Congenital hypertrophic pyloric stenosis is a common disease in the neonatal period. It is predominantly male, with a male-to-female ratio of about 4-5:1, or even up to 9:1. It is mostly seen in the first child, accounting for 40-60% of the total number of cases. The diagnosis can be established based on the typical clinical manifestations, the three main signs such as gastric peristaltic waves, pyloric masses and ejection vomiting. The most reliable diagnosis is based on palpation of the pyloric mass. Diagnosis of pyloric mass: 1. Gastroesophageal reflux Due to the hypoplastic lower esophageal sphincter, the gastric cardia lacks muscle tone and is often in an open state. The sick child mostly vomits within a few days after birth, especially after feeding the sick child is placed flat vomiting occurs, such as standing the sick child upright can be prevented. Barium meal X-ray fluoroscopy to see the cardia open, the contrast agent reflux into the esophagus can confirm the diagnosis. 2, improper feeding due to feeding too much, too fast, or artificial feeding due to bottle tilt bottle gas into the stomach, or improper placement after feeding, etc., are common causes of vomiting in newborns. If the vomiting is caused by improper feeding, too much milk should be fed too quickly, and the vomiting can be stopped by carrying the baby in your arms after feeding and gently patting the back so that the gas accumulated in the stomach is expelled. 3, esophageal hiatal hernia refers to the abdominal organs (mainly the stomach) through the diaphragmatic esophageal hiatus into the thoracic cavity caused by the disease. Esophageal hiatal hernia is the most common type of diaphragmatic hernia, reaching more than 90%. Patients with esophageal hiatal hernia can be asymptomatic or mildly symptomatic, and the severity of their symptoms is independent of the size of the hernia sac and the severity of esophageal inflammation. It is important to distinguish between hiatal hernia and reflux esophagitis, which can exist simultaneously or separately. The pyloric mass is hypertrophic, especially in the cricoid muscle, but also in the longitudinal muscle and elastin fibers. The pylorus is olive-shaped, hard and elastic. It is more rigid when the muscle is in spasm. It is usually 2-2.5 cm long, 0.5-1 cm in diameter, and 0.4-0.6 cm thick, with larger masses in older children. However, the size was not related to the severity of symptoms and the duration of the disease. The surface of the mass is covered with peritoneum and is smooth, but the blood supply is partially obstructed by pressure, so the color appears pale. The thickened muscle layer squeezed the mucosa in longitudinal folds, making the lumen narrow, and the mucosal edema and later inflammation made the lumen even smaller, so that only a 1-mm probe could be passed through the pylorus on the autopsy specimen. The lumen of the narrow pyloric duct gradually widens as it moves toward the gastric sinus, while the hypertrophic muscular layer gradually thins, with no precise demarcation between the two. However, in the duodenal side, the boundary is obvious, because the muscle layer of the gastric wall is not continuous with the duodenal muscle layer, and the hypertrophic pyloric mass abruptly terminates and projects into the duodenal lumen, resembling a cervical-like structure. Histological examination showed hyperplasia and hypertrophy of the muscular layer, disorganized arrangement of muscle fibers, and edema and congestion of the mucosa. Due to pyloric obstruction, the proximal stomach is dilated, the wall is thickened, the mucosal folds are increased and edematous, and the retention of gastric contents often leads to mucosal inflammation and erosion, and even ulceration.