gastric muscle defect
Introduction
Introduction Most of the muscle wall defects in the stomach wall are congenital gastric wall muscle defects. Congenital defects of gastric musculature refers to the muscle wall defects caused by embryonic developmental disorders. Congenital gastric wall muscle defects are rare in clinical practice and are the most common cause of spontaneous gastric perforation in neonates. The mortality rate is extremely high, and it is still 35% to 72%.
Cause
Cause
The cause of muscle wall defect in the stomach wall:
(1) Causes of the disease
There are several theories about the causes of congenital gastric wall muscle defects.
1. Embryonic development abnormality During the development of the embryo, the ring muscle of the stomach wall first occurs, starting at the lower end of the esophagus, gradually developing to the fundus and the large curved part of the stomach. At the 9th week of the embryo, the oblique muscle appears, and finally the longitudinal muscle is formed. If a developmental disorder occurs at a certain stage, it will result in a muscular layer defect in the stomach wall.
2. Gastric wall ischemia In perinatal respiratory disorders, hypothermia and hypoxemia, the baby can re-distribute the modern compensatory blood, increasing the blood supply to vital organs such as the brain and heart, and the blood of the stomach and intestines. The supply is significantly reduced, causing ischemic necrosis of the gastrointestinal tract.
3. Increased intragastric pressure is the main factor that promotes perforation. The submucosal tissue of newborns is fragile, the elastic fibers are underdeveloped, and gastric expansion is prone to occur. If the stomach contents of the child are delayed, breastfeeding, sucking, and swallowing air during crying, the gastric pressure can be increased, the stomach can be dilated, and finally the muscle wall defect of the stomach wall is broken.
(two) pathogenesis
The main pathological changes were muscle wall defects in the stomach wall. The most common site was the large curvature of the stomach, followed by the anterior wall of the stomach, the cardia, the bottom, the small curve, the posterior wall, and the pylorus. The size of the defect range is not equal. There are only mucosa, submucosa and serosa at the defect. Any factors that increase the intragastric pressure after birth, such as: swallowing air, milking or crying, vomiting, gastric lavage, mask pressure, oxygen, etc. can cause a sudden increase in intragastric pressure, and the lesion is protruding outward, showing a diverticulum kind. If the pressure is constantly increasing, it will affect the blood circulation, causing necrosis of the stomach wall which is deficient in the muscular layer. The edges of the perforations are irregular and appear black and yellow necrosis. Abnormal mucosa, muscle layer and blood vessels near the perforation. The muscle layer of the perforated margin gradually became thinner, and the muscle layer of the perforation was interrupted and absent. The mucosa near the hole is thinned, the lower layer of the mucosa is thin, and the stomach gland is poorly developed. The abnormal size of the vascular wall in the mucosa and submucosal tissues is monolayer, blood vessel congestion, dilatation, and hemorrhage. No inflammatory changes. The perforations vary in size and can be multiple.
Examine
an examination
Related inspection
Gastric examination, gastroscopy, electronic gastroscope, gastroscope
Diagnosis of gastric wall muscle defect:
Congenital gastric wall muscle defect is not easy to diagnose before perforation. The general condition of the child is good after birth, no obvious prodromal symptoms, and a history of normal fetus. It usually occurs 3 to 5 days after birth. There are also individual cases as early as the 2nd day or late to the 8th day. Acute onset, sudden onset of acute abdomen, refusal of milk, vomiting, vomit is yellow-green or brown, low crying, listlessness, progressive bloating, difficulty breathing, bruising. In the advanced stage, there may be manifestations of peritonitis, fever, intestinal paralysis, dehydration, electrolyte imbalance, and shock. Physical examination revealed shortness of breath, loss of bowel sounds, obvious abdominal distension, abdominal wall venous engorgement, abdominal, waist, scrotal skin edema, disappearance of liver dullness, and positive abdominal dullness. After perforation for 12 hours, the abdominal wall may appear purple, bright and edema, and mild muscle tension and other peritonitis. Abdominal puncture can suck out gas or pus, feces, and the like. Perforation often occurs within 1 week after birth, and most of it is 3 to 5 days.
Early neonates, especially premature infants, suddenly develop progressive bloating 3 to 5 days after birth, accompanied by vomiting, difficulty breathing, cyanosis, liver dullness disappeared, and bowel sounds disappeared. The disease may be considered. If perforated, the abdominal X-ray is a large amount of gas and liquid. In the standing position, the diaphragm is elevated, and there is a large amount of free gas in the infraorbital and abdominal cavity. The liver and spleen shadows on both sides moved to the sides of the mid-abdominal spine, the stomach bubble disappeared, and the intestinal inflated was less. The fluid accumulates in the lower abdomen, showing a fluid level across the entire abdomen. When the perforation or perforation is small, only the gastric dilatation is weak and the shape is special. Barium meal angiography showed weak gastric peristalsis, marked expansion, and delayed pyloric opening.
Diagnosis
Differential diagnosis
Differential diagnosis of gastric wall muscle defects:
1. Perforation caused by gastric perforation, mechanical damage, intestinal obstruction, etc. caused by other causes in the neonatal period.
2. Children with meconium peritonitis often have no meconium, or less meconium discharge, X-ray shows intestinal adhesion, intestinal lumen inflation, multiple fluid level, less free gas in the abdominal cavity, underarm, normal stomach bubble . Calcification is sometimes seen.
Diagnosis: Congenital gastric wall muscle defect is not easy to diagnose before perforation. The general condition of the child is good after birth, no obvious prodromal symptoms, and a history of normal fetus. It usually occurs 3 to 5 days after birth. There are also individual cases as early as the 2nd day or late to the 8th day. Acute onset, sudden onset of acute abdomen, refusal of milk, vomiting, vomit is yellow-green or brown, low crying, listlessness, progressive bloating, difficulty breathing, bruising. In the advanced stage, there may be manifestations of peritonitis, fever, intestinal paralysis, dehydration, electrolyte imbalance, and shock. Physical examination revealed shortness of breath, loss of bowel sounds, obvious abdominal distension, abdominal wall venous engorgement, abdominal, waist, scrotal skin edema, disappearance of liver dullness, and positive abdominal dullness. After perforation for 12 hours, the abdominal wall may appear purple, bright and edema, and mild muscle tension and other peritonitis. Abdominal puncture can suck out gas or pus, feces, and the like. Perforation often occurs within 1 week after birth, and most of it is 3 to 5 days.
Early neonates, especially premature infants, suddenly develop progressive bloating 3 to 5 days after birth, accompanied by vomiting, difficulty breathing, cyanosis, liver dullness disappeared, and bowel sounds disappeared. The disease may be considered. If perforated, the abdominal X-ray is a large amount of gas and liquid. In the standing position, the diaphragm is elevated, and there is a large amount of free gas in the infraorbital and abdominal cavity. The liver and spleen shadows on both sides moved to the sides of the mid-abdominal spine, the stomach bubble disappeared, and the intestinal inflated was less. The fluid accumulates in the lower abdomen, showing a fluid level across the entire abdomen. When the perforation or perforation is small, only the gastric dilatation is weak and the shape is special. Barium meal angiography showed weak gastric peristalsis, marked expansion, and delayed pyloric opening.
