Peptic ulcer in children

Introduction to Pediatric Peptic Ulcer Pepticulcer is not common in early childhood, and there are many cases in adolescents. In recent years, due to the wide application of endoscopes in the clinic, the incidence rate has increased. Children in all age groups can become ill, to newborns and the elderly. More common. Gastric ulcers often occur in small infants, mostly stress ulcers, and duodenal ulcers occur mostly in older children. The average incidence of duodenal ulcer in children is about 3 to 5 times higher than that of gastric ulcer. There are more boys than girls, and the general statistics are about 2:1. It is reported that 21% to 50% of adult cases begin in childhood. 1.6% started before the age of 4. Acute peptic ulcer in children is more than chronic ulcer, secondary to more than primary. Often secondary to severe hypoxia or severe infections (sepsis, pneumonia, gastroenteritis, meningitis), severe malnutrition, large amounts of long-term use of corticosteroids, extensive burns (Curlign's ulcer), neurological damage (cranial When damage, encephalitis, brain tumors and the like are involved in the thalamus, especially in the late stage of the disease, Rokitansky-Cushing's ulcer may be complicated. basic knowledge Sickness ratio: 0.1% Susceptible people: young children Mode of infection: non-infectious Complications: anemia, gastric perforation, pyloric obstruction

Pediatric peptic ulcer etiology

Causes

There are many causes of peptic ulcer, such as heredity, spirit, environment, diet, smoking, endocrine and other factors. So far, there is no conclusion. The pathogenesis tends to be attack factor-defense factor imbalance theory. Under normal circumstances, gastric mucosa secretes mucus, good Defensive factors such as blood transport, vigorous cell renewal ability and regulation mechanism of gastric juice secretion are superior, or balanced with attack factors such as hydrochloric acid, pepsin, and Hp. Once the attack factor is enhanced and/or the defense factor is weakened, ulcers may form. It is currently believed that among the above factors, two major environmental factors are important for the onset of most ulcer patients, namely the use of Helicobacter pylori infection and aspirin (ASA) or other non-steroidal anti-inflammatory drugs (NSAIDs). The cause of familial ulcer disease is related to heredity and is also associated with cross-infection of Helicobacter pylori in family members.

Harmful factors causing peptic ulcer

The basic factor in the development of peptic ulcer is an increase in gastric acid-pepsin secretion.

Gastric acid (20%):

In 1910, Schwartz put forward the famous saying "no acid and no ulcer", which is still correct. Gastric acid is secreted by parietal cells of gastric mucosa. There are three receptors on the parietal cells, namely acetylcholine receptor, gastrin receptor and histamine receptor. These three receptors produce an acid-secreting effect after stimulation with the corresponding substances acetylcholine, gastrin and histamine, and vagal activity is also associated with gastric acid secretion.

1 wall cell acid secretion process can be divided into 3 steps:

A. Histamine, a cholinergic transmitter or gastrin binds to a corresponding receptor on the membrane side of the cell bottom.

B. Mediated by the second information (AMP, Ca2), the stimulation signal is transmitted from the intracellular to the apical membrane of the cell.

C. Under stimulation, transfer H-K-ATPase to secretory microtubules, pump H from the cytosol to the gastric cavity to produce gastric acid. In general, histamine, acetylcholine and gastrin promote gastric acid secretion separately. In addition, there is synergy.

2 Normal daily average gastric juice secretion of 1000 ~ 1500ml, hydrochloric acid 40mmol / L, duodenal ulcer (DU) patients daily gastric secretion of 1500 ~ 2000ml, hydrochloric acid 40 ~ 80mmol / L, and gastric ulcer (gaseric ulcer , GU) patients daily gastric secretion and hydrochloric acid in the normal range, gastric acid secretion changes with age, the gastric juice is alkaline when the child is born, 24 to 48h free acid secretion peak, which is considered to be from the mother gastrin There is a direct relationship between the placenta, 2 days later, the mother's gastrin is reduced, the stomach acid is reduced, and it rises after 10 days, and the low level is 1 to 4 years old, and gradually increases after 4 years old, so the newborn can develop acute gastric ulcer after 2 days of birth. Gastric perforation, due to increased gastric acid secretion with age, older children with more peptic ulcers than infants.

3 reasons for increased gastric acid:

A. The number of parietal cells increased: 1.09 × 109 for normal males and 0.82 × 109 for females, and 1.8 × 109 for DU (more than 1 fold), and GU was 0.8 × 109 (close to normal).

