Sphincter of Oddi dysfunction(English) sphincter of Oddi dysfunction) - a disease (clinical condition) characterized by partial obstruction of the ducts of bile and pancreatic juice in the sphincter of Oddi. Dysfunctions of the sphincter of Oddi, according to modern concepts, include only benign clinical conditions of non-calculous etiology. It can have both a structural (organic) and functional nature, associated with a violation of the motor activity of the sphincter.

According to the Rome Consensus on Functional Disorders of the Digestive Organs (Rome II Criteria), the term “sphincter of Oddi dysfunction” is recommended to be used instead of the terms “postcholecystectomy syndrome”, “biliary dyskinesia” and others.

Spasm of the sphincter of Oddi

Spasm of the sphincter of Oddi(English) spasm of sphincter of Oddi) - disease of the sphincter of Oddi, classified by ICD-10 with code K83.4. According to the 1999 Rome consensus, it is classified as a dysfunction of the sphincter of Oddi.

Postcholecystectomy syndrome

Postcholecystectomy syndrome(English) postcholecystectomy syndrome) - dysfunction of the sphincter of Oddi, caused by a violation of its contractile function, preventing the normal outflow of bile and pancreatic secretions into the duodenum in the absence of organic obstacles, resulting from cholecystectomy. Occurs in approximately 40% of patients who underwent cholecystectomy due to gallstones. It is expressed in the manifestation of the same clinical symptoms that were before the cholecystectomy operation (phantom pain, etc.). Classified by ICD-10 with code K91.5. The 1999 Rome consensus does not recommend the term “postcholecystectomy syndrome.”

Clinical picture

The main symptoms of sphincter of Oddi dysfunction are attacks of severe or moderate pain lasting more than 20 minutes, repeated for more than 3 months, dyspepsia and neurotic disorders. A feeling of heaviness in the abdominal cavity, dull, prolonged pain in the right hypochondrium without clear irradiation are often observed. Mostly the pain is constant, not colicky. In many patients, attacks occur quite rarely at first, lasting several hours, and in the intervals between attacks the pain disappears completely. Sometimes the frequency and severity of pain attacks increases over time. During the period between attacks, pain persists. The relationship between painful attacks and food intake is expressed differently in different patients. Most often (but not necessarily), pain begins within 2-3 hours after eating.

Sphincter of Oddi dysfunction can occur at any age. However, it most often occurs in middle-aged women. Dysfunction of the sphincter of Oddi very often occurs in patients who have undergone cholecystectomy (removal of the gallbladder). In 40–45% of patients, the cause of complaints is structural disorders (strictures of the biliary tract, undiagnosed stones of the common bile duct, etc.), in 55–60% - functional ones.

Classification

According to the 1999 Rome Consensus, there are 3 types of biliary dysfunction of the sphincter of Oddi and 1 type of pancreatic dysfunction.

1. Biliary type I, includes:

• the presence of typical attacks of biliary pain (repeated attacks of moderate or severe pain in the epigastric region and/or in the right hypochondrium lasting 20 minutes or more;
• expansion of the common bile duct by more than 12 mm;
• with endoscopic retrograde cholangiopancreatography (ERCP), slow release of the contrast agent with a delay of more than 45 minutes;
• 2 or more times the normal level of transaminases and/or alkaline phosphatase, with at least two liver enzyme tests.

2. Biliary type II, includes:

• typical attacks of biliary pain;
• meeting one or two other Type I criteria.

50–63% of patients in this group have manometric confirmation of sphincter of Oddi dysfunction on manometric examination. In patients with biliary type II, disorders can be both structural and functional.

3. Biliary type III characterized only by attacks of biliary pain without any objective disorders characteristic of type I. When manometry of the sphincter of Oddi of patients in this group, dysfunction of the sphincter of Oddi is confirmed in only 12–28% of patients. In biliary group III, sphincter of Oddi dysfunction is usually functional in nature.

4. Pancreatic type manifested by epigastric pain characteristic of pancreatitis, radiating to the back and decreasing when the torso is tilted forward, and is accompanied by a significant increase in serum amylase and lipase. In the group of patients with these symptoms and the absence of traditional causes of pancreatitis (cholelithiasis, alcohol abuse, etc.), manometry reveals sphincter of Oddi dysfunction in 39–90% of cases.

Diagnostic tests

Instrumental diagnostic methods

Non-invasive

• Ultrasound examination to determine the diameter of the common bile and/or pancreatic ducts before and after the introduction of stimulants.
• Hepatobiliary scintigraphy.

Invasive

• Endoscopic retrograde cholangiopancreatography.
• Sphincter of Oddi manometry (“gold standard” for diagnosing sphincter of Oddi dysfunction).

Treatment

Treatment uses drug therapy aimed at eliminating pain and symptoms of dyspepsia, preventing complications and concomitant damage to other organs.

Papillosphincterotomy

Papillosphincterotomy(sometimes called sphincterotomy) - a surgical intervention aimed at normalizing bile outflow and/or the functioning of the sphincter of Oddi and consisting in dissection of the major duodenal papilla. It is also used to remove stones from the bile ducts.

Currently, it is performed endoscopically and, in this case, is called endoscopic papillosphincterotomy. Usually performed simultaneously with endoscopic retrograde cholangiopancreatography.

See also

Sources

• Vasiliev Yu. V. Dysfunction of the sphincter of Oddi as one of the factors in the development of chronic pancreatitis: treatment of patients. Journal "Difficult Patient", No. 5, 2007.
• Kalinin A.V. Dysfunctions of the sphincter of Oddi and their treatment. RMJ, August 30, 2004.

Notes

Wikimedia Foundation. 2010.

Definition

PHES is a symbol for various disorders, recurrent pain and dyspeptic symptoms that occur in patients after cholecystectomy.

Spasm of the sphincter of Oddi, dyskinesia of the extrahepatic bile ducts, stomach and duodenum, microbial contamination, gastro-duodenitis, long cystic duct after cholecystectomy may be the cause of some of the symptoms included in PCES, which should be deciphered based on the examination results.

Survey

One time

General blood test

General urine test

ASAT, AlAT

ALP, GGTP

Study of portions A and C of duodenal contents, including bacteriological

Coprogram, feces for dysbacteriosis and helminths

One time

Esophagogastroduodenoscopy with mucosal biopsy

Duodenal intubation to obtain portions A and C

Ultrasound of the abdominal organ (complex)

Sigmoidoscope

: surgeon, coloproctologist.

Diet therapy is differentiated depending on the timing of the postoperative period, clinical manifestations of PCES, body weight, lithogenicity of bile - for life.

Drug treatment

Cisapride or dompsridone 10 mg 3-4 times a day, or debridate 100-200 mg 3-4 times a day for 2 weeks. +

Erythromycin 0.25 g 4 times a day for 7 days +

Maalox or Remagel, or gastrin-gel, or phosphalugel, 15 ml 4 times a day 1.5-2 hours after meals for 4 weeks.

If indicated, antibacterial therapy can be continued and intensified; it is possible to use multienzyme drugs (Creon, pancitrate, festal, digestal, etc.)

10 days.

Patients are subject to medical examination depending on the diagnosed disease, but not according to PCES.

Disappearance of pain and dyspeptic syndromes, absence of changes in laboratory parameters (remission), reduction of clinical manifestations of the disease, restoration of ability to work.

