant tenderness in the lower left abdomen, may have muscle tension or palpable hard colonic tube.

　　Systemic symptoms include fever, fatigue, anemia; in severe cases, there may be dehydration, electrolyte disorder, acid-base imbalance, etc., weight gain, and growth and development delay are also the earliest clinical manifestations of pediatric UC. There may be extra-intestinal manifestations such as arthritis, joint pain, iridocyclitis, liver enlargement, etc.

　　Ulcerative colitis can be classified as follows:

　　1. Degree

　　It is divided into mild, moderate, severe, and extremely severe according to clinical manifestations.

　　(1) Mild: Patients have less than 4 diarrhea episodes a day, mild or no hematochezia, no fever, pulse quickening, anemia, and normal ESR.

　　(2) Moderate: Between moderate and severe.

　　(3) Severe: Diarrhea more than 6 times a day,明显黏液血便, body temperature above 37.5°C, pulse quickening, hemoglobin less than 100g/L, ESR more than 30mm/h.

　　(4) Severe: If the blood in the stool is more than 10 times a day on the basis of severe indicators, plasma protein is less than 30g/L, and accompanied by severe toxicity or consumption, it is considered severe.

　　2. Classification

　　It is divided into initial type, acute fulminant type, chronic recurrent type, chronic persistent type. The initial type refers to the first onset without a history of past illness, with severe symptoms accompanied by systemic toxic symptoms, which may be accompanied by toxic megacolon, intestinal perforation, sepsis, and other complications. In addition to the fulminant type, all types have varying degrees of classification and interconversion.

　　3. Lesion range

　　It is divided into proctitis, recto-sigmoid colonitis, left hemicolitis, right hemicolitis, regional colitis, and total colitis.

　　4. Degree of lesion activity

　　It is divided into active phase and remission phase.

　　Infantile total colitis accounts for about 62%, and common complications include intestinal bleeding, intestinal stricture, intestinal perforation, sepsis, and toxic megacolon.

　　Second, Crohn's disease

　　Symptoms depend on the location of the lesion and the degree of inflammation. Abdominal pain is the most common complaint in CD, usually located around the umbilicus, often occurring during or after meals, causing children to be unwilling to eat or even have anorexia. Only the abdominal pain in the ileal terminal lesion is located in the lower right abdomen. Diarrhea is common in 90% of children, which can be caused by various factors, such as large-scale intestinal mucosal dysfunction, bile salt malabsorption, overgrowth of bacteria, inflammatory protein loss, etc. Diarrhea occurs after meals accompanied by abdominal pain, and patients with colonic involvement have hematochezia. Intestinal involvement is watery stool, and electrolytes need to be monitored simultaneously. CD hematochezia is less common than UC. CD in the upper gastrointestinal tract is less common, but there are also confirmed gastric duodenal lesions by endoscopy and histological examination, which are often difficult to differentiate from other diseases such as gastroesophageal reflux, Helicobacter pylori infection, peptic ulcer, etc.

　　The etiology and pathogenesis of this disease are not yet fully clear, and it is relatively difficult to prevent from a preventive perspective. However, infection factors, dietary allergy factors, and psychological factors can be prevented by taking corresponding measures.

　　For children with gastrointestinal diseases, the issues to be paid attention to in diet are generally similar. The principles of treatment and diet are the same. For example, eat less spicy things, smoke, alcohol, and try to eat less spicy, sweet, sour things, and less greasy and greasy things. For ulcerative colitis, some cold remedies, so-called aspirin-like non-steroidal anti-inflammatory drugs should be particularly cautious and try not to eat them. Because these drugs may trigger the aggravation of the disease.

Protein electrophoresis, skin test, fibrinogen, stool routine, endoscopy, smear, erythrocyte sedimentation rate (ESR), C-reactive protein test (CRP), serum immunoglobulin measurement, prothrombin time (PT)

The purpose of laboratory examination in inflammatory bowel disease is to:

① Exclude infectious colitis.

② Understand the activity of the disease, suggest disease remission or early prediction of recurrence.

③ Guide the formulation of treatment plans, evaluate the efficacy, and predict the outcome.

④ Understand the impact of ulcerative colitis on the function of other organs.

