I. Overview of inflammatory bowel disease
Inflammatory bowel disease (IBD) is a chronic non-specific intestinal inflammatory disease with unknown etiology, including Crohn’s disease (CD) and ulcerative colitis (UC). Because of the unknown etiology, the large clinical variation in individual patient performance, and the lack of specific clinical tests, there are many misdiagnoses and mismanagement in practice, and the risk of clinical diagnosis and treatment is high. Crohn’s disease is mainly a chronic non-caseating granulomatous inflammatory disease that can involve all parts of the gastrointestinal tract from the oral cavity to the anus, but the ileocecal region is the most frequent site, with wall-piercing inflammation, mostly segmental, “jumping” and asymmetric distribution; ulcerative colitis is mainly a chronic non-specific inflammatory disease of the colon, with lesions mainly The lesions mainly involve the mucosa and submucosa of the colon, starting from the distal end of the colon and progressing retrograde to the proximal end in a “backwards” fashion, even involving the whole colon and terminal ileum, with a continuous distribution.
The incidence of Crohn’s disease is higher in European Caucasians, and the incidence in the United States is about 100/100,000 people, while it is less common in China than in Europe and the United States, but the incidence in China has gradually increased in recent years, which may be related to the rapid economic development in China in recent years, resulting in changes in the living habits and dietary habits of the country and environmental pollution.
The etiology of Crohn’s disease is currently believed to be related to the following aspects.
(i) Genetic
There is a clear familial aggregation in the development of Crohn’s disease, usually with a significantly higher incidence in first-degree relatives than in the general population, and a certain genetic predisposition. There are also racial differences in the disease, with a high incidence in Caucasians and a low incidence in Blacks and Asians. The genetic susceptibility site for Crohn’s disease is located on chromosome 16 and is involved in the regulation of cytokines, inflammatory chemokines and receptors. HLA-DR7 and others are positively associated with the development of Crohn’s disease, while HLA-DR3 is negatively associated.
(ii) Infection
Lesions of Crohn’s disease often occur at the site of greatest bacterial exposure. Associated bacteria and their products, including Mycobacterium avium subsp. paratuberculosis, Listeria monocytogenes, and measles virus, have been detected in diseased intestinal segments of patients with the disease. The therapeutic effect of metronidazole in Crohn’s disease also suggests a partial role of infection in the pathogenesis.
(iii) Immunity
Patients with Crohn’s disease have abnormal humoral and cellular immunity. Specific autoantibodies such as anti-colonial epithelial antibodies, anti-ASCA cell wall antibodies, anti-neutrophil plasmatic antibodies (ANCA), elevated circulating immune complex (CIC) and complement C2 and C4 can be detected in the serum. In tissue culture, the patient’s lymphocytes are toxic and can kill normal colonic epithelial cells, and the cytotoxic effect disappears after removal of the diseased intestinal segment.
The pathological manifestation of Crohn’s disease is a proliferative lesion that penetrates all layers of the intestinal wall. The lesions are often confined to the small intestine, especially the terminal ileum, followed by the colon and ileum, and occasionally the stomach, duodenum, or esophagus. The pathological changes are non-caseous necrosis of the intestinal wall and mesenteric lymph nodes, total wall inflammation of the intestinal wall, segmental distribution of the lesions, congestion or thickening and stiffening of the intestinal wall, tubular shape of the intestinal canal in the affected area, accompanied by plasma membrane fibrin deposits or adhesions of the adjacent intestinal canal; the early mucosa shows small shallow ulcers, which later develop into longitudinal or transverse ulcers. The submucosa is highly widened, lymphocytes are heavily colonized, and nodulopathy-like granuloma is formed. The submucosal edema and cellular infiltration form islet-like protrusions, which, together with ulcer healing and scar contraction, result in pebble-like changes on the mucosal surface. The fissure in the intestinal wall is a penetrating ulcer that causes adhesions and abscesses to form between the intestinal canal and the intestinal canal, and between the intestinal canal and organs or tissues, which can develop into an internal fistula.
