Pyloric mass

Introduction Congenital hypertrophic pyloric stenosis is a common disease in the neonatal period. The success of the treatment of pyloric stenosis is one of the great achievements of surgery in this century. There are different morbidity rates depending on geography, seasonality and ethnicity. The European and American countries are higher, about 2.5 to 8.8 , and the Asian region is relatively low. The incidence rate in China is 3 . Mostly male, the ratio of male to female is about 4 to 5:1, and even as high as 9:1. More common in the first child, accounting for 40 to 60% of the total number of cases. According to the typical clinical manifestations, three major signs such as gastric peristalsis, sputum and pyloric mass and jet vomiting can be seen, and the diagnosis can be confirmed. The most reliable diagnosis is based on a pyloric mass.

Cause

The cause of the pyloric mass:

In order to clarify the etiology and pathogenesis of pyloric stenosis, a lot of research work has been carried out over the years, including pathological examination, establishment of animal models, detection of gastrointestinal hormones, virus isolation, genetic research, etc., but the cause is still inconclusive.

(1) Genetic factors: plays a very important role in etiology. The onset is obviously familial, and even a mother and 7 sons are ill, and the single-oval twins are more common than the double-oval twins. The incidence of children with a history of pyloric stenosis in parents can be as high as 6.9%. If the mother has this medical history, the probability of her child disease is 19%, and her female is 7%; the father has a history of 5.5% and 2.4%, respectively. Studies have shown that the genetic mechanism of pyloric stenosis is polygenic, neither recessive nor non-sexual, but a directed gene consisting of a dominant gene and a sexually modified multifactor. This genetic tendency is affected by certain environmental factors, such as social class, diet, and various seasons. The incidence is high in spring and autumn, but the relevant factors are unknown. It is common in high-weight male infants, but it has nothing to do with the length of gestational age.

(B) nerve function: mainly engaged in the pyloric myenteric plexus researchers, found that ganglion cells do not mature until 2 to 4 weeks after birth, therefore, many scholars believe that neuronal dysplasia is the mechanism that causes pyloric muscle hypertrophy, While denying the theory of lesions caused by degeneration of pyloric ganglion cells in the past, histochemical analysis was used to determine the activity of enzymes in pyloric ganglion cells. However, there were also disagreements. It was observed that ganglion cells with pyloric stenosis were not identical to fetuses. If the ganglion cell dysplasia is the cause, the premature infant should have more morbidity than the full-term infant, but there is no difference between the two. In recent years, it is suggested that the structural changes and dysfunction of peptidergic nerve may be one of the main causes. The number of neuropeptides containing enkephalin and vasoactive intestinal peptide in the ring muscle was significantly reduced by immunofluorescence technique, and the tissue was determined by radioimmunoassay. The substance P content is reduced, and it is speculated that changes in these peptide nerves are associated with pathogenesis.

(3) Gastrointestinal hormones: There are experiments to give pentagastrin gastrin to pregnant dogs. As a result, the proportion of pyloric stenosis in the puppies is very high. It was found that the concentration of serum gastrin in pregnant women was relatively high at the end of pregnancy from March to April. According to this, pregnant women in the late pregnancy due to emotional anxiety caused by elevated serum gastrin concentration, and through the placenta into the fetus, the fetal genetic genetic role, causing long-term pyloric obstruction, pyloric expansion and stimulate G cells secrete gastrin, Thus the disease. However, other scholars repeatedly measured gastrin, some reported increased, and some did not change abnormally. Even in cases of elevated gastrin, it is not possible to infer whether it is the cause or result of pyloric stenosis, because in some cases 1 week after surgery, gastrin returned to normal levels, and some increased. In recent years, gastrointestinal stimulating hormone has been studied, and the concentrations of prostaglandins (E2 and E2a) in serum and gastric juice have been determined, suggesting that the content of gastric juice in children is significantly increased, suggesting that the pathogenesis is that the local hormone concentration in the pylorus muscle layer is increased and the muscles are continuously stressed. State, and cause disease. There have also been studies on serum cholecystokinin, and there have been no abnormal changes.

