Intestinal stenosis

　　The etiology is not completely clear. It is common in patients with celiac disease, and some patients also have lymphoma and intestinal adenoma. Whether these diseases are the etiology of this condition remains to be clarified. It is generally believed that it is due to developmental disorders during the stage of re-penetrating the intestinal canal in the embryonic period; some believe it is due to circulatory disorders in the fetal intestine, which obstructs its normal development. Intestinal stenosis is more common in membranous stenosis, with the degree of stenosis being relatively mild, often only a narrow ring, while short-segmental stenosis is rare.

　　The ulcers in this disease are mostly multiple, with the most common involvement being the jejunum, followed by the ileum, and occasionally occurring in the duodenum or colon. The ulcers are generally deep, reaching the muscular layer, thus easily causing perforation or contraction of the serosal surface scar. Under the microscope, villous atrophy of the small intestine can be seen, with infiltration of lymphocytes, plasma cells, histiocytes, and neutrophils at the base and around the ulcers. The edges of the ulcers sometimes show metaplasia of gastric mucosa. The intestinal mucosa between the ulcers is normal or shows inflammatory changes. The etiology of duodenal atresia and stenosis, as well as jejuno-ileal atresia and stenosis, will be elaborated below.

　　Duodenum atresia and stenosis: During the 5th week of embryogenesis, the excessive proliferation of epithelial cells in the intestinal canal leads to the occlusion of the intestinal lumen, resulting in a temporary filling period. By the 9th to 11th week, the filled epithelial cells undergo cavitation, forming many vesicles, which then fuse together to re-penetrate the intestinal lumen, forming a normal intestinal canal by the 12th week. If the re-penetrating of the intestinal canal is obstructed, it can lead to atresia or stenosis, which is the main etiology of duodenal atresia (Tandler's theory). It often occurs with other malformations, such as Down syndrome, malrotation of the intestines, annular pancreas, esophageal atresia, and malformations of the anal-rectal, cardiovascular, and urinary systems. The presence of multiple system malformations suggests that this is related to a systemic developmental defect in the early embryonic stage, rather than simply due to local maldevelopment of the duodenum.

　　Ileal and jejunal atresia and stenosis are considered in recent years to be caused by intestinal circulatory disorders. In the fetal period, after the intestinal tract has formed, certain abnormal pathological changes occur in the intestines, such as intestinal torsion, intussusception, inflammation, perforation, adhesion by bands, and malformation of blood vessel branches, which cause circulatory disorders in the mesentery, thereby affecting the blood supply of a segment of the small intestine, leading to aseptic necrosis and (or) perforation, absorption, and repair of the intestinal tract, resulting in atresia or stenosis of the intestinal tract at the corresponding site.

　　1. Peritonitis and sepsis, as well as malnutrition.

　　2. Postoperative complications:

　　(1) Anastomotic obstruction: It is the most common postoperative complication, including functional and mechanical obstruction.

　　(2) Anastomotic leak.

　　(3) Necrotizing enterocolitis.

　　Duodenal atresia and stenosis often occur in the second part of the duodenum, most commonly at the distal end of the ampulla, and a few at the proximal end. Common types include: ① Diaphragm type: The intestinal tract maintains continuity externally, and there is an intact diaphragm in the lumen, which can be single or multiple; or the diaphragm may be funiculated into the distal end of the obstruction site to form a windbag-like change; or there is a small hole in the center of the diaphragm. ③ Blind segment type: The continuity of the intestinal tract is interrupted, and the two blind ends are completely separated or only connected by a fibrous band, and the mesentery also has a wedge-shaped defect. This type is less common. ③ Duodenal stenosis: There is circumferential mucosal hyperplasia in the intestinal tract, and the intestinal wall at this location has no functional dilation, and there may also be a constricted segment of the intestinal tract near the ampulla. The duodenum and stomach near the proximal obstruction are significantly dilated, the intestinal wall is thickened, the nerve plexus between the intestinal walls is degenerative, the distal intestinal tract at the time of intestinal atresia is atrophic and small, the intestinal wall is thin, there is no gas in the intestinal lumen, and there may be gas in the distal intestinal lumen during intestinal stenosis.

　　The normal full length of the small intestine in patients with ileal atresia and stenosis is the same as that of normal individuals, which is 250-300cm for mature individuals and 160-240cm for immature individuals. The atresia cases are significantly shorter than normal, only 100-150cm, or even shorter. The proximal intestinal lumen of atresia is extremely dilated due to the accumulation of contents, with a diameter of 3-4cm, thickened intestinal wall, poor peristaltic function, poor blood supply, and even necrosis and perforation. The distal intestinal tract of atresia is small and collapsed, with a diameter less than 4-6mm, no gas in the lumen, and only a small amount of mucus and desquamated cells. There may be concurrent meconium peritonitis. Associated malformations include malrotation of the intestine, intussusception, abdominal wall defect, anal atresia, congenital heart disease, and Down syndrome, etc.

　　The timing of vomiting and the degree of abdominal distension in children with intestinal stenosis vary with the degree of stenosis, and can manifest as chronic incomplete intestinal obstruction. Severe stenosis may present similarly to intestinal atresia.