Ulcerative colitis is widely distributed throughout the world, with the highest incidence in northern and eastern European Caucasians, the highest incidence in Jews, and a relatively low incidence in blacks and yellows. The incidence of ulcerative colitis in China is lower than abroad, but in recent years the incidence has tended to increase gradually. The disease can be seen at any age, but it is most common between the ages of 20 and 30, and is slightly more common in men than in women.
Similar to Crohn’s disease, the etiology of ulcerative colitis is not clear, and it is thought that it may be related to the following causes.
(i) Heredity
The incidence of the disease in identical twins is 6%-16%, while the incidence in dizygotic twins is only 0-5%, the incidence in whites is 3 times that of blacks, and the incidence in Jews is 3-5 times that of non-Jews.
(ii) Infection
The association of microbial infections with the disease has been one of the current research hotspots, but until now no direct specific pathogens have been identified. Some studies have shown that ulcerative colitis may be associated with double streptococci, Shigella, RNA viruses, etc. Certain microbial pathogens or their toxins can cause an intestinal inflammatory response similar to that of ulcerative colitis, suggesting that microbial infection may be one of the etiologies.
(iii) Environmental factors
The incidence of this disease is higher in the more socio-economically developed countries, and with the continuous development of our economy, the incidence of this disease in China is also increasing year by year. The incidence of this disease is higher in people with higher socio-economic status, indoor work and less usual activities, while it is lower in poor areas and manual workers. Epidemiological investigations have found that the incidence of ulcerative colitis decreases after appendectomy, and the mechanism is unclear. Smoking seems to have a protective effect on ulcerative colitis, probably because nicotine reduces the permeability of the intestinal mucosa, decreases the level of prostaglandin E2, and inhibits the activity of natural killer cells and neutrophils, but smoking can worsen Crohn’s disease. The relationship between oral contraceptives, NSAID and this disease is still controversial.
(iv) Immunity
The disease often has abnormalities in immune regulation. The number of IgA, IgG and IgM producing plasma cells in the mucosa of the lesion is increased, and specific antibodies, anti-colonic epithelial antibodies and ANCA can be detected in the serum of some patients, and the detection rate is higher in patients with primary sclerosing cholangitis. The presence of circulating immune complexes in the serum, activating complement or through lymphocyte cytotoxicity, leads to mucosal inflammation.
Most scholars believe that the pathogenesis of ulcerative colitis is based on a genetic background and that infections or environmental factors are only causative factors that cause hypersensitivity of the intestinal mucosa to antigens and dysfunctional immune regulation, ultimately leading to chronic inflammation and tissue damage in the patient’s colonic mucosa, which is difficult to self-limit.
Ulcerative colitis lesions are mainly located in the rectum and sigmoid colon, and may extend retrogradely to the descending colon or even the entire colon, and if the terminal ileum is involved, it is called “inverted ileitis”. The inflammation is mainly located in the mucosal layer, but can also involve the submucosal layer, and rarely reaches the muscular layer, with a uniform and continuous distribution of lesions. The earliest lesions occur in the crypt at the base of the intestinal glands, where a large number of inflammatory cells infiltrate and form a crypt abscess, after which many small abscesses join together and the process of inflammation and necrosis increases, resulting in ulceration. In the early stage, the colonic mucosa is edematous, congested, hemorrhagic and granular, characterized by fragile mucosa that bleeds easily when touched, followed by the formation of small oval-shaped shallow ulcers that first develop along the longitudinal axis of the colon and then fuse into a large, extensive irregular ulcer. Microscopically, we can see intestinal glandular crypt erosions and ulcers with cellular infiltration at the edges, mainly lymphocytes and plasma cells, with a decrease in cupular cells; during acute attacks or with secondary infection, a large number of neutrophils are seen. The lesioned intestinal wall had vascular proliferation in the lamina propria, and hemorrhage and thrombosis were seen. Inflammation is slightly less severe in the subacute phase. During the repair process, there is granulomatous proliferation, epithelial regeneration and fibrous scar formation. In the chronic phase the mucosa is mostly atrophied and the submucosa is scarred. A large amount of scarring is formed when the ulcer heals, which can lead to shortening of the colon or narrowing of the intestinal lumen, often causing pseudopolyposis or even cancer in the later stages. In addition, there are complications such as peritonitis, per colorectal abscess and fistula formation caused by ulcer perforation.
