Clinical guidelines for cholecystitis. Algorithm for managing patients with cholelithiasis

DEFINITION. Gallstone disease (GSD) is a disease characterized by the formation of stones in the gallbladder (cholecystolithiasis), the common bile duct (choledocholithiasis), which can occur with symptoms of biliary (biliary, hepatic) colic in response to transient stone obstruction of the cystic or common bile duct, accompanied by spasm of smooth muscles, intraductal hypertension.

In ecologically developed countries, cholelithiasis develops in 10-15% of the population. Between the ages of 21 and 30, cholelithiasis affects 3-4% of the population, from 41 to 50 years - 5%, over 60 years - up to 20%, over 70 years - up to 30%. The predominant gender is female (2-5:1), although there is a tendency for the incidence to increase in men.

ETIOLOGY AND PATHOGENESIS

Factors predisposing to the formation of gallstones (primarily cholesterol): female gender; age (the older the patient, the higher the likelihood of cholelithiasis); genetic and ethnic characteristics; nature of nutrition - excessive consumption of fatty foods high in cholesterol, animal fats, sugar, sweets; pregnancy (history of multiple births); obesity; starvation; diseases of the ileum - short colon syndrome, Crohn's disease, etc.; the use of certain medications - clofibrate, estrogens, somatostatin, etc.

The main cause of stone formation is a violation of the physico-chemical composition and stagnation of bile, infections of the biliary tract. In its normal state, cholesterol is insoluble in water; maintaining the homogeneity of bile depends on the concentration of cholesterol, bile acids and lysolycetin. The basis for the formation of stones is increased secretion of cholesterol.

Classification of gallstones

By localization:

in the gallbladder

in the common bile duct

in the hepatic ducts

By number of stones:

single

multiple

By composition:

• cholesterol - contain mainly cholesterol, have a round or oval shape, layered structure, diameter from 4-5 to 12-15 mm; typical location - gallbladder

  pigment (bilirubin) are characterized by small sizes, usually multiple; hard, fragile, completely homogeneous, located both in the gallbladder and bile ducts

  mixed (found most often) - often multiple, of the most varied forms; they contain cholesterol, bilirubin, bile acids, proteins, glycoproteins, various salts, and microelements.

Classification of cholelithiasis according to clinical course:

latent form (stone carriage);

primary chronic cholecystitis;

biliary colic;

chronic recurrent cholecystitis.

Clinic

Often, cholelithiasis is asymptomatic (a latent course is observed in 60-80% of people with stones in the gall bladder and in 10-20% of people with stones in the common bile duct), and stones are discovered accidentally during an ultrasound. The diagnosis of cholelithiasis is made on the basis of clinical data (the most common option in 75% of patients is biliary colic) and ultrasound results.

The main clinical manifestation of cholelithiasis is biliary colic (usually due to transient stone obstruction of the cystic duct).

It is characterized by acute visceral pain localized in the epigastric or right hypochondrium; less often, pain occurs only in the left hypochondrium, precordial region, or lower abdomen, which significantly complicates diagnosis.

In 50% of patients, pain radiates to the back and right scapula, interscapular region, right shoulder, and less often to the left half of the body.

The duration of biliary colic ranges from 15 minutes to 5-6 hours. Pain lasting more than 5-6 hours should alert the doctor regarding complications, especially acute cholecystitis.

The pain syndrome is accompanied by increased sweating, a grimace of pain on the face and a forced position - on the side with the legs tucked to the stomach. Sometimes nausea and vomiting occur. The onset of pain may be preceded by the consumption of fatty, spicy foods, alcohol, physical activity, and emotional experiences. Pain is associated with overstretching of the gallbladder wall due to increased intravesical pressure and spastic contraction of the sphincter of Oddi or cystic duct. With biliary colic, an increase in body temperature is possible, however, prolonged and significant hyperthermia (above 38 ° C) in combination with symptoms of intoxication (asthenovegetative syndrome, dryness and coated tongue) usually indicate the addition of acute cholecystitis. The presence of jaundice is usually considered a sign of biliary obstruction.

When collecting anamnesis, it is necessary to especially carefully question the patient regarding episodes of abdominal pain in the past, since as cholelithiasis progresses, episodes of biliary colic recur, become protracted, and the intensity of pain increases.

Nonspecific symptoms are also possible, for example, heaviness in the right hypochondrium, flatulence, and dyspeptic symptoms.

It is possible to identify a symptom of muscle protection, increased pain during palpation in the right hypochondrium and tapping the edge of the palm along the right costal arch, as well as Murphy’s symptom (involuntary holding of breath at the height of inspiration during palpation of the gallbladder due to increased pain). The addition of acute cholecystitis is characterized by the appearance of specific inflammatory symptoms from the biliary system.

bladder (see article “chronic acalculous cholecystitis”).

DIAGNOSTICS

A thorough history taking and physical examination (identifying typical signs of biliary colic, symptoms of an inflamed gallbladder).

Performing ultrasound as a first-line method or other studies to visualize gallstones. However, even if stones are not detected by available methods, the likelihood of their presence in the common bile duct is assessed as high if the following clinical and laboratory signs are present: jaundice; dilation of the bile ducts, including intrahepatic ones, according to ultrasound data; altered liver tests (total bilirubin, ALT, AST, gamma-glutamyl transpeptidase, alkaline phosphatase, the latter increases when cholestasis occurs due to obstruction of the common bile duct).

Laboratory testing is necessary to identify persistent obstruction of the biliary tract or the addition of acute cholecystitis.

One of the important diagnostic goals should be considered the differentiation of the uncomplicated course of cholelithiasis (asymptomatic stone carriage, uncomplicated biliary colic) and the addition of possible complications (acute cholecystitis, acute cholangitis, etc.), requiring more aggressive treatment tactics.

Laboratory research

For the uncomplicated course of cholelithiasis, changes in laboratory parameters are not typical.

With the development of acute cholecystitis and concomitant cholangitis, the appearance of leukocytosis (11-15x10 9 / l), an increase in ESR, an increase in the activity of serum aminotransferases, cholestasis enzymes - alkaline phosphatase, γ-glutamyl transpeptidase (GGTP), bilirubin level up to 51-120 µmol/l (3 -7 mg%).

Mandatory laboratory tests

general clinical studies: clinical blood test. Leukocytosis with a shift of the leukocyte formula to the left is not typical for biliary colic. It usually occurs when acute cholecystitis or cholangitis occurs; reticulocytes;

coprogram;

general urinalysis;

blood plasma glucose

Lipid metabolism indicators: total blood cholesterol, low-density lipoproteins, very low-density lipoproteins.

Liver function tests (their increase is associated with choledocholithiasis and biliary tract obstruction): AST; ALT; y-glutamyl transpeptidase; prothrombin index; alkaline phosphatase; bilirubin: total, direct, serum albumin;

Pancreatic enzymes: blood amylase, urine amylase.

Additional laboratory tests

Hepatitis virus markers:

HB s Ag (hepatitis B virus surface antigen); anti-HB c (antibodies to hepatitis B nuclear antigen); anti-HCV (antibodies to the hepatitis C virus).

Instrumental studies

If there is a clinically justified suspicion of cholelithiasis, an ultrasound scan is first necessary.

The diagnosis of cholelithiasis is confirmed using computed tomography (gallbladder, bile ducts, liver, pancreas) with quantitative determination of the Hounsfield attenuation coefficient of gallstones (the method allows one to indirectly judge the composition of stones by their density), magnetic resonance cholangiopancreatography (allows one to identify invisible Ultrasound of stones in the bile duct, sensitivity 92%, specificity 97%), ERCP (a highly informative method for studying extrahepatic ducts if a stone in the common bile duct is suspected or to exclude other diseases and causes of obstructive jaundice).

Mandatory instrumental studies

Ultrasound of the abdominal organs is the most accessible method with high sensitivity and specificity for detecting gallstones: for stones in the gall bladder and cystic duct, the sensitivity of ultrasound is 89%, the specificity is 97%; for stones in the common bile duct - sensitivity less than 50%, specificity 95%. A targeted search is required: expansion of intra- and extrahepatic bile ducts; stones in the lumen of the gallbladder and bile ducts; signs of acute cholecystitis in the form of thickening of the gallbladder wall more than 4 mm and identification of a “double contour” of the gallbladder wall.

Survey radiography of the gallbladder area: the sensitivity of the method for detecting gallstones is less than 20% due to their frequent X-ray negativity.

FEGDS: carried out to assess the condition of the stomach and duodenum, to examine the major duodenal papilla if choledocholithiasis is suspected.

Differential diagnosis

Biliary colic must be differentiated from the following 5 conditions.

Biliary sludge: sometimes a typical clinical picture of biliary colic is observed. The presence of bile sediment in the gallbladder on ultrasound is characteristic.

Functional diseases of the gallbladder and bile ducts: during the examination, no stones are found, signs of impaired contractility of the gallbladder (hypo- or hyperkinesia), spasm of the sphincter apparatus according to direct manometry (dysfunction of the sphincter of Oddi) are detected. Pathologies of the esophagus: esophagitis, esophagospasm, hiatal hernia. Characterized by pain in the epigastric region and behind the sternum in combination with typical changes during FEGDS or X-ray examination of the upper gastrointestinal tract.

Peptic ulcer of the stomach and duodenum. Pain in the epigastric region is characteristic, sometimes radiating to the back and decreasing after eating, taking antacids and antisecretory drugs. FEGDS is necessary.

Diseases of the pancreas: acute and chronic pancreatitis, pseudocysts, tumors. Typical pain is in the epigastric region, radiating to the back, provoked by food intake and often accompanied by vomiting. The diagnosis is helped by identifying increased activity in the blood serum of amylase and lipase, as well as typical changes according to the results of radiological diagnostic methods. It should be taken into account that cholelithiasis and biliary sludge can lead to the development of acute pancreatitis.

Liver diseases: characterized by dull pain in the right hypochondrium, radiating to the back and right shoulder blade. The pain is usually constant (which is not typical for the pain syndrome associated with biliary colic) and is accompanied by enlargement and tenderness of the liver on palpation. The diagnosis is made by determining liver enzymes in the blood, markers of acute hepatitis and imaging studies.

Diseases of the colon: irritable bowel syndrome, inflammatory lesions (especially when the hepatic flexure of the colon is involved in the pathological process). Pain syndrome is often caused by motor disorders. The pain is often relieved by bowel movements or passing gas. Colonoscopy or irrigoscopy can distinguish functional changes from organic ones.

Diseases of the lungs and pleura. Characteristic manifestations of pleurisy are often associated with cough and shortness of breath. An X-ray examination of the chest is necessary.

Skeletal muscle pathologies. There may be pain in the right upper quadrant of the abdomen associated with movements or taking a certain position. Palpation of the ribs may be painful; Increased pain is possible with tension in the muscles of the anterior abdominal wall.

TREATMENT

Indications for hospitalization

To the surgical hospital:

recurrent biliary colic;

acute and chronic cholecystitis and their complications;

acute biliary pancreatitis.

To the gastroenterology hospital:

chronic calculous cholecystitis - for detailed examination and preparation for surgical or conservative treatment;

exacerbation of cholelithiasis and the condition after cholecystectomy (chronic biliary pancreatitis, dysfunction of the sphincter of Oddi).

Duration of inpatient treatment: chronic calculous cholecystitis - 8-10 days, chronic biliary pancreatitis (depending on the severity of the disease) - 21-28 days.

Treatment includes diet therapy, the use of medications, external lithotripsy methods and surgery.

Non-drug treatment

Diet therapy: at all stages, 4-6 meals a day are recommended with the exclusion of foods that increase bile secretion, secretion of the stomach and pancreas. Avoid smoked meats, refractory fats, and irritating seasonings. The diet should include a large amount of plant fiber with the addition of bran, which not only normalizes intestinal motility, but also reduces the lithogenicity of bile. With biliary colic, fasting is necessary for 2-3 days.

Drug therapy

Oral litholytic therapy is the only effective conservative method for the treatment of cholelithiasis. Bile acid preparations are used to dissolve stones: ursodeoxycholic acid (Ursofalk, Ursosan) and chenodeoxycholic acid.

Ursodeoxycholic acid slows down the absorption of cholesterol in the intestine and promotes the transfer of cholesterol from stones to bile.

Chenodeoxycholic acid inhibits the synthesis of cholesterol in the liver and also helps dissolve cholesterol stones. Treatment with bile acid preparations is carried out and monitored on an outpatient basis.

Strict patient selection criteria make this method available to a very small group of patients with an uncomplicated course of the disease - approximately 15% with cholelithiasis. High cost also limits the application of this method. The most favorable conditions for the outcome of oral lithotripsy are:

in the early stages of the disease;

for uncomplicated cholelithiasis , rare episodes of biliary colic, moderate pain syndrome;

in the presence of pure cholesterol stones (“float up” during 3 oral cholecystography);

if there are non-calcified stones in the bladder (CT attenuation coefficient less than 70 Hounsfield units);

■ with stone sizes no more than 15 mm (when combined with shock wave lithotripsy - up to 30 mm), the best results are observed with stone diameters up to 5 mm; with single stones occupying no more than 1/3 of the gallbladder;

■ with preserved contractile function of the gallbladder. Contraindications to the use of conservative therapy for cholelithiasis:

Complicated cholelithiasis, including acute and chronic cholecystitis, since the patient is indicated for rapid sanitation of the biliary tract and cholecystectomy.

Disabled gallbladder.

Frequent episodes of biliary colic.

Pregnancy.

Severe obesity.

An open ulcer of the stomach or duodenum.

Concomitant liver diseases - acute and chronic hepatitis, liver cirrhosis.

Chronic diarrhea.

Gallbladder carcinoma.

The presence of pigmented and calcified cholesterol stones in the gallbladder.

Stones with a diameter of more than 15 mm.

Multiple stones occupying more than 50% of the gallbladder lumen.

Patients are prescribed chenodeoxycholic acid at a dose of 15 mg/kg/day or ursodeoxycholic acid at a dose of 10 mg/kg/day once, the entire dose in the evening before bed, with plenty of water. The most effective and often recommended treatment regimen is a combination of taking chenodeoxycholic acid at a dose of 7-8 mg/kg and ursodeoxycholic acid at a dose of 7-8 mg/kg once at night. The duration of treatment ranges from 6 to 24 months with continuous use of drugs. Regardless of the effectiveness of litholytic therapy, it reduces the severity of pain and reduces the likelihood of developing acute cholecystitis. Treatment is carried out under the control of the condition of the stones according to ultrasound every 3-6 months. After the stones dissolve, ultrasound is repeated after 1-3 months.

After dissolving the stones, it is recommended to take ursodeoxycholic acid for 3 months at a dose of 250 mg/day. The absence of positive dynamics according to ultrasound data after 6 months of taking the drugs indicates the ineffectiveness of oral litholytic therapy and indicates the need to discontinue it.

Antibacterial therapy. Indicated for acute cholecystitis and cholangitis (see article “chronic acalculous cholecystitis”).

Surgical treatment

In asymptomatic cases of cholelithiasis, as well as in a single episode of biliary colic and infrequent pain episodes, a wait-and-see approach is most justified. If indicated, oral lithotripsy may be performed in these cases.

Indications for surgical treatment for cholecystolithiasis:

■ the presence of large and small stones in the gallbladder, occupying more than 1/3 of its volume;

course of the disease with frequent attacks of biliary colic, regardless of the size of the stones;

disabled gallbladder;

Cholelithiasis complicated by cholecystitis and/or cholangitis;

combination with choledocholithiasis;

GSD complicated by the development of Mirizzi syndrome;

ZhKB , complicated by dropsy, empyema of the gallbladder; GSD complicated by perforation, penetration, fistulas;

GSD complicated by biliary pancreatitis;

GSD accompanied by obstruction of the common patency

bile duct.

Methods of surgical treatment: laparoscopic or open cholecystectomy, endoscopic papillosphincterotomy (indicated for choledocholithiasis), extracorporeal shock wave lithotripsy.

Cholecystectomy. It is not indicated for asymptomatic stone carriers, since the risk of surgery outweighs the risk of developing symptoms or complications. However, in some cases, laparoscopic cholecystectomy is considered justified even in the absence of clinical manifestations (Indications for cholecystectomy in asymptomatic stone carriers are a calcified “porcelain” gallbladder; stones larger than 3 cm; upcoming long stay in a region with a lack of qualified medical care; sickle cell anemia ; the patient's upcoming organ transplantation).

If there are symptoms of cholelithiasis, especially frequent ones, cholecystectomy is indicated. Preference should be given to the laparoscopic option in the maximum possible number of cases (less pain, shorter hospital stay, less trauma, shorter postoperative period, better cosmetic result).

The question of the timing of cholecystectomy for acute cholecystitis remains controversial to this day. Deferred (after 6-8 weeks) surgical treatment is considered traditional, followed by conservative therapy with the mandatory prescription of antibiotics to relieve acute inflammation. However, data have been obtained indicating that early (within a few days from the onset of the disease) laparoscopic cholecystectomy is accompanied by the same frequency of complications, but can significantly reduce the treatment time.

There are practically no absolute contraindications to laparoscopic procedures. Relative contraindications include acute cholecystitis with a disease duration of more than 48 hours, peritonitis, acute cholangitis, obstructive jaundice, internal and external bile fistulas, liver cirrhosis, coagulopathy, unresolved acute pancreatitis, pregnancy, morbid obesity, severe pulmonary heart failure.

Shock wave lithotripsy is used very limitedly, as it has a fairly narrow range of indications and a number of contraindications and complications. Extracorporeal shock wave lithotripsy is used in the following cases. The presence in the gallbladder of no more than three stones with a total diameter of less than 30 mm. The presence of stones that “pop up” during oral cholecystography (a characteristic sign of cholesterol stones). Functioning gallbladder according to oral cholecystography. Reduction of the gallbladder by 50% according to scintigraphy.

It should be borne in mind that without additional treatment with ursodeoxycholic acid, the recurrence rate of stone formation reaches 50%. In addition, the method does not prevent the possibility of developing gallbladder cancer in the future.

Endoscopic papillosphincterotomy is indicated primarily for choledocholithiasis.

FORECAST

The effectiveness of conservative treatment turns out to be quite high: with proper selection of patients, complete dissolution of stones is observed after 18-24 months in 60-70% of patients, but relapses of the disease are not uncommon.

Literature

CHRONIC AALCTIC CHOLECYSTITIS (CAC)

DEFINITION. Chronic acalculous cholecystitis is a chronic recurrent inflammation of the gallbladder wall, accompanied by a violation of its motor-tonic function.

In ICD 10 revision of cholecystitis occupies the heading K 81

ETIOLOGY AND PATHOGENESIS

Infection plays a leading role in the development of chronic cholecystitis; the causative agent of the infection usually enters through the hematogenous and lymphogenous routes, less often through the ascending route, i.e. from the duodenum. The development of toxic and allergic inflammation in the gallbladder is observed. It is also possible that the wall of the gallbladder is damaged by pancreatic enzymes that enter there due to increased pressure in the ampulla of the common bile duct. Such forms of cholecystitis are classified as enzymatic.

The role of viral hepatitis in the pathogenesis of chronic inflammation of the biliary system is noted.

In middle-aged and older people, a negative role is played by circulatory disorders in the wall of the gallbladder, which develop against the background of severe atherosclerotic lesions of the gallbladder arteries, and less often - with systemic vascular lesions.

A significant role in the pathogenesis of chronic cholecystitis is played by a violation of the motor-evacuation function of the gallbladder (dyskinesia), which can both contribute to the development of a chronic inflammatory process and be a consequence of it (secondary dyskinesia)

CLASSIFICATION

Functional disorders (dyskinesia)

Inflammatory (cholecystitis, cholangitis)

Exchange (ZhKB)

Developmental anomalies (absence of a bladder, bifurcation, constrictions, diverticula, aplasia and hypoplasia of internal and external ducts)

Combined

CLINIC

Clinical manifestations of gallbladder dyskinesia and chronic cholecystitis are diverse and do not have reliable symptoms and specific features. The classic one is the “right hypochondrium symptom” (N.A. Skuya) - pain in the upper right half of the abdomen, if it is not a symptom of another disease.

It is generally accepted that the nature of complaints in chronic cholecystitis determines the type of dyskinesia. It is classically believed that with hyperkinetic dyskinesia, fairly intense paroxysmal pain in the right hypochondrium, reminiscent of colic, is observed.