X. International Classification of Diseases (ICD-10)

1. Chronic pancreatitis of alcoholic etiology Code K 86.0

2. Other chronic pancreatitis (chronic pancreatitis of unspecified etiology, infectious, recurrent) Code K 86.1

Definition

Chronic pancreatitis (CP) is a progressive disease of the pancreas, characterized by the appearance of signs of an acute inflammatory process during an exacerbation, the gradual replacement of the organ parenchyma with connective tissue and the development of insufficiency of the exo- and endocrine functions of the gland.

Chronic pancreatitis in the clinic is divided into obstructive, calcific, parenchymal. Its pathomorphological basis is the combination of destruction of the acinar apparatus with a progressive inflammatory process leading to atrophy, fibrosis (cirrhosis) and disorders in the pancreatic ductal system, mainly due to the development of micro- and macrolithiasis.

Survey

Mandatory laboratory tests

One time

General blood test

General urine test

Total bilirubin and fractions

ASAT, AlAT

ALP, GGTP

Blood amylase

Blood lipase

Coprogram

Blood sugar

Blood calcium

Total protein and fractions

Mandatory instrumental studies

One time

Plain X-ray of the abdominal cavity

Ultrasound of the abdominal organs (comprehensive)

Twice

Ultrasound of the pancreas

Additional studies according to indications

Twice

Laparoscopy with targeted biopsy of the pancreas

CT pancreas

Coagulogram

Blood sugar after taking glucose (sugar curve)

Consultations with specialists are mandatory: surgeon, endocrinologist.

Characteristics of therapeutic measures

The first three days severe exacerbation- hunger and, if indicated, parenteral nutrition.

With duodenostasis- continuous aspiration of acidic gastric contents using a thin tube, intravenously every 8 hours with ranitidine (150 mg) or famotidine (20 mg);

orally - buffer antacids in the form of a gel (Maalox, Remagel, phosphalugel, gasterin gel) every 2-3 hours; intravenously – polyglucin 400 ml per day, hemodez 300 ml per day, 10% albumin solution 100 ml per day, 5-10% glucose solution 500 ml per day.

For intractable pain syndrome- parenterally 2 ml of 50% analgin solution with 2 ml of 2% papaverine solution or 5 ml of baralgin or a synthetic analogue of somatostatin - sandostatin (50-100 mcg 2 times a day subcutaneously, or intravenous drops of lidocaine (in 100 ml of isotonic sodium chloride solution 400 mg of the drug).

After relief of severe pain, usually from the 4th day from the start of treatment:

Small meals with limited animal fat;

Before each meal, multienzyme preparation Creon (1-2 capsules) or pancitrate (1-2 capsules);

Gradual withdrawal of analgesics, infusion therapy and parenteral administration of drugs, some of them are prescribed orally:

ranitidine 150 mg or famotidine 20 mg 2 times a day,

Domperidone or cisapride 10 mg 4 times a day over 15 minutes. before meals, or

debridate 100-200 mg 3 times a day for 15 minutes. before meals.

Duration of inpatient treatment- 28-30 days (in the absence of complications).

Requirements for treatment results

The onset of complete clinical remission or remission with a defect (presence of pseudocysts, incompletely eliminated pancreatic steatorrhea with uncompensated duodenostasis) is possible.

Patients with chronic pancreatitis are subject to dispensary observation (re-examination and examination in an outpatient setting twice a year).

XI. International Classification of Diseases (ICD-10)

1. Alcoholic fatty liver (fatty liver) Code K 70.0

2. Alcoholic hepatitis (acute, chronic) Code K 70.1

3. Alcoholic fibrosis and liver sclerosis (the outcome of previous fatty degeneration and hepatitis) Code K 70.2

4. Alcoholic cirrhosis of the liver Code K 70.3

Despite the diversity of diagnoses, they are all united by common etiological and pathogenetic connections with alcohol intoxication. The formation of diseases is determined by the duration of the medical history and the toxicity of the alcoholic drink. Essentially, there are 3 types of alcoholic liver damage:

a) fatty liver;

b) acute and chronic hepatitis (fatty degeneration with necrosis of hepatocytes and mesenchymal reaction);

c) cirrhosis of the liver.

Survey

Mandatory laboratory tests

One time

General blood test

General urine test

Reticulocytes

Total bilirubin and fractions

Blood cholesterol

ASAT, AlAT, GGTP

Uric acid in the blood

Creatinine

Blood sugar

Blood calcium

Blood amylase

Coprogram

Blood group

Rh factor

Mandatory instrumental studies

Ultrasound of the abdominal organs (comprehensive)

Esophagogastroduodenoscopy

Additional Research

One time

Percutaneous liver biopsy

Liver

Electrocardiography

Laparoscopy

Blood immunoglobulins

Serological markers of hepatitis A, B, C, D virus

Consultations with specialists are mandatory: narcologist, neurologist, infectious disease specialist.

Characteristics of therapeutic measures

1. Abstain from drinking alcohol.

2. 10-day course of intensive therapy:

a) intravenous administration of 300 ml of a 10% glucose solution with the addition of 10-20 ml of essentiale (1 ampoule contains 1000 mg of essential phospholipids), 4 ml of a 5% solution of pyridoxine or pyridoxal phosphate, 5-10 ml of hophnthol, 4 ml of a 5% solution of thiamine (or 100-200 mg of cocarboxylase), 5 ml of 20% solution of piracetam (nootropil).

The course of treatment is 5 days;

b) intravenous hemodez 1,200 ml (or hemodez-N, or gluconeodez). Three infusions per course;

c) vitamin B 12 (cyanocobalamin, oxycobalamin) 1000 mcg intramuscularly daily for 6 days;

d) creon or pancitrate orally (capsules) or other multienzyme drug with food;

e) folic acid 5 mg per day and ascorbic acid 500 mg per day orally.

2 month course(carried out after completion of intensive therapy) includes:

Essentiale (2 capsules 3 times a day after meals) or hofitol (1 tablet 3 times a day)

Creon or pancitrate (1 capsule 3 times a day with food) picamilon (2 tablets 3 times a day).

Against the background of such therapy, symptomatic treatment is carried out, including for possible complications (portal hypertension, ascites, bleeding, encephalopathy, etc.).

Duration of inpatient treatment

Alcoholic liver dystrophy - 5-10 days.

Alcoholic acute hepatitis - 21-28 days.

Alcoholic chronic hepatitis with minimal activity - 8-10 days.

Alcoholic chronic hepatitis with pronounced activity - 21-28 days.

Alcoholic cirrhosis of the liver, depending on the severity scale - from 28 to 56 days.

All patients, regardless of diagnosis, are subject to dispensary observation in an outpatient setting.

Requirements for treatment results

Ensure remission of the disease in conditions of abstinence from drinking alcohol.

Remission includes elimination of hepatitis activity with normalization of laboratory parameters.

XII. International Classification of Diseases (ICD-10)

1. Gallstone disease (cholelithiasis) Code K 80

2. Gallstones with acute cholecystitis Code K 80.0

3. Gallstones without cholecystitis (cholecystolithiasis) Code K 80.2

4. Bile duct stones (choledocholithiasis) with cholangitis (not primary sclerosing) Code K 80.3

5. Bile duct stones with cholecystitis (choledocho- and cholecystolithiasis) (any variants) Code K 80.4

Definition

Gallstone disease is a disease of the hepatobiliary system caused by impaired metabolism of cholesterol and (or) bilirubin and characterized by the formation of stones in the gall bladder and (or) bile ducts. There are cholesterol and pigment stones.