⑤ It provides an objective basis for the differential diagnosis of this disease and other diseases. However, in the diagnosis and evaluation of ulcerative colitis, laboratory indicators are not specific and can only be part of the comprehensive analysis of the disease.

1. Hematological examination

(1) Hemoglobin and plasma proteins: In mild cases, hemoglobin levels are usually normal or only slightly decreased. In moderate to severe cases, there may be mild to moderate decreases, or even severe anemia and hypoproteinemia with edema. The decrease in hemoglobin can be attributed to chronic inflammatory bleeding and protein loss, iron and other hematopoietic substances deficiency or malabsorption, especially the ileal lesions in Crohn's disease are prone to vitamin and mineral malabsorption and bone marrow hematopoiesis inhibition related to chronic inflammation. In addition, although the patient's renal function is normal, insufficient erythropoietin secretion plays an important role in the formation of anemia in inflammatory bowel disease.

(2) White blood cell count: The majority of patients have normal counts, while moderate to severe patients may have slight increases. A few severe patients can reach up to 30×10^9/L, sometimes with an increase in neutrophils as the main feature. In severe cases, neutrophil nuclear left shift and toxic granules may occur. The increase in white blood cell count in ulcerative colitis may be related to the activity of inflammation, and systemic application of glucocorticoids can also increase granulocytes. In addition, the use of immunosuppressants during treatment may cause a decrease in lymphocyte count.

(3) Platelet count: During the recurrence of ulcerative colitis and Crohn's disease, the platelet count can increase. For relatively mild to moderate ulcerative colitis, the platelet count greater than 400×10^9/L is more common in severe patients, but this index has not been widely applied to the diagnosis of inflammatory bowel disease.

2. Fecal examination

(1) Routine fecal examination:肉眼观以糊状黏液脓血便为最常见，重症者粪质极少，少数患者以血便为主，伴有少量黏液或无黏液，镜检可见大量红细胞，脓细胞，还可见嗜酸性粒细胞，急性发作期粪便涂片中常见有大量多核的巨噬细胞。The most common finding is pasty, mucous, purulent, and bloody stools. In severe cases, the fecal matter is very little. A few patients have mainly bloody stools, accompanied by a small amount of mucus or no mucus. Microscopic examination shows a large number of red blood cells, pus cells, and also eosinophils. During the acute attack, a large number of multinucleated macrophages are commonly found in the fecal smear.

(2) Pathogenic examination: The purpose of the pathogenic examination of inflammatory bowel disease is to exclude infectious colitis, which is an important step in the diagnosis of the disease. The content of the pathogenic examination includes:

① Bacterial culture: It should be examined repeatedly multiple times. If satisfied with the clinical diagnosis, it is necessary to perform more than 3 times continuously, such as for research cases, it should be more than 6 times.

② Examination of tissue-destroying ameba trophozoites: Take fresh feces, especially bloody mucous stools, and perform repeated examinations multiple times (same as bacterial culture).

③ Fecal egg collection: Collect all the feces each time, perform egg collection and hatching, and do it continuously for multiple times (same as bacterial culture), which can exclude chronic schistosomiasis and other parasitic infections.

④ Virological examination: During the acute onset of the disease, it is recommended to use an electron microscope or immunoelectron microscope to find viral particles in the feces, or use immunological methods to find viral-specific antigens, in order to exclude opportunistic viral infections.

3. ESR (erythrocyte sedimentation rate) examination: During the active phase, the ESR of patients with inflammatory bowel disease is generally increased. ESR can generally reflect the activity of the disease. According to foreign reports, the average ESR of patients in remission is 18 mm/h, 43 mm/h for mild activity, 62 mm/h for moderate activity, and 83 mm/h for severe activity.

The change of ESR reflects the change in the concentration of certain proteins in the serum during the active phase of the disease. When the concentration of certain proteins in the serum changes, especially r-globulin, fibrinogen, and Y-globulin, as well as the hematocrit, ESR will change. Due to the long half-life of serum proteins related to ESR, if the clinical symptoms improve quickly, ESR often does not decrease until several days after the symptoms are relieved, so ESR cannot reflect the changes in the patient's condition in a timely manner.