(4) Muscle functional hypertrophy: Some scholars have observed through careful observation that some infants born 7 to 10 days will force the curd block to pass through the narrow pyloric tube. It is believed that this mechanical stimulation can cause mucosal edema to thicken. On the other hand, it also causes dysfunction of the cerebral cortex to the internal organs, causing paralysis of the pylorus. Two factors contribute to the formation of severe obstruction of the pyloric stenosis and symptoms. However, there are also negative opinions. It is not appropriate to think that pyloric fistula first causes functional hypertrophy of pyloric muscles, because hypertrophic muscles are mainly ring muscles, and sputum should cause some early symptoms, but early in some vomiting episodes In the case of surgery, a mass has usually been formed, and the size of the mass has nothing to do with the length of the disease. Pyloric obstruction is manifested when muscle hypertrophy reaches a certain critical value.

(V) Environmental factors: The incidence rate has obvious seasonal peaks, mainly in spring and autumn. In the biopsy tissue sections, there are white blood cell infiltration around the ganglion cells. It is speculated that it may be related to viral infection, but the detection of coxsackie virus in the blood, feces and pharynx of the child and his mother was not detected. There was no change in the detection of serum neutralizing antibodies. No pathological changes were observed in animals infected with Coxsackie virus, and the study is continuing.

The main pathological change is hypertrophy of the pyloric muscle layer, especially in the ring muscle, but also in the longitudinal muscles and elastic fibers. The pylorus is olive-shaped and hard and elastic. It is harder when the muscles are paralyzed. It is generally 2 to 2.5 cm long, 0.5 to 1 cm in diameter, and 0.4 to 0.6 cm in thickness. It is larger in older children. However, the size has nothing to do with the severity of the symptoms and the length of the disease. The surface of the mass is covered with a peritoneum and is very smooth, but the blood supply is partially blocked because of the pressure, so the color appears pale. Ring muscle fibers increase and hypertrophy, muscles are like gravel hard, thick muscle layer squeezes the mucous membranes as vertical folds, making the lumen narrow, mucosal edema, inflammation later, making the lumen more small, pylorus on the autopsy specimen Only 1mm probe can be passed. When the narrow pyloric tube moves to the antrum of the stomach, the cavity gradually tapers and the thick muscle layer gradually becomes thinner, and there is no precise boundary between the two. However, the lateral boundary of the duodenum is obvious. Because the muscularis of the stomach wall is not continuous with the muscular layer of the duodenum, the hypertrophic pyloric mass suddenly terminates and protrudes into the duodenal cavity, resembling a cervical-like structure. Histological examination showed muscle hyperplasia, hypertrophy, disordered muscle fibers, mucosal edema, and congestion.

Due to pyloric obstruction, proximal gastric dilatation, wall thickening, increased mucosal folds and edema, and due to retention of gastric contents, often lead to mucosal inflammation and erosion, and even ulcers.

an examination

Related inspection

Gastrointestinal CT examination, fiberoptic examination, gastric ultrasound, gastric barium meal angiography

Examination and diagnosis of pyloric mass:

According to the typical clinical manifestations, three major signs such as gastric peristalsis, sputum and pyloric mass and jet vomiting can be seen, and the diagnosis can be confirmed. The most reliable diagnosis is based on a pyloric mass. If the lumps are not accessible, a real-time ultrasound or barium meal check can be performed to help confirm the diagnosis.

(1) Ultrasound examination: The diagnostic criteria for the three indicators reflecting the pyloric mass are pyloric muscle thickness 4 mm, pyloric tube length 18 mm, and pyloric tube diameter > 15 mm. A stenosis index of more than 50% has been proposed as a diagnostic criterion. Can also pay attention to observe the opening and closing of the pyloric tube and food passage, it was found that a few cases of pyloric tube open normal: called non-obstructive pyloric hypertrophy, follow-up observation of the mass gradually disappeared.