This section groups diseases etiologically and pathogenetically associated with cholelithiasis and its complications, incl. with infection of the biliary tract. Diagnosis and treatment depend on the completeness of the examination.

Survey

Mandatory laboratory tests

One time

Blood cholesterol

Blood amylase

Blood sugar

Coprogram

Blood group

Rh factor

Bacteriological examination of duodenal contents

Twice

General blood test

General urine test

Total bilirubin and its fractions

AsAT, AlAT, ShchF, GGTP

C-reactive protein

Mandatory instrumental studies

One time

X-ray of the abdominal cavity

X-ray examination of the chest

Ultrasound of the liver, gall bladder, pancreas and spleen

Endoscopic retrograde cholangiopancreatography (according to indications)

Electrocardiography

Additional Research are carried out depending on the expected diagnosis and complications.

Surgeon.

Characteristics of medicinal events.

Acute calculous cholecystitis.

Antibacterial therapy options (one is most often used):

Drug treatment:

1. Ciprofloxacin (individual regimen), usually 500 mg orally 2 times a day (in some cases, a single dose can be 750 mg, and the frequency of use can be 3-4 times a day).

The duration of treatment is from 10 days to 4 weeks. The tablets should be swallowed whole, on an empty stomach, with a small amount of water. According to indications, therapy can be started with intravenous administration of 200 mg 2 times a day (preferably drip).

2. Doxycycline, orally or intravenously (drip) is prescribed on the 1st day of treatment 200 mg/day, on subsequent days - 100-200 mg/day, depending on the severity of the clinical course of the disease. Frequency of administration (or intravenous infusion) is 1-2 times/day.

The duration of treatment is from 10 days to 4 weeks.

3. Cephalosporins, for example, fortum or kefzol, or claforan IM 2.0 g every 12 hours, or 1.0 g every 8 hours.

The course of treatment is on average 7 days.

4. Septrin orally 960 mg 2 times a day with an interval of 12 hours (or intravenously drip) at the rate of 20 mg/kg trimethoprim and 100 mg/kg sulfamethoxazole per day, frequency of administration - 2 times, duration of treatment - 2 weeks. The solution for intravenous infusion should be prepared ex tempore for 5-10 ml (1-2 ampoules) of septrin, using 125-250 ml of solvent (5-10% glucose solutions or 0.9% sodium chloride solution).

The duration of treatment with antibacterial agents also includes the postoperative period.

The choice of antibacterial drug is determined by many factors. It is important not to use drugs that have hepatotoxic effects. For a purulent process, the drug of choice is meronem (500 mg intravenously every 8 hours).

Symptomatic medications, as well as antibacterial agents, are prescribed in the preoperative period to fully prepare for surgery:

domperidone (Motilium) or cisapride (Coordinax) - 10 mg 3-4 times a day, or

debridate (trimebutine) - 100-200 mg 3-4 times a day, or meteospasmil 1 caps. 3 times a day.

Doses, regimens and drugs with symptomatic effect are determined by many factors, taking into account an individual approach to their prescription.

If it is impossible to take the drug orally, a drug with a symptomatic effect is prescribed parenterally. For example, papaverine hydrochloride or no-shpu 2 ml of a 2% solution IM 3-4 times a day. Sometimes, for severe pain, baralgin (5 ml) is used as an injection.

For all of the above diseases, there are indications for surgical treatment (cholecystectomy, papillosphincterotomy, etc.).

Duration of inpatient treatment

In the preoperative period - no more than 7 days, in the postoperative period - no more than 10 days, outpatient observation for a year.

Requirements for treatment results

Ensure relief of symptoms of the disease in the postoperative period - elimination of cholekinesis disorders and active inflammation in the biliary tract (remission). The absence of remission is considered in other sections (codes K 91.5 and 83.4).

Acute calculous cholecystitis with choledocholithiasis, obstructive jaundice and cholangitis

Drug treatment is carried out regardless of emergency treatment measures in connection with diagnosed choledocholithiasis.

1. Antibacterial agents

Cefotaxime (claforan, etc.) or ceftazidime (Fortum, etc.), or cefoperazone (cefobid, etc.), or cefpiramide (tamycin), or ceftriaxone (ceftriaxone Na, etc.) 1-2 g IM or IV / 3 times a day for 8-10 days with a transition to oral cefuroxime (Zinnat, etc.) 250 mg 2 times a day until complete remission occurs.

2. Detoxification agents

Hemodesis (250-400 ml intravenous drip daily for 5 days), new Alvezin (1000-2000 ml intravenous drip daily for 3 days) and other measures as indicated.

Duration of inpatient treatment

In the preoperative and postoperative periods within 3-4 weeks, outpatient observation in the absence of complications for a year.

Requirements for treatment results

Ensure remission of cholangitis. The absence of remission is considered in other sections (codes K 91.5 and K 83.4).

XIII. International Classification of Diseases (ICD-10)

1. Cholecystitis (without cholelithiasis) Code K 81.

2. Acute cholecystitis (emphysematous, gangrenous, purulent, abscess, empyema, gallbladder gangrene) Code K 81.0

3. Chronic cholecystitis Code K 81.1

Definition

Survey

Mandatory laboratory tests

One time

Blood cholesterol

Blood amylase

Blood sugar

Blood type and Rh factor

Coprogram

Bacteriological, cytological and biochemical study of duodenal contents

Twice

Community blood test

General urine test

Bilirubin and its fractions

ASAT, AlAT

ALP, GGTP

Total protein and protein fractions

C-reactive protein

Mandatory instrumental studies

One time

Ultrasound of the liver, gallbladder, pancreas

Duodenal sounding (ECD or other options)

Esophagogastroduodenoscopy

X-ray examination of the chest

Additional Research

They are carried out depending on the expected diagnosis and complications.

Mandatory consultations with specialists: surgeon

Characteristics of therapeutic measures

Depending on the disease being diagnosed.

Acute acalculous cholecystitis and exacerbation of chronic bacterial cholecystitis(Ciphers K 81.0 and K 81.1)

Drug therapy (antibacterial treatment options using one of them)

1. Ciprofloxacin orally, 500-750 mg 2 times a day for 10 days.

2. Doxycycline orally or intravenously. On the 1st day, 200 mg/day is prescribed, on subsequent days 100-200 mg/day, depending on the severity of the disease. Duration of taking the drug is up to 2 weeks.

3. Erythromycin orally. The first dose is 400-600 mg, then 200-400 mg every 6 hours. The course of treatment, depending on the severity of the infection, is 7-14 days. The drug is taken 1 hour before meals or 2-3 hours after meals.

4. Septrin (bactrim, biseptol, sulfatone) 480-960 mg 2 times a day with an interval of 12 hours. The course of treatment is 10 days.

5. Cephalosporins for oral administration, for example, cefuroxime axetil (Zinnat) 250-500 mg 2 times a day after meals. The course of treatment is 10-14 days. (Correction of therapy is possible depending on the clinical effect and the results of the study of duodenal contents)

Symptomatic drug therapy (used according to indications)

1. Cisapride (Coordinax) or domperidone (Motilium) 10 mg 3-4 times a day or debridate (trimebutine) 100-200 mg 3-4 times a day, or meteospasmil 1 caps. 3 times a day. The duration of the course is at least 2 weeks.