4.血清急性期反应蛋白的监测：炎性肠病活动期，尤其是重症患者，可出现急性期反应，急性期反应即应激反应，是机体对各种感染或损伤，包括炎症性肠病的一种基本反应，其涉及许多免疫和炎症过程，以及许多器官的功能改变，这种反应常伴有某些在肝脏合成的血清蛋白质含量异常，如a1-酸性糖蛋白，C-反应蛋白，a1-抗 胰蛋白酶 ，纤维蛋白原，a2-巨球蛋白和补体C3等，这些血清蛋白质称为急性期反应蛋白(acute phase response protein)或急性期蛋白(acute phase protein)，其血清含量的监测，对于了解病情活动和评价严重程度有一定价值。

C-反应蛋白(CRP)是一种非特异性急性期反应蛋白，它作为炎性肠病实验室指标的重要优势在于能对炎症发生和消退做出快速反应，其浓度可出现高达1000倍的变化，血清中CRP含量可反应病情活动性，病变范围和严重程度，Sharma等发现29例炎性肠病患者缓解期CRP40µg/ml，患者对内科治疗反应差，如治疗期间CRP>70µg/ml，常是重度或内科治疗失败,提示需手术切除病变肠管的患者，但CRP在炎性肠病的诊断价值不及克罗恩病时敏感。

CRP本身选择性地附着于细胞膜上，并与游离DNA结合，CRP在血液循环中的半衰期较短，只有l9h，因此，在炎症缓解后其血清含量很快回落，白细胞介素-1，白细胞介素-6，肿瘤坏死因子a以及转移生长因子p等细胞因子，能促进肝细胞合成CRP。

5.免疫学检查： 炎性肠病患者，其体液免疫和细胞免疫功能有改变，因此，常被归类为自身免疫性疾病，本病的免疫学检查，有助于了解本病的发生机制和判断病情活动性，可作为本病诊断的辅助指标。

(1)体液免疫：溃疡性结肠炎活动期，血清中IgG,，IgA，IgM可升高，尤其是血清IgA升高反映了肠道黏膜免疫系统的恢复。

(2)细胞免疫：克罗恩病的病程经过中细胞免疫占主导作用，疾病活动期外周血中辅助性T细胞/抑制性T细胞(Th/Ts)比值增高，随着病情缓解，Th/Ts逐渐下降，动态监测Th/Ts比值的变化对估计克罗恩病患者的活动性及疗效颇有价值。

6.Coagulation function tests: In the active phase of ulcerative colitis, in addition to changes in platelet count, there may also be changes in some coagulation factors. In acute fulminant cases, vitamin K deficiency can cause a decrease in prothrombin (factor II) and a mild to moderate decrease in factors VII and X, resulting in an elongation of prothrombin time (PT). In patients with extensive lesions, an increase in factor V, VIII, and plasma fibrinogen (factor I) may be seen. However, in the active phase of ulcerative colitis, local blood flow is in a hypercoagulable state. Due to inflammatory stimulation, the number of platelets in the blood increases, adhesion is enhanced, and platelets tend to aggregate, with blood cells adhering to them, forming firm thrombi in the mucosal surface blood vessels. This is one of the theoretical bases for the clinical use of anticoagulants.

7.Liver function tests: When inflammatory bowel disease is complicated with liver damage, serum alanine aminotransferase, alkaline phosphatase, bilirubin, and sulfobromophthalein sodium test may be abnormal. It is particularly worthy of attention that the detection of protein metabolism in ulcerative colitis patients is important, especially during the active phase, where there may be a decrease in serum albumin (albumin, A), an increase in globulin (globulin, G), and a decrease in the albumin/globulin ratio (A/G). Serum protein electrophoresis shows a decrease in albumin, an increase in alpha-2 and Y-globulin, and in severe cases, an increase in alpha-2 globulin and a decrease in Y-globulin. The decrease in serum albumin during the active phase of ulcerative colitis is related to protein loss at the site of intestinal inflammation and malnutrition. Some authors have pointed out that the serum albumin content has a good negative correlation with the amount of intestinal protein loss. The increase in globulin is related to the increase in acute phase reactant proteins. Abnormal protein metabolism in ulcerative colitis reflects the activity, severity, extent, and course of the disease to some extent.