B. Gastrin: human gastrin G17 (highest gastric antrum) or G34 (highest duodenum), no increase in gastrin in DU patients, it is suggested that the increase of gastric acid secretion in DU patients may be related to parietal cells Gastrin stimulating sensitivity, Isenberg and Grossman, have injected 8 different doses of gastrin into patients with DU and non-ulcer (NUD), resulting in a maximum effective gastric acid secretion (MAO), a half effective amount of gastrin NDU The mean value was 148.2±30.3, and the DU was 60.5±9.6, indicating that the excessive acid secretion of DU patients is caused by the sensitivity of parietal cells to gastrin.

C. Other factors driving the increase of gastric acid secretion: nerve, endocrine, paracrine and other factors can affect the increase of gastric acid secretion, and the tension of the secretion of basic gastric acid secretion in patients with peptic ulcer increases, and the sensitivity also increases.

Pepsin (15%):

The main cells of the gastric wall secrete pepsinogen, and according to immunochemical typing, they are divided into proproteinase I (PGI) and proproteinase II (PGII). There are five subtypes of PGI, which are distributed in the main cells of the stomach, and PGII is present in the stomach. Gastric sinus, the application of radioimmunoassay can measure the increase of PGI in the blood of 30% to 50% DU patients.

When it reaches 130g/L, its risk of DU is 3 times higher than that of normal people, and the risk of GU is increased by 3 times when PGII is increased.

The digestion of pepsin is closely related to gastric acid. When the pH of gastric acid is 1.8-2.5, the activity of pepsin is optimal. When pH>4, pepsin loses activity and does not digest, so digestion must be sufficient. The acid can make the pepsin be activated when the pH reaches 3 or less. The stomach acid and pepsin act together to produce ulcers, but gastric acid is the main factor. The pepsin content in the gastric juice is very small when the child is born, and then slowly increases until the puberty reaches the adult level.

Bile acid salt (10%):

The relationship between bile and gastric ulcer has been reported. In the dysmotility of the gastric antrum or duodenum, bile nausea causes gastric mucosal damage, especially bile and pancreatic juice mixed with each other in the duodenum to form lysolecithin. Destruction of the gastric mucosal barrier, so that the hydrogen ions are reversely dispersed to damage the gastric mucosa. It is believed that the damage of bile to the gastric mucosa is mainly caused by bile acid (bile salt), which increases the reverse diffusion of hydrogen ions in the stomach. The effect of reducing the potential difference of mucosa is closely related to the acidic environment and the concentration of bile in the stomach. Animal experiments show that the reverse diffusion of hydrogen ions in the high concentration of bile and pH=2, the most significant reaction, low concentration and pH= The reaction was mild under conditions of 8.

Bile acid stimulates mast cells to release histamine. Histamine can dilate the blood vessels of the gastric mucosa and increase the permeability of the capillary wall, leading to mucosal edema, hemorrhage, inflammation and erosion. Under such circumstances, the mucosa can easily develop into ulcers.

Helicobacter pylori infection (20%):

Hp is closely related to chronic gastritis. Inhibition of Hp increases the rate of healing of primary peptic ulcer. The recurrence rate of ulcers after Hp elimination is significantly reduced. The elimination of bacteria and the regression of gastroduodenal inflammation are related to the recurrence of ulcers in many studies. According to the literature, more than 90% of patients with gastroduodenal ulcer who have not taken ASA and other NSAIDs have chronic active gastritis caused by Hp infection, only about 5% to 10% of patients with duodenal ulcer and 30 % of patients with gastric ulcer have no clear evidence of Hp infection, and the 1-year recurrence rate of peptic ulcer after eradication of Hp is <10%, and the recurrence rate of Hp() after healing of peptic ulcer is about 50%, 2 years. The recurrence rate is almost 100%, so there is no acid and no ulcer, and there is a tendency to be replaced by "no Hp infection without ulcer" or both.

The alteration of Hp infection in gastric mucosa may be related to Hp products (cytotoxin, urease) and inflammatory process. Hp infection and mucosal inflammation may destroy the integrity of gastric and duodenal mucosal barrier, DU does not It is rare to have Hp, but it is unclear why only a small number of patients infected with Hp develop peptic ulcer. What is the pathogenesis? It is thought that it may be related to the following:

1Hp strain: Different Hp strains have different pathogenicity and produce different clinical results. The Hp strain with cell vacuolating toxin (CagA, VagA) is infected, which increases the chance of ulceration. It has been found that children with ulcers have infected this. The proportion of bacteria is very high.