2. Chofitol 2-3 tablets. 3 times a day before meals or allohol, 2 tablets. 3-4 times a day after meals or other drugs that increase choleresis and cholekinesis. The duration of the course is at least 3-4 weeks.

3. Digestal or festal, or Creon, or Panzinorm, or another multienzyme drug, taken for 3 weeks before meals, 1-2 doses for 2-3 weeks.

4. Maalox or phosphalugel, or Remagel, or Protab, or another antacid drug, taken in one dose 1.5-2 hours after meals.

Duration of inpatient treatment – 7-10 days, outpatient - at least 2 months. Patients require clinical observation.

Requirements for treatment results

Remission of the disease consists of eliminating the symptomatic manifestations of the disease with restoration of the function of the gallbladder and duodenum.

XIV. International Classification of Diseases (ICD-10)

1. Fibrosis and cirrhosis of the liver Code K 74

2. Primary bilnar cirrhosis of the liver, unspecified Code K 74.5

3. Portal hysterectomy (with complications) Code K 76.6

4. Chronic liver failure Code K 72

Definition

Liver cirrhosis (LC) is characterized by a violation of the structure of the organ due to the development of fibrosis and parenchymal nodes. Liver cirrhosis is often the outcome of chronic hepatitis. Clinical classification takes into account the etiology, as well as the severity of portal hypertension and liver failure.

Survey

Mandatory laboratory tests

One time

Blood potassium and sodium

Blood group

Rh factor

Serum iron

Fecal occult blood test

Viral markers (HBsAg, HBeAg, antibodies to hepatitis B, C, D virus)

Twice

Total and direct bilirubin

Blood cholesterol

Blood urea

Community blood test

Reticulocytes

Platelets

Total protein and protein fractions

ASAT, AlAT

ALP, GGTP

General urine test

Fibrinogen

Mandatory instrumental studies

Ultrasound of the liver, gallbladder, pancreas, spleen and vessels of the portal system

Esophagogastroduodenoscopy

Additional studies (if indicated)

Histological examination of the biopsy specimen

Blood copper

Ceruloplasmin

Antismooth muscle, antimitochondrial and antinuclear antibodies (if studies for viral markers are negative and there is a suspicion of autoimmune and primary biliary cirrhosis)

Blood α-fetoprotein (if hepatoma is suspected)

Paracetamol and other toxic substances in the blood according to indications

Coagulogram

Blood immunoglobulins

Biochemical, bacteriological and cytological examination of ascitic fluid

Percutaneous or targeted (laparoscopic) liver biopsy

Paraabdominocentesis

Consultations with specialists according to indications: ophthalmologist, surgeon, gynecologist,

Characteristic therapeutic measures

Liver cirrhosis, compensated

(Child-Pugh class A - 5-6 points: bilirubin< 2 мг%, альбумин >3.5 g%, prothrombin index 60-80, no hepatic encephalopathy and ascites).

Basic therapy and elimination of dyspepsia symptoms.

Pancreatin (Creon, pancitrate, mezim and other analogues) 3-4 times a day before meals, one dose, course - 2-3 weeks.

Subcompensated liver cirrhosis

(Child-Pugh class B - 7-9 points: bilirubin 2-3 mg%, albumin 2.8-3.4 g%, prothrombin index 40-59, grade I-II hepatic encephalopathy, small transient ascites).

Diet with restriction of protein (0.5 g/kg b.w.) and sodium chloride (less than 2.0 g/day)

Spironolactone (veroshpiron) orally 100 mg per day continuously. Furosemide 40-80 mg per week. constantly and according to indications.

Lactulose (normaze) 60 ml (on average) per day constantly and according to indications.

Neomycip sulfate or ampicillin 0.5 g 4 times a day. Course 5 days every

Decompensated liver cirrhosis

(Class C according to Chanld-Pyo - more than 9 points: bilirubin > 3 mg%, albumin 2.7 g% or less, prothrombin index 39 or less, grade III-1V hepatic encephalopathy, large torpid ascites)

Ten-day course of intensive therapy.

Therapeutic paracentesis with a single removal of ascitic fluid and simultaneous intravenous administration of 10 g of albumin per 1.0 liter of removed ascitic fluid and 150-200 ml of polyglucin.

Enemas with magnesium sulfate (15-20 g per 100 ml of water), if there is constipation or evidence of previous esophageal-gastrointestinal bleeding.

Neomycip sulfate 1.0 g or ampicillin 1.0 g 4 times a day. Course 5 days.

Orally or through a naso-gastric tube, lactulose 60 ml per day. Course 10 days.

Intravenous drip administration of 500-1000 ml per day of hepasteryl-A. Course - 5-

7 infusions.

Course of prolonged continuous therapy

Basic therapy with the elimination of symptoms of dyspepsia (multi-enzyme drug before dosing continuously), spironolactone (veroshpiron) orally 100 mg per day continuously, furosemide 40-80 mg per week; constantly oral lactulose (iormase) 60 ml (on average) per day, constantly neomycin sulfate or ampicillin 0.5 g 4 times a day. Course 5 days every 2 months.

Basic therapy, including diet, regimen and medications, is prescribed for life, and intensive therapy for the period of decompensation, and, in connection with complications, symptomatic treatment.

Features of drug treatment of some forms of liver cirrhosis

Liver cirrhosis varied in the outcome of autoimmune hepatitis

1) Prednisolone 5-10 mg per day - a constant maintenance dose.

2) Azathioprine 25 mg per day in the absence of contraindications – granulocytopenia and thrombocytopenia.

Liver cirrhosis, developed and progressing against the background of chronic active

viral hepatitis B or C.

Alpha interferon (during viral replication and high hepatitis activity).

Primary biliary cirrhosis

1) Ursodeoxycholic acid 750 mg per day continuously

2) Cholestyramine 4.0-12.0 g per day, taking into account the severity of skin itching.

Liver cirrhosis due to hemochromatosis (pigmented cirrhosis of the liver)

1) Deferoxamine (desferal) 500-1000 mg per day intramuscularly along with bloodletting (500 ml weekly until the hematocrit is less than 0.5 and the total iron-binding capacity of the blood serum is less than 50 mmol/l)

2) Insulin taking into account the severity of diabetes.

Liver cirrhosis in Wilson-Konovalov disease

Penicillamine (cuprenil and other analogues). The average dose is 1000 mg per day, continuous use (the dose is selected individually).

Duration of inpatient treatment- up to 30 days.

Requirements for treatment results

1. Provide stable compensation for the disease

2. Prevent the development of complications (bleeding from the upper

digestive tract, hepatic encephalopathy, peritonitis).

XV. International Classification of Diseases (ICD-10)

1. Syndromes of the operated stomach (dumping, etc.). Code K 91.1 i.e.

consequences of gastric surgery

Definition

The consequences of gastric surgery include functional and structural disorders after gastrectomy and various types of vagotomy and anastomosis, manifested by astheno-vegetative, dyspeptic and often pain syndromes.

