Biliary dyskinesia is a violation of the motor and evacuation functions of the bile ducts and gallbladder in the absence of organic changes in them.

Etiology and pathogenesis. Dyskinesias are subdivided into primary and secondary. The reason primary dyskinesias are considered functional changes in the biliary system, which are based on violations of neurohumoral regulation. Secondary dyskinesias usually accompany gastrointestinal diseases - chronic gastroduodenitis, chronic

pancreatitis - or are the result of previous diseases (acute viral hepatitis, dysentery, salmonellosis, etc.). Dis-kinetic disorders of the biliary tract are largely due to the state of the ANS, which regulates the rhythmic activity of the gallbladder and its sphincter, bile ducts. On the other hand, a close relationship was established between the rhythm of the biliary tract and the activity of the antrum of the stomach, duodenum. Dyskinesias are often combined with impaired motility of the upper gastrointestinal tract, manifested by duodenogastric, gastroesophageal refluxes, and duodenospasm. A well-known role in the regulation of the motility of the biliary tract belongs to intestinal hormones - gastrin, cholecystokinin, secretin, etc.

The clinical picture. Dyskinesias of the biliary tract are manifested by pain in the right hypochondrium and dyspeptic disorders. Distinguish dyskinesias hypotonic and hypertensive. Hypotonic form characterized by a decrease in the muscle tone of the gallbladder. It is, as a rule, enlarged, slightly reduced. The sphincter of Oddi is often spasmodic. Children complain of dull, aching pains in the right hypochondrium and around the navel, rapid fatigue. With ultrasound scanning, it is possible to visualize an enlarged gallbladder, sometimes its functional bends or deformities. After ingestion of a food irritant, the bladder usually contracts, but less than normal. The hypotonic form is much more common than the hypertensive (in about 80% of cases). This is due to insufficient cholecystokinin levels due to frequent damage to the duodenum and the proximal small intestine, where this intestinal hormone is produced.

When hypertensive form dyskinesia, there is an accelerated emptying of the gallbladder. Clinically, this form is also characterized by pain in the right hypochondrium and around the navel, nausea. An ultrasound scan reveals an accelerated emptying of the gallbladder and a decrease in its size. Ultrasound of the liver with dyskinesias can also reveal one or another degree of cholestasis.

Treatment dyskinesia depends on their shape. For both forms, a diet is shown (table number 5 according to Pevzner). For hypotonic dyskinesia, products containing plant fiber are recommended, for hypertensive dyskinesia, restriction of mechanical and chemical food irritants, as well as antispasmodics - no-shpa, papaverine. Physiotherapeutic procedures give a good effect: with hypotonic dyskinesia - tonic procedures (galvanization, faradization), with hypertensive - sedative-type procedures (electrophoresis with novocaine, papaverine).

Chronic cholecystitis

Chronic cholecystitis occurs in children quite often. It accounts for about 15% of all cases of diseases of the gastroenterological sphere.

Etiology and pathogenesis chronic cholecystitis are quite complex.

The microbial factor plays an important role, but it is necessary to bear in mind the violation of the passage of bile and the mechanism of bile formation. The latter depends on three factors: active secretion of bile acids by hepatocytes with their subsequent transport into the tubules; active transport of inorganic ions; and finally, electrolytes.

Disruption of each of these mechanisms leads to a change in the composition of bile and disruption of its transport. The bile passage is also significantly affected by the condition of the duodenum and the sphincter apparatus. With duodenostasis, intraduodenal pressure is significantly higher than in the ducts of the biliary system, which leads to the reflux of the contents of the duodenum into the common bile duct, causing

rhenium of the common bile duct, and forms aseptic cholecystitis. With duodenitis, the inflammatory process spreads to the nipple fatter (papillitis), causes a spasm of the sphincter of Oddi, which leads to an increase in pressure in the biliary system and cholestasis.Infection can join these processes.

The clinical picture. The course of chronic cholecystitis is undulating. Pain attacks occur after food errors, physical activity, stressful situations. Pains are accompanied by nausea and vomiting, dyspeptic stools. In the interictal period, patients feel well. Chronic cholecystitis can proceed without bright attacks, sluggishly - patients complain of constant pain in the right hypochondrium, heartburn, nausea, flatulence, loss of appetite. Due to the violation of the secretory and motor function of the gastrointestinal tract, fermentation processes occur in the intestine, the stool becomes unstable - constipation is replaced by liquefied feces with a putrid odor. Children develop hypovitaminosis, general intoxication, and as-tenization.

Diagnostics. The diagnosis of chronic cholecystitis is made on the basis of clinical data, ultrasound scanning, and la-paroscopy.

Treatment with an uncomplicated course, it consists in prescribing a diet, antibiotic therapy (with signs of infection), spasmolytics, means that ensure the normal passage of bile and its products (cholekinetics and choleretics). Cholekinetics include magnesium sulfate, xylitol, sorbitol, choleretics - allochol, cholenzyme, ni-codine, oxafenamide. A good effect is also given by herbal preparations - flamin (immortelle preparation), kholagogum, kholagol. With a long persistent course of chronic cholecystitis with frequent exacerbations occurring with fever, changes in the blood, it is necessary to resolve the issue of removing the gallbladder.

Diseases of the pancreas

Acute pancreatitis

Pancreatitis is an inflammatory-degenerative disease of the pancreas with an acute or chronic course.

Etiology and pathogenesis. The triggering factors for the onset of acute pancreatitis can be acute viral infections (mumps, Coxsackie B virus, chickenpox, viral hepatitis A and B), abdominal trauma (a typical injury is a fall on the handlebars of a bicycle), biliary tract disease, gastroduodenitis, gastric ulcer and duodenum. Diseases of the biliary tract contribute to the ingress of bile into the pancreatic duct due to abnormalities or obstruction of stones, with phenomena of duodenostasis and increased intraduodenal pressure. Bile activates pancreatic enzymes, inducing autolytic processes.

Negative medicinal effects (steroid hormones, salicylic drugs) can also play a known role in the origin of acute pancreatitis.

There are two main mechanisms for the development of the pathological process in acute pancreatitis - autolytic processes in the tissues of the pancreas and an increase in the concentration of enzymes in the blood. The following mechanism of autolysis is assumed: under the influence of any of the listed etiological factors, trypsinogen is activated, turning into trypsin, and the amount of trypsin exceeds the ability of the pancreas to inactivate it with an inhibitor. Violation of this balance leads to the activation of other proteolytic enzymes, which causes autolysis of small areas of pancreatic tissue at first, and then generalization of the process occurs.

Hyperenzymemia plays a significant role in the genesis of clinical manifestations of acute pancreatitis.

In infectious diseases, acute pancreatitis develops if an infectious agent enters the pancreas by lymphogenous or hematogenous routes. The mechanism of traumatic injury to the pancreas is not well understood. It is known that when the body is bent, the gland is compressed by the anterior mesenteric vessels. In this position, a shock wave passing through the abdominal cavity can lead to hemorrhage or tissue damage: It is known that autoantibodies form against the tissue of the damaged organ.

The clinical picture. The main clinical symptom of acute pancreatitis is abdominal pain, more often of a cramping character, localized in the epigastrium or in the navel. The duration of the pain is from several minutes to several days. The pain can be localized in the left hypochondrium, radiate to the back and shoulders, and is often combined with nausea and vomiting. Children become restless, looking for the most comfortable position. With severe pancreatitis, collapse may occur. Physical examination reveals a slight bloating, possibly induration of the abdominal wall in the epigastric region. Palpation of the pancreas is almost impossible. In acute pancreatitis, as a rule, tachycardia, a drop in blood pressure, deafness of heart sounds are noted. Abdominal effusion may occur. Intestinal symptoms are observed - an increase in stool up to 3-4 times a day, its liquefaction, on palpation of the abdomen - a splash noise (Obraztsov-Strazhesko symptom).

Diagnostics. Acute pancreatitis is diagnosed based on clinical and laboratory findings. Of laboratory research, the main thing is to determine the levels in the blood of enzymes of the pancreas - amylase, lipase, trypsin and its inhibitor. An increase in the level of enzymes takes place in the first days of the illness, and sometimes in the first hours.

Minor hyperglycemia and glucosuria are also noted. An ultrasound scan reveals an increase in size, induration, and swelling of the organ.

Treatment. In acute pancreatitis, general rest and physiological rest of the pancreas are very important. The patient is transferred to parenteral nutrition. During fasting, it reduces

xia gastric secretion, the release of stimulants of pancreatic function decreases. Prescribe an abundant drink of alkaline mineral waters (degassed). Gastric juice is aspirated through a nasogastric tube. In order to prevent shock, albumin, 5% glucose solution is injected intravenously. To prevent autolysis of the pancreatic parenchyma, antienzyme drugs are administered - counterkal, which suppresses the activity of trypsin, chymotrypsin, plasmin, kallikrein, thromboplastin. The drug is administered intravenously, but drip in 200-300 ml of isotonic sodium chloride solution. Gordox, traskolan have the same effect. Aminocaproic acid is also used - it inhibits fibrinolysis, the activity of kinins, has an antiallergic effect (intravenously, 5% solution in isotonic solution, drip), M-anticholinergics (gastrocepin - 1 mg / kg).

Chronic pancreatitis

Etiology and pathogenesis. Chronic pancreatitis can occur as a consequence of acute pancreatitis, in particular as one of the manifestations of mumps, as well as against the background of diseases of the liver, biliary tract, stomach and duodenum. Chronic food overloads, the use of strong broths, coffee, chocolate, fatty foods, smoked meats are also important. According to A.V. Mazurin, 35% of children with chronic pancreatitis have exogenous constitutional obesity. A well-known role in the development of chronic pancreatitis is played by intoxication, poisoning (cobalt, mercury, lead, etc.), prolonged use of glucocorticoids.

The mechanism of development of the pathological process in the pancreas in chronic pancreatitis largely depends on the etiological reasons. In case of mumps, a viral infection affects the interstitium of the gland, followed by cell degeneration, the formation of areas of adipose tissue and, later, sclerosis. The process of development of chronic pancreatitis against the background of gastroduodenitis, dyskinesia of the biliary tract, accompanied by duodenostasis and increased pressure in the duodenum, which causes difficulty in the outflow and stagnation of pancreatic secretion (swelling of the Vater's nipple, spasm of the sphincter of Oddi) looks different. Duodenopancreatic reflux, which promotes the penetration of enterokinase into the pancreatic ducts, which activates trypsinogen and closes the pathological chain described above, can play an important role in duodenal pathology. Acute pancreatitis).

The clinical picture. Chronic pancreatitis has an undulating course. During an exacerbation, children complain of pain in the upper abdomen, more often of a paroxysmal nature, accompanied by nausea and vomiting. The pains can be shingles, radiating to the left shoulder, the phrenicus symptom is positive on the left. On palpation of the abdomen, pain zones can be identified: the area of \u200b\u200bthe anterior abdominal wall, onto which the pancreas and bile ducts are projected.

gi (Shoffard zone), in the left hypochondrium - on the line connecting the navel with the middle of the left costal arch (Mayo-Robson point), etc. The general condition of the child is disturbed - subfebrile condition, loss of appetite, increased stool up to 3-4 times a day , bloating, rumbling along the small intestine. In feces, the amount of fatty acids increases and<леточного крахмала, стул может быть обильным и зловонным. Вследствие нарушения процессов всасывания ребенок прогрессивно те­ряет в весе. При стихании обострения выраженность вышеописанных симптомов уменьшается, но полностью они не купируются.

Diagnostics. A special place in the diagnosis of chronic pancreatitis is occupied by the determination of the activity of pancreatic enzymes in the duodenal contents, blood, urine. The important tests are secretin and pancreozymin, which are functional pancreatic tests. The introduction of secretin causes a decrease in the content of bicarbonates, an increase in the content of amylase, lipase, and increases the activity of trypsin in the blood. Pancreozymin does not increase the content of amylase and lipase in the blood, but increases proteolytic activity. In some patients, there is an increase in the content of trypsin inhibitor in the blood. For diagnostic purposes, ultrasound scanning of the gland is also used.

Treatment. Therapy of chronic pancreatitis is aimed at eliminating inflammation and enzymatic autolysis of gland tissues, maximizing its functional sparing, and restoring impaired function. During an exacerbation, fat intake is limited; milk protein is preferred and food is steamed. Jam, honey, sugar are recommended. If necessary, the patient is transferred to parenteral nutrition for several days. Used, as in acute pancreatitis, antienzyme drugs - counter-calories, gordox, traskolan. They are injected intravenously in an isotonic solution or in a glucose solution. The calculation is based on 1 kg of body weight. In addition, rheopolyglucin (10 mg / kg), 5% glucose is recommended. If indicated, prednisone is prescribed (2 mg / kg / day).

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abstract

On Topic: Biliary dyskinesia

Performed by an intern doctor

Ostankova A. Yu.

Semipalatinsk

Biliary dyskinesia (BAD) is a dysfunction (motility) of the gallbladder and (or) ducts.

Primary dyskinesia occurs due to a violation of the cortical regulatory mechanisms; secondary - according to the principle of viscero-visceral reflexes, mainly with pathology of the pyloroduodenal zone. Depending on the tone of the sphincter apparatus and the kinetics of the gallbladder, hyper- and hypotonic, hyper- and hypokinetic types are distinguished.

DWP is the most common pathology of the hepatobiliary system in children of preschool and school age. In the structure of cholepathies, it is more than 8%, it occurs either in combination with other diseases of the gastrointestinal tract, or without them. Girls get sick 3-4 times more often than boys. dyskinesia gallbladder rehabilitation

Dyssynergism of the motility of the gallbladder and its sphincters (Oddi, Lutkens), as well as changes in the homeostasis of intestinal hormones, are of great importance in the pathogenesis of DWP. These disorders occur when the general adaptive mechanisms of regulation are weakened, as a result of which a psychovegetative syndrome is formed against the background of hereditary or acquired inferiority of the biliary system.

Dysfunction of the gallbladder and duct motility leads to the development of cholestasis, the essence of which is reduced to disorders of the hepatic-intestinal circulation of bile and its components, changes in the physicochemical and bacteriostatic properties of bile, which causes pain, dyspeptic syndromes and the development of complications in the form of cholecystitis or cholelithiasis.

Age aspect. The first signs of the disease appear in preschool-school age, the peak incidence is at 7-9 years.

The family aspect. Patients with DVP are more common in families where there are conflict situations leading to the development of neurosis in children. The importance of hereditary factors in the occurrence of IDH has not been directly proven, but it must be borne in mind that the child's body may have a hereditary predisposition to the weakness of the adaptive mechanisms, manifested by frequent colds, allergic reactions, and neurological disorders.

Diagnostic criteria

Supporting signs:

1) pain in the right hypochondrium and (or) near the navel, short-term, paroxysmal, sometimes radiating to the right shoulder (with hypertensive type) or constant, aching (with hypotonic type);

2) dyspeptic phenomena: decreased appetite, belching, nausea, bitterness in the mouth, bloating and recurrent stool disorders (with hypertensive type) or constipation (with hypotonic type);

3) positive blistering symptoms, the appearance or intensification of pain with:

palpation in the area of \u200b\u200bthe gallbladder projection (Kera's symptom);

percussion in the area of \u200b\u200bthe gallbladder projection (Lekene symptom);

palpation in the area of \u200b\u200bthe gallbladder during inhalation and abdominal retraction, when the patient suddenly interrupts inhalation (Murphy's symptom);

tapping along the costal arch on the right (Grekov-Ortner symptom);

palpation and percussion in the epigastric region, especially at inspiratory height;

palpation in the choledocho-pancreatic zone of Shoffard, located to the right and slightly up from the navel.

Optional signs:

1) changes in the functions of the central and autonomic nervous system (headache, fatigue, irritability, pathological dermographism, distal hyperhidrosis);

2) change in the function of the cardiovascular system in the form of:

tachy or bradycardia;

extrasystoles;

muffled heart sounds;

systolic murmur of a functional nature;

paroxysmal tachycardia with a tendency to increase blood pressure (with hypertensive type of DVP);

sick sinus syndrome and lowering blood pressure (with hypotonic type of venous thrombosis).

Laboratory and instrumental research methods

Basic methods:

general blood and urine tests (normal);

Ultrasound of the biliary tract;

fractional duodenal intubation (in the absence of an ultrasound device), where 5 phases are distinguished, each of which has a certain duration in time.

1st phase - the duration of the release of bile from the duodenum, consisting of duodenal juice, bile from the common bile duct and an admixture of pancreatic juice. The duration of the phase is 10-20 minutes.

2nd phase - the closure time of the sphincter of Oddi after the introduction of magnesium sulfate or other choleretic agents into the duodenum (4-8 minutes). If the sphincter of Oddi gapes, then bile flows immediately into the duodenum, with a spasm, there is no bile for more than 8 minutes (hypertonicity of the sphincter of Oddi).

3rd phase - the time for the appearance of light bile from the common bile duct until the appearance of gallbladder bile (3-6 minutes). With hypotension of the biliary tract, the time is lengthened.

4th phase - secretion of dark colored gallbladder bile (20-30 min). With hypotension of the gallbladder, this period is lengthened by more than 30 minutes.

5th phase - secretion of bile (light color) from the hepatic ducts. The time is not indicated, since bile is secreted constantly during the day;

chemical, physical, bacteriological analyzes of bile (no signs of inflammation).

Additional methods: determination in the blood of the level of bilirubin, enzymes (alanine aminotransferase, lactate dehydrogenase), thermal imaging method.

Survey stages

In the family doctor's office: collection and analysis of anamnestic data, with special attention should be paid to the socio-psychological climate in the family; an objective examination of the child by organs and systems.

In the clinic: general blood and urine tests; Ultrasound of the biliary tract; duodenal intubation; chemical, physical and bacteriological analysis of bile; biochemical blood test (protein and its fractions, CRP, sialic acid, bilirubin, ALT, ASAT, LDH).

Course, complications, prognosis

Clinical course options

The variety of clinical manifestations of DVP is caused by combined disorders of the stomach, duodenum and other parts of the intestine. Paroxysmal short-term pain in the right hypochondrium is characteristic of the hypertensive form, and it is associated with negative emotions. In the intervals between attacks of pain, children do not present complaints. An abundance of dyspeptic symptoms (nausea, bitterness in the mouth, decreased appetite), aching constant pain in the right hypochondrium is characteristic of hypotonic dyskinesia, which is much more common than hypertensive.

The course of the disease is characterized by undulation - periods of exacerbation and remission.

The severity of the condition is determined by the severity of pain, dyspeptic syndromes, as well as the nature of the combined lesion of other parts of the gastrointestinal tract.

Duration of illness. The acute period with adequate treatment lasts 3-4 days, after which the pain and dyspeptic syndromes disappear. The duration of the disease itself is on average 2-3 years.

Complications: cholecystitis, gallstone disease, gastroduodenitis.

The forecast is favorable.

Differential diagnosis

Conducted with:

cholecystitis (the presence of general neurotic reactions, the absence of symptoms of intoxication, a temperature reaction, signs of inflammation according to the analysis of bile and blood testifies to DVP);

gallstone disease (the conclusion is based on the data of the clinic, echoscopy, and in the absence of ultrasound, on the data of X-ray examination);

gastroduodenitis (the results of gastrofibroscopy are of decisive importance).

Diagnosis formulation

Secondary DVP. Hypertensive (hypotonic) type, exacerbation phase.

Primary DVP. Hypokinetic type with weakness of the sphincter of Oddi, remission phase.

Therapeutic tactics

Patients are treated at home.

1. With a hypotonic type of DVP, the following are prescribed:

full-fledged frequent (5-6 times a day) meals; in the acute period of the disease, refractory fats, foods rich in cholesterol, spices, fatty meat, butter dough, canned food are excluded from the diet; frying food is not allowed (diet No. 5 according to Pevzner); at the same time, patients should receive a sufficient amount of choleretic products (cream, eggs, butter and especially vegetable oil, fruits, berries, vegetables);

choleretic agents: holosas - 1 teaspoon 3 times a day, allochol - 1 tablet 3 times a day, cholenzym - 0.5-1 tablet 3 times a day, oxyphenamide - 0.25 tablets 3 times a day before food; especially indicated for constipation choleretic tea (immortelle flowers 4 parts, trefoil leaves 3 parts, coriander fruits 2 parts, mint leaves 2 parts: one tablespoon of the mixture is brewed in 500 ml of boiling water, infused for 20 minutes, filtered, give 100 ml 2-3 once a day 30 minutes before meals);

tonic agents: aloe extract (up to 5 years old - 5-10 drops, at an older age - 1/2 teaspoon 3 times a day), apilak - 0.005-0.01 g 3 times a day under the tongue, tincture lemongrass - 10-15 drops 1-3 times a day before meals, ginseng - 10-15 drops 3 times a day before meals, Eleutherococcus extract - 10-20 drops 2-3 times a day before meals, pantocrine - 0, 05-0.075 g 2 times a day, vitamin B1 - inside 10-15 mg 3 times a day, i.m. 2.5% solution, 0.5-1 ml 1 time a day, B6 - inside 5-10 mg 2-3 times a day, intramuscularly 0.5-1 ml once a day;

physiotherapy: galvanization, darsonvalization, diadynamic currents to the gallbladder area;

physiotherapy exercises, toning the abdominal wall.

2. In case of hypertensive type of DVP, the following are prescribed:

antispasmodics: no-shpa - 1 / 2-1 tablet 3 times a day, papaverine - 0.01-0.015 g 3 times a day, platifillin - 0.0025-0.005 g 3 times a day, aminophylline - 0.05-0 , 1 g 3 times a day, typhene - 0.01-0.02 g 2 times a day, halidor - 0.05-0.1 g 2 times a day;

sedatives: sodium bromide - 2% solution, 1 dessert spoon 3 times a day, valerian infusion - 10-15 drops 3 times a day;

physiotherapy: ozokerite, paraffin, diathermy, electrophoresis of novocaine, magnesium sulfate;

reflexology;

sparing exercise therapy (not in the acute period).

The criteria for the correctness of treatment: the disappearance of pain, dyspeptic, neurological syndromes; normal functioning of the gallbladder and ducts with repeated echoscopy or duodenal intubation.

Indications for hospitalization: unclear diagnosis; the impossibility of providing parents with the entire complex of prospective examinations and treatment due to social conditions, low family culture; serious condition of the patient; the nature of the primary disease, against the background of which there was DVP; unsuccessful home treatment in the first 3 days.

Treatment measures at the hospital stage:

creating a protective regime for the child;

ensuring a strict diet, taking into account the nature of the process;

regular physiotherapy activities;

if necessary - revision of the diagnosis.

Rehabilitation of children in remission consists in carrying out:

dispensary observation for 3 years after the illness;

remediation of chronic foci of infection;

anti-relapse treatment after stabilization of the pathological process: for 2 months for 10 days, choleretic drugs are taken monthly, or tyubazh (blind probing) are carried out 2 times a week; for this, the child is given (preferably in the morning) 15 ml of a 33% solution of magnesia sulfate, heated to 40-50 ° C, or 2 egg yolks with 1 tablespoon of sugar (a glass of warm mineral water can be used), after which the child is placed for 1 hour on the right side with a warm heating pad; after the specified time has elapsed, the child must take 10 deep breaths;

vitamin therapy (B1, B2, B6) in the autumn and spring periods for 2-3 weeks;

physiotherapy in the spring period of the year, the course is 10 procedures, the choice of the type of physiotherapy depends on the type of dyskinesia (see above);

physiotherapy exercises; with the disappearance of pain, dyspeptic syndromes - physical education at school in the main group.

Childcare Tips for Parents

Parents should master a set of physical therapy exercises from an instructor in a polyclinic, provide dietary nutrition - more frequent (5-6 times) meals with limited animal refractory fats (lard, mutton fat, etc.), and also monitor compliance with hygiene measures with the obligatory rinsing of the mouth after meals.

Prevention

Primary prevention:

proper organization of food;

elimination of moments that can cause a neurosis in a child;

timely detection and treatment of giardiasis, helminthic invasion, gastrointestinal diseases;

rehabilitation of chronic foci of infection.

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Content

Introduction

Etiology and pathogenesis of DVP

Diagnostics of the veins

Literature

Introduction

Biliary dyskinesia is a disorder of the contractile function of the biliary system, mainly the gallbladder and extrahepatic biliary tract, leading to impaired biliary excretion.

There are two main types of dyskinesia: hypomotor (hypokinetic, hypotonic) and hypermotor (hyperkinetic, hypertensive).

Hypomotor dyskinesia of the biliary tract is more common, in which there is a decrease in the evacuation function of the gallbladder, which leads to its stretching and stagnation of bile. There is a decrease in the function of the gallbladder with relatively constant moderate pain in the right hypochondrium, slightly decreasing after eating.

With hypermotor dyskinesia, pain in the right hypochondrium is intense, paroxysmal. The onset of pain is usually associated with an error in diet, alcohol intake, emotional stress.

When diagnosing, it is important to establish the form of dyskinesia, as well as determine the presence or absence of concomitant cholecystitis. The form of dyskinesia is established based on the characteristics of the manifestation of the disease. Ultrasound results play an important role. Duodenal intubation is also used.

Etiology and pathogenesis of DVP

The following factors are distinguished, leading to biliary dyskinesia (GB):

Neurocirculatory dysfunction of various origins;

Postponed acute viral hepatitis;

Constitutional features of a child with autonomic dystonia and a sedentary lifestyle;

Neuroses;

Food allergy, atopic diathesis;

Any chronic pathology of the gastrointestinal tract (especially inflammatory);

Hereditary predisposition, although it probably still more often comes down to family characteristics of the lifestyle, in particular, nutrition;

Chronic foci of infection in the body (ENT pathology, etc.);

Poisoning, ecopathology, long-term abuse of food in industrial canning products;

Endocrine diseases (obesity, thyrotoxicosis, diabetes mellitus).

VA Galkin (1996) writes: the concept of gallbladder dyskinesias as purely functional disorders is currently being revised. Not only with hypomotor, but also with hypermotor forms of dyskinesia, organic changes take place at the level of the hepatocyte, which is a kind of primary factor contributing to the disruption of the activity of not only the intra-, but also extrahepatic biliary tract, including the gallbladder. This pathology is a specific type of cholestasis. However, the role of vegetative-vascular (neurocirculatory) dystonia in the development of biliary dyskinesia is not excluded. So, two main factors lead to the disorder of the gallbladder motility:

1. violation of the functional state of the hepatocyte and hence - dyscholia (change in the composition of bile);

2.Disorders of neurogenic regulation of the muscular wall of the gallbladder, both central (neurocirculatory dysfunction, neuroses) and peripheral (with pathology of the gastrointestinal tract by the type of viscero-visceral reflexes from interoceptors) genesis.

At the same time, it was found that gallbladder dyskinesias can also be caused by a violation of the secretion of enteric hormones (cholecystokinin, motilin, etc.) in chronic pathology of the duodenum and small intestine, as well as apudopathy. Violation of the rhythm of the flow of bile into the intestine reduces the bactericidal properties of the upper gastrointestinal tract, leads to dysbacteriosis, intestinal dyskinesia. Long-term dyskinesia, causing stagnation and infection of bile, the reflux of intestinal contents into the gallbladder (reflux), leads to cholecystitis. With the predominance of the tone of the sympathetic part of the nervous system, the patient is characterized by hypotonic dyskinesias (80% of all dyskinesias), with parasympathicotonia - hypertensive.

The clinical picture of DVP depending on the form

Clinical manifestations of biliary dyskinesia are caused by impaired motor function of the biliary tract, which, on the basis of complaints, anamnesis and data from an objective examination of patients, can be divided into local and general symptoms.

Hypertensive-hyperkinetic form of biliary dyskinesia it is observed more often in persons with vagotonia and is characterized by recurrent acute colic, sometimes very intense pain in the right hypochondrium with irradiation to the right scapula, shoulder (resembles hepatic colic) or, conversely, to the left half of the chest, heart region (resembles an attack of angina pectoris). Cardiac manifestations in diseases of the gallbladder were described by S.P. Botkin as a vesicocardial reflex (Botkin's symptom). The pain, as a rule, occurs suddenly, repeats several times a day, is of a short-term nature, is not accompanied by an increase in body temperature, an increase in ESR and leukocytosis. Sometimes attacks are accompanied by nausea, vomiting, and intestinal dysfunction. It is possible that such patients develop vasomotor and neurovegetative syndromes: sweating, tachycardia, hypotension, feeling of weakness, headache.

Patients associate the onset of pain attacks in the right hypochondrium not so much with errors in food, but with psycho-emotional overstrain. Pain syndrome in hyperkinetic form of biliary dyskinesia is a consequence of a sudden increase in pressure in the gallbladder, which is reduced with acute hypertension of the sphincters of Lutkens or Oddi.

Most patients note increased irritability, fatigue, mood swings, sleep disturbances, pain in the heart, and palpitations.

When examining patients, the skin is not changed; the subcutaneous fat layer is expressed normally, often even enlarged. Palpation is sometimes noted soreness (positive symptom of Zakharyin) in the projection area of \u200b\u200bthe gallbladder - Shoffard's zone (at the intersection of the lower edge of the liver with the outer edge of the right rectus muscle of the abdominal wall). Sometimes there may be positive symptoms of Vasilenko, Kera, Murphy, Mussey-Georgievsky on the right, right phrenicus symptom. Zakharyin-Ged's skin hyperesthesia zones are absent in most cases.

Outside of the period of exacerbation, palpation of the abdomen shows slight pain in the projection of the gallbladder and the epigastric region. Pain points, characteristic of chronic cholecystitis, are mild or absent. Possible functional changes in other digestive organs (pylorospasm, hypokinesia of the stomach, duodenostasis, hypo- and hyperkinesia of the colon), cardiovascular and endocrine systems. In the interictal period, a feeling of heaviness in the right hypochondrium sometimes remains. The pain usually intensifies after psycho-emotional overload, during menstruation, after physical exertion, the use of spicy and cold foods.

Hypotonic-hypokinetic form of biliary dyskinesia observed more often in persons with a predominance of the tone of the sympathetic part of the autonomic nervous system. It is characterized by a feeling of fullness and constant dull, aching pain in the right hypochondrium without clear localization, which intensify after excessive psychoemotional stress, and sometimes food intake. Pain syndrome in hypokinesis is due to the predominant stretching of the infundibular part of the gallbladder. This is facilitated by the release of anticholecystokinin, an excessive amount of which significantly reduces the formation of cholecystokinin in the duodenum. A decrease in the synthesis of cholecystokinin, which is a cholekinetic agent, further slows down the motor function of the gallbladder.

Patients often complain of poor appetite, belching, nausea, bitter taste in the mouth, bloating, constipation (less often diarrhea). On palpation, slight pain is determined with deep palpation in the Shoffard zone.

Dyskinesia of the biliary tract can occur latently and with less pronounced local clinical symptoms in the presence of general neurological symptoms. On the basis of complaints, anamnesis, an objective examination, a preliminary diagnosis can be made. To establish the final diagnosis, it is necessary to carry out a number of laboratory and instrumental research methods.

Hypotonic-hyperkinetic form of biliary dyskinesia

It is known that very often biliary dyskinesias, especially secondary ones, occur with a dilated stagnant gallbladder against the background of spasm of the sphincter of Oddi. Most often it occurs with an increased tone of the parasympathetic division of the autonomic nervous system and high acid production in the stomach. These are the patients:

1. constitutional vagotonics;

2. non-ulcer dyspepsia;

3. type B gastritis - chronic primary gastroduodenitis (pre-ulcer condition);

4. peptic ulcer;

5. chronic recurrent pancreatitis;

6.traumatic brain injury.

With all these diseases, especially with a peptic ulcer, there is a spasm of the sphincter of Oddi, since peptic ulcer disease is a clear representative of the disease of the sphincters (pyloric pulp and sphincter of Oddi). It is also known that increased acidification of the duodenum contributes to the spasm of the sphincter of Oddi, and anti-acid drugs (antacids, H 2 histamine blockers, inhibitors of H + / K + -ATPase) indirectly help relieve spasm of the sphincter of Oddi.

In the presence of a spasm of the sphincter of Oddi, bile stagnation occurs in the gallbladder, and after a certain time - its dilation. The appointment and long-term use of myogenic antispasmodics (papaverine, no-spa) and non-selective M-anticholinergics (atropine, platifillin, metacin) aggravate hypomotor dyskinesia of the gallbladder. This is especially true for peptic ulcers, since until recently, patients with peptic ulcer disease received courses of treatment consisting of myogenic antispasmodics and non-selective M-anticholinergics. The dilatation of the gallbladder and the stagnation of bile in it are further aggravated by the appointment of H-anticholinergics - ganglion blockers (benzohexonium, pyrylene, gangleron), which are currently practically not used. This factor should be regarded as a very positive moment in the treatment of patients with peptic ulcer.

Patients with stagnant gallbladder with spasm of the sphincter of Oddi have their own characteristics of pathogenesis, clinical picture, diagnosis and treatment in comparison with previously described forms of dyskinesia. They usually complain of heaviness and pulling pain in the right hypochondrium, dry mouth, constipation (usually sheep's stool), mood instability, irritability, fatigue. The latter complaints are especially pronounced in their presence and in the underlying disease.

On examination, a scalloped tongue (tooth prints) is determined, which indicates stagnation of bile in the gallbladder. On palpation, as usual, there is sensitivity in the Shoffard zone (positive symptom of Zakharyin), sometimes it is possible to palpate an enlarged gallbladder. There is certainly a positive symptom of Mussi-Georgievsky and Frenicus is on the right. Palpation reveals spasmodic, moderately painful sections of the colon, and tight filling of the sigmoid colon with feces.

Patients with a hypomotor-hyperkinetic form of dyskinesia are very difficult to duodenal intubation, since the sphincter of Oddi is often poorly disclosed in them. Therefore, they must be prepared very carefully one day before the study and immediately before duodenal intubation. During the day, the day before probing, patients must take antispasmodics, mainly not myogenic antispasmodics (no-shpa, halidor), but antispasmodic drugs that have a selective relaxing effect on the sphincter of Oddi and do not affect the relaxation of the gallbladder muscles. Before going to bed, the patient should take a double dose of buscopan (20 mg) or gastrocepin (100 mg) and 50-100 g of honey with tea, preferably green.

While examining the patients of our polyclinic who are registered with the diagnosis "DVP", we note the following:

1. In 63 children from 5 to 15 years old, based on the nature of complaints, history, clinical picture, physical examination, laboratory studies and ultrasound diagnostics revealed IDD (dyskinesia of the gallbladder hypotonic type with dyscholia, hyperkinetic type and cholestasis syndrome.

2. The analysis of pain syndrome revealed that diffuse pain in primary school age occurs 2.1 times more often than in senior school age and 1.5 times less often than in preschool age. Pain in the right hypochondrium in primary school age occurs 1.2 times less often than in senior school age and 2.2 times more often than in preschool age.

3. The analysis of the dyspeptic syndrome revealed that nausea is observed in 48.4% of preschoolers, 57.8% of younger children and 56.9% of older school children. Vomiting in primary school age occurs 1.6 times more often than in senior school age and 1.3 times less often than in preschool age.

Diagnostics of the veins

Diagnostics based on the analysis of complaints, examination data and the results of additional research methods. Ultrasound is a valuable diagnostic method for this pathology. Ultrasound can reveal the nature of motor disorders of the gallbladder, diagnose biliary tract anomalies (kink, torsion, etc.). Very often, it is these structural features of the biliary tract or gallbladder that are the direct cause of dyskinesias.

With dyskinesia of the biliary tract, diet therapy is prescribed within the framework of the dietary table N5. Considering the role of reflex influences in the genesis of ID, an important role is played by the organization of a rational regimen, adequate sleep, limitation of psycho-emotional overload and stress.

The principles of VBD therapy, taking into account the variant of gallbladder dyskinesia, are presented in Table 1.

Table 1. Principles of differentiated therapy for LAD

Hyperkinetic dyskinesia of DWVP	Hypokinetic dyskinesia of DVP
1. Sedation therapy: sodium bromide, persen, valerian tincture, seduxen, tazepam and other tranquillizers	1. Toning therapy: aloe extract, ginseng tincture, pantocrinum, eleutherococcus
2. Choleretics: convaflavin, cholezym, nicodine, oxafenamide, allochol, berberine, etc.	2. Cholekinetics: magnesium sulfate, sorbitol, xylitol, mannitol, raw egg yolk, vegetable oils
3. Hydrocholeretics: urotropin, salicylic sodium, mineral waters of low mineralization (Smirnovskaya, Slavyanovskaya, Essentuki N4 and N20) 3 ml / kg body weight per day	3. Hydrocholeretics: mineral waters of high mineralization: Essentuki 17, Naftusya, Arzni, Batalinskaya, carbonated in a cold form.
4. Physiotherapy: thermal procedures: paraffin and ozokerite applications, dia and inductothermy, electrophoresis of papaverine, platifillin, dibazol	4. Physiotherapy: faradization of the right phrenic nerve, galvanization of the gallbladder, diadynamic therapy
4. Medicinal herbs: common barberry, immortelle, corn silk, peppermint	Medicinal herbs with cholekinetic action: mountain ash, chamomile flowers, centaury grass and collections from them

From the very first days of treatment, the state of the autonomic nervous system is corrected. In case of hypertensive and hyperkinetic type of DVP, sedatives are prescribed: bromides, valerian infusion, motherwort. In case of hypotonic and hypokinetic type of JVP, tonic preparations are used: extract of Eleutherococcus, Leuzea, tincture of ginseng, aralia, lemongrass.

Antibiotic therapy for this pathology is not indicated. When prescribing chemotherapy drugs in connection with another concomitant disease, it is necessary to take into account the possible adverse effect of these drugs on the function of the biliary system. If giardiasis or other helminthic invasion is detected, anthelmintic therapy is mandatory.

Choleretic agents play a special role. According to their mechanism of action, they are subdivided into choleretics (increase the formation of bile) and cholekinetics (promote the release of bile from the bladder into the intestinal lumen).

Choleretics include: allochol, cholenzyme, cholecin, liobil and other preparations with bile acids; nicodine, oxafenamide, tsikvalone (synthetic drugs); immortelle, corn stigmas, tansy, rose hips, cholagol, olimetin (herbal preparations); valerian preparations, mineral water (increased bile secretion due to the water component).

To cholekinetics about carry: magnesium sulfate, sorbitol, xylitol, berberine bisulfate (increase the tone of the gallbladder and reduce the tone of the biliary tract); antispasmodics, aminophylline (relax the sphincters of the biliary system).

The choice of drugs to restore the functions of bile formation and bile secretion depends on the type of dyskinesia.

For hypertensive type of JVP, oxafenamide, nicodine, mineral waters of low mineralization are used (Slavyanovskaya, Smirnovskaya, Essentuki 4, 20, Narzan in hot or heated form 5-6 times a day). For herbal medicine, chamomile flowers, peppermint, licorice root, valerian root, motherwort herb, dill fruits are used.

With a hypotonic type of DVP, flamin, cholecystokinin, magnesium sulfate, pancreozymin are prescribed; mineral waters of high mineralization (Essentuki 17, Arzni, etc., room temperature or slightly warmed up 30-60 minutes before meals, depending on the secretion of the stomach). Herbal medicine: corn stigmas, immortelle flowers, chamomile, nettle leaves, rose hips, St. John's wort, oregano.

With the hyperkinetic type of DVP, antispasmodics are used in a short course, potassium and magnesium preparations, mineral waters of low mineralization in a heated form 5-6 times a day. Herbal medicine: chamomile flowers, peppermint, licorice root, valerian root, motherwort herb, dill fruits.

For hypokinetic type of DVP, sorbitol, xylitol, cholecystokinin, pancreosimin, magnesium sulfate, mineral waters of high mineralization at room temperature or slightly warmed up 30-60 minutes before meals are recommended. Herbal medicine as in hypotonic type. In case of intrahepatic cholestasis, tubazh (tubeless drainage of the biliary system, or "blind" probing) is performed 1-2 times a week. Prescribe tonic drugs, choleretics and cholekinetics. With increased activity of the hepatic enzyme ALT, choleretics are not prescribed.

Treatment of children with DVP is carried out until the complete elimination of bile stagnation and signs of impaired bile outflow. In case of severe pain, it is advisable to treat the child for 10-14 days in a hospital setting, and then in a local sanatorium.

Timely diagnosis of disorders of the biliary tract function and proper treatment of children, depending on the type of violations identified, allows to prevent the formation of further inflammatory diseases of the gallbladder, liver, pancreas and prevents early stone formation in the gallbladder and kidneys.

Elimination of the causative factor that caused the disease is of decisive importance in the treatment of secondary IDS. Treatment of giardiasis, gastroduodenal pathology, autonomic dysfunctions, etc.

Hofitol is one of the drugs we use for the treatment of DVP in children. This is a herbal medicinal product that has a complex effect on the gastrointestinal tract, including regulating bile-forming and biliary functions, and, in addition, has a hepatoprotective effect. This herbal preparation is an extract of the fresh leaves of the field artichoke. Chophytol improves the antitoxic function of the liver, exhibits antioxidant activity, and has a mild diuretic effect. Contains the following active ingredients, which determine its systemic action: caffeolyquic acids, flavonoids, sequiterpenlactone, inulin, cynarases enzymes, vitamins of groups A, B, C, macro- and microelements, including Fe, P, Mn. Choleretic action of Chophytol is carried out by normalizing the processes of bile formation, bile secretion and tone of the gallbladder and biliary tract. The hepatoprotective properties of this drug were studied and confirmed by scientists Gebhardt and Mitarb in an experimental model on an isolated colony of hepatocytes labeled with radioactive C14-acetate in 1995. The hepatoprotective effect is associated with an increase in the outflow of bile, an improvement in the antitoxic function of the liver, and an effect on its enzyme system. The detoxifying effect of Hofitol on the liver is carried out by enhancing the binding of glucurone and sulfo groups, which leads to an improvement in the protein-synthetic function of the liver and, consequently, to a decrease in the formation of end products of nitrogen metabolism (urea, creatinine). Chophytol has a multifaceted effect on fat metabolism: it reduces cholesterol synthesis by hepatocytes, normalizes intracellular phospholipid metabolism, and reduces atherogenic cholesterol fractions. The mechanism of the therapeutic action of chophytol on the kidneys is associated with renal vasodilation, which leads to an improvement in glomerular filtration, increased excretion of the end products of hepatic detoxification and gives a mild diuretic effect. The antioxidant effect is carried out as a result of the normalization of enzymes of the antioxidant defense of the cell, activation of respiratory enzymes (oxidoreductases), stabilization of cell membranes, and normalization of intracellular synthesis of cholesterol and lipids. Due to its diverse pharmacological action, chophytol has quite wide indications for use in children:

Acute and chronic hepatitis (including infectious);

Fatty hepatosis, liver cirrhosis;

Dyskinesia of the biliary tract, including those with dyscholia syndrome;

Chronic intoxication (hepatotoxic substances, nitro compounds, alkaloids, heavy metal salts);

Chronic nephritis;

Lipid metabolism disorders;

Chronic and subacute renal and hepatic failure.

Hofitol can be used in children from the first months of life. There are forms in the form of a solution for oral administration (for young children), tablets and a solution for injection.

In our clinic, the following dosages of chophytol are used in children:

For children from 0 to 12 months, 0.3–0.5 ml (5–10 drops) of solution 3 times a day;

Children 1–5 years old, 0.5–1 ml (10–20 drops) of solution 3 times a day;

Children 6–12 years old, 0.5 teaspoon of solution or 1 tablet 3 times a day;

Children over 12 years old take 0.5-1 teaspoon of solution or 1-2 tablets 3 times a day.

conclusions

So, in conclusion, we can say the following:

1. Dyskinesia of the biliary tract in children is the most common pathology of the biliary system. The term "dyskinesias" literally translates to "movement disorders" and refers to an abnormal, uncoordinated function of smooth muscles.

2. In the hypertensive form of DVP, children complain of paroxysmal, stabbing pain in the right hypochondrium or in the right side. Young children point to the umbilical zone. Radiation of pain to the right shoulder and scapula is very rarely observed. A rather characteristic symptom for this condition is a sharp colicky pain in the right side when running fast or walking fast, which is explained by additional stretching of the capsule of an already enlarged liver with an increased inflow of venous blood. This symptom is especially pronounced in physical education lessons or in training, during outdoor games, dancing.

3. The hypotonic form of DVP is characterized by an almost constant, aching dull pain in the right side. Emotional stress, nutritional errors can increase pain.

4. There are also primary DVP and secondary DVP, which is present in a variety of pathological conditions - diseases of the gastrointestinal tract, kidneys, central nervous system, etc. labile form of DZHVP (75%), less often - stable (25%). The stable form of DGVP is more common in organic diseases of the stomach, 12-PC, ZhVP, labile - in the case of FGD.

5. In the development of DVT, the decisive factor is the dysregulation of the function of the VHL by the nervous system, both the CNS and the ANS. This is confirmed by the data of neurophysiological examination - in the hypertensive type of venous thrombosis, parasympathicotonia is observed predominantly, and in hypotonic venous thrombosis - sympathicotonia with normal or excessive autonomic support.

6. The main complaint of children with IDH is pain syndrome, which does not have a clear and distinct characteristics. Pain is often provoked by stressful situations, intermittent, short-lived, not intense. Their localization is more often in the area of \u200b\u200bthe right hypochondrium.

7. Indispensable companion of the disease is dyspepsia. Children have decreased appetite, they are often worried about nausea. Often, young patients do not tolerate fatty and sweet foods: after eating them, they develop nausea and vomiting. Sometimes older children complain of a bitter taste in their mouth. Unstable stools appear.

8. During an objective examination, the doctor reveals areas of pain on palpation in the right hypochondrium, increased pain when tapping the edge of the palm along the edge of the costal arch. In most children, the liver is enlarged and its edge is palpable 1-2 cm below the costal arch.

9. Treatment of children with DVP is carried out until the complete elimination of bile stagnation and signs of impaired bile outflow. In case of severe pain, it is advisable to treat the child for 10-14 days in a hospital setting, and then in a local sanatorium.

10. Timely diagnosis of biliary tract dysfunctions and proper treatment of children, depending on the type of detected violations, prevents the formation of further inflammatory diseases of the gallbladder, liver, pancreas and prevents early stone formation in the gallbladder and kidneys.

Literature

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2. Denisov M. Yu. Practical gastroenterology for a pediatrician: Reference guide, 1999.

3. Pediatric gastroenterology (selected chapters) / Under. ed. A. A. Baranova, E. V. Klimanskaya, G. V. Rimarchuk, 2002.

4. Diseases of the digestive system in children / Under. ed. A. A. Baranova. 1996.

5. Zaitseva OV, Vovk AN Dysfunctional disorders of the biliary tract in children: a modern view of the problem // Consilium medicum. Pediatrics. 2003. No. 2. P. 26–29.

6. Clinical guidelines for ultrasound diagnostics in pediatrics / Under. ed. M. I. Pykova, K. V. Vatolina, 1998.

7. Korovina N. A., Zakharova I. N. Cholepathy in children and adolescents: A guide for a doctor, 2003.

8. International classification of functional disorders of the digestive system. Rome Consensus on Functional Disorders of the Digestive System, 1999.

9. Minushkin ON Dysfunctional disorders of the biliary tract: pathophysiology, diagnostics and therapeutic approaches, 2004.

10. Minushkin ON Report on clinical testing of the drug Odeston in patients with chronic cholecystitis, 2002.

11. Nasonova SV, Tsvetkova LI Experience of using odeston in the treatment of chronic diseases of the gallbladder and biliary tract // Ros. zhurn. gastroenterol., hepatol., coloproctol. 2000. No. 3.

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16. Yakovenko E. P., Grigoriev P. Ya. Chronic diseases of the extrahepatic biliary tract: Diagnostics and treatment, 2000

This is a violation of the timely full outflow of the produced bile into the duodenum.

Etiology:

Primary causes (with congenital malformations of the biliary tract (doubling of the gallbladder and ducts, congenital narrowing, constrictions and septa in the gallbladder, etc.))

Secondary causes (dysfunction (contraction) of the biliary tract associated with various diseases).

Clinic:

Symptoms: abdominal pain, loss of appetite, nausea, intolerance to fatty foods, sometimes vomiting when overeating fatty and sweet foods, bitter taste in the mouth, unstable stools (alternating constipation and diarrhea), signs of disorders of the autonomic nervous system.

1. Hypermotor (or hyperkinetic) DWP.

It occurs with excessive spastic contraction of the gallbladder. Characterized by sharp short-term attacks of pain (colic) in the right side. The pain increases with brisk running and walking (usually in physical education classes), in stressful situations and when the diet is disturbed. Patients with hypermotor JVP do not tolerate fatty, fried and egg yolks.

2. Hypomotor (or hypokinetic) DVP.

The gallbladder contracts sluggishly. Characterized by dull, aching pain in the right side, rather similar to a feeling of bursting, heaviness, discomfort. The pain intensifies with a violation of the diet or with emotional stress. Constipation is common in children with hypomotor veins.

3. Mixed JVP.

Combines signs of both hypomotor and hypermotor forms. It behaves unpredictably in different situations. Diagnostics:

From the history and examination.

Ultrasound of the gallbladder and biliary tract (+ ultrasound with breakfast)

Duodenal intubation

X-ray examination

Gastroscopy; scintigraphy

Treatment:

Hypermotor type: diet (table number 5 according to Pevzner or hepatic table); drugs that relax smooth muscles (no-shpa, papaverine); calming the nervous system (valerian, motherwort); magnesium preparations (panangin, asparkam); mineral water; physiotherapy (exercise therapy, electrophoresis with magnesium)

Hypomotor type: daily regimen; diet; tonics (preparations of Eleutherococcus, ginseng), B vitamins; choleretic agents (flamin (immortelle flowers), cholenzym, hophytol (artichoke)); homeopathic remedies (hepel, galstina); Tubage improves the outflow of bile from the liver and gallbladder, reduces viscosity and liquefies bile.

Prevention:

- adherence to a healthy lifestyle, proper nutrition. You should strictly maintain the intervals between meals, do not get carried away with spicy and pickled dishes, alcohol, carbonated drinks.

44. Chronic cholecystitis in children. Causes. Clinic. Diagnostics. Treatment. Forecast.

This is an inflammatory disease lasting more than 6 months, affecting the walls of the gallbladder mainly in the neck area, usually proceeding with impaired circulation of bile.

Causes:

Infectious, allergic genesis of the disease is allowed, primary aseptic (chemical) inflammation, as a result of prolonged dyscholia. Enzymatic genesis, due to damage to the epithelium of the mucous membrane of the biliary tract by pancreatic enzymes. The infection enters the bile duct by the lymphogenous, hematogenous and ascending route.

Clinic:

Subfebrile condition and moderate leukocytosis. During the period of exacerbation, severe intoxication is possible. Pain syndrome: intense and prolonged abdominal pain, more often of a paroxysmal nature, arising either independently of food intake or after eating fatty foods, physical activity. Bole are not associated with the season of the year. The main localization of pain is the right hypochondrium and in the "vesicular" points. Symptoms are positive - Ortner, Murphy, soreness at the Kera point, Lepine's symptom. In older children, atypical localization of pain syndrome is possible - pain in the heart, pain in the epigastric region or behind the sternum (esophalgic form). Dyspeptic syndrome: nausea, vomiting that does not bring relief, tendency to constipation. The most pronounced clinic with cholecystocholangitis.

Diagnostics:

Duodenal intubation (On examination, bile is cloudy, heterogeneous, sometimes with flakes, contains a large amount of mucus; microscopy of bile reveals a large number of leukocytes (more than 10 in p / sp), amorphous salts of bile acids, salts of calcium bilirubinate, cholesterol)

Blood test (an increase in the level of Ig-M, G, as well as an increase in the activity of serum alkaline phosphatase.)

Cholecystography (violations of the motor function of the bile ducts, a sharp decrease in concentration function, an increase in the size of the bile ducts, deformation of its "neck" - "an apple on a thin leg")

Ultrasound (congenital changes in the gallbladder, changes in the walls of the bladder, their thickening and compaction, separation of the walls (symptom of layering)).

Treatment:

In a hospital setting during an exacerbation

Bed rest; diet table number 5; choleretic products (vegetable juices, vegetable oil, eggs); choleretic drugs; antibiotic therapy (ampicillin with eubiotic)

Forecast:

Cholecystectomy; uncomplicated cholecystitis has an excellent prognosis, with very low mortality; some complications may develop (gallbladder cancer, jaundice, pancreatitis, perforation).

Dyskinesias of the biliary tract(dysfunctional disorders of the biliary tract) are changes in the tone of the gallbladder, bile ducts and their sphincters, manifested by a violation of the outflow of bile into the duodenum, accompanied by pain in the right hypochondrium.
Dyskinesias of the biliary tract are divided into primary and secondary. Primary is understood as biliary dyskinesias without the presence of proven organic changes in the extrahepatic biliary system; they account for only 10-15%. Secondary dysfunctional disorders of the biliary tract occur in acalculous cholecystitis, cholelithiasis (GSD), hepatitis, cirrhosis of the liver, diseases of the stomach and duodenum, after surgical removal of the gallbladder (cholecystectomy) and resection of the stomach, in pregnancy, premenstrual tension syndrome, diabetes mellitus, , when treated with somatostatin.
The following factors play a role in the mechanisms of development of biliary dyskinesias:

Violations of autonomic nervous regulation (increased tone of the parasympathetic or sympathetic department);

Central nervous regulation disorders;

Pathological (interoreceptive) reflexes from various parts of the digestive tract;

Hormonal regulation disorders.

There are the following clinical forms of biliary dyskinesia:
1. By localization: a) gallbladder dysfunction; b) dysfunction of the sphincter of Oddi.
2. By causation: a) primary; b) secondary.
3. By functional state: a) hypotonic-hypokinetic form; b) hypertensive-hyperkinetic form.
The clinical picture. The main clinical symptoms in dysfunctional disorders of the biliary tract are pain, dyspepsia, and neurotic disorders. With a hypotonic-hypokinetic form, there is a feeling of heaviness in the abdominal cavity, dull, prolonged pain in the right hypochondrium without clear irradiation (spread). They subside after eating, choleretic drugs, duodenal intubation. Nausea, bitterness in the mouth, vomiting, unstable stools (constipation, less often diarrhea) are also characteristic. In hypertensive-hyperkinetic form of pain, cramping, short-term, with typical irradiation. There may be nausea, vomiting, spastic constipation, signs of vagotonia (increased function of the parasympathetic nervous system).
The clinical picture of sphincter of Oddi dysfunction is characterized by recurrent attacks of severe or moderate pain for more than 20 minutes, repeated for more than 3 months and localized:
in the epigastrium or right hypochondrium with irradiation to the back and right scapula (biliary type);
in the left hypochondrium with irradiation to the back, decreasing when bending forward (pancreatic type);
shingles (combined type).
Pain can be combined with the following symptoms: onset after eating; appearance at night; nausea and / or vomiting.
Patients with sphincter of Oddi dysfunction are classified:
I group- diagnosed dysfunction (manometry is optional).
Criteria:
A. Classic attack of biliary pain.
B. An increase in the activity of ALT and / or ALP in 2 times, identified at least twice.
B. Slowing down the evacuation of the contrast medium with endoscopic retrograde cholangiopancreatography (ERCP) for more than 45 minutes.
D. Expansion of the common bile duct more than 12 mm.
II group- suspected dysfunction (manometry is necessary).
Typical pain and one or two criteria of the first group.
III group- possible dysfunction (manometry is necessary if surgery is expected).
Characteristic pains without other changes.
To diagnose dysfunctional disorders of the biliary tract, the following are used:
1. Non-invasive methods:
study of the level of hepatic and / or pancreatic enzymes during a painful attack;
provocative pain tests (for example, the Nardi test);
Ultrasound with an assessment of the function of the gallbladder and sphincter of Oddi;
quantitative scintigraphy of the liver and biliary tract.
duodenal intubation;
X-ray methods (cholecystography, intravenous cholangiography) are rarely used today, they provide information on the concentration and contractile function of the gallbladder;
fibrogastroduodenoscopy (FGDS): the state of the large duodenal papilla, the presence of diseases of the stomach and duodenum.
2. Invasive methods:
ERCP;
endoscopic manometry of the sphincter of Oddi.
Treatment. In dysfunctional disorders of the biliary tract, especially in primary forms, psychotherapy, the use of psychotropic and vegetative-stabilizing drugs are of particular importance.

Medication depends on the type of dyskinesia. When hypotonic-hypokinetic dyskinesia is prescribed:

a diet rich in dietary fiber and vegetable oil, with an increase in foods with cholekinetic effects; tyubazhi ("blind tyubazh"); duodenal intubation with intraduodenal injection of mineral water 0.3-1 l (with severe hypotension - 1-2 times a week); physiotherapy exercises; choleretics and cholekinetics in courses of 1 month; motor controllers; drinking treatment with mineral waters (water of medium mineralization, cool (30-350 C), 1 glass 3 times a day 15-30 minutes before meals).

With secondary dyskinesias, it is necessary to treat the underlying disease. In some cases, according to indications, invasive methods of treating sphincter of Oddi dysfunction are used: endoscopic balloon dilatation; injection of botulism toxin into the sphincter; setting the times of a stent catheter into the bile duct; excision of the sphincter.

INTESTINAL OBSTRUCTION

28) intestinal obstruction: concept, classification, etiopathogenesis, diagnosis.
intestinal obstruction- a disease characterized by a partial or complete violation of the movement of contents through the digestive tract.
classification:by the factor of congenitality: congenital and acquired.
by the mechanism of occurrence: a) dynamic (functional): 1) spastic 2) paralytic b) mechanical: 1) obstructive, 2) strangulation 3) mixed.
by the level of obstruction: a) small intestinal: 1) high 2) low, b) colonic
downstream: acute, chronic
by stage: a) initial-2-12 hours (neuroreflex), b) intermediate (toxic) -12-36 hours, c) late (peritonitis) - later 36 hours.

Etiology:allocate predisposing and producing factors. Congenital predisposing factors include: 1) malrotation syndrome, 2) common mesentery of the cecum and ileum, 3) Dolichosigma (lengthening of the sigmoid colon), 4) Long mesentery, ligaments, large pockets (Treyz). Acquired predisposing factors include: 1) adhesions, 2) scars, 3) inflammatory infiltrates, 4) foreign bodies, 5) gallstones and fecal stones, 6) helminthiasis, 7) operative defects.
producing factors: 1) a sharp change in the motor activity of the gastrointestinal tract (food load, starvation, drug stimulation, dyskinesia, infectious diseases, enterocolitis) 2) increased intra-abdominal pressure during exercise.
Pathogenesis: three theories: 1) the theory of stercoremia (toxic) - with the development of ileus, intoxication gradually increases due to the absorption of toxins from the stagnant intestinal contents in the adducting segment of the intestine (above the place of obstruction)
2) the theory of biochemical changes - it is based on the dyscrasia of digestive juices. Normally, about 10 liters of digestive juices are secreted in the digestive tract. Their loss with vomiting, combined with impaired absorption and digestion processes, aggravate the loss of nutrients from the body. All this causes profound disturbances of protein, carbohydrate, lipid, water-electrolyte and vitamin metabolism, acid-base state of the body.
3) Nerve-reflex theory - from the leading loop into the central nervous system comes powerful afferent impulses with intestinal obstruction. First, a focus of excitation is formed, then a focus of inhibition. Disturbed blood circulation of the intestinal wall, trophism, paresis deepens.
stages of pathogenesis: 1) violation of mesenteric and organ hemocirculation (ischemia of the intestinal wall)
2) development of proximal microbial hypercolonization of the intestine (intensive reproduction of intestinal microflora)
3) development of the syndrome of enteric insufficiency with violation of all intestinal functions. 4) disorders in the immune system of the gastrointestinal tract
5) development and progression of peritonitis 6) progression of endogenous intoxication
7) the development of multiple organ failure
Diagnostics:includes an assessment of the patient's complaints and anamnesis, examination, palpation, abdominal percussion. It is important to have a rectal examination, assessment of changes from the OAC, OAM, biochemical blood test. From special methods - fluoroscopy (graphy) of the abdominal cavity, assessment of the passage of barium or irrigoscopy. They can use fibrogastroduodenoscopy, colonoscopy, ultrasound, CT and NMR tomography, mesentericography, gastrointestinal scintigraphy.

29) General principles of treatment of acute intestinal obstruction, indications for surgical treatment, types of operations.
Canned food should be treated with an effect on the links of the pathogenesis of intestinal obstruction. Principles: First, decompression of the proximal gastrointestinal tract should be ensured by aspiration of the contents through a nasogastric or nasointestinal (installed during surgery) tube. The setting of a cleansing and siphon enema, when they are effective ("erosion" of dense feces), allows you to empty the colon located above the obstacle and, in some cases, to resolve the obstruction. In case of tumor large bowel obstruction, intubation of the narrowed section of the intestine is desirable to unload the adductor. Secondly, it is necessary to correct water-electrolyte disturbances and eliminate hypovolemia. The general rules for such therapy are set out in Chapter III, here we only note that the volume of infusion therapy carried out under the control of CVP and diuresis (catheterization of one of the central veins and the presence of a catheter in the bladder is desirable) should be at least 3-4 liters. It is imperative to replenish the potassium deficiency, since it contributes to the aggravation of intestinal paresis. Thirdly, in order to eliminate hemodynamic disorders, in addition to adequate rehydration, rheologically active agents should be used - rheopolyglucin, pentoxifylline, etc. blood plasma. Fifthly, it is necessary to influence the peristaltic activity of the intestine: with increased peristalsis and cramping pain in the abdomen, antispasmodics are prescribed (atropine, platifillin, no-shpu, etc.), with paresis - means that stimulate the motor-evacuation ability of the intestinal tube: intravenous administration of a hypertonic solution sodium chloride (at the rate of 1 ml / kg of the patient's body weight), ganglion blockers, proserin, uretide, polyhydric alcohols, for example, sorbitol, Bernard's currents to the anterior abdominal wall). And, finally, last (but not least), measures are vital to ensure detoxification and prevention of purulent-septic complications. For this purpose, in addition to the transfusion of significant amounts of liquid, it is necessary to use the infusion of low molecular weight compounds (hemodez, sorbitol, mannitol, etc.) and antibacterial agents.
indications for surgical treatment:
1) in the presence of signs of peritonitis.
2) in the presence of obvious signs or suspicion of strangulated or mixed intestinal obstruction.
In other cases: a medical and diagnostic reception is carried out, with a negative one, an operative treatment is performed, with a positive one, a conservative one. Reception includes: subcutaneous injection of atropine, performing perirenal novocaine blockade, washing the stomach, introducing a siphon enema. It is assessed in the following way: if gases have moved away, there was a chair, the abdomen has decreased in size, the pain syndrome has disappeared, the reception is considered positive.

Types of operations: Most authors divide all surgical interventions for intestinal obstruction into three groups:
- elimination of the cause of mechanical intestinal obstruction (unwinding during volvulus, disinvagination during intussusception, dissection of strangulated adhesions, bowel resection, etc.);
- the imposition of various kinds of anastomoses to bypass obstacles;
- the imposition of an intestinal fistula above the obstacle.
Each method of surgery requires an individual approach, taking into account the type of obstruction, the nature of changes in the intestine, etc.
For a favorable outcome of surgery for intestinal obstruction, correct management of patients in the postoperative period is of great importance. Here, if necessary, the fight against hemodynamic disorders, disorders of water-salt, protein and carbohydrate metabolism continues, measures are taken to restore peristalsis as soon as possible.

30) Dynamic intestinal obstruction: causes, clinical picture, diagnosis, treatment.
Causes:paralytic obstruction develops peritonitis, acute pancreatitis, perforation of the hollow organ, hypokalemia after operations on the abdominal organs and drainage of the abdominal cavity. Its occurrence is possible after the resolution of spastic obstruction, with dysentery, dyspepsia and damage to the vagus nerve.
reasonsspastic obstruction can be reflexes from other organs of the chest and abdominal cavities, retroperitoneal space, lesions of the central nervous system (dorsal tabes), spasm of the mesenteric vessels (abdominal toad), lead poisoning, nicotine, morphine.
Clinic:The disease is characterized by a sudden onset. The leading symptom is severe cramping pains. The pain is not localized and usually spreads throughout the abdomen. During the period of labor, the patient rushes about on the bed, screams. Dyspeptic disorders are not typical. Stool and gas retention is not observed in all patients, they are never persistent. The general condition of the patient is disturbed slightly. The abdomen has a normal configuration on examination. Sometimes the abdominal wall is elongated and the abdomen takes on a scaphoid shape.
diagnostics: includes an assessment of the patient's complaints and anamnesis, examination, palpation, abdominal percussion. It is important to have a rectal examination, assessment of changes from the OAC, OAM, biochemical blood test. From special methods - fluoroscopy (graphy) of the abdominal cavity, assessment of the passage of barium or irrigoscopy. They can use fibrogastroduodenoscopy, colonoscopy, ultrasound, CT and NMR tomography, mesentericography, gastrointestinal scintigraphy.

An overview X-ray examination of the abdomen reveals a spastic-atonic state of the intestine. Sometimes, along the course of the small intestine, small Kloyber bowls are visible, located in a chain from the left from top to bottom and to the right. In a contrast study of the gastrointestinal tract with barium, the delayed passage of the barium suspension through the small intestine is determined.
treatment:conservative. Patients are prescribed antispasmodics, physiotherapeutic procedures, warmth on the stomach, and the underlying disease is treated. Held medical and diagnostic reception according to Vishnevsky, allowing early differentiation of mechanical KN from dynamic, with a negative result, surgical treatment is performed, with a positive one, conservative. Reception includes: subcutaneous injection of atropine, performing perirenal novocaine blockade, washing the stomach, introducing a siphon enema. It is assessed in the following way: if gases have departed, there was a chair, the stomach has decreased in size, the pain syndrome has disappeared, the reception is considered positive.
2) 250 ml of liquid barium sulfate is given orally.
3) infusion therapy is performed.
4) an assessment of the passage of barium is carried out - during its passage (after 6 hours into the colon, after 24 hours into the direct), the diagnosis of intestinal obstruction is removed, and the patient is subjected to a detailed examination.