8.Electrolyte and acid-base balance examination: Generally, the blood electrolytes and acid-base balance of ulcerative colitis patients are normal. Severe diarrhea may cause hypokalemia, hyponatremia, and metabolic acidosis. Frequent vomiting may cause hypokalemia, hypochlorhydria, hyponatremia, and metabolic alkalosis.

9.Skin test: Hyporesponsive to both phytohemagglutinin skin test and tuberculin skin test.

10.X-ray examination: Barium enema and barium meal are one of the important means for diagnosing IBD, especially gas-barium double contrast imaging can better show small mucosal lesions and improve the diagnostic rate.

(1)UC: The early manifestations can be normal or only show large mucosal folds, blurred intestinal margins. In severe cases, the mucosa may appear brush-like or serrated, with ulcers, pseudopolyps, disappearance of colonic pouches, stiffness of the intestines, shortening into a tubular shape, and narrowing of the intestinal lumen.

(2)CD: In the early stage, the CD can be normal or only show irregular thickening, distortion, and thickening of the mucosa. In typical cases in the late stage, ulcers, fissures, fistulas, and a road-stone-like reticular change can be seen. There may be intermittent narrowing of intestinal segments accompanied by expansion of adjacent intestinal segments or normal intestinal segments between the affected segments, showing a skip-like distribution.

11. Endoscopic examination: Pediatric colonoscopy can reach the ileocecal region, can observe the entire colon, determine the location, extent, and degree of the lesions, and take tissue biopsies at multiple sites to improve the diagnostic rate.

(1) UC: The lesions start from the rectum and show diffuse distribution, mucosal congestion and edema, rough and granular, increased fragility, easy to bleed, ulcers of varying sizes, shallow, with purulent or purulent bloody exudates. Chronic inflammation is manifested as mucosal hyperplasia, pseudopolyps, luminal stenosis, and the lesions develop continuously from the distal colon to the proximal colon, or to the entire colon.

(2) CD: Mucosal congestion and edema, not easy to bleed, round, elliptical, or linear fissure longitudinal distribution, known as 'aphthous ulcer', or pavement-like change, inflammatory polyps, intestinal lumen stenosis, skip distribution of lesions, normal adjacent tissue, anal fissures, fistulas.

12. Histopathological changes

(1) UC: The findings vary with the activity and remission of the lesion. In the active phase, the mucosa shows inflammatory reaction, crypt deformation, infiltration of lymphocytes, polymorphonuclear cells, and plasma cells into the lamina propria, reduction of goblet cells, formation of crypt abscesses, ulceration of abscesses, and formation of ulcers. In the remission phase, there is intestinal epithelial hyperplasia and atrophy of glandular epithelium.

(2) CD: Segmental transmural inflammation, with two main histological features: one is fissured ulcers that can reach the peritoneal membrane of the abdominal wall, and the other is non-caseating necrotic granulomas containing multinucleated giant cells and epithelioid cells, few in number, scattered distribution, and incomplete in structure.

　　For children with gastrointestinal diseases, the issues to be paid attention to in diet are all similar. The principles of treatment and diet are the same. For example, eat less刺激性 things, smoke, alcohol, spicy, sweet and sour things, eat less greasy and greasy things..

　　First, treatment

　　The goal of IBD treatment is to control chronic non-specific inflammatory attacks and maintain remission. The focus of treatment is to block each important link of the pathogenesis. The first consideration in the treatment of IBD is: ① The location and extent of the disease, which is closely related to the choice of treatment methods, drug response, and prognosis. ② The activity and severity of the disease: Different stages and degrees of lesions should adopt different countermeasures and estimate the prognosis. ③ The course of the disease, the initial treatment response is good, while the recurrence is poor. ④ The patient's overall condition and the presence of complications, which help in the selection of different treatment methods, prognosis estimation, and quality of life evaluation. There are three principles of treatment: ① Early control of symptoms; ② Maintain remission, prevent recurrence; ③ Evaluate the effectiveness of internal medicine treatment, determine the boundaries of internal and external medicine treatment, and prevent complications.

