Acute pancreatitis: clinical guidelines

List of Abbreviations

BP – blood pressure

MBF – major duodenal papilla

SPP – suppurative-necrotic parapancreatitis

PC – purulent complications

GI – gastrointestinal tract

RF – respiratory failure

Du – duodenum

CSG – clinical-statistical group

CT – computed tomography

APFC/ANC – acute peripancreatic/necrotic collections

IMV – invasive mechanical ventilation

MRI – magnetic resonance imaging

OF – organ failure

AP – acute pancreatitis

ICU – intensive care unit

PA – pancreatic abscess

P – pancreas

PI – peripancreatic infiltrate

PP – pancreatic pseudocyst

ERCP – endoscopic retrograde cholangiopancreatography

ESR – erythrocyte sedimentation rate

CRP – C-reactive protein

SIRS – systemic inflammatory response syndrome

SIRS – systemic inflammatory response syndrome

US – ultrasound examination

UV – ultraviolet irradiation

EGD – esophagogastroduodenoscopy

EST – endoscopic retrograde papillosphincterotomy with lithoextraction

ACS – abdominal compartment syndrome

IAP – intra-abdominal pressure

SOFA – Sequential Organ Failure Assessment

Terms and Definitions

Interstitial oedematous pancreatitis – characterized by diffuse (or sometimes local) enlargement of the pancreas due to inflammatory edema.

Necrotizing pancreatitis (pancreatic necrosis) – diffuse or focal areas of non-viable pancreatic parenchyma, which are typically combined with necrosis of retroperitoneal adipose tissue.

Sterile pancreatic necrosis – pancreatic necrosis that does not contain pathogenic microflora and is not accompanied by the development of purulent complications.

Acute peripancreatic fluid collection – an acute peripancreatic collection of fluid without signs of necrosis of the pancreatic parenchyma and retroperitoneal adipose tissue in the first 4 weeks of the disease, lacking a well-defined wall.

Acute necrotic collection – a collection containing variable amounts of both fluid and necrotic tissue in the pancreatic parenchyma and/or retroperitoneal adipose tissue within the first 4 weeks of the disease, lacking a well-defined wall.

An acute peripancreatic fluid collection («acute peripancreatic fluid collection», «acute necrotic collection») is an exudative-proliferative inflammatory process in the pancreas and surrounding tissues, accompanied by an acute collection of fluid (with or without pancreatic necrosis) located within or near the pancreas and lacking a wall of granulation or fibrous tissue. It occurs in phase IB of acute pancreatitis and has the following outcomes: complete resolution and resorption (usually by the 4th week of the disease), formation of a pancreatic pseudocyst, and development of purulent complications.

A pancreatic pseudocyst («acute pseudocyst», PP) is a collection of fluid (with or without sequestra) bounded by fibrous or granulation tissue, occurring after an attack of acute pancreatitis. It develops after 4 weeks from the onset of the disease, in the phase of aseptic sequestration of necrotizing pancreatitis. As a rule, it is the outcome of an infiltrate. The cyst contents can be aseptic and infected. Bacterial contamination of the cyst contents is often clinically silent, but the probability of its infection is always higher in the presence of sequestra.

Walled-off necrosis («walled-off necrosis») is a mature, encapsulated collection of pancreatic and/or peripancreatic necrosis with the development of a well-defined inflammatory capsule that occurs later than 4 weeks from the onset of the disease.

Infected pancreatic necrosis («infected pancreatic necrosis», purulent-necrotic parapancreatitis) is bacterially contaminated necrosis of the pancreatic tissue and retroperitoneal adipose tissue with their purulent melting and sequestration. It is determined by the presence of at least one of the following signs: gas bubbles in the zone of pancreatic necrosis detected by computed tomography; a positive bacteriological result of peritoneal fluid for aerobic and facultatively anaerobic opportunistic microorganisms in an aspirate obtained by fine-needle aspiration; a positive bacteriological result of peritoneal fluid for aerobic and facultatively anaerobic opportunistic microorganisms in discharge obtained during a sanitation surgery.

Organ failure («organ failure») is an impairment of organ function requiring medical intervention to maintain homeostasis.

Multiple organ failure («multiple organ failure») is a progressive failure (dysfunction) of two or more systems in critically ill patients, making it impossible to maintain homeostasis without medical intervention and having a high probability of a fatal outcome.

Persistent organ failure («persistent organ failure») is the failure of a single organ system for 48 hours or more.

Transient organ failure («transient organ failure») is the failure of a single organ system for less than 48 hours. [1-8].

1. Brief information on the disease or condition

1.1 Definition of the disease or condition

Acute pancreatitis (AP) is an aseptic inflammation of a demarcation type, based on necrosis of pancreatic acinar cells and enzymatic aggression with subsequent expanding necrosis and dystrophy of the gland, in which damage to surrounding tissues and distant organs, as well as systems, and the addition of a secondary purulent infection are possible.

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

The following etiological forms of acute pancreatitis are distinguished:

• Acute alcoholic-alimentary pancreatitis – 55%.

• Acute biliary pancreatitis (occurs due to bile reflux into the pancreatic ducts with biliary hypertension, which arises, as a rule, due to cholelithiasis, sometimes from other causes: diverticulum, papillitis, opisthorchiasis, etc.) – 35%.

• Acute traumatic pancreatitis (due to pancreatic trauma, including surgical or post-ERCP) 2–4%.