Hypokinetic dyskinesia is characterized by a feeling of heaviness, fullness in the area of ​​the right hypochondrium, and severe dyspeptic syndrome. Although the nature of the complaints may vary.

Violation of the motor-evacuation function of the biliary tract - this is an uncoordinated, excessive or insufficient contraction of the gallbladder and sphincters 0di, Lutkens, Mirizzi .

Classification of functional disorders of the biliary tract:

Primary dyskinesias causing disruption of the outflow of bile and/or pancreatic secretions into the duodenum in the absence of organic obstacles

Gallbladder dysfunction

Sphincter of Oddi dysfunction

Secondary dyskinesia of the biliary tract, combined with organic changes in the gallbladder and sphincter of Oddi

Causes of impaired gallbladder emptying:

Primary

Impaired function of the smooth muscles of the gallbladder (decreased muscle mass or receptor sensitivity)

Discoordination of the functions of the gallbladder and cystic duct

Secondary

Hormonal disorders - pregnancy, premenstrual syndrome, somatostatin treatment

Postoperative conditions - gastric resection, anastomosis, vagotomy

Systemic diseases - diabetes, liver cirrhosis, celiac enteropathy, myotonia

Presence of inflammation and stones in the gallbladder

ABOUT The main clinical dyskinesias are considered in the “Roman criteria”. According to the Rome Criteria -3 of 2006, the term dyskinesia of the gallbladder is renamed separately into dyskinesia of the gallbladder, biliary zone of the f. Oddi, pancreatic zone of the f. Oddi. Rome-3 has developed a definition of biliary pain: localized in the epigastrium and/or right upper quadrant of the abdomen, recurs, episodes last 30 minutes or more, increases to constant Additional symptoms: nausea and vomiting, irradiation to the back and/or right subscapular region, leads to waking up at night. There is endocrine (spastic) dyskinesia, which manifests itself in women during the premenstrual period against the background of hyperfolliculinemia. The influence of age, gender, professional, hereditary, social, household, dietary factors, constitutional characteristics, as well as the influence of concomitant pathology on the functional activity of the biliary tract is known. The influence of concomitant pathology is great. Thus, in patients with diabetes mellitus and obesity, a decrease in the contractile function of the gallbladder is observed. In patients with duodenal ulcer, hypermotor dyskinesia of the biliary tract is formed.

According to domestic terminology, dyskinesias are classified depending on the presence or absence of morphological changes in the wall of the gallbladder. Dyskinesia can be primary (functional), without morphological changes in the wall of the gallbladder, i.e. caused by changes in the functional state of the central nervous system, hormonal disorders, visceral reflexes in diseases of the abdominal organs and secondary, associated with morphological changes in the wall of the gallbladder as a result of inflammatory processes in it (cholecystitis).

Based on the nature of disturbances in the motor-evacuation function of the gallbladder, hypo- and hyperkinetic forms of dyskinesia are distinguished.

DIAGNOSTICS

Diagnostic tests for diseases of the biliary tract

Screening

• Duodenal sounding (motility, concentration, sphincter of Oddi tone, inflammation - mucus, leukocytes, bile cells, chromatic sounding - bile acids, cholesterol)

  Determination of bilirubin, alkaline phosphatase, ALT, AST, amylase and blood lipase during or no later than 6 hours after the end of a painful attack

Clarifying

Ultrasound with assessment of biliary and sphincter of Oddi function

ERCP with sphincter of Oddi manometry

Hepatobiliscintigraphy with 99m Tc

Drug tests (with cholecystokinin, morphine - prostigmine provocation test)

Computed tomography

Nuclear magnetic resonance

The diagnosis of chronic cholecystitis is made clinically and echographically. The main diagnostic criterion for chronic cholecystitis is ultrasound echolocation of the gallbladder. The severity of the inflammatory process is indicated by the thickness and density of the gallbladder wall (normally, the wall thickness does not exceed 3 mm).

Strengthening the echostructure of the gallbladder ( compaction), deformation is regarded as a sign of organic changes in the wall of the gallbladder, characteristic of chronic cholecystitis; and a thickening of the gallbladder wall of more than 3 mm, a double contour, is regarded as an exacerbation of the chronic inflammatory process in it.

1. The thickness of the gallbladder wall is more than 4 mm in persons without pathology of the liver, kidneys, or heart failure, in this case a presumptive conclusion is expressed, and if the wall thickness is more than 5 mm, an affirmative one.

2. The presence of a sonographic Murphy sign;

3. An increase in the size of the gallbladder by more than 5 cm from the upper limit of normal for patients of this age.

4. The presence of a shadow from the walls of the gallbladder;

5. The presence of paravesical echo inactivity (fluid), which is more typical for an acute process.

True cholecystitis is a relatively uncommon disease. Under the guise of cholecystitis there are endless dyskinesias of the biliary tract, of which, of course, there are much more. Therefore, to make a diagnosis of chronic cholecystitis, a careful comparison and scrupulous analysis of anamnestic, clinical and echographic data is required.

To diagnose the type of dyskinesia, it is advisable to use methods of fractional chromatic duodenal sounding (FCDS) with methylene blue and ultrasound echolocation with a choleretic test.

Criteria for diagnosing gallbladder dysfunction caused by hypofunction of the gallbladder muscles:

1. The presence of prolonged, often constant pain in the right hypochondrium, often in combination with one or more of the following signs:

nausea, vomiting

stool disorder

2. Hypomotor dyskinesia of the gallbladder

Criteria for diagnosing gallbladder dysfunction caused by incoordination of gallbladder function:

1. The presence of biliary pain (paroxysmal pain in the right hypochondrium or epigastrium lasting at least 20 minutes) combined with one or more of the following signs:

irradiation to the back or right shoulder blade

Occurs after meals and at night

nausea, vomiting

2. Gallbladder dysfunction

3. Absence of structural changes in the biliary system

Examples of clinical diagnoses

Exacerbation of chronic cholecystitis with severe disturbances in the motor-evacuation function of the gallbladder according to the type of hypokinesia

TREATMENT

In the treatment of chronic illness, antibacterial drugs, choleretic, myospasmolytics, anticholinergics are used; in the treatment of dysfunctions of the gallbladder and biliary tract, depending on the type of disorder - choleretic prokinetics, myotropic antispasmodics, anticholinergics, sedatives.

Indications for the use of choleretic drugs:

Choleretics (allochol, cholenzim, hofetol, cyqualon, nicodin, hepatofalk planta, etc.) in combination with enzymes for the correction of intestinal disorders are prescribed in the remission phase and in the phase of fading exacerbation of chronic acalculous cholecystitis. The therapeutic effect of choleretics is due to the fact that, by increasing the secretion of bile, they increase its flow through the bile ducts, which reduces the intensity of the inflammatory process and prevents the spread of ascending infection

Choleretics with a high content of bile acids (decholin, libil, cholenzyme, dehydrocholic acid, etc.) to preserve the myceliality of bile are prescribed for the prevention of cholelithiasis;

Cholekinetics (magnesium sulfate, sorbitol, xylitol, olimethine, holosas ) It is advisable to use for hypokinesia of the gallbladder and bile stasis , after cholecystectomy.

Contraindications to the use of choleretic drugs :

with severe exacerbation of the inflammatory process in the gallbladder and bile ducts. Choleretic drugs are prescribed 3-5 days after the exacerbation has stopped.

for chronic hepatitis (to avoid stimulation of hepatocytes).

With hyperkinetic dyskinesia of the gallbladder.

with chronic pancreatitis in the acute stage.

Condition after cholecystectomy

If there are unpleasant sensations in the right hypochondrium, or congestion in the extrahepatic bile ducts, mineral water can be taken as a choleretic agent. If necessary, it is possible to prescribe nicodine, cyclone, as choleretic drugs with an antibacterial effect.

Options for antibacterial therapy for exacerbation of chronic cholecystitis:

1. Ciprofloxacin– 500 - 750 mg - 2 times a day, 7-10 days.

2. Tetracycline drugs: Doxycycline(Vibramycin - Poland) in therapeutic doses.

3. Erythromycin 200 - 400 mg X 4 times a day, 7-14 days or rovamycin 1.5 IU x 2 times a day per os.

Therapy can be adjusted depending on the clinical effect and the results of studies of duodenal contents.

At the end of an exacerbation, a course of choleretic drugs is added to antibacterial drugs or immediately after a course of antibiotic therapy: allochol, 2 tablets. 3 - 4 times a day after meals, hofitol 2 drops. 3 times a day or other drugs that enhance choleresis and cholekinesis.

Adequate therapy of chronic cholecystitis and correction of motor-evacuation disorders of the gallbladder provide a certain opportunity to prevent the development of cholelithiasis.

At hypokinetic dyskinesia of the gallbladder It is recommended to use tubes with mineral water, sorbitol, prokinetics (Motilium 10 mg 3-4 times a day), choleretics, cholecystokinetics, physical therapy, active motor mode, swimming. The drug of choice for hypokinetic dyskinesia of the gallbladder is Hofetol, which enhances the contractility of the gallbladder by 3.5-5 times or more.

For hyperkinesia of the gallbladder the use of myotropic antispasmodics (dicetel, duspatalin, meteospasmil, no-shpa, golidor, etc.), anticholinergics (platifillin, buscopan 1-2 drops 3-4 times a day) is indicated. Taking such myotropic antispasmodics as dicetel, duspatalin, meteospasmil justified when hypermotor dyskinesia of the gallbladder is combined with IBS.

Literature

Practical hepatology \under. Ed. N.A. Mukhina - Moscow, 2004. - 294 pp.

Vetshev P.S. Gallstone disease and cholecystitis // Clinical perspectives of gastroenterology, hepatology. - 2005. - No. 1 - P 16-24.

Peter R., McNally “Secrets of Gastroenterology”, Moscow, 2004.

Lychev V.G. “Fundamentals of clinical gastroenterology”, Moscow, N-Novgorod, 2005

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K80 Gallstone disease.

Information about the discovery of gallstones was found in ancient sources. Gall stones were used as ritual decorations and in cult rites. Descriptions of the signs of cholelithiasis are given in the works of Hippocrates, Avicenna, and Celsus. There is information that the founders of ancient medical science, Galen and Vesalius, discovered gallstones during autopsies of corpses.

The French physician Jean Fernel (J. Fernel) in the 14th century described the clinical picture of cholelithiasis, and also established its connection with jaundice.
The German anatomist A. Vater in the 18th century described the morphology of gallstones and indicated that the cause of their formation was thickening of bile. Chemical research on gallstones was first undertaken by D. Galeati in the mid-18th century.
The information about gallstone disease accumulated by that time was summarized by the German anatomist and physiologist A. Haller in his works “Opuscula pathologica” and “Elementa physiologiae corporis humani” in the middle of the 8th century.
A. Haller divided all gallstones into two classes: 1) large, ovoid, usually single, consisting of “a tasteless yellow substance that, when heated, melts and can burn,” and 2) smaller, dark-colored, multifaceted, which are found not only in the bladder, but also in the bile ducts. Thus, the modern classification of gallstones, dividing them into cholesterol and pigment stones, was actually justified a long time ago.
Haller's contemporary F.P. de la Salle isolated a substance “similar to fat wax” from gallstones, represented by thin silvery plates. At the end of the 18th and beginning of the 19th centuries, cholesterol was isolated in its pure form by A. de Fourcroy, and from bile by the German chemist L. Gmelin and the French chemist M. Chevreul; the latter called it cholesterol (from the Greek chole - bile, stereos - volumetric).

In the middle of the 19th century, the first theories of the origin of gallstones appeared, among which two main directions stood out:
1) the root cause of the formation of stones is a disturbed condition of the liver, which produces pathologically altered bile,
2) the root cause is pathological changes (inflammation, stasis) in the gallbladder.
The founder of the first direction is the English doctor G. Thudichum. An adherent of the second was S.P. Botkin, who pointed out the importance of inflammatory changes in the development of cholelithiasis and described in detail the symptoms of the disease and therapeutic approaches.
One of the first experimental models of calculous cholecystitis was created by P. S. Ikonnikov in 1915.

At the end of the 19th century, the first attempts at surgical treatment of cholelithiasis were made: in 1882, Karl Langenbach (C. Langenbuch) performed the world's first cholecystectomy, and in Russia this operation was first performed in 1889 by Yu. F. Kosinsky.
S. P. Fedorov, I. I. Grekov, A. V. Martynov made a great contribution to the development of biliary tract surgery.
In 1947 “postcholecystectomy syndrome” has been described, which implies the persistence of symptoms or their appearance after removal of the gallbladder. It should be noted that there is significant clinical heterogeneity of this concept, and research in this direction continues to this day.

At the end of the 20th century, traditional cholecystectomy was replaced by less invasive methods - laparoscopic cholecystectomy (first performed in Germany by E. Muguet in 1985, and cholecystectomy from a mini-access, or “mini-cholecystectomy” (M. I. Prudkov, 1986 g., Vetshev P.S. et al., 2005). Robot-assisted technology for laparoscopic cholecystectomy is currently being actively implemented.
At the end of the 20th and beginning of the 21st, important discoveries were made in the field of studying genetic predisposition to cholelithiasis. Experience has been gained in the successful use of ursodeoxycholic acid in the dissolution of gallstones. In recent years, the problem of cholelithiasis has attracted increased attention due to the “epidemic of excess weight” and the increasing incidence of stone formation in children and adolescents.

Source: diseases.medelement.com

MINISTRY OF HEALTH OF THE REPUBLIC OF BELARUS

BELARUSIAN STATE MEDICAL UNIVERSITY

1st DEPARTMENT OF SURGICAL DISEASES

S.I. Leonovich, A.I. Protasevich

GALLSTONE DISEASE.

ACUTE AND CHRONIC
CALCULOUS CHOLECYSTITIS

Reviewers: head. 2nd department of surgical diseases, Dr. med. sciences, prof.
S.I. Tretiak; beginning department Military Field Surgery, BSMU, Ph.D. honey. Sciences, Associate Professor
S.A. Zhidkov

Approved by the University Scientific and Methodological Council
as methodological recommendations 06/09/2004, protocol No. 8

Leonovich S.I.

L 47 Gallstone disease. Acute and chronic calculous cholecystitis: Method. recommendations / S.I. Leonovich, A.I. Protasevich - Mn.: BSMU, 2004. - 42 p.

The main theoretical issues related to cholelithiasis are reflected. The etiology, pathogenesis, pathological anatomy and clinical picture of cholelithiasis and its complications are covered. Modern methods of diagnosis and treatment are presented.

UDC 616.366-033.7-036.11/.12(075.8)

BBK 54.13ya73

© Design. Belarusian State
Medical University, 2004

Topic of the lesson: Cholelithiasis. CHRONIC AND ACUTE CALCULOUS CHOLECYSTITIS

Total lesson time: 5 o'clock.

Motivational characteristics of the topic. Gallstone disease (GSD) and its complications are of significant theoretical and practical interest to doctors of various specialties. Treatment of cholelithiasis still remains the prerogative of surgeons, but a number of situations require a common solution with the involvement of therapists, endoscopists, radiologists and other specialists.

According to the National Institutes of Health, cholelithiasis affects 10–15% of the adult population worldwide. The emergence of new technologies in the diagnosis and treatment of this pathology requires the doctor to constantly improve his knowledge.

Lesson objectives: based on previously obtained data on normal and pathological anatomy, physiology and pathophysiology of the liver, gallbladder and bile ducts, study the etiology, pathogenesis, clinical picture, diagnosis, treatment tactics for cholelithiasis and its complications.

Lesson objectives

Understand the normal and pathological anatomy of the gallbladder, bile ducts, sphincter of Oddi.

To become familiar with the main etiological factors of cholelithiasis, to find out the pathogenesis of chronic acute calculous cholecystitis.

Understand the main clinical manifestations of cholelithiasis and its complications, learn how to collect anamnesis and complaints for this pathology.

Familiarize yourself with the principles of clinical examination of patients, learn to diagnose various syndromes and symptoms of cholelithiasis.

Learn to evaluate the results of laboratory and instrumental diagnostic methods for chronic and acute calculous cholecystitis, choledocholithiasis, stenosis of the major duodenal papilla, cholangitis.

Master treatment tactics and types of treatment for cholelithiasis.

Requirements for the initial level of knowledge

To successfully and completely master the topic, you must repeat:

normal and topographic anatomy of the liver, gallbladder, bile ducts;

physiology of bile formation and excretion, synthesis and metabolism of cholesterol.

Test questions from related disciplines

Bile formation, principles, regulation of the formation and secretion of bile.

What are the functions of the gallbladder?

What are the structure and functions of the choledochoduodenal junction (papilla of Vater, sphincter of Oddi)?

What is the morphological and functional relationship of the gallbladder, bile ducts, pancreas and duodenum?

Test questions on the topic of the lesson

Gallstone disease. Concept, etiology, epidemiology, types of stones, pathogenesis.

Clinical manifestations of cholelithiasis.

Laboratory and instrumental methods for diagnosing cholelithiasis, indications and data assessment.

Treatment of chronic calculous cholecystitis. Types of operations.

Treatment of acute calculous cholecystitis. Types of operations.

Alternative methods of treating cholelithiasis, types, indications for use.

Choledocholithiasis, concept, clinic, diagnosis, treatment options.

LBD stenosis, concept, clinical picture, diagnosis and treatment.

Cholangitis, classification, pathogenesis, clinical picture, diagnosis, treatment principles.

Mirizzi syndrome, concept, clinic, diagnosis, treatment.

Biliary fistulas, pathogenesis, clinical picture, diagnosis, treatment.

Methods of intraoperative examination of the bile ducts.

Gallbladder cancer, classification, clinical forms, clinic, diagnosis, treatment, prognosis.

TRAINING MATERIAL

Memorable dates from the history of biliary surgery

1867 - J.S. Bobbs - first cholecystomy.

1882 - C. Langenbuch - the first planned cholecystectomy.

1882 - H. Marcy - first choledocholithotomy.

1887 - N.D. Monastyrsky - formation of cholecystojejunostomy.

1889 - Yu.F. Kosinsky - the first cholecystectomy in Russia.

1891 - R. Abbe - for the first time in the world, carried out external drainage of the common bile duct through the stump of the cystic duct.

1900 - W.S. Halsted - used hidden drainage to replace the common bile duct defect.

1931 - P.L. Mirizzi - proposed and performed the first intraoperative cholangiography.

1935 - P. Huard - percutaneous transhepatic cholangiography was first used.

1951 - H. Wilgegans - designed an endoscope for examining the common bile duct (choledochoscopy).

1968 - McCune - introduction of endoscopic retrograde cholangiopancreatography into practice.

1974 - Nakajima M., Kawai K., Classen M. - introduction of endoscopic papillosphincterotomy into practice.

1984 - Ph. Mouret - the first video laparoscopic cholecystectomy.

Physiology of bile formation

Every day, the liver continuously secretes up to 1,000 ml of bile. The main components of bile: water (liver bile - 98%, cystic bile - 84%), bile salts (liver bile - up to 1.4 g%, cystic bile - up to 11.5 g%), cholesterol (liver bile - up to 0. 2 g%, cystic bile - 1.6 g%), phospholipids (liver bile - 0.25 g%, cystic bile - 0.35 g%), bilirubin (liver bile - up to 140 mg%, cystic bile - up to 360 mg%) . Bile also contains proteins, fatty acids, bicarbonates, electrolytes, and mucin.

Cholesterol in bile is present in a free, non-esterified form; in the aqueous environment of bile it can be transported only through the formation of vesicles or micelles with bile acids and phospholipids.

Bile phospholipids are represented by lecithin (90%), lysolecithin (3%), phosphatidylethanolamine (1%). Phospholipids are hydrolyzed in the intestine and do not participate in the enterohepatic circulation.

The main part of bilirubin (up to 85%) is formed from hemoglobin of erythrocytes, a smaller part is synthesized from hemoproteins of other tissues (myoglobin, cytochrome, catalase, etc.). Unconjugated bilirubin in blood plasma is bound to albumin, which transports it to hepatocytes. In a conjugation reaction, it is converted into bilirubin mono- and diglucuronide (a water-soluble substance) and is secreted into bile. Bilirubin is not included in the enterohepatic circulation and, under the influence of enzymes in the colon, is converted into stercobilin and urobilinogen.

