Cholelithiasis: Clinical Guidelines

Applies toadults2024 editionK80.0, K80.1, K80.2, K80.3…

Clinical guidelines of the Russian Ministry of Health, adults. 2024 edition, ICD-10 codes: K80.0, K80.1, K80.2, K80.3…. The page features a concise version by WhiteCoat Pro and the full official text.

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Brief for Practice

WhiteCoat Pro editorial summary based on the 2024 guideline text. Each item links to the original section — verify against it before prescribing.

Cholelithiasis is a chronic disease characterized by the formation of stones in the biliary tract; it can be asymptomatic or complicated by colic, cholecystitis, choledocholithiasis, cholangitis, and biliary pancreatitis. The main objectives are to confirm the presence of stones, identify complications, and timely select endoscopic or surgical treatment.

Key points

The diagnosis of cholelithiasis is confirmed by visualization of gallstones using any instrumental method; the clinical form of the disease is determined based on a combination of clinical, laboratory, and instrumental data. → in text
In asymptomatic cholecystolithiasis, treatment and special follow-up are not required, except for cases where prophylactic cholecystectomy is indicated due to an increased risk of gallbladder cancer. → in text
Biliary colic lasting more than 6 hours raises suspicion of acute cholecystitis; elevated bilirubin and/or alkaline phosphatase requires ruling out a common bile duct stone, while fever with chills suggests cholecystitis or cholangitis. → in text
In acute calculous cholecystitis, early cholecystectomy, preferably laparoscopic, is preferred within the first 72 hours from symptom onset after preparing the patient for surgery. → in text
In choledocholithiasis, endoscopic papillosphincterotomy and stone extraction serve as the primary methods of duct clearance; if a stone is impacted in the major duodenal papilla or in the presence of cholangitis, decompression is performed within 24 hours, and in other cases, no later than 72 hours. → in text
In severe cholecystitis or high operative and anesthetic risk, a staged approach is possible: first, gallbladder decompression or drainage, followed by delayed cholecystectomy. → in text
Physical activity and restriction of easily digestible carbohydrates are important for preventing stone formation; after bariatric surgery or on a low-calorie diet up to 800 kcal/day, ursodeoxycholic acid at 1000–1500 mg/day is used for 3–12 months as determined by the physician. → in text

Diagnostics

Take the medical history: inquire about biliary pain, colic episodes, previous acute cholecystitis, pancreatitis, jaundice, fever, and chills. Dyspeptic symptoms after fatty meals should not be considered as symptoms of cholecystitis per se. → in text
Perform a physical examination and assess tenderness in the right upper quadrant, Murphy's sign, and other signs of cholecystitis, as well as signs of jaundice, cholangitis, and pancreatitis. In patients with stones without clinical signs of cholecystitis, the diagnosis is established based on imaging data (Level of Reliability of Evidence C, Level of Credibility of Evidence 5). → in text
If acute cholecystitis and other complicated forms of cholecystolithiasis are suspected, perform a complete blood count with leukocyte differential (Level of Reliability of Evidence C, Level of Credibility of Evidence 5). If acute cholecystitis or cholangitis is suspected, determine C-reactive protein (Level of Reliability of Evidence C, Level of Credibility of Evidence 5). → in text
Determine ALT, AST, alkaline phosphatase, GGT, total and conjugated bilirubin, and pancreatic amylase (Level of Reliability of Evidence C, Level of Credibility of Evidence 5). In the absence of elevated AST, ALT, alkaline phosphatase, GGT, and bilirubin and no dilation of the common bile duct, the probability of choledocholithiasis is very low. → in text
As the primary imaging method, perform comprehensive abdominal ultrasound with evaluation of the liver, gallbladder, bile ducts, and pancreas (Level of Reliability of Evidence C, Level of Credibility of Evidence 5). When acute cholecystitis is suspected, ultrasound is also the first-line examination (Level of Reliability of Evidence C, Level of Credibility of Evidence 4). → in text
If ultrasound is inconclusive in a patient with biliary pain or signs of cholecystitis, perform MRCP (Level of Reliability of Evidence B, Level of Credibility of Evidence 2) or endoscopic ultrasound (Level of Reliability of Evidence C, Level of Credibility of Evidence 5). When the common bile duct is dilated and liver function tests are abnormal without stone visualization on ultrasound, MRCP or endoscopic ultrasound is recommended to confirm or rule out choledocholithiasis (Level of Reliability of Evidence A, Level of Credibility of Evidence 2). → in text

Treatment

Prescribe therapeutic nutrition: avoid long intervals between meals, alcohol, carbonated beverages, spicy, salty, smoked, and marinated foods, as well as high-fat foods; tolerance to fats and egg yolks is evaluated individually. → in text
For biliary colic without contraindications, use NSAIDs until symptoms resolve (Level of Reliability of Evidence B, Level of Credibility of Evidence 1) and add an antispasmodic (Level of Reliability of Evidence B, Level of Credibility of Evidence 3). Studies have used diclofenac 75 mg intramuscularly, ketoprofen 200 mg intravenously, or indomethacin 50 mg in suppositories. → in text
In acute cholecystitis and complicated choledocholithiasis, administer infusion therapy with monitoring of blood pressure, heart rate, and urine output (Level of Reliability of Evidence C, Level of Credibility of Evidence 5). In severe cases, target parameters are: mean arterial pressure >65 mmHg, urine output >0.5 mL/kg/h, venous oxygen saturation >70%; vasopressors are indicated for persistent hypotension after adequate fluid resuscitation. → in text
In Grade I acute cholecystitis, systemic antibiotics are not recommended (Level of Reliability of Evidence C, Level of Credibility of Evidence 5). In Grades II–III, systemic antibiotic therapy is indicated (Level of Reliability of Evidence C, Level of Credibility of Evidence 5); piperacillin/tazobactam, 3rd–4th generation cephalosporins, carbapenems, monobactams, or fluoroquinolones may be used, taking into account severity, healthcare-associated infection risks, and renal and hepatic function. → in text
In complications of cholecystolithiasis, surgical treatment is indicated (Level of Reliability of Evidence C, Level of Credibility of Evidence 4). Following biliary colic, elective or early cholecystectomy is performed to prevent acute cholecystitis (Level of Reliability of Evidence A, Level of Credibility of Evidence 1). → in text
In acute calculous cholecystitis, early, preferably laparoscopic, cholecystectomy is performed within the first 72 hours (Level of Reliability of Evidence B, Level of Credibility of Evidence 1). In case of gallbladder perforation and diffuse peritonitis, emergency surgery is required within the next 2–3 hours after establishing the diagnosis. → in text
In choledocholithiasis, endoscopic papillosphincterotomy with stone extraction is performed (Level of Reliability of Evidence B, Level of Credibility of Evidence 1). For common bile duct stones larger than 1 cm, after controlled papillosphincterotomy, balloon dilation is added, and mechanical lithotripsy if necessary (Level of Reliability of Evidence A, Level of Credibility of Evidence 1). → in text
If complete endoscopic stone extraction is not possible, complete the procedure by placing a plastic biliary stent or nasobiliary drain (Level of Reliability of Evidence B, Level of Credibility of Evidence 2). If retrograde decompression is ineffective, percutaneous transhepatic drainage is performed (Level of Reliability of Evidence C, Level of Credibility of Evidence 5). → in text

When to refer and how to monitor

Biliary colic, acute cholecystitis, choledocholithiasis with cholangitis, obstructive jaundice, or acute biliary pancreatitis are indications for hospitalization in a surgical inpatient department. → in text
All patients with suspected acute cholecystitis must be examined by a surgeon; the diagnosis of colic or acute cholecystitis is an indication for urgent hospitalization. → in text
In moderate or severe acute cholecystitis, as well as in choledocholithiasis with cholangitis or obstructive jaundice, the patient is immediately referred to the surgical department of a level II–III medical facility where transpapillary endoscopic intervention is available. → in text
If conservative treatment is ineffective within 24–48 hours, the patient is transferred from a level I medical facility to a level II facility or interdistrict surgical department where laparoscopic cholecystectomy and transpapillary intervention are available. → in text
If endoscopic papillosphincterotomy or percutaneous transhepatic drainage cannot be performed, a patient without severe purulent cholangitis is immediately referred to a specialized facility with the necessary equipment and specialists. → in text

Frequently asked questions

Is it necessary to operate on asymptomatic gallbladder stones?

Usually no: treatment and special follow-up are not prescribed. Elective prophylactic cholecystectomy is required in the presence of risk factors for gallbladder cancer, including stones $\ge$3 cm in patients older than 50 years, duration of cholecystolithiasis over 20 years, porcelain gallbladder, adenomas, and polypoid lesions $\ge$8 mm. → in text

How to relieve biliary colic?

In the absence of contraindications, NSAIDs are prescribed until symptoms resolve, and an antispasmodic is added. Studies have used diclofenac 75 mg intramuscularly, ketoprofen 200 mg intravenously, and indomethacin 50 mg in suppositories. → in text

When should acute cholecystitis or choledocholithiasis be suspected after colic?

Pain persisting for more than 6 hours requires ruling out acute cholecystitis. Elevated bilirubin and/or alkaline phosphatase indicates the need to rule out a common bile duct stone; fever with chills after colic is characteristic of cholecystitis and/or cholangitis. → in text

How to diagnose acute cholecystitis according to the Tokyo Guidelines?

A suspected diagnosis requires at least one local sign of inflammation and at least one systemic sign, or characteristic imaging findings. A definitive diagnosis requires signs from all three groups: local, systemic, and imaging. → in text

Within what timeframe should the bile ducts be decompressed in cholangitis?

In choledocholithiasis with cholangitis or gallstone impaction in the major duodenal papilla, decompression is performed within 24 hours of diagnosis. In other cases, drainage is performed no later than 72 hours; in Grade II–III cholangitis, decompression is performed immediately in parallel with conservative therapy. → in text

Status: Applied · approved by the Scientific and Practical Council of the Russian Ministry of Health
Database ID: 877, edition 1 (ID 877_1)
Publication date: December 25, 2024
Age category: adults
ICD-10 codes: K80.0 K80.1 K80.2 K80.3 K80.4 K80.5 K80.8 K82.0 K82.1 K82.2 K82.3 K82.4 K82.8 K83.1 K83.3 K83.8 K87.0 K91.5
Specialties: Surgery Gastroenterology
Developers: All-Russian Public Organization "Russian Society of Surgeons"
Russian Gastroenterological Association
Association "Endoscopic Society "REndo"
Official text: Ministry of Health of Russia Guidelines — 877_1

Condensed Clinical Guidelines: Cholelithiasis

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All abridged clinical guidelines: 259

Beginning of abbreviated version — open

Complications and Related Pathologies of the Gallbladder (GB)

GB Wall Perforation:
In gangrenous cholecystitis: perforation occurs most frequently in the region of the GB fundus.
In calculous cholecystitis: occurs due to pressure necrosis of the GB wall by a gallstone, most commonly in the region of the GB neck.
GB Fistula:
Etiology: perforation of the GB wall.
Classification (types): cholecystoduodenal, cholecystoenteric, cholecystogastric, cholecystodermal, biliodigestive, biliobiliary, biliary, gallstone fistula.

Cholesterolosis of the GB:
Metabolic disease of the GB.
Pathogenesis: diffuse or focal accumulation of lipids (predominantly free and esterified cholesterol) in the gallbladder wall.

Brief Information on the Disease: Cholelithiasis

Cholelithiasis (gallstone disease, syn. cholelithiasis) is a chronic genetically predisposed disease characterized by the formation of stones in the biliary tract.

Clinical Variants of Cholelithiasis:

Asymptomatic course:
Presence of stones in the GB with absence of biliary colic attacks, acute cholecystitis (AC) attacks, acute pancreatitis, signs of choledocholithiasis, and other complications.

Note: Clinical symptoms may be present, but they are caused by concomitant gastric and intestinal motility disorders.
Complicated course:
Presence of stones at various sites with the development of biliary colic attacks and/or acute cholecystitis (AC) attacks, acute pancreatitis, biliary tract obstruction, cholangitis, and other complications.

Etiology and Pathogenesis (Types of Gallstones)

Two main types of stones are distinguished.

These are cholesterol and pigment stones (pigment stones are covered on the next page):

1) Cholesterol stones:
Composition: cholesterol >50% (in "pure cholesterol" stones — >90%). They also include a glycoprotein matrix and calcium bilirubinate.
Characteristics of "pure cholesterol" stones: larger size, solitary, yellowish-white, floating (float in bile); frequently radiolucent — not visible on plain radiography, readily detected by ultrasound.

Classification of Gallstones (Continued)

Cholesterol stones: initially radiolucent, though calcium may be deposited on their surface over time.

Pigment stones: cholesterol content <20%. Main components: calcium bilirubinate, calcium polymers, and mucins.

Pigment stones are divided into 2 subtypes:

Black stones:
Composition: predominantly calcium bilirubinate (unconjugated bilirubin salt).
Characteristics: usually multiple, easily friable, size <5 mm. Radiopaque in 50–75% of cases.
Pathogenesis: commonly form in hemolysis and liver cirrhosis.

Brown stones:
Composition: calcium bilirubinate, mucins, cholesterol, calcium palmitate, and stearate. Bacterial components may be present in the core.
Characteristics: soft, layered, variable radiodensity.
Pathogenesis: form against the background of chronic inflammation in the intra- and extrahepatic bile ducts.

Epidemiology

Cholesterol stones are found in the vast majority of patients (70–80%).

Black pigment stones are found in 15–20%.

(The main risk factors for cholelithiasis are listed in Appendix A3).

Pathogenesis of Stone Formation and Biliary Sludge

Initial stages of cholelithiasis: nucleation → crystallization → biliary sludge → microolith formation.

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List of Abbreviations

ALT – alanine aminotransferase

AST – aspartate aminotransferase

GGT – gamma-glutamyl transferase

GD – gallstone disease

GB – gallbladder

CT – computed tomography

HAI – healthcare-associated infections

LC – laparoscopic cholecystectomy

HC – healthcare organization

MRI – magnetic resonance imaging

MRCP – magnetic resonance cholangiopancreatography

ICU – intensive care unit

CBD – common bile duct

CHD – common hepatic duct

AC – acute cholecystitis

OC – open cholecystectomy

US – ultrasound examination

UDCA – ursodeoxycholic acid

ChE – cholecystectomy

PTBD – percutaneous transhepatic biliary drainage

PTGBD – percutaneous transhepatic gallbladder drainage

ALP – alkaline phosphatase

EUS – endoscopic ultrasonography

EST – endoscopic papillosphincterotomy

ERCP – endoscopic retrograde cholangiopancreatography

Terms and Definitions

Cholelithiasis (gallstone disease, syn. cholelithiasis) is a chronic disease with a genetic predisposition characterized by the formation of stones in the biliary tract.

Acute calculous cholecystitis is an acute inflammatory lesion of the gallbladder (GB) developing against the background of cholelithiasis.

Chronic calculous cholecystitis is a chronic inflammatory lesion of the GB developing against the background of cholelithiasis.

