Colon duplication anomaly

　　There are many theories about the etiology of colon duplication anomalies, but each theory cannot fully explain the cause of duplication anomalies at various locations. The etiology may be polygenic, and the etiology of different locations and different pathological changes may be different.

　　1. The theory of primitive gut cavitation disorder: After the 5th week of embryonic development, the rapid proliferation of epithelial cells in the primitive gut cavity causes the intestinal cavity to appear temporarily occluded. Later, the occluded intestinal cavity epithelial cells appear many cavities, making the occluded intestinal cavity communicate again, that is, the cavitation period appears. If there is a developmental disorder at this time, the intestinal tubes may appear interspaces parallel to the digestive tract, which may form intestinal cystic-type duplication anomalies.

　　2. The theory of diverticular-like external pouch: At 8-9 weeks of embryonic development, the distal colon forms a temporary diverticulum-like external pouch due to the outward proliferation of epithelial cells covered by connective tissue. This pouch gradually disappears later. If it remains, the diverticulum-like external pouch at the original location can develop into a cystic-type colon duplication anomaly.

　　3. The theory of chordomere-ectoderm separation disorder: At 3 weeks of embryonic development, the notochord forms between the inner and outer germ layers. If there is abnormal adhesion between the inner and outer germ layers at this time, the notochord is divided into two parts, left and right, at this location. The notochord and vertebral body form a cord-like enteric nerve tube through the outer germ layer between the notochord and the digestive tract. When the inner germ layer develops into the digestive tract later, the part of the intestine pulled by the cord-like adhesion bulges ventrally to form a diverticulum-like bulge. This location may develop into a duplication anomaly later. Since the adhesions occur on the dorsal side of the primitive gut, the duplication anomalies are also located on the mesenteric side. The cord-like adhesions can affect the development of the vertebral body, so this type of duplication anomaly is often accompanied by vertebral body developmental anomalies, such as hemivertebrae, butterfly vertebrae, etc. Li Long et al. divided intestinal duplication anomalies into two types, and the mesenteric-type duplication anomaly is exactly located between the two mesenteries, accounting for 91.6%. It is associated with thoracic vertebral anomalies and proposed that this type is caused by a disorder in the separation of the notochord and the primitive gut.

　　4. Theory of primitive gut ischemic necrosis: Many scholars believe that after the primitive gut development is completed, due to ischemic necrotic lesions in the primitive gut, changes such as intestinal atresia, stenosis, and short colon occur. The residual intestinal tract fragments that receive blood supply from nearby vessels can develop into duplicated malformations by themselves. Therefore, some children with colon duplication malformation may be accompanied by malformations such as intestinal atresia, stenosis, and short colon.

　　In addition to its clinical manifestations, colon duplication malformation can also cause other diseases. The main complications of this disease include the following:

    1. Nutritional absorption disorder, leading to anemia.

　　2. Intestinal dysfunction, causing irregular diarrhea.

　　3. Perforation may be accompanied by severe peritonitis.

　　(1) Extraintestinal cystic type duplicated malformation: This is the most common type of duplicated malformation. It manifests as round or oval cystic masses not in communication with the colon lumen, tightly attached between the two leaves of the colon mesentery. The size of the cysts varies greatly, with the smaller ones only 1 cm in diameter and the larger ones occupying most of the abdominal cavity. The cysts are filled with colorless or pale yellow mucosal secretions. When the cysts grow to a certain extent, they can compress the main intestinal tract or trigger intussusception. In cases where the inner wall of the cyst cavity is lined with ectopic gastric mucosa or pancreatic tissue, they may be corroded by gastric acid or pancreatic enzymes, leading to peptic ulcers, causing bleeding or perforation within the cyst cavity, and resulting in peritonitis.

　　(2) Cystic type duplicated malformation within the intestinal wall: Cysts occur within the muscular layer of the jejunum or ileum or beneath the mucosa, and are not in communication with the colon lumen. This type is more common in the distal ileum or ileocecal region. Zhao Li and others reported 13 cases of cystic malformation within the intestinal wall, with 11 cases (84.6%) located within 5 cm from the ileocecal valve in the distal ileum. This type of cyst protrudes into the intestinal lumen as it slightly increases in size, and can block the intestinal lumen early, causing obstruction or triggering intussusception. The diameter of the cyst is rarely more than 4 cm.

　　(3) Tubular type duplicated malformation: There are two morphological types of tubular type duplicated malformation.

　　① Long tubular malformation: The malformation presents as a long tubular shape, attached to the mesentery side, and runs in parallel with the main intestinal tract. The malformation wall has a completely normal intestinal tract structure and often shares the mesentery and blood supply with the main intestinal tract. The length of the malformation varies, with the shorter ones several centimeters long and the longer ones up to 50-70 cm, even involving the entire colon. Most of the malformation intestinal tracts are blind-ended at the proximal end, with the distal end opening into the main intestinal tract. The lumen is lined with gastric mucosa or pancreatic tissue, which is more common than the cystic type, and the malformation is not connected to the main intestinal tract, or the distal end is blind-ended, and the proximal end opens into the main intestinal tract. The cavity is filled with a large amount of mucosal secretions, forming a large tubular cyst, which can displace or compress the main intestinal tract, causing intestinal obstruction.

　　② Diverticular malformation: The malformation is in the shape of a diverticulum, extending from the mesentery of the main intestinal tract to any part of the abdominal cavity. The terminal is in a free state, adherent to the intestinal tract or organ it contacts, and the proximal intestinal segment of varying length opens into the main intestinal tract. This type of malformation can have its own independent mesentery and blood supply, and can be completely resected during surgery.