Survey

Mandatory laboratory tests

One time

Community blood test

General urine test

Hematocrit

Reticulocytes

Serum iron

Common bilirubin

Blood sugar and sugar curve

Total protein and protein fractions

Blood cholesterol, sodium, potassium and calcium

Coprogram

Urine diastasis

Histological examination of the biopsy specimen

Feces for dysbacteriosis

Mandatory instrumental studies

One time

Esophagogastroduodenoscopy with biopsy

Sigmoidoscopy

Ultrasound of the liver, gallbladder and pancreas

Electrocardiography

Mandatory consultations with specialists: surgeon, endocrinologist.

Characteristics of therapeutic measures

With dumping syndrome - rational nutrition and lifestyle.

Combinations of drugs

1.Debridate 100-200 mg 3 times a day or meteospasmil 1 cap. 3 times a day, or egloil (sulpiride) 50 mg 3 times a day 30 minutes before meals.

2. Imodium (lopsramide) 2-4 mg after diarrheal stool, but not more than 12 mg per day.

3. Creon or pancitrate, or mezim, one dose at the beginning of meals 4-5 times a day.

4. Maalox or protab, or phosphalugel, or another antacid drug, or sucralfate (Venter, sucrat gel) one dose per 30 minutes. before meals 4 times a day.

5. Vitamins B, (I ml). B, (1 ml), nicotinic acid (2 ml), folic acid (10 mg), ascorbic acid (500 mg), hydroxycobalamin (200 mcg) one dose daily.

According to indications, tube enteral or parenteral nutrition is performed.

Continuous maintenance therapy in an outpatient setting (prescription for

patient)

1) Dietary regime.

2) Multienzyme preparations (Creon or pancitrate, or mezim, or pancreatin).

3) Antacids (Maalox, Remagel, etc.) and cytoprotectors (Venter, Sucrat gel).

4) Preventive multivitamin courses.

5) Courses of antibacterial therapy for decontamination of the small intestine twice a year.

Duration of inpatient treatment- 21-28 days, and outpatient - for life.

Requirements for results treatment

1. Clinical, endoscopic and laboratory remission with restoration of all parameters to normal

2. Incomplete remission or improvement, when the symptoms of the disease are not completely relieved.

This refers to severe dumping syndrome, in which complete and stable remission cannot be achieved, even with adequate treatment.

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Archive - Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2007 (Order No. 764)

Chronic cholecystitis (K81.1)

General information

Brief description

Cholecystitis- an inflammatory disease that causes damage to the wall of the gallbladder, the formation of stones in it and motor-tonic disorders of the biliary system.

Protocol code:H-S-007 "Cholelithiasis, chronic cholecystitis with cholecystectomy"

Profile: surgical

Stage: hospital
ICD-10 code(s):

K80.2 Gallstones without cholecystitis

K80 Gallstone disease (cholelithiasis)

K81 Cholecystitis

Classification

Risk factors and groups

Cirrhosis;
- infectious diseases of the biliary tract;
- hereditary blood diseases (sickle cell anemia);
- old age;
- pregnant women;
- obesity;
- medications that lower blood cholesterol levels actually increase cholesterol levels in bile;
- rapid weight loss;
- stagnation of bile;
- hormone replacement therapy in postmenopause;
- women taking birth control pills.

Diagnostics

Diagnostic criteria: constant pain in the epigastrium radiating to the right shoulder and between the shoulder blades, which intensifies and lasts from 30 minutes to several hours. Nausea and vomiting, belching, flatulence, aversion to fatty foods, yellowish tint to the skin and whites of the eyes, low-grade fever.

List of main diagnostic measures:

1. General blood test (6 parameters).

2. General urine analysis.

3. Determination of glucose.

4. Determination of capillary blood clotting time.

5. Determination of blood group and Rh factor.

7. Histological examination of tissue.

8. Fluorography.

9. Microreaction.

11. HbsAg, Anti-HCV.

12. Determination of bilirubin.

13. Ultrasound of the abdominal organs.

14. Ultrasound of the liver, gall bladder, pancreas.

15. Esophagogastroduodenoscopy.

16. Consultation with a surgeon.

List of additional diagnostic measures:

1. Duodenal sounding (ECD or other options).

2. Computed tomography.

3. Magnetic resonance cholangiography.

4. Cholescintigraphy.

5. Endoscopic retrograde cholangiopancreatography.

6. Bacteriological, cytological and biochemical study of duodenal contents.

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Treatment

Treatment tactics

Treatment goals: surgical removal of the gallbladder.

Treatment

Cholecystectomy, intraoperative drainage according to Pinovsky and in the postoperative period - ERCP, PST.
Antibacterial therapy for the prevention of postoperative purulent complications. Dressings. If stones are detected in the gallbladder, surgical intervention is performed to prevent possible complications.

After preparing the patient, the operation begins with laparoscopy. If the hepatoduodenal zone is intact, the operation is performed laparoscopically.

Indications for cholecystectomy using laparoscopic technique:

Chronic calculous cholecystitis;

Polyps and cholesterosis of the gallbladder;

Acute cholecystitis (in the first 2-3 days from the onset of the disease);

Chronic acalculous cholecystitis;

Asymptomatic cholecystolithiasis (large and small stones).

If the common bile duct is enlarged or there are stones in it, laparotomy and classic cholecystectomy are performed. In the postoperative period, antibacterial and symptomatic therapy is carried out.

Emergency surgery is indicated for symptoms of peritonitis and a tense, enlarged gallbladder.

Early cholecystectomy compared with delayed cholecystectomy does not have a significant difference in terms of complications, but early cholecystectomy reduces hospital stay by 6-8 days.

Antibacterial treatment options using one of them:

1. Ciprofloxacin orally, 500-750 mg 2 times a day, for 10 days.

2. Doxycycline orally or intravenously. On the 1st day, 200 mg/day is prescribed, on subsequent days 100-200 mg/day, depending on the severity of the disease.

Duration of taking the drug is up to 2 weeks.

4. For the treatment and prevention of mycosis during long-term massive antibiotic therapy - itraconazole oral solution 400 mg/day, for 10 days.

5. Anti-inflammatory drugs 480-960 mg 2 times a day with an interval of 12 hours.

Symptomatic drug therapy (used according to indications):

3. Multienzyme drug taken before meals, 1-2 doses, for 2-3 weeks. Therapy can be adjusted depending on the clinical effect and the results of studies of duodenal contents.

4. Antacid drug, taken one dose 1.5-2 hours after meals.

List of essential medications:

1. *Trimepyridine hydrochloride injection solution in ampoule 1%, 1 ml

2. *Cefuroxime 250 mg, 500 mg tablet.

3. *Sodium chloride 0.9% - 400 ml

4. *Glucose solution for infusion 5%, 10% in a bottle of 400 ml, 500 ml; solution 40% in ampoule 5 ml, 10 ml

5. *Itraconazole oral solution 150 ml - 10 mg\ml

6. *Diphenhydramine solution for injection 1% 1 ml

7. Polividone 400 ml, fl.

8. *Aminocaproic acid 5% - 100ml, fl.

9. *Metronidazole solution 5mg/ml 100ml

11. *Drotaverine solution for injection 40 mg/2ml

12. *Thiamin injection solution 5% in 1 ml ampoule

13. *Pyridoxine 10 mg, 20 mg tablet; injection solution 1%, 5% in 1 ml ampoule

14. *Riboflavin 10 mg tablet.