Bile acids are cholic and chenodeoxycholic acids (primary bile acids). They bind to glycine and taurine and decompose in the intestine to secondary bile acids - deoxycholic and lithocholic. Cholic, chenodeoxycholic, and deoxycholic acids are absorbed in the intestine and enter the liver through the portal vein system, being re-excreted into bile (enterohepatic circulation). Only 5–10% of bile acids in bile are excreted in the feces. Bile acids perform the following functions in the body: the formation of micelles for the transport of water-insoluble substances (cholesterol, fat-soluble vitamins), activation of pancreatic lipase, stimulation of intestinal motility.

Anatomy and physiology of the gallbladder

The gallbladder (GB) is a pear-shaped sac, 3 to 9 cm long, capable of holding about 60–80 ml of fluid. It consists of a bottom, a body and a neck, which continues into the cystic duct. The saccular expansion of the neck of the gallbladder is called Hartmann's pouch. The gallbladder has three layers: serous, muscular and mucous. In the usual location of the gallbladder, the serous membrane covers only its free surface, the part facing the liver is covered with loose connective tissue, it contains the so-called Luschke's passages. Luschke's ducts begin from the small intrahepatic bile ducts and reach the mucous membrane of the gallbladder (the latter circumstance must be taken into account when performing cholecystectomy). In the wall of the gallbladder there are also branched invaginations of the mucous membrane, penetrating through the entire muscular layer and in contact with the serosa (Rokitansky-Aschoff sinuses). They play an important role in the development of biliary peritonitis without perforation of the gallbladder.

The gallbladder is supplied with blood from the cystic artery, which in most cases arises from the right hepatic artery. Smaller blood vessels enter from the liver through the gall bladder bed. Blood from the gallbladder flows through the cystic veins into the portal vein system. In the mucous membrane of the gallbladder and under the peritoneum there are lymphatic vessels that pass through the lymph node at the neck of the gallbladder (Moscagni node) to the nodes along the common bile duct and then into the thoracic lymphatic duct. Innervation of the gallbladder and bile ducts is carried out due to the hepatic and cystic nerve plexuses (celiac nerve plexus), as well as due to the left vagus nerve and the right phrenic mixed nerve, which causes irradiation of pain during inflammation in this area to the right shoulder girdle and the right half neck.

When eating food, the gallbladder contracts 1-2 times, and bile enters the intestines, where it participates in the digestive process. The most significant effect is produced by the gastrointestinal hormone cholecystokinin-pancreozymin (CCK-PZ), which is formed in the chromaffin cells of the duodenum and, to a lesser extent, also in the ileum and jejunum. CCK-PZ is produced when food enters the duodenum and signals the liver and gall bladder about the need for further digestion - stimulating contraction of the gall bladder, increased bile secretion by the liver, and relaxation of the sphincter of Oddi. In addition, CCK-PZ stimulates the secretory function of the pancreas. Nervous stimuli have less effect on gallbladder motility.

Gallstone disease (GSD)- metabolic disease of the hepatobiliary system, characterized by the formation of stones in the hepatic bile ducts (intrahepatic cholelithiasis), in the common bile duct (choledocholithiasis) or in the gallbladder (cholecystolithiasis) (P.Ya. Grigoriev, 1993).

International Classification of Diseases - 10

Diseases of the gallbladder, bile ducts and pancreas (K80 – K87)

K80 Gallstone disease [cholelithiasis].

K80.0 Gallstones with acute cholecystitis.

K80.1 Gallstones with other cholecystitis.

K80.2 Gallstones without cholecystitis.

K80.3 Bile duct stones with cholangitis.

K80.4 Bile duct stones with cholecystitis.

K80.5 Bile duct stones without cholangitis or cholecystitis.

Etiology, epidemiology and pathogenesis of cholelithiasis

In developed countries, cholelithiasis is one of the most common diseases. According to various authors, in Germany, gallstones occur in 10–15% of the population; in Russia, every 19 people aged 41 to 50 are affected, and every seventh person over the age of 71 is affected. In women, cholelithiasis occurs 3–5 times more often than in men.

There are several types of stones depending on their chemical composition:

cholesterol;

pigment (contain mainly bilirubin and its polymers);

calcareous (calcium);

mixed.

Theories of the pathogenesis of cholelithiasis

The most substantiated theories of gallstone formation:
1) infectious; 2) stagnation of bile; 3) lipid metabolism disorders.

Each of these theories reflects a certain part of the lithogenesis process.

The formation of cholesterol stones occurs only in the presence of bile oversaturated with cholesterol, and a decrease in the motor activity of the gallbladder, an increase in mucus secretion, and the presence of infection are also important. Factors influencing the formation of cholesterol stones:

gender - women get sick 3–5 times more often than men, which is probably due to hormonal differences (estrogens stimulate liver receptors for lipoprotein, promote the absorption of cholesterol and its secretion into bile);

genetic and ethnic factors;

age - as you get older, the risk of developing stones increases;

food - high-calorie food containing a significant amount of cholesterol, easily digestible carbohydrates, animal fats;

pregnancy - decreased contractile activity of the gallbladder and hormonal changes;

diseases of the terminal ileum, taking certain medications.

The causes of pigment stones are less studied. It is believed that they are formed due to:

liver damage, leading to the appearance of pigments of a pathological structure, which easily combine with calcium ions and precipitate;

increased formation of unbound bilirubin (hemolytic diseases, liver diseases);

transformation of normal pigments into insoluble compounds under the influence of pathological processes in the bile ducts (infection, surgical manipulations).

Pigment stones often form in the common bile duct.

It is customary to distinguish three stages of gallstone disease: physicochemical (there are signs of increased lithogenicity of bile, there is no clinical, radiological or sonographic picture of the disease), latent (there are stones in the gall bladder, which do not manifest themselves clinically, but are detected radiographically and during ultrasound examination) , clinical (calculous cholecystitis).

The clinical manifestations of cholelithiasis are very diverse, which led to the identification of the following forms of the disease:

latent (patients do not complain);

dyspeptic chronic (the main complaints are a feeling of heaviness in the stomach, a feeling of pressure in the epigastric region, heartburn, flatulence);

chronic pain (occurs without pronounced pain attacks, moderate aching pain in the epigastrium and right hypochondrium, intensifies in connection with food);

biliary colic and chronically relapsing form (manifested by sudden and recurring painful attacks);

angina pectoris form (in elderly people suffering from coronary heart disease - resembles an attack of angina pectoris, after cholecyst-ectmia the attacks disappear).

Chronic calculous cholecystitis

Depending on the severity of pain, dyspeptic, inflammatory syndromes, the following are distinguished:

chronic calculous cholecystitis in remission;

chronic calculous cholecystitis in the acute stage.

There are primary chronic calculous cholecystitis, residual chronic calculous cholecystitis (a history of acute cholecystitis), chronic recurrent cholecystitis (repeated painful attacks).

Chronic calculous cholecystitis is manifested primarily by pain - dull pain in the right hypochondrium and attacks of biliary colic. Other symptoms (feeling of heaviness in the right hypochondrium, heartburn, nausea, vomiting, constipation, intolerance to fatty foods) are nonspecific and may be caused by other diseases.

Biliary colic is a symptom complex that occurs as a result of the movement of a stone to the neck of the gallbladder. As a result, irritation of the gallbladder mucosa occurs and intravesical pressure increases.

Clinically, biliary colic is manifested by an attack of intense pain in the right hypochondrium and epigastrium, with irradiation to the shoulder, neck, and right scapula. Less commonly, the pain radiates to the left, to the region of the heart, simulating an attack of angina. Simultaneously with the pain, nausea and vomiting appear, which does not bring noticeable relief. An attack of biliary colic can be triggered by eating fatty foods, spices, physical stress, and sometimes emotional factors.

We can talk about biliary colic only when the pain syndrome is quickly (within 6 hours from the onset of the attack) relieved by the use of antispasmodics and analgesics, and the patient has no or mild inflammatory syndrome. If there is an inflammatory syndrome, and the pain syndrome is not relieved by the administration of antispasmodic analgesics within 6 hours, the patient should be assumed to have acute cholecystitis or an exacerbation of chronic cholecystitis.

Inspection. When examining a patient, one can identify signs that may suggest cholelithiasis (gender, age, obesity, metabolic disorders, signs of chronic liver disease).

Palpation. The examination of the abdomen is performed in a supine position, legs slightly bent at the knees, arms at your sides. During an attack of biliary colic, flatulence and restriction of respiratory movements are possible. Particular importance is given to identifying pain when examining certain points. A number of symptoms characteristic of various forms of cholelithiasis have been described.

Kehr's symptom is pain when inhaling during palpation of the right hypochondrium.

Ortner-Grekov symptom - tapping the edge of the palm on the right costal arch causes pain.

Boas's symptom is the detection of an area of ​​hyperesthesia in the lumbar region.

Murphy's symptom - pressing evenly with the thumb on the area of ​​the gallbladder, the patient is asked to take a deep breath; at the same time, he “takes away” his breath and there is pain in this area.

The Mussi-Georgievsky symptom is pain on palpation between the legs of the sternocleidomastoid muscle.

Laboratory research

In the case of chronic calculous cholecystitis without exacerbation and biliary colic, there may be no changes in general and biochemical blood tests.

If an inflammatory syndrome is detected (leukocytosis, an increase in the number of band neutrophils, an increase in ESR), acute cholecystitis should be suspected.

An increase in the concentration of AST, ALT, alkaline phosphatase and bilirubin indicates that the patient has complications of cholelithiasis (acute cholecystitis, choledocholithiasis, cholangitis, etc.).

AND instrumental diagnostic methods

Ultrasound examination abdominal cavity is the method of choice in diagnosing cholelithiasis.

The sensitivity of the method for chronic uncomplicated calculous cholecystitis is 95%, specificity is 90–95%. The study is accessible and safe for the patient. Signs of cholelithiasis are the detection of stones in the gallbladder, manifested by intense echoes with a distinct acoustic shadow, spreading and blocking the image of the structures lying behind them. Acute cholecystitis is characterized by the presence of stones (in the cervical area, not dislodged) in combination with signs of inflammation of the gallbladder (increase in size, thickening of the wall, appearance of “layering” of the wall), changes in the wall of the gallbladder (thickening). The method allows, although with less sensitivity and specificity, to assess the condition of the bile ducts (size, condition of the walls, presence of cholangioliatasis).

X-ray examination of the gallbladder
and bile ducts

Unlike kidney stones, only 10% of gallstones are visible on plain radiography. The possibility of their detection is due to the calcium content in them.

X-ray contrast examination (oral and intravenous cholecystocholangiography) is based on the ability of the liver to secrete iodine-containing substances with bile. The study is informative only in the case of preserved liver function and the absence of bilirubinemia, has a low degree of reliability of the results, and may be accompanied by complications. All this significantly limits the use of the above methods.

Biliary tract scintigraphy

The technique is based on the uptake of labeled 99m Tc by liver cells and the release of the latter into bile. The resolution of bile duct scintigraphy in jaundice is significantly inferior to other imaging methods.

Computed tomography (CT)

Standard CT has low accuracy in diagnosing gallstones, but it can help distinguish cholesterol stones from stones containing calcium, which is important for deciding whether a patient should undergo shock wave lithotripsy or litholytic therapy. CT is used mainly to assess the condition of the tissues around the gallbladder and ducts, determine the dilation of the bile ducts and the level of their obstruction, and damage to the pancreas. Spiral CT allows you to conduct a study quickly (15–30 s), assess the condition of the liver vessels and ducts, and obtain a three-dimensional image.

Magnetic resonance imaging (MRI)

WITH The method is based on recording the energy released from protons ordered in a magnetic field upon transition to a lower energy level.

If the information content of ultrasound and CT is insufficient, the use of magnetic resonance cholangiopancreatography (MRCP) makes it easier to identify dilated bile ducts, space-occupying lesions and stones. The study is highly informative for diagnosing bile duct obstruction and establishing its cause.

Laparoscopy

Visual examination of the abdominal organs using optical instruments is a fairly effective diagnostic method for damage to the liver, gallbladder and bile ducts. In case of cholelithiasis, the need for laparoscopy most often arises in the differential diagnosis of jaundice, suspected tumor of the bile ducts or gallbladder. Despite the high diagnostic value of laparoscopy, the indications for it must be strictly justified, since the latter is an invasive procedure and may be accompanied by the development of severe complications.

Endoscopic retrograde cholangiopancreatography (ERCP)

WITH Using an endoscope, a large duodenal papilla is detected, which is cannulated. A radiopaque contrast agent is injected retrogradely, under the control of an endoscope and in an X-ray room. The study allows you to assess the condition of the entire biliary system, in some cases the pancreatic duct.

The main indication is to determine the causes of obstructive jaundice and pain syndrome when other research methods are uninformative: clinical, laboratory, sonographic, etc.

Performing ERCP may be accompanied by the development of complications typical for diagnostic gastroduodenoscopy - reaction to drugs, aspiration, cardiopulmonary complications, perforation of a hollow organ, as well as specific complications - pancreatitis, cholangitis, bleeding.

Percutaneous transhepatic cholangiogarphy (PTCH)

First performed in 1937 (P.Huard) by puncturing the dilated bile ducts and administering lipiodol. Before the advent of ultra-thin Chiba needles, the procedure was accompanied by a significant number of complications (bleeding and bile leakage into the abdominal cavity).

Currently, PCCG, along with ERCP, is the method of choice in the diagnosis of obstructive jaundice, and in patients after gastrectomy according to Billroth II, it is the only possible one.

The intervention is carried out in an operating room equipped with an X-ray unit. The puncture is performed in the VIII or IX intercostal space on the right along the mid-axillary line after anesthesia of the skin, subcutaneous tissue, and intercostal muscles. After inserting the needle, the mandrel is removed and a contrast agent is injected. It is possible to perform a puncture under ultrasound guidance.

Examination of a patient with chronic calculous cholecystitis should include mandatory ultrasound examination of the gallbladder, bile ducts, liver and pancreas; fibrogastro-duodenoscopy (if it is impossible to perform, radiography of the stomach and duodenum); ECG; general blood and urine analysis, biochemical blood test (total protein, bilirubin, urea, creatinine, electrolytes, AST, ALT, alkaline phosphatase, amylase, markers of viral hepatitis), coagulogram, determination of blood group and Rh factor. If there is a suspicion of damage to the bile ducts and pancreas, the additional methods described above for their examination are necessary.

Patients with concomitant pathology should be examined to adjust treatment or determine contraindications to surgery.

Differential diagnosis

Principles of treatment of cholelithiasis

Treatment of gallstones

The presence of gallstones requires immediate treatment. This is due to the presence of clinical manifestations of the disease (pain, dyspeptic disorders, etc.) and the risk of complications.

In the case of stone-carrying stones (accidentally detected stones, absence of a clinic), two approaches are possible: 1) surgical treatment using minimally invasive methods to prevent possible complications;
2) observation. Active treatment of stones in the absence of contraindications to surgical treatment is more justified.

Currently, the main treatment method for this pathology is surgery. Non-surgical treatments for cholelithiasis have limited indications, a high relapse rate and should only be used in a limited number of patients.

Tactics for chronic calculous cholecystitis outside of exacerbation are planned surgical intervention. The emergence of minimally invasive cholecystectomy techniques and progress in the field of anesthesiology and intensive care have significantly reduced the number of contraindications to surgery.

Patients with a clinical picture of biliary colic or chronic calculous cholecystitis should be hospitalized in the surgical department, where they receive conservative therapy aimed at stopping the attack. Treatment includes: 1) ensuring rest and creating functional rest for the organ (bed rest, fasting);
2) relief of pain syndrome (novocaine blockades - perinephric, round ligament of the liver, administration of non-narcotic analgesics, antispasmodics); 3) infusion therapy. There is evidence of the effectiveness of non-steroidal anti-inflammatory drugs (diclofenac, indomethacin) and antiplatelet agents (pentoxifylline). Antibacterial therapy is prescribed for patients with concomitant pathology and a high risk of developing acute cholecystitis (2nd-3rd generation cephalosporins or alternative regimens - fluoroquinolone, clindamycin, amoxiclav, etc.). Simultaneously with treatment, patients undergo an emergency examination, including assessment of the state of the cardiovascular and pulmonary systems, liver and kidney function, and correction of treatment for concomitant pathologies. When an attack is stopped, surgical treatment is performed without discharging the patient from the hospital. If additional therapy for concomitant pathology is necessary, surgery is performed after treatment in a therapeutic hospital.

Surgical methods for treating chronic
calculous cholecystitis

Traditional (open) cholecystectomy.

Cholecystectomy from a mini-access (laparoscopically assisted cholecystectomy).

Video laparoscopic cholecystectomy.

Traditional laparotomic cholecystectomy.

X olecystectomy involves removal of the gallbladder along with stones after separate ligation or clipping of the cystic artery and duct. First performed by the German surgeon Langebuch in 1882, in Russia for the first time by Yu.F. Kosinsky - 1889.

To perform cholecystectomy, upper median laparotomy and oblique subcostal approaches of Kocher and Fedorov are currently used.

There are two options for performing cholecystectomy: “from the bottom” and “from the neck” (antegrade and retrograde cholecystectomy).

Cholecystectomy “from the bottom” is performed in the case of infiltrative-inflammatory changes in the cervical area, when there are difficulties in identifying and isolating the cystic artery and duct. With this option of cholecystectomy, there is more pronounced bleeding from the gallbladder tissue and there is a danger of small stones moving from the gallbladder. In this case, however, there is less chance of damage to the bile ducts.

IN While performing a traditional cholecystectomy, it is possible to carry out intraoperative diagnosis of biliary tract pathology: examination, palpation of the extrahepatic bile ducts, cholangiomanometry and cholangio-debitometry, intraoperative cholangiography, choledochoscopy, intraoperative ultrasound, diagnostic choledochotomy. Completion of the operation depends on the identified changes (external drainage, biliodigestive anastomosis, transduodenal papillosphincterotomy).

The disadvantages of the operation are significant surgical trauma, a long period of temporary disability, a cosmetic defect, the possibility of developing early (wound suppuration, eventration, etc.) and late (ventral hernia) postoperative complications.

Laparoscopic cholecystectomy

The first cholecystectomy without opening the abdominal cavity was performed by the French surgeon Philippe Mouret in 1987 in Lyon.

Under general anesthesia, a Veress needle is inserted into the abdominal cavity and carbon dioxide is injected (creating carboxyperitoneum). The laparoscope and instruments are then inserted at typical points. The cystic duct and gallbladder vessels are isolated and clipped. The gallbladder is isolated from the bed using electrocoagulation and removed.

During laparoscopic cholecystectomy, instrumental palpation of the common bile duct is possible, and, if necessary, intraoperative cholegraphy and choledoscopy. The possibility of performing laparoscopic choledocholithotomy and choledochoduodenoanastomosis has been shown.

Laparoscopic cholecystectomy is the “gold” standard for the treatment of chronic calculous cholecystitis.

There are, however, a number of contraindications to performing this surgical intervention:

severe cardiopulmonary disorders;

uncorrectable hemostasis disorders;

peritonitis;

late stages of pregnancy;

obesity degree II–III;

pronounced scar-inflammatory changes in the area of ​​the gallbladder neck and hepatoduodenal ligament;

acute pancreatitis;

obstructive jaundice;

biliodigestive and biliobiliary fistulas;

gallbladder cancer;

previous operations on the upper floor of the abdominal cavity.

These contraindications are not absolute. The introduction of new treatment technologies, such as the gas-free lifting method, expanding the capabilities of video-laparoscopic intraoperative examination of the biliary tract (cholegraphy, choledochoscopy, intraoperative ultrasound) and treatment significantly reduces this list.

The undoubted advantages of laparoscopic cholecystectomy: low trauma, good cosmetic effect, significant reduction in mortality and the level of postoperative complications, rapid rehabilitation and reduction in temporary disability.

Mini-access cholecystectomy

Cholecystectomy with this technique is performed from a small incision in the abdominal wall - 3–5 cm. Adequate access for surgery is created using a special set of mini-assistant instruments (ring-shaped retractor, a set of hook-mirrors and a lighting system). An additional set of instruments allows for a number of diagnostic and therapeutic manipulations on the common bile duct (cholangiography, choledochotomy, choledoduodenostomy, common bile duct drainage).

Cholecystectomy from a mini-access, according to some authors, is comparable to LCE in terms of the level of morbidity and quality of life of operated patients.

Non-surgical treatments for gallstones

Oral litholytic therapy.

Contact litholytic therapy.

Extracorporeal shock wave lithotripsy followed by oral litholytic therapy.