　　(4) Thoracic and abdominal cavity repeated malformations: Thoracic and abdominal cavity repeated malformations account for 2% to 6% of gastrointestinal duplication, and can originate from any part of the gastrointestinal tract in the abdomen. The chest and abdominal duplication of the colon often originates from the jejunum, and the malformation is a long tubular shape that originates from the mesenteric side of the main intestinal tract, passes through a certain abnormal foramen or esophageal hiatus behind the peritoneum, and enters the posterior mediastinum. The malformation terminal can extend to the top of the pleura, and attach to the cervical vertebra or upper thoracic vertebra. Thoracic and abdominal cavity repeated malformations are associated with spinal malformations, such as hemivertebrae, vertebral fusion, anterior cleft of the spine, or neural tube cysts in the spinal canal.

　　Repeated malformations in the thoracic and abdominal cavities can also exist separately in the thoracic and abdominal cavities, and there is no connection between them. Although such cases are rare, they are easy to misdiagnose or miss in clinical practice. Therefore, after the diagnosis of repeated malformation in any part, careful examination should be made to see if there is a second malformation.

　　2. Classification according to mesenteric blood supply: Li Long and others classified the colon duplication malformation according to the relationship between the intestinal tract and the mesenteric blood supply of the main intestinal tract, and divided it into conjoined type and mesenteric type.

　　(1) Conjoined type (Type I): The aorta separates from the marginal artery of the mesentery to emit blood vessels to both intestinal walls, and the two blood vessels respectively run from the two layers of peritoneum side to the supplied intestinal tract. The blood vessels supplying the main intestinal tract do not pass through the duplicated intestinal tract, and the interruption of the blood supply of the duplicated intestinal tract does not affect the blood supply of the main intestinal tract. This type accounts for 75.3% of duplication malformations, with the cystic type being the most common, and only 6.2% are associated with thoracic vertebral malformations.

　　(2) Mesenteric type (II): The duplicated intestinal tract is located between the two layers of peritoneum in the mesentery. When the artery crosses over the duplicated intestinal tract from both sides to reach the main intestinal tract, the short branches entering the duplicated intestinal tract do not affect the blood supply of the main intestinal tract. This type accounts for 24.7% of duplication malformations, with tubular type being the most common. The incidence of thoracic vertebral malformations is as high as 91.6%.

　　The pathological morphology of colon duplication malformation (colonic duplication) is divided into cystic type and tubular type. The cystic type mostly occurs in the cecum and sigmoid colon, and its pathological manifestation is similar to that of the cystic type of small intestine. This disease is a congenital malformation, and there is no effective preventive measure. In order to prevent the occurrence of serious complications, early surgical treatment should be performed for patients with symptoms.

　　1. X-ray examination: Abdominal flat film can show the compression and displacement of the intestinal tract, and in cases of incomplete intestinal obstruction, gastrographic examination shows arched pressure marks in the intestinal tract. Barium meal examination may show a defect in the filling of a group of colonic barium or compression, especially the areas near the ileocecal valve and the terminal ileum should be noted. If there is a filling of tubular or diverticular barium outside the colon and ileum, and it appears with peristalsis, it has important diagnostic value.

　　X-ray film of the spine shows abnormal vertebral bodies, and further myelography, magnetic resonance imaging, or CT examination should be performed to determine whether there is an enterocystoma in the spinal cord canal.

　　2. Ultrasound examination: Abdominal ultrasound examination shows abdominal mass as cystic, and makes a judgment on its location and size, which is conducive to diagnosis and differential diagnosis.

　　3. Radionuclide imaging: When there is ectopic gastric mucosa in the duplicated intestinal tract, after intravenous injection of 99mTc, abdominal scanning can often show a radioactive accumulation area at the location of the duplicated intestinal tract, but it needs to be distinguished from Meckel's diverticulum, and it should be noted that negative results cannot negate the diagnosis.

　　4. Laparoscopic examination: If laparoscopic examination is possible, it can accurately determine the location and type of the lesion.

　　Diet should be light, easy to digest, and low in residue. It should not be too greasy, and spicy and irritant foods should not be eaten.

　　Eat more fresh fruits and vegetables. It is also not advisable to stay up late every day. More exercise should be done.

　　Pay attention not to eat too much spicy oil, mustard, chili, and other irritant foods.

　　Pay attention not to eat too greasy things, and also pay attention to eat less of things like hairtail fish and crabs.

　　Endoscopic treatment For sites with small bleeding volume and where the colonoscope can reach, endoscopic treatment can be performed. There are various treatment methods, such as spraying hemostatic drugs (thrombin, adrenaline) under the endoscope, and then compressing the bleeding with the tip of the endoscope; hemostasis under the endoscope by high-frequency coagulation, microwave, or laser, and the combination of endoscopic drug therapy and physical therapy. It is necessary to pay attention to the risks of endoscopic treatment, as intestinal perforation may occur during inappropriate electrocoagulation and laser treatment.

　　Interventional therapy under angiography: When colonic vascular malformations with bleeding are shown by selective angiography, pituitrin can be injected through the angiography catheter to stop bleeding, but blood pressure and heart rate should be closely observed, or absorbable gelatin sponge can be used to block under superselection. Some may bleed again after vascular intervention; due to the single blood supply of the colon, the collateral circulation is not rich, and ischemic colitis or intestinal necrosis may occur after embolization treatment, with an incidence rate of 10% to 25%, and the consequences are serious.