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Related diseases and their treatment

Descriptions of diseases

Titles

Description

Postcholecystectomy syndrome is a syndrome of functional restructuring of the biliary system after surgery. It includes impaired motility of the sphincter of Oddi (muscular sphincter of the outlet of the common bile duct into the duodenum) and impaired motor function of the duodenum itself. Most often, a violation of the tone of the sphincter of Oddi occurs, such as hypotension or hypertension. However, postcholecystectomy syndrome also includes conditions whose causes were not eliminated during surgery. These are stones left in the ducts, stenosing papillitis or bile duct stenosis, bile duct cysts and other mechanical obstructions in the bile ducts that could have been removed during surgery, but for various reasons went unnoticed. As a result of surgery, damage to the bile ducts, narrowing and cicatricial changes in the bile ducts could occur. Sometimes incomplete removal of the gallbladder occurs, or the pathological process develops in the stump of the gallbladder duct.

Classification

There is no generally accepted classification of postcholecystectomy syndrome. More often in everyday practice the following systematization is used:
1. Relapses of stone formation of the common bile duct (false and true).
2. Strictures of the common bile duct.
3. Stenosing duodenal papillitis.
4. Active adhesive process (limited chronic peritonitis) in the subhepatic space.
5. Biliary pancreatitis (cholepancreatitis).
6. Secondary (biliary or hepatogenic) gastroduodenal ulcers.

Symptoms

* heaviness and dull pain in the right hypochondrium.
* intolerance to fatty foods.
* belching with bitterness.
* heartbeat.
* sweating.

Reasons

The cause of postcholecystectomy syndrome can be diseases of the gastrointestinal tract that have developed as a result of the long-term existence of cholelithiasis, which continue to occur after surgical treatment. These are chronic pancreatitis, hepatitis, cholangitis, duodenitis and gastritis. It is believed that the most common cause of postcholecystectomy syndrome is stones in the bile ducts. Stones may be undetected and left in the ducts during surgery or newly formed. Patients complain of pain in the right hypochondrium, which is paroxysmal in nature and is accompanied or not accompanied by jaundice. During an attack, darkening of the urine may be detected. With retained stones, the first signs of the disease appear soon after surgical treatment, but newly formed stones take time.
The cause of postcholecystectomy syndrome may be a violation of the tone and motor function of the duodenum or duodenal obstruction.

Treatment

Treatment of patients with postcholecystectomy syndrome should be comprehensive and aimed at eliminating those functional or structural disorders of the liver, biliary tract (ducts and sphincters), gastrointestinal tract and pancreas, which underlie the suffering and were the reason for consulting a doctor.
Frequent split meals (5–7 times a day), a low-fat diet (40–60 g per day of vegetable fats), and the exclusion of fried, spicy, and sour foods are prescribed. Drotaverine and mebeverine can be used for pain relief. In cases where all medical options have been tried, and there is no effect of treatment, surgical treatment is performed to restore the patency of the bile ducts. To eliminate relative enzymatic deficiency and improve fat digestion, enzyme preparations containing bile acids (festal, panzinorm forte) are used in average daily doses. The presence of hidden, and even more so obvious, disorders of fat digestion implies long-term use of enzymes for both therapeutic and preventive purposes. Therefore, the duration of the course of treatment is individual. Often, removal of the gallbladder is accompanied by a violation of the intestinal biocenosis. To restore the intestinal microflora, antibacterial drugs (doxycycline, furazolidone, metronidazole, intetrix) are first prescribed in short 5-7 day courses (1-2 courses). Then treatment is carried out with drugs that restore the intestinal microbial landscape, promoting the growth of normal microflora (for example, bifidumbacterin, Linex). For 6 months after removal of the gallbladder, patients should be under medical supervision. It is advisable to recommend sanatorium-resort treatment no earlier than 6–12 months after surgery.

Source: kiberis.ru

Magazine issue: December 2008

A.A. Ilchenko
Central Research Institute of Gastroenterology, Moscow

Diagnosis of cholelithiasis (GSD) at the stage of formed gallstones is the reason for high operational activity in this disease. Despite the introduction into clinical practice of less invasive technologies compared to abdominal cholecystectomy, some patients experience so-called postcholecystectomy disorders, referred to as postcholecystectomy syndrome (PCES).

Despite the fact that PCES is included in the modern classification of diseases ICD-10 (code K.91.5), there is still no precise understanding of the essence of this syndrome.
According to the 1999 Rome Consensus on Functional Disorders of the Digestive Organs, the term “postcholecystectomy syndrome” usually refers to dysfunction of the sphincter of Oddi, caused by a violation of its contractile function, preventing the normal outflow of bile and pancreatic secretions into the duodenum in the absence of organic obstacles. One could agree with such an interpretation if there were no close anatomical and functional relationship between the biliary system and other digestive organs. Removal of the gallbladder is an exclusively forced measure, and the pathology of the gallbladder that led to cholecystectomy, as a rule, develops over a long period of time and is almost always associated with pathology of other digestive organs, primarily the pancreaticoduodenal zone. Therefore, it is difficult to imagine that the loss of the gallbladder will not affect the course of pathological processes that developed before the operation.
Based on this, from a practical point of view, it is advisable to consider PCES from the perspective of taking into account the entire complex of pathological conditions associated with long-term cholelithiasis. In this regard, the following main groups of reasons for the development of PCES can be distinguished:

1. Diagnostic errors associated with identifying pathology associated with the biliary system, which were made at the preoperative stage and/or during surgery.
2. Technical errors and tactical errors made during the operation.
3. Functional disorders that developed after removal of the gallbladder or aggravated by cholecystectomy.
4. Exacerbation and/or progression of diseases of the hepatopancreatoduodenal zone that existed before surgery.

First group
Functional disorders of the biliary tract are an indispensable attribute of cholelithiasis, ensuring its formation and progression. In case of cholelithiasis, the most important are disturbances in the coordinated work of the Lutkens sphincter and the sphincter of Oddi. Therefore, diagnosis of biliary dysfunctions and their correction before surgery contribute to a more rapid adaptation of the body to the loss of gallbladder functions. Underestimation of functional disorders at the preoperative stage in the early postoperative period can manifest itself in various types of dysfunction of the sphincter of Oddi (biliary, pancreatic or mixed types).
Structural changes in the biliary tract are usually represented by stenosis of the terminal part of the common bile duct or stenotic papillitis, which are formed as a result of trauma to the mucous membrane and the sphincter apparatus directly by migrating microliths or small stones. Identification of these and other changes (cholangitis, choledocholithiasis and others) before surgery is of particular importance, as it determines not only clinical symptoms, but also the management tactics of a patient preparing for cholecystectomy.
Surgery is the last diagnostic stage, therefore, clarification of the nature of pathological changes during surgery must be carried out as fully as possible using modern methods of intraoperative diagnostics - intraoperative cholangiography, direct cholangioscopy, and in recent years, intraoperative sonography. As a result of such diagnostic errors, pathological changes in the common bile duct remain unrecognized. For example, incomplete examination of the bile ducts without x-ray monitoring of their condition leads to the fact that in half of the cases stones in the duct system go unnoticed.

Second group
This group of errors is the main reason for the formation of the so-called “true postcholecystectomy syndrome” and repeated operations on the biliary tract, and they are described in detail in practical surgical manuals.