Cholecystolithiasis is the presence of stones in the GB.

Cholangiolithiasis is the presence of stones in the bile ducts.

Hepatolithiasis is the presence of stones in the intrahepatic bile ducts.

Choledocholithiasis is the presence of a stone(s) in the common bile duct (CBD).

Cholangitis is an inflammatory lesion of the bile ducts.

Biliary sludge is a mobile sediment in the gallbladder consisting of cholesterol crystals and calcium salts fixed on mucin. Sludge is potentially reversible, but is considered a condition preceding gallstone formation.

«Complex» choledocholithiasis is a concept combining clinical situations associated with the detection of large (>15 mm) and/or multiple stones in the GB, or their localization in the intrahepatic biliary tract, Mirizzi syndrome, a narrow pancreatic segment of the CBD, which make it difficult to grasp and extract stones during endoscopic retrograde transpapillary intervention.

Gallbladder obstruction – a condition not associated with cholelithiasis and characterized by the difficulty or impossibility of bile outflow from the gallbladder due to complete or partial obstruction, stenosis, stricture of the gallbladder and/or cystic duct. Partial non-calculous obstruction is known in the literature as "cystic duct syndrome" or "organic syphopopathy".

Gallbladder hydrops – a disease of the GB manifested by its overdistension and filling of its lumen with milk-colored or colorless mucous and/or watery contents. As a rule, it is a non-inflammatory process caused by obstruction (blockage) of the GB and/or cystic duct. The most frequent cause is the presence of a stone in the neck of the GB or in the cystic duct.

Gallbladder perforation – or perforation of the GB wall; develops in patients with its gangrenous form, or due to pressure sore of the GB wall by a gallstone in calculous cholecystitis. In the first case, perforation most often occurs in the fundus of the GB, in the second – in the neck of the GB.

Gallbladder fistula – the etiological factor is perforation of the GB wall; the following are distinguished: cholecystoduodenal fistula, cholecystoenteric fistula, cholecystogastric fistula, cholecystodermal fistula, biliodigestive fistulas, biliobiliary biliary fistula, biliary fistula, and bile fistula.

Gallbladder cholesterosis is a metabolic disease of the GB characterized by diffuse or focal accumulation of lipids in its wall, predominantly in the form of free and esterified cholesterol.

1. Brief information on the disease or condition

1.1 Definition of the disease or condition

Cholelithiasis (gallstone disease, syn. cholelithiasis) is a chronic disease with a genetic predisposition characterized by the formation of stones in the biliary tract.

Asymptomatic cholelithiasis: the presence of stones in the GB in the absence of biliary colic attacks, attacks of acute cholecystitis (AC), acute pancreatitis, clinical, laboratory, and instrumental signs of choledocholithiasis and other complications. This form of the disease may feature clinical symptoms caused by concomitant gastric and intestinal motility disorders.

Complicated cholelithiasis: the presence of gallstones of various localizations with the development of biliary colic attacks and/or attacks of AC, acute pancreatitis, development of biliary obstruction, cholangitis, and other complications.

1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)

There are two main types of stones:

1) Cholesterol stones. The cholesterol content in them is >50% (>90% in so-called "pure cholesterol stones"). In addition, they consist of a glycoprotein matrix and calcium bilirubinate. Pure cholesterol stones are larger, single, yellowish-white, floating, and usually radiolucent. However, calcium may deposit on their surface over time.

2) Pigment stones. The cholesterol content in them is <20%, and the main components are calcium bilirubinate, calcium polymers, and mucins. Pigment stones are subdivided into 2 subtypes:

a. Black – consisting predominantly of calcium bilirubinate (unconjugated bilirubin salt), usually multiple, fragile, <5 mm in size, radiopaque in 50–75% of cases. They more commonly form in the setting of hemolysis and liver cirrhosis.

b. Brown (consisting of calcium bilirubinate, mucins, cholesterol, calcium palmitate, and stearate). They are soft, layered, and of varying radiodensity. Bacterial component inclusions may be found in the core of the stone. They form against the background of a chronic inflammatory process in the intra- and extrahepatic bile ducts.

The vast majority of patients (70–80%) have cholesterol stones, and 15–20% have black pigment stones.

The main risk factors for cholelithiasis are presented in Appendix A3.

The initial stages of stone formation are nucleation, crystallization, biliary sludge, and microlith formation. Biliary sludge is characterized by the formation of a thick layer of mucin gel in which lecithin-cholesterol crystals, cholesterol monohydrate, and calcium bilirubinate are precipitated. The development of sludge is associated with decreased GB motility. Sludge can be reversible and recurrent. Approximately 14% of such patients develop gallstones. Biliary sludge can cause complications characteristic of cholelithiasis – biliary colic, AC, acute pancreatitis, and possibly chronic idiopathic pancreatitis [1, 2].

Among the morphological variants of chronic calculous cholecystitis, special types are distinguished – xanthogranulomatous, hyalinizing, and lymphocytic. Xanthogranulomatous cholecystitis is a variant of chronic cholecystitis in which ongoing inflammation leads to extensive thickening and fibrosis extending beyond the GB wall. In this case, complications such as abscess formation and fistula formation are more frequently recorded [3]. Hyalinizing cholecystitis is a form of chronic cholecystitis in which GB wall structures are replaced by dense hyaline sclerosis. Hyalinization is found in 1.6% of GB tissue samples obtained during cholecystectomy (ChE); focal or diffuse calcification ("porcelain gallbladder") is also frequently identified. This form of cholecystitis is associated with an increased risk of GB carcinoma [4]. In lymphocytic or follicular cholecystitis, a lymphocytic inflammatory response predominates (>30 intraepithelial lymphocytes per 100 biliary epithelial cells are identified), sometimes in the form of follicles protruding into the lumen. Overall, these patients have a higher incidence of distal biliary tree strictures. Risk factors have not been clearly established [5].

1.3 Epidemiology of the Disease or Condition

The prevalence rates of gallstone disease (GSD) in different countries are determined by the genetic characteristics of the local population, as well as, apparently, lifestyle features predisposing to metabolic disorders, in particular, a relatively high intake of simple carbohydrates [6-9]. In countries with a Western lifestyle (Europe, North America, Russia), GSD is recorded at a frequency of ≈ 10-15%, and among individuals with signs of metabolic syndrome at a frequency of ≈ 20-30%. In Africa, Asian countries, and Japan, the prevalence of GSD is lower at 3.5-5%. Among certain ethnic groups, the incidence of GSD is extremely high: in Mexican and Chilean Indian populations, it reaches 45-80%.

In the presence of a family history burdened by GSD, the incidence increases by 4-5 times. The prevalence of GSD clearly correlates with age. In countries with a Western lifestyle, the detection rate of GSD in older age reaches 30%, although the maximum frequency of complications occurs at the age of 40-69 years. The prevalence of GSD is higher in women. However, with age, sex differences in morbidity diminish: while in the 30-39 age group the female-to-male prevalence ratio is 2.9:1, in the 40-49 age group it is 1.6:1, and in the 50-59 age group it is 1.2:1. The risk of developing GSD increases during pregnancy; with recurrent pregnancies, the probability of gallstone formation increases by 10-11 times. Biliary sludge is detected in 20-30% of pregnant women, and gallstones in 5-12%. Cases of spontaneous stone dissolution after childbirth have been reported; sludge is also often reversible. Among patients with diabetes mellitus, the prevalence of GSD is increased by 3 times; with liver cirrhosis, by 2-5 times. Under conditions of rapid weight loss and after bariatric surgery in the absence of prophylactic UDCA, the probability of developing GSD can be >30%.

In Russia, about 160 thousand patients with acute cholecystitis are hospitalized annually, more than 100 thousand patients undergo surgery, and more than 150 thousand patients are operated on for chronic cholecystitis.

The incidence rate of acute cholecystitis in the Russian Federation is 136 cases per 100 thousand adult population. In the structure of hospitalized patients with acute abdominal conditions, acute cholecystitis ranks second (23.6%) after acute pancreatitis (24.9%), and cholecystectomy in the structure of emergency and urgent surgeries (25.0%) ranks second after appendectomy (39.0%). In-hospital mortality for acute cholecystitis is 1.0%, and postoperative mortality is 1.4%. Postoperative mortality for chronic cholecystitis does not exceed 0.1% [10].

1.4 Features of Coding the Disease or Condition

K80 – Cholelithiasis (gallstone disease):

K80.0 – Calculus of gallbladder with acute cholecystitis

K80.1 – Calculus of gallbladder with other cholecystitis

K80.2 – Calculus of gallbladder without cholecystitis

K80.3 – Calculus of bile duct with cholangitis

K80.4 – Calculus of gallbladder with cholecystitis

K80.5 – Calculus of bile duct without cholecystitis or cholangitis

K80.8 – Other forms of cholelithiasis

K82.0 – Obstruction of gallbladder

K82.1 – Hydrops of gallbladder

K82.2 – Perforation of gallbladder

K82.3 – Fistula of gallbladder

K82.4 – Cholesterosis of gallbladder

K82.8 – Other specified diseases of gallbladder

K83.1 – Obstruction of bile duct

K83.3 – Fistula of bile duct

K83.8 – Other specified diseases of biliary tract

K87.0* – Disorders of gallbladder and biliary tract in diseases classified elsewhere

K91.5 – Postcholecystectomy syndrome

1.5 Classification of the disease or condition

Gallstone disease (GSD) may present in the following main forms:

1. Uncomplicated course:

- asymptomatic cholecystolithiasis;

- chronic calculous cholecystitis;

- asymptomatic choledocholithiasis;

2. Complications:

- cholecystolithiasis/choledocholithiasis with attacks of biliary colic;

- gallbladder hydrops;

- acute calculous cholecystitis (catarrhal, phlegmonous, gangrenous, emphysematous);

- choledocholithiasis with acute cholecystitis;

- choledocholithiasis with acute pancreatitis;

- choledocholithiasis with acute cholangitis;

- cholangiolithiasis with cholangitis;

- Mirizzi syndrome;

- cholecystoenteric fistula;

- gallstone ileus.

The diagnosis takes into account the localization of stones, the clinical form of the disease, and the nature of surgical interventions, if any were performed.

1.6 Clinical presentation of the disease or condition

The «classic type» of patient with cholesterol gallstones is a middle-aged, hypersthenic woman with overweight and a history of pregnancies. However, one should keep in mind the increasing prevalence of GSD among young people and even children with metabolic syndrome [8].

Asymptomatic cholecystolithiasis. Asymptomatic course is characterized by the presence of stones in the gallbladder and no history of attacks of biliary colic, acute cholecystitis, acute pancreatitis, or clinical, laboratory, and instrumental signs of choledocholithiasis. This course is observed in 66-75% of cases [9].

Chronic calculous cholecystitis. Chronic cholecystitis develops as a consequence of incomplete resolution of inflammation after previous attacks of acute cholecystitis. Lithogenic bile and local dysbiosis apparently play a role in its maintenance and progression. The term «chronic» reflects not so much the duration of the pathological process as the acuteness and degree of inflammation. Due to the lack of clear universally accepted diagnostic criteria, the degree of certainty of the diagnosis of chronic calculous cholecystitis may vary [11, 12]. Chronic calculous cholecystitis may present with mild aching pain in the right upper quadrant, occurring or intensifying 1-4 hours after eating, especially fatty foods. Abdominal palpation may reveal moderate tenderness at the gallbladder point. Murphy, Vasilenko, Ortner, Mussi-Georgievsky, and Shchetkin-Blumberg signs are absent.

Complicated course of GSD is characterized by the presence of gallstones of various localizations with attacks of biliary colic, acute cholecystitis, obstructive jaundice, cholangitis, acute pancreatitis, and fistula formation. Clinical symptoms are caused by the development of inflammation against the background of biliary tract obstruction due to stone migration into the gallbladder neck, cystic duct, or common bile duct.

Cholecystolithiasis/choledocholithiasis with attacks of biliary colic. Biliary (hepatic) colic is the most frequent manifestation of the complicated course of GSD. The cause of colic is the impaction of a stone in the gallbladder neck, cystic duct, or migration into the common bile duct. Obstruction and reflex spasm cause an increase in intraluminal pressure and the onset of visceral pain. Typically, biliary colic develops 1-1.5 hours after consuming fatty, fried foods, or an unusually large meal after prolonged restriction, and is associated with increased gallbladder contraction under the influence of cholecystokinin. Colic can also be triggered by bumpy rides, trunk flexion, physical exertion, and psycho-emotional stress. Biliary colic often occurs at night, several hours after falling asleep. During biliary colic, nausea and pain rapidly increase, reaching a «plateau»; the pain is pronounced, fairly constant, and distending in nature. The pain is localized in the epigastric region and the right upper quadrant, and may radiate to the right scapula, interscapular region at the level of the lower thoracic vertebrae, right shoulder and right half of the neck, and sometimes to the chest or sternal area. The term «colic», meaning severe spasmodic pain, does not accurately reflect the nature of biliary colic, as the pain does not exhibit wave-like intensification. The duration of biliary colic ranges from a few minutes to several hours. Typically, the pain is accompanied by (and may be preceded by) nausea and vomiting, which lack pathological impurities and do not bring relief. Autonomic reactions frequently develop, manifesting as tachycardia or bradycardia, blood pressure fluctuations, transient intestinal paresis, urges to defecate, and a rise in body temperature to subfebrile values. The patient cannot find a position that relieves the pain. Palpation reveals moderate, poorly localized tenderness in the right upper quadrant; Ortner's sign may be positive, while peritoneal irritation signs are absent. The attack resolves with the administration of nonsteroidal anti-inflammatory drugs, antispasmodics, or spontaneously (abruptly terminating). Biliary colic attacks may be masked (in such cases, the term «biliary pain attack» is applicable).

If a biliary colic attack lasts >6 hours, the development of acute cholecystitis should be suspected. If serum bilirubin and/or alkaline phosphatase (ALP) levels are elevated, the presence of a stone in the common bile duct should be ruled out. The onset of fever with chills after a colic attack generally indicates the development of acute cholecystitis and/or cholangitis.

In most cases, biliary colic should be differentiated from dyspepsia syndrome and coronary syndrome [13]. Pain attacks caused by stone obstruction of the gallbladder neck and biliary tract may be interpreted not as biliary colic, but as dyspepsia or chest pain. Consequently, some cases of acute cholecystitis remain unrecognized.

Acute calculous cholecystitis. The development of acute calculous cholecystitis is frequently preceded by a prolonged episode of biliary colic. As inflammation develops, pain intensifies, spreading to the right upper quadrant and epigastric region, and may radiate to the interscapular region, right scapula, or shoulder. The pain is constant or cramping in character, dull, and sometimes excruciating. Dyspnea may occur due to the forced limitation of respiratory depth. Fever is typically low-grade (38–39 °C) accompanied by chills. Palpation of the abdomen reveals a more localized area of tenderness at the gallbladder point; in the majority of patients, Murphy's, Ortner's, Vasilenko's, and Mussey-Georgievsky's signs are positive, along with signs of peritoneal irritation in the right upper quadrant and symptoms of dynamic intestinal obstruction (anorexia, repeated vomiting, abdominal distension, decreased bowel sounds). Jaundice may develop later due to the involvement of adjacent liver tissue, bile ducts, and lymph nodes in the inflammatory process. In the absence of gallbladder perforation, signs of generalized peritonitis are absent. A complete blood count generally reveals neutrophilic leukocytosis with a left shift. A biochemical blood test may show moderate hyperbilirubinemia (usually no more than a 4-fold increase in total bilirubin; higher values indicate the likely presence of choledocholithiasis), a moderate increase in transaminase activity, and elevated C-reactive protein levels.

In most cases, the duration of an acute cholecystitis attack is 1–4 days. Spontaneous resolution of the inflammatory process is possible, or it may progress with the development of life-threatening complications.

The severity of acute cholecystitis symptoms is highly variable, making it difficult to rule out the disease based solely on clinical findings. Criteria for establishing the diagnosis of acute cholecystitis, according to the Tokyo Guidelines 2013/2018, are provided in Appendix G2.

Complicated choledocholithiasis. Complications develop against the background of impaired bile/pancreatic juice outflow and superimposed infection. In a complicated course, choledocholithiasis may manifest as attacks of biliary colic, obstructive jaundice, acute cholecystitis, cholangitis, or acute pancreatitis.

Choledocholithiasis with obstructive jaundice. Characteristic symptoms include jaundice, pruritus, dark urine, and acholic stools. In some cases, these symptoms appear 12–24 hours after a severe pain attack (biliary colic). Palpation may reveal tenderness in the right upper quadrant, with positive Ortner's and Murphy's signs [14, 15].
Choledocholithiasis/cholangiolithiasis with cholangitis. The course of cholangitis can be chronic, acute, or fulminant. The classic manifestation of acute cholangitis is Charcot's triad: pain and tenderness upon palpation in the right upper quadrant of the abdomen, hectic fever with chills, and obstructive jaundice; in more severe cases and with a fulminant course, Reynolds' pentad is observed, which includes the addition of hypotension and altered mental status [16]. Pain may be the only symptom or may be entirely absent (especially in elderly patients). Jaundice is noted in 60–70% of cases and fever in 90% of cases [17, 18]. Neutrophilic leukocytosis with a left shift, elevated C-reactive protein levels, increased serum transaminase activity, and laboratory markers of cholestasis are characteristic.
Choledocholithiasis with acute pancreatitis. Acute obstructive pancreatitis, developing due to the migration of a gallstone into the distal common bile duct, is characterized by a severe clinical course and an elevated blood level of conjugated bilirubin. The development of pancreatic pain is often preceded by an attack of biliary colic. Subsequently, spontaneous passage of the stone and improvement in the patient's condition are possible. If the stone does not pass, the severity of the condition and the serum conjugated bilirubin level increase; without surgical intervention, the prognosis is unfavorable.
Mirizzi syndrome. There are no pathognomonic symptoms, and approximately one-third of cases are asymptomatic. The most frequent symptoms include jaundice, right upper quadrant or epigastric pain, hyperthermia, nausea, vomiting, dark urine, and decreased appetite. The duration of symptoms and gallstone disease history, combined with the identification of characteristic anatomical changes using imaging modalities, allows for an intuitive suspicion of Mirizzi syndrome [19, 20].

2. Diagnostics, medical indications and contraindications for diagnostic methods

The main criterion for diagnosing gallstone disease is the detection of gallstones using any instrumental imaging method of the gallbladder and biliary tract.

Regarding the clinical forms of gallstone disease, there is no single diagnostic method; it is necessary to rely on a comprehensive set of clinical, laboratory, and instrumental data [23–28].

Diagnostic criteria

- presence of complaints characteristic of chronic cholecystitis or complications of gallstone disease, a history of gallstone detection, previous attacks of biliary colic and/or acute cholecystitis, and acute biliary pancreatitis;

- detection of symptoms characteristic of chronic cholecystitis, biliary colic, and acute cholecystitis;

- laboratory examination (detection of signs of a complicated course of gallstone disease – markers of inflammation and cholestasis);

- instrumental examination (detection of gallstones, assessment of their location and size, and signs of gallstone disease complications).

2.1 Complaints and Anamnesis

Gallstone disease in the form of gallbladder stones is characterized by the absence of specific complaints. It may be completely asymptomatic or present with dyspeptic complaints reflecting concomitant delayed gastric emptying (a feeling of fullness in the epigastric region, nausea, and in some cases, vomiting after fatty meals) and small intestinal bacterial overgrowth syndrome (bloating). Such complaints should not be regarded as symptoms of gallstone disease itself.

In gallstone disease with chronic cholecystitis, complaints typically include aching pain in the right upper quadrant of the abdomen in response to fatty foods, which often intensifies in the evening and at night. The pain may be accompanied by nausea and radiate to the right shoulder girdle, beneath the right scapula, and to the lower thoracic spine. There is no elevation in body temperature or signs of intoxication. The pain may persist for weeks. A history of previous acute cholecystitis and episodes of biliary colic is frequently reported [27].

Complaints and anamnestic data characteristic of patients with biliary colic, cholecystitis, cholangitis, and acute obstructive pancreatitis are described in subsection 1.6.

2.2 Physical Examination

Gallstone disease in the form of gallbladder stones without cholecystitis is asymptomatic. However, to assess the probability of gallstone disease during patient evaluation, older age, female gender, features of metabolic syndrome, dyslipidemia, type 2 diabetes mellitus, history of pregnancies, rapid weight loss, symptoms of liver disease, inflammatory bowel disease, and hemolytic anemia should be taken into account.

Symptoms identified during the physical examination of patients with complications of gallstone disease – biliary colic, cholecystitis, cholangitis, and acute obstructive pancreatitis – are described in subsection 1.6 [27–31].

All patients with gallstones in the gallbladder without clinical signs of cholecystitis are recommended to have gallstone disease diagnosed based on the detection of gallstones via imaging methods – past and/or present – in order to determine management tactics or dynamic surveillance [27].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Commentary. There is no single diagnostic method for gallstone disease with gallbladder stones and chronic cholecystitis; this diagnosis is recommended to be established taking into account the full range of clinical and laboratory data [25, 26].

It is necessary to take into account the data of:

- medical history (characteristic complaints, previous attacks of acute calculous cholecystitis);

- physical examination (detection of tenderness upon palpation at the gallbladder point in the absence of symptoms of biliary colic and acute cholecystitis);

- instrumental examination (detection of gallbladder wall thickening on ultrasound (US), and tenderness upon transducer pressure at the gallbladder point).

2.3 Laboratory Diagnostics

All patients with suspected acute cholecystitis and other complicated forms of gallstone disease are recommended to undergo a complete (clinical) blood count with determination of leukocyte count and differential leukocyte count (A12.05.119, A12.05.121) to determine the presence of an inflammatory process and its severity [32–34, 279].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Commentary. In acute cholecystitis, the complete (clinical) blood count most frequently reveals neutrophilic leukocytosis with a left shift and an elevated ESR. In elderly patients, leukocytosis is detected in half of the cases. Leukocytosis is also characteristic of the development of cholangitis.

All patients with suspected acute cholecystitis and cholangitis are recommended to determine the serum C-reactive protein level to confirm an acute inflammatory process [25, 28–32].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. In acute cholecystitis and cholangitis, an elevated serum C-reactive protein (CRP) level is detected in the majority of cases, and to a greater extent in elderly patients, which may be explained by the higher incidence of severe disease. An increase in C-reactive protein is also characteristic of the development of cholangitis.

All patients with suspected acute cholecystitis (AC), choledocholithiasis, or cholangitis are recommended to undergo a routine general biochemical blood test determining the activity of alanine aminotransferase and aspartate aminotransferase (ALT and AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), total and conjugated bilirubin levels, and pancreatic amylase activity to confirm the diagnosis [32–34, 279].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

Comment. Routine biochemical blood test parameters are of great importance in diagnosing concomitant acute pancreatitis and choledocholithiasis and in selecting treatment tactics. In the absence of elevated serum AST, ALT, ALP, GGT, and bilirubin activity, and no dilation of the common bile duct (CBD) on ultrasound, the probability of choledocholithiasis is very low. The specificity of a total bilirubin increase up to 4 mg/dL (68 µmol/L) for choledocholithiasis is 75%; however, such an increase in bilirubin is observed in only 2/3 of cases. These patterns are reflected in the choledocholithiasis probability scoring system (Appendix G1). An increase in serum amylase activity may indicate the development of an episode of biliary pancreatitis.

2.4 Instrumental Diagnostics

All patients with a history of characteristic manifestations of gallstone disease (GSD), elderly patients with abdominal pain of unclear origin, and patients with signs of an infectious process of an unspecified primary localization at the pre-hospital/hospital stage are recommended to undergo an ultrasound examination (US) of the abdominal organs with an assessment of the state of the liver, gallbladder, bile ducts, and pancreas (A04.16.001 Ultrasound examination of the abdominal organs (comprehensive)) to rule out GSD and its complications (AC, choledocholithiasis, cholangitis, acute pancreatitis) [23–25].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

Comment. Abdominal ultrasound is the method of choice in the diagnosis of cholecystolithiasis; it is a safe and inexpensive imaging method with a diagnostic accuracy of about 95%, although it depends on the operator's experience. Gallstones appear on ultrasound as echogenic structures with posterior acoustic shadowing that shift with changes in body position (if differentiation from polyps and tumors is necessary, the patient should be examined in various positions: supine, left lateral decubitus, or standing). Ultrasound allows for the assessment of the size and location of stones, the presence of inflammatory changes in the gallbladder wall, and the dilation of the ductal system. Ultrasound also allows for the detection of stones in the CBD, although the sensitivity of this method in diagnosing choledocholithiasis is significantly lower than that for gallbladder stones and substantially depends on the operator's experience [35–37]. The detection of stones in the CBD and its dilation on transabdominal ultrasound are the best predictors of choledocholithiasis, especially with concomitant signs of obstructive jaundice and cholangitis (Appendix G1). In the absence of ultrasound data indicating CBD dilation and the presence of stones within its lumen, and with normal biochemical test results, the probability of choledocholithiasis is very low.

All patients with a history of biliary colic attacks and/or signs of cholecystitis and insufficient diagnostic value of abdominal ultrasound are recommended to undergo magnetic resonance cholangiopancreatography (MRCP) to detect gallstone disease [38–50].

GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)

All patients with a history of biliary colic attacks and/or signs of cholecystitis and insufficient diagnostic value of abdominal ultrasound for detecting gallstone disease, along with MRCP, may be recommended endoscopic ultrasonography (EUS) of the pancreatobiliary zone [46].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. MRCP is highly informative in detecting stones around 5 mm in size; EUS has a higher sensitivity in detecting stones <5 mm and biliary sludge. Both of these methods are highly informative in diagnosing choledocholithiasis and bile duct strictures (sensitivity is 97-98% and 93-95%, respectively) and simultaneously allow for a fairly accurate assessment of the state of the pancreas. Disadvantages compared to transabdominal ultrasound include relative cost, insufficient availability of these studies, the invasive nature of EUS, and contraindications for MRCP in individuals with pacemakers and metal implants.

All patients with suspected AC based on clinical data are recommended to undergo abdominal ultrasound (A04.16.001) as a first-line diagnostic step to confirm the diagnosis [35, 36, 38–42].

GPP CLOE 4Grade of Recommendation C (Level of Evidence – 4).

Comment. Signs of AC according to ultrasound include gallbladder wall thickening ≥ 4 mm, the presence of a double contour, and fluid in the pericholecystic space. Since wall thickening, a double contour, and the presence of pericholecystic fluid can be caused by other reasons (e.g., ascites), the most specific and reliable sign is the sonographic Murphy's sign (marked tenderness upon probe pressure over the gallbladder area during inspiration). The positive predictive value of detecting sonographic Murphy's sign or gallbladder wall thickening in the presence of gallstones for the diagnosis of acute cholecystitis is 92-95% [42].

Patients with an atypical clinical picture of AC, insufficient diagnostic value of abdominal ultrasound, or the impossibility of its performance, as well as for differential diagnosis of the disease and suspected complications, are recommended to undergo computed tomography (CT) of the abdominal organs with intravenous bolus contrast enhancement (if technically feasible) [51–57].

GPP CLOE 4Grade of Recommendation C (Level of Evidence – 4).

Comment. CT makes it possible to detect an enlarged gallbladder, wall thickening, submucosal edema, mucosal thickening with extension of the process to the gallbladder bed tissue, increased density of pericholecystic adipose tissue (as a sign of acute inflammation), the presence of fluid in the pericholecystic space, pericholecystic abscess, and gas within the gallbladder. The sensitivity of CT for detecting complications of AC is significantly higher than that of ultrasound (85% vs 68%). CT and ultrasound are complementary methods for assessing the state of the gallbladder [53–56].

The disadvantages of CT examination include: difficulties in detecting gallstones, difficulties in interpreting gallbladder wall thickening and adjacent fatty tissue, which may not be related to gallbladder disease. One must also take into account that this research method is associated with patient exposure to ionizing radiation and incurs additional financial costs.

Patients with AC in cases of insufficient diagnostic value of abdominal ultrasound and abdominal CT with intravenous bolus contrast enhancement are recommended to undergo magnetic resonance imaging (MRI) of the abdominal organs (if technically feasible) for differential diagnosis and detection of disease complications [52, 278].

Level CLevel 5Level of recommendation evidence C (reliability level of evidence – 5).

Comment. MRI plays a significant role in detecting gallbladder perforation, pericholecystic abscess, and cholecystoenteric fistulas; it has a major advantage over ultrasound and CT because it provides specific information about the causes, degree of inflammation, presence or absence of gallbladder wall necrosis or abscess, and other complications of AC. MRI criteria for acute uncomplicated cholecystitis include 6 criteria: (a) presence of stones in the gallbladder, often localized in its neck or cystic duct; (b) gallbladder wall thickening (greater than 3 mm); (c) gallbladder wall edema; (d) gallbladder enlargement (diameter greater than 40 mm); (e) presence of pericholecystic fluid; (f) presence of fluid around the liver (the so-called "C" sign – a small amount of fluid between the liver and the right diaphragmatic dome or abdominal wall, distinct from pericholecystic fluid). Detection of one or more of these MRI criteria indicates the presence of AC with a sensitivity of 88% and specificity of 89%.

Patients with AC upon detection of choledocholithiasis via abdominal ultrasound or other methods and an elevated total bilirubin level >4 mg/dL (68 µmol/L) are recommended to undergo endoscopic retrograde cholangiopancreatography (ERCP) (A06.14.007 Retrograde cholangiopancreatography) to visualize the ductal system during endoscopic stone extraction from the CBD, endoscopic nasobiliary drainage, or endoscopic stenting [60].

Level CLevel 5Level of recommendation evidence C (reliability level of evidence – 5).

Comment. Taking into account the invasive nature and risk of complications, ERCP should be used only during a planned endoscopic intervention, and not for exclusively diagnostic purposes, although the sensitivity of this method in detecting CBD calculi is high.

All patients with CBD dilation detected during ultrasound, CT, or MRI and laboratory abnormalities (elevated transaminases, ALP, GGT, total bilirubin >4 mg/dL (68 µmol/L)) in the absence of clear visualization of a CBD stone are recommended to undergo MRCP or EUS of the pancreatobiliary zone (A04.14.003 Endosonography of the pancreatobiliary zone) to confirm or rule out choledocholithiasis [215–217].

Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)

Comment. Endoscopic ultrasound (EUS) of the pancreatobiliary zone and MRCP – diagnostic methods allowing highly accurate detection of common bile duct (CBD) stones >5 mm in size. These investigations are indicated in cases of intermediate probability of choledocholithiasis (Appendix G1). A systematic review showed that the sensitivity and specificity of EUS are 95% and 97% respectively, while these figures for MRCP are – 93% and 96%, respectively.

Performance of peroral transpapillary cholangioscopy using an ultra-slim endoscope is recommended for guidance during contact intraductal lithotripsy (laser or electrohydraulic), as well as a diagnostic method when a combination of choledocholithiasis with other biliary duct pathology is suspected (strictures of unclear etiology, tumor biopsy, primary sclerosing cholangitis, etc.) [224–232].

GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)

Comment. The advantages of routine peroral transpapillary cholangioscopy in choledocholithiasis, including for monitoring the effectiveness of lithoextraction compared to ERCP, have not been confirmed by prospective studies [224, 225].

The use of cholangioscopy is justified in contact lithotripsy of large calculi as a navigational technique, as well as for direct visualization of the bile ducts and targeted biopsy when combined biliary pathology is suspected [226–232].

2.5 Other Procedures

Not required.

3. Treatment, including drug and non-drug therapies, diet therapy, and pain management

All patients with asymptomatic cholecystolithiasis are not recommended to receive treatment or special follow-up, except for the cases listed in the "Surgical Treatment" section [62–66].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Comment. No special randomized controlled trials have been conducted to evaluate the superiority of cholecystectomy over conservative therapy or an expectant approach in asymptomatic cholecystolithiasis. The probability of symptom development under an expectant approach is 0.7-2.5% per year, while complications such as acute cholecystitis, acute pancreatitis, obstructive jaundice, and cholangitis develop in 0.1-0.3%. Cholecystectomy does not significantly affect life expectancy, as the risk of surgical intervention in these cases balances the potential benefits.

In complicated gallstone disease—biliary colic, acute cholecystitis, choledocholithiasis with cholangitis, obstructive jaundice, or acute biliary pancreatitis—hospitalization in a surgical department is indicated.

For chronic cholecystitis, treatment may be carried out on an outpatient basis.

3.1. Diet therapy

All patients with gallstone disease are recommended medical nutrition therapy [67].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Even in asymptomatic gallstone disease, foods with a mucosal-irritant effect must be excluded from the diet – canned foods and marinades, alcohol; carbonated drinks, spicy, salty, and smoked foods, vegetables rich in essential oils (radish, black radish, turnip, onion, garlic), and the consumption of chocolate and baked goods should be limited. Long intervals between meals should be avoided. An individualized approach based on tolerance is adopted regarding the intake of fats and egg yolks; a high-fat intake is recommended to be avoided. Among animal fats, butter is preferred as it is the most easily digestible.

In patients with acute cholecystitis or complicated choledocholithiasis, fasting is recommended in the preoperative period and on the day of surgery. In the postoperative period, recommended is early enteral nutrition with a gradual increase in the frequency and volume of fluid and food intake [68].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

3.2. Conservative treatment

In all patients with formed gallstones, oral dissolution therapy (litholysis) using ursodeoxycholic acid** (UDCA**) preparations is not recommended [59, 69–74].

Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)

Comment. A meta-analysis demonstrated the efficacy of UDCA** preparations in dissolving small (<10 mm) non-calcified calculi, which are cholesterol stones in the vast majority of cases, provided that gallbladder contractility is preserved (with UDCA** intake for over 6 months, stones were dissolved in 63% of patients). However, UDCA** treatment has been shown not to reduce the frequency of symptoms and complications of cholelithiasis; furthermore, there is a high risk of stone recurrence (25–64% after 5 years and 49–80% after 10 years). In most cases, recurrent stones are accompanied by clinical manifestations; on average, one-third of patients require cholecystectomy within 3 years. Three months after UDCA** treatment, only 26% of patients were free from colic (vs. 33% in the placebo group).

The incidence of cholelithiasis complications after completing the course of therapy was 2% per year, which is comparable to the population of patients who did not receive UDCA**.

In complicated cholelithiasis, UDCA** treatment cannot be considered an alternative to cholecystectomy indicated for such patients [59, 74].

Extracorporeal shock wave lithotripsy is not recommended for the treatment of patients with cholecystolithiasis [75–80].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Comment. Randomized controlled trials, cohort studies, and systematic reviews have shown that the efficacy of extracorporeal shock wave lithotripsy in treating cholelithiasis is insufficiently high; even with careful patient selection, stone clearance is achieved in approximately half of the cases. Stone recurrence with clinical symptoms occurs, resulting in approximately one-third of patients undergoing cholecystectomy within the next 3 years. The results of studies evaluating the incidence of biliary pain and pancreatitis attacks following this intervention are contradictory.

In all patients with a biliary colic attack in the absence of contraindications, the administration of a non-steroidal anti-inflammatory drug (ATC code M01A non-steroidal anti-inflammatory and antirheumatic products) is recommended until symptom resolution [81–96, 283].

GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)

In all patients with a biliary colic attack, the additional administration of antispasmodics in the absence of contraindications (ATC codes A03A, A03B) is recommended until symptom resolution [81–96].

GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)

Comment. Among antispasmodics (ATC codes A03A, A03B), various rapid-onset drugs may be used, in particular, hyoscine butylbromide (in standard doses orally, intravenously, in suppositories), platifylline** (in standard doses subcutaneously), drotaverine** (in standard doses intramuscularly, intravenously), mebeverine** (orally). The administration of antispasmodics helps relieve pain and likely reduces the risk of acute cholecystitis. The additional administration of a non-steroidal anti-inflammatory drug provides more effective analgesia and, as shown by randomized controlled trials, reduces the risk of acute cholecystitis. Such treatment improves tolerance to early cholecystectomy (performed within the first 24 hours of colic onset). Clinical studies have successfully used diclofenac** (75 mg intramuscularly), ketoprofen** (200 mg intravenously), and indometacin (50 mg in suppositories). When using non-steroidal anti-inflammatory drugs, the risk of renal impairment and other adverse effects must be considered.

In all patients with dyspeptic symptoms associated with cholelithiasis, it is recommended to use antispasmodics (ATC A03E, A05AX, A03AA, A03BB), peripheral dopamine receptor antagonist prokinetics (ATC A03FA), and antifoaming agents (ATC A03AX) [19, 100, 284, 285].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Drugs of these classes can help normalize the motility of the stomach and initial segments of the small intestine and reduce gas formation. It is advisable to use antispasmodics (ATC A03E – Antispasmodics and anticholinergics in combination with other drugs, A05AX – Other drugs for biliary tract therapy, A03AA – Synthetic anticholinergic agents, esters with a tertiary amino group, A03BB – Semisynthetic belladonna alkaloids, quaternary ammonium compounds) with the most selective action on the smooth muscle of the gastrointestinal tract and biliary tract: hymecromone (orally "on demand" 200–400 mg orally for discomfort, or in courses of 200–400 mg 3 times a day half an hour before meals for 14 days), mebeverine** (orally 200 mg 2 times a day in courses of 10–30 days), trimebutine (orally 200 mg 3 times a day in courses of 1 month), hyoscine butylbromide (10–20 mg orally or in suppositories 3 times a day in courses of 10–30 days). When symptoms of delayed gastric emptying predominate, it is advisable to prescribe prokinetics (ATC A03FA Gastrointestinal motility stimulants) – domperidone (10 mg 3 times a day before meals for up to 7 days), itopride (50 mg 3 times a day before meals for 1 month or more). In case of a tendency to flatulence, antifoaming agents (ATC A03AX Other drugs for functional gastrointestinal disorders) can be used – simethicone, guaiazulene in combination with dimethicone (guaiazulene + dimethicone) in standard doses orally, the combination of alverine + simethicone ("on demand" 1 tab. orally for discomfort and bloating, or course treatment 1 tab. 2–3 times a day before meals for 14–30 days).

In patients with acute cholecystitis and complicated forms of choledocholithiasis, parenteral administration of antispasmodics (ATC Papaverine and derivatives) is recommended for pain relief until symptoms resolve or early cholecystectomy is performed [103, 280-281].

GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)

In patients with acute cholecystitis and complicated forms of choledocholithiasis, recommended infusion therapy aimed at correcting metabolic disorders (B05BB Solutions affecting the water-electrolyte balance) [14, 285].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Initial treatment of acute cholecystitis and complicated choledocholithiasis is carried out using infusion therapy (ATC Solutions affecting the water-electrolyte balance), with monitoring of blood pressure, pulse, and urine output rate. It should be taken into account that with conservative treatment of acute cholecystitis, clinical manifestations of the disease subside in approximately 50% of patients, whereas in the rest the disease either progresses or inflammatory symptoms persist for a long time, which delays recovery times.

The full range of therapy for severe forms of acute cholecystitis and complicated choledocholithiasis is best carried out in an intensive care unit (ICU) with monitoring of basic hemodynamic parameters: cardiac output, urine output rate, blood pressure and central venous pressure, body temperature, and other indicators. Crystalloid plasma substitutes (B05BB Solutions affecting the water-electrolyte balance) can be used for infusion therapy.

Control parameters for the effectiveness of treatment in the ICU are: CVP between 8 and 12 mm Hg, mean arterial pressure > 65 mm Hg, venous blood saturation > 70%, urine output rate > 0.5 ml/kg/h. Vasopressors are indicated for persistent hypotension despite adequate infusion therapy.

Treatment is carried out against the background of correction of comorbid conditions, for which specialized specialists are engaged [104, 107–112].

In patients with mild acute cholecystitis (Grade 1 according to TG13/18), the administration of systemic antibacterial drugs is not recommended [28, 113].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Nevertheless, the administration of systemic antibacterial drugs even in mild acute cholecystitis contributes to a more favorable course of the disease [110].

In patients with moderate and severe acute cholecystitis (Grade II-III according to TG13/18), the administration of systemic antibacterial drugs is recommended to prevent the progression of inflammation and the development of complications [104, 110–112, 114–116].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. In patients with acute cholecystitis receiving systemic antibacterial drugs, it is recommended to give preference to drugs with good penetration into the biliary tract [114-117].

In II-III degree severity of the inflammatory process (TG 13/18), it is advisable to prescribe therapy based on a combination of penicillins (J01C, J01D), including combinations with beta-lactamase inhibitors (piperacillin+tazobactam), 3rd or 4th generation cephalosporins (cefepime**, ceftazidime** (possibly in combination with metronidazole**); carbapenems (imipenem+cilastatin**, meropenem**, doripenem); monobactams (aztreonam, possibly in combination with metronidazole**) fluoroquinolones (J01MA) (ciprofloxacin**, levofloxacin**, moxifloxacin** (possibly in combination with metronidazole** J01XD01).

In grades I and II (TG 13/18) of acute cholecystitis severity, antibiotic therapy can be completed within 24 hours after cholecystectomy. In complicated cases, the duration of antibiotic therapy is extended to 4-7 days after the elimination of the source of infection and resolution of bile outflow disorders [113, 155, 218].

If microbiological blood culture reveals gram-positive microorganisms (Enterococcus spp., Streptococcus spp.), the duration of antibiotic therapy after the elimination of the infection focus should be at least 14 days.

In patients with choledocholithiasis complicated by cholangitis, recommended antibacterial therapy to relieve the inflammatory process [155].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Comment. When choosing antibiotics, it is recommended to consider their pharmacokinetics and pharmacodynamics, biliary penetration, renal and hepatic function, local microbiological monitoring data, as well as the presence of allergies and other adverse events. Empirical antibacterial therapy is carried out until the results of bacteriological studies of body fluids and antibiotic susceptibility testing are obtained; after that, the therapy should be adjusted using the de-escalation principle.

The following groups of drugs are indicated as empirical antibacterial therapy:

Penicillin group¹: Piperacillin + Tazobactam (for Grade II and III (TG 13/18), as well as for healthcare-associated infections (HCAIs));
1st–2nd generation cephalosporins: Cefazolin**², Cefoxitin (for Grade I (TG 13/18));
3rd generation cephalosporins: Ceftriaxone** ± Metronidazole**, Cefotaxime** ± Metronidazole** (for Grade I (TG 13/18)), Ceftazidime** ± Metronidazole** (for Grade II and III (TG 13/18), as well as for HCAIs), or Cefoperazone + sulbactam** (for Grade II (TG 13/18));
4th generation cephalosporins: Cefepime** (for Grade III (TG 13/18), as well as for HCAIs);
Carbapenems: Ertapenem** (for Grade I–III (TG 13/18), as well as for HCAIs), Imipenem + cilastatin**, Meropenem**, Doripenem (for Grade III (TG 13/18), as well as for HCAIs);
Monobactams: Aztreonam ± Metronidazole** (for Grade III (TG 13/18), as well as for HCAIs);
Fluoroquinolones³: Ciprofloxacin** ± Metronidazole**, Levofloxacin** ± Metronidazole**, Moxifloxacin** (for Grade I–II (TG 13/18));
Vancomycin** (infection caused by Enterococcus spp. in Grade III (TG 13/18) or HCAIs) [155].

¹Ampicillin-sulbactam is not recommended when resistance rates exceed 20%.

²Local microbiological monitoring data are required for prescription.

³Prescribed when susceptibility is known or in case of allergy to beta-lactam antibiotics.

Antibacterial therapy in patients with septic shock should be initiated within 1 hour of diagnosis; in other cases, within 6 hours of the diagnosis of acute cholangitis [233].

The recommended duration of antibiotic therapy after achieving source control in patients with acute cholangitis is 4–7 days. In verified bacteremia with gram-positive coccal infection, the duration of antibacterial therapy should be at least 2 weeks [155].

3.3. Surgical treatment

All patients with complications of gallstone disease are recommended surgical treatment [118–125].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Comment. The choice of surgical procedure and its timing are determined depending on the nature of the complications.

Following a history of biliary colic, elective cholecystectomy (A16.14.009 Cholecystectomy, A16.14.009.002 Laparoscopic cholecystectomy) is recommended electively or as early as possible after relief of the colic attack, to prevent acute cholecystitis attacks [126–128].

GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)

Comment. The risk of progression from biliary colic to acute cholecystitis (AC) reaches 10%. Furthermore, following an episode of colic, the recurrence rate of colic (20–50%), development of AC, acute obstructive pancreatitis, obstructive jaundice, and cholangitis remains quite high within the first year (0.5–3%). With subsequent episodes of colic, the risk of complicated forms of AC increases. Early laparoscopic cholecystectomy (LC) helps avoid complications that occur during the waiting period for elective cholecystectomy (CE). None of the conservative therapy methods (extracorporeal shock wave lithotripsy, ursodeoxycholic acid [UDCA]**) have a significant impact on reducing the risk of biliary colic and AC.

All patients at risk of gallbladder cancer due to gallstone disease are recommended to undergo elective prophylactic cholecystectomy to prevent this disease [129–140].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Comment. The risk of gallbladder cancer is elevated in the following patient groups: aged over 50 years with stone size ≥3 cm; with a history of gallstone disease >20 years; with hyalinizing cholecystitis, focal or diffuse gallbladder calcification ("porcelain gallbladder"); with polypoid gallbladder lesions ≥8 mm in size; with gallbladder adenomas; in the presence of stones in individuals with a family history of gallbladder cancer (gallbladder cancer in first-degree relatives); with hereditary nonpolyposis colorectal cancer [129–140].

Acute calculous cholecystitis

When determining the surgical strategy for AC, it is advisable to use the AC severity criteria according to the Tokyo Guidelines 2013, which classify AC severity into Grade I, II, and III (Appendix G3) [141].

Patients with acute calculous cholecystitis are recommended to undergo early cholecystectomy (within the first 72 hours from symptom onset), preferably via a laparoscopic approach (A16.14.009.002 Laparoscopic cholecystectomy), as soon as appropriate conditions for surgery are prepared, to prevent potential complications [142–148, 282].

GCR BLoE 1Grade of Recommendation B (Level of Evidence – 1)

Comment. Currently, an active surgical strategy is preferred, where the decision for surgery is made immediately upon diagnosing Grade I and Grade II AC. Patients with AC of young and middle age, without severe comorbid conditions, with a disease duration of no more than 3 days, and with the absence of gross cicatricial-infiltrative changes in the gallbladder neck and extrahepatic bile duct pathology according to ultrasound are recommended to undergo urgent cholecystectomy –[142–148, 282].

In the absence of CE, approximately one-third of patients develop complications and recurrences of AC, which ultimately necessitates CE [142–148, 282].

If surgery is unjustifiably delayed into the first 5–7 days or the second week, an infiltrate in the subhepatic space often develops, involving the altered gallbladder (with phlegmonous or gangrenous inflammation), greater omentum, loops of the small and large intestine, and elements of the hepatoduodenal ligament, which complicates cholecystectomy and increases the risk of intraoperative complications [142–143, 282].

Performing surgery within the first 3 days of disease onset is associated with fewer technical difficulties, a lower risk of intra- and postoperative complications, lower mortality, and reduces the total duration of treatment and rehabilitation [146–150, 282].

Laparoscopic cholecystectomy is the standard intervention for the definitive resolution of cholecystolithiasis.

In 2023, 101.9 thousand patients with AC underwent surgery in the Russian Federation, of whom 1.4 thousand died. The proportion of laparoscopic surgeries for AC in the Russian Federation has increased from 68.4% to 72.6% since 2021. Mortality after open cholecystectomy (OC) was 4.31%, and after LCE it was 0.27% [10]. Numerous studies have shown that LCE carries a low risk of adverse outcomes and has clear advantages over open surgery in many respects: lesser tissue trauma and postoperative pain intensity, lower mortality, shorter hospital stay, earlier recovery of working capacity, and a less noticeable cosmetic defect [142–150].

Early LCE is defined differently across studies. For some authors, early LCE – is an operation performed in patients with symptoms for less than 72 hours, while for others – with symptoms for less than 7 days, but within 4-6 days after diagnosis, which roughly corresponds to 10 days from symptom onset. Most experts believe that early CE should be performed as soon as appropriate conditions for surgical intervention are established [142–148, 282].

If a patient is admitted later than the optimal time frame (72 hours), the feasibility of laparoscopic cholecystectomy is determined by a surgical board.

Patients with acute calculous cholecystitis complicated by gallbladder perforation and diffuse or widespread peritonitis are recommended to undergo emergency surgery (A16.14.009 Cholecystectomy, A16.14.009.002 Laparoscopic cholecystectomy) to save life [102–103, 152–153, 282].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Emergency surgery is performed within the next 2–3 hours from the moment of diagnosing destructive cholecystitis complicated by localized or generalized peritonitis. Preoperative preparation is carried out during this time.

Patients with acute calculous cholecystitis and suppurative cholangitis, especially with a clinical presentation of septic shock, are recommended to undergo intensive preoperative preparation for 6–12 hours with antibacterial therapy, followed by biliary tract decompression [154–155].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

To prevent potential complications, all patients are recommended to undergo laparoscopic cholecystectomy in accordance with the principles of the Critical View of Safety (CVS) [156–157].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. A key safety element of any cholecystectomy technique is the dissection of the gallbladder neck and 1/3 of the body with identification of the cystic duct and cystic artery orifices. Only after ensuring that only two tubular structures—the cystic duct and cystic artery—approach the gallbladder part isolated on all sides and separated from the liver bed, can one proceed to their clipping and transection. During laparoscopic cholecystectomy, this step must be clearly visible on the monitor screen as the critical view of safety. To clarify anatomical relationships, operative cholangiography (A06.14.003) through the cystic duct or gallbladder neck, intraoperative ultrasound, or ICG fluorescence imaging (if technically available) can be used. If difficulties arise during surgery in patients with acute calculous cholecystitis, it is recommended to review the anatomical landmarks, invite a more experienced surgeon, switch to a fundus-first cholecystectomy, or convert to an open procedure.

If a bile duct injury is identified during laparoscopic cholecystectomy in a patient with acute calculous cholecystitis and indications for an open procedure are established, conversion (switching from a laparoscopic to an open laparotomy approach) is recommended to be performed by a surgeon experienced in reconstructive hepatobiliary surgery [156–158].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

If the surgical team lacks experience in reconstructive hepatobiliary surgery in a patient with a bile duct injury, it is recommended to leave a drain in the subhepatic space (laparoscopic abdominal drainage) and refer the patient to a medical facility experienced in managing such injuries [156–158].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

In patients with acute calculous cholecystitis and anatomical variations of the biliary tract or a high risk of cholecystectomy in complex intraoperative situations, it is recommended to perform cholecystostomy (A16.14.006, A16.14.006.001) with possible delayed cholecystectomy or subtotal cholecystectomy (laparoscopic or open – A16.14.009, A16.14.009.001, A16.14.009.002) to safely complete the operation [105–106, 156–157, 159, 282].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. If Mirizzi syndrome is suspected, separation of the gallbladder neck from the common hepatic duct and common bile duct should be avoided. It is recommended to transect the gallbladder neck transversely and inspect its lumen from the inside. In this case, the duct wall defect can be sutured using viable remnants of the gallbladder neck over a T-tube in the common hepatic and common bile ducts. If the duct wall is completely destroyed, it is better to complete the procedure with external drainage of the proximal and distal bile duct stumps [160–161].

For patients with acute calculous cholecystitis at high operative and anesthetic risk due to decompensation of comorbidities (ASA ≥3), age, complications of gallstone disease, or severe inflammatory-infiltrative changes, with severe acute cholecystitis (Grade III), it is recommended to perform staged surgical treatment [141, 219–223, 282].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Comment. Performing urgent cholecystectomy under these conditions is associated with an unjustifiably high risk of intra- and postoperative complications. Conservative management only delays the surgery and leads to pericholecystic complications. In patients with a high operative and anesthetic risk (ASA ≥3) (Appendix G4) and a charlson comorbidity index (CCI ≥6) (Appendix G6) with Grade 1–2 acute cholecystitis, a two-stage treatment approach is possible, utilizing predominantly minimally invasive technologies: a) Stage I – gallbladder decompression or drainage (A16.14.006.002 Ultrasound-guided percutaneous transhepatic cholecystostomy (PTC), cholecystocholangiosostomy); b) Stage II – delayed surgery – laparoscopic cholecystectomy or open cholecystectomy. Such staged surgery is generally performed in the "cooling-off period" after the resolution of inflammatory-infiltrative changes in the gallbladder and adjacent tissues, and after the treatment of comorbid conditions. Delayed cholecystectomy is defined differently by various authors: either as a procedure performed within 7 to 45 days, or as a procedure performed at least 6 weeks after the initial diagnosis. The optimal timing for delayed cholecystectomy after percutaneous transhepatic cholecystostomy remains unresolved.

In patients with acute calculous cholecystitis complicated by obstructive jaundice without signs of peritonitis, urgent endoscopic papillosphincterotomy (EPST) (A16.14.042) and stone extraction from the common bile duct (A16.14.008.001 Endoscopic lithoextraction from the common bile duct) is recommended followed by cholecystectomy, preferably laparoscopic, performed either in a single stage or within the next few days. In selected cases, percutaneous transhepatic cholangiocystostomy (PTCCS) as the first stage, is recommended followed by endoscopic correction of duct pathology and elective laparoscopic cholecystectomy [162–165].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. If technical conditions allow, single-stage procedures can be performed, such as laparoscopic cholecystectomy + EPST with stone extraction via the "rendezvous" technique.

For acute cholecystitis patients presenting with an impacted stone in the major duodenal papilla, suppurative cholangitis, or acute biliary pancreatitis, ERCP and EPST are recommended on an emergency basis.

If simultaneous clearance and adequate decompression of the bile ducts are not feasible, bilioduodenal stenting or nasobiliary drainage is recommended. Cholecystectomy is recommended during the same hospital admission, provided there is adequate decompression of the bile ducts and resolution of cholangitis and acute pancreatitis.

When the clinical presentation is dominated by acute destructive cholecystitis, or when endoscopic restoration of bile flow is impossible or ineffective, a single-stage surgery is recommended: cholecystectomy, choledocholithotomy, and external drainage of the common bile duct (A16.14.020) as indicated [154, 165–167].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Open choledochostomy remains an important step in biliary tract surgery even in the era of endoscopy and laparoscopic surgery, although its use has decreased with the widespread adoption of ERCP and EPST. Nevertheless, there are patients who require open choledocholithotomy and T-tube placement.

Morbidity and mortality rates depend primarily on the presence or absence of acute suppurative cholangitis rather than on the performance of choledochostomy. This procedure remains an important tool in the arsenal of surgeons dealing with biliary surgery. Indications for choledochotomy include: obstructive jaundice at the time of surgery; palpable stones in the ducts; common bile duct diameter greater than 10 mm; presence of acute cholangitis. The intervention may be completed with external biliary diversion via the cystic duct stump or common bile duct drainage. In some cases, under particularly favorable conditions (unchanged duct wall, confidence in complete stone removal, previously performed EPST), it is acceptable to conclude the duct intervention without external drainage.

There is no significant difference in mortality between laparoscopic choledocholithotomy and endoscopic methods of bile duct clearance. There is no significant difference in residual stone rates and failure rates between the laparoscopy groups and the preoperative or intraoperative ERCP groups [166].

Choledocholithiasis / cholangiolithiasis

In patients with intrahepatic gallstones, it is recommended that treatment tactics be formulated by a multidisciplinary team [59, 168–176].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. For asymptomatic intrahepatic bile duct stones, watchful waiting is an option. This tactical approach is justified because the probability of developing clinical manifestations within the next 15 years is relatively low, at around 11%. The most characteristic clinical manifestations are biliary colic, obstructive jaundice, and fever.

When clinical manifestations are present, it is advisable to develop management strategies within a multidisciplinary team of specialists (a gastroenterologist, a surgeon (optimally – specializing in liver and biliary surgery), an endoscopist, a percutaneous biliary intervention specialist) [59, 168–176]. When symptoms appear, a multidisciplinary approach is required to discuss potential endoscopic or percutaneous interventions; combined techniques (such as the "rendezvous" procedure, combining percutaneous and endoscopic interventions); or liver resection in cases of localized strictures and stones or localized parenchymal atrophy. Active intervention reduces the likelihood of recurrent cholangitis and new stone formation.

In cases of diffuse stone distribution, oral or percutaneous transhepatic intraductal cholangioscopy-guided lithotripsy is practiced, which frequently achieves complete stone dissolution, although recurrences are quite common [251].

For the treatment of choledocholithiasis, ultrasound- and fluoroscopy-guided percutaneous transhepatic procedures should be used (hepatic duct drainage, balloon dilation with stone extraction, lithotripsy, stricture dilation) [252].

All patients with choledocholithiasis are recommended to undergo transpapillary endoscopic intervention – EPST and endoscopic extraction of stones from the common bile duct [166, 238-239].

GCR BLoE 1Grade of Recommendation B (Level of Evidence – 1)

Comment. EPST with common bile duct stone extraction has the following advantages over traditional surgical methods: minimally invasive, low complication and mortality rates, adequate decompression of the bile ducts, broad technical capabilities for stone extraction, the possibility of permanent or temporary bile duct stenting to prevent stone impaction, bile diversion into the gastrointestinal lumen, and no need for forced oral return of bile [166, 238-239].

In patients with uncomplicated choledocholithiasis and large common bile duct stones (>1 cm), it is recommended to perform balloon dilation following controlled EPST [60, 240-248], supplemented by mechanical lithotripsy if necessary.

GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)

Comment. According to a systematic review of 9 RCTs, the combination of EPST and large-balloon dilation compared with EPST alone in patients with common bile duct stones >1 cm more frequently achieved complete stone removal with comparable complication rates. Additionally, the groups with supplementary balloon dilation showed a lower need for mechanical lithotripsy [60, 240–248].

For patients with large and complex choledocholithiasis, as a potential alternative or in case of failure of EPST combined with balloon dilation and mechanical lithotripsy, it is recommended to use oral transpapillary cholangioscopy-guided intraductal lithotripsy (A03.14.002) [230, 249-250].

GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)

Comment. The first RCT comparing these treatment options demonstrated a higher rate of complete stone clearance with intraductal laser lithotripsy [249]. The ASGE conducted a meta-analysis and systematic review of 183 cohort studies (13,588 patients), which showed comparable success and complication rates between these approaches [60].

Further studies corroborate findings regarding the higher rate of technical success of intraductal lithotripsy under the guidance of peroral transpapillary cholangioscopy for complex choledocholithiasis, with comparable complication rates and treatment costs. However, these studies are limited by small sample sizes [230, 250].

In patients with concurrent uncomplicated cholecystolithiasis and choledocholithiasis, it is recommended to perform cholecystectomy and common bile duct stone extraction [166, 239, 253–261].

GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)

Commentary. The following treatment modalities for cholecystocholedocholithiasis have been described:

Single-stage

§ Laparoscopic cholecystectomy and choledocholithotomy

§ Laparoscopic cholecystectomy and intraoperative endoscopic sphincterotomy with stone extraction

Two-stage

§ First stage: endoscopic sphincterotomy, stone extraction. Second stage: laparoscopic cholecystectomy

§ First stage: laparoscopic cholecystectomy. Second stage: endoscopic sphincterotomy, stone extraction

Randomized controlled trials and meta-analyses of these strategies have revealed no differences in the rate of successful common bile duct stone extraction, complications, and mortality. Single-stage laparoscopic cholecystectomy and choledocholithotomy are associated with slightly shorter hospital stays [166, 239, 253–261].