2 The genetic susceptibility of the host: The incidence of DU in O-type blood is 30% to 40% higher than that in other blood types, and the possibility of DU in blood-type substances is not 40% to 50%. Some studies have considered Hp infection and Different blood group antigens are two independent factors in the occurrence of DU.

3 Inflammatory reaction: neutrophils cause oxidation reaction, Hp surface protein activates monocytes and macrophages, secretes IL-1, TNF, and synthesizes platelet activating factor to produce serious pathological reactions.

4 acid secretion reaction: It has been reported that Hp infection, food peptone, etc. can cause the release of gastrin from the gastric antrum G cells, and the bacteria return to normal after elimination. More thought: Hp infection leads to inflammation of the antrum, making the antrum Gastrin release increases, somatostatin secretion decreases and gastric acid secretion increases.

5 Gastric epithelial metaplasia of the duodenum: Hp causes duodenal gastric mucosal metaplasia, which reduces the secretion of duodenal bicarbonate and increases gastric acid secretion.

Others believe that the cellular vacuolating toxin produced by Hp is released and activated in gastric juice. Through the pylorus to the intestinal tract, the activated vacuolar toxin causes vacuolization of duodenal epithelial cells before being digested by some proteases in the intestine, so Duodenal ulcer is caused in the absence of Hp in the duodenum.

Drug factor (5%):

There are three more important drugs that cause peptic ulcer:

1 Aspirin (ASA).

2 non-steroidal anti-inflammatory drugs (NSAIDs), such as indomethacin, phenylbutazone.

3 Adrenal cortex hormone, ASA and most other NSAIDs and peptic ulcer interactions in several aspects: small doses can cause platelet dysfunction, a small dose can cause acute superficial gastric mucosal erosion caused by bleeding, about 2 /3 Patients with long-term use of NSAIDs have gastroduodenal mucosal lesions, most of which are superficial lesions. About 1/4 of patients with long-term use of drugs have ulcer disease, but the mechanism of gastric ulcer caused by ASA/NSAIDs is still unclear. It is believed that these drugs directly damage the gastric mucosa, in addition to increasing the reverse diffusion of hydrogen ions, it can also inhibit prostaglandin synthesis, increase gastric acid, pepsin secretion, gastric mucosal blood supply disorders, and gastric mucosal barrier function.

Genetic factors (5%):

The 1GU and DU siblings were 1.8 times and 2.6 times higher than the general population. GU was susceptible to GU and DU was susceptible to DU. The family history of children with DU was obvious in children. The PUD of O-type blood was higher than other blood types by about 35%, mainly DU, and ulcer with bleeding, perforation, comorbidity with O-type more common, the investigation found that DU children more than men, 48.08% are DU family history, family incidence rate 1 family> 2 family members> 3 family members The incidence of grade 1 family members is 11 times higher than that of the general population. O-type blood is more common, accounting for 44.23% of children, and the symptoms are severe.

2HLA is a complex genetic polymorphism system. The gene locus is on the short arm of chromosome 6 and many diseases have been found to be associated with certain HLA antigens. HLA-B5, HLA- is found in HLA serotyping. B12, HLA-BW35 has a correlation with DU, HLA-DQAl*03 gene is associated with DU. Shanghai Lujin Hospital detected HLA-DQAl gene in children with duodenal ulcer, and the frequency of *03 allele in children with DU was obvious. Below normal healthy children, the *03 gene has an important resistance to DU.

3 pepsinogen (PG) is a precursor of pepsin, secreting PGI, PGII. Family survey found that half of serum of patients with DU increased PGI content. In high PGI offspring, 50% also showed high PGI, indicating that patients with PGI were single chromosome. Dominant inheritance supports the presence of DU genetics.

Mental factors:

Fifteen years ago, patients with gastrostomy found that human gastric mucosa responded differently with people's emotional changes. When excited, gastric mucosa was congested, gastric juice secretion increased, stomach movement increased, and depression and despair, gastric mucosa pale The stomach movement slows down. Modern research has found that when the body is in a state of stress or stress, it can produce a series of physiological, neuroendocrine, neurobiochemical, and gastrointestinal functions, including gastric juice secretion, and gastrointestinal exercise will be in the mood. Changes under the influence of hypnosis and biofeedback inhibition.