　　There is no satisfactory drug treatment plan for intestinal stenosis. Adrenal cortical hormones may have some therapeutic effect, but the long-term efficacy remains to be evaluated. For those with concurrent intestinal perforation or massive hemorrhage for whom medical treatment is ineffective, surgical treatment can be performed.
　　　　

    Preventive measures should be taken specifically according to the causes of intestinal strangulation, which can effectively prevent and reduce the occurrence of intestinal strangulation.

　　1. Patients with abdominal wall hernia should be treated promptly to avoid intestinal strangulation caused by incarceration.

　　2. Strengthen health education, promote good hygiene habits, and prevent and treat enterobiasis.

　　3. Patients with abdominal large surgery and peritonitis should be well-gastrostomized, and surgical manipulation should be gentle to minimize or avoid peritoneal infection.

　　4. Early detection and treatment of intestinal tumors.

　　5. Early mobilization after abdominal surgery.

　　Barium X-ray examination or endoscopic examination may reveal small intestinal ulcers, and if other diseases can be ruled out, this disease should be considered. Biopsy of the jejunal mucosa by mouth may sometimes yield diagnostic specimens, but attention should be paid to avoid causing intestinal perforation. Surgical exploration and biopsy of the resected intestinal specimen postoperatively are reliable diagnostic methods.

　　It is also important to differentiate this disease from other diseases. For example, bacterial dysentery, viral diarrhea, and Campylobacter jejuni enteritis. Bacterial dysentery is caused by Shigella, and diarrhea is often accompanied by purulent or mucous stools, less in quantity, and often with tenesmus, fever, and chills. Microscopic examination of feces can reveal a large number of pus cells, red blood cells, and phagocytes. Atypical dysentery in infants and children should be differentiated by etiological diagnosis. Viral diarrhea is diarrhea caused by intestinal virus infection, characterized by high communicability. Rotavirus, picornavirus, and other infections often present with vomiting followed by diarrhea, mostly watery with mucus, and occur mainly in autumn and winter. Other viral diarrhea is more common in summer and autumn, with symptoms of nausea, vomiting, and respiratory symptoms, pharyngitis, and possible paralysis, often affecting the neck and back muscles. Green watery stools or egg-shaped watery stools are common in children under one year old. Antibiotic treatment is generally ineffective, and the course of the disease usually resolves spontaneously within 5 to 7 days. Serological and viral isolation are used for further differentiation. Campylobacter jejuni enteritis is a mild disease caused by Campylobacter jejuni, which is similar to viral enteritis. Severe cases may be similar to ulcerative colitis or Crohn's disease. It presents with fever, watery or mucous stools, foul odor, and bile-like color, with purulent stools in severe cases, similar to dysentery, which usually recovers within one week. Children often have abdominal colic and may have seizures during high fever. The disease often occurs in contact with poultry, livestock, or consumption of unsterilized milk or raw water. Darkfield microscopy can detect the arrow-like active motility of Campylobacter, and bacterial culture is used for further diagnosis.

　　Therapeutic diet for congenital small intestinal atresia and intestinal stenosis:

　　Nutritional support: During the fasting period, water, electrolytes, and intravenous hyperalimentation are administered daily through the vein. Generally, it is only possible to start eating by mouth after 7 to 14 days postoperatively, when the intestinal function has recovered. The initial feeding volume is 5 to 10 ml, administered every 2 hours. If the child does not vomit, the feeding volume can be gradually increased. After 4 to 5 days since the start of feeding, the child can usually return to normal feeding.

　　There is no satisfactory drug treatment plan for this disease. Only some patients may respond to gluten-free diet, while most scholars still recommend that all patients with the disease should follow a gluten-free diet. Adrenal corticosteroids may have some therapeutic effect, but the long-term efficacy remains to be evaluated. For those with concurrent intestinal perforation or massive hemorrhage who do not respond to medical treatment, surgical treatment can be considered.

　　1. Preoperative preparation: For patients with good general condition, supplement an appropriate amount of 2:1 10% glucose solution with Ringer's solution or normal saline before surgery. Perform nasogastric decompression, intravenous vitamin C and K, inject antibiotics, and then perform surgery. If dehydration and electrolyte imbalance exist, correct dehydration and acidosis, provide oxygen and keep warm, transfuse an appropriate amount of fresh plasma or whole blood, and prepare for 3-4 hours before surgery.