When determining the surgical strategy for acute cholangitis, it is advisable to use the Tokyo Guidelines (Tokyo Guidelines 2013/2018) (Appendix G5), according to which the severity of acute cholangitis is classified into Grade I, II, and III [262].

In patients with choledocholithiasis complicated by stone impaction in the major duodenal papilla or acute cholangitis, it is recommended to perform biliary decompression within 24 hours of diagnosis. In other cases, biliary drainage is recommended no later than 72 hours after diagnosis (A16.14.042, A16.14.008.001, A16.14.020.004, A16.14.032.002) [263–265].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Commentary. To date, no randomized controlled trials have investigated the optimal timing of biliary decompression in complicated choledocholithiasis. The authors of a systematic review including 2 prospective and 7 retrospective non-randomized studies concluded that in patients with acute cholangitis, endoscopic retrograde cholangiopancreatography and biliary decompression performed within 48 hours of diagnosis are associated with a twofold reduction in mortality and hospital stay compared to groups in which decompression was performed later [263].

The findings of this review formed the basis of the corresponding ESGE recommendation [264]. The Russian Consensus on Current Issues in the Diagnosis and Treatment of Obstructive Jaundice Syndrome recommends performing biliary decompression within 24 hours of hospitalization in the presence of biliary pancreatitis or cholangitis (100% of experts agreed with this statement), appealing to the TG18 recommendations. In other cases, the consensus recommends deciding on the timing and methods of biliary drainage within no more than 72 hours [234].

TG18 state that for Grade I cholangitis, biliary decompression is recommended if initial therapy fails within 24 hours, while for Grade II and Grade III cholangitis, it is recommended immediately and in parallel with conservative therapy [265].

If single-stage complete endoscopic stone extraction is not feasible in patients with complicated choledocholithiasis, it is recommended to conclude the endoscopic procedure with biliary stenting using a plastic stent (218050 Non-absorbable polymer biliary stent***) or endoscopic nasobiliary drainage [239, 266–268].

GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)

Commentary. The placement of a plastic stent facilitates the gradual reduction of stone size due to the erosion of its surface "soft" fractions and also simplifies the procedure of repeat stone extraction [60, 234, 239, 266–268].

The placement of uncovered metal stents in patients with complicated choledocholithiasis is not recommended [234].

In patients with choledocholithiasis complicated by Grade III cholangitis (TG13) or coagulopathy, it is recommended to perform endoscopic biliary stenting without endoscopic sphincterotomy and stone extraction as the first stage of treatment [264, 269].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

Commentary. Endoscopic sphincterotomy is associated with an increased risk of bleeding compared with endoscopic stenting. In critically ill patients and those with coagulopathy, the development of bleeding can significantly worsen the course of the disease, so biliary decompression in cholangitis should be performed in stages. Endoscopic biliary stenting performed as the first stage aims to relieve cholangitis, while definitive treatment of choledocholithiasis—endoscopic sphincterotomy with stone extraction—is performed as a second stage after the resolution of organ dysfunction and correction of coagulopathy [264, 269].

If retrograde biliary decompression is impossible or unsuccessful in patients with complicated choledocholithiasis, it is recommended to perform percutaneous transhepatic biliary drainage [234, 269-270].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

Commentary. Antegrade methods of biliary decompression in cholangitis demonstrate comparable technical success rates, complication rates, and mortality in comparative studies with retrograde methods, but are associated with longer hospital stays [264].

When analyzing non-comparative studies of endoscopic sphincterotomy and percutaneous transhepatic cholangiography/drainage, the latter approach was associated with a higher number of complications (predominantly hemorrhagic) with comparable mortality. However, in these studies, percutaneous transhepatic cholangiography/drainage was more frequently performed for malignant jaundice [271].

Performing access to the bile ducts under ultrasound guidance helps increase the safety of percutaneous transhepatic cholangiography/drainage [269]. Antegrade access can also be used as an adjunct to facilitate retrograde cannulation of the common bile duct within the rendezvous technique [272].

If endoscopic sphincterotomy or percutaneous transhepatic cholangiography/drainage cannot be performed in a specific hospital and the patient has no severe purulent cholangitis, it is recommended to immediately transfer the patient to a specialized medical facility with the necessary equipment and staff [234, 265].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Commentary. Transabdominal surgical interventions for complicated choledocholithiasis are indicated if minimally invasive interventions and transfer of the patient to a higher-level hospital are not possible [234].

Following the resolution of obstructive jaundice caused by choledocholithiasis in the presence of concomitant cholecystolithiasis, it is recommended to perform cholecystectomy to prevent recurrent choledocholithiasis [273–277].

GCR ALOE 2Grade of Recommendation A (Level of Evidence – 2)

Commentary. Regarding cholecystolithiasis after endoscopic common bile duct stone extraction, a watchful waiting strategy and a prophylactic cholecystectomy strategy have been evaluated. Studies conducted have shown higher mortality in the watchful waiting groups during up to 5 years of follow-up. It has also been demonstrated that prophylactic cholecystectomy reduces the risks of acute cholecystitis, recurrent biliary colic, and recurrent choledocholithiasis (including with cholangitis and obstructive jaundice). The question of the need for prophylactic cholecystectomy in patients with resolved choledocholithiasis but without stones in the gallbladder remains ambiguous [273–277].

The issue of performing cholecystectomy after the resolution of obstructive jaundice caused by choledocholithiasis is decided on an individual basis, either electively after discharge or during the same hospitalization, depending on the specific situation. In difficult cases, the decision is made by a medical board.

4. Medical Rehabilitation and Sanatorium-Resort Treatment

In all patients with chronic calculous cholecystitis, even in remission, it is not recommended to undergo sanatorium-resort treatment with mineral waters [68].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Commentary. Sanatorium-resort treatment for calculous cholecystitis is not recommended because mineral waters generally have a choleretic effect, which can provoke an attack of biliary colic and acute cholecystitis.

Following cholecystectomy, it is recommended to consider referring patients for sanatorium-resort treatment [68].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Commentary. After cholecystectomy, rehabilitation can be carried out in 2-3 weeks in local sanatoriums specializing in the treatment of gastrointestinal diseases, rehabilitation centers, health resorts, as well as at resorts with low- and medium-mineralized waters (sodium bicarbonate, sodium-calcium bicarbonate, sodium chloride bicarbonate, sulfate-calcium-magnesium-sodium, and others, heated to 42-44°C, 30-60 minutes before meals).

Medical rehabilitation for patients after cholecystectomy, primarily for complications of acute cholecystitis and the postoperative course, is recommended to be started as early as possible and carried out concurrently with treatment [177–180].

Leveled of Evidence CLevel of Data Reliability 2Level of evidence C (level of data reliability – 2)

Comment. Rehabilitation is carried out in specialized care departments (stage I), inpatient medical rehabilitation departments (stage II), and in outpatient rehabilitation departments, day hospital rehabilitation departments, or sanatorium rehabilitation departments (stage III).

Upon the development of functional insufficiency after the completion of surgical treatment or conservative therapy (at the end of the first stage of rehabilitation), the patient may be referred for rehabilitation to the second or third stage of rehabilitation in accordance with the assessment of their self-care ability and rehabilitation potential.

Rehabilitation is organized by a multidisciplinary rehabilitation team consisting of a surgeon, exercise therapy physician, medical psychologist, occupational therapist, and physical rehabilitation specialist. At the first stage, the attending physician is a surgeon, and all rehabilitation measures are coordinated with them and with the anesthesiologist-intensivist (if the patient is in the ICU). Other specialists may be involved if necessary.

The most serious rehabilitation problems for patients with severe forms of acute cholecystitis and a complicated postoperative course include:

ICU-acquired syndrome;
Immobilization syndrome, motor deprivation, and sensory deprivation;
Nutritional deficiency;
Cognitive dysfunction;
Pain;
Stress.

A prolonged stay in the ICU or a medical organization for severe acute cholecystitis may lead to motor deficit (loss of the ability to walk), muscle atrophy, pressure ulcers, cachexia, and other problems that can lead not only to functional impairment but also to disability. The actions of the rehabilitation team should be aimed at preventing the negative impact of the hospital environment on the patient's functioning.

There is no data on the superiority of specific physiotherapy methods in acute cholecystitis; physiotherapy may be considered as an alternative and complementary method to basic therapy. Verticalization of the patient should be carried out in accordance with profile guidelines and taking into account surgical contraindications.

Patients with pain syndrome should be provided with pain management measures. In the absence of contraindications, a multimodal analgesic regimen is appropriate (organized jointly with a medical psychologist and an occupational therapist), including opioid analgesics (N02A), non-steroidal anti-inflammatory drugs (M01A), and paracetamol**.

5. Prevention and Dispensary Observation

All individuals with risk factors for cholesterol gallstone formation are recommended to undergo prevention through maintaining adequate physical activity, a balanced diet with a restriction on easily digestible carbohydrates (glucose, sugar, added fructose) [181].

GCR BLEL 3Grade of Recommendation B (Level of Evidence – 3)

Comment. A higher level of physical activity during 5-year follow-up is associated with a reduced risk of gallstone formation with clinical manifestations of gallstone disease. When recommending a physical activity regimen, one should be guided by WHO recommendations and the patient's general health status.

All patients who have undergone bariatric surgery and/or are following a low-calorie diet (≤800 kcal/day) with a low fat content are recommended a temporary prescription of #UDCA** until body weight stabilizes in order to prevent cholesterol gallstone formation [59, 182–184].

GCR BLoE 1Grade of Recommendation B (Level of Evidence – 1)

Comment. According to systematic reviews and meta-analyses, #UDCA** reduced the risk of gallbladder stone formation both during a low-calorie high-fat diet for weight loss and after bariatric surgery (average relative risk 0.33). A dose of #UDCA** of 1000–1500 mg per day has a more pronounced preventive effect compared to a dose of 500-750 mg per day. It is advisable to start #UDCA** intake simultaneously with the transition to a low-calorie diet and in the first days to weeks after bariatric surgery. The duration of UDCA** intake, according to accumulated observations, ranges from 3 to 12 months, depending on the rate of weight loss and at the physician's discretion. The risk of both asymptomatic and clinically manifest cholelithiasis is reduced. Taking UDCA** after sleeve gastrectomy reduces the incidence of cholecystectomy from 7 to 2.3% [147, 182]. Following a low-calorie high-fat diet with UDCA** intake is accompanied by a lower risk of stone formation compared to following a low-calorie low-fat diet [184].

All patients with gallstone disease prior to cholecystectomy should be assigned to dispensary observation group III; during the dispensary check-up stage, risk factors must be corrected and in-depth preventive counseling provided [185]. Regarding the potential reduction in mortality, such patients should be assigned to dispensary group A ("mortality potentially preventable by primary prevention measures") [186]. The frequency of visits by a gallstone disease patient to a physician is determined individually depending on the course of the disease. When symptoms appear, a consultation with a gastroenterologist and a surgeon is indicated to determine the plan for further in-depth examination and indications for cholecystectomy. An indicator of remission is the absence of signs of complications (colic, acute cholecystitis, choledocholithiasis, etc.). Following successful litholytic therapy and in the absence of recurrent colic, a stay in gastrointestinal-profile sanatoriums (e.g., Borjomi, Erino, Monino, Zheleznovodsk, Krainka, Truskavets) is possible. The use of spa and resort factors should be cautious and carried out taking into account individual tolerance.

All patients with gallstone disease who have undergone cholecystectomy belong to dispensary observation group II. In this group, after cholecystectomy and discharge from the hospital, joint follow-up by a general practitioner (therapist) and a surgeon is recommended in the first month after surgery; thereafter, consultations and additional studies are performed as indicated, depending on the course of the postoperative period and the appearance of clinical symptoms.

6. Organization of Medical Care

All patients with suspected acute cholecystitis must be examined by a surgeon;
Diagnosis of biliary colic and acute cholecystitis serves as an indication for urgent hospitalization of patients to a surgical inpatient facility;
If ongoing conservative treatment is ineffective within 24–48 hours, the patient's transfer is indicated from a level I medical organization to a level II medical organization or to an interdistrict surgical department, or where there is the possibility of performing laparoscopic cholecystectomy and transpapillary endoscopic intervention, if necessary;
Patients with moderate or severe acute cholecystitis must be immediately referred to surgical departments of level II or III medical organizations;
Patients with choledocholithiasis complicated by cholangitis and obstructive jaundice must be immediately referred to surgical departments of level II or III medical organizations where transpapillary endoscopic intervention can be performed;
The duration of inpatient treatment for patients with acute cholecystitis is determined by the possibility of relief of the acute attack, performance of cholecystectomy on an urgent or delayed basis, development of complications, and the course of the postoperative period;
In asymptomatic choledocholithiasis, elective treatment in a surgical hospital is indicated;
In chronic calculous cholecystitis, the indications for referring the patient for surgical treatment and the level of the surgical hospital are determined by the surgeon taking into account examination data and concomitant diseases.

7. Additional Information

The outcome of the disease or condition may be influenced by:

Purulent-necrotic and other complications of acute cholecystitis (cholangitis, obstructive jaundice, peritonitis, sepsis, gastrointestinal bleeding, etc.);
Polyvalent allergy;
History of leukemia, oncological diseases, tuberculosis, or positive test results for HIV infection, hepatitis B and C, syphilis;
Pronounced congenital defects confirmed by history and/or physical examination, leading to impaired normal functioning and requiring correction (congenital heart defects, gastrointestinal tract, urogenital system, skeleton; Marfan syndrome, Klinefelter syndrome, Edwards syndrome, Opitz syndrome, Goldenhar syndrome, and others);
Cardiovascular diseases: post-infarction cardiosclerosis, silent myocardial ischemia, pericarditis, aortic aneurysm, grade III hypertension, effort angina, unstable angina, Prinzmetal's angina;
Clinically significant rhythm and conduction disorders (atrial fibrillation/flutter, frequent ventricular extrasystole of bi(tri)geminy type, ventricular tachycardia, complete left bundle branch block, trifascicular block, ventricular fibrillation, sinoatrial block greater than degree I, atrioventricular block degree II–III, Frederique syndrome);
Chronic heart failure stage III–IV according to NYHA;
Chronic cor pulmonale in the decompensation stage;
Bronchial asthma;
Pulmonary embolism;
Acute myocardial infarction;
Acute cerebrovascular accident;
Transient ischemic attack;
Acute pneumonia, pleurisy;
Systemic connective tissue diseases according to medical history — systemic sclerosis, systemic lupus erythematosus, systemic vasculitis, antiphospholipid syndrome, dermatomyositis, sarcoidosis, rheumatic fever, and others;
Type I and type II diabetes mellitus;
Obesity with a body mass index of 40 or more (grade III);
Acute renal failure;
Chronic kidney disease with a glomerular filtration rate of less than 30 mL/min;
Gastric and duodenal ulcer in the acute stage, liver cirrhosis;
Multiple sclerosis and other demyelinating diseases;
Any psychiatric disorders according to medical history;
Hematological diseases according to medical history;
Drug addiction or chronic alcoholism according to medical history;
Pregnancy, lactation period.