Oral litholytic therapy

The method is based on the introduction of exogenous bile acids into the patient's body. The main drugs are ursodeoxycholic and chenodeoxycholic acids. Ursodeoxycholic acid prevents the absorption of cholesterol in the intestine and promotes the transfer of cholesterol from stones into bile. Chenodeoxycholic acid inhibits cholesterol synthesis in the liver and also helps dissolve cholesterol stones. The most effective treatment is a combination of these drugs.

The technique has a number of limitations and disadvantages:

only cholesterol stones of limited size are dissolved in 60–80% of cases (the need to perform a CT scan - the optimal attenuation coefficient is less than 70 Hounsfield units, stone diameter is less than 1.5 cm);

long-term treatment (more than 2 years);

relapse rate - 50%;

the functional activity of the gallbladder must be preserved (the need for additional research);

the cost of treatment is significantly higher than that of surgical treatment.

Extracorporeal shock wave lithotripsy

The method is based on generating a high-energy shock wave (usually piezoelectric) and directing it at the stone under ultrasound control. The method can be used in patients with a functioning gallbladder, a single stone up to 2 cm in diameter. The axis of the shock wave should not pass through the lung. The resulting stone fragments ideally pass through the cystic and common bile ducts into the duodenum. Lithotripsy is currently, as a rule, supplemented by oral administration of litholytic drugs. The disadvantages of the method are frequent complications from the bile ducts and pancreas, a fairly high frequency of relapses, and the need to take medications for a long time (see above).

Contact dissolution of gallstones

The essence of the method is to introduce a liquid dissolving drug directly into the gallbladder and ducts. If there are stones in the gallbladder, the patient undergoes percutaneous transhepatic puncture of the gallbladder under X-ray or ultrasound control. A catheter is inserted into the gallbladder through a needle and guidewire. Methylterzbutyl ether is injected through the catheter and the substance is immediately aspirated back. Treatment duration is from 4 to 12 hours.

Since the gallbladder is not removed, as with the methods described above, the relapse rate reaches 50–60%. Complications associated with the development of chemical inflammation of the gallbladder and absorption of the drug in the gastrointestinal tract are possible.

Acute calculous cholecystitis

Acute calculous cholecystitis is an acute inflammation of the gallbladder, one of the most common complications of cholelithiasis, developing in approximately 20–25% of patients with chronic calculous cholecystitis.

In terms of the absolute number of deaths, acute cholecystitis exceeds acute appendicitis, strangulated hernias, and perforated gastroduodenal ulcers, only slightly inferior to acute intestinal obstruction. Overall postoperative mortality ranges from 2–12%, does not tend to decrease and reaches 20% in older people.

Acute acalculous cholecystitis occurs in the practice of emergency surgery in no more than 2–5% of cases - mainly, these are vascular lesions of the gallbladder in people with widespread atherosclerosis, diabetes mellitus, as well as acute inflammation against the background of a septic condition, severe trauma, etc. .p.

Pathogenesis

In the pathogenesis of acute calculous cholecystitis, certain sequentially developing changes can be traced: increased intravesical pressure, microcirculatory disorders, progressive hypoxia of the gallbladder wall, infection, the appearance of morphological signs of the inflammatory process in the bladder wall with varying severity of destructive changes.

It is generally accepted that the development of acute calculous cholecystitis is associated with occlusion of the cystic duct, which occurs as a result of either obstruction by a small calculus from the inside, or due to external compression by a calculus wedged into Hartmann's pouch, swelling of the neck of the gallbladder. Obstruction of the cystic duct and inflammation of the bladder wall alter the absorption capabilities of the gallbladder mucosa, which leads to biliary hypertension. Biliary hypertension leads to arteriovenous shunting of blood in the bladder wall and the development of hypoxic changes. Microcirculation disorders, in turn, contribute to a decrease in tissue resistance and infection.

Classification

There is no single classification that includes pathomorphological and clinical variants of acute cholecystitis.

There are primary acute cholecystitis (first identified), when it is the first clinical manifestation of cholelithiasis, and recurrent.

Morphological classification of acute cholecystitis.

Catarrhal - the inflammatory process is limited to the mucous and submucosal layers, swelling and slight infiltration of the wall by neutrophils are noted.

Phlegmonous - all layers of the wall are edematous, diffusely infiltrated with neutrophils, there are mucosal defects, the vessels of the gallbladder wall are full-blooded and thrombosed.

Gangrenous- extensive areas of necrosis of all layers of the gallbladder wall.

Perforated.

Clinically, acute calculous cholecystitis is divided into complicated and uncomplicated. Complications of acute calculous cholecystitis are divided depending on:

the nature of the damage to the bile ducts (choledocholithiasis, stenosis of the papilla of Vater, cholangitis, bile duct strictures);

localization of the pathological process - empyema of the gallbladder, acute obstructive cholecystitis, perivesical infiltrate, perivesical abscess, liver abscess, hydrocele of the gallbladder;

lesions of other organs and systems - acute pancreatitis, peritonitis, liver abscesses, biliary cirrhosis.

Clinic

People of any constitution, gender and age get sick, but the main group consists of women aged 45 years and older. Most patients have a history of chronic calculous cholecystitis.

Main syndromes for acute calculous cholecystitis:

pain (characteristic attack with typical irradiation);

inflammatory (symptoms of intoxication and infection);

dyspeptic;

peritoneal.

Clinical symptoms- enlarged and painful on palpation gallbladder, muscle tension in the right hypochondrium, symptoms of Murphy, Ortner-Grekov, Kera, Mussi-Georgievsky.

The disease begins acutely with pain in the right hypochondrium and epigastrium, the pain usually occurs late at night or in the morning, radiates to the back below the angle of the right shoulder blade, to the right shoulder or, less commonly, to the left half of the body, and may resemble an attack of angina. An attack can be triggered by a late, heavy dinner or fatty foods. Characterized by increased sweating, pain and a motionless position on the side with legs tucked to the stomach. Often patients apply a heating pad to the right hypochondrium. Typical signs are nausea, vomiting, fever up to 38°C, and bloating. The clinical course of acute cholecystitis to a certain extent corresponds to the nature of morphological changes in the gallbladder. Yes, when catarrhal form inflammation, the patient’s general condition does not suffer: body temperature is normal, intoxication is not expressed, moderate pain in the right hypochondrium, nausea, and flatulence are noted. Vomiting is not typical. Palpation of the abdomen reveals moderate pain in the right hypochondrium without symptoms of peritoneal irritation. The gallbladder is rarely palpated - 10–15% of cases. Phlegmonous form The disease is characterized by a clear clinical picture in the form of intense pain with characteristic irradiation. The patient has severe weakness, fever, dry mouth, tachycardia up to 100 beats per minute. Dyspeptic syndrome is characterized by nausea, repeated vomiting, and bloating. There is pain on palpation of the abdomen in the right hypochondrium and epigastrium, an enlarged painful gallbladder is palpated.

The most pronounced clinical manifestations are with gangrenous and gangrenous-perforative form of acute cholecystitis. Signs of general intoxication come first: patients are adynamic, dehydrated, tachycardia more than 100 beats per minute, fever. On objective examination, the abdomen is painful in all parts, and there are symptoms of peritoneal irritation.

If obstruction of the cystic duct and sterility of bile in the bladder persist, the latter can be absorbed, and the cavity of the gallbladder remains filled with clear liquid - hydrocele. When the contents of the cavity are infected, empyema of the gallbladder develops, the course of which can be acute or chronic.

X A typical symptom of hydrocele of the gallbladder is the presence of a mobile, elastic, painless gallbladder in the absence of jaundice, signs of inflammation and intoxication. With empyema of the gallbladder, after conservative therapy, the patient’s condition normalizes, but pain on palpation in the gallbladder area remains, low-grade fever, and moderate inflammatory syndrome remain.

Features of the flow acute calculous cholecystitis in elderly and senile patients - rapid progression of destructive changes in the gallbladder involving the extrahepatic bile ducts in the process, discrepancy between the clinical picture and morphological changes. The clinical picture is not always pronounced: the temperature may be low, pain and symptoms of the disease are either mild or absent, and symptoms of intoxication prevail. These patients, as a rule, have concomitant pathology from other organs and systems, and a “mutual burden” syndrome often develops. Among the atypical forms of acute cholecystitis, the so-called cardiac form is described, in which the pain syndrome manifests itself in the form of pain in the heart or behind the sternum (cholecystocoronary syndrome - S.P. Botkin). Most often, such pain is observed in people of older age groups.

Diagnostics

Laboratory diagnostics

A general blood test reveals leukocytosis with an increase in the number of band neutrophils and an increase in ESR.

Biochemical blood test - possible increase in the content of AST, ALT, alkaline phosphatase, bilirubin.

Mandatory laboratory tests in patients with acute calculous cholecystitis: general clinical blood test, blood glucose, bilirubin, ALT, AST, amylase, creatinine, urea, coagulogram, blood test for RW, blood group and Rh factor, general analysis and urine diastasis, markers of viral hepatitis.

Instrumentaldiagnostics

ABOUT The main diagnostic method is ultrasonography.

Signs of acute calculous cholecystitis:

increased size of the gallbladder (more than 10 cm in length and 4 cm in width);

thickening of the walls (over 3 mm);

doubling (layering) and indistinctness of the walls;

the presence in the lumen of a hyperechoic suspension and stones fixed in the neck;

signs of acute perivesical changes;

positive ultrasound Murphy sign.

The ability of dynamic ultrasonography to assess the effectiveness of conservative therapy is valuable.

Plain radiography of the abdominal organs in 10% of cases it can detect stones in the gallbladder; its use is justified in the case of an unclear clinical picture for the purpose of differential diagnosis (acute intestinal obstruction, perforation of a hollow organ).

Application of laparoscopy in difficult cases, it allows you to clarify ultrasonography data, especially in the presence of cholecystopancreatitis. It is important to be able to carry out not only diagnostic but also therapeutic measures (decompression of the gallbladder, sanitation of the abdominal cavity).

Scintigraphy of the biliary tract. If acute cholecystitis is suspected, scintigraphy can be used to assess the patency of the cystic duct. The absence of an image of the gallbladder with a patent common bile duct and the appearance of a radioisotope in the intestine is highly likely to indicate acute cholecystitis.

Examination of a patient with acute calculous cholecystitis requires mandatory ultrasound of the abdominal organs, FGDS, chest x-ray, ECG (if indicated - abdominal x-ray, CT).

Differential diagnosis is carried out with: 1) acute appendicitis; 2) acute pancreatitis; 3) perforated ulcer; 4) myocardial infarction;
5) right-sided pleuropneumonia; 6) right-sided renal colic;
7) abdominal aortic aneurysm.

Treatment

Prehospital stage

A diagnosis or reasonable assumption of the presence of acute cholecystitis, especially in the case of established cholelithiasis, is an indication for sending the patient to a surgical hospital. If the diagnosis of acute cholecystitis is not cleared, the use of local heat (a heating pad) on the abdominal area, as well as the use of enemas and laxatives, is contraindicated. If the patient refuses hospitalization, he and his relatives must be warned in writing about the possible consequences with a corresponding entry in the medical record. In the event of a patient’s unauthorized departure from the emergency department of a surgical hospital before the diagnosis is determined, the doctor of the emergency department is obliged to report this to the clinic at the patient’s place of residence for an active examination by the surgeon of the polyclinic at home.

Inpatient treatment

According to the course, acute calculous cholecystitis is divided into three groups: widespread (urgent), progressive, regressive (Gri-shin I.N., Zavada N.V.)

Common acute calculous cholecystitis corresponds to gangrene and (or) perforation of the gallbladder with local peritonitis. In this case, emergency surgical intervention is indicated (traditional cholecystectomy, sanitation and drainage of the abdominal cavity, and, if indicated, external drainage of the biliary tract).

The remaining patients undergo intensive conservative treatment during the first day, aimed at stopping the inflammatory process and restoring the natural outflow of contents from the gallbladder. As part of this treatment, an emergency ultrasound examination is performed, which provides objective information about the size of the gallbladder, the condition of its walls, the presence and location of stones and perivesical complications.

Conservative therapy. Standard conservative treatment of acute calculous cholecystitis includes dehydration infusion therapy with crystalloid and colloid solutions, analgesics (analgin, tramadol, ketanov, etc.), antispasmodics (no-spa, papaverine, baralgin), anticholinergic drugs (atropine), novocaine blockade of the round ligament liver, subxiphoidal or perinephric novocaine blockade, correction of concomitant pathology. For prolonged administration of novocaine and antibacterial drugs, catheterization of the round ligament of the liver is used.

Taking into account rheological disturbances, increased surface tension of blood plasma and erythrocyte membranes, as well as increased coagulation activity in acute calculous cholecystitis, the use of drugs that improve microcirculation (pentoxifylline, rheopolyglucin, etc.) is recommended. There are reports of the effective use of non-steroidal anti-inflammatory drugs (indomethacin, diclofenac) for the treatment of acute calculous cholecystitis.

The use of antibacterial drugs is justified in cases of suspected destructive (phlegmatic or gangrenous) cholecystitis, cholangitis, extravesical complications, as well as in patients with a high surgical risk for the prevention of purulent-inflammatory complications. The peculiarity of conservative therapy for acute calculous cholecystitis is that the latter is often preoperative preparation.

Progressive acute calculous cholecystitis is determined in the absence of effect from conservative therapy within 48–72 hours from the start of treatment or in the presence of clinical and ultrasound signs of destructive cholecystitis and progression of local and general symptoms of inflammation. Such patients are indicated for urgent surgical treatment (48–72 hours from the moment of admission to the hospital).

For regressive acute calculous cholecystitis With conservative treatment, clinical symptoms resolve and laboratory parameters return to normal. In this case, patients continue to undergo conservative treatment and a comprehensive examination, while the indications for delayed or planned surgical treatment are clarified.

ABOUT selection operation in the vast majority of cases - traditional or laparoscopic cholecystectomy with intraoperative revision of the biliary tract.

The problem of choosing treatment tactics in patients of senile age and with a high surgical and anesthetic risk is a difficult one. Features of the course of acute calculous cholecystitis in elderly and senile patients are the rapid progression of destructive changes in the gallbladder with the involvement of extrahepatic bile ducts in the process, the discrepancy between the clinical picture and morphological changes. These patients, as a rule, have concomitant pathology from other organs and systems, and a “mutual burden” syndrome often develops.

In such patients, two-stage treatment is possible. At the first stage, if conservative therapy is unsuccessful and there is a high risk of radical treatment, the patient undergoes cholecystostomy, then, after compensation of the condition, cholecystectomy is performed.

Complications of calculous cholecystitis

Choledocholithiasis- presence of stones in the extrahepatic bile ducts. According to various authors, it occurs in 20–30% of patients with cholelithiasis. Bile duct stones in 70–90% of cases are cholesterol, migrated from the gallbladder.

Clinical manifestations of choledocholithiasis occur in two thirds of patients.

N The most typical are: pain syndrome (the localization and nature of pain does not differ from those in biliary colic), dyspeptic syndrome (nausea, vomiting, bloating, etc.), inflammatory syndrome, cholestasis syndrome and obstructive jaundice. The occurrence of inflammation of the ducts against the background of impaired bile outflow is characterized by the classic Charcot triad (jaundice, fever, chills).

Laboratory indicators with “silent” bile duct stones, they either do not differ from the norm or change slightly. Possible leukocytosis, increased levels of bilirubin and transaminases, increased activity of cholestasis enzymes - alkaline phosphatase and γ-glutamyltransferase. With complete or partial obstruction with the development of ascending cholangitis, a pronounced increase in all of the listed indicators is observed.

Instrumental diagnostics

Standard ultrasound examination reveals choledocholithiasis in 40–70% of cases. This is due to the small size of the calculus, the absence of ultrasound shadow, air overlay, and the absence of dense echo structures. An indirect sign of blockage of the bile ducts is their expansion, revealed during the study. A promising direction for diagnosing choledocholithiasis is the use of endoscopic ultrasound.

The main highly informative preoperative methods for diagnosing choledocholithiasis: ERCP, PCCG, magnetic resonance cholangiopancreatography, CT.

Bile duct stones, even if asymptomatic, can cause numerous complications, which necessitates treatment.

Complications of bile duct stones

Obstruction of the bile duct, obstructive jaundice.

Cholestasis, cholangitis.

Liver abscess, sepsis.

Secondary biliary cirrhosis.

Biliary fistulas.

Acute pancreatitis.

Intestinal obstruction.

Cholangiocarcinoma.

Treatment

IN
The choice of treatment option for chronic calculous cholecystitis in combination with choledocholithiasis will depend on the severity of clinical manifestations, the time of diagnosis (before surgery, during surgery), and the presence of other complications (stenosis of the spinal cord, cholangitis, obstructive jaundice).

Two-stage treatment

Sanitation of the biliary tract - ERCP, papillosphincterotomy, stone extraction (Dormia basket).

Cholecystectomy is preferably laparoscopic.

One-stage treatment

During open or laparoscopic cholecystectomy, choledochotomy and choledocholithotomy are performed.

Completion of choledocholithotomy.

A blind suture of the common bile duct is confidence in the sanitation of the bile ducts and the absence of stenosis of the BDK.

Blind suture of the common bile duct + external drainage of the biliary tract according to Halsted-Pikovsky (through the stump of the cystic duct).

Choledochoduodenoanastomosis - with multiple stones, a wide atonic duct, a history of pancreatitis, stenosis of the lumbar duct.

External drainage using a T-shaped drainage (according to Kehr) - changes in the duct wall, multiple stones.

When detecting residual or recurrent choledocholithiasis in the postoperative period, EPST and sanitation of the hepaticocholedochus are indicated. If impossible, standard laparotomy, choledocholithotomy, choledochoduodenostomy or external drainage of the common bile duct according to Pikovsky.

Stenosis of the major duodenal papilla

WITH Tenoses of Vater's juice, for the most part, are secondary and occur against the background of cholelithiasis due to the passage or herniation of stones. Less commonly, the causes of stenosis of the terminal part of the common bile duct are inflammatory changes in the head of the pancreas or duodenum.

Clinical manifestations of stenosis are varied and sometimes nonspecific. Typical attacks of biliary colic or pain in the right hypochondrium and epigastrium, dyspeptic syndrome. When bile outflow is impaired, signs of cholestasis, cholangitis and obstructive jaundice occur.

Laboratory tests: leukocytosis, increased levels of bilirubin and trans-aminases, cholestasis syndrome (alkaline phosphatase and γ-glutamyltransferase), possibly increased activity of amylase and lipase.

Instrumental diagnostics: ERCP, endoscopic ultrasound, MRI (dilation of the common bile duct, slower outflow of contrast, slow contractions of the duodenal nipple). Endoscopic manometry allows the most complete assessment of the condition of the BDK, however, the method is quite complex and is not widely used.

Treatment

In the presence of jaundice and cholangitis - two-stage: 1) EPST, sanitation of the hepaticocholedochus; 2) planned cholecystectomy. It is possible to perform traditional cholecystectomy, choledocholithotomy, and biliodigestive anastomosis.

Cholangitis - inflammation of the bile ducts

The disease was first described by J.M. Charkot (1877) in the form of a triad of symptoms: fever with chills, jaundice and pain in the upper abdomen. B.M. Reynolds (1959) added to Charcot's triad signs of toxic shock in the form of clouding of consciousness and arterial hypotension arising from the accumulation of purulent bile in the ducts due to obstruction of the terminal part of the common bile duct.

The most common cause of cholangitis is choledocholithiasis, less often it occurs against the background of stenosis or strictures of the biliary tract. Currently, there is an increase in the incidence of tumor obstruction as a cause of cholangitis.

The pathophysiology of cholangitis involves three components: cholestasis, increased ductal pressure, and bacterial infection.

Normally, intestinal microorganisms are constantly present in the bile in small quantities (duodenobiliary reflux). When the bile ducts are obstructed, they multiply, and with complete obstruction, the concentration of microorganisms in the bile approaches their concentration in the feces. The bile microflora in cholangitis corresponds to the intestinal microflora.

An increase in intraductal pressure leads to bivenous reflux of bacteria and endotoxin into the central bloodstream, causing biliary sepsis.

The main organs affected by the development of cholangitis are the cardiovascular system (microcirculation disorders), kidneys (failure due to hypovolemia), liver and lungs. Endotoxemia in cholangitis leads to the rapid development of secondary immunodeficiency and disseminated intravascular coagulation syndrome. 10–30% of patients with obstructive suppurative cholangitis develop septic shock.