• Other etiological causes: autoimmune processes, vascular insufficiency, vasculitis, drugs (**hydrochlorothiazide, systemic hormonal agents, **mercaptopurine), infectious diseases (mumps, hepatitis, cytomegalovirus), allergic factors (varnishes, paints, building material odors, anaphylactic shock), dyshormonal processes during pregnancy and menopause, diseases of adjacent organs (gastroduodenitis, penetrating ulcer, tumors of the hepatopancreatoduodenal region) – 6–8%.

In children, the causes of acute pancreatitis are most often the following factors:

• Congenital anomalies, such as choledochal cyst and pancreatobiliary junction malformations.

• Periampullary obstruction: cholelithiasis, pancreas divisum, tumors.

• Pancreatic trauma.

• Metabolic disorders: type I, IV, and V hyperlipoproteinemia, alpha-1 antitrypsin deficiency, hypercalcemia, diabetes mellitus.

• Genetic predisposition associated with CFTR and PRSS1 gene mutations.

• Drugs (L-asparaginase, glucocorticoids, valproic acid, azathioprine, etc.).

• Infections: mumps, measles, Epstein-Barr virus infections, etc.

• Systemic diseases: Reye's syndrome, cystic fibrosis, chronic intestinal pseudo-obstruction, sepsis, multiple organ failure.

• In some cases, the etiological factor cannot be established (so-called idiopathic pancreatitis).

The leading role in the pathogenesis of toxemia in acute pancreatitis belongs to pancreatic enzymes: trypsin, lipase, phospholipase A2, lysosomal enzymes, which cause oxidative stress, lipid distress syndrome, capillary thrombosis, hypoxia, acidosis, hypermetabolism, cell membrane and endothelial damage.

Primary aggression factors:

• pancreatic enzymes: trypsin, chymotrypsin – cause proteolysis of tissue proteins;

• phospholipase A2 destroys cell membranes;

• lipase hydrolyzes intracellular triglycerides to fatty acids and, combining with calcium, leads to lipolytic necrosis in the pancreas, retroperitoneal tissue, and the mesentery of the small and large intestine;

• elastase destroys the vascular wall and interstitial connective tissue structures, leading to necrosis.

Secondary aggression factors. Pancreatic enzymes activate the kallikrein-kinin system with the formation of biologically active substances: bradykinin, histamine, serotonin, which lead to increased vascular permeability, microcirculatory disorders, edema, increased exudation and microthrombosis, ischemia, hypoxia, and tissue acidosis.

Tertiary factors. Macrophages, mononuclear cells, neutrophils against the background of microcirculatory disorders, systemic inflammatory response, hypoxia produce cytokines (interleukin 1, 6, and 8, tumor necrosis factor, platelet-activating factor, prostaglandins, thromboxane, leukotrienes, nitric oxide), which contributes to the suppression of immune status. Fourth-order aggression factors. Cytokines, enzymes, metabolites of various nature formed in the pancreas, adipose tissue, intestinal wall, and abdominal cavity increase the permeability of the intestinal wall, intestinal flora translocation occurs, and they facilitate the entry of toxins into the portal and systemic circulation and the lymphatic system, damaging target organs: the liver, lungs, kidneys, heart, brain, intestines, and the mucosa of the stomach and intestines [2,3,5,6].

Aggression factors and organ dysfunctions create a "mutual aggravation" syndrome.

Phases of acute pancreatitis. Edematous (interstitial) pancreatitis accounts for 80–85% of the disease structure. It is characterized by a mild severity of the disease and rare development of local complications or systemic disorders, and has no phase course.

Necrotizing pancreatitis occurs in 15–20% of AP patients, clinically always manifests with moderate or severe disease, and has a phase course with two peaks of mortality – early and late. The early phase, which usually lasts during the first two weeks, is followed by a second or late phase, which can drag on for a period from weeks to months. It is advisable to consider these two phases separately, since each phase corresponds to a specific clinical form and, consequently, a specific therapeutic and diagnostic algorithm.

Phase I – early, in turn, is subdivided into two periods:

- IA phase, as a rule, is the first week of the disease. This period is characterized by the formation of necrosis foci of varying volume in the pancreatic parenchyma or surrounding tissue, and the development of endotoxemia. Endotoxemia manifests as mild or profound systemic disorders in the form of single or multiple organ failure. The maximum period for the formation of necrosis in the pancreas is usually three days; after this period, it does not progress further. However, in severe pancreatitis, the period of its formation is much shorter (usually 24–36 hours). An accumulation of enzymatic effusion occurs in the abdominal cavity (enzymatic peritonitis and parapancreatitis), which is one of the sources of endotoxemia. Moderate severity of the disease manifests as transient dysfunction of individual organs or systems. In severe forms of the disease, the clinical picture may be dominated by symptoms of organ (multiple organ) failure: cardiovascular, respiratory, renal, hepatic, etc.

- IB phase, as a rule, is the second week of the disease. It is characterized by the body's reaction to the formed foci of necrosis (both in the pancreas and in the parapancreatic tissue). Clinically, symptoms of resorptive fever prevail, and a peripancreatic infiltrate is formed.

Phase II is the late, sequestration phase (usually starting from the 3rd week of the disease and lasting for several months). Sequestra in the pancreas and retroperitoneal tissue usually begin to form from the 14th day of the disease onset. When large fragments of necrotic pancreatