Postoperative complications of pyloric stenosis

Pyloric stenosis mostly occurs in infants. If the child still vomits and spits up frequently one month after birth, it may be caused by this reason. Pyloric stenosis may be caused by incomplete functional development of the pyloric nerves. This situation may cause eating problems for children, and they may suffer from malnutrition. This requires parents to always pay attention to their children's physical changes and seek medical attention in time for any abnormalities.

Surgical Procedure

If the duodenum is inadvertently entered, the enamel membrane should be closed with a good suture and covered with an omentum patch. If the muscle incision is damaged or if the mucosal injury is extensive, the incised muscle should be sutured. Make a second parallel muscle incision at 45 to 180 degrees of the original incision.

Postoperative precautions

Postoperative gastric obstruction will last for 8 to 12 hours, and all patients will experience varying degrees of gastric relaxation. Therefore, glucose, water, or electrolyte solution can be given 6 to 6 hours after surgery. At the beginning, feed in small amounts (15 to 30 ml every 2 to 3 hours). The amount and concentration of the diet can be gradually increased over the next 24 hours. A small amount of vomiting is not uncommon (20%) and should not cause panic unless the vomiting is persistent. If gastric outlet obstruction persists for 10 to 14 days after surgery, the possibility of incomplete pylorostomy should generally be considered.

Etiology hypothesis

Although the cause of hypertrophic pyloric stenosis is unknown, several hypotheses have been proposed. In 1960, Lynn suspected that cheese production through the narrow pyloric duct caused edema and swelling leading to complete obstruction. If this hypothesis is correct, why don't all newborns have the disease? So a familial or genetic tendency must exist. Postnatal pyloric hypertrophy in response to congenital delayed opening of the pyloric sphincter has been suggested as a possible pathogenic mechanism. Recently, researchers have pointed out that the lack of nitric oxide production is a factor in the pathogenesis of hypertrophic pyloric stenosis. Nitric oxide acts as a smooth muscle relaxant and appears to play an important role in the relaxation of the mammalian digestive tract. Studying pyloric tissue obtained from nine newborns with hypertrophic pyloric stenosis, Vanderwinden and colleagues found a reduced capacity for nitric oxide synthesis. The researchers suggest that decreased nitric oxide production may be responsible for the pyloric spasm observed in HPS.