Second, the clinical manifestations of Crohn’s disease
The clinical manifestations of Crohn’s disease are varied and are related to the location, extent, severity and duration of the intestinal lesions and the presence of complications. In typical cases, the disease starts slowly in youth, often lasting several months and years, with active and remission periods of varying length, alternating with each other, and progressive development during recurrent episodes.
(a) The symptoms of intestinal tract are mainly as follows
1, abdominal pain: the vast majority of patients have abdominal pain, mostly vague in nature, with paroxysmal aggravation or recurrent episodes, mostly in the right lower abdomen, associated with terminal ileal lesions, followed by peribulbar or total abdominal pain. Postprandial abdominal pain is associated with gastrointestinal reflexes. The possible plasma membrane involvement, peri-intestinal abscesses, intestinal adhesions, intestinal obstruction, intestinal perforation, acute peritonitis and toxic megacolon in Crohn’s disease can cause abdominal pain. A few first diagnoses are confirmed by surgical findings of acute abdomen as appendicular Crohn’s disease or intestinal obstruction due to Crohn’s disease, which will be discussed in detail later.
2, diarrhea: a common symptom of the disease, most of the stool 2 to 6 times a day, can be paste or watery, generally no pus or mucus, such as lesions in the rectum, there may be pus and blood and the feeling of urgency.
3, blood in the stool: compared with ulcerative colitis, there is less fresh blood in the stool, and the amount is usually not large.
4, abdominal mass: some cases may have abdominal masses, mostly in the right lower abdomen and around the umbilicus.
5, extra-intestinal fistula: can be the first symptom of some patients, extra-intestinal fistula can be seen in many parts of the abdominal wall and perineum, but most commonly in the right lower abdomen, related to the site of Crohn’s disease. Patients first appear subcutaneous abscess, with hypothermia and other symptoms of systemic toxicity, abscess cut drainage first out of the pus, after a few hours to a few days visible intestinal fluid or fecal juice outflow, and thereafter repeatedly does not heal.
6.Anal symptoms: Occasionally, there are those with vague pain in the anus, perianal abscess and anal fistula formation as the first symptoms.
(B) Its systemic symptoms are mainly as follows
1, systemic symptoms of toxicity: fever is the most typical manifestation, active intestinal inflammation and tissue destruction toxin absorption can cause fever, 1/3 of patients can have moderate fever or low fever, often intermittent, in acute severe cases or with septic complications, more can appear high fever, chills and other toxemia symptoms. In addition, most of the patients have nausea, vomiting, poor nutrition and other systemic symptoms.
2, malnutrition: due to intestinal malabsorption and excessive consumption, often cause patients wasting, anemia and hypoproteinemia, etc.. There are also patients in the case of unknown diagnosis of hormone abuse to control the symptoms of malnutrition.
3, other systemic pathologies: Crohn’s disease can also be combined with other systemic pathologies, mostly related to autoimmunity and malnutrition, including arthralgia (inflammation), herpetic ulcers, erythema nodosum, noma, inflammatory eye disease, active hepatitis, fatty liver, cholelithiasis, sclerosing cholangitis, peribiliary cholangitis, renal calculi, thrombophlebitis, ankylosing spondylitis, vasculitis, leukodystrophy, amyloidosis, osteochondrosis. amyloidosis, osteoporosis and pestle finger, etc. The onset of the disease at a young age may affect the development of the affected children.
4, complications: 40% of Crohn’s disease patients can have varying degrees of intestinal obstruction, and recurrent, acute intestinal perforation accounted for 10% to 40%. In addition, the anal area and rectal lesions, extra-intestinal fistulas are also common, Crohn’s disease may induce toxic megacolon and carcinoma, the incidence of carcinoma literature reports a wide range.