(B) barium meal examination: the main basis for diagnosis is pyloric lumen growth (> 1cm) and narrow (<0.2cm). It can also be seen that the stomach is dilated, the gastric peristalsis is enhanced, and the pyloric mouth is closed, which is "bird-like", and the gastric emptying is delayed. Some patients followed up and reviewed the cases after pyloric muscle incision. This sign has been seen for several days. Later, the pyloric tube becomes shorter and wider, and may not return to normal. After the examination, the expectorant should be aspirated through the gastric tube and washed with warm saline to avoid vomiting and aspiration pneumonia.

Symptoms appear 3 to 6 weeks after birth, but also earlier, and very few occur after 4 months. Vomiting is the main symptom, initially only back to milk, followed by jet vomiting. Occasionally, vomiting occurs at the beginning. As the obstruction worsens, vomiting is performed almost every time after feeding. The vomit is mucus or milk. When the stomach stays for a long time, the curd is spit out and contains no bile. In a small number of cases, due to irritative gastritis, the sputum contains fresh or degenerative blood. It has been reported that in cases of pyloric stenosis, a large number of hematemesis of gastric ulcer in the neonatal period of high gastric acid, and duodenal ulcers have also been reported. After vomiting, the baby still has a strong appetite, and if he is still breastfeeding, he can still suck hard. The symptoms of immature children are often atypical, and jet vomiting is not significant.

As vomiting intensifies, due to insufficient intake of milk and water, the body weight does not increase at first, followed by a rapid decline, the urine volume is significantly reduced, and the bowel movement is performed once a few times, the amount is small and the quality is hard, and occasionally the brownish green is discharged, which is called hunger. Stool. Due to malnutrition, dehydration, the baby is obviously thin, the skin is loose and wrinkled, the subcutaneous fat is reduced, and the depression is distressed. At the beginning of the onset, vomiting loses a lot of stomach acid, which can cause alkalosis, slow and slow breathing, and may have symptoms such as throat and hand, foot and ankle. After dehydration is severe, kidney function is low, acidic metabolites are retained in the body, and some alkaline substances are neutralized. Therefore, there are few people with obvious alkalosis. Late cases of severe malnutrition are hard to see.

Place your abdomen in a comfortable position. You can lie on your mother's lap. The abdomen is fully exposed. Under bright light, when you are feeding sugar water, you can see the stomach and peristaltic waves. The waveform appears under the left costal margin. Slowly over the upper abdomen, one or two waves advance, and finally disappear to the right side of the umbilicus. The examiner is located on the left side of the baby. The technique must be gentle. The left hand is placed on the outer edge of the rectus abdominis of the right costal margin. Press the rectus abdominis with the index finger and the ring finger. Use the middle finger to gently touch the deep part to touch the olive. Smooth and hard pyloric mass, 1 to 2 cm in size. After vomiting, the stomach is emptied and the abdominal muscles are temporarily relaxed. Occasionally, the tail or right kidney of the liver is mistaken for a pyloric mass. However, if the abdominal muscles are not slack or the stomach is dilated, it may not be able to be removed. After the stomach tube is emptied, the sugar water is fed while sucking and checking. It is necessary to check repeatedly with patience. According to experience, most cases can reach the mass.

Laboratory tests can find that infants with clinically dehydrated water have varying degrees of hypochlorine alkalosis, elevated blood Pco2, elevated pH and low serum chlorine. It must be recognized that metabolic alkalosis is often accompanied by low potassium, and the mechanism is still unclear. A small amount of potassium is lost with the gastric juice. When the sputum poisoning, the potassium ions move into the cells, causing high potassium in the cells, while the extracellular potassium is increased, and the potassium in the renal distal convoluted epithelial cells is increased, so that the blood potassium is lowered.

Differential diagnosis

Symptom identification of pyloric mass confusing:

Differential diagnosis of pyloric mass: should be differentiated from various diseases such as improper feeding, systemic or local infection, pneumonia and congenital heart disease, central nervous system disease that increases intracranial pressure, progressive kidney disease, infectivity Gastroenteritis, various intestinal obstructions, endocrine diseases, and gastroesophageal reflux and esophageal hiatus hernia.

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