Third group
After cholecystectomy, hypertonicity of the sphincter of Oddi develops, and in the first month after surgery, this pathology is observed in 85.7% of patients. Hypertonicity of the sphincter of Oddi is clinically accompanied by biliary hypertension, cholestasis, pain in the right hypochondrium, and in some cases a clinical picture of exacerbation of biliary pancreatitis develops.
The mechanism of development of hypertonicity of the sphincter of Oddi is associated with the shutdown of the regulatory role of the Lutkens sphincter and the muscular activity of the gallbladder, since the tone of the sphincter of Oddi reflexively decreases during contraction of the gallbladder, which ensures the coordinated activity of the entire sphincter apparatus of the biliary tract. A decrease in the reaction of the sphincter of Oddi in response to cholecystokinin after cholecystectomy was experimentally established. Dysfunction of the sphincter of Oddi in the form of its hypertonicity after cholecystectomy is usually temporary and manifests itself, as a rule, during the first months after surgery. Motor dysfunction of the sphincter of Oddi is one of the causes of acute or chronic abdominal pain and dyspeptic syndrome in the postoperative period. It should be noted that the quality of life after cholecystectomy in patients with reduced contractile function of the gallbladder before surgery is better than in those with preserved or increased function. It is known, for example, that in patients with the so-called disabled gallbladder, dilatation of the common bile duct is rarely observed both before and after surgery. Gradual adaptation leads to the fact that such patients rarely develop PCES.

Fourth group
Chronic biliary insufficiency accompanying cholelithiasis persists even after removal of the gallbladder. Moreover, these changes are detected in 100% of patients in the first 10 days after surgery and in 81.2% of patients do not disappear after cholecystectomy for a long time. It is noteworthy that chronic biliary insufficiency is determined already in the initial stages of cholelithiasis. So, according to O.V. Delyukina, in patients with biliary sludge in the form of a suspension of hyperechoic particles, it was detected in 91.7%, with mild severity in 50%, and moderate severity in 41.7%.
The deficiency of bile acids after cholecystectomy is compensated to a certain extent by accelerating their enterohepatic circulation. However, a significant acceleration of enterohepatic circulation is accompanied by suppression of the synthesis of bile acids, which leads to an imbalance in the ratio of its main components and a violation of the solubilizing properties of bile.
Removal of the gallbladder is accompanied by a restructuring of the processes of bile formation and bile excretion. According to R.A. Ivanchenkova, after cholecystectomy, choleresis increases due to both acid-dependent and acid-independent fractions. An increase in bile secretion occurs within 2 weeks after cholecystectomy. Increased choleresis is the main cause of cholagenic diarrhea after cholecystectomy.
Among the organs of the hepatopancreatoduodenal zone, removal of the gallbladder most affects the function of the pancreas. The development of chronic pancreatitis of biliary etiology is facilitated by frequently occurring functional disorders (dysfunction of the sphincter apparatus of the biliary tract) or organic diseases of the ductal system that disrupt the passage of bile (narrowing, compression by cysts or enlarged lymph nodes, stones localized in the terminal part of the common bile duct, inflammatory processes, especially with localization in its distal parts, etc.). In this regard, exacerbation of chronic pancreatitis in patients who have undergone cholecystectomy occurs quite often. According to V.A. Zorina et al. who examined patients 4-10 days after cholecystectomy, 85% of patients showed increased levels of b1-antitrypsin in the blood serum, and in 34.7% of cases the levels were more than 2 times higher than the norm.
Chronic gastritis is the most common pathology of the digestive system. It is believed that its role in the formation of postcholecystectomy syndrome is small and is determined mainly by functional disorders. Chronic gastritis is often associated with Helicobacter pylori (HP). In this regard, the need for anti-Helicobacter therapy in patients undergoing cholecystectomy is being discussed. The accumulated experience indicating that anti-Helicobacter therapy, carried out, for example, before gastrectomy, significantly reduces the number of postoperative complications, convinces of the same need in connection with the upcoming cholecystectomy.
The need for anti-Helicobacter therapy is also confirmed by recent studies indicating a possible connection between Helicobacter pylori infection and biliary pathology and hepatobiliary cancer, in particular. According to F. Fukuda et al. who examined 19 patients with hepatobiliary cancer and 19 patients with benign diseases of the hepatobiliary system, using PCR they detected Helicobacter pylori DNA in bile samples in 52.6% and 15.7% of cases, respectively. The first evidence of the presence of HP in the bile and mucous membrane of the gallbladder in humans was obtained, as well as data from experimental studies on animals confirming the role of enterohepatic Helicobacter (H. bilis, H. hepaticus, H. rodentium) in biliary lithogenesis. Resolving the issue of the role of Helicobacter in the etiology of biliary pathology can significantly change approaches to the management of patients with biliary tract diseases, including the issue of preventing postcholecystectomy syndrome.
Chronic duodenitis and bacterial overgrowth syndrome (SIBO). Cholecystectomy is accompanied by a decrease in the bactericidal properties of bile, which leads to excessive bacterial growth in the duodenum. This is also facilitated by a decrease in the barrier function of the stomach due to hyposecretion of hydrochloric acid. Chronic biliary insufficiency, a decrease in the bactericidal properties of bile and the addition of SIBO lead to significant digestive disorders, which causes the development of corresponding symptoms and requires drug correction.
Thus, analyzing the nature of the pathological processes associated with cholecystectomy, we can give the following definition of postcholecystectomy syndrome: PCES - a set of functional and/or organic changes associated with the pathology of the gallbladder or ductal system, aggravated by cholecystectomy or developed independently as a result of technical errors in its implementation.
Such a definition directs the doctor to a more thorough examination of patients before surgery in order to identify various concomitant pathologies of both the digestive organs and other organs and systems, and allows us to understand the pathogenetic connection between surgical intervention and the clinical symptoms that develop after it.
Analysis of clinical symptoms made it possible to identify the following variants of the course of PCES:

Dyspeptic variant - with symptoms of dyspepsia in the form of nausea, a feeling of bitterness in the mouth and unexpressed pain;
pain variant – with pain syndrome of varying severity;
icteric variant - periodically subecteric skin and sclera with or without pain;
clinically asymptomatic variant - with the absence of complaints, with the presence of changes in biochemical blood parameters (increased levels of alkaline phosphatase, bilirubin, AST, ALT, amylase) and/or dilatation of the CBD according to ultrasound data of more than 6 mm.

The results of a survey of 820 patients with PCES showed that the dyspeptic variant was the most common compared to others (Figure).

Diagnostics
To diagnose PCES, methods are used to identify functional and structural disorders of the biliary tract, occurring both independently and in association with other diseases of the digestive system. Laboratory (determination of levels of GGTP, alkaline phosphatase, bilirubin, AST, ALT, amylase) and instrumental (ultrasound, endoscopy) diagnostic methods are used as screening methods. As additional methods - endoscopic retrograde cholangiopancreaticography (ERCP), including with sphincter of Oddi manometry, dynamic cholescintigraphy, magnetic resonance cholangiography, endoscopic ultrasonography, staged chromatic duodenal sounding and other methods.
A thorough examination of patients with PCES using highly informative diagnostic methods allows for timely and adequate correction of anatomical and functional disorders that developed after removal of the gallbladder or aggravated by cholecystectomy.

Treatment
In most cases, conservative treatment allows for correction of the main pathophysiological disorders in PCES, however, at various times after cholecystectomy, indications for surgical treatment may appear.
Nutritional therapy is important in the early postoperative period. Dietary recommendations include frequent (up to 6 times a day) and small meals. It is necessary to limit fat to 60-70 g per day. If pancreatic function is preserved, up to 400-500 g of carbohydrates per day can be included in the diet. In order to ensure adequate functional adaptation of the digestive organs to loss of gallbladder function, it is advisable to expand the diet as early as possible (depending on concomitant diseases). The basic principles of conservative therapy are to restore the normal biochemical composition of bile, the outflow of bile and pancreatic secretions into the duodenum, as well as to treat diseases associated with pathology of the biliary tract.
In the presence of chronic biliary insufficiency, replacement therapy with ursodeoxycholic acid (UDCA) is necessary. Our experience shows that the use of UDCA in an average daily dose of 10-15 mg per 1 kg of body weight effectively reduces the degree of biliary insufficiency and the severity of dyscholia. The dose and duration of treatment with UDCA are determined by the degree of biliary insufficiency and the dynamics of changes in the cholate cholesterol coefficient during therapy.
To ensure adequate bile outflow, myotropic antispasmodics are indicated: hymecromone - 200-400 mg 3 times a day or mebeverine hydrochloride 200 mg 2 times a day, or pinaveria bromide 50-100 mg 3 times a day for 2-4 weeks.
Drugs of this group have a mainly antispasmodic effect and do not affect the nature of pathological changes in the liver. In this regard, hepabene deserves attention - a combined preparation of plant origin, consisting of fumaria extract and milk thistle extract.
Fumaria officinalis extract, containing the alkaloid fumarin, has a choleretic effect, has an antispasmodic effect, reduces the tone of the sphincter of Oddi, facilitating the flow of bile into the intestines.
Milk thistle fruit extract (Fructus Silybi mariani) contains silymarin, a group of flavonoid compounds including isomers: silibinin, silydianin and silicristin. Silymarin has a hepatoprotective effect: it binds free radicals in liver tissue, has antioxidant membrane-stabilizing activity, stimulates protein synthesis, promotes the regeneration of hepatocytes, thus normalizing various liver functions in acute and chronic liver diseases. During therapy with hepabene, the biochemical composition of bile is stabilized, and the cholesterol saturation index of gallbladder bile decreases. The dual mechanism of action of hepabene (antispasmodic and hepatoprotective) makes it one of the drugs of choice in patients with PCES. Gepabene is prescribed 1-2 capsules 3 times a day, the course of treatment is 1-3 months.
In the presence of bacterial overgrowth syndrome, antibacterial drugs are prescribed - co-trimoxazole, intetrix, furazolidone, nifuroxacid, ciprofloxacin, erythromycin, clarithromycin, which are used in standard doses. The course of treatment is 7 days. If necessary, several courses of antibacterial therapy are carried out with a change in drugs in the next course. Non-absorbable antibiotics may be very promising in the treatment of SIBO. The first clinical trials of using rifaximin show that the drug normalizes the bacterial microflora and reduces the symptoms of duodenal hypertension, which is also important in patients with PCES. After the antibacterial course, probiotics are prescribed (bifiform, bifidumbacterin, sporobacterin, etc.), prebiotics - hilak-forte, which normalizes the intestinal microflora, stimulates the regeneration of epithelial cells of the intestinal wall damaged by deconjugated bile acids.
To bind excess bile and other organic acids, especially in the presence of chologenic diarrhea, the use of aluminum-containing antacids 10-15 ml (1 sachet) 3-4 times a day 1-2 hours after meals for 7-14 days is indicated. According to indications, it is possible to use enzyme preparations (pancreatin, etc.).
In the late postoperative period, a number of complications may arise that require repeated operations. Recurrence of stones is quite rare and occurs if there are reasons that contribute to their formation (impaired outflow of bile and secretion of lithogenic bile). Common bile duct stones are removed using balloon dilatation, papillotomy, or papillosphincterotomy. In some cases, these operations are combined with contact lithotripsy. Recurrence of strictures, according to E.I. Halperin, is the most common complication and accounts for 10-30% after operations on scarred bile ducts. Restenosis of the major duodenal papilla also develops after papillosphincterotomy, which may raise the question of the advisability of choledochoduodenoanastomosis.

Prevention
Prevention measures consist of a comprehensive examination of patients in the process of preparing for surgery in order to identify and timely treatment, primarily of diseases of the hepatopancreatoduodenal zone. A technically competent and complete operation, if necessary using intraoperative diagnostic techniques, is important and is aimed at preventing postoperative complications and postcholecystectomy syndrome in particular. One of the main conditions for the prevention of PCES is timely surgical intervention before the development of complications of the disease, as well as preoperative preparation to the required extent in order to correct the identified disorders. However, high operational activity in cholelithiasis is associated with high economic health care costs (table). In this regard, the most effective way to prevent cholelithiasis and, as a consequence, PCES, is to identify and treat patients with cholelithiasis in the early (pre-stone stages). For this purpose, the Central Research Institute of Gastroenterology has developed a modern clinical classification of cholelithiasis:
Stage I - initial or prestone: As studies have shown, the use of short courses of therapy aimed at eliminating biliary dysfunction and restoring the normal biochemical composition of bile can be an effective means of primary prevention of cholelithiasis.

Literature
1. Galperin E.I., Volkova N.V. Diseases of the biliary tract after cholecystectomy. M.: Medicine. 1998; 272.
2. Tarasov K.M. Clinical and laboratory assessment of biliary insufficiency in patients who underwent cholecystectomy. Author's abstract. Candidate of Medical Sciences Moscow, 1994; 22.
3. Delyukina O.V. Motor dysfunctions of the biliary tract and features of the biochemical composition of bile in biliary sludge, methods for their correction. Author's abstract. Ph.D. honey. Sci. Moscow, 2007; 25.
4. Guide to gastroenterology / Ed. F.I. Komarov and A.L. Grebeneva. M.: Medicine, 1995; 2.
5. Zorina V.A., Kononova N.Yu., Zubkovskaya N.S., Kononov Yu.N. Study of the activity of antitrypsins in a comprehensive assessment of the effectiveness of balneotherapy for postcholecystectomy conditions. Materials of the 7th International Slavic-Baltic Scientific Forum “St. Petersburg - Gastro-2005”. Gastroenterology of St. Petersburg. 2005; 1-2: M52.
6. Fukuda K., Kuroki T., Tajima Y., et al. Comparative analysis of Helicobacter DNAs and biliary pathology in patients with and without hepatobiliary cancer // Carcinogenesis. 2002; 23: 1927-31.
7. Lin T.T., Yeh C.T., Wu C.S., Liaw Y.F. Detection and partial sequence analysis of Helicobacter pylori DNA in the bile samples // Dig. Dis. Sci. 1995; 40:3:2214-2219.
8. Kawaguchi M., Saito T., Ohno H. et al. Bacteria closely resembling Helicobacter pylori detected immunohistologically and genetically in resected gallbladder mucosa // J. Gastroenterol. 1996; 31: 1: 294-298.
9. Maurer KJ, Ihrig MM, Rogers AB. et al. Identification of cholelithogenic enterohepatic helicobacter species and their role in murine cholesterol gallstone formation // Gastroenterology. 2005 Apr;128:4:1023-33.
10. Vikhrova T.V. Biliary sludge and its clinical significance. Author's abstract. Candidate of Medical Sciences Moscow, 2003; 28.