　　1. Internal medicine treatment

　　(1) General treatment: Maintain nutrition and water-electrolyte balance. For severe cases, provide high-calorie, high-protein, a variety of vitamins, and low-fat, low-fiber diet. Supplement a variety of trace elements, blood transfusion, plasma, and human serum albumin to correct hypoproteinemia and correct acid-base balance. For those with frequent vomiting, apply an appropriate antispasmodic agent. For concurrent infections, add antibiotics such as metronidazole (Flagyl).

　　(2) Drug treatment: Glucocorticoids (GCS) are suitable for moderate to severe cases, with definite anti-inflammatory and immunosuppressive effects. It is contraindicated in patients with fistula formation and abscess in CD.

　　① Prednisone and prednisolone: 1-2mg/(kg·d), 2-3 times a day, for a total of 2-3 weeks, gradually reduce the dose as symptoms improve, alternate day or intermittent therapy [1mg/(kg·d)], lasting for 4-6 weeks, then gradually reduce the dose to stop the medication, with a total course of 2-3 months.

　　② Hydrocortisone and methylprednisolone (methylprednisolone):

　　A. Intravenous administration: Suitable for intravenous administration in severe cases that are ineffective with oral medication. Hydrocortisone 10mg/(Kg·d), methylprednisolone (methylprednisolone) 1-1.5mg/(kg·d), administered intravenously in divided doses for 10-14 days. Pay attention to sepsis, hypokalemia, fever, and intestinal perforation.

　　B. Local treatment: Suitable for local mild to moderate cases from the rectum to the left half of the colon. Hydrocortisone 25-50mg per dose, prednisolone sodium succinate (succinate hydrocortisone) 25-50mg per dose, added to 50ml of normal saline, retained enema for at least 1 hour, 1-2 times a day, for a course of 10-14 days. The foam agent, 5ml rectally injected, can reach the sigmoid colon. Suppositories are effective for the rectum and are convenient to carry.

　　C. Infusion of adrenal cortical hormones into mesenteric arteries: It has achieved good results in the treatment of UC cases in Japan.

　　(3) Sulfasalazine (sulfosalicylic acid azo-sulfapyridine): Sulfasalazine (SASP) is the main drug for treating mild to moderate inflammatory bowel disease (IBD), and it is also one of the only effective drugs for maintaining remission. After oral administration, 75% of it is decomposed by colonic cells, breaking the azo chain into 5-aminosalicylic acid (5-ASA) and SP. The former is the effective component for treatment, with the functions of inhibiting local inflammation, clearing free radicals' damage to tissues, and inhibiting immune reactions. It is commonly used for UC and colon CD. The dosage is 50-75mg/(kg·d), 2-3 times a day, and gradually reduced to maintenance dose after the condition stabilizes, with a course of 2 years. Adverse reactions include gastrointestinal discomfort, nausea, vomiting, headache, rash, decreased platelet count and function, decreased folic acid absorption, and a few cases of bone marrow suppression. It is not suitable for long-term high-dose administration.

　　(4) Mesalazine (5-ASA, 5-aminosalicylic acid): It has stronger anti-inflammatory effects than sulfasalazine (SASP), reduces adverse reactions, and is suitable for those who cannot tolerate sulfasalazine (SASP) or for those whose SASP therapy is not effective. The dosage is 20-30mg/kg per day, divided into 3 doses, and after symptom relief, the maintenance dose (half of the treatment dose) is adjusted.

　　4-aminosalicylic acid (4-ASA) is effective for ulcerative colitis (UC).

　　Pantasa is composed of 2 molecules of 5-aminosalicylic acid (5-ASA) connected by an azo chain, which can release 2 molecules of 5-aminosalicylic acid (5-ASA) in the colon, reducing the dosage by 50% and reducing adverse reactions.

　　(5) Immunosuppressants: Often used for patients who cannot tolerate sulfasalazine (SASP), are dependent on adrenal cortical hormones, and have extensive lesions that cannot be operated on. When used, regular white blood cell count and platelet count checks are required.

