Widespread infiltration in the pelvis
Introduction
Introduction Rectal cancer spread out of the intestinal wall when there is extensive infiltration in the pelvic cavity (or recurrence in the pelvic cavity after surgery), which can cause soreness in the waist and ankle, and a feeling of swelling. Invasive cervical cancer is often found in gynaecological examinations and confirmed by pathological biopsy. Some cervical cancer is asymptomatic and abnormal in the naked eye, pay attention to identification. The occurrence of colorectal cancer is the result of multiple genetic changes caused by various factors of genetic and environmental factors in the colonic mucosal epithelium. Many epidemiological studies of colorectal cancer have shown that the possible causes of colorectal cancer are socio-economic development, lifestyle changes, especially changes in dietary structure, and other factors such as environment and genetics.
Cause
Cause
(1) Causes of the disease
The occurrence of colorectal cancer is the result of multiple genetic changes caused by various factors of genetic and environmental factors in the colonic mucosal epithelium. Many epidemiological studies of colorectal cancer have shown that the possible causes of colorectal cancer are socio-economic development, lifestyle changes, especially changes in dietary structure, and other factors such as environment and genetics.
1. Dietary factors: Epidemiological studies have shown that dietary factors are an extremely important factor in the pathogenesis of cancer, because 70% to 90% of cancers are related to environmental factors and lifestyle, and 40% to 60% of them. % of environmental factors are related to diet and nutrition to a certain extent.
(1) High-fat diet: A worldwide survey found that in countries with high colorectal cancer in North America, Western Europe, and Australia, people eat more than 120g of fat per day. In countries such as Poland, Spain, and Yugoslavia, where the incidence of colorectal cancer is high, the daily consumption of fat per person is 60-120g. In Colombia, Sri Lanka, Thailand and other places with low colorectal cancer, the daily fat consumption per person is only 20 to 60 g. The incidence of colorectal cancer in high and low incidence areas can vary by more than 6 times. The middle and low-incidence areas can differ by about 3 times. The fat content of Americans with high colorectal cancer accounts for 41.8% of total calories, and is mainly saturated fat. The Japanese with low colorectal cancer (the incidence of colorectal cancer is about 1 times lower than that of the United States), and the fat in the diet accounts for 12.2% of the total calories, and is mainly unsaturated fat. The correlation between the time trend of colorectal cancer incidence and dietary structure in Shanghai, China also shows that the change of colon cancer incidence rate is closely related to dietary structure changes. As the survey shows, the per capita consumption of some major foods in Shanghai in the 1980s increased significantly compared with the 1950s, with pork being tripled, eggs 2.2 times, and fresh vegetables 1.6 times. In 1992, Shanghai City consumed 86.4g of fat per person per day, accounting for 31.2% of heat energy sources; 58.7g and 22.4% of suburbs were respectively. At the same time, the age-standardized incidence rate of male colorectal cancer in Shanghai was 21.5/100,000, which was similar to the incidence of the same period in the internationally equivalent of the colorectal cancer in Spain and Poland.
Some animal studies have also confirmed that high fat intake can increase the risk of colorectal cancer. Reddy et al used induced dimethylhydrazine (DMH) to induce colorectal tumors in rats. The induction rate was 17% to 36% in the diet group containing 5% fat, and 64% to 67% in the diet group containing 20% fat. Significant difference. The results suggest that giving animals a high-fat diet can increase the incidence of colorectal tumors, make tumors appear earlier, increase the degree of malignancy and metastasis of tumors, and significantly shorten the survival time of tumor animals.
The reason why high-fat diets increase the incidence of colorectal cancer is:
A fat diet may cause colorectal cancer by altering the concentration of bile acid in the stool.
2 high fat and glucuronidase, ornithine dehydroxylase, nitroreductase, azooxygenase, lipoxygenase, cyclooxygenase activity, promote carcinogens, carcinogen production.
3 High-fat dieters often consume more meat, and meat can produce carcinogenic heterocyclic amines during frying or baking, which may lead to colorectal cancer.
(2) Low-fiber diet: Dietary fibre refers to plant polysaccharides and lignin that cannot be hydrolyzed by human digestive enzymes in plant foods. Higginson has noted that colon cancer in Africa is rarely associated with large consumption of whole grains and little constipation. La Vecchia et al. reported in 1988 that eating more fresh vegetables had a protective effect on colorectal cancer (RR=0.5). Yang Gong, from Zhejiang Medical University in China, also found in a controlled study that there was a significant negative correlation between the risk of taking fresh vegetables (especially cruciferous vegetables), fresh fruits and colorectal cancer, and dose-response. The relationship was very significant (P < 0.01). Analysis of the relationship between nutrients and colorectal cancer found that dietary fiber played an important protective role; while the intake of saturated fatty acids and monounsaturated fatty acids was positively correlated with the risk of colon cancer (P<0.01), but There was no significant correlation with rectal cancer.