Features of the course of cholelithiasis during pregnancy

During pregnancy, the risk of developing biliary colic and acute cholecystitis increases, which is explained by the development of bile stasis in the gallbladder and increased lithogenicity of bile. Biliary sludge and gallbladder stones appear for the first time during pregnancy in 5% of cases. Approximately every fourth pregnant woman with biliary sludge or gallstones develops attacks of biliary colic and/or acute cholecystitis [187]. Moderate increase in physical activity had no positive effect on the risk of stone formation [188]. Indications for cholecystectomy frequently arise within the first year after childbirth. In the presence of asymptomatic cholecystolithiasis, cholecystectomy is recommended before a planned pregnancy, as the risk of a complicated course increases significantly, and the consequences can be fatal for the fetus. With unjustified refusal of surgical treatment, the incidence of colic is very high (92%, 64%, and 44% in the first, second, and third trimesters, respectively), as well as the development of acute pancreatitis and cholangitis. In the asymptomatic course of gallstone disease during pregnancy, special therapeutic measures are not required; the prescription of UDCA** preparations for the prevention of formation or dissolution of gallstones during pregnancy is contraindicated.

All pregnant patients with gallstone disease in the presence of urgent indications for cholecystectomy are recommended to undergo this surgery regardless of the trimester of pregnancy [189–196].

Level CLevel 3Level of recommendation evidence C (reliability level of evidence – 3).

Comment. Urgent cholecystectomy is not contraindicated during pregnancy and ranks second in frequency among non-obstetric surgical interventions in pregnant women. Urgent cholecystectomy in pregnant women is not associated with an increased rate of preterm labor or a negative impact on fetal health.

In pregnancies up to 20 weeks, laparoscopic cholecystectomy is optimal; at later stages, cholecystectomy should be performed via mini-access or an open approach to prevent life-threatening complications [190–194].

All pregnant patients with gallstone disease and clinically manifest choledocholithiasis are recommended to undergo endoscopic papillary sphincterotomy with stone extraction during ERCP (A16.14.042, A16.14.008.001). Depending on anatomical features, size, and number of common bile duct stones, the surgeon may decide to supplement the procedure with endoscopic balloon dilation of the sphincter of Oddi [195–199].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Pregnancy is an independent risk factor for acute pancreatitis. ERCP and endoscopic lithoextraction should be performed by experienced specialists to minimize radiation exposure, the risk of pancreatitis, electrical trauma to the uterus, and other complications. Special measures are required to reduce the X-ray dose.

If pregnant women have choledocholithiasis complicated by obstructive jaundice in late pregnancy, percutaneous transhepatic cholangiography (PTC) can be used as an alternative to EST to resolve the jaundice, along with balloon dilation of the sphincter of Oddi to remove stones from the bile ducts.

To avoid high radiation exposure during ERCP, ultrasound-guided PTC can be performed to resolve jaundice.

Features of the course of cholecystitis in patients over 65 years of age and in those with diabetes mellitus

In elderly patients and those with diabetes mellitus, the prevalence of gallstone disease increases significantly; severe acute cholecystitis and gallbladder gangrene develop more frequently. Diagnosis becomes more challenging due to age-related changes in pain perception and alterations in the inflammatory response [6, 27, 200, 201]. Pain may lack typical features or be completely absent in every 8th patient, while vomiting and fever (usually not exceeding 38 °C) are observed in less than half of the cases. Murphy's sign is elicited in less than half of patients; the frequency of abdominal muscle guarding and peritoneal irritation signs is lower. Leukocytosis is observed in about half of the cases, although it can reach higher values than in younger patients, as can C-reactive protein levels, which may be explained by the more frequent development of severe forms of the disease [202-207]. Diagnostic principles are the same as in the general population. At the first stage of additional examination—comprehensive abdominal ultrasound—classic signs of acute cholecystitis are detected in only half of the cases. The diagnostic accuracy of CT and MRI in the elderly is insufficiently studied.

In complicated gallstone disease, cholecystectomy is the preferred treatment method; advanced age per se is not a contraindication for surgery, but individual operative and anesthetic risks must be taken into account. Performing cholecystectomy is quite safe even at 75–80 years of age, although the rate of conversion to open cholecystectomy, complication rates, and hospital stay duration are somewhat higher [204, 205]. With concomitant choledocholithiasis, EST is more effective than conservative therapy [206]. Performing cholecystectomy during the current hospitalization has a more favorable effect on long-term prognosis than conservative treatment—even after adjusting for comorbidities [206, 207]. Cholecystectomy can also be performed when other complications of gallstone disease develop (acute pancreatitis, obstructive jaundice) as soon as the general condition is stabilized [206, 207].

Features of the course of cholecystitis in liver cirrhosis.

In Child-Pugh class A and B liver cirrhosis, laparoscopic cholecystectomy is preferred, carrying a lower risk of complications than open cholecystectomy [208]. In Child-Pugh class C liver cirrhosis, the complication rate of cholecystectomy (both laparoscopic and open) is higher, as is the rate of conversion to open cholecystectomy [209, 210]. In severe liver damage and severe cholecystitis, endoscopic cholecystoduodenal stenting may be performed [211].

Criteria for Evaluating the Quality of Medical Care

№	Quality criteria	Performance assessment (yes/no)
Diagnostic stage
1.	A general (clinical) blood test with differential leukocyte count was performed.	yes/no
2.	A general therapeutic blood chemistry panel was performed, assessing ALT, AST, ALP, GGT, total and direct bilirubin, and pancreatic amylase activity.	yes/no
3.	An abdominal ultrasound evaluating the liver, gallbladder, bile ducts, and pancreas was performed at the pre-hospital or in-hospital stage.	yes/no
5.	The diagnosis of gallstone disease and its complications was established using instrumental methods.	yes/no
Treatment stage
6	Spasmolytics (ATC Papaverine and its derivatives) were prescribed parenterally to patients with acute cholecystitis.	yes/no
7	Infusion therapy was prescribed to patients with acute cholecystitis and complicated forms of choledocholithiasis.	yes/no
8	Systemic antibacterial therapy was administered for moderate and severe acute cholecystitis.	yes/no
9	Antibacterial therapy was administered for acute cholangitis.	yes/no
10	Early cholecystectomy, preferably via a laparoscopic approach, was performed for acute calculous cholecystitis.	yes/no
11	Emergency surgery was performed upon diagnosing acute cholecystitis complicated by perforation and diffuse or generalized peritonitis.	yes/no
12	Staged surgical treatment was performed in patients with acute cholecystitis who have a high operative and anesthetic risk due to decompensation of comorbidities (ASA ≥3), advanced age, gallstone disease complications, or pronounced inflammatory-infiltrative changes, in severe acute cholecystitis (Grade III).	yes/no
13	EST with endoscopic lithoextraction from the common bile duct was performed for choledocholithiasis.	yes/no
14	Bile duct decompression was performed within 24 hours of diagnosing choledocholithiasis complicated by impaction of a stone in the major duodenal papilla or by acute cholangitis.	yes/no
15	Endoscopic stenting of the common bile duct or nasobiliary drainage was performed when one-stage complete endoscopic lithoextraction was impossible in patients with complicated choledocholithiasis.	yes/no
16	Percutaneous transhepatic cholangiographic drainage was performed when retrograde biliary decompression was impossible or unsuccessful in patients with complicated choledocholithiasis.	yes/no

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Appendix A1. Working Group Composition

Revishvili A.Sh., Academician of the RAS, Professor (Moscow)

Ivashkin V.T., Academician of the RAS, Professor (Moscow)

Gulyaev A.A., MD, Professor (Moscow)

Zharkova M.S., PhD (Moscow)

Korolev M.P., MD, Professor (Saint Petersburg)

Lapina T.L., PhD, Associate Professor (Moscow)

Okhlobystin A.V., PhD, Associate Professor (Moscow)

Sheptulin A.A., MD (Moscow)

Shirokova E.N., MD (Moscow)

Shulpekova Yu.O., PhD (Moscow)

Yartsev P.A., MD (Moscow)

Anischenko M.A., PhD (Moscow)

Bronstein G.P., surgeon (Moscow)

Vetshev P.S., MD, Professor (Moscow)

Vetsheva N.N., MD (Moscow)

Emelyanov S.I., Corr. Member of the RAS, Professor (Moscow)

Kaminsky M.N., PhD (Khabarovsk)

Kriger A.G., MD, Professor (Moscow)

Mamoshin A.V., MD (Moscow)

Natroshvili A.G., MD (Moscow)

Natroshvili I.G., MD (Kislovodsk)

Olovyanny V.E., MD (Moscow)

Pribytkova O.V., PhD (Chelyabinsk).

Prudkov M.I., MD, Professor (Yekaterinburg)

Sazhin A.V., Corr. Member of the RAS, Professor (Moscow)

Fedorov E.D., MD, Professor (Moscow)

Shulutko A.M., MD, Professor (Moscow)

Appendix A2. Methodology for Developing Clinical Guidelines

The purpose of these guidelines is to provide practitioners with modern concepts of the etiology and pathogenesis of cholelithiasis, and to introduce current algorithms for its diagnosis and treatment.

Target audience of these clinical guidelines:

1. Surgeons

2. Endoscopists

3. Gastroenterologists

4. General practitioners (family physicians)

5. General practitioners

6. Diagnostic imaging specialists

Table 1. Level of Evidence (LoE) grading scale for diagnostic methods (diagnostic interventions)

LoE	Definition
1	Systematic reviews of studies with reference-standard control or systematic reviews of randomized controlled trials with meta-analysis.
2	Individual studies with reference-standard control or individual randomized controlled trials and systematic reviews of studies of any design, except randomized controlled trials, with meta-analysis.
3	Studies without sequential reference-standard control, or studies with a reference standard not independent of the evaluated method, or non-randomized comparative studies, including cohort studies.
4	Non-comparative studies, case reports.
5	Only mechanism of action rationale or expert opinion is available.

Table 2. Levels of evidence with indication of the classification used for levels of evidence (LE).

LoE	Definition
1	Systematic review of randomized clinical trials with meta-analysis.
2	Individual randomized clinical trials and systematic reviews of studies of any design, except for randomized clinical trials, with meta-analysis.
3	Non-randomized comparative studies, including cohort studies.
4	Non-comparative studies, case reports, case series, or case-control studies.
5	Only justification of the intervention mechanism of action (preclinical studies) or expert opinion is available.

Table 3. Grades of recommendation (GR) with indication of the classification used for grades of recommendation.

GoR	Definition
A	Strong recommendation (all considered efficacy criteria (outcomes) are important, all studies are of high or moderate methodological quality, and their conclusions on the outcomes of interest are consistent).
C	Conditional recommendation (not all considered efficacy criteria (outcomes) are important, not all studies are of high or moderate methodological quality, and/or their conclusions on the outcomes of interest are inconsistent).
C	Weak recommendation (lack of adequate quality evidence (all considered efficacy criteria (outcomes) are unimportant, all studies are of low methodological quality, and their conclusions on the outcomes of interest are inconsistent).

Procedure for updating clinical guidelines

The mechanism for updating clinical guidelines provides for their systematic revision at least once every three years, as well as upon the emergence of new evidence-based medicine data on the diagnosis, treatment, prevention, and rehabilitation of specific diseases, or in the presence of justified additions/comments to previously approved clinical guidelines, but no more frequently than once every 6 months.

Appendix A3. Reference Materials

These clinical guidelines have been developed taking into account the following regulatory and legal documents:

Order of the Ministry of Health and Social Development of the Russian Federation dated June 2, 2010 No. 415n "On approval of the Procedure for providing medical care to the population for gastroenterological diseases"
Order of the Ministry of Health of the Russian Federation dated May 10, 2017 No. 203n "On approval of criteria for assessing the quality of medical care."
Order of the Ministry of Health and Social Development of the Russian Federation dated July 2, 2007 No. 461 "On approval of the standard of medical care for patients with cholelithiasis (for specialized care)"

Factors predisposing to biliary sludge and gallstone formation.

Cholesterol stones
Factors	Mechanisms
1. Demographic/genetic factors: higher prevalence in Northern Europe and North America compared to Asia; familial predisposition, predisposition in type IIa, IIb, III, and IV dyslipidemia.	Hereditary traits of enzymes controlling the synthesis and transport of bile components (mutations in ABCG8, ABCG5, ABCB4, ABCB11, ApoB100 and ApoE4, CYP7A1, mucin, Lith13, and HMG-CoA reductase genes). In most cases, the disease has a polygenic origin.
2. Metabolic factors: diet high in fat and simple carbohydrates; obesity, metabolic syndrome, diabetes mellitus.	↑ formation and secretion of cholesterol into bile; ↓ gallbladder motility;
3. Weight loss during 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 bile acids.
4. Female sex, estrogen therapy	Estrogens stimulate hepatic lipoprotein receptors, ↑ cholesterol uptake from the intestine and its secretion into bile; ↓ conversion of cholesterol to its esters; ↓ bile acid secretion.
5. Impaired gallbladder emptying: prolonged total parenteral nutrition; prolonged fasting, low-fat diet; spinal cord injuries, autonomic neuropathy; pregnancy; medication effects (octreotide**); bariatric surgery (in the absence of preventative cholecystectomy).	Bile stasis creates conditions for cholesterol nucleation.
6. Fibrate therapy.	↑ secretion of cholesterol into bile.
7. Bile acid metabolism disorders: chronic liver diseases; terminal ileum disease.	↓ bile acid secretion; ↑ deoxycholic acid pool.
Pigment stones
Demographic/genetic factors (residence in rural areas, in Asian countries); Chronic hemolysis; Liver cirrhosis (most commonly alcoholic); Cystic fibrosis; Chronic bacterial and parasitic cholangitis; Diseases/resection of the ileum, intestinal bypass anastomoses; Gilbert's benign hyperbilirubinemia.	↑ secretion of mucins, immunoglobulins. Deconjugation of bilirubin in bile under the influence of bacterial ß-glucuronidase (E. coli) and parasites (Ascaris lumbricoides, Opisthorchis felineus) Deconjugation of bilirubin in bile under the influence of cholangiocyte ß-glucuronidase (especially when the gallbladder epithelial function of maintaining bile pH is impaired). ↑ absorption of deconjugated bilirubin in the colon. Hydrolysis of bile phospholipids to lysolecithin and fatty acids, which participate in the formation of the stone matrix.
Ceftriaxone crystallization in bile**

Appendix B. Physician Action Algorithms

Diagnosis of acute cholecystitis.