　　2. Surgical method

　　(1) Single-type jejunoileal atresia surgery: Perform intestinal resection and end-to-end or end-to-oblique anastomosis for single jejunoileal atresia. After laparotomy, determine the location and type of atresia, the diameter and peristaltic condition of the proximal dilated intestinal tract, and whether there is inflammation, necrosis, or perforation. Then, check the diameter and length of the distal atresia intestinal tract, whether the mesentery is absent, and whether the colon is ectopic (malrotation). Excise 15-20cm of the proximal dilated intestinal tract, squeeze the intestinal contents into the atresia segment before excision. Cover the cut end of the intestinal tract with saline gauze. Lightly lift the blind pouch of the atresia distal end, insert a thin silicone tube or needle into the blind pouch, slowly inject normal saline, causing the distal small intestine to dilate until the saline enters the cecum. If suspected of associated colonic atresia, inject saline into the colon until the rectum to exclude multiple atresia. Withdraw the silicone tube, obliquely excise 2-3cm of the distal blind pouch intestinal tract, making the serosal side intestinal wall 45° oblique, continue to cut the serosal side intestinal wall to make the intestinal tract diameter close to the proximal intestinal tract. Suture with 5-0 non-traumatic silk thread, making one U-shaped suture on each side of the mesentery and serosal side through the muscularis mucosae. Use the single-layer interrupted inversion suture method. First suture the posterior wall, with the suture needle entering from the submucosa, exiting the serosa, passing through the opposite intestinal wall serosa, and exiting the submucosa. Tighten and tie the knot. Complete the end-to-oblique anastomosis of the anastomotic mouth and suture the mesenteric defect.

　　After anastomosis, check whether the anastomotic mouth is unobstructed or leaking, straighten the intestinal tract, and check for any concomitant anomalies. For meconium peritonitis, only release the adhesion sites that may cause obstruction, and do not over-operate. For malrotation of the intestine, perform Ladd surgery.

　　(2) Proximal jejunal atresia surgery: High jejunal atresia may lead to the expansion and thickening of the jejunal beginning even the duodenum. Simple intestinal anastomosis may cause postoperative obstruction due to poor peristaltic function of the preserved intestinal tract. It is necessary to first truncate or excise part of the dilated intestinal tract to promote the recovery of postoperative peristalsis.

　　①Proximal jejunal truncal成形术 and end-to-end anastomosis: Raise the blocked proximal jejunum, plan the length and range of truncal jejunal dilatation according to the diameter of the distal intestinal tract. Then, excise part of the jejunal serosal side wall to form a tail shape. Suture the intestinal wall to stop bleeding while excising, or use an automatic suture machine to suture. Excise the blind end of the distal intestinal tract and perform end-to-end or end-to-back anastomosis. To prevent obstruction caused by excessive curvature of the duodenojejunal flexure after jejunojejunostomy, the Treitz ligament needs to be released. Raise the transverse colon, incise the retroperitoneum 2-3cm transversely at the beginning of the jejunum, and expose the Treitz ligament. Tie and cut off each part attached to the jejunal wall, bluntly free the beginning of the jejunum to move the duodenal flexure downward, and suture the retroperitoneal incision longitudinally with fine silk thread. Pay attention to avoid the superior mesenteric artery and vein on the right side of the Treitz ligament during the operation and do not damage them.

　　② Anastomosis of Proximal Dilated Intestinal Tract by Folding and Suturing: The duodenojejunal flexure is fully mobilized, and the dilated intestinal wall is folded inward on the mesenteric side to reduce the caliber of the intestinal lumen. A continuous seromuscular layer suture with a 5-0 silk thread and a needle distance of 1 cm is performed. An end-to-end anastomosis is performed with the distal intestinal tract. After the anastomotic orifice is completed, one U-shaped suture passing through the seromuscular layer is placed on each side of the mesentery and the opposite mesentery to strengthen the anastomotic orifice to prevent leakage. This technique is recommended by Delorimier and Touloukian (1993). The advantage is to increase the surface area of the small intestinal mucosa, which is especially beneficial for cases that may develop short bowel syndrome.

　　③ Resection and Anastomosis of Dilated Intestinal Tract with Stent Tube: After the proximal dilated intestinal tract is resected and sutured, an end-to-end anastomosis is performed, and the silicone nasogastric tube (or gastrostomy tube) is placed into the distal intestinal lumen through the anastomotic orifice. The advantage is that it fully relieves pressure after surgery, ensuring the patency and healing of the anastomotic orifice. The disadvantage is that it increases the operation time, and the silicone tube may compress the small intestine.

　　(3) Apple Peel-like (Apple-Pee1) Aplasia Surgery: This type of aplasia is located in the proximal jejunum, with the distal intestinal mesentery free, and the small intestine surrounds the vascular branches in a spiral shape. The distance between the two blind ends of the atresia is large, increasing the difficulty of anastomosis during surgery. The general condition of the child is usually good, and the tail of the dilated proximal jejunum is trimmed and shaped, and anastomosed end-to-end or end-to-oblique with the distal intestinal tract. The anastomotic orifice is sutured with a single-layer interrupted mucosal inversion method, and the course of the intestinal tract is carefully straightened after anastomosis to prevent torsion. In children with low birth weight, multiple congenital malformations, or poor overall condition, a simple surgical technique should be adopted, and Santulli stoma surgery can be performed. The dilated proximal intestinal tract is anastomosed to the distal intestinal tract in a T-shaped lateral side-to-side manner, and a stoma is created in the proximal segment of the intestinal tract. Bishop-Koop stoma surgery can also be performed, with the proximal intestinal tract and the distal jejunum anastomosed in an inverted T-shaped end-to-side manner, and a stoma is created in the distal intestinal tract. Parenteral nutrition is given postoperatively, and the stoma closure surgery is performed 2 to 3 months later after the overall condition of the body improves.