The possible mechanism by which a high-fiber diet can reduce the incidence of colorectal cancer is:
1 dietary fiber can increase the volume of feces, dilute carcinogens, and shorten the intestinal transit time, reduce the contact between colonic mucosa and fecal carcinogens, thereby reducing the risk of colon cancer.
2 By inhibiting reabsorption, dilution and adsorption, chelation, reducing the deoxycholic acid concentration in the intestine, affecting intestinal lipid metabolism.
3 change the intestinal flora, affect the structure and function of intestinal mucosa, and affect the growth rate of mucosal epithelial cells, and mediate the pH of the intestine (usually the pH of feces in low-incidence areas of colorectal cancer is lower than that in high-incidence areas).
4 through mucin to strengthen the mucosal barrier, reduce intestinal toxic substances on the intestinal epithelium.
(3) Nitrosamine compounds: Many of the nitrosamine compounds are strong carcinogens, and tumors of various organs can be induced in animal experiments. Generally, small doses of nitrosamines can cause cancer if exposed for a long time. Nitrosamine compounds are widely found in food additives and preserved foods such as meat, fish, and vegetables treated with nitrite (such as bacon, ham, salted fish, etc.). Animal experiments have confirmed that nitrosamines can be converted into sputum by intestinal bacteria to cause colorectal cancer. Domestic Yanggong and other studies have found that the positive correlation between pickled foods is a separate risk factor for colorectal cancer. The risk of colon cancer ingested more than 3 times a week was 2.2 times (P < 0.01) for less than one case, 2.3 times for rectal cancer (P < 0.01), and 2.1 times for left colon cancer. Semi-colon cancer is 1.8 times.
(4) Vitamins: Case-control studies showed that carotene, vitamin B2, vitamin C, and vitamin E were all associated with a reduction in the relative risk of developing colorectal cancer. Statistical tests showed significant levels and showed a dose-response relationship. For example, Chiu et al. reported in 2003 that high intakes of vitamin C, carotene, and vitamin E were associated with a reduced risk of colon cancer. Mc Cullough et al. reported a follow-up observation of 60,866 men and 668,83 female participants in 2003, suggesting that vitamin D can reduce the risk of colorectal cancer in men (RR=0.71, 95% CI=0.51, 0.98), calcium in There is a protective effect in the development of colorectal cancer (RR=0.87, 95% CI=0.67, 1.12).
(5) Frying fried foods: The portion of the food roasted (fried) coke (especially meat) contains a carcinogen heterocyclic amine which acts on the colon and may cause colorectal cancer. The case-control study reported by Yang Gong et al. suggests that the carcinogenic effect of fried foods is also an independent risk factor. The risk of colon cancer ingested more than 3 times a week was 2.3 times (P < 0.01) for less than one case, 2.6 times for rectal cancer (P < 0.01), and 2.6 times for left colon cancer. Semi-colon cancer is 1.9 times.
(6) Onion and garlic: The protective effect of onion and garlic on tumor has been widely recognized, and the growth inhibition effect of this kind of food on tumor has been confirmed many times in the experiment. Garlic oil can significantly reduce the damage of colonic mucosal cells caused by dimethyl cholestyramine, and can reduce the induction rate of colorectal cancer in mice by 75%. Domestic Yanggong reported that the risk of colon cancer in high-incubation garlic food was 74% in the low-intake group (P<0.05), but the correlation with rectal cancer was not certain (OR=0.81, P>0.05). .
(7) Trace elements and minerals:
1 Selenium: Selenium is a trace element in the human body. It is a strong antioxidant. One of its most important biological functions is to inhibit the peroxidation reaction, and the peroxidation reaction can promote the carcinogen to the deoxyribonucleic acid. Several large-scale studies have found that mortality from multiple cancers, including nodules and rectal cancer, is inversely related to selenium intake in local diets. However, the influence of inorganic elements such as selenium on the etiology of human tumors may be affected by other food components (or interactions, or mixed, biased, etc.), so some people think that these factors may be just some accompanying factors, but not directly Affect the risk of colorectal cancer in the population.
2 Calcium: Animal experiments have shown that calcium can improve the toxic effects of deoxycholic acid on intestinal epithelium. Some scholars believe that the increase of the concentration of bile acids and free fatty acids in the intestine can promote the occurrence of colorectal cancer, and calcium can be combined with them to form insoluble saponified compounds, so that their stimulation and toxic effects on the intestinal epithelium are alleviated. Many epidemiological studies have also suggested that high calcium intake protects against the development of colorectal cancer. Yang Gong and other 1994 nutritional epidemiological studies showed that the protective effect of dietary calcium on colorectal cancer is not only related to intake, but also closely related to the food source of calcium. Among them, animal dietary calcium is related to the risk of reducing the incidence of colorectal cancer, while plant dietary calcium is not related to this. It is speculated that the calcium ions of different food sources may be different from the organic components of food, and may cause differences in the effects of calcium from different food sources.