The most widespread classification of cholangitis according to the clinical course (E.I. Galperin, 1977): acute form - Reynolds pentad, signs of a systemic reaction, septic shock; acute relapsing form - episodes of exacerbations alternate with periods of clinical remission; chronic form - the clinical picture is nonspecific (weakness, fatigue, low-grade fever, slight jaundice). It is customary to divide cholangitis depending on the morphological changes in the ducts (catarrhal, phlegmonous, gangrenous, etc.), according to the degree of prevalence of the process (segmental intrahepatic and extrahepatic, widespread, total), according to the nature of the microflora (aerobic, anaerobic, mixed), by the nature of the complications (without purulent complications, with liver abscesses, with systemic inflammatory response syndrome, with sepsis, with severe sepsis, septic shock).

Cholangitis Clinic: pain syndrome (right hypochondrium), Charcot triad, Reynolds pentad, possible development of multiple organ failure and disseminated intravascular coagulation syndrome.

Laboratory tests: leukocytosis, cholestasis and cytolysis syndromes (increased bilirubin, transaminases, alkaline phosphatase, γ-glutamyl transferase).

It is necessary to perform blood cultures, determine hemostatic parameters and kidney function.

Instrumental methods: ultrasound, MRI, ERCP, PPCP.

Basic principles of treatment of cholangitis

Timely implementation of biliary decompression and restoration of bile duct patency.

Carrying out intensive therapy aimed at reducing intoxication, reducing the manifestations of multiple organ failure, and stabilizing the patient’s condition.

Timely and adequate antibacterial therapy.

Biliary decompression can be carried out using EPST (papillosphyterotomy, removal of stones with a Dormia basket, stent installation, nasobiliary drainage) or PPCS. After restoration of bile outflow, resolution of jaundice and intoxication, the patient undergoes open or laparoscopic cholecystectomy with correction of bile duct pathology.

It is also possible to perform laparoscopic cholecystectomy with revision of the biliary tract, choledochoscopy, and removal of stones.

If minimally invasive decompression is impossible (large, unremovable stones), traditional open surgery, choledochotomy, restoration of bile outflow, external drainage of the bile ducts, followed by planned cholecystectomy are performed.

The choice of tactics depends on the patient’s condition and the severity of cholangitis and the severity of endotoxemia.

Antibacterial therapy for acute cholangitis is prescribed upon admission, the choice of drug is carried out empirically, and further correction is possible taking into account the microflora. The main causative agents of cholangitis are gram-negative intestinal flora (Escherichia coli and Klebsiella) and anaerobes (bacteroides). Taking into account the ability of antibiotic accumulation in bile and minimal hepatotoxicity, the use of inhibitor-protected penicillins and cephalosporins, ureidopenicillins, III-IV generation cephalosporins, fluoroquinolones and carbopenems is considered optimal. The use of metronidazole is also rational.

All patients with moderate and severe purulent intoxication are indicated for targeted detoxification. The most common methods are plasmapheresis (removal of endotoxin, cytokines, circulating immune complexes) and enterosorption (binding of endotoxin in the intestine, limiting its penetration into the portal bloodstream). It is possible to use hemosorption, xenospleen, etc. Research is underway to develop specific methods of detoxification, in particular, the use of human antiserum to endotoxin, endotoxin antagonists - polymyxin B, lactulose.

Mirizzi syndrome

The Argentine surgeon P. Mirizzi in 1948 first described a narrowing of the common hepatic duct, as well as a fistula between the gallbladder and the extrahepatic bile duct.

It is customary to distinguish between two forms of Mirizzi syndrome: acute and chronic. The first form most often manifests itself as a narrowing of the lumen of the hepaticocholedochus, the second is characterized by the presence of a fistula between the gallbladder and the extrahepatic bile duct.

Pathogenesis

Against the background of acute calculous cholecystitis, compression of the extrahepatic bile ducts occurs with a calculus located in Hartmann's pouch (clinically - acute calculous cholecystitis and obstructive jaundice). With conservative treatment, the acute process may resolve, but compression and inflammation around the hepaticocholedochus lead to the formation of a narrowing of the latter (stricture). Over time, the walls of the bile duct and gallbladder come closer together and, under the influence of stones, a communication occurs between them (vesicocholedocheal fistula); as a rule, at this stage the stricture is eliminated. Through this pathological formation, stones from the gallbladder exit into the common bile duct (bladder-rider).

Diagnostics

Clinical manifestations of Mirizzi syndrome depend on the form of the disease. Patients with the acute form present complaints characteristic of acute calculous cholecystitis, complicated by obstructive jaundice; The duration of the disease is usually short, and choledocholithiasis is uncommon. The chronic form of the syndrome is characterized by a long course of cholelithiasis, choledocholithiasis, and obstructive jaundice with exacerbations.

The main diagnostic method is ERCP.

Acute form of Mirizzi syndrome (X-ray signs of stricture)

Dilation of the bile ducts above the narrowing.

Symptoms of a “break” in contrasting pro-currents.

Deviation of the deformed part of the duct.

Absence of stones near the narrowing zone.

Limited deformation not exceeding 1 cm.

Chronic form of Mirizzi syndrome (cholecystocholedocheal fistula)

Contrasting the gallbladder through a pathological anastomosis with the hepaticocholedochus.

Lack of contrast enhancement of the cystic duct.

Gallbladder deformity.

Choledocholithiasis, stenosis of the major duodenal papilla.

The most dangerous manifestations of Mirizzi syndrome, which pose a threat to the patient’s life, are obstructive jaundice and acute cholecystitis.

The choice of surgical method depends on the intraoperative picture and intraoperative cholangiography data. In the 1st form, cholecystectomy and drainage of the bile ducts (prevention of stricture progression) according to Keur are most often performed. If irreversible narrowing of the bile ducts is detected, hepaticojejunostomy may be performed.

If a cholecystocholedochal fistula is detected, it is possible to perform a subtotal cholecystectomy or resection of the gallbladder with closing the defect in the fistula area and drainage of the hepaticocholedochus according to Kehr. In case of significant destruction of the wall of the extrahepatic ducts, the operation of choice is hepaticojejunostomy.

Biliary fistulas

A biliary fistula is a persistent, constant or intermittent, complete or partial release of bile outward (external biliary fistula), into hollow organs (internal biliary fistula), completely or partially bypassing its natural path into the intestine (Kalchenko I.I., 1966).

External biliary fistulas can form as a result of the inflammatory process in the gallbladder and the abscess breaking out through all layers of the abdominal wall; after cholecystostomy and cholecystectomy in the presence of an obstruction in the terminal part of the common bile duct (choledocholithiasis, stenosis of the central bile duct, pancreatitis), if the bile ducts are damaged during cholecystectomy and gastrectomy.

When identifying a biliary fistula, it is necessary to clarify its type (complete or incomplete), the causes of formation, and the condition of the bile ducts.

Diagnostics: fistula probing, fistulocholangiography, ERCP.

Treatment. In the presence of a spontaneous biliary fistula due to perforation of the gallbladder and breakthrough of the abscess outward, a radical operation is indicated - cholecystectomy after sanitation of the fistula and abscess cavity.

For fistulas caused by biliary hypertension, it is necessary to perform EPST and remove stones from the ducts.

Treatment of injuries to the bile ducts and their complications (external biliary fistula, post-traumatic stricture, obstructive jaundice, cholangitis) currently represents a serious medical and social problem. These patients are indicated for reconstructive biliodigestive operations (hepaticojejunostomy on a Roux-en-Y loop), and in some situations, placement of a biliary plastic stent.

Internal biliary fistulas. The main reason is the long course of calculous cholecystitis. The inflamed gallbladder fuses with a section of the intestine (usually the duodenum, less often the colon), then a fistula is formed. A biliary fistula can also form as a result of penetration into the gallbladder or duct of an ulcer of the stomach and duodenum, as well as an ulcer of the colon with nonspecific ulcerative colitis or Crohn's disease. The most common are biliodigestive fistulas; rare anatomical variants are cholecystohepatic, biliovasal, biliopericardial and other fistulas.

Clinic. Recognition of internal biliary fistulas presents significant clinical and radiological difficulties. Symptoms that allow one to suspect the presence of this complication include: 1) a sharp decrease and rapid disappearance of a previously identified infiltrate in the right hypochondrium or a decrease in the size of the gallbladder, especially if loose stools mixed with blood and pus appear at the same time; 2) sudden disappearance of pain, high fever and decrease in jaundice; 3) development of signs of intestinal obstruction and passage of gallstones larger than 1 cm in feces; 4) signs of persistent cholangitis occurring without intense jaundice.

Fistulas can be asymptomatic and close after the stone passes into the intestine; in this case, they are diagnosed during surgery.

Cholecystocolic fistulas can manifest as severe cholangitis due to reflux of intestinal contents. The entry of bile acids into the colon causes diarrhea and weight loss.

Diagnostics. It is possible to contrast the bile ducts with oral administration of contrast (cholecystoduodenal fistula) or with irrigography (cholecystocolic). The method of choice is ERCP.

Surgical treatment: cholecystectomy with mandatory revision of the bile ducts, closure of the intestinal wall defect.

Gallstone obstruction

A gallstone with a diameter of more than 2.5 cm that enters the intestine through a fistula can cause acute intestinal obstruction. Obstruction usually occurs in the ileum, but cases of acute intestinal obstruction caused by gallstones at the level of the duodenum, sigmoid and rectum have been described.

Older women with a history of chronic calculous cholecystitis are more likely to suffer. Clinic: paroxysmal pain, nausea, vomiting, bloating, non-passage of gas and stool. Diagnosis is established on the basis of data from plain radiography of the abdominal cavity and ultrasound. If conservative treatment fails and there are signs of obstructive intestinal obstruction, it is indicated surgical intervention. The stone is lowered into the rectum and removed; for fixed stones, enterotomy is necessary.

The decision to perform cholecystectomy and closure of the biliary fistula is made individually at the same time, depending on the patient’s condition, surgical findings and the qualifications of the surgeon, since the elimination of the fistula during surgery for gallstone intestinal obstruction significantly increases the risk of surgical intervention in elderly and senile patients.

Gallbladder cancer

WITH leaves 1–7% of all malignant neoplasms, in the group of patients with bilio-pancretoduodenal localization - 10–14%. Histologically, adenocarcinoma is detected in 80% of cases.

The frequency of combination of gallbladder cancer with gallstone disease reaches, according to some authors, 75–90%, increasing in proportion to the duration of cholelithiasis.

Benign tumors of the gallbladder are also considered precancerous diseases; they are divided into epithelial (papillomas, adenomas), non-epithelial (fibromas, fibroids) and mixed (myxomas, adenomyomas, etc.). The most common are papillomas and adenomas, malignancy is more common in formations more than 1.5 cm in diameter, the frequency of malignancy is 10–33%.

Classification. The International Classification of Gall Bladder Cancer is used according to TNM criteria, which takes into account the location and extent of the primary tumor, the presence or absence of metastases in regional lymph nodes, and the presence or absence of distant metastases.

Primary tumor (T)

TX - the primary tumor cannot be assessed.

T0 - there are no signs of a primary tumor.

Tis - intraepithelial cancer without spreading to the submucosal layer.

T1 - the tumor spreads in the mucosal (T1a) or muscular (T1b) layers.

T2 - the tumor extends to the perimuscular connective tissue, but does not invade the serosa or liver tissue.

T3 - the tumor invades the serous membrane or spreads into the liver to a depth of 2 cm, or grows into one of the surrounding organs.

T4 - the tumor grows into the liver to a depth of more than 2 cm and/or into two or more neighboring organs.

Regional lymph nodes (N)

NX - regional lymph nodes cannot be assessed.

N0 - no signs of lymph node involvement.

N1 - metastases in lymph nodes located near the cystic and common bile duct and/or the portal of the liver.

N2 - metastases in lymph nodes located near the head of the pancreas, duodenum, portal vein, celiac and/or superior mesenteric artery.

Distant metastases (M)

Mx - the presence of distant metastases cannot be assessed.

M0 - no distant metastases.

M1 - there are distant metastases.

Diagnostics

Gallbladder cancer is characterized by the absence of pathognomonic clinical signs and significant polymorphism of symptoms.

Clinical forms of gallbladder cancer (Aliev M.A., 1986)

Pseudocholelithiasis- complaints and symptoms characteristic of chronic, less often acute calculous cholecystitis are noted.

Tumor- the presence of a tumor in the right hypochondrium or a typical “minor signs” syndrome.

Jaundice - the main symptom is obstructive jaundice.

Dyspeptic- complaints of nausea, vomiting, and stool disorders bring the patient to the doctor.

Septic - persistent fever, sometimes hectic fever.

Metastatic(“silent”) - metastases are initially detected in the liver and other organs.

Symptoms of cancer can be masked by complications of gallstone disease or the tumor itself - acute cholecystitis, cholangitis, liver abscesses, intestinal obstruction, bleeding during tumor growth.

Differential diagnosis gallbladder cancer is carried out with chronic cholecystitis, benign tumors of the gallbladder, tumors of the hepatobiliopancreatoduodenal zone.

Before surgery, an accurate diagnosis can be established in 10–45% of cases.

Instrumentaldiagnostics

Ultrasound. The examination can reveal thickening of the gallbladder wall and the presence of tissue masses associated with the gallbladder. The use of endosonography increases the sensitivity and specificity of the method.

CT is used mainly to determine the extent of the tumor process.

Laparoscopy - allows you to establish a diagnosis when a tumor has invaded the organ wall, perform a targeted biopsy, assess the extent of the process and avoid a trial laparotomy.

If jaundice occurs, ERCP or PCCG may be used.

Laboratory diagnostics is of secondary importance and is based on the identification of anemia, cytolysis syndrome, cholestasis and liver failure.

It is possible to identify tumor markers of liver and biliary tract diseases - α-fetoprotein, carbohydrate antigen CA19-9.

Treatment

In 25–30% of patients with gallbladder cancer, when the diagnosis is made, radical treatment is impossible due to the prevalence of the process. Only 10–15% of initially identified patients can undergo radical surgery.

The stage of the tumor determines the tactics and scope of surgery; the age and general condition of the patient are also taken into account. Operations are traditionally divided into palliative and radical.

Radical operations

Stage I (T1) - cholecystectomy with regional lymphadenectomy.

Stage II (T2) - cholecystectomy, resection of the gallbladder bed of at least 2–3 cm, lymphadenectomy.

Stage III (T3) - cholecystectomy, anatomical resection of IV–V liver segments, lymphadenectomy.

Palliative operations

Stage IV (T4) - operations are aimed at eliminating complications - restoration of bile outflow, resolution of intestinal obstruction, etc. (average life expectancy after palliative operations is 2–8 months).

Superradical operations have also been proposed for patients with stage IV of the process - removal of the gallbladder with right-sided hemihepatectomy and pancretoduodenal resection.

The options for chemotherapy, radiotherapy and radiation therapy for gallbladder cancer still appear limited.

Considering the difficulties of early diagnosis and unsatisfactory results of treatment of gallbladder cancer, the main thing is prevention of this terrible disease. Prevention consists of timely detection and treatment of gallstone disease.

Assignments for student independent work

As a result of independent study of literature, you need to know:

normal and topographic anatomy of the gallbladder, bile ducts, major duodenal papilla and pancreas;

etiology and pathogenesis of cholelithiasis and its main complications;

clinical picture of various forms of cholelithiasis;

basic laboratory methods for diagnosing cholelithiasis;

instrumental methods for diagnosing cholelithiasis, indications for their use;

therapeutic tactics for various forms of cholelithiasis.

To prepare for the lesson you need:

clearly understand the goals and objectives of the upcoming lesson;

familiarize yourself with the contents of the lecture “Cholelithiasis, acute and chronic calculous cholecystitis”, given at the department;

familiarize yourself with the contents of these guidelines;

complete control tasks to check the results of self-study on the topic of the lesson.

Tests

Complications of cholelithiasis can be all pathological conditions, except: a) acute pancreatitis; b) obstructive jaundice;
c) duodenostasis, d) obstructive small intestinal obstruction; e) cholangitis.

Biliary colic is characterized by: 1) intense pain in the right hypochondrium; 2) irradiation of pain to the right shoulder blade; 3) Shchetkin–Blumberg sign in the right hypochondrium; 4) Ortner's symptom; 5) high temperature. Choose the correct combination of answers: a) 1, 2, 4; b) 2, 3, 4; c) 4, 5; d) 3, 4; e) 2, 3, 5.

The clinical picture of acute cholangitis is usually characterized by: 1) hectic temperature; 2) pain in the right hypochondrium; 3) jaundice; 4) girdle pain; 5) bloating and uncontrollable vomiting. Choose the correct combination of answers: a) 1, 2, 4; b) 1, 2, 3; c) 3, 4, 5; d) 4, 5; e) 1, 4, 5.

For the diagnosis of choledocholithiasis, it is most advisable to use: 1) transabdominal ultrasound scanning; 2) intravenous cholegraphy; 3) ERCP; 4) duodenal intubation; 5) plain radiography of the abdominal cavity. Choose the best combination of answers: a) 1, 2;
b) 1, 2, 3; c) 1, 3; d) 3, 4; e) 2, 4, 5.

The most substantiated theories of stone formation in the gallbladder are: 1) infectious; 2) theory of stagnation in the gallbladder; 3) metabolic disorders; 4) allergic; 5) the theory of “protective” colloids. Choose the best combination of answers: a) 1, 2; b) 1, 2, 3; c) 1, 3; d) 3, 4; e) 2, 4, 5.

The optimal method for diagnosing chronic calculous cholecystitis: a) ERCP; b) laparoscopy; c) ultrasonography; d) spiral CT;
e) duodenal intubation.

Acute obstructive cholangitis is manifested by: 1) jaundice; 2) chills; 3) an increase in the level of alkaline phosphatase in the blood; 4) leukocytosis;
5) enlarged liver. Correct answer: a) 1, 2, 3, 5; b) 1, 2, 3, 4; c) 1, 2, 4, 5; d) everything is correct; d) everything is wrong.

Indications for intraoperative cholangiography: 1) detection of stones in the common bile duct by palpation; 2) suspicion of cicatricial narrowing of the large duodenal nipple; 3) presence of jaundice before surgery; 4) increase in the diameter of the common bile duct; 5) jaundice at the time of surgery. Correct answer: a) 1, 2, 3, 4; b) 1, 3, 4; c) 3, 4; d) 1, 3, 4, 5; d) all answers are correct.

Treatment indicated for a patient with an attack of biliary colic caused by gallstones: a) emergency surgery; b) conservative treatment; c) urgent surgery after stopping the attack; d) antienzyme therapy; e) laparoscopic cholecystostomy.

Characteristic signs of obstructive jaundice against the background of choledocholithiasis will be: 1) hyperbilirubinemia; 2) leukopenia; 3) bilirubinuria;
4) positive stool reaction to stercobilin; 5) high level of alkaline phosphatase in the blood. Correct answers: a) 1, 3, 5; b) 2, 3, 5; c) 3, 4, 5; d) everything is correct; d) everything is wrong.

To diagnose obstructive jaundice and find out its cause, everything is used except: a) studies of AST and ALT; b) infusion cholegraphy; c) laparoscopy; d) ERCP; e) percutaneous transhepatic cholangiography.

If stones are detected in the gall bladder, cholecystectomy is indicated in the following cases: a) in all cases; b) with a latent form of the disease; c) with decreased ability to work; d) surgery is contraindicated for elderly and senile patients; e) surgery is contraindicated in patients under 18 years of age.

Jaundice due to choledocholithiasis is not characterized by: a) bilirubinemia; b) urobilinuria; c) increased alkaline phosphatase in the blood; d) normal activity of AST and ALT; e) absence of stercobilin in feces.

A complication of cholelithiasis requiring emergency surgical intervention is: a) diffuse peritonitis; b) cicatricial stricture of the common bile duct; c) choledocholithiasis; d) enterovesical fistula; d) jaundice.

Which disease most often has to be differentiated from chronic cholecystitis: a) stomach cancer; b) duodenal ulcer; c) chronic gastritis; d) gastric ulcer;
e) chronic pancreatitis?

Cholecystectomy for cholelithiasis is indicated when: 1) there is no filling of the gallbladder on the cholangiogram; 2) stones that cause repeated colic; 3) gallstones, causing dyspepsia; 4) stones, often leading to relapses of cholecystitis; 5) more than five stones on the cholecystogram. Correct would be: a) 1, 2; b) 4; c) 1, 2; d) 3, 4, 5 that's right.

Intraoperative methods for examining extrahepatic bile ducts do not include: a) palpation of the common bile duct; b) cholangiomanometry;
c) intravenous cholegraphy; d) choledochoscopy; e) intraoperative cholangiography.

Hepatic colic is not characterized by: a) pain in the right hypochondrium radiating to the back; b) phrenicus symptom; c) Murphy's symptom; d) severe muscle tension and pain in the right hypochondrium; e) Ortner's symptom.

Which of the complications of cholelithiasis requires emergency surgical intervention: 1) acute catarrhal cholecystitis; 2) cholecystopancreatitis; 3) choledocholithiasis; 4) obstructive jaundice; 5) biliary colic? Choose the best combination of answers: a) 1, 4, 5; b) 2, 4; c) 1, 2, 3, 4;
d) everything is correct; d) everything is wrong.

A 50-year-old patient, six months after cholecystectomy performed for chronic calculous cholecystitis, again began to experience pain in the right hypochondrium, periodically accompanied by yellowing of the sclera. An ultrasound examination of the abdominal cavity failed to detect any obvious pathology in the extrahepatic bile ducts. Which of the following methods is most informative for diagnosis in this case: a) infusion cholegraphy; b) oral cholecystography:
c) ERCP; d) liver scan; e) computed tomography?

Which of the following signs is the most reliable in diagnosing cholelithiasis: a) positive Courvoisier’s sign; b) positive Murphy's sign; c) the presence of ultrasound signs of stones; d) increase in serum bilirubin above 30 µm/l; e) high levels of AST and ALT?

Obstructive jaundice is characterized by the following symptoms: 1) increased direct bilirubin in the blood serum; 2) increase in indirect bilirubin in blood serum; 3) bilirubinuria; 4) hypercholesterolemia; 5) increase in stercobilin in feces. Choose the correct combination of answers: a) 1, 3, 5; b) 1, 3, 4; c) 2, 3, 4; d) 2, 3, 4, 5; d) 2, 3.

Gallstone disease is dangerous: 1) the development of liver cirrhosis;
2) cancerous degeneration of the gallbladder; 3) secondary pancreatitis;
4) development of destructive cholecystitis; 5) possible obstructive jaundice. Correct will be: a) everything is correct; b) 3, 4, 5; c) 1, 5; d) 1, 3, 4, 5; e) 2, 3, 4, 5.

The formation of cholesterol stones in the gallbladder is promoted by: 1) pregnancy; 2) metabolic disorders; 3) taking aspirin; 4) age; 5) floor; 6) constitution; 7) increased amount of bile acids. Correct would be: a) 1, 2, 3, 4, 7; b) 1, 2, 3, 4, 6, 7; c) everything is correct; d) 1, 2, 4, 5, 6; 7;
e) 2, 3, 4, 5, 7.

In acute cholecystitis, differential diagnosis must be made with: 1) acute pancreatitis; 2) perforated duodenal ulcer; 3) acute appendicitis; 4) right-sided pleuropneumonia;
5) chronic pancreatitis in the acute stage. Choose the best combination of answers: a) 1, 2, 4; b) 1, 2, 3; c) 2, 3, 5; d) 3, 4, 5; d) everything is correct

An accurate diagnosis of acute calculous cholecystitis can be made based on: 1) the patient’s complaints; 2) medical history; 3) ultrasound scanning of the gallbladder and pancreas; 4) infusion cholangiography; 5) retrograde cholangiopancreatography. Correct answers: a) 1, 2, 3; b) 2, 3, 4; c) 3, 4, 5; d) 2, 4, 5; e) 4, 5.

Complications of acute calculous cholecystitis include everything except: a) varicose veins of the esophagus; b) obstructive jaundice; c) cholangitis; d) subhepatic abscess; d) peritonitis.

A patient with gangrenous cholecystitis is shown: a) emergency surgery; b) delayed operation; c) conservative treatment; d) surgery in the absence of effect from conservative therapy; e) decision-making depends on the age of the patient.

What is the advantage of performing cholecystectomy from the cervix: 1) conditions are created for bloodless removal of the gallbladder; 2) the path of purulent bile entering the common bile duct is interrupted; 3) it is possible to avoid the migration of stones from the bladder to the common bile duct; 4) allows you to refrain from choledochotomy; 5) eliminates the need for intraoperative cholangiography? Correct answers: a) 1, 2, 4; b) 1, 3, 4; c) 2, 4, 5; d) 1, 2, 3; e) 1, 2, 5.

Acute calculous cholecystitis usually develops due to:
1) entry of infected bile into the gallbladder; 2) stagnation of bile in the gallbladder; 3) the presence of stones in the gall bladder; 4) thrombosis of the cystic artery; 5) obstruction of the cystic duct. Correct answer: a) 1, 2; b) 1, 2, 3, 4; c) 2, 4, 5; d) 3, 4, 5; e) 4 and 5.

In acute destructive cholecystitis, cholecystostomy is indicated for: a) concomitant edematous pancreatitis; b) an elderly patient; c) in case of severe general condition of the patient; d) the presence of infiltrate in the neck of the gallbladder; e) concomitant cholangitis.

Absolute contraindications for performing laparoscopic cholecystectomy: 1) intrahepatic location of the gallbladder; 2) elderly and senile age of the patient; 3) acute calculous cholecystitis; 4) presence of choledocholithiasis; 5) reasonable suspicion of gallbladder cancer; 6) acute pancreatitis; 7) late stages of pregnancy. Correct answer: a) everything is correct; b) everything is wrong; c) 1, 5, 7; d) 2, 3, 4, 5, 6; e) 5, 6, 7.

Answers

1-in; 2-a; 3-b; 4-in; 5-b; 6-in; 7-g; 8-d; 9-b; 10-a; 11-b; 12-a; 13-b; 14-a; 15-b; 16-d; 17-v; 18-g; 19-d; 20-in; 21-v; 22-b; 23-d; 24-g; 25-d; 26-a; 27-a; 28-g; 29-d; 30-d; 31-v; 32-d.

Situational tasks

1. A 30-year-old patient consulted a general practitioner at a clinic with complaints of periodic pain in the right hypochondrium. The pain goes away on its own within 5–20 minutes and is not accompanied by fever or dyspeptic symptoms. At the time of examination there is no pain, the abdomen is soft and painless. The doctor sent the patient for an ultrasound (see figure). Your presumptive diagnosis. Recommend treatment.

2. A 58-year-old patient was delivered on the third day from the onset of pain in the right hypochondrium, the temperature rose to 38 degrees. Previously, there were repeated attacks of such pain that lasted 5–7 days. General condition is satisfactory. The abdomen is tense and painful in the right hypochondrium, where a painful infiltrate up to 10 cm in diameter is palpated. There are no symptoms of peritoneal irritation. Ultrasound: gallbladder 120 by 50 mm, in the neck area a stone 15 mm, does not move when changing body position, gallbladder wall up to 8 mm. Make a diagnosis. Recommendations for treatment.

3. A 60-year-old patient was admitted with severe jaundice, which began after an attack of severe pain in the right hypochondrium. He has been suffering from cholelithiasis for three years. Attacks of pain occur 3-4 times a year after breaking the diet. There was no jaundice or fever during attacks before. The sclera and skin are jaundiced, the abdomen is soft, moderately painful in the right hypochondrium. Ultrasound - gallbladder 7520 mm, wall 2 mm, in the lumen there are many stones up to 8 mm; Common bile duct up to 16 mm, extra- and intrahepatic ducts are expanded. FGDS - there is no bile in the duodenum, the major duodenal papilla is not changed. What complications of cholelithiasis did the patient develop? What additional diagnostic methods should be used? Treatment.

4. A 45-year-old female patient periodically complains of pain in the right hypochondrium, not associated with eating. Ultrasound examinations repeatedly reveal gallbladder polyps up to 5 mm, but no stones were found. What are your tactics?

5. A 58-year-old patient was admitted to the clinic on the second day of the disease with complaints of pain in the right hypochondrium, nausea, and vomiting of bile. The abdomen is tense and painful in the right hypochondrium, positive Murphy, Ortner, Mussi-Georgievsky symptoms. Leukocytosis - 1510 9 /l. Ultrasound picture of acute calculous cholecystitis. After conservative treatment, there is an improvement within 24 hours, slight pain in the right hypochondrium remains, leukocytosis is 910 9 /l. What is your treatment strategy?

6. A 48-year-old female patient was admitted with a clinical picture of acute cholecystitis. The patient was prescribed conservative treatment. Three hours after admission, the abdominal pain intensified, and the Shchetkin-Blumberg sign was positive in the right hypochondrium and right iliac region. What complication developed in the patient? What are the treatment tactics?

7. A 57-year-old patient was admitted with moderate pain in the right hypochondrium, radiating to the scapula. History of chronic calculous cholecystitis. There were no changes in the general blood test results. There is no jaundice. Palpation reveals an enlarged, slightly painful gallbladder. The temperature is normal. What is your diagnosis? Therapeutic tactics.

8. A 56-year-old patient, suffering from cholelithiasis for a long time, was admitted on the 3rd day from the onset of exacerbation of the disease. Complex conservative therapy did not lead to an improvement in the patient's condition. As observation progressed, significant abdominal bloating, cramping pain, and repeated vomiting mixed with bile were noted. X-ray of the abdominal cavity: pneumatosis of the small intestine, aerocholia. Your proposed diagnosis, treatment tactics.

9. An 80-year-old patient suffers from frequent attacks of calculous cholecystitis with severe pain. There is a history of two myocardial infarctions and arterial hypertension. Two months ago I suffered a cerebral infarction. There are no signs of peritonitis. Which treatment method should be preferred?

10. A 55-year-old patient who underwent cholecystectomy 2 years ago was admitted with a clinical picture of obstructive jaundice. When performing ERCP, there are signs of choledocholithiasis. What treatment method is indicated for the patient?

11. A patient who underwent endoscopic papillosphincterotomy has intense pain in the epigastric region radiating to the lower back, repeated vomiting, muscle tension in the anterior abdominal wall. Leukocytosis is pronounced and serum amylase levels are increased. What is your diagnosis? What are the treatment tactics?

Answers to situational problems

1. Gallstone disease, attacks of hepatic colic. Elective laparoscopic cholecystectomy is recommended.

2. Acute phlegmonous calculous obstructive cholecystitis. Urgent surgical treatment is indicated - cholecystectomy; if there are contraindications, two-stage treatment (cholecystostomy under local anesthesia).

3. Choledocholithiasis, obstructive jaundice. ERCP, endosonography. Endoscopic papillosphincterotomy, stone extraction, after resolution of jaundice - planned cholecystectomy.

4. The risk of developing gallbladder cancer and the presence of clinical manifestations of polyps - indications for surgical treatment - laparoscopic cholecystectomy.

5. The patient is indicated for surgical treatment - delayed cholecystectomy after additional examination.

6. The patient developed perforation of the gallbladder with the development of widespread peritonitis. An emergency operation is indicated - cholecystectomy, sanitation and drainage of the abdominal cavity, and, if indicated, placement of tampons and external drainage of the biliary tract.

7. The patient probably has hydrocele of the gallbladder; planned surgical treatment is indicated - cholecystectomy.

8. The patient probably has acute gallstone intestinal obstruction; if conservative treatment is ineffective, emergency surgery is indicated - laparotomy, enterotomy, stone removal.

9. The patient is prescribed conservative therapy; if ineffective, cholecystostomy is indicated.

10. Performing endoscopic papillosphyterotomy, sanitation of the hepaticocholedochus using a Dormia basket and a Fogarty catheter.

11. The patient has developed acute pancreatitis; complex conservative treatment is indicated.

Basic literature

Surgical diseases: Textbook / Ed. M.I. Cousin. – 3rd ed. reworked and additional – M: Medicine, 2002. – 784 p.

Further reading

Grishin I.N.. Cholecystectomy: Practical guide. – Mn.: Higher. school, 1989. – 198 p.

Gallstone disease / S.A. Dadwani, P.S. Vetshev, A.M. Shulutko, M.I. Prudkov; Moscow honey. acad. them. THEM. Sechenov, Ural. state honey. acad. – M.: Publishing house. House Vidar - M, 2000. - 139 p.

Korolev B.A., Pikovsky D.L.. Emergency surgery of the biliary tract. – M.: Medicine, 1990. – 240 p.

non-infectious diseases in outpatient clinics... BelMAPO, 2004. – 42 p. Leonovich, S. I. Gallstonedisease. Spicy And chroniccalculouscholecystitis: method. recommendations / S. I. Leonovich, A. ...

1. Abstract of the dissertation

   ... acutecalculouscholecystitis; GENDER at chroniccalculouscholecystitis acutecholecystitis to the number of operations for chroniccholecystitis...activity at gallstoneillnesses And acutecholecystitis like the way...

2. VOLGOGRAD ORDER OF THE RED BANNER OF LABOR BYKOV Alexander Viktorovich MODERN APPROACHES TO DIAGNOSIS AND SURGICAL TREATMENT OF CHOLELITHIS DISEASE 14

   Abstract of the dissertation

   ... acutecalculouscholecystitis; GENDER at chroniccalculouscholecystitis; ratio of the number of operations at acutecholecystitis to the number of operations for chroniccholecystitis...activity at gallstoneillnesses And acutecholecystitis like the way...

3. Clinical history

   Document

   17 Diagnosis of the referring institution: Gallstonedisease, chroniccalculouscholecystitis. Surgical operations: 287 Cholecystectomy... chronic. At acutecholecystitis Usually the onset of an attack is not as violent as with. gallstoneillnesses ...

Gallstones without cholecystitis (K80.2)

Gastroenterology

General information

Brief description

PROFILE COMMISSION FOR THE SPECIALTY “GASTROENTEROLOGY” OF THE MINISTRY OF HEALTH OF THE RUSSIAN FEDERATION

RUSSIAN GASTROENTEROLOGICAL ASSOCIATION

Cholelithiasis

Definition

Gallstone disease (GSD, syn. cholelithiasis) is a chronic disease with a genetic predisposition, in which the formation of stones in the bile ducts is observed.

When stones form in the gall bladder (GB), they talk about “cholecystolithiasis”, in the common bile duct - about “choledocholithiasis”, in the intrahepatic ducts - about “intrahepatic cholelithiasis” (Figure 1).

Figure 1. Possible localization of gallstones.

Basic code according to ICD-10

K80 Gallstone disease.

History of the study of the disease

Information about the discovery of gallstones was found in ancient sources. Gall stones were used as ritual decorations and in cult rites. Descriptions of the signs of cholelithiasis are given in the works of Hippocrates, Avicenna, and Celsus. There is information that the founders of ancient medical science, Galen and Vesalius, discovered gallstones during autopsies of corpses.

The French physician Jean Fernel (J. Fernel) in the 14th century described the clinical picture of cholelithiasis, and also established its connection with jaundice.
The German anatomist A. Vater in the 18th century described the morphology of gallstones and indicated that the cause of their formation was thickening of bile. Chemical research on gallstones was first undertaken by D. Galeati in the mid-18th century.
The information about gallstone disease accumulated by that time was summarized by the German anatomist and physiologist A. Haller in his works “Opuscula pathologica” and “Elementa physiologiae corporis humani” in the middle of the 8th century.
A. Haller divided all gallstones into two classes: 1) large, ovoid, usually single, consisting of “a tasteless yellow substance that, when heated, melts and can burn,” and 2) smaller, dark-colored, multifaceted, which are found not only in the bladder, but also in the bile ducts. Thus, the modern classification of gallstones, dividing them into cholesterol and pigment stones, was actually justified a long time ago.
Haller's contemporary F.P. de la Salle isolated a substance “similar to fat wax” from gallstones, represented by thin silvery plates. At the end of the 18th and beginning of the 19th centuries, cholesterol was isolated in its pure form by A. de Fourcroy, and from bile by the German chemist L. Gmelin and the French chemist M. Chevreul; the latter called it cholesterol (from the Greek chole - bile, stereos - volumetric).

In the middle of the 19th century, the first theories of the origin of gallstones appeared, among which two main directions stood out:
1) the root cause of the formation of stones is a disturbed condition of the liver, which produces pathologically altered bile,
2) the root cause is pathological changes (inflammation, stasis) in the gallbladder.
The founder of the first direction is the English doctor G. Thudichum. An adherent of the second was S.P. Botkin, who pointed out the importance of inflammatory changes in the development of cholelithiasis and described in detail the symptoms of the disease and therapeutic approaches.
One of the first experimental models of calculous cholecystitis was created by P. S. Ikonnikov in 1915.

At the end of the 19th century, the first attempts at surgical treatment of cholelithiasis were made: in 1882, Karl Langenbach (C. Langenbuch) performed the world's first cholecystectomy, and in Russia this operation was first performed in 1889 by Yu. F. Kosinsky.
S. P. Fedorov, I. I. Grekov, A. V. Martynov made a great contribution to the development of biliary tract surgery.
In 1947 “postcholecystectomy syndrome” has been described, which implies the persistence of symptoms or their appearance after removal of the gallbladder. It should be noted that there is significant clinical heterogeneity of this concept, and research in this direction continues to this day.

At the end of the 20th century, traditional cholecystectomy was replaced by less invasive methods - laparoscopic cholecystectomy (first performed in Germany by E. Muguet in 1985, and cholecystectomy from a mini-access, or “mini-cholecystectomy” (M. I. Prudkov, 1986 g., Vetshev P.S. et al., 2005). Robot-assisted technology for laparoscopic cholecystectomy is currently being actively implemented.
At the end of the 20th and beginning of the 21st, important discoveries were made in the field of studying genetic predisposition to cholelithiasis. Experience has been gained in the successful use of ursodeoxycholic acid in the dissolution of gallstones. In recent years, the problem of cholelithiasis has attracted increased attention due to the “epidemic of excess weight” and the increasing incidence of stone formation in children and adolescents.

Etiology and pathogenesis

Etiology and pathogenesis

The cause of stone formation is excess concentration of bile. There are two main types of stones (Figure 2):

1) Cholesterol. The cholesterol content in them is >50% (and even >90% in the so-called “pure cholesterol stones”). They also contain bile pigments, calcium salts, the matrix consists of mucus glycoproteins. For pure cholesterol stones, they are usually larger in size, single, yellowish-white. A calcium shell may form on the surface of cholesterol stones.

2) Pigment. Their cholesterol content<20%, они состояь преимущественно из кальция билирубината и полимероподобных комплексов кальция и гликопротеинов слизи. Пигментные камни, в свою очередь, разделяют на 2 подтипа:

a. Black(consisting predominantly of calcium bilirubinate, usually multiple, easily crumbling, size<5 мм, рентгенопозитивные в 50-75% случаев). Образование черных камней наиболее характерно для гемолиза и цирроза печени.

b. Brown(consisting of calcium salts of unconjugated bilirubin, mucin glycoproteins, cholesterol, palmitate and calcium stearate; soft, layered, X-ray negative). The formation of brown stones is characteristic of a chronic inflammatory process in the intra- and extrahepatic bile ducts. Inclusions of bacterial components may be found in the core of the stone, which confirms a possible connection with infection.

Drawing 2 . Types of gallstones: A) cholesterol, B) black pigmented, C) brown pigmented.

Stones up to 1 cm in size are conventionally designated as “small”, 1-2 cm - “medium” and >2 cm - large, although during instrumental diagnostics errors in assessing the size of stones are possible.

The mechanisms of gallstone formation in the presence of certain risk factors for the development of biliary sludge and cholelithiasis are presented in Table 1.

Table 1. Factors predisposing to the formation of biliary sludge, cholesterol and pigmented gallstones.

Cholesterol stones
Factors	Mechanisms
1. Demographic/genetic factors: Highest prevalence among North American Indians, Chilean Indians, Hispanic Chileans Higher prevalence in Northern Europe and North America compared to Asia Lowest prevalence in Japan Family predisposition	Secretion of cholesterol into bile, decreased secretion of PL associated with genetic factors
2. Obesity, metabolic syndrome	Secretion of cholesterol into bile, ↓ motility of the gallbladder due to decreased sensitivity to cholecystokinin
3. Type 2 diabetes mellitus	Same
4. Losing weight on the background of a low-calorie, especially very low-calorie diet (≤800 kcal per day)	Mobilization of cholesterol from tissues with its secretion into bile; ↓ enterohepatic circulation of the gastrointestinal tract. Estrogens stimulate hepatic lipoprotein receptors, the uptake of cholesterol from food and its secretion into bile; ↓ conversion of cholesterol into its esters; inhibit the secretion of fatty acids into bile
5. Female gender	Same
6. Taking estrogen medications	Same
7. Age over 40	Secretion of cholesterol into bile, ↓ pool and secretion of fatty acids, secretion of mucins?
8. Decreased motility of the gallbladder with the formation of biliary sludge: A. Long-term total parenteral nutrition B. Fasting B. Pregnancy D. Effect of drugs (in particular, octreotide)	↓ emptying the gallbladder
9. Clofibrate therapy	secretion of cholesterol into bile
10. Decreased secretion of fatty acids A. Primary biliary cirrhosis B. CYP7A1 gene defect B. Lesion of the terminal part of the ileum	↓ FA content in bile
11. MDR3 gene defect	↓ PL content in bile
12. Mixed disorders A. High-calorie diet - high in fat and simple carbohydrates. The latter plays a major role B. Spinal cord injuries	secretion of cholesterol into bile ↓ FA content in bile ↓ emptying the gallbladder
Pigment stones
1. Demographic/genetic factors: Asia, rural residence 2. Chronic hemolysis 3. Alcoholic cirrhosis of the liver 4. Pernicious anemia 5. Cystic fibrosis 7. Age 8. Ileal disease/resection, bypass	Secretion of mucins, immunoglobulins Deconjugation of bilirubin Increased absorption of unconjugated bilirubin due to fatty acids entering the colon

Formation of cholesterol stones

According to modern concepts, the first stage in the formation of cholesterol stones is biliary sludge.

Cholesterol (CH) is one of the main components of bile; in the aqueous phase it is in a suspended state - in the form of mixed micelles or vesicles including cholesterol, phospholipids (PL), and bile acids (BA). CS and PL are secreted by hepatocytes into bile in the form of single-layer vesicles, which then turn into mixed micelles.

Under conditions of a relative excess of cholesterol (“lithogenic bile”), unstable, cholesterol-enriched vesicles are formed, which merge into larger multi-lamellar structures - crystal precipitates.

The formation of lithogenic bile is the most important stage of stone formation. Immediate causes of the formation of lithogenic bile:

1) increased formation of cholesterol:

Due to the increased activity of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase, an enzyme that determines the rate of cholesterol synthesis in

liver
- due to increased uptake of cholesterol by liver cells from the bloodstream and its transfer into bile (in particular, due to the consumption of high-calorie foods rich in carbohydrates and cholesterol);

2) changed ratio of cholesterol, PL, FA:

Due to the hereditary characteristics of the activity of enzymes that control the synthesis and transfer of these components (Table 2, Figure 3),

Due to a decrease in the synthesis of fatty acids in the liver and disruption of their enterohepatic circulation.

The main factor determining the rate of FA uptake from the bloodstream and their transfer into bile is the activity of FA transporters on the canalicular membrane.

hepatocyte - facing the bile canaliculus.

Table 2. Changes in the ratio of cholesterol, PL and FA in bile in the presence of genetic changes in the activity of enzymes that control the metabolism and transport of cholesterol.

The enzyme and its activity due to genetic characteristics	Relative content in bile
	HS	FL (lecithin)	LCD
ABCG5/G8 (members 5, 8 of class G superfamily of ATP-binding cassette transporters)		Normal	Normal
↓ CYP7A1 (subunit 7A1 of cytochrome P450)	Normal	Normal	↓
↓ MDR3 (ABCB4) (multidrug resistance protein (member of class 4 ATP-binding cassette transporter superfamily))	Normal	↓	Normal

Figure 3. A cassette of transporters of bile components on the canalicular membrane of the hepatocyte.

Contribution of genetic factors emphasize the high frequency of detection of gallstones in first-degree relatives of patients with cholelithiasis, as well as the high prevalence of cholelithiasis in certain nationalities.

In patients with cholelithiasis, an increase in cholesterol content in food leads to an increase in the secretion of cholesterol into the bile. In the absence of cholelithiasis, the secretion of cholesterol does not increase even against the background of a cholesterol-enriched diet. Thus, genetic factors, coupled with a high-calorie and cholesterol-rich diet, create the basis for the development of cholelithiasis.

The role of genetic factors is supported by twin studies. In monozygotic twins, the contribution of genetic factors can be estimated at 25%, environmental conditions at 13%, and individual lifestyle characteristics at 62%.

A polymorphism of the gene encoding the structure of the ABCG5/G8 protein - the intrahepatic cholesterol transporter - has been described, in which its secretion into bile is increased (Table 2).

The high risk of cholelithiasis in certain nationalities is associated with the characteristics of mitochondrial DNA, in which the rate of conversion of cholesterol into fatty acids is reduced and the ratio of cholesterol/fatty acids in bile is increased.

Apparently, in most cases, cholelithiasis is of polygenic origin, but there may also be cases of monogenic inheritance. Thus, with a mutation of the CYP7A1 gene with a deficiency of cholesterol 7-hydroxylase, which catalyzes the first stage of the conversion of cholesterol into FAs, a relative deficiency of FAs is observed. Homozygous carriers of the mutant CYP7A1 gene always develop hypercholesterolemia and cholelithiasis. Heterozygotes are only predisposed to these abnormalities.

With a mutation in the MDR3 (ABCB4) gene, which encodes the PL export pump on the canalicular membrane of hepatocytes, their transport into bile is inhibited; as a result, hypersaturation of bile with cholesterol and the formation of stones in different parts of the biliary system are observed. Thus, an excess of cholesterol in relation to FA and PL is more often associated with hypersecretion of cholesterol, but it can also be caused by insufficient secretion of FA and PL.

Conditions in which FA metabolism is disrupted, additionally contribute to the oversaturation of bile with cholesterol. Increased hydroxylation of cholic acid leads to the replacement of its pool with an increased pool of deoxycholic acid. Excessive intake of deoxycholate into the bile is accompanied by hypersecretion of cholesterol.

Necessary conditions for the formation of stones(Figure 4).

1. Oversaturation of bile with cholesterol. This is a necessary, but not sufficient condition for stone formation. In most cases, the residence time of bile in the gallbladder is not long enough for cholesterol crystals to settle and grow.

2. Nucleation of cholesterol monohydrate crystals, which can occur in the presence of provoking factors and/or lack of interfering factors. According to modern concepts, nucleation is promoted by mucins and non-mucin glycoproteins (in particular, immunoglobulins), and apolipoproteins A-I, A-II and some other glycoproteins are prevented. Apparently, the nucleation of the cholesterol monohydrate crystal and its growth occurs in the mucin gel layer. The fusion of bubbles forms liquid crystals, which then turn into solid crystals. Further growth occurs due to the sedimentation of lamellar structures and bubbles oversaturated with cholesterol.

3. Decreased motility of the gallbladder - due to decreased sensitivity to cholecystokinin and/or autonomic neuropathy. If the gallbladder completely “throws out” the supersaturated bile, the stones will not be able to grow. In many patients with cholelithiasis, the motility of the gallbladder is reduced.

Figure 4. Stages of formation of cholesterol stones [according to N.J. Greenberger, G. Paumgartner, 2015, as modified].

Biliary sludge can be characterized as the formation of a thick layer of mucous material consisting of lecithin-CS crystals, cholesterol monohydrate, calcium bilirubinate, mucin gel. During sludge, a semilunar layer of sediment usually forms in the lowest part of the gastrointestinal tract, which has a characteristic ultrasonic appearance. For the development of biliary sludge, an imbalance between the production and degradation of mucin and the nucleation of bile components against the background of a supersaturation of cholesterol and calcium with bilirubinate are necessary.

Biliary sludge can be considered as a step preceding the formation of cholesterol stones. According to observations, over the next 2 years, sludge disappears in ≈18% of cases, in 60% it disappears and appears again, in 14% gallstones form, and in 6% of cases attacks of biliary colic occur.

Sludge often develops when the contractile function of the gallbladder is impaired and is associated with almost the same factors as cholelithiasis (Table 1).

Formation of pigment stones

Pigment stones are more often observed in people of Asian origin, rural populations, with chronic hemolysis, bacterial contamination of the biliary tract, diseases involving the ileum (in particular, Crohn's disease), anastomosis, cystic fibrosis, cirrhosis of the liver, Gilbert's syndrome (see Table 1 ).

During hemolysis, the excretion of conjugated bilirubin into bile increases, then it undergoes deconjugation in the biliary tract under the influence of endogenous glucuronidase.

The formation of pigment stones is also facilitated by dysfunction of the gallbladder epithelium in maintaining the pH of bile and the formation of bilirubin salts, as well as the production of phospholipase A by bacteria, which catalyzes the hydrolysis of bile PL to lysolecithin and fatty acids involved in the formation of the matrix of pigment stones.

Epidemiology

GSD is characterized by a fairly high prevalence in countries with a Western lifestyle (Europe, North America, Russia): this disease is registered with a frequency of ≈ 10-15%. Such a high frequency, in addition to the contribution of genetic factors, is explained by dietary patterns and consumption of increased amounts of simple carbohydrates.

In Africa, Asian countries and Japan, the prevalence of cholelithiasis is lower - 3.5-5%.

The NANESH III epidemiological study noted significant racial differences in the incidence of cholelithiasis, highlighting the important contribution of genetic factors to the pathogenesis of the disease. Among some nationalities, the incidence of gallstones is extremely high: among Mexicans and Chilean Indians, the probability of developing gallstones during their lifetime reaches 45-80%.

The main risk factors for the development of cholelithiasis:

1) age. The incidence of cholelithiasis clearly correlates with age. In countries with a Western lifestyle, the incidence of cholelithiasis in old age reaches 30%.

However, the maximum frequency of clinical manifestations of cholelithiasis is recorded at the age of 40-69 years.

2) female. The risk of developing cholelithiasis in women is approximately 2-3 times higher, which is associated with the influence of estrogens on lithogenic potential. However, differences in the incidence of men and women are smoothed out with age: in the age group of 30-39 years, the ratio of the risk of developing cholelithiasis in women and men is 2.9:1, at the age of 40-49 years - 1.6:1, at the age of 50- 59 years old - 1.2:1.

3) pregnancy. The risk of developing cholelithiasis increases during pregnancy, especially with repeated pregnancies (the likelihood of stone formation increases by 10-11 times). During pregnancy, biliary sludge develops in 20-30% of patients, stones - in 5-12% of cases. However, cases of spontaneous dissolution of stones after childbirth have been reported.

4) hormone replacement therapy in postmenopause (the risk of cholelithiasis increases by 3.7 times).

5) taking estrogen - in both sexes.

6) family history of cholelithiasis (the risk is increased by 4-5 times).

7) obesity, hypertriglyceridemia. Among people with metabolic syndrome, cholelithiasis is detected in ≈ 20% of cases.

8) diabetes mellitus (the risk is increased by 3 times).

9) liver cirrhosis (risk increased 10 times).

10) the use of drugs that affect the concentration of cholesterol in bile, motility of the biliary tract or are capable of crystallization in bile (somatostatin, fibrates, ceftriaxone).

11) rapid weight loss, bariatric interventions (probability of developing cholelithiasis >30%).

12) damage to the terminal ileum.

13) sufficiently long total parenteral nutrition.

In recent decades, there has been an increase in the incidence of cholelithiasis in children and adolescents; the most likely reason for this is the "overweight epidemic."

Clinical picture

Symptoms, course

Clinical picture

The “classic type” of a patient with cholelithiasis is a woman over 40 years old, with a hypersthenic build, with increased body weight and a history of childbirth. However, it should remember the increasing incidence of morbidity in young people and even children with increased body weight.

GSD can be asymptomatic. Clinical manifestations occur with the development of inflammation or obstruction of the bile ducts - with the migration of stones to the neck of the gallbladder, into the cystic or common bile duct.

The main clinical manifestations of cholelithiasis are attacks of biliary colic and acute cholecystitis.

It is also possible to develop cholangitis and attacks of acute biliary pancreatitis. The possibility of developing chronic biliary pancreatitis remains a matter of debate.

Biliary (biliary, hepatic) colic- the most common and characteristic manifestation of cholelithiasis. The cause of colic is the wedging of a stone into the neck of the gallbladder or its entry into the cystic duct or common bile duct. Obstruction and reflex spasm cause an increase in intraluminal pressure and the appearance of visceral pain.

In typical cases, biliary colic develops 1-1.5 hours after eating fatty, fried foods or an unusually large amount of food after a long period of restriction, quickly increases in intensity, reaching a “plateau”, while it is pronounced and quite constant, bursting (Figure 5) . The name “colic”, meaning severe cramping pain, does not accurately reflect the nature of biliary colic, since it does not have a wave-like intensifying nature. In the English-language literature, the term “biliary pain” is used to refer to such attacks (see Table 5).

The displacement of the stone can also be provoked by a shaking ride or bending of the body. The duration of biliary colic can range from several minutes to several hours. The pain is localized in the epigastrium and right hypochondrium, and can radiate under the right scapula, into the interscapular space, at the level of the lower thoracic vertebrae, into the right shoulder and neck on the right (Figure 6). Often accompanied by nausea, vomiting, which does not bring relief, and vegetative manifestations - tachycardia or bradycardia, changes in blood pressure, symptoms of intestinal paresis or the urge to stool, an increase in body temperature to subfebrile values. The patient is tossing about in bed. The attack resolves with the administration of antispasmodics or spontaneously. The pain ends quickly, less often - gradually.

Figure 5. Differences between biliary “colic” and intestinal and renal colic in the nature of pain.

Figure 6. Localization of pain in diseases of the biliary tract and pancreas.

Often, biliary colic develops at night, a few hours after falling asleep. According to the findings of researchers from Denmark, pain in the right upper quadrant of the abdomen at night is quite specific to bile duct pathology.

Attacks of biliary colic can be mild and recur quite often; in such cases, the diagnosis is sometimes formulated as “exacerbation of chronic calculous cholecystitis.” However, in many cases it is more correct to regard the symptoms as a manifestation of repeated colic associated with obstruction of the cervix of the gallbladder.

If an attack of biliary colic lasts > 6 hours, the development of acute cholecystitis should be suspected (see below). When serum bilirubin increases and/or serum alkaline phosphatase (ALP) levels should exclude common bile duct stone. The addition of fever with chills after an attack of colic, as a rule, means the development of complications - acute cholecystitis, acute pancreatitis, cholangitis.

Acute cholecystitis usually develops due to obstruction of the cervix/cystic duct by a stone. In case of symptomatic cholelithiasis, acute cholecystitis is observed with a frequency of up to 10%.

Inflammation is triggered by three factors:

1) mechanical effects of increased intraluminal pressure and stretching, which leads to wall ischemia;

2) the chemical effect of lysolecithin, released from bile lecithin under the action of phospholipase, as well as other tissue factors;

3) bacterial infection, the signs of which are clearly detected in 50-85% of patients (in acute cholecystitis, E. coli, Klebsiella spp., Streptococcus spp., Clostridium spp. are most often sown from bladder bile).

Acute cholecystitis usually begins as an attack of biliary pain, which becomes increasingly widespread and affects the right hypochondrium. As with biliary colic, pain may radiate to the interscapular region, right scapula, or shoulder (Figure 6). In 60-70% there are indications of the presence of similar symptoms in the past, which resolved spontaneously. Signs of peritoneal irritation gradually appear:

More distinct localization and increasing nature of pain,

It intensifies with shaking and deep breathing,

Symptoms of ileus (anorexia, repeated vomiting, bloating, decreased peristaltic sounds),

Characteristic symptoms determined by palpation (Table 3).

Low grade fever (38-39° C) is more typical, but high fever with chills is possible. In a later period - with inflammation of the bile ducts and lymph nodes - jaundice may occur. In the absence of such a complication as perforation of the gallbladder, signs of diffuse peritonitis are usually not observed.

A general blood test reveals leukocytosis (usually within 10-15x1012/l with a shift to the left), a biochemical analysis can reveal moderate hyperbilirubinemia (total bilirubin is usually<85,5 мкмоль\л, прямой < 5 мг\дл) и умеренное повышение трансаминаз.

Based on clinical data alone, it is difficult to accurately exclude the development of acute cholecystitis; Additional research methods are important (see below).

Table 3. Abdominal palpation data in acute cholecystitis.

Techniques	Data
Palpation in the right upper quadrant of the abdomen	Soreness - in almost all patients (in old age, with diabetes mellitus, at the stage of gangrene, soreness may not be detected)
Palpation of the gallbladder	Detection of an enlarged, tense gallbladder in 25-50% of patients
Pressing with a finger followed by a sharp release of the abdominal wall Percussion in the projection of the gallbladder	Severe pain (the patient screams) - Shchetkin-Blumberg symptom
Inserting fingers under the costal arch at the height of inspiration or when coughing	Severe pain (the patient groans, reflex laryngospasm is possible) - Murphy's symptom

Delayed diagnosis of acute cholecystitis is fraught with the risk of death dangerous complications- empyema, gangrene, perforation of the gallbladder, development of biliary peritonitis. Empyema and developing gangrene are characterized by increased pain in the right hypochondrium and increased body temperature against the background of acute cholecystitis, an increase in leukocytosis >15 x 10 9 /l with a shift in the leukocyte formula to the left, despite adequate antibacterial therapy. As the degree of gangrenous changes increases, the pain may subside. A detailed discussion of complications is beyond the scope of this review.

Diagnostics

A preliminary diagnosis of cholelithiasis is based on questioning, medical history, examination, and identification of typical risk factors for this disease (see Table 1).

To confirm the diagnosis, it is necessary to resort to radiation diagnostic methods to visualize stones and determine the form of the disease (Table 6).

Ultrasound of the liver and biliary tract (ultrasound)- method of choice in the diagnosis of gallstones due to high sensitivity in detecting gallstones, safety and wide availability. Ultrasound does not have sufficient sensitivity in diagnosing choledocholithiasis, which is largely due to the depth of the terminal portion of the common bile duct. An indirect sign of choledocholithiasis - dilation of the common bile duct - is not always observed.

If cholelithiasis is suspected, it is necessary to resort to ultrasound (class C of clinical recommendations).

Ultrasound signs of acute cholecystitis, see below in this section for more details.

Ultrasound can determine the so-called “ non-functioning" residential complex-containing a minimal amount of bile (wrinkled) or, on the contrary, stretched and not contracting in response to a choleretic breakfast.

Allows you to detect gallstones with sufficient calcium content (this method detects 10-15% of cholesterol stones and about 50% of pigment stones). Radiography is also used in recognizing emphysematous cholecystitis, porcelain gallstones, calcareous bile, and gallbladder paresis.

Cholecystography with oral contrast is currently used very rarely, usually to assess the patency of the cystic duct and contractility of the gallbladder.

Cholangiography with intravenous contrast is also practically not used due to insufficiently clear contrasting of the bile ducts.

Percutaneous transhepatic cholangiography (PTCH) is an alternative method of contrasting the biliary tree in cases where other methods (MR-CPG, ERCP) are not applicable. Puncture of the biliary tree is usually performed in the 10th or 11th intercostal space (there is a risk of damage to the pleura). The transvesical approach carries a higher risk of bile leakage. The overall rate of severe complications of the procedure is 2-4%.

Endoscopic retrograde cholangiography (ERCG)- an invasive method, during which the major papilla is cannulated with contrasting of the common bile duct. If a stone/s are detected in the common bile duct, endoscopic papillosphincterotomy and lithoextraction can be performed simultaneously. Due to its technical complexity and traumatic nature, ERCG today is not used only for diagnostic purposes (if choledocholithiasis is suspected). ERCG during planned endoscopic papillosphincterotomy in order to provide access to the papillotome and visualize the process.

X-ray examinations with contrast can determine the so-called “disabled” - not amenable to contrast - ZhP. The reasons for this may be:

Total filling of the gastrointestinal tract with stones,

Cystic duct obstruction due to stone blockage or stenosis,

Sclerosis, wrinkling, calcification of the gallbladder.

Magnetic resonance cholangiopancreatography (MR-CPG) has a high diagnostic value in recognizing choledocholithiasis (about 90-95%), but stones of<3 мм могут не обнаруживаться. Это исследование нельзя проводить пациентам с кардиостимуляторами/дефибрилляторами, несовместимыми с проведением МРТ, что служит существенным препятствием, особенно в когорте пожилых больных.

Endoscopic ultrasound (endoUS)) pancreato-biliary zone has even a slightly higher diagnostic value in recognizing choledocholithiasis (about 98%) than MR-CPG, since it allows you to identify very small stones, sludge, strictures of the terminal part of the common bile duct. The limitations of this method are its invasiveness and the ability to evaluate the ductal system only in the area where it enters the duodenum.