(iii) Laboratory tests.
1, blood tests: white blood cells are often increased, red blood cells and hemoglobin are often decreased, which is related to blood loss, malnutrition, bone marrow suppression, and reduced absorption of iron, folic acid and vitamin B12. Blood sedimentation is increased and C-reactive protein is elevated, but may decrease significantly after disease progression is effectively controlled. There may be an increase in mucin, a decrease in albumin, and a decrease in serum potassium, sodium, calcium and magnesium.
2. Stool routine: red and white blood cells can be seen, and the occult blood test may be positive.
Immunological examination: positive serum antibodies (IgG and IgA) against phosphopeptide mannan of Saccharomyces cerevisiae cell wall is a more specific serological marker of Crohn’s disease, anti-neutrophil cytoplasmic IgG (antineutrophil IgG) antibodies (ANCA) are positive. Anti-neutrophil cytoplasmic IgG antibodies (ANCA) positive rate is about 5%-10%, higher than the normal population of 3%-4%. Elevated TNF-α in serum is associated with disease activity, and other cytokines (IL-1, IL-6, IL-8, etc.) may be increased.
(iv) Imaging.
Imaging is important for the diagnosis of Crohn’s disease, especially when the intestinal lumen is narrowed making endoscopy inaccessible. The whole gastrointestinal tract and colon air-barium double imaging can understand the lesions of the terminal ileum and other parts of the small intestine, which show inflammatory lesions of the gastrointestinal tract, such as fissure ulcers, mucosal fold destruction, pebble sign, pseudo-polyps, fistula formation, etc. The lesions are segmental-like distribution, single or multiple irregular stenosis or dilatation, and air-barium double imaging can improve the positive diagnosis rate. Abdominal CT and magnetic resonance examination have some diagnostic value in determining whether there are intestinal collaterals with thickened and separated intestinal walls and intra-abdominal abscesses. Ultrasound examination of the abdomen shows varying degrees of intestinal peristalsis, intestinal wall thickening and stenosis, and proximal intestinal dilatation.
(v) Endoscopy and biopsy.
Mucosal congestion and edema with round or linear ulcers, pebble-like changes, stiff intestinal lumen strictures or inflammatory polyp-like manifestations, normal or mildly congested mucosa between lesions, and jumpy distribution can be seen. Ultrasound endoscopy helps to determine the extent and depth of the lesion and to detect intra-abdominal masses or abscesses. Biopsy reveals fissure-like ulcers, non-caseating necrotic nodular granulomas, lymphocytic aggregates in the lamina propria and submucosa, normal crypt structure, and no reduction in cupped cells.
Third, the diagnosis of Crohn’s disease and misdiagnosis prevention
The diagnosis of Crohn’s disease, especially the initial diagnosis, is difficult. When summarizing the reasons for the increasing incidence of Crohn’s disease year by year, academician Lai Jieshou of Nanjing General Hospital of Nanjing Military Region pointed out that the increasing level of diagnosis of the disease in China is also an important reason. To diagnose the disease, the mind must first have knowledge of the disease, and the possibility of making a diagnosis of this disease is possible only if the possibility of this disease is thought of. If the physician only knows about appendicitis, then the right lower abdominal pain is basically likely to be diagnosed only as appendicitis. Therefore, in clinical practice, if patients present with diarrhea, abdominal pain, especially chronic abdominal pain, accompanied by abdominal masses, the possibility of Crohn’s disease should be considered. If there are also intestinal obstruction, perianal lesions, intestinal fistulas and other immune diseases, imaging and endoscopy should be done for identification, specifically Crohn’s disease should be carefully differentiated from the following diseases.
(i) Ulcerative colitis
Clinically, sometimes Crohn’s disease is very difficult to differentiate from ulcerative colitis, which can generally be judged from the following.