3 Other inorganic elements: Studies have shown that potassium, iron, phosphorus and kidney, the risk of colorectal cancer is negatively correlated, zinc, magnesium, copper may affect the metabolism of carcinogens or degrade certain enzymes, which is related to the inhibition of cancer . But there is still a lack of more evidence to support. Some authors believe that these inorganic elements may have a mixed effect with some "vegetable" dietary factors (such as dietary fiber, vitamin C, etc.), or just some accompanying factors. Therefore, the impact of these inorganic elements on the pathogenesis of colorectal cancer needs further research.
2. Occupational factors: Although it is generally believed that colorectal cancer is not an occupational disease, the relationship between occupational factors and the incidence of colorectal cancer still needs our attention. As reported by Donham et al. 1980, workers producing asbestos insulation in colorectal cancer patients are more common, and animal experiments have confirmed that asbestos fibers swallowed can penetrate the intestinal mucosa. In addition, in the metal industry, cotton yarn or textile industry and leather manufacturing industries, the standardized mortality and mortality of colorectal cancer is also higher. Domestic Gao Yutang passed the study on the relationship between occupation and tumor incidence in Shanghai in 1990, and pointed out that the ratio of standardized colon cancer incidence (SIR) of various professional and technical personnel was significantly higher (male = 135, P < 0.01; female = 147, P < 0.01). Female commercial workers had a colon cancer SIR=132, P<0.05. Colon cancer of male production workers, transport workers, etc. SIR=90, P<0.05.
3. Physical activity: In addition to occupational exposure and socio-economic factors related to occupation, physical activity is also closely related to the occurrence of colorectal cancer. Gerhardsson et al reported a 14-year follow-up of 16477 people in 1988, suggesting that the relative risk of colon cancer in the low-physitivity group (less active at work and at leisure) was significantly higher (RR=3.6, 95% CI=1.3). , 9.8); the relative risk of low physical activity was lower at work (RR=1.6, 95% CI=0.8, 2.9); the relative risk was also low in the group with only leisure activities (RR=1.6, 95% CI= 1.0, 2.7). In the analysis of occupational physical activity, it was found that the risk of colon cancer in the occupational category with long-term or frequent sitting position was 1.4 times higher than that of some occupations with strong physical activity (95% CI=1.0, 1.9), and the relationship with cecal cancer was more Close (OR = 2.1, 95% CI = 1.1, 4.0). There is a perception that a reduction in physical activity can extend the passage of feces in the intestine, thereby increasing the chance of carcinogens coming into contact with the intestinal mucosa. Another view is that bowel movements are affected by prostaglandins, and physical activity can stimulate the production and secretion of prostaglandins. Therefore, lack of physical activity can increase the risk of colon cancer. The results of the case-control study also support the protective effect of physical activity on the prevention of colorectal cancer, especially colon cancer.
4. Genetic factors: It is estimated that genetic factors may play an important role in at least 20% of patients with colorectal cancer. The Lovett study found that the general population in London had a risk of colorectal cancer in their lifetime of 1 in 50, but the risk of colorectal cancer in first-degree relatives (including parents, siblings, children) rose to 1/17; When a first-degree relative, a second-degree relative (including grandparents, grandparents, aunts, aunts, aunts, aunts, aunts, aunts, grandsons, grandchildren, grandchildren) suffer from colorectal cancer, the risk is 1/12; The first-degree relatives have a 1/10 risk of colorectal cancer before the age of 45; the risk of colorectal cancer in two first-degree relatives can be as high as 1/6. Since then, research on the genetic predisposition of colorectal cancer has become a hot topic. There are currently two hereditary syndromes that are predisposed to colorectal cancer.
(1) "familial adenomatous polyposis" which accounts for 1% of the total number of rectal cancers. This is an autosomal dominant hereditary disease. If it is not treated, it will turn cancer into colorectal cancer in the future.
(2) "Hereditary nonpolyposis colorectal cancer (HNPCC)", which accounts for 5% to 10% of the total number of rectal cancers.
This is also an autosomal dominant hereditary syndrome characterized by early onset of colorectal cancer, frequent lesions in the proximal colon, and multiple primary colorectal cancers. About 80% of the first-degree relatives of the patient will develop the disease. This syndrome is associated with germline mutations of five known DNA mismatch repair genes (hMSH2, hMLH1, hPMS1, hPMS2, hMSH6) and has a microsatellite instability characteristic phenotype. The genetic epidemiology study of colorectal cancer also found that the genetic background affecting the pathogenesis of colorectal cancer may be different. The relationship between colon cancer and heredity is closer than that of rectal cancer, and different age groups (such as 40 years old group and >40 year old group) The relationship between colorectal cancer and genetic factors is different. Among them, young people (40 years old) with colorectal cancer are closely related to heredity. These studies provide a basis for identifying high-risk populations of colorectal cancer, and we should cause family members with a family history of colorectal cancer, especially those with a colorectal cancer age of 40 years or younger (especially first-degree relatives). highly valued.
5. Disease factors
(1) Colorectal adenoma: Colorectal adenoma is a precancerous lesion. Most studies suggest that more than 80% of colorectal cancers occur on pre-existing adenomas. Therefore, the adenomas found in the examination should be removed to prevent the occurrence of colorectal cancer in the future. However, more than 30% of patients with colorectal adenomas will have new adenomas, so strict follow-up is needed.
(2) Ulcerative colitis: This disease is more common in Europe and the United States, but the incidence of the disease has also increased in the past 20 years. Ekbom et al. studied 3117 patients with ulcerative colitis diagnosed between 1922 and 1983 and found that the incidence of colorectal cancer among them was 5.7 times (relative risk). This relative risk is related to the lesion. Ulcerative inflammatory lesions were limited to the rectum, the lowest, only 1.7 times, 2.8 times in the left colon, and 14.8 times in the total colon. The risk of colorectal cancer is also associated with the onset age of ulcerative colitis. 40% of those 15 years of age will develop colorectal cancer, compared with 30% of those who start after 35 years of age. Heimann et al reported 52 cases of ulcerative colitis undergoing surgical resection, and the patient had ulcerative colitis for an average of 21 years (8 to 46 years). Multi-primary colorectal cancer is common in ulcerative colitis, and 10 of Heimann's 52 cases have 2 colorectal cancers, 5 cases have 3 cancers, and 1 case has 5 cancers. Therefore, 31% have multiple primary and simultaneous primary tumors. Colorectal cancer. In addition, in 52 cases, poorly differentiated colorectal cancer accounted for 42%, significantly more than in general colorectal cancer. Some authors have reported that patients with ulcerative colitis with a wide range of lesions have been ill for more than 10 years, and the risk of colorectal cancer is several times higher than that of the general population. In the first 10 years after the onset of the disease, the risk of colorectal cancer is estimated to be 0% to 3%; the likelihood of colorectal cancer increases to 12% to 15% after the second 10 years; in the third After 10 years, it will increase to 50%. Rosen et al believe that patients with a history of ulcerative colitis 7 years are at high risk for colorectal cancer, and should be given a full colonoscopy every year. If there is no atypical hyperplasia in pathological examination for 2 consecutive years, it can be changed to a full colonoscopy every 2 years. Patients with ulcerative left colonitis can have a full colonoscopy from the 15th year of the disease and check every 2 years. Patients with ulcerative rectal and sigmoid colon can be censused as in the general population. Choi et al reported that 41 of 2050 cases of ulcerative colitis had colorectal cancer, and 19 of them were regularly examined for colorectal cancer. Most of them were early cancer, and the 5-year survival rate was 77.2%. The other 22 cases were not monitored. The examination showed that the tumors were mostly advanced and the 5-year survival rate was 36.3%. However, it should be pointed out that the purpose of regular inspection is not only to detect cancer at an early stage, but also to prevent the occurrence of colorectal cancer by early colectomy when there is a trend of canceration. Langholz et al reported that after follow-up and colectomy for patients with ulcerative total colitis, there is no difference in the likelihood of colorectal cancer in the lifetime and the likelihood of colorectal cancer in all local populations (3.5% and 3.7%, respectively). ), prompting positive medical treatment, reasonable monitoring and examination, and timely surgery after finding the lesions can reduce the risk of colorectal cancer in such patients.
(3) Crohn's disease: Crohn's disease is a chronic inflammatory disease that mostly invades the small intestine and sometimes affects the large intestine. The risk of colorectal cancer in patients with Crohn's disease for a long time and before the age of 30 is estimated to be 4 to 40 times higher than that of the general population. From the disease to cancer, the average is 20 years. Cancer tends to occur in the intestines of the inflammatory stenosis. The difference between colon cancer and general colon cancer in these patients is that the average age of cancer is 49 years old, 10 years earlier than the general population with colorectal cancer; more than 10% are multiple primary colorectal cancer; mucinous adenocarcinoma accounts for 50% ( Only 9% of colorectal cancer in the general population is mucinous adenocarcinoma. Rosen et al. advocated that colonoscopy and biopsy should be performed every two years from the 15th year of the onset of the disease, and should be checked once a year from the 20th year onwards.
(4) Schistosomiasis: A national survey of malignant tumor deaths published in 1980 confirmed that the distribution of colorectal cancer mortality was significantly associated with the distribution of schistosomiasis deaths. In 1980, Huang Yujian et al. counted the mortality of colorectal cancer in various areas according to the prevalence of schistosomiasis in one of the epidemic areas of schistosomiasis, Shanghai Qingpu County, and found that the schistosomiasis overweight epidemic area (schistosomiasis infection rate >50%), severely endemic areas (Infection rate 30% to 49%), moderate endemic area (infection rate 10% to 29%) and mildly endemic area (infection rate <10%), colorectal cancer mortality rate was 19.16/100,000, 16.55/10 10,000, 12.44/100,000 and 9.73/100,000, statistical analysis showed that schistosomiasis infection was significantly associated with colorectal cancer (P<0.05). In 1988, Li Ying based on the 1974-1976 Zhejiang Cancer Death Retrospective Survey and the 1975-1978 Chinese Malignant Tumor Survey Data and the Chinese Schistosomiasis Atlas, the correlation between schistosomiasis endemic areas and colorectal cancer morbidity and mortality. The relationship between schistosomiasis and colorectal cancer mortality in 12 provinces and autonomous regions in southern China and 10 counties in Jiaxing, Zhejiang Province was found to be 0.706 and 0.903, respectively, suggesting that schistosomiasis may be associated with High incidence of colorectal cancer. But this view is still controversial. There is insufficient evidence on colorectal cancer and schistosomiasis in several epidemiological studies conducted by colorectal cancer in China. Epidemiological and pathological studies of schistosomiasis and colorectal polyps in Haining, Zhejiang Province also suggest that polyp carcinogenesis has nothing to do with the presence or absence of schistosomiasis eggs in polyps. In addition, the results of the colorectal cancer screening conducted in Jiashan and Haining, Zhejiang Province, do not support schistosomiasis as a risk factor for colorectal cancer.
(5) cholecystectomy: Some authors have reported that the risk of colon cancer can be increased after cholecystectomy, especially proximal colorectal cancer. Caprilli's (1988) case-control study of 318 cases of colorectal cancer showed an increased risk of colon cancer in men after cholecystectomy (RR = 2.75, P < 0.05), whereas women's risk decreased (RR). = 9.18, P < 0.02). However, some studies have not observed the same phenomenon.
6. Other carcinogenic factors
(1) Obesity: There are some case-control studies and cohort studies suggesting that obesity is positively associated with the risk of colon cancer, but the association with rectal cancer is not yet certain. For example, Nomura et al reported a 5-year cohort study of 8006 Japanese men aged 45-68 years and found that body mass index [BMI, weight/height (kg/m), also known as Quetelet index] 26, suffering from colon cancer The risk was significantly increased (RR = 3.0), but the same association was not observed for rectal cancer. Graharm also reported that obesity can significantly increase the risk of colon cancer (male OR = 2.2, 95%, CI = 1.2, 4.1; female OR = 1.8, 95%, CI = 1.0, 3.4). However, some studies have not found a link between high BMI and colorectal cancer, and even the opposite.
From the etiology point of view, perhaps obesity is a concomitant form of high risk status of colon cancer, and the connection between obesity and cancer is affected by many factors, such as diet, drinking, smoking, physical activity, hypertension, diabetes, sex hormone balance. The situation, etc., should be considered in the evaluation of the role of obesity in the pathogenesis of cancer.
(2) pelvic radiation therapy: Some patients believe that the risk of colorectal cancer after cervical cancer radiotherapy is 4 times higher than the average person. For example, Martins reported that the average interval from radiotherapy to colorectal cancer was 15.2 years, 32% occurred within 10 years after radiotherapy, and 28% occurred 20 years after radiotherapy. Fudan University Affiliated Tumor Hospital showed that the median interval from radiotherapy to colorectal cancer was 19 years, 36% occurred within 10 years after radiotherapy, and 36% occurred after 20 years. The cancer is located in the large intestine within the range of the original radiation field, and is mostly rectal cancer. Because cervical cancer is a common cancer in China, radiotherapy is the most commonly used treatment, and because of its good curative effect, most patients can survive for a long time (10-year survival rate can reach about 65%), thus having the opportunity to form radiation. Colorectal cancer. In this regard, women and surgeons must fully understand, in order to facilitate timely diagnosis and treatment.
(3) Other factors: In addition to the above, for smokers, those with a history of breast cancer or female germline cancer, those with a history of kidney cancer or bladder cancer, those who have undergone ureter-sigmoid anastomosis, those with immunodeficiency, and those with diabetes Patients should also be aware that they are at higher risk of colorectal cancer than the general population.
(B) the pathogenesis: comprehensive domestic data, the location of colorectal cancer in the rectum accounted for 56% to 70%, sigmoid colon 12% to 14%, descending colon 3%, splenic flexion 0.6% to 3%, transverse colon 2% to 4% Liver curvature 0.7% to 3%, ascending colon 2% to 13%, cecum 4% to 10%. Slater reported a progressive decrease in the incidence of left colon and rectal cancer over time, while the incidence of transverse colon and right colon cancer increased.
Gross pathology
(1) Gross classification of early colorectal cancer: Early colorectal cancer refers to cancer lesions confined to the large intestinal mucosa and submucosa, generally no lymph node metastasis, but 5% to 10% of cases may have local lymph node metastasis.
Early colorectal cancer is divided into 3 types:
1 polyp bulge type (type I): can be divided into pedicle type (Ip), yati broad base type (Ips), pedicle-free type (Is). This type is mostly intramucosal cancer.
2 flat bulge type (IIa type): generally in the form of cents. This type is mostly submucosal cancer.
3 flat bulge with ulcer type (IIa + IIc type): also known as type III, generally small disc-shaped, edge bulge, central depression, this type is rare, only seen in submucosal cancer.
(2) Middle and late stage colorectal cancer classification: The middle and late stage colorectal cancer is divided into the following 4 types.
1 bulge type: the tumor protrudes into the intestinal lumen, and is nodular, polypoid or cauliflower-like bulge. The boundary is clear, and there is a pedicle or a broad base. Infiltration is more shallow and limited, and the superficial muscle layer has cancer infiltration.
2 ulcer type: the surface of the tumor forms a deep ulcer, and the ulcer is generally deeper than the muscle layer. According to the shape and growth of the ulcer, it is further divided into:
A. Localized ulcer type: The tumor looks like a crater, with irregular deep ulcer formation, varying in size, and the tumor tissue at the edge of the ulcer is surrounded by a levee.
B. Infiltrating ulcer type: The tumor mainly grows into the deep layer of the intestinal wall, and the central necrosis of the tumor forms a deep ulcer with a large bottom.
3 infiltrating type: the tumor diffuses into the various layers of the intestinal wall, so that the intestinal wall thickens and hardens, and the circumference of the intestine is obviously reduced, forming a ring-shaped stenosis.
4 gel-like type: the shape of the tumor is different, it can be bulging, ulcer or diffuse infiltration, but the appearance and cut surface are translucent jelly.
2. Type of histology
(1) Papillary adenocarcinoma: The cancer cells are composed of a papillary structure of varying thickness, the nipple is slender, and the cancer cells are columnar and may have different degrees of differentiation.
(2) tubular adenocarcinoma: The cancerous tissue is mainly composed of glandular tubular structures, and can be classified into highly differentiated, moderately differentiated and poorly differentiated adenocarcinoma according to the degree of differentiation.
(3) Mucinous adenocarcinoma: This type is characterized by the appearance of a large amount of mucus in the cancerous tissue. There is a large "mucus lake" formed, or a cystic adenocarcinoma structure, which is filled with mucus.
(4) signet ring cell carcinoma: cancer cells are mostly small and medium round cells, the cytoplasm is filled with mucus, the nucleus is on one side, and the whole cell is in the shape of a ring.
(5) Undifferentiated carcinoma: The cancer cells in the tumor are diffuse into pieces or in a mass, and do not form a glandular structure or other tissue structure. The undifferentiated cancer cells have a large nucleoplasmic ratio and a nuclear abnormality.
(6) Adenosquamous carcinoma (adenosperm cell carcinoma): Adenocarcinoma in the tumor appears mixed with squamous cell carcinoma. The adenocarcinoma partially has adenoid structure, while the squamous cell carcinoma has poor differentiation and keratinization.
The above tissue types may coexist in two or more histological types within the same tumor. Among them, tubular adenocarcinoma is the most common account of 66% to 80%, followed by mucinous adenocarcinoma, signet ring cell carcinoma, and papillary adenocarcinoma, respectively, 16%, 3% to 7.5%, 5%. Adenosquamous carcinoma and undifferentiated carcinoma are rare.
3. Dispersion method
(1) Hematogenous dissemination: Hematogenous dissemination generally depends on several factors:
1 degree of differentiation of cancer.
2 Local anatomy of the primary lesion.
The deeper the cancer cells invade the intestinal wall, the more chances of blood transfer. Hematogenous spread usually occurs in the later stages. Cancer cells are first transferred to the liver via the portal vein. There is very little liver metastasis (<1%) in the early stage of colorectal cancer, mainly in middle and advanced cancer. The Japan Colorectal Cancer Research Association (1990) collected 5,826 cases of colorectal cancer surgery in the country, and 406 cases (7%) had liver metastases. Venous involvement of colorectal cancer is closely related to the location of the lesion. 42.6% of rectal cancers with lesions located 6 cm below the anus had venous involvement, which was higher than the incidence of rectal cancer in the middle and upper segments. In addition, the chance of venous invasion of rectal cancer is greater than that of colon cancer, so its prognosis is generally worse than colon cancer.
(2) Adjacent organ spread: Colon cancer can invade the retroperitoneal space, such as the uterus, ovaries, and kidneys, but invasive duodenum and pancreas are rare. Rectal cancer invades the small intestine, sigmoid colon, bladder, uterus and vagina.
(3) lymph node (tube) dissemination: the most common form of dissemination of colorectal cancer. The rate of lymph node metastasis is closely related to the pathological type and degree of differentiation of colorectal cancer. Dukes reported that lymph node metastasis rates of high, moderate, and poorly differentiated cancer in 2238 colorectal cancers were 30%, 47.1%, and 81.3%, respectively. Since there is no lymphatic vessel in the mucosa, there is no lymphatic metastasis in mucosal cancer. Lymphatic vessels are distributed from the submucosal layer, which means that lymphatic metastasis may occur. Colon cancer usually first metastasizes to the para-lymph node. Figures 2 and 3 show the lymph nodes of the colon and rectum.
It shows that the drainage of the rectum has a potential channel. Miles reported up-diffusion of the lymphatic vessels along the supraorbital and inferior mesenteric vessels and transferred to the superior rectal artery and the inferior mesenteric lymph nodes; the lateral dissemination terminated in the intra-orbital lymph nodes; the downward dissemination terminated in the inguinal lymph nodes. Spratt reported that patients with colorectal cancer had a 5-year survival rate of 24% with 1 to 5 lymph node metastases, and a 5-year survival rate of only 9% with 6 to 10 lymph node metastases (Fig. 4, 5).
(4) Peritoneal dissemination: colorectal cancer is less disseminated and abdominal cavity. When tumor cells penetrate the intestinal wall and reach the serosa, it is easy to spread to the entire abdominal cavity. It is more common in patients with right colon cancer, and the occurrence of peritoneal dissemination The rate is about 10%.
(5) dissemination of the nerve bundle membrane: colorectal cancer cells easily invade the myometrial nerves of the intestinal wall, infiltrating the small channels between the local perineural membrane and the neuroendothelium. This infiltration is associated with local recurrence. 81% of patients with nerve infiltration had local recurrence, while only 30% of those without nerve infiltration had local recurrence. There were 398 cases of 523 cases of colorectal cancer without neuroinvasion in Shanghai Cancer Hospital. The 5-year survival rate was 60.55%, and there were 125 cases of nerve infiltration. The 5-year survival rate was 22.4% (P<0.005).
4. Clinical pathological staging
(1) Dukes staging: This staging was founded by Dukes, a famous British colon cancer expert. In 1935, Dukes divided the colorectal cancer into three phases A, B, and C based on the maximum depth of tumor infiltration.
Stage A: The tumor is limited to the intestinal wall.
Stage B: The tumor has invaded the intestinal wall.
Stage C: Regardless of which layer the tumor invades, it is C stage as long as it is accompanied by lymph node metastasis.
Dukes then divided the C phase into C1 and C2 phases, of which C1: no high lymph node metastasis; C2: high lymph node metastasis. The staging method is simple and easy to master, and has been used for many years.
After Dukes, many people have revised their staging and proposed various "improved Dukes staging." In 1967, Turnbull added a D phase reflecting the distant transfer based on the Dukes staging. More cited today is the staging method proposed by Astler and Coller in 1954 and revised in 1978. This staging method involves more detailed factors such as tumor infiltration depth, lymph node metastasis and distant metastasis. In the modified Astler-Coller staging system, stage A is the tumor invasion and mucosa and submucosa. In stage B1, the tumor invades the muscularis propria, and in stage B2, the tumor invades the serosal layer. If the tumor penetrates the serosa, it enters the adjacent structure. B3. Tumors with lymph node metastasis, according to the depth of invasion of the primary tumor, staged in stage C1 (tumor invasion of the full thickness of the muscularis layer or involving part of the muscularis propria, with lymph node metastasis), C2 (tumor invasion of the full thickness of the muscle Layer and involving the serosa, with lymph node metastasis), C3 (tumor invading the serosa or involving adjacent structures, with lymph node metastasis). There is a distant transfer for the D phase.
(2) Staging of colorectal cancer in China: It was proposed in the first national colorectal cancer seminar held in Hangzhou in 1978. In 1990, it was recommended in the "Specifications for the diagnosis and treatment of common malignant tumors in China" compiled by the National Cancer Prevention Office and the China Anti-Cancer Association. The clinical pathological staging of colorectal cancer in China is as follows: Stage I (Dukes A stage): The depth of invasive cancer does not penetrate the muscular layer and there is no lymph node metastasis.
Stage I0 (A0) - lesions are limited to the mucosa.
Stage I1 (A1) - cancer invades the submucosa.
Stage I2 (A2) - cancer invades the muscular layer of the intestinal wall.
Stage II (Dukes B): The cancer has reached the serosal or parenteral adjacent tissue, but no lymph node metastasis.
Stage III (Dukes C): There has been lymph node metastasis.
Stage III1 (C1) - mesenteric or near-intestinal mesenteric lymph node metastasis.
Stage III2 (C2) - lymph node metastasis at the mesenteric artery.
Stage IV (Dukes D): including all invasive lesions, or distant organs (liver, lung, bone, etc.) metastases, or distant lymph nodes (such as supraclavicular lymph nodes), or widespread peritoneal dissemination. Completely removed or unremovable.
(3) TNM clinical staging: The TNM staging proposed by the International Anti-Cancer Alliance in 1997 is as follows:
T (primary focus):
Tx - the original condition cannot be assessed.
To - no evidence of primary tumor.
Tis - carcinoma in situ: intraepithelial or intramucosal cancer does not penetrate the mucosal muscle layer and reaches the submucosa.
T1 - cancer invades the submucosa.
T2 - cancer invades the muscularis root layer of the intestinal wall.
T3 - The cancer has penetrated the intrinsic muscle layer to the subserosal, or the primary lesion is located in the colon and rectum without serosal layer, and the cancer has invaded the colon or rectal tissue.
T4 - The cancer has penetrated the peritoneum or directly invaded other organs (T4 is also involved in the other large intestine after penetrating the serosa, such as when the cecum invades the sigmoid colon).
N (regional lymph node): Nx - regional lymph nodes cannot be assessed. No - no lymph node metastasis. N1 - 1 to 3 regional lymph node metastasis. N2 - 4 regional lymph node metastasis. Note: There are cancer nodules > 3 mm in diameter in the adipose tissue of the para-rectal or para-colonial lymph nodes, but the lymph node metastasis is classified when there is no residual lymph node structure in histological examination. However, if the cancer nodule is 3 mm, it is classified as a spread of the discontinuity of the primary lesion, and belongs to T3.
M (distant transfer): Mx - unable to assess whether there is a distant transfer. Mo - no distant transfer. Ml - there is a distant transfer.
Staging: Phase 0 - TisNoMo. Phase I - T1 ~ 2 NoMo. Phase II - T3 ~ 4 NoMo. Phase III - any T, N1 ~ 2Mo. Phase IV any T, any N, Ml. Note: Phase 0 and Phase I are equivalent to Dukes A; Phase II is equivalent to Dukes B, in which T3NoMo has a better prognosis, while T4NoMo has a poorer prognosis; Phase III is equivalent to Dukes C, in which N1 has a better prognosis than N2.
Examine
an examination
Related inspection
Pelvic inflation angiography
Symptoms caused by local infiltration: rectal cancer spread out of the intestinal wall when there is extensive infiltration in the pelvic cavity (or recurrence in the pelvic cavity after surgery), which can cause pain in the waist and ankle, swelling feeling; when the tumor infiltrates or compresses the sciatic nerve or closes Sciatic nerve pain or obturator neuralgia may also occur in the sacral nerve root (lumbosacral plexus); vaginal bleeding or hematuria may occur when the tumor invades the vagina and bladder mucosa; colon cancer may invade and contact with the small intestine After the formation of internal hemorrhoids, there may be postprandial diarrhea, which discharges the symptoms of not completely digesting the food; if the tumor involves the ureter, hydronephrosis may occur. If the bilateral ureter is involved, it may cause urinary closure and uremia, and the pelvic recurrence after rectal cancer operation. And the common cause of death.
Diagnosis
Differential diagnosis
Soreness or pain in the waist when you are tired: The soreness or pain in the lower back is caused by the disease of the lumbar muscle strain. When you are tired, the pain or pain will increase. It is a clinical manifestation of lumbar muscle strain. Chronic lumbar muscle strain is a common clinical disease, frequently-occurring disease, and more pathogenic factors. The main symptoms are waist pain, increased fatigue during the day, and can be alleviated after rest. Over time, muscle fiber degeneration, even a small amount of tear, formation of scar or fiber Suspension or adhesion, leaving long-term chronic low back pain. The treatment is mainly based on non-surgical treatment. If various non-surgical treatments are ineffective, surgery can be performed.
Pain in the lumbosacral region: Scar adhesions caused by chronic pelvic inflammation and pelvic congestion can cause lower abdominal swelling, pain, and lumbosacral pain. Often exacerbated after exertion, after sexual intercourse and before and after menstruation.