　　① Azathioprine: Used for refractory CD; ineffective for treatment with adrenal cortical hormones, sulfasalazine (SASP), and metronidazole (灭滴灵); serious adverse reactions appear in patients with long-term dependence on adrenal cortical hormones (such as prednisone use for more than half a year); concurrent with various fistulas and perianal lesions, can be used with adrenal cortical hormones to maintain remission. Preoperative application stabilizes the condition, and postoperative application prevents recurrence. Dosage: 1-2mg/(kg·d), course of treatment 2-3 months. Foreign reports show that 2/3 of the cases were remitted within 7 years.

　　② Mercaptopurine (6-MP): 1.5mg/(kg·d), twice daily. Foreign reports show a CD remission rate of 67% and an anastomotic healing rate of 50%.

　　③ Cyclosporin: Used for refractory and intractable acute severe IBD, especially suitable for children with poor general condition who have not improved after 7 to 10 days of high-dose intravenous injection of adrenal cortical hormones. The dose is 1-2mg/(kg·d), administered intravenously, followed by oral administration of 4-8mg/(kg·d). Many studies have shown its effectiveness, especially for those who are preparing for surgery but have not yet undergone surgery. The most effective for young children with early diagnosis. Treatment for 6-8 weeks in the acute phase and then gradually reduced, while starting other immunosuppressive treatments.

　　(6) Traditional Chinese medicine treatment: Local Chinese medicine retention enema combined with traditional Chinese medicine dialectical treatment is effective for UC, as reported in Beijing, the retention enema of Xilie powder, Yunnan Baiyao, and procaine had a relief rate of 74.1%; in Guangzhou, the enema of Sanhuang decoction combined with Chinese medicine dialectical treatment had a relief rate of 66.7% and so on.

　　(7) Antibiotics: Antibiotics are ineffective for IBD itself and are only used for secondary infections such as severe and toxic megacolon. Commonly used antibiotics include ampicillin (ampicillin), metronidazole (灭滴灵), gentamicin, and sulfonamides, etc.

　　2. Nutritional support therapy

　　Most IBD patients suffer from protein-energy malnutrition, often with deficiencies in various nutrients including vitamins, minerals, and trace elements. Therefore, attention should be paid to the nutritional treatment of IBD. Enteric nutrition, such as elemental diet or total parenteral nutrition, should be given according to the condition. Elemental diet improves the nutritional status of patients, changes the intestinal flora, absorbed in the jejunum, can reduce the amount of food and digestive enzymes reaching the lesion segment of the intestines; reduce the stimulation of exogenous allergens such as protein in food to the lesion; can alleviate symptoms, improve activity indicators (Hb, ESR, plasma protein, etc.), and restore and promote the growth and development of children.

　　Elemental diet components: glucose, corn syrup, malt syrup, amino acids, casein hydrolysate, egg white casein, corn oil, skim milk, lactose, etc. Sugar, protein, and fat are mixed into a solution in a certain proportion according to different formulas. The total amount is calculated according to the needs of different individuals and administered in divided doses (e.g., every 3 to 4 hours), or infused continuously through a nasogastric tube for 24 hours. The course of treatment can last for several months.

　　For severe or deteriorating IBD children, for those who are ineffective to drugs and whose condition is active, it is necessary to improve the general condition and correct nutritional metabolism disorders before surgery to adapt to surgery. For those who cannot eat after surgery, incomplete obstruction, fistula formation, or severe perianal lesions, total parenteral nutrition (TPN) and complete intestinal rest should be adopted.

　　3, Biological treatment

　　Biological therapy drugs have only been developed in recent years. They mainly rely on the central position of immune effector cells, macrophages, especially T lymphocytes in immune response, and intervene at the molecular level of cells in key steps of differentiation, transcription, and expression. Especially for the blocking of various pro-inflammatory factors and the promotion and supplementation of anti-inflammatory factors, in order to achieve the purpose of eliminating inflammatory reactions. The most studied is TNF-α, and the treatment of refractory CD with TNF-α monoclonal antibody has achieved remarkable efficacy, and the drug has been approved for marketing in countries such as the UK and the US. There are reports on clinical trials of recombinant IL-10 for CD, but the subsequent clinical reports are not satisfactory. Recently, the use of IL-12, IL-8 antagonists, IFN-γ monoclonal antibody, IL-1ra, and ICAM has been reported, and the efficacy is yet to be observed.