Crohn’s disease manifests itself differently from other gastrointestinal diseases, often with vague pain in the right lower abdomen or around the navel, rotten stools, usually without obvious purulent stools, sometimes with abdominal masses, fistula formation and intestinal obstruction manifestations, and may be accompanied by fever and malnutrition, as well as joint, skin, eye, oral mucosa, liver and biliary tract lesions.
(ii) Intestinal tuberculosis
It is sometimes difficult to differentiate from Crohn’s disease clinically. The intestinal tuberculosis lesions mainly involve the ileocecal region of the intestine and the adjacent colon, and do not have a segmental distribution, while fistulas and perianal lesions occur less frequently. It is often associated with tuberculosis of other organs, a positive tuberculin test, elevated ADA activity in the blood, and effective anti-tuberculosis therapy. The diagnosis is confirmed by the presence of caseous necrosis in the lesion tissue on pathological examination.
(iii) Other infectious diseases
Bacterial and parasitic enteritis can lead to abdominal pain, diarrhea, mucus and blood stools, such as bacterial dysentery, amebic dysentery, schistosomiasis, etc. They can be identified by detailed history taking and stool culture.
(iv) Tumor
Colon cancer, small intestinal lymphoma, sarcoma, etc. can be diagnosed by endoscopic tissue biopsy.
Since the etiology of Crohn’s disease is unknown and there are still no specific diagnostic indicators, the diagnosis of the disease is still an exclusive diagnosis based on clinical manifestations, so there is a high risk of definite diagnosis and a high rate of misdiagnosis in clinical practice. The way to avoid diagnostic risk is similar to other diseases requiring exclusive diagnosis, on the one hand, it is necessary to avoid missing diagnosis, and the prerequisite for avoiding missing diagnosis is to be able to think about whether Crohn’s disease may be present when typical or atypical clinical manifestations appear, especially when the original treatment regimen is not effective, and to promptly review one’s diagnostic strategy to see if there is any missing diagnosis or missing diagnosis, and to make efforts to On the other hand, it is necessary to avoid misdiagnosis, which is often due to the lack of knowledge of the doctor, or too conceited, or too confident in the diagnosis made by an authoritative hospital or an authoritative expert, because Crohn’s disease is an exclusive diagnosis, so even if there are more typical clinical manifestations, it is still necessary to conduct some exclusive diagnostic tests. As the treatment strategies for the two diseases are completely different, it is extremely risky to treat Crohn’s disease when the diagnosis is not known, and the two diseases may coexist. In addition, Crohn’s disease needs to be differentiated from some systemic diseases such as immunoglobulin deficiency, intestinal leukoaraiosis, and also from Meckel’s diverticulum.
Fourth, the treatment of Crohn’s disease and surgical risk prevention
Since the cause of Crohn’s disease is still unclear, there is no curative therapy. Therefore, the principle basis of treatment is carried out by blocking the inflammatory response and regulating the immune function. The principles are to control the symptoms of the disease as early as possible, to promote remission, to maintain treatment and mitigate recurrence, to prevent and control complications and to master the timing of surgical treatment. In general, Crohn’s disease is mainly treated with medication in most cases, and surgical treatment is mainly to address its complications, but a foreign rheological survey shows that about 78% of Crohn’s disease patients will experience at least one abdominal surgical procedure in their lifetime, so as a general surgeon you should and must be aware of this disease whose incidence is increasing year by year in China. A small number of young surgeons think that they only need to know about the surgical part of the disease, but this is very wrong. If young general surgeons are still growing up thinking that surgery is all or most of surgery, then this is extremely irresponsible to the patient and to themselves, because this one-sided understanding can bring great risk to the treatment of the disease.
The drugs used to treat Crohn’s disease are broadly classified as follows.