During stress, gastric acid secretion increases, pancreatic secretion decreases, and gastric emptying rate decreases significantly. Patients with ulcers are more fearful of stress than healthy people.

Mark and other analysis found that: ulcer patients are suspicious, stubborn, have a strong sense of dependence, poor ability to handle things, immature, impulsive, easy to feel lonely, poor self-control, easy to be under pressure and anxiety, life events Frequent reactions are often made, and the incidence of peptic ulcers in school-age children is increased, which is related to the excessive burden of learning, and the increasing complexity of mental stress and psychological factors.

Food factors: In the rice-rice area of southern China, the incidence of peptic ulcer is higher than that of the northern region where the noodle food is dominant. Eating cold drinks, eating spicy food or overeating, not eating breakfast, eating greed at night, eating fried food Bad habits such as sparkling drinks cause direct damage to the gastric mucosa.

Defensive factors of peptic ulcer

1. Gastric mucosal barrier: The gastric mucosal barrier is composed of the cell membrane of the epithelial cells of the mucosa and the tight junction of the intercellular space. The process of mucosal resistance to hydrogen ion reverse osmosis has three parts:

1 Maintain a gradient difference between the concentration of hydrogen ions in the gastric juice and the concentration of hydrogen ions in the tissue fluid of the stomach wall.

2 resist the reverse diffusion of hydrogen ions and other harmful substances such as bile, drugs, pepsin damage to the mucosa.

3 epithelial and mucosal / submucosal blood circulation of nutrient mucosa and promote healing.

2, mucosal barrier function: the surface of the gastric mucosa is covered with a layer of mucus, secreted by mucosal epithelial cells and cervical mucosal cells at the gastric crypt, containing macromolecular substances such as glycoprotein, mucopolysaccharide, protein, phospholipid, etc. It is 10 to 20 times that of epithelial cells, so that the mucous membrane below it is isolated from the contents of the stomach cavity, blocking the damage of hydrogen ions and pepsin.

3, bicarbonate secretion: the proximal end of the stomach and duodenal mucosa can also secrete a small amount of bicarbonate into the mucosal layer, neutralizing the acid on the surface of the mucosal layer, so that the surface of the epithelial cells can maintain the pH range of 6-8. Resist the reverse dispersion of hydrogen ions.

4, gastric mucosal blood supply and epithelial cell regeneration capacity: stomach, duodenal mucosa is rich in blood supply, transporting sufficient nutrients to mucosal cells and continuously removing metabolites, so that epithelial cells are updated in time, animal experiments confirmed mucosa After the injury, it can be repaired quickly within 30 minutes, so the balance between shedding and renewal is maintained, thus maintaining the integrity of the mucosa. When the gastric mucosa is insufficiently supplied, the mucosa is ischemic necrosis, and the cell regeneration is delayed, it may form. ulcer.

5, prostaglandin effect: gastric mucosal epithelial cells have a continuous synthesis and release of endogenous prostaglandins (PG), mainly PGE2, the latter has the effect of preventing various harmful substances on the digestive tract epithelial cell damage and acid necrosis, This effect is called cytoprotection and is expressed as:

1 Protect the gastric mucosa from toxic substances.

2 reduce the gastrointestinal bleeding caused by NSAIDs, any substance that does not dissociate and dissolve in fat at acidic pH, it is easy to enter the mucosal cells in the stomach, once it enters the cell, it will dissociate due to the change of pH, and it is transparent. Decreased sex, retention in mucosal cells to play a toxic role, such as NSAIDs, the mechanism of PG cell protection:

A. Promote gastric mucosal epithelial cells to secrete mucus and HCO3-.

B. Inhibition of basic gastric acid and gastric acid secretion after meals.

C. Strengthen the blood circulation and protein synthesis of the mucosa.

D. Promote the release of surface active phospholipids, thereby enhancing the water flow on the surface of the gastric mucosa.

E. Scavenging oxygen free radicals, non-steroidal anti-inflammatory drugs inhibit prostaglandin synthesis, so it can induce ulcers. In addition to prostaglandins, some brain gut peptides such as somatostatin, pancreatic polypeptide, enkephalin, etc. also have cytoprotective effects.