Appendix B. Algorithms of physician actions — Cholelithiasis

Appendix C. Patient Information

Appendix B1. General Information

The main cause of acute inflammation of the gallbladder (acute cholecystitis) is cholelithiasis. In this case, a gallstone blocks the outflow of bile from the gallbladder, causing a spasm of the muscle fibers of the gallbladder wall coupled with inflammation. Precipitating factors for stone impaction include eating fatty, fried foods, eating after a long interval, and body jarring. In rarer cases, acute cholecystitis occurs in the absence of gallstones, but against the background of another severe disease or an intestinal infection. Signs of acute cholecystitis include pain in the right upper quadrant and epigastric region radiating to the right scapula, at the level of the lower thoracic vertebrae, to the right half of the neck, and fever; nausea and vomiting are also frequently observed. The development of acute cholecystitis may be preceded by a sudden attack of biliary colic with similar pain localization, frequently occurring at night.

Every patient diagnosed with cholelithiasis should follow dietary rules restricting fatty foods to prevent the development of biliary colic and cholecystitis, avoid long intervals between meals, and be aware of their main clinical symptoms. If signs suggesting biliary colic and acute cholecystitis occur, a physician must be called. For a correct diagnosis, analyzing clinical symptoms alone is insufficient; it is necessary to perform blood tests, an ultrasound examination of the abdominal cavity, and sometimes more complex diagnostic procedures. If confirmed, the patient must remain under the observation of a surgeon in a surgical hospital. In the acute phase of the process (the first 1-2 days), a strict sparing diet is recommended, and subsequently, as the condition improves, the diet is expanded. Antispasmodics, anti-inflammatory drugs, and antibiotics are used to treat acute cholecystitis. If no improvement occurs, surgical treatment is required (typically, removal of the gallbladder). Even upon complete resolution of inflammation, "in the cold period," cholecystectomy is indicated due to the high risk of recurrence. Chronic cholecystitis may develop as a consequence of incomplete resolution of inflammation following an episode of acute cholecystitis; its symptoms are insufficiently defined, and mild aching pain in the right upper quadrant, worsening after fatty food consumption, may be present.

Appendix B2. Postoperative Period Recommendations

After surgery, the patient should adhere to relatively simple and feasible restrictions for 1–2 months. They are quite simple to follow, especially considering that ignoring them is fraught with rather unpleasant and undesirable consequences.

Diet

After surgery for cholecystitis, food at home should be pureed and porridge-like. Milk and milk kissels, liquid porridges (preferably on water), chicken and vegetable broth, and vegetable purees are allowed. Dietary nutrition is prescribed to the patient for the first 2–3 months after surgery. The diet affects the composition of the intestinal microflora and the activity of its functions. It is necessary to follow these principles:

Fractional and frequent meals; single-moment consumption of large food portions is contraindicated;

Food should not be hot or cold, but only slightly warmed;

A balanced diet providing the body with a full range of nutrients, vitamins, and minerals, since immune stimulation and strengthening are required during the recovery period;

Exclusion of foods that promote fermentation and gas formation in the digestive tract; the diet should not contain legumes, heavy animal fats, any varieties of cabbage, smoked foods, marinades, and pickles, and the consumption of alcoholic and carbonated beverages is not recommended.

During the first two weeks, the following are excluded from the diet:

smoked, salted, fatty, fried, and spicy dishes;

sausages;

spices, mayonnaise, ketchup;

bakery products;

alcohol (until complete recovery).

The patient is strongly advised to monitor their weight. Since physical activity is significantly reduced in the postoperative period, it is easy to gain excess weight, which is highly undesirable. To restore normal microflora, dairy and fermented milk products and abundant fluid intake are beneficial for the body. Meat and fish should not be consumed in the first weeks after surgery, but broths and pureed meat/fish minced dishes are acceptable. It is better to give up bread and bakery products; an excellent alternative can be crispbreads with a minimum of fiber and carbohydrates.

Vegetables (carrots, beets) and bananas are well tolerated by the body, whereas citrus fruits are best avoided. At the same time, for immune support, the body needs vitamin C, which can be obtained from other foods or taken in tablet form, along with other vitamins and multivitamin-mineral complexes. The end of the diet should not be abrupt. It is recommended to gradually expand the diet. By no means should one abruptly relapse into previously excluded foods. In general, the postoperative diet is not strict, so it will be useful to follow the habits already established over several months thereafter. This will only benefit the organism.

Physical activity after cholecystitis surgery

Over the following 6 weeks, muscle fusion occurs, against which the risk of adhesions and hernias remains. Lifting heavy objects and vigorous physical exertion are strictly prohibited. At the same time, it is noted that daily slow-paced walking of 2–3 kilometers in the afternoon helps prevent adhesions. Therapeutic exercises are prescribed. Notably, the best recovery of muscle tissue occurs in those individuals who previously led an active lifestyle and kept their bodies toned. After a few months, one can return to moderate loads, gradually supplementing therapeutic exercises with general exercises.

take short walks on foot;

after the formation of the postoperative scar, visit the swimming pool and perform simple physical exercises;

for those who lead an active lifestyle, as well as overweight patients, wear a special abdominal binder.

Appendix G. Assessment Scales, Questionnaires, and Other Evaluation Tools

Appendix G1. Risk Stratification for Choledocholithiasis

Source: Ansaloni L, Pisano M, Coccolini F, et al. 2016 WSES guidelines on acute calculous cholecystitis. World J Emerg Surg 2016;11:25, DOI 10.1186/s13017-016-0082-5.

Type: rating scale

Purpose: determination of choledocholithiasis risk category

Predictors
Very high risk	Detection of common bile duct stone on ultrasound
Very high risk	Serum total bilirubin >4 mg/dL
High risk	Common bile duct diameter >6 mm (with intact gallbladder)
High risk	Serum total bilirubin 1.8–4 mg/dL
Moderate	Abnormalities in other liver function tests (other than bilirubin)
	Age >55 years
	Clinical signs of biliary pancreatitis

Key:

Risk stratification class for choledocholithiasis
High	Presence of any very strong predictor
Low	All predictors absent
Intermediate	All other cases

Appendix G2. Diagnostic criteria for acute cholecystitis (TG18/TG13 diagnostic criteria for acute cholecystitis)

Source: Okamoto K., Suzuki K., Takada T. Tokyo Guidelines 2018: flowchart for the management of acute cholecystitis J Hepatobiliary Pancreat Sci (2018) 25:55-72 https://doi.org/10.1002/jhbp.516

Type: rating scale

Purpose: diagnosis of acute cholecystitis

Section A	Criteria
Local signs of inflammation	Murphy's sign
Local signs of inflammation	Mass in the right upper abdominal quadrant, pain, or tenderness
Section B
Systemic signs of inflammation	Fever
	Elevated C-reactive protein level
	Leukocytosis
Section C
Imaging findings	Characteristic signs of acute cholecystitis*

*for example, presence of pericholecystic fluid, enlarged gallbladder, thickened walls, double-contour walls, gallstones/sludge in the lumen

Key (interpretation): Probable AC diagnosis: ≥1 item in section A + ≥1 item in sections B or C. Definite AC diagnosis: ≥1 item in sections A, B, and C

Appendix G3. Severity grading criteria for acute cholecystitis (TG18/TG13 severity grading for acute cholecystitis)

Source: Okamoto K., Suzuki K., Takada T. Tokyo Guidelines 2018: flowchart for the management of acute cholecystitis J Hepatobiliary Pancreat Sci (2018) 25:55-72 https://doi.org/10.1002/jhbp.516

Type: rating scale

Purpose: To determine the severity of acute cholecystitis

Grade I – mild cholecystitis
Criteria for severe cholecystitis and signs of organ dysfunction listed below are absent. Mild inflammatory changes of the gallbladder are noted.
Grade II – moderate cholecystitis (presence of ≥1 of the following):
Leukocytosis >18 × 10⁹ /L
Palpable tender mass in the right upper quadrant
Duration of symptoms >72 h
Marked local inflammation and complications (gangrenous cholecystitis, pericholecystic abscess, liver abscess, biliary peritonitis, emphysematous cholecystitis)
Grade III – severe cholecystitis (presence of ≥1 of the following):
Cardiovascular dysfunction: hypotension requiring dopamine infusion ≥5 mcg/kg/min or norepinephrine at any dose
Neurological dysfunction: depressed level of consciousness
Respiratory dysfunction: PaO₂/FiO ratio <300
Renal dysfunction: oliguria or serum creatinine >2.0 mg/dL
Hepatic dysfunction: PT-INR >1.5
Hematological dysfunction: thrombocytopenia <100 × 10⁹/L

Key:

Grade 1: Criteria for Grade II and III and signs of organ dysfunction are absent. Mild inflammatory changes of the gallbladder are observed

Grade 2: presence of ≥1 sign of Grade II

Grade 3: presence of ≥1 sign of Grade III

Appendix G4. American Society of Anesthesiologists Physical Status Classification System (ASA physical status classification system)

Source: https://www.asahq.org/standards-and-practice-parameters/statement-on-asa-physical-status-classification-system

Type: index

Purpose: To determine the physical status of patients

Classification	Definition	Examples
ASA I	A normal healthy patient	Healthy, non-smoking, minimal alcohol use.
ASA II	A patient with mild systemic disease	Patients with mild systemic disease without significant functional limitations. Examples include, but are not limited to: smoker, social alcohol drinker, pregnant, obesity (<30 BMI <40), well-controlled diabetes mellitus, controlled arterial hypertension, mild pulmonary disease.
ASA III	Patient with severe systemic disease	Patients with moderate or severe systemic disease that results in substantial functional limitations. Examples include, but are not limited to: poorly controlled arterial hypertension or suboptimally controlled diabetes mellitus, COPD, morbid obesity (BMI ≥40), active hepatitis, alcohol dependence or abuse, implanted pacemaker, moderate reduction of left ventricular ejection fraction, end-stage renal disease undergoing regularly scheduled dialysis. History (>3 months) of myocardial infarction, stroke, transient ischemic attack, coronary artery disease, or stenting.
ASA IV	Patient with severe systemic disease that is a constant threat to life	Examples include (but are not limited to): myocardial infarction, stroke, transient ischemic attack, coronary artery disease or stenting, ongoing myocardial ischemia or severe heart valve dysfunction, sharp decrease in ejection fraction, sepsis, disseminated intravascular coagulation (DIC), acute or chronic renal failure with irregular hemodialysis.
ASA V	Moribund patient who is not expected to survive without the operation	Examples include (but are not limited to): ruptured aortic aneurysm, severe polytrauma, intracranial hemorrhage, acute intestinal ischemia with concomitant severe cardiac pathology or multiple organ failure.
ASA VI	Declared brain-dead patient whose organs are being removed for donor purposes.
The addition of modifier "E" denotes emergency surgery. An emergency is defined as existing when delay in treatment of the patient would lead to a significant increase in the threat to life or body part. Examples include: ASA I E, II E, III E, or IV E. ASA class V is generally always ASA V E. ASA class VI E does not exist.

Key (interpretation): ASA I – normal healthy patient; ASA II – patient with mild systemic disease; ASA III – patient with severe systemic disease; ASA IV – patient with severe systemic disease that is a constant threat to life; and ASA V – moribund patient not expected to survive without the operation. An additional sixth class, ASA VI, is assigned to brain-dead patients whose organs are being removed for donor purposes.

Appendix G5. Severity assessment criteria for acute cholangitis (TG18/TG13 severity assessment criteria for acute cholangitis)

Source: Kiriyama S, Kozaka K, Takada T, et al. Tokyo Guidelines 2018: diagnostic criteria and severity grading of acute cholangitis (with videos). J Hepatobiliary Pancreat Sci. 2018;25(1):17-30. doi:10.1002/jhbp.512

Type: rating scale

Purpose: To determine the severity of acute cholecystitis

Grade I – mild cholecystitis
Does not meet the criteria for Grade II or III acute cholangitis listed below
Grade II – moderate acute cholangitis (presence of ≥2 of the following):
Blood leukocyte count >12 × 10⁹/L or <4 × 10⁹/L
Fever ≥39^◦C
Age ≥75 years
Hyperbilirubinemia ≥5 mg/dL
Hypoalbuminemia (<0.7 × lower limit of normal)
Grade III – severe cholecystitis (presence of ≥1 of the following):
Cardiovascular dysfunction: hypotension requiring dopamine infusion ≥5 mcg/kg/min or norepinephrine at any dose
Neurological dysfunction: depressed level of consciousness
Respiratory dysfunction: PaO₂/FiO <300
Renal dysfunction: oliguria or serum creatinine >2.0 mg/dL
Hepatic dysfunction: PT-INR >1.5
Hematological dysfunction: thrombocytopenia <100 × 10⁹/L

Key:

Grade 1: Criteria for Grade II and III are absent

Grade 2: presence of ≥2 signs of Grade II

Grade 3: presence of ≥1 sign of Grade III

Appendix G6. Charlson Comorbidity Index

Charlson Comorbidity Index, CCI

Source: Charlson ME, Pompei P, Ales KL, MacKenzie CR: A New Method of Classifying Prognostic Comorbidity in Longitudinal Studies: Development and Validation. Journal of Chronic Diseases 40:373-383, 1987

Type: Index

Purpose: To determine the physical status of patients

Key: summation of points for each item + 1 point for each decade of age starting at 50 years (maximum 4 points).

10-year survival calculation = 0.983^ (e ^{CCI × 0.9}), where CCI = Charlson Comorbidity Index

Parameter	Definition	Score
Myocardial infarction	History of definite or probable MI (ECG changes and/or enzyme changes)	1
Congestive heart failure		1
Peripheral artery disease	Intermittent claudication or previous bypass surgery for chronic arterial insufficiency, history of gangrene or acute arterial insufficiency, untreated thoracic or abdominal aneurysm (≥6 cm)	1
Cerebrovascular disease	History of stroke with minor or no residuals and transient ischemic attacks	1
Dementia		1
Chronic pulmonary disease		1
Connective tissue disease		1
Peptic ulcer disease	Any treatment for peptic ulcer disease or history of ulcer bleeding	1
Mild liver disease	Mild = chronic hepatitis (or cirrhosis without portal hypertension)	1
Diabetes mellitus without end-organ damage		1
Hemiplegia		2
Moderate or severe renal disease	Severe = on dialysis, post-kidney transplant, uremia, moderate = creatinine >3 mg/dL (0.27 mmol/L)	2
Diabetes with end-organ damage		2
Solid tumor without metastasis		2
Leukemia		2
Lymphoma		2
Moderate or severe liver disease	Severe = cirrhosis and portal hypertension with history of variceal bleeding, moderate = cirrhosis and portal hypertension without history of variceal bleeding	3
Metastatic solid tumor		6
AIDS		6

Scales and calculators from this guideline

Charlson Comorbidity Index (CCI)Cumulative severity of comorbid conditions and prognosis Dopamine calculatorCalculation of dopamine infusion rate (mcg/kg/min → ml/h) with automatic Child-Pugh scoreAssessment of liver cirrhosis severity and prognosis Norepinephrine calculatorCalculation of norepinephrine infusion rate in ml/h based on dose in mcg/kg/min, weight NYHA functional classClassification of chronic heart failure severity ASA (physical status before surgery)ASA classification of anesthetic risk

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