(i) Aminosalicylates
Sulfasalazine (SASP) and 5-aminosalicylic acid (5-ASA) are suitable for patients in the chronic phase or mild to moderate active phase. 4g-6g/d of SASP, divided into 3-4 doses, usually 3-4 weeks to take effect, and gradually reduce to maintenance 1g-2g/d after remission, maintenance medication for about 1 to 2 years. Small bowel Crohn’s disease can be treated with 5-ASA, and the current 5-ASA dosage forms are mesalazine, olsalazine, and balsalazide. For rectal, sigmoid and descending colon lesions can be given rectally with SASP or 5-SAS preparations 2g to 4g/d enema, or with suppositories 0.5g/only, 1 to 2 times/d. Severe liver and kidney diseases, infants and children, hemorrhagic constitution and those who are allergic to aminosalicylates should not apply aminosalicylates.
(ii) Adrenocorticosteroids
Hormone therapy can be used for patients with moderate or severe Crohn’s disease in the active stage. Commonly used dose of prednisone (prednisone) 30mg ~ 60mg / d, 10d ~ 14d, about 80% of patients can be relieved of symptoms, later can gradually reduce the drug to 5mg ~ 15mg / d, maintenance 2-3 months. For those who cannot take it orally, hydrocortisone or methylprednisolone can be given intravenously. For rectal, sigmoid or descending colon lesions, drug retention enema can be used, such as hydrocortisone succinate 100mg, 5% procaine 100mg, plus saline 100ml, slow enema, once a night, also can be combined with SASP, 5-ASA or stannous dispersion, during the use of drugs should be alert to intestinal perforation, hemorrhage, peritonitis and abscess formation and other complications. Due to the serious side effects of corticosteroids and their inaccurate efficacy in maintaining remission, it is generally recommended to withdraw them as soon as the acute attack is controlled.
(iii) Immunosuppressants
Sulfonamides or hormonal agents may be used instead of other immunosuppressive agents. Azathioprine is commonly used, and it usually takes about 3 months to take effect. Because of the risk of tumor induction, it should not be used in people with high risk of tumor and should not be used in women during pregnancy. Other drugs include cyclosporine A, methotrexate, FK506, etc.
(iv) Antibiotics
Intestinal bacterial infection is closely related to the severity and recurrence of the disease. Metronidazole can counteract the destructive effect of anaerobic bacteria on intestinal mucosa and reduce the activity index of the disease, but it is easy to relapse after reducing the dose. Other successful treatment with ciprofloxacin and clarithromycin has been reported.
(V) Intestinal probiotics
Normal flora in the intestine, especially mixed (Lactobacillus and Bifidobacterium) preparations have positive significance in improving Crohn’s disease.
(vi) Biological agents for the treatment of infliximab
It is anti-tumor necrosis factor (TNF-α) monoclonal antibody, intravenous drip once 5mg/Kg body weight, the remission rate after 4 weeks up to 48%, every 8 weeks drip can effectively prevent recurrence, it also has significant effect on perianal and abdominal fistula, can reduce the amount of hormone. The main side effects are: allergic reactions; induction of autoantibodies; induction of non-Hodgkin’s lymphoma and rheumatoid arthritis; and a significantly higher rate of infection. The effectiveness of other biological agents such as natalizumab, IFN-α, NF-κB agents, and epithelial cell growth factor still needs further study. Since immunomodulatory biologics are highly targeted and have few side effects in the treatment of Crohn’s disease, their application prospects are very promising, and related research is one of the current research hotspots.
(VII) Others
As Crohn’s disease is a chronic disease, protein-energy malnutrition is very likely to occur during the course of the disease, and supportive therapy is very important to enhance nutrition, correct metabolic disorders, and improve anemia and hypoproteinemia. Recently, there is a new understanding of the clinical nutrition of Crohn’s disease. Some studies have shown that the remission rate of Crohn’s disease patients taking elemental diet can be as high as 85%, and there is no significant difference in the remission rate and 1, 3 and 5-year relapse rate compared with adrenocorticotropic hormone. Antispasmodic, analgesic, antidiarrheal and infection control also contribute to disease remission, but care must be taken to be alert to the risk of inducing toxic megacolon when applying anticholinergic drugs such as atropine. There have also been studies and reports on the use of rebaudioside alone or in combination for the treatment of Crohn’s disease.