(6) Epidermal growth factor: Epidermal growth factor (EGF) is a polypeptide secreted from the salivary gland, duodenal mucus in the Brunner gland, pancreas and other tissues. It has been reported that EGF is specific to the gastric mucosa in the gastrointestinal tract. Receptor binding plays a cytoprotective role. For example, after exogenous EGF, it can significantly reduce the damage of gastric mucosa caused by harmful substances such as ethanol and aspirin. Preliminary clinical observation can promote ulcer healing after oral administration of EGF in patients with peptic ulcer. .

EGF protects gastric mucosa and promotes ulcer healing. It may be involved in the regulation of EGF involved in gastric mucosal epithelial cell regeneration, stimulates digestive tract mucosal DNA synthesis, promotes epithelial regeneration and recovery, and has also reported that EGF can increase gastric mucosal blood flow.

Pathogenesis

Duodenal ulcer is mostly located in the ball, which is more common in large curved and anterior wall. The surface of the ulcer is generally less than 1cm. The gastric ulcer can be seen in the antrum, body and bottom. The angle of the ulcer and the antrum of the stomach are more common. The depth of the injury can be The mucosal muscle layer is reached, and the erosion is limited to the mucosal surface. The ulcer base can be divided into 4 layers, the surface is covered with a membrane formed by white blood cells, red blood cells and cellulose exudates, and the second layer is cellulose-like necrotic tissue, the third layer. For the inflammatory granulation tissue of the blood vessel, the fourth layer is fibrous tissue. The ulcer healing process is to first generate granulation tissue from the basal part, and then the epithelial tissue surrounding the ulcer grows into and differentiates into the surface of the newly grown granulation tissue, and finally covers the ulcer surface. Basal granulation tissue hyperplasia, followed by the formation of fibrous scar tissue, ulcers with large or multiple recurrences, due to fibrous tissue contraction, can deform the duodenal bulb.

Pediatric peptic ulcer prevention

1. Pay attention to the combination of work and rest, reasonably arrange the children's study and life, and don't let the children get too tired and nervous.

2, to prevent hunger and satiety, regular quantitative meals, to avoid the burden of the gastrointestinal tract when it is light and heavy.

3, nutritional balance, do not emphasize high nutrition. Eat high-protein, low-fat and digestible foods. At the same time correct the eclipse habits of children.

4, do not eat irritating food for a long time, but eat cold drinks, such as ice cream.

5, eat slowly, do not let the children eat while eating, or eat while reading books and television.

Pediatric peptic ulcer complications Complications anemia, gastric perforation, pyloric obstruction

1. Bleeding: When the ulcer destroys the blood vessels in the stomach wall or the duodenal wall, it can cause bleeding. When the amount of bleeding is small, it is manifested as fecal occult blood positive. When the ulcer destroys the large blood vessels, it will cause massive hemorrhage, which is manifested as hematemesis or black stool. Due to the action of stomach acid, the amount of blood vomiting is too much, and the vomiting can be bright red immediately, and then the tar-like stool is discharged, which can seriously cause hemorrhagic shock.

2, anemia: children with ulcer disease long-term diet is not good, absorption is not good, coupled with the inflammation of ulcers, acute or chronic blood loss caused by anemia, mostly vegetative small cell anemia, also known as iron deficiency anemia, these Children are weak and easy to develop various infections.

3, perforation: ulcers can penetrate the stomach wall or duodenum and ulcer perforation, substances in the stomach or duodenum such as stomach acid, food, bacteria, air, etc. into the abdominal cavity caused by diffuse peritonitis, this child is extremely extreme Irritable, pale, severe abdominal pain, and even shock.

4, pyloric obstruction: more common in older children, when the ulcer of the stomach occurs close to the pylorus of the stomach, the stimulation of the inflammatory reaction, the sphincter sputum, or the inflammatory edema around the ulcer, hindering the passage of food through the pylorus, can occur temporarily Pyloric obstruction; such as repeated attacks and healing of ulcers, forming scars over time, adhesion to surrounding tissues and causing persistent pyloric obstruction.

Pediatric peptic ulcer symptoms common symptoms gastrointestinal symptoms upper gastrointestinal bleeding abdominal pain bloating nausea bloody appetite loss black stool

1, primary peptic ulcer

The clinical manifestations of peptic ulcer in children are various, and the symptoms of different ages are quite different.

(1) Neonatal period: the main features of sudden upper gastrointestinal bleeding or perforation, often acute onset, mainly due to hematemesis, blood in the stool, abdominal distension and peritonitis, easily misdiagnosed, this period is mostly acute stress Ulcer, the mortality rate is higher, the most common incidence 24 to 48 hours after birth.

(2) Infant and child: In this period, children with more acute onset, irritability, poor appetite, sudden hematemesis, melena, may have loss of appetite in the early stage, repeated vomiting and abdominal pain, growth retardation.

(3) Preschool age: The primary ulcer gradually increases. The symptoms of abdominal pain are obvious in this period. Most of them are located in the umbilical cord. They are intermittent, and the relationship with diet is not clear. It is also nausea, vomiting, acid reflux, anemia and upper gastrointestinal bleeding. common.

(4) School age: Duodenal ulcer is more common, with increasing age, clinical performance is close to adults, abdominal pain above symptoms, abdominal pain in the umbilical cord, sometimes night pain, or pantothenic acid, hernia or chronic anemia, a few People show painless black stools, fainting, and even shock.

2, secondary peptic ulcer

Secondary peptic ulcer is mostly related to stress factors or taking non-steroidal anti-inflammatory drugs. The common stress factors in children are severe systemic infection, shock, sepsis, surgery, trauma, etc. The ulcer caused by severe burn is called curling. Ulcer, craniocerebral surgery called cushing ulcer, the mechanism of stress-induced ulcers is still unknown, presumably related to the submucosal small blood vessels contraction caused by superficial mucosal ischemia, partly due to the destruction of gastric mucosal barrier caused by H reverse osmosis, followed by It is abnormal in gastric acid secretion, and may also be related to prostaglandins. Generally speaking, secondary ulcers are more serious. Some scholars have reported 54 cases of secondary ulcers in children, of which 55.5% (30/54) are associated with bleeding. Perforation accounted for 14.8% (8/54), shock accounted for 11.1% (6/54), pain or vomiting accounted for 9% (5/54), premenstrual ulcer accounted for 62.9% (34/54), secondary ulcer The clinical feature is that it lacks obvious clinical symptoms and is found only when bleeding, perforation or shock occurs, so the mortality rate is as high as 10% to 77%.

Pediatric peptic ulcer examination

1. Detection of Helicobacter pylori:

Mainly divided into two aspects:

(1) Invasive method: Hp culture was performed by gastroscopically taking gastric mucosa living tissue, rapid urease measurement, and bacterial staining examination.

(2) Non-invasive method: Determination of Hp-IgG in serum as a screening index for Hp and urea breath test. Positive breath test indicates active Hp infection, but 13C-expiratory test requires certain equipment and is expensive. Clinical application is limited, while the 14C-expiratory test is less expensive, but because it is a radionuclide, it should not be used in children.

2, gastric acid secretion test: gastric acid secretion test is difficult in children, and the test is not meaningful for the diagnosis of most peptic ulcer, so it is rarely used clinically, but for the refractory ulcer can determine its gastric acid secretion function, such as continuous rise High, should pay attention to whether there is gastrinoma (Zollinger-Ellison syndrome).

3. Fecal occult blood test: It is a simple and meaningful test, which has practical value for judging the activity of small amount of bleeding or bleeding.

4, endoscopy: endoscopy is the most important means of diagnosis of peptic ulcer, ulcers seen under the endoscope as a circular or elliptical lesions, a few linear, clear boundaries, the center is covered with gray-white moss, surrounding The mucosa is slightly elevated or in the same plane. According to the course of the disease, the ulcer is divided into three cycles: active phase, healing phase, and scar phase.

5, X-ray barium meal check: Because the X-ray can pass through the stomach wall, but can not pass through the expectorant, so after eating the expectorant, the contour of the stomach and duodenum can be seen on the screen, if in the stomach Or the duodenal wall is found on the wall of the duodenum, which can determine the diagnosis of ulcer disease. This is called direct sign. The so-called shadow is the filling effect of the tincture in the ulcer, that is, under fluoroscopy, in the stomach and duodenum. The prominent shadow appearing on the wall, because the pediatric ulcer is shallow and small, the duodenal ulcer is mostly on the posterior wall of the ball. This position is difficult to observe. Therefore, the typical ulcer is not easy to find, most children with ulcers Can only be inferred by indirect signs, such as the duodenal bulb stimuli, that is, when the tincture passes through the ball, the speed is too fast, the pyloric fistula is limited to tenderness, the barium meal perspective, the duodenal ulcer detection rate About 75%, the gastric ulcer examination rate is less than 40%, so the negative examination of barium meal can not say that the child does not have ulcer disease, because the expectorant does not absorb, no damage to the body, the operation method is simple, the child is easy to accept, so to So far, the perspective of barium meal is still pediatric The preferred method of examination for the diagnosis of ulcer disease.

6, fiber gastroscopy: this test can be used for HP infection detection and gastric juice analysis, because ultra-small diameter gastroscope has been used in clinical, pediatric pharyngeal reflex is weak, gastroscope is easier to pass the pharynx, the success rate is higher, will not occur Accidents, so older children are easy to accept this method of examination, through the gastroscope, can directly observe the location, number, shape and edge of the lesion, so the detection rate of ulcer disease can be as high as 90% to 95%, and can Do a biopsy and a Helicobacter test for no lesions.

7. Electrogastrogram examination: As with electrocardiogram and electroencephalogram, the electrode is used to record the gastric electrical activity through the electrogastrogram. Therefore, the child is painless and can be accepted by children of all ages. Electrogastrogram and gastroscope Check and control, the coincidence rate is 53% to 60%, this examination can only be used for screening for ulcer disease, and the diagnosis cannot be confirmed.

Diagnosis and diagnosis of peptic ulcer in children

diagnosis

Because the symptoms of peptic ulcer in children are not typical, therefore, for clinical recurrent abdominal pain with unknown causes, long-term vomiting, melena, hematemesis, chronic anemia or gastrointestinal symptoms on the basis of serious systemic diseases, Peptic ulcers may be considered and further examination is required. It can be diagnosed according to laboratory tests.

Differential diagnosis

1. Abdominal pain:

Abdominal pain is a common clinical symptom in pediatrics. It is mainly caused by organic or functional abnormalities of the digestive system and other organ diseases. In addition to peptic ulcers, the following diseases also often cause abdominal pain. Such as reflux esophagitis, can occur after sternal pain, acute, chronic gastritis and duodenitis symptoms are similar to ulcer disease, acute and chronic inflammation of the small intestine and large intestine and functional dysfunction, liver, gallbladder, pancreas and urinary When the reproductive system is acute, chronic inflammation, and respiratory system infections occur in abdominal lymphadenitis, abdominal pain symptoms also occur. As long as the clinical examination, comprehensive consideration, combined with the pain characteristics and accompanying symptoms of different organs can make a judgment of.

2, hematemesis (hematemesis):

Hematemesis is a more serious symptom of digestive tract disease, so it is very important to judge the location of bleeding and the amount of bleeding. In addition to peptic ulcer, it is also seen in esophageal ulcer, esophageal varices, acute and chronic gastritis, twelve. Refers to enteritis, biliary bleeding, acute pancreatitis complicated by gastric mucosal injury, and systemic diseases, such as blood diseases, allergic purpura, neonatal hemorrhagic disease, etc. In addition, attention should also be paid to pseudohematemesis from the non-digestive tract, for example, Nasal, pharyngeal hemorrhage and hemoptysis, spit out after swallowing, very similar to gastrointestinal bleeding, but careful examination can identify, the amount of bleeding can be estimated, for example, the blood of vomiting is brown, indicating less bleeding, Such as vomiting dark red blood, showing a large amount of blood, bleeding amount up to 20% of the systemic blood volume, hemorrhagic shock can occur, infant gastrointestinal bleeding more than 3 ~ 10ml, adults more than 50 ~ 100ml, large red Or black tar-like stool, check the bloody substance of the gastric juice and fecal occult blood, you can judge whether the bleeding stops.

3, blood in the stool (hematochezia):

Blood in the stool is a common symptom of digestive diseases. The amount of blood in the stool varies greatly. A small amount of bleeding is difficult to identify with the naked eye. It can only be confirmed by concealed occult blood, and a large amount of bleeding can cause serious consequences. The bleeding site is often related to the color of blood. Most of the bleeding above the ileocecal valve is black tar-like stool, colon bleeding is mostly dark red, rectal or anal bleeding is mostly bright red, and there are many diseases causing bleeding, relying on detailed medical history, laboratory examination, combined with imaging Learning, especially endoscopy, for comprehensive analysis, can generally make a correct diagnosis.

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