Clinical recommendations for the treatment of pyloric stenosis in infants. Pyloric stenosis in infants: full symptoms of the disease, diagnosis and treatment methods

– cicatricial stenosis of the pylorus, predominantly of ulcerative origin, due to which the movement of chyme into the intestine is disrupted, nutritional status, water-electrolyte balance and homeostasis of the body suffer. Symptoms are characterized by vomiting and severe dehydration, emaciation, pain and a feeling of fullness in the stomach, and dyspeptic symptoms. To make a diagnosis, clinical and biochemical blood tests, gastrography, endoscopy, ultrasound, and ECG are used. Treatment includes conservative (gastric decompression, intestinal and parenteral nutrition, antiulcer therapy) and surgical measures.

General information

Pyloric stenosis is an organic narrowing of the outlet of the stomach, which forms during a complicated course of gastric ulcer, less often - with neoplasms of the stomach. This pathological condition develops in no more than 15% of patients with ulcerative lesions of the stomach and duodenum. Among all complications of peptic ulcer, pyloric stenosis accounts for about one third of cases. At least 20% of patients with this pathology are men. The disease develops in working age and old age. In recent years, the incidence of pyloric gastric stenosis has been decreasing, which is associated with the development of more effective antiulcer treatment methods (proton pump inhibitors, H2-histamine receptor blockers). This clinical problem is especially relevant for specialists in the field of gastroenterology and surgery. Congenital pyloric stenosis is the subject of study in pediatrics and is discussed in the corresponding section of the site.

Causes of pyloric stenosis

The most common cause of pyloric stenosis is a recurrent gastric ulcer. A repeated inflammatory process with ulceration, especially if not treated, first leads to swelling and spasm of the stomach walls, and then to the formation of cicatricial strictures and a slowdown in the passage of food from the stomach to the initial parts of the small intestine. As a result of this, the stomach becomes overfilled with digestive juices and food masses, which is compensated by increased muscle contractions of its walls and myocyte hyperplasia. Hypertrophy and stenosis of the pylorus gradually develops - an organic pathology characterized by narrowing of the pylorus and slower gastric emptying. Most often, this outcome is caused by a callous or penetrating gastric ulcer, less often by a scarring ulcer.

However, compensatory mechanisms during pyloric stenosis are quickly depleted, and therefore the stomach soon becomes significantly overstretched and increases in size, its peristalsis weakens, and congestion worsens. Vomiting of food eaten the day before occurs, leading to the loss of large amounts of fluid, electrolytes, and nutrients. With decompensation of pyloric stenosis, the patient experiences severe metabolic alkalosis (caused by the loss of chloride ions), water-electrolyte imbalance, and protein metabolism disorders. Loss of potassium leads to weakness of all muscles, but paralysis of the diaphragm and myocardium is of primary importance, which ends in cessation of breathing and cardiac activity. Hypocalcemia is marked by the development of seizures.

More rare causes of the formation of pyloric stenosis include a bleeding and perforated ulcer of the stomach or duodenum (they are characterized by postoperative pyloric stenosis), stomach cancer and other tumors of this localization.

Symptoms of pyloric stenosis

Characteristic clinical signs of pyloric stenosis include vomiting of food eaten the day before (sometimes several days before), the sound of splashing on an empty stomach (which indicates congestion), and peristalsis in the epigastrium visible through the anterior abdominal wall. The severity of clinical signs depends on the stage of the disease (compensated, subcompensated or decompensated).

Against the background of compensated pyloric stenosis, a slight narrowing of the gastric outlet is observed, which is accompanied by a moderate increase in its contractility. The usual symptoms of a peptic ulcer include a feeling of fullness and heaviness in the stomach, belching with acid and heartburn, vomiting food eaten with an admixture of acid, which brings relief to the patient. Food taken shortly before the attack is visualized in the vomit. There is no weight loss or it is insignificant.