Regarding the selection of drugs for Crohn’s disease, emphasis should be placed on the use of individualized protocols, with drug therapy adapted to the acute and remission phases, and appropriate drugs should be selected for treatment according to the severity of the disease, the different stages of the disease and the different lesion sites. In general, light patients in the active phase can be treated with aminosalicylates alone, which are the first-line drugs in the active phase, and attention should be paid to choosing different dosage forms according to different parts of the lesion. Steroid hormone is one of the first choice to control the disease activity during the active phase, but attention should be paid to the application of the starting dose should be sufficient, and the dose should be reduced immediately after the disease control to avoid the occurrence of adverse reactions caused by hormones. For patients with refractory or complicated fistula formation, second-line therapeutic agents, i.e. immunosuppressive agents or biologics, can be used. Patients with concomitant infection need to be combined with antibiotics, which need to be selected according to the patient’s condition, stool and drainage fluid pathogenic bacteria culture results, but metronidazole is currently clear by more certain efficacy.
One of the preferred drugs in the maintenance phase is 5-ASA, steroids in principle need to be withdrawn as soon as possible after the control of symptoms, but 10% to 15% of patients relapse after withdrawal, the need for hormonal drugs to maintain, the minimum dose available to maintain a few months, but as far as possible, do not take long-term. Maintenance therapy with immunosuppressants and reagents has also been reported. The principles of drug selection for Crohn’s disease are presented here, and there are more books and literature available on the subject, so I will not repeat them here. In recent years, a “step-down therapy” program has been proposed, advocating the administration of the biologic agent infliximab early in the active phase of the disease, which is based on the increasing evidence of the effectiveness of infliximab in clinical treatment. This is based on the increasing clinical evidence for the effectiveness of infliximab, although the application of the “step-down” regimen still requires the selection of appropriate patients and is available to interested readers.
The purpose of devoting such a large section to the pharmacological treatment of patients with Crohn’s disease is to suggest that surgeons should have a holistic approach to the treatment of Crohn’s disease. Crohn’s disease is an autoimmune disease, a systemic disease, except that the most significant lesions are reflected in the GI tract, and surgical treatment is only one part of its overall treatment. For Crohn’s disease, surgical treatment only addresses its complications and does not treat its primary disease. Therefore, before the occurrence of complications that require surgical treatment, the development of the disease should be actively controlled to prevent the occurrence of complications, and relevant medications should continue to be given after surgical treatment of complications in order to inhibit their recurrence.
The surgical treatment of Crohn’s disease is only for its complications, such as obstruction, bleeding, perforation, abscesses, inflammatory masses, internal and external intestinal fistulas, etc. The surgical procedures performed for these complications are similar to those performed for similar cases of other causes, mainly resection of the complicating intestinal segment or repair of the organ that has eroded into a fistula (bladder, vagina, etc.). treatment. Since the surgery is performed for complications and does not cure their primary disease, this differs from another inflammatory bowel disease, ulcerative colitis, in which there is no recurrence of intestinal lesions after total colectomy, whereas after resection of intestinal lesions in Crohn’s disease, there is still a possibility of recurrence of other residual intestinal lesions. According to the literature, the recurrence rate of cases that do not continue medication treatment after surgery is 65% to 90% at 1 year and 80% to 100% at 3 years after endoscopic review.
The recurrence rate according to the clinical symptoms is lower, 20%-25% per year, and the reoperation rate is 25%-30% in 5 years and 45%-50% in 20 years, and most patients eventually need reoperation, and 25% need a second reoperation. This is second only to the incidence of short bowel syndrome due to loss of the small bowel due to vascular disease. The preservation of the small bowel during surgery for Crohn’s disease and the active prevention of postoperative recurrence are the main focus and special points of surgical treatment. Professor Evers of Texas State University Medical Center, USA, in his chapter on small bowel in Hitchcock Surgery, points out that “when surgically treating Crohn’s disease with complications, it should be limited to a small segment with complications and no more of the intestine should be removed, even if the lesion can be observed by the nake