　　4, Surgical treatment

　　(1) UC:

　　① Indications for surgery:

　　A, Acute onset: Severe or explosive cases, with perforation, bleeding, toxic megacolon.

　　B, Chronic lesions: Recurrent episodes, chronic consumption, protein loss, limited growth and development in children, and long-term use of high-dose corticosteroids.

　　C, Malignancy: Severe condition, widespread and persistent lesions, and younger onset are more prone to cancer.

　　D, Severe extraintestinal complications, perianal complications that are difficult to cure.

　　② Surgical methods:

　　A, Total colectomy, rectal resection, and ileostomy: For patients with severe illness and systemic failure, ileostomy can be performed first, and then total colectomy and rectal resection can be performed in the second stage when the condition improves, which can根治 the lesion while permanent stoma brings lifelong trouble and pain.

　　B, Total colectomy and ileorectal anastomosis: More suitable for children, which can preserve the rectum, but needs to prevent recurrence, can take salicylate sulfapyridine (SASP) or local enema, needs long-term follow-up, rectaloscopy tracking.

　　C, Total colectomy and homemade ileostomy: The ileum is sutured laterally before stoma creation, and an artificial pouch or valve is artificially created to store feces.

　　(2) CD: The vast majority (85%) of CD patients require surgery, about 50% undergo reoperation after recurrence, and careful consideration is needed for surgical indications, methods, timing, and preoperative and postoperative management.

　　① Indications for surgery: Perforation, bleeding, obstruction, fistula, abscess formation, and toxic megacolon, etc., as well as refractory cases with ineffective medical treatment.

　　② Surgical methods:

　　A, Local resection: Often used for colonic CD, limited small intestinal lesions such as stricture, fistula, abscess. The resected intestinal segment should be as short as possible to avoid malabsorption and short bowel syndrome.

　　B, Short circuit technique: For duodenal CD, gastrojejunostomy; for colonic CD, total colectomy with ileostomy, etc.

　　C, perianal complications: abscess drainage, fistula resection.

　　5, Treatment Plan

　　Currently, there is no pediatric treatment plan, and the principles of classic foreign schemes are referred to. Ideal treatment must follow certain conventions, adopt standardized treatment plans based on the determination of disease course, type, stage, degree, location, and the presence or absence of complications. The following plans are for reference.

　　The goal of treatment is to induce remission, maintain remission, ensure growth and development, and try to make children have a normal life. Most IBD children have intermittent attacks, with intervals ranging from several months to several years, and the earliest onset age can be in infancy.

　　Second, prognosis

　　The prognosis of ulcerative colitis patients depends on the type of disease, the presence or absence of complications, and the conditions of treatment. Long-term observation of pediatric patients shows that about 10% of children achieve long-term remission after the first attack; still 20% of children have recurrent attacks; 50% of children have mild symptoms for a long time, and 20% of children have persistent severe symptoms. The surgery rate for patients with total colitis is high. Unlike adult patients, about 1/3 of rectal and sigmoid colitis children have their lesions spread to the proximal side within the first 5 years of onset. Observations show that only about 20% of pediatric patients have their quality of life unaffected. Due to the high incidence of colon cancer in ulcerative colitis, strict long-term follow-up observation should be conducted for pediatric patients.

　　1, UC

　　About 90% of children have moderate to severe disease, extensive lesions, and rarely achieve complete remission. Radical surgery can cure the disease, and about 20% to 30% need immediate surgery during the acute severe stage. Almost all severe cases eventually require surgical treatment. After 10 years, UC patients have a risk of colon cancer, which increases year by year. Therefore, for children with a disease course of more than 10 years, a fiberoptic colonoscopy and biopsy should be performed every 6 to 12 months. The reported mortality rate of surgery abroad is 20%, and the incidence of cancer is 3% to 5%.

　　2, CD

　　The prognosis of pediatric CD is poor. Alternating between remission and exacerbation is a characteristic of the disease, and about 70% of children require surgical treatment. The ileal type has a poorer prognosis than the simple colonic type, with higher rates of surgery, recurrence, reoperation, and mortality. The causes of death are often recurrence, abscess, perforation, and severe malnutrition.