Computed tomography does not allow us to judge with sufficient reliability the presence of stones in the bile ducts, because detects stones that contain sufficient amounts of calcium and absorb X-rays (no more than 50%).

Bilioscintigraphy - a radioisotope study with 99m Tc labeled iminodiacetic acids (HIDA, DIDA, DISIDA, etc.) is based on the rapid uptake of a radiopharmaceutical administered in high concentration from the blood and its excretion into the bile. Lack of sufficient visualization of the gallbladder with normal visualization of the distal biliary tract may indicate cystic duct obstruction, acute or chronic cholecystitis, or previous cholecystectomy.

Table 6. Instrumental methods for diagnosing cholelithiasis.

Diagnostic advantages of the method	Factors limiting information content	Comments
Ultrasound of the gallbladder
Easy to do and affordable	Gas formation Severe obesity Ascites	Method of choice in stone detection
Accuracy of gallstone detection (>95%)
Simultaneous scanning of the gallbladder, liver, bile ducts, pancreas
A “real-time” study that allows assessing the volume and contractility of the gallbladder
Can be used for jaundice, pregnancy
Allows you to detect even very small stones in the gallbladder
Plain radiography of the abdominal cavity
Low cost Availability	Insufficient sensitivity. Contraindications during pregnancy	Pathognomonic signs - with calcified stones, emphysematous cholecystitis, “porcelain” gallbladder, calcareous bile, gallbladder paresis
Radioisotope scanning (HIDA, DIDA, etc.)
Accurate identification of cystic duct obstruction Simultaneous assessment of bile ducts	Contraindications for pregnancy. Serum bilirubin >6-12 mg/dl. Cholecystogram has low resolution	Indicated to confirm the diagnosis if acute cholecystitis is suspected; less sensitive and specific for chronic cholecystitis. Allows you to identify signs of dyskinesia (“acalculous cholecystopathy”), especially when administering CCK to assess gastric emptying
Magnetic resonance cholangiopancreatography (MR-CPG) Endoscopic ultrasound
High sensitivity in detecting common bile duct stones	Accuracy of MR-CPG in detecting stones<3 мм недостаточная.	Methods of choice in the presence of dilated common bile duct according to ultrasound and/or elevated liver tests (suspicion of choledocholithiasis)

*Gall bladder

Instrumental methods in the diagnosis of acute calculous cholecystitis

The presence of acute cholecystitis cannot be convincingly excluded without resorting to additional methods, in particular ultrasound and cholecystoscintigraphy (their sensitivity is 88% and 97%, respectively).

Signs of acute cholecystitis according to additional methods:

Ultrasound: severe pain when compressed by a sensor directly in the projection of the gallbladder (“ultrasound Murphy’s sign”), the presence of fluid around the gallbladder, thickening of its wall (≥4 mm). The most specific and reliable of these signs

- “ultrasound Murphy’s sign”, since wall thickening and the presence of fluid may be due to other reasons (for example, ascites);

Cholecystoscintigraphy: lack of visualization of the gallbladder (due to occlusion of the cystic duct).

Differential diagnosis

Differential diagnosis of pain in the right upper quadrant of the abdomen, which is typical for cholelithiasis, sometimes presents significant difficulties. Table 4 presents the main nosological forms between which a distinction should be made. This is especially true in relation to coronary heart disease.

Table 4. Differential diagnosis of pain in the right upper quadrant of the abdomen.

Disease	Characteristics of pain	Additional Research
Biliary pain	Constant in nature, rapidly increasing in intensity until a “plateau” is reached, lasts 4-6 hours, can radiate to the suprascapular region on the right	Ultrasound of the abdominal organs
Acute cholecystitis	Longer lasting (> 6 hours) biliary pain with local tenderness, muscle tightness, fever and/or leukocytosis	Ultrasound of the abdominal organs and/or bilioscintigraphy with iminodiacetic acid
Dyspepsia	Bloating, nausea, belching, poor tolerance to fatty foods
Duodenal ulcer	Pain 2 hours after eating, relieved by food or antacids	Endoscopic examination of the upper gastrointestinal tract
Liver abscess	Pain associated with fever and chills; palpable liver, pain and muscle tension in the right hypochondrium	Chest X-ray cells (pleural effusion on the right). Computed tomography of the abdomen
Myocardial infarction	Pain/discomfort in the right upper quadrant or epigastric region; may resemble biliary pain	Electrocardiography, activity of cardiac-specific enzymes in the blood. AST<150 Ед/л, АЛТ может быть в норме.

An attack of biliary colic must be differentiated from manifestations of lower myocardial infarction, the beginning of an attack of pancreatitis, as well as intestinal colic. Therefore, a full physical examination of the patient with an assessment of the condition of all systems is important.

To exclude myocardial infarction, especially in persons with risk factors for coronary artery disease, it is advisable to register an ECG.

An attack of pancreatitis is characterized by intense girdling pain and repeated vomiting.

With intestinal colic, defecation and the passage of gas usually lead to pain relief.

Complaints of vaguely expressed bursting pain (discomfort) in the epigastric region, dyspeptic symptoms, regurgitation, bloating after eating fatty foods should not be confused with biliary colic; These symptoms are common in cholelithiasis, but are not specific to it. Such symptoms are often referred to as “poor tolerance to fatty or rich foods” and are associated with an impaired response to enterohormones - cholecystokinin and YY-peptide.

In the presence of typical biliary pain, it is necessary to immediately conduct an ultrasound examination of the abdominal organs. Ultrasound has 99% specificity for detecting gallstones; it is a safe and fairly cheap research method. However, in a small proportion of patients, despite the presence of typical biliary pain, stones cannot be detected. If there is a reasonable suspicion of the presence of biliary pain, biliary dyskinesia can be suspected. Dyskinesia is characterized by a low contraction fraction of the gallbladder (<50%) по данным холецистосцинграфии с холецистокинином.

Table 5 shows some signs that make it easier to differentiate acute calculous cholecystitis from other diseases.

Table 5. Signs that allow you to differentiate acute calculous cholecystitis from other diseases.

	Difference from symptoms of acute cholecystitis	Additional methods data
Intestinal obstruction	Cramping nature of pain Localization uncharacteristic for cholecystitis Increased peristalsis “Splashing noise”, positive sign of Valya	Plain fluoroscopy of the abdomen: distension of intestinal loops and fluid levels
Perforation of peptic ulcer	Ulcerative history Acute onset with “dagger” pain No vomiting	Plain fluoroscopy of the abdominal cavity: free gas in the abdominal cavity
Acute pancreatitis	More severe general condition Girdle nature of the pain Sharp pain in the epigastric region and less pronounced pain in the right hypochondrium	Increased activity of pancreatic amylase in blood and urine
Appendicitis	General condition is usually less heavy The pain is less intense No irradiation to the right shoulder girdle, shoulder and scapula Single vomiting	Ultrasound of the abdominal organs: signs of appendicitis
Pyelonephritis, paranephritis	Dysuria Pasternatsky's symptom Urological history	Urinalysis, excretory urography, chromocystoscopy, etc.: signs of urinary tract damage

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Treatment

Principles of treatment

In asymptomatic cases, it is most advisable to adhere to the tactics of monitoring the patient without active treatment (class C of clinical recommendations). In the absence of symptoms, the risk of developing symptoms or complications requiring surgical treatment is quite low (1-2% per year).

Lifestyle, nutrition

Maintaining normal body weight and a balanced diet helps prevent the development of acute cholecystitis. The calorie content of the diet should be moderate, food intake should be fractional (5-6 times a day with breaks of no more than 4-5 hours, except at night). It is advisable to adhere to a diet enriched with dietary fiber (fresh fruits and vegetables), grains (grain bread, oats, brown rice, cut products), beans and lentils are healthy, and among meat products, preference should be given to those containing less fat - chicken, turkey ( without skin), fish (not too oily). It is better to choose fermented milk products with a reduced fat content, and reduce the consumption of dairy products to a minimum. Fried foods, smoked foods, baked goods and foods rich in simple carbohydrates should be avoided (the latter increase the risk of stone formation). Regular physical activity helps prevent weight gain.

Surgical treatment

The main method of surgical treatment of cholelithiasis that occurs with clinical symptoms remains cholecystectomy. Cholecystectomy not only prevents complications of acute cholecystitis, but also the development of gallbladder cancer in the long term.

Numerous studies have shown that cholecystectomy carries a low risk of adverse outcomes, and the risk of recurrence of symptoms with this method of treatment is the lowest. The laparoscopic technique has clear advantages over open surgery in many respects: less noticeable cosmetic defect, lower cost, earlier return to function, lower mortality, less tissue damage and pain in the postoperative period and shorter hospital stay. .

In recent years, the technique of single-port laparoscopic cholecystectomy has been developed - through one trocar access in the paraumbilical area, which gives minimal cosmetic effect. Surgery through a single-port access is most optimal in cases of uncomplicated chronic calculous cholecystitis.

Indications for cholecystectomy are presented in Table 7.

If necessary cholecystectomy during pregnancy(in cases of acute cholecystitis, pancreatitis, or the inability to eat food in adequate quantities due to the onset of symptoms), the risk of surgical intervention for the mother and fetus is lowest in the second trimester.

Table 7. Indications for cholecystectomy and optimal timing for surgery (in the absence of contraindications).

States	Timing of surgery
Recurrent attacks of biliary colic	As planned (class B clinical recommendations)
Biliary dyskinesia (?)*	As planned
Calcified (“porcelain”) GB	As planned
Acute cholecystitis (complicated forms or lack of improvement with conservative treatment)	Urgent (within the next 48-72 hours) (class A clinical recommendations)
Previous acute cholecystitis	As planned, optimally - in the next 4-6, maximum - 12 weeks (class C of clinical recommendations)
Choledocholithiasis	After removing the stone from the common bile duct (simultaneous cholecystectomy and extraction are also practiced) common bile duct stone)
Attack of biliary pancreatitis (high probability of recurrence of acute pancreatitis)	In real hospitalization, but after the symptoms of pancreatitis have subsided (class A of clinical recommendations)

*Note. In Russia, the practice of performing cholecystectomy for biliary dyskinesia (“acalculous cholecystopathy”) has not yet developed; the operation is performed only in isolated cases.

In recent years, as surgical techniques have improved, previously accepted contraindications to laparoscopic cholecystectomy have disappeared. In particular, laparoscopic surgery is not contraindicated in acute cholecystitis, in old age, in chronic obstructive pulmonary disease (excluding severe cases), in Child-Pugh class A and B liver cirrhosis (but not in severe decompensation), in obesity, in pregnancy. , if there is a history of indications for abdominal interventions.

The need to switch to open access surgery during laparoscopic intervention occurs in 5-25% of cases, and the most common reason for this is the difficulty of establishing the anatomical relationships of various structures.

According to a meta-analysis, mortality with laparoscopic intervention is 8.6-16 per 10,000, with open access - 66-74 per 10,000 patients. At the same time, the incidence of damage to the common bile duct during laparoscopy is higher - 36-47 cases per 10,000 and 19-29 cases per 10,000 patients, respectively.

Percutaneous cholecystolithotomy It is performed under general anesthesia and under the control of fluoroscopy and ultrasound. After puncture of the abdominal wall, a small incision is made in the gallbladder, through which stones are removed or destroyed using contact electrohydraulic or laser lithotripsy. Subsequent inflation of the catheter inside the bladder prevents bile leakage. The recurrence rate of stone formation is high. Advantages over cholecystectomy have not been shown. Intervention is carried out only in selected cases.

Cholecystostomy (including minicholecystostomy) It is performed extremely rarely, only in special circumstances - in patients with a very high operational risk, for whom the operation is performed for health reasons, so it should be the least traumatic. The intervention is performed under local anesthesia. After applying a purse-string suture, the contents are aspirated and stones are removed. Significant disadvantages of the intervention are the inability to detect and remove impacted stones, the likelihood of missing incipient complications - areas of incipient gangrene, stones of the common bile duct, cholangitis.

The concept of postcholecystectomy syndrome

In 10-15% of patients who undergo cholecystectomy, various digestive symptoms persist or reappear (Figure 7). To refer to such conditions, the collective term “post-cholecystectomy syndrome” is sometimes used. From a practical point of view, one should strive to avoid such a generalized formulation, since in 95% of cases a specific cause of symptoms can be identified, and, accordingly, the correct treatment tactics can be chosen.

Figure 7. The frequency of manifestations of “postcholecystectomy” disorders [data from the article by Jensen SW. Postcholecystectomy Syndrome. Internet page

http://emedicine.medscape.com/article/192761].

There are early and delayed forms of postcholecystectomy syndrome. The first include residual stones of the cystic duct or common bile duct, cholangitis, consequences of intraoperative damage to the bile ducts, and leakage of bile. The second includes relapse of stone formation in the ducts, strictures, inflammation of the cystic duct/gastric stump, stenosis of the papilla of Vater, dyskinesia of the sphincter of Oddi, formation of neuroma, as well as manifestations of diseases of neighboring organs (for example, gastroesophageal reflux, chronic pancreatitis, irritable bowel syndrome, diverticular diseases, intestinal ischemia), which are mistakenly attributed to the consequences of surgery.

The development of diarrhea after cholecystectomy may be due to both innervation disturbances due to surgical trauma and changes in the synchronization of the supply of bile acids with meals (“chologenic diarrhea”). In most patients, after cholecystectomy, the normal rhythm of bile secretion is restored. On an empty stomach, bile acids are retained in the proximal part of the small intestine, and after eating, due to peristaltic contractions, they move to the distal parts, where they are reabsorbed.

In the examination plan for patients with “postcholecystectomy syndrome,” it is advisable to include, in addition to routine studies, the modern methods of radiodiagnosis described above, which are characterized by high image detail. In case of chronic diarrhea, the examination is carried out according to the traditional plan for this syndrome.

Minimally invasive interventions

Contact chemical litholysis method- using percutaneous injection of methyl tert-butyl ether into the gallbladder, causing the dissolution of stones - used in selected university clinics in Germany, Italy and the USA with the permission of local ethical committees. Methyl tert-butyl ether is not registered as a medicinal product at the state level either abroad or in Russia. Its introduction, depending on the access to the stone, carries a fairly high risk of complications. The recurrence rate of stone formation is also quite high. To date, contact litholysis is not practiced in Russian clinics.

Percutaneous shock wave lithotripsy- a non-invasive method in which local application of high-energy waves (electro-hydraulic, electro-magnetic or piezoelectric) leads to crushing of stones. Lithotripsy can be used if there are ≤ 3 stones with a total diameter in the gallbladder<30 мм «всплывающего» типа и при условии сохранения функции ЖП (сокращение ЖП на 50% по данным сцинтиграфии).

Due to the limited conditions under which this method is effective, a fairly high frequency of complications (colic, acute cholecystitis, pancreatitis, choledocholithiasis with the development of obstructive jaundice, micro- and macrohematuria, liver hematomas, gallbladder) is used very limitedly. Without additional treatment with ursodeoxycholic acid, the recurrence rate of stone formation in the next 1-2 years reaches 50%.

Conservative treatment of cholelithiasis

For cholelithiasis, oral stone dissolving agents can be used - ursodeoxycholic acid (UDCA) preparations. However, they are effective only in a limited part of patients (about 10% of all patients with cholelithiasis).

UDCA reduces bile cholesterol saturation and also appears to create a lamellar liquid crystalline phase that extracts cholesterol from stones. The dose of UDCA for the treatment of cholelithiasis is 10-15 mg/kg body weight per day.

The clinical effectiveness of therapy with bile acid preparations is shown in the presence of clinically manifest (infrequent attacks of biliary pain) X-ray negative gallstones less than 15 mm in size, provided that the gallbladder function is preserved (filled with stones no more than 1/3). The highest dissolution rate (>70%) is achieved in patients with small (<5 мм) флотирующими рентгенонегативными камнями. В этих случаях при назначении УДХК в течение 3 месяцев удается достичь уменьшения выраженности билиарной боли более чем у половины пациентов. При приеме УДХК в дозе 10 мг/кг массы тела в день в течение 1 года растворение камней происходит примерно у 60% пациентов. Рецидивы в ближайшие 5 лет наблюдаются в ≈25% случаев. Поэтому наиболее целесообразно ограничивать назначение УДХК случаями, когда у пациента имеются противопоказания к оперативному лечению или он не дает согласия на проведение холецистэктомии (класс С клинических рекомендаций).

UDCA treatment is carried out under ultrasound control every 3-6 months. The absence of signs of a decrease in the number and size of stones after 6 months of treatment indicates the ineffectiveness of therapy.

Pigment stones are not amenable to dissolution by UDCA.

Chenodeoxycholic acid preparations are not currently used in Russia.

For relief of biliary colic You can use antispasmodics of various classes, which are advisable to administer parenterally to obtain a quick effect.

It has a powerful antispasmodic effect even when taken orally hyoscine butyl bromide- antispasmodic with selective N-, M3-cholinolytic action. Numerous studies have examined the effect of this drug in the treatment of biliary pain, as well as abdominal pain of other origins (the effectiveness was confirmed in a meta-analysis). The antispasmodic effect of hyoscine on the sphincter of Oddi has been proven. The effect of hyoscine after oral administration occurs already in the 15th minute, which is important for the rapid relief of painful biliary pain. Dosage regimen: “on demand” 10-20 mg orally or in suppositories, or course treatment 10-20 mg 3 times a day before meals for 10-30 days. Class B of clinical recommendations for the relief of biliary pain.

To relieve dyspeptic symptoms, often accompanying cholelithiasis (“poor tolerance to fatty and rich foods”), antispasmodics, antifoaming agents, as well as hymecromone, which has a cholecystokinin-like effect (class B of clinical recommendations for the relief of biliary pain), are used.

Alverine+simethicone thanks to the combined composition, it helps not only to relieve spasm and pain (alverine, a selective antispasmodic), but due to the presence of an optimal dose of an antifoam in the composition, it helps to quickly relieve flatulence, which is characteristic of patients with diseases of the biliary tract. Dosage regimen: “on demand” 1 table. (60 mg+300 mg) orally for discomfort and bloating, or a course of treatment of 1 table. 2-3 times a day before meals for 14-30 days or longer (class B of clinical recommendations for the relief of flatulence).

Hymecromone- a highly selective antispasmodic of the sphincter of Oddi, a synthetic analogue of umbelliferone contained in the fruits of anise and fennel, which have been used since ancient times as antispasmodics. Hymecromone has a cholecystokinin-like relaxing effect on the sphincter of Oddi. In blind studies, gimecromone showed significant effectiveness in relieving biliary pain. The drug is not contraindicated for cholelithiasis or cholecystolithiasis. The action of hymecromone is realized only at the level of the bile ducts; absorption into the systemic circulation does not exceed 3%, which largely explains the high selectivity of action on the sphincter of Oddi.

By relaxing the sphincter of Oddi and improving the flow of bile into the duodenum, hymecromone can help reduce the lithogenicity of bile. It may be added to UDCA therapy to dissolve gallstones.

Dosing regimen of hymecromone: on-demand intake of 200-400 mg orally for discomfort, or course treatment of 200-400 mg 3 times a day half an hour before meals for 14-30 days or longer. Class B clinical guidelines.

Application prokinetics(domperidone, itopride, trimebutine), affecting the upper gastrointestinal tract, in cholelithiasis is justified by the fact that such patients often experience dyspeptic symptoms, and the motility of the biliary tract is closely related to the motility of the stomach and duodenum.

Trimebutine as an agonist of peripheral μ-, κ- and δ-opiate receptors, it has a prokinetic and at the same time a distinct antispasmodic effect, which gives it the properties of a universal modulator of motility in all parts of the digestive tract. Studies show that trimebutine quickly (within an hour) relieves abdominal pain and dyspeptic disorders in gastrointestinal diseases (class C of clinical recommendations). Trimebutine dosage regimen: course treatment of 100-200 mg 3 times a day, regardless of meals, for 30 days. or longer. The drug is well tolerated.

The risk of developing gallstone cancer against the background of cholelithiasis is increased compared to the population without gallstones. The highest risk (about 20%) is observed with “porcelain” gallbladder, therefore, if this condition is detected, prophylactic cholecystectomy is indicated.

Figure 8. Natural course of cholelithiasis (addition of symptoms and development of complications over time).

Information

Sources and literature

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