Congenital gastric outlet obstruction

　　1. Etiology

　　The cause is still unclear. It is speculated that the development of the endodermal tube is interrupted before the 8th week of embryogenesis, leading to rupture and atresia. After 8 weeks, the elongated endoderm connects to form a septum. Some people also believe it is related to the abnormal cavitation process of the digestive tract. At present, most scholars believe that the etiology of the disease is similar to that of congenital intestinal atresia and stenosis, occurring during the embryonic period.

　　Cavity formation disorder during the development of the foregut. Some believe that there may be vascular malformations, infarction leading to gastric necrosis forming occlusion and stenosis; in recent years, some have reported that the fetus has an epidermolysis bullosa through fetal endoscopy, which may involve the pyloric mucosa and form scars leading to pyloric atresia and stenosis. Some have collected 81 cases with familial pyloric atresia, considering it an autosomal recessive hereditary disease. In type 4, the most common is pyloric membrane atresia or stenosis, which, together with pyloric antrum membrane atresia or stenosis, is also called gastric diaphragm. This section focuses on the introduction of this disease.

　　2. Pathogenesis

　　The diaphragm in the stomach is usually located 1.5-3 cm before the pylorus or close to the pylorus, and there may also be two diaphragms, one located several centimeters away from the pylorus in the duodenum, separating the stomach and duodenum. The diaphragm may have a hole (narrowing) or no hole (occlusion). It is 2-3 mm thick and consists of mucosa, submucosal tissue, and muscular layer. Both sides are covered with mucosa, and the space is filled with loose connective tissue.

　　Complications may include malnutrition, growth and development disorders, dehydration, alkalosis, anemia, and others. The course of the disease is long, and the patient gradually appears general fatigue, weight loss, weight loss, less urine, constipation, and sometimes symptoms such as mental disorders and tetany.

　　The disease is more common in premature infants, most of whom have a history of polyhydramnios, a large diaphragmatic orifice that can pass through food, and may be asymptomatic. If the diaphragmatic orifice is small or secondary inflammation causes mucosal edema to narrow the orifice, it can cause obstruction symptoms, and vomiting occurs soon after birth, vomiting after feeding, showing ejection vomiting containing milk and milk clots, without bile and blood. Vomiting is often intermittent, accompanied by decreased appetite, weight loss, generally lower than the standard weight by 10% to 15%, and some even lower by 25% to 40% or more. Crying and restlessness after eating, vomiting after relief, and intractable vomiting can lead to dehydration, alkalosis, malnutrition. Physical examination shows abdominal distension in the upper abdomen, with gastric shape, gastric peristalsis waves, flat middle and lower abdomen, and if the diaphragmatic orifice is absent (completely occluded), symptoms of high obstruction may appear earlier. If there are two diaphragms, the lower stomach and upper duodenum isolated will become dilated, filled with secretions, forming a cystic mass that can be felt in the upper abdomen.

　　The etiology of congenital pyloric stenosis is not yet fully clear, so there is no effective preventive measure. Some scholars believe that the disease is an autosomal recessive hereditary disease, and genetic counseling should be done well.

　　1. Blood examination

　　There is a decrease in plasma protein and hemoglobin, and alkalosis is common; blood sodium, potassium, chloride, calcium, and blood pH should be checked.

　　2. X-ray examination

　　Visible gastric bubble shadow, no air-filled shadow in the middle and lower abdomen, normal size of the stomach, a narrowing can be seen 1-2 cm before the pylorus, the normal pyloric sphincter and duodenal bulb shadow can be displayed through the diaphragmatic orifice, the diaphragmatic septum in the stomach is completely occluded and can be confirmed through upper gastrointestinal barium meal, gastroscopy diagnosis, barium swallow examination, the antrum of the stomach is blind-ended, and the small colon can be displayed by barium enema.

　　1. Protect the gastric mucosa, avoid high salt, hard, hot, excessive drinking and eating, eat less and more meals, eat at regular times and in fixed amounts, and eat easily digestible food.

　　2. The food should be fresh, and more fresh vegetables and fruits should be eaten to increase the intake of high-quality protein.

　　3. Patients with gastric outlet obstruction often have symptoms such as fullness and pain in the epigastrium, which are caused by indigestion; common symptoms such as nausea, vomiting, and anorexia should be treated with light, appetizing, and easy-to-digest foods.

　　4. After the operation for gastric outlet obstruction, the diet should be adjusted to high-nutrition and low-irritating foods. It is better to choose staple foods that the patient is accustomed to, and add millet porridge and glutinous rice porridge, which is beneficial and harmless. The side dishes should be fresh meat, eggs, vegetables, and fruits. After the operation, the patient should have 3 to 5 meals a day, and the amount of food should gradually increase. Many patients can recover to the preoperative food intake after half a year. If there are phenomena of nausea and vomiting after meals, there is no need to be anxious, just sit for a while or take a slow walk, and the symptoms can be relieved. You can also take a decoction of 10 grams of ginger frequently.

　　1. Treatment

　　Surgical treatment should be performed for all types of pyloric atresia and stenosis. Blind-end atresia should be treated with duodenal-jejunal anastomosis or end-to-side anastomosis, which is anatomically and physiologically reasonable and has a good effect. For those with atresia or stenosis of the pylorus or pyloric sinus, a valve resection and pyloroplasty should be performed, and a multi孔 gastrointestinal decompression tube should be sent to the duodenal segment during surgery. In the neonatal period, due to the small lumen of the pylorus and the edema and hypertrophy of the valve, it is not easy to resect the valve, and a pyloroplasty can be performed by simply incising the valve, which can also achieve a good effect.

　　2. Prognosis

　　The cure rate of this disease in the past was 80%, and we have collected 29 cases which were all cured. From 1976 to 1987, China Medical University treated a total of 10 cases, including 5 cases of pyloric valve stenosis and 5 cases of pyloric sinus stenosis. Two neonates had a very small central aperture of the pyloric valve, about 0.2cm, and were admitted with high intestinal obstruction. The diagnosis was confirmed by barium meal gastrointestinal examination and intraoperative determination. All cases were treated by surgery, and all were cured and discharged after a smooth postoperative course. Four cases were followed up for 2 to 12 years, and the children fully recovered to normal 1 to 2 months after discharge, with good growth and development and intelligence.