When pyloric stenosis passes into the subcompensation stage, the patients' condition worsens, they note rapid weight loss and increased severity of symptoms. There are complaints of severe pain and a feeling of significant heaviness in the epigastrium, rotten belching, vomiting after almost every meal (sometimes with food taken many hours ago). Since after vomiting there is a marked improvement in the general condition, some patients induce it artificially. Immediately after eating, gastric peristalsis increases, which leads to stomach colic, rumbling in the stomach, and diarrhea. Patients also complain of constant weakness, fatigue, and drowsiness, which are associated with impaired nutritional status.

In the stage of decompensation, the symptoms of pyloric stenosis come first, masking the signs of peptic ulcer disease that prevailed before. The patients are cachectic and very weakened. The pain in the stomach becomes less intense, but almost constantly I am bothered by rotten belching and repeated profuse vomiting of food eaten several days ago. Loss of fluid through vomit leads to severe dehydration, which is manifested by thirst and a decrease in the rate of diuresis, dry skin and mucous membranes. This stage is characterized by stool instability - diarrhea is replaced by constipation. The overfilled stomach is visible through the anterior wall of the abdomen, its convulsive ineffective contractions are recorded, and a splashing noise is constantly heard over the epigastric region. At this stage of pyloric stenosis, irreversible dystrophic changes in the wall of the stomach usually occur, so it is most often impossible to restore its motor-evacuation function.

Diagnosis of pyloric stenosis

All patients who are at risk for the formation of pyloric stenosis (the presence of an ulcer of the pyloroduodenal localization, a history of suturing of gastric perforation, frequent relapses of ulcerative defects, male gender) should immediately contact a gastroenterologist when the first signs of impaired motor and evacuation function of the stomach appear.

One of the simplest and most accessible methods for diagnosing motor-evacuation dysfunction of the stomach is ultrasound. Ultrasound examination of the abdominal organs will allow you to visualize a full stomach, and sometimes a hypertrophied muscle layer in the pyloric region. However, to establish the severity and stage of the disease, more accurate techniques are needed, such as gastrography and endoscopy.

In the stage of compensation for pyloric stenosis, X-rays of the stomach reveal a slight increase in the size of the stomach cavity and activation of its peristalsis. Visualization of cicatricial ulcerative stenosis of the pylorus is possible. The removal of contrast into the intestines is delayed for no more than 12 hours. When performing endoscopy, stenosis of the pyloric zone is clearly visible; in this area, the gastric lumen may narrow down to 0.5 cm. Gastric peristalsis is enhanced, the mucous membrane is hypertrophied.

The following radiological signs indicate a subcompensated stage of pyloric stenosis: a significant increase in the stomach cavity, the presence of contents in it even on an empty stomach, decreased contractility. The images show three layers - contrast agent, air and mucus. Emptying the stomach takes from 12 hours to 24 hours. When performing fibrogastroscopy, an expansion of the gastric cavity is also noted in combination with a narrowing of the pyloric region to 0.3 cm.

Decompensation of pyloric stenosis on gastrography is manifested by significant overdistension of the stomach, very sluggish peristalsis, and pronounced stenosis of the outlet sections. Complete evacuation of the contrast agent does not occur even after 24 hours. The endoscopic picture is complemented by signs of mucosal atrophy.

Electrogastrography reveals a decrease in the contractility of the stomach of varying degrees of severity (from rare peaks of activity in the compensation stage to the almost complete absence of motor function during decompensation of pyloric stenosis).

All patients with pyloric stenosis require a blood test for the level of hemoglobin and hematocrit, electrolytes and ions, and nitrogenous waste. The acid-base state of the blood must be assessed. If a patient is diagnosed with hypokalemia, an ECG is necessary to timely detect cardiac arrhythmias.

Treatment of pyloric stenosis

Treatment of pyloric stenosis is carried out in a hospital setting and requires mandatory surgical intervention (preferably in the early stages of the disease, when complete restoration of the motor function of the stomach is possible). Conservative measures are used exclusively for preoperative preparation purposes.

Immediately after the patient enters the department, a gastric tube is inserted and stagnant stomach contents are evacuated (so-called gastric decompression). It is recommended to pass the probe beyond the level of stenosis, followed by fractional introduction of food into the small intestine. If this cannot be done (usually at the stage of decompensation, critical pyloric stenosis does not make it possible to insert a probe into the intestine), it is recommended to switch to full intravenous nutrition.

