Ulcerative colitis (UC) is a chronic nonspecific inflammatory disease of unknown origin occurring in the colon, with common clinical manifestations such as diarrhea, mucopurulent stools, abdominal pain, and concomitant systemic discomfort (e.g., fever, anemia, hypoproteinemia, malnutrition). The cause and mechanism remain unclear and may be an inflammatory injury to the intestinal mucosa caused by multifactorial interactions. Current studies have shown that it is mainly due to bacterial/food antigens in the intestinal lumen, combined with individual genetic susceptibility, impaired intestinal mucosal barrier function, and altered environmental factors (diet, smoking, air pollution, mental stress, psychological changes) that cause abnormal intrinsic and acquired immune responses in the intestinal mucosal tissues, and a large infiltration of activated T cells, macrophages and dendritic cells in the intestinal mucosal tissues, which secrete high levels of A large number of activated T cells, macrophages and dendritic cells infiltrate the intestinal mucosal tissue, secreting high levels of pro-inflammatory cytokines (such as TNF-a, IFN-g, IL-2, IL-17A), leading to an imbalance of immune balance in the intestinal mucosal tissue, inducing apoptotic necrosis of intestinal epithelial cells and inflammatory damage such as intestinal mucosal erosion, ulcer formation and glandular fossa abscess. In recent years, with the in-depth research on the pathophysiological mechanism of UC and the clinical application of endoscopic diagnostic techniques, pathological histology, microbial immunology, and molecular biotechnology, the diagnosis and treatment of UC have been greatly promoted from the traditional 5-aminosalicylic acid (5-ASA) preparations to the use of targeted bioimmunotherapy ( Such as infliximab, trade name: class gram), to bring a new dawn of clinical treatment, so that the patient’s condition has been effectively controlled, the quality of life has been significantly improved. According to Truelove and Witts criteria, the diagnosis of severe UC should meet the following criteria: diarrhea 3 6 times/d with obvious mucus and blood stool, temperature > 37.8℃, pulse > 90 beats/min, hemoglobin < 105g/L, sedimentation > 30 mm/h, C-reactive protein (CRP) > 30 mg/L. This scoring system is crude and This scoring system is crude and cannot accurately quantify the score. In recent years, the Mayo scoring system is mostly used internationally, and the score is mainly based on the patient’s stool frequency, bloody stool, endoscopic mucosal manifestations, and physician’s assessment, each of which has a score of 0, 1, 2, or 3. A total score of ≤2 is considered in remission, 3 – 5 is mild, 6 – 10 is moderate, and 11 – 12 is severe. Typically 20% of patients with UC are clinically mild, 71% are moderate, and 9% are severe. Active severe UC is a fatal disease with a mortality rate of up to 15% and a still high surgical treatment rate of 35% – 40%. Ten percent of severe UC may develop into toxic megacolon (TMC) with a poor prognosis. Therefore, for patients with severe UC, timely diagnosis should be made, which is especially important for clinical treatment and prognostic regression. Second, clinical treatment strategies 1. general clinical management and treatment for patients with severe UC require hospitalization and, if necessary, ICU monitoring; necessary psychotherapy; normal diet is generally advocated, and severe cases may receive parenteral and parenteral nutrition therapy; timely screening for food intolerance (allergen determination) and avoidance of immunoreactive food intake; timely correction of water-electrolyte disorders, anemia, and hypoproteinemia. Timely exclusion of intestinal pathogenic microbial infections, such as bacteria (e.g., Escherichia coli, Salmonella, Shigella, Staphylococcus aureus, Mycobacterium tuberculosis, Clostridium difficile), viruses (e.g., CMV), parasites (ameba, schistosomiasis), etc.; antibiotics are generally not recommended, but are required for co-infections; for those with significant increase in platelets, hypercoagulability, or even the possibility of venous For those with significantly increased platelets, hypercoagulable state, or even possible venous thrombosis, subcutaneous injection of heparin can be considered to prevent thrombosis; use analgesic, antispasmodic, and nonsteroidal anti-inflammatory drugs with caution, especially anticholinergic drugs, narcotics, colonoscopy, and barium enema angiography are prohibited for TMC patients. If abdominal pain occurs, consider using hot compresses, paracetamol tablets, dulcolax, etc. Avoid anticholinergics; 5-ASA drugs should be suspended in patients with severe UC and can be used as maintenance treatment after remission; perform imaging examinations in a timely manner necessary to exclude intestinal perforation, intestinal obstruction, TMC and perianal abscess; if TMC occurs, stable vital signs and no sepsis can be treated conservatively, and if there is no remission for 48 – The main mechanism is to inhibit T-cell IL-2 and IL-2R expression, prevent T-cell proliferation and differentiation, and limit the release of inflammatory mediators (such as IFN-g, TNF-a) by binding to receptors on the surface of immune cells. TNF-a) release, effectively inducing remission and controlling disease progression. Clinical observation found that 60% of UC patients with clinical symptoms disappeared after 5 days of hormone therapy, and 15% of symptoms were improved, but 25% of patients still did not respond to hormone therapy. In general, hormone therapy is effective in patients (50% – 75%) within 1 week, so the clinical focus is on the first 3 – 5 days of treatment, if the temperature does not decrease after 3 – 5 days of treatment, it may be ineffective, for those who do not respond to hormone therapy, they may receive cyclosporine A (CyA), biological agents or surgery. For patients with severe UC, it is important to master the indications for the use of hormone therapy, real-time monitoring, dynamic observation of changes in the systems, and prevention of side effects. Common side effects include metabolic system (elevated blood glucose, hypertension, hypercholesterolemia, hypokalemia, suppression of adrenocortical function), skeletal-muscular system (osteoporosis, skeletal head necrosis, myopathy, delayed growth), skin (seated sores, polycythemia, skin tags), eye (cataract, glaucoma), nervous system (neuropathy, insomnia, psychiatric abnormalities), infections, and other lesions (full moon face, buffalo back, weight gain, peptic ulcer). 2) CsA: CsA inhibits T cell activation and secretion of pro-inflammatory cytokines (IL-2, TNF-a, IFN-g) and reduces the inflammatory response of the intestinal mucosa. It was first started in the United States at Mt Sinai Hospital in New York City in severe UC patients with ineffective hormones, and intravenous CsA treatment (4 mg/kg) was found to have good clinical efficacy in some patients, with a mean response time of 5.8 days, which spared 73% of the severe patients from intestinal surgical resection. Later, in a comparative clinical study abroad, it was found that CsA (4 mg/kg, iv) treatment resulted in clinical remission in 64% – 73% of critically ill UC patients with no side effects. Further studies later found that intravenous treatment with 2 mg/kg of CsA in patients with severe UC achieved similar clinical effects, controlled clinical symptoms, induced healing of intestinal mucosal ulcers, and reduced the toxic side effects of CsA compared to 4 mg/kg dose. Currently, CsA is advocated for patients with severe UC, especially for hormone-ineffective or hormone-dependent patients, with a rapid onset of action in 1 week. For those who are not effective with hormone therapy (7-10 d), the short-term efficiency of CsA treatment is 75%-80%, and the long-term efficiency is 60%. In general, patients with severe UC are routinely treated with intravenous CsA at a dose of 2 – 4 mg/kg-d for 1 – 2 weeks. Clinical studies have shown that the use of 2 mg/kg/d is effective and reduces its toxicity; once symptoms are controlled, treatment is switched to oral CsA (4 mg/kg-d) in two doses for 3 months. During the use of CsA, the blood concentration is closely monitored, and the intravenous use should be checked 2 times in the 1st week, and the concentration is maintained at the effective concentration. Then 1 dose/week (first 4 weeks), then 1 dose/2 weeks (last 8 weeks) until discontinuation. Blood levels of CsA are measured by exsanguination: 150 – 250 ng/ml (2 mg/kg-d) or 300 – 350 ng/ml (4 mg/kg-d). Test serum magnesium and cholesterol levels in time for clinical use to prevent toxic side effects. Correct hypomagnesium (< 1.5 mg/dL), hypocholesterolemia (< 120 mg/dL) before use. It should also be closely monitored to prevent the occurrence of infections (e.g., pneumocystis). 3) Biologic agents: Class K was the first biologic agent to be used clinically for the treatment of UC. It is a human-mouse chimeric IgG1 monoclonal antibody synthesized by genetic engineering technology, which has been clinically applied in patients with Crohn's disease, UC, rheumatoid arthritis and psoriasis, showing good anti-inflammatory effects. Foreign literature reports that classical gram treatment can induce clinical symptom remission in UC patients, induce healing of intestinal mucosal ulcers, maintain clinical symptom remission, improve patients' quality of life, and reduce surgical intervention. In China, classical grams have been used clinically on a large scale in patients with Crohn's disease, and clinical treatment has been attempted in recent years in patients with UC. Its main mechanisms of action include direct neutralization of TNF-a bioactivity in blood circulation and tissues, induction of apoptosis and necrosis of inflammatory cells, inhibition of the release of pro-inflammatory cytokines, reduction of leukocyte infiltration in intestinal mucosal tissues, and induction of Treg and suppressive cytokine secretion with immunomodulatory effects. Currently, in clinical practice, patients with active severe UC who are ineffective or dependent on hormones can be treated with selective classical gram therapy at a dose of 5 mg/kg (iv, 2h), and if ineffective, try 10 mg/kg, and if still ineffective, consider surgical treatment. Therefore, gram-like therapy can be used as a remedial measure before surgical resection treatment. Recently, gastroenterologists from Europe have recommended the early use of gram-like therapy for UC patients, especially those with persistent symptoms, hormone dependence/ineffectiveness, and elevated CRP, to achieve clinical remission as soon as possible, to promote healing of intestinal mucosal ulcers, to maintain clinical remission in a hormone-free state, to improve patients' quality of life, and to reduce complications, and to use gram-like therapy as a remedial treatment option prior to surgical treatment It can be used as a remedial treatment option before surgical treatment. The side effects of classical gram treatment mainly include antibodies (30% - 61%), intravenous infusion reactions (such as headache, dizziness, nausea, local skin irritation, chest pain, dyspepsia, etc.), anti-dsDNA, ANA, similar drugs causing systemic lupus erythematosus, T-cell lymphoma, occasional upper respiratory and urinary tract bacterial infections, Mycobacterium tuberculosis infections, fungal infections, and nerve demyelination. 3. Surgery: Although there is significant clinical progress in drug treatment of UC, some patients still need surgery, clinical statistics show that 5% - 25% of UC patients need surgery, which will seriously affect the quality of life of patients, and even cause death. The absolute indications for surgery are necrotic hemorrhage of the intestinal wall, intestinal perforation, cancer, and ineffective medical drug therapy; the relative indications are hormone dependence, growth retardation, severe systemic complications, and toxic megacolon. There are no clinically valid indicators to predict the indication for surgery. Although many clinicians consider whether to undergo surgery based on changes in the patient's condition, especially the presence of cryptitis/crypt abscess, worsening inflammatory ulcers of the intestinal mucosa, hormone nonresponse, elevated CRP, extensive lesions, worsening bloody stools, and increased frequency of diarrhea, surgery is ultimately chosen in most cases after failure of pharmacological therapy, which severely affects quality of life. Serious UC is a fatal disease that seriously affects human life, can not simply be called "benign lesions", can not simply understand that surgical treatment can "cure". In general, patients with UC who are medically ineffective, dependent, or severely ill are treated with total colorectal resection (small bowel abdominoplasty) or ileal pouch-anal anastomosis (IPAA, ileal J-pouch anastomosis). bowel obstruction, postoperative bleeding, anastomotic lesions (strictures, fistulas, abscesses, cancer), decreased quality of life, medical costs, and even death. Therefore, close nursing management is needed after surgery to avoid complications, and to inform patients that "surgical treatment" is not a complete cure for the disease, postoperative complications should be explained to patients in detail, as well as how to deal with the prognosis of regression, etc. In recent years, with the in-depth understanding of the pathogenesis of UC, the clinical treatment of UC has also brought new light. The clinical treatment of UC has also brought a new light. For patients with severe disease, glucocorticoid therapy can be chosen. If symptoms are relieved, conventional immunosuppressive drugs (azathioprine, AZA; 6-mercaptoguanine, 6-MP) or 5-ASA can be used for maintenance treatment; if ineffective or dependent, CsA or IFX treatment can be shifted; if still ineffective, surgical treatment is required. Despite the great development of medical technology in recent years, the pathogenesis of UC is still unclear, which limits the early diagnosis and effective treatment of UC. Therefore, we should strengthen basic research to promote the translation of basic research results to clinical treatment and improve the level of treatment.