Drug treatment includes antiulcer therapy (proton pump inhibitors, H2-histamine receptor blockers, etc.), correction of water balance and electrolyte levels, acid-base status of the blood, and nutritional status of the patient (parenteral nutrition). To normalize gastric motility, prokinetics are used (their use is justified at the stage of compensation for pyloric stenosis and in postoperative treatment).

Surgical treatment of pyloric stenosis is aimed at eliminating stenotic deformation of the stomach and restoring its normal functioning. For this purpose, a truncal vagotomy is performed with gastroenteroanastomosis; endoscopic vagotomy and pyloroplasty; trunk vagotomy with gastrectomy of the antrum of the stomach; hemigastrectomy; gastroenterostomy. The choice of type of surgical intervention depends on the stage of pyloric stenosis and the general condition of the patient.

The prognosis for early treatment of pyloric stenosis is usually favorable. The possibility of death is associated with the decompensated stage of the disease, general exhaustion, and old age. The only method of preventing pyloric stenosis in adults is the early detection and treatment of gastric and duodenal ulcers.

Congenital hypertrophic pyloric stenosis

Version: MedElement Disease Directory

Congenital hypertrophic pyloric stenosis (Q40.0)

Congenital diseases, Gastroenterology

general information

Short description

Congenital pyloric stenosis(congenital hypertrophic pyloric stenosis, congenital hypertrophic pyloric stenosis) - congenital narrowing of the pyloric canal The pyloric canal (pyloric canal) is the final part of the stomach adjacent to the pylorus (the narrowed part of the stomach at the point of its transition into the duodenum).
due to a malformation of all layers of the pyloric section of the stomach with thickening of the mucous membrane in the pyloric section, impaired innervation of the pyloric muscles and excessive growth of connective tissue in them.

Classification

When classifying, the degree of obstruction of the pyloric canal is indicated, the presence of complications is noted (gastric pneumatosis, dehydration and its type, erosion of the stomach and esophagus).

Etiology and pathogenesis

It is a multifactorial disease, the development of which is played by hereditary predisposition.
May occur as a result of intrauterine viral infections (cytomegalovirus, herpetic), as well as gestosis Preeclampsia (pregnancy toxicosis) is the general name for pathological conditions that occur during pregnancy and complicate its course.
, stress and other environmental influences on the mother’s body.

Morphologically, pyloric stenosis is manifested by a thickening of the wall of the pyloric canal up to 3-7 mm (normal 1-2 mm). In healthy children in the first weeks of life, the pylorus The pylorus is the narrowed part of the stomach at the point of its transition to the duodenum.
It has a round shape, resembling an onion and pink color. In the case of pyloric stenosis, it lengthens and takes on an olive shape, cartilaginous density and a white color.
Histologically, hypertrophy is detected Hypertrophy is the growth of an organ, its part or tissue as a result of cell proliferation and an increase in their volume
muscle fibers (mainly the circular layer), connective tissue septa thicken, swelling occurs, and later sclerosis of the mucous and submucosal layers with impaired differentiation of connective tissue structures.

Epidemiology

Congenital pyloric stenosis occurs in the population with a frequency of 0.5:1000 to 3:1000. Moreover, the frequency of cases of this disease in boys (1:150) significantly exceeds this figure in girls (1:750). For every 1 case of congenital pyloric stenosis in girls, there are 4-7 cases in boys.

Risk factors and groups

There is an established relationship between parental consanguinity and the incidence of congenital hypertrophic pyloric stenosis. More often this defect occurs in the first child.
In 6.9% of cases, a family-hereditary predisposition was identified. If there is a sick boy in the family, the risk for future brothers is 4%, for sisters - 3%. For future brothers and sisters of a sick girl, the risk is 9 and 4%, respectively.

Clinical picture

Symptoms, course

The disease develops gradually.
At the age of 2-3 weeks, the child begins to regurgitate, which at the 3-4th week of life turns into profuse vomiting. Vomit in the early stages can sometimes contain an admixture of bile, but as the degree of narrowing of the pylorus increases, the bile in the vomit disappears. Then “fountain” vomiting appears when the volume of vomit exceeds the volume of the last feeding. Vomit has a sour, stagnant odor.
The child loses weight, his subcutaneous tissue becomes thinner, and after a short period of time he begins to weigh less than at birth. Dystrophy with a typical clinical picture is steadily progressing. The body develops a deficiency of microelements (iron, calcium, phosphorus) and vitamins.

The disease may have an acute course, with severe disturbances of homeostasis Homeostasis is the relative dynamic constancy of the internal environment (blood, lymph, tissue fluid) and the stability of the basic physiological functions (blood circulation, respiration, thermoregulation, metabolism, etc.) of the body.
. In this case, the loss of body weight reaches 15-20%. The child is characterized by lethargy, adynamia, skin with a gray color and pronounced marbling, tachycardia, rare urination, constipation (although dyspeptic, “hungry” stools may also be observed). Since the child loses hydrochloric acid and chlorine, this disease is characterized by alkalosis.
Anemia develops, water-electrolyte metabolism is disrupted, and the blood thickens.
In severe cases of pyloric stenosis, hemorrhagic syndrome with gastric bleeding, catarrhal-hemorrhagic esophagitis and antral gastritis may occur.
Symptoms increase more slowly with insufficiency of the cardiac part of the stomach and reflux esophagitis: frequent regurgitation is observed, vomiting “fountain” is less common, and disturbances in the acid-base state are less pronounced.

When examining the child, note:
- symptoms of malnutrition Hypotrophy is an eating disorder characterized by varying degrees of underweight
and dehydration;
- enlargement of the epigastric region compared to the sunken lower abdomen;
- peristalsis of the stomach visible to the eye in the form of an hourglass (especially during feeding). You can induce peristalsis by lightly stroking the epigastric area.
- sometimes it is possible to palpate the thickened pylorus.

The child has scanty, dark green stools (due to insufficient milk entering the intestines and the predominance of bile and intestinal gland secretions in the chyme).
Urination is rare with a reduced amount of urine excreted; concentrated urine.
As a result of vomiting, asphyxia and aspiration pneumonia may occur. Purulent-septic complications such as osteomyelitis, pneumonia, and sepsis may be added to the disease.

Diagnostics

Pyloric stenosis should be suspected if the following symptoms are present:
1. Fountain vomiting from 2-3 weeks of age with a constant frequency.
2. The amount of milk released during vomiting is greater than the amount of milk sucked.
3. A sharp decrease in body weight - body weight is less than at birth.
4. Significantly reduced number of urinations (about 6).
5. Presence of severe constipation (in most cases).
6. The appearance of the hourglass symptom after feeding.
7. Sharp pallor of the skin.
8. The child is lethargic, calm, his condition is progressively worsening.

Instrumental diagnostics

Mandatory studies: Ultrasound and gastroduodenoscopy.

Ultrasound allows you to see the pyloric olive in longitudinal and transverse sections, determine the nature of gastric peristalsis and observe the movement of gastric contents through the pyloric canal.

Normally, in children of the first months of life, there is no content in the stomach on an empty stomach, the length of the pylorus does not exceed 18 mm, the lumen of the pyloric canal is well visualized, the thickness of the muscle layer of the wall is no more than 3-4 mm, the diameter of the pylorus is no more than 10 mm.

With hypertrophic pyloric stenosis, during an ultrasound scan on an empty stomach, a large amount of liquid contents is detected in the stomach, peristalsis is deep, “pulling”. When a peristaltic wave passes, the pyloric canal is rigid and does not open; its length averages 21 mm (from 18 to 25 mm), the outer diameter of the pylorus is 14 mm (from 11 to 16 mm).
On a longitudinal section, the circular muscle is represented by two parallel hypoechoic stripes, between which there is an echogenic strip of the mucous membrane. On a cross section, the circular muscle is visualized as a hypoechoic ring around an echogenic circle of the mucous membrane. The thickness of the muscle averages 5 mm (range 3 to 6 mm).

EGDS in case of pyloric stenosis, it allows to detect gastric dilatation, sharp narrowing and rigidity of the pyloric canal, and often cardia insufficiency. Liquid contents are often found in the stomach on an empty stomach, the walls of the stomach are hypertrophied, peristalsis is increased, or the stomach is atonic; erosions can be found on the gastric mucosa.

Additional Research

X-ray examination of the stomach with barium

Direct radiological signs: changes in the shape, size and function of the antropyloric part of the stomach.

If the narrowing of the pylorus is pronounced, as a result of gastric peristalsis, the contrast agent fills only the initial part of the pyloric canal, without penetrating into the duodenum (symptom of “anthropyloric beak”). The wall of the stomach hangs over the narrowed pyloric canal at the base of the “beak”; as a result, a kind of intussusception (intrusion) of the thickened pylorus into the lumen of the antrum occurs - a symptom of “shoulders” or “braces”.

For less severe stenosis Stenosis is a narrowing of a tubular organ or its external opening.
The X-ray image shows the entire pyloric canal. It is significantly elongated (the “antennae” or “flagellum” symptom).
The symptom of “parallel lines”, which are formed by expanded folds of the mucous membrane, is a sign indicating a narrowing of the pyloric canal due to muscle hypertrophy and thickening of the mucous membrane.

Identification of at least one of the listed direct signs allows us to consider the diagnosis of congenital hypertrophic pyloric stenosis verified.
Indirect signs indicate changes in the evacuation function, as well as a change in the pattern of gas distribution along the intestinal loops.

The most significant of them:
1. Reducing the amount of gas in the intestinal loops with a distended stomach;
2. Segmenting rapid peristalsis of the stomach, sometimes like an “hourglass”: the elongated and narrowed pylorus does not contract. Even with increased peristaltic contractions of the stomach, its contents do not move into the duodenum for a long time - a symptom of delayed evacuation. 24-72 hours after ingestion of barium, some of it is still observed in the stomach.

Laboratory diagnostics

Mandatory studies: complete blood count, hematocrit, urinalysis.

Additional Research: biochemical blood test (potassium, sodium, chlorine, acid-base status).

Differential diagnosis

Differential diagnosis is carried out with diseases accompanied by persistent vomiting:
- pylorospasm;
- chalasia and achalasia of the esophagus;
- rare malformations: narrowing of the esophagus, esophageal atresia, duodenal atresia;
- hypoxic-ischemic damage to the central nervous system;
- adrenogenital syndrome;
- hypoaldosteronism;
- meningitis and other infectious and inflammatory diseases.

At congenital prepyloric stenosis a clinical picture very similar to pyloric stenosis is observed, characterized by high intestinal obstruction. The final diagnosis is made on the basis of ultrasound, endoscopy, and x-ray examination.

When carrying out differential diagnosis, one should exclude pylorospasm. In contrast to pyloric stenosis, pylorospasm:
- vomiting from birth, irregular.
- the amount of milk sucked is greater than the amount of milk released during vomiting;

The child’s body weight at the time of examination is greater than at birth, it is normal or slightly behind (in most cases);

The number of urinations is moderately reduced (10-15), there is no oliguria;
- spastic constipation is possible, but sometimes the stool is independent;
- when eating food there is no visible peristalsis of the stomach (in most cases);
- the skin is not too pale;
- the child is noisy, his condition is not significantly disturbed.

In diagnosis and differential diagnosis stenosis and esophageal diverticulum The leading role is played by esophagoscopy and x-ray examination.

Vomiting can also be caused by a double esophagus or a congenital short esophagus. The diagnosis is confirmed by endoscopy and x-ray examination, and no abnormalities on the part of the pylorus are detected.

Complications

Trophic disturbance, dehydration.

Treatment

Currently, the main treatment method for pyloric stenosis is surgery.

Surgery

Once the diagnosis is established, all children undergo extramucosal pyloromyotomy according to Frede-Ramstedt.
Preoperative preparation of children in serious condition includes infusion rehydration, correction of water-salt metabolism and acid-base status (reopolyglucin, 5% glucose solution, 5% albumin solution, amino acid solutions, panangin, ascorbic acid, calcium preparations and vitamins, saline solution, Ringer). In the case of 12-hour preparation, enteral nutrition is not prescribed. When longer preparation is necessary, the baby is fed with expressed breast milk or an adapted formula of 10 ml every 2 hours.

Non-drug treatment
On the first day after surgery, the baby should be fed 10-20 ml of expressed breast milk every 2 hours, gradually increasing the feeding volume (by 100 ml every day). Transfer to breastfeeding is possible if the condition improves by 6-7 days after surgery.

Drug treatment
In the first days after surgery, infusion therapy with solutions of amino acids, glucose, microelements, and vitamins is carried out. This is necessary to correct metabolic disorders and obtain sufficient nutrition.

In the treatment complex, drugs are used that protect the mucous membrane (Maalox, Phosphalugel, etc.), vitamins, biological products (Bifiform, Linex), enzymes (Creon, Pancitrate, etc.). In the case of the addition of purulent-septic diseases (pneumonia, sepsis, osteomyelitis), the prescription of antibacterial agents is indicated.

Forecast

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Causes of pyloric stenosis

With pyloric stenosis, there is an abnormal narrowing of the pylorus (lower section) of the stomach. In this case, food, even in liquid form, cannot move further, and the digestion process is disrupted. Everything remains in the stomach and is subsequently released in vomit. At the same time, the baby does not receive the necessary nutrients, weakening before our eyes. In addition, fluid is lost through vomiting, which leads to dehydration and dry mucous membranes.

As a rule, the pathology is congenital and is more common in boys. The reason is underdevelopment or abnormal development of the lower part of the stomach, in which the pyloric muscles are lined with inelastic connective tissue. The sphincter remains small, stretches with difficulty and passes solid food and liquids very poorly.

The appearance of the disease is preceded by the following factors:

endocrine diseases of the mother (for example, increased gastrin levels);
heredity;
taking antibiotics and other medications during pregnancy;
severe toxicosis in the first trimester;
infectious diseases suffered after conception, incl. such as rubella, herpes virus.

In addition to acute pyloric stenosis, there is a protracted form of the pathology. It has 3 stages: compensation, subcompensation and decompensation.

The severity of symptoms and the rate of development of clinical manifestations are influenced by the degree of narrowing of the canal and the condition of the baby’s stomach.

In older children, an acquired form of the pathology occurs. Its causes are chemical burns of the internal walls of the stomach, severe peptic ulcer disease. The disease is much more difficult to treat than with a congenital anomaly.

Symptoms in newborns

Pyloric stenosis in newborns has pronounced symptoms, and an experienced neonatologist can immediately make an accurate diagnosis. In the first week of the baby's life, the mother may experience frequent regurgitation and single bouts of vomiting. At 2-3 weeks, vomit erupts in a stream.

Clinical manifestations of pyloric stenosis increase at an accelerated pace, the child changes literally before our eyes. The pathology is characterized by:

Complications of congenital pathology - erosion on the walls of the stomach, its distension. Possible consequences of frequent vomiting are pneumonia, asphyxia. In severe cases, doctors diagnose sepsis, a degenerative condition.

Diagnostic methods

To make a diagnosis, a clinical examination is performed, which includes palpation to determine the size of the gastrointestinal tract, the degree of fullness of the stomach, and assess the severity of other pathological symptoms. An ultrasound and blood test are required. With pyloric stenosis in the blood, an increase in hematocrit, hypokalemia, and hypochloremia are observed.

An unpleasant research method for children is endoscopy of the upper parts of the digestive system. Using an endoscope, specialists examine the stomach and determine the volume of its contents.

At an older age, radiography may be indicated, with the help of which it will be possible to determine the severity of the anatomical defect.

The difference between pyloric spasm and pyloric stenosis

When diagnosing, it is important to differentiate between functional and structural abnormalities. Pyloric stenosis is classified as a pathology of internal organs; it is manifested by a pronounced narrowing of the pyloric zone. Pylorospasm, in which food also passes sparingly through the lower part of the stomach, is classified as a functional disorder associated with abnormalities in the innervation of the organ (we recommend reading: pylorospasm in newborns: causes, symptoms and treatment). The anomaly is also differentiated from intestinal obstruction, atresia, and hiatal hernia.

Sometimes, to make an accurate diagnosis, doctors prescribe antispasmodics, which help determine the causes of obstruction. After taking them, with pyloric spasm, the baby becomes much better; with pyloric stenosis, the condition does not change or worsens as the child grows and the anomaly progresses.

The main differences between pylorospasm and pyloric stenosis are given in the table:

Symptoms	With pylorospasm	With pyloric stenosis
Children's age	From birth	Vivid manifestations occur in the baby at 2-3 weeks of life
Volume and frequency of vomiting	Mild, frequent vomiting (but not after every meal)	Fountain after every feeding
Daily number of urinations	To 10	Significantly reduced
Chair	Constipation, possibly diluted	Persistent constipations
Body mass	Same as at birth or slightly reduced	Significantly reduced
Child's anxiety	Constant (neurological factor)	Rarely

Treatment regimen

Pyloric stenosis is treated surgically. The pediatric surgeon selects treatment tactics taking into account the age, symptoms, well-being of the newborn, and the presence of other pathologies. Typically, surgical intervention is planned; if the child’s condition is serious, the operation can be performed urgently.

Intervention stages:

preparatory with general strengthening therapy (administration of glucose and electrolyte solutions to support the baby’s body);
direct surgery preserving the integrity of the stomach;
rehabilitation measures, feeding in small portions with a gradual increase in dosage according to the age of the newborn.

The most sparing operation is considered to be pyloromyotomy according to Frede-Ramstedt (pictured). Surgeons cut through the connective tissue of the stomach layer by layer and reach the pylorus. Then the muscle ring is sequentially opened, which leads to independent straightening of the mucous membrane.

After the operation, the stomach gradually narrows, the clinical picture of the pathology subsides. Additionally, work is carried out with the nerve endings, which allows you to consolidate the effect of the treatment. With this intervention, the gastric mucosa is not damaged, which helps reduce the risk of postoperative complications.

What to do for prevention?

The health of the baby born depends on the nature of the pregnancy, so it is very important to plan and prepare for conception.

Preventive measures that minimize the risk of pyloric stenosis:

whether the expectant mother has been vaccinated against rubella, hepatitis, and other viral diseases (a doctor will advise) - vaccines should be administered six months before conception;
regular examinations and tests during pregnancy;
strengthening the expectant mother’s immunity, taking medications strictly as prescribed by the doctor.

After the baby is born, a caring mother pays attention to his well-being, notes any deviations in behavior, bad mood, and whims. Symptoms of pyloric stenosis will definitely alert you and will be a reason for a visit to the doctor. If you seek medical help in a timely manner, any dangerous consequences of the pathology will be prevented.

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This is one of the most common causes of partial high obstruction in children in the first weeks and months of life. Thickening of the pylorus during pyloric stenosis was first noted by M. Hirschprung in 1887. It is regarded as a defect in the innervation of the pyloric sphincter. At first, a deficiency of innervation causes a spastic state of the sphincter, and then, under its influence, degeneration of the smooth muscle fibers of the pylorus occurs. Smooth muscle fibers are large, with a large core.

In some cases, atypia of the pyloric mucosa is detected - dystopia and the formation of multiple cystic cavities in the thickness of the muscle layer. The nerve nodes of the muscle layer are surrounded by fibrous tissue, the nerve cells are wrinkled, the glial elements are hyperplastic, and the bundles of nerve fibers in the serosa are deformed. In recent years, the genetic nature of this developmental defect has been proven. The relative risk of pyloric stenosis among relatives is quite high, and is higher in the sons of patients, which indicates a partial dependence of the inheritance of the defect on gender.

The pylorus thickens, lengthens, becomes dense and glassy, and its lumen sharply narrows. Clinical manifestations become most noticeable by the beginning of the third week of the child’s life and progress. The most striking clinical manifestation of pyloric stenosis is the characteristic “fountain” vomiting. It is observed 1 - 1.5 hours after feeding. Its contents are curdled milk without any admixture of bile with a sour odor and an acidic reaction. The amount of vomit exceeds the amount of food eaten before, as it remains in the stomach from previous feedings. In some cases, streaks of blood can be seen in the vomit. Sometimes quite severe stomach bleeding occurs.

Constipation appears, urination becomes less frequent. Prolonged persistent vomiting leads to exhaustion. The child’s face has sunken eyes, the skin becomes flabby and dry due to constant dehydration. A characteristic sign of pyloric stenosis is increased gastric peristalsis, visible through the thinned abdominal wall in the form of an hourglass: two rounded protrusions with a bridge in the center appear in the epigastric region, gradually smoothing out and disappearing. Peristalsis is better detected after feeding. It can be provoked by lightly stroking the epigastrium with your fingers. Laboratory data indicate blood thickening (decreased blood volume, increased hemoglobin, hematocrit), hypochloremia, hypokalemia, metabolic alkalosis.

At x-ray examination pay attention to an increase in the size of the stomach, the presence of a high level of fluid on an empty stomach, and reduced gas filling of the intestinal loops. X-ray contrast examination is performed in a vertical position 30-40 minutes after giving a contrast agent (5% aqueous suspension of barium in breast milk in the volume of a single feeding). Segmenting peristalsis of the stomach and the absence of primary evacuation into the duodenum are visible. An X-ray in the lateral projection reveals a narrowed pyloric canal, a “beak” symptom. All radiographs should be taken with the child in an upright position. Typically, no further testing is required.

Recently, for the diagnosis of pyloric stenosis, fibroesophagogastroscopy. In this case, the expanded folded antrum of the stomach is visible, the lumen of the pyloric canal is sharply narrowed to the size of a pinhead, and does not open when inflated with air (unlike pylorospasm). In addition, fiberoscopy makes it possible to examine the esophagus and determine the severity of reflux esophagitis, which often accompanies pyloric stenosis. It is also possible ultrasound diagnostics pyloric stenosis. An experienced ultrasound operator not only detects the presence of a hypertraffic pylorus, but can measure its length and width, the length of the pyloric canal, the thickness of the muscle layer and mucous membrane. The advantage of the method is its non-invasiveness and lack of radiation exposure.

Treatment

The radical method of treating pyloric stenosis is surgery. Since 1912, extramucosal pyloromyotomy according to Frede-Ramstedt has been generally accepted. The intervention is preceded by preoperative preparation aimed at correcting hypovolemia, alkalosis, and hypokalemia. During the operation, the anatomical obstacle is removed and the pyloric patency is restored. 3-6 hours after the operation, the child begins to drink a 5% glucose solution, then 5-10 ml of milk after 2 hours.

In the next day, the amount of milk is increased daily by 100 ml (10 ml per feeding). By the 6th day, the feeding volume is increased to 60 - 70 ml with an interval of 3 hours, after which the child is transferred to normal feeding. In the first days after surgery, the deficiency of fluid, electrolytes, protein and other ingredients is replenished through infusion therapy and auxiliary parenteral nutrition, as well as the administration of microenemas (5% glucose solution and Ringer-Locke solution in equal quantities of 30 ml, 4 times a day in warm form).

One of the complications of the operation may be injury to the mucous membrane of the duodenum. Damage is detected when the stomach wall is compressed and its contents move through the pylorus. When perforation occurs, air bubbles and sometimes intestinal contents appear in the lower corner of the wound. The discovered hole is sutured with one or two sutures in the transverse direction. Repeated pyloromyotomy is performed on the opposite side of the sphincter. The prognosis is favorable. Children require clinical observation for further treatment of malnutrition, anemia, and hypovitaminosis.

Bychkov V.A., Manzhos P.I., Bachu M. Rafik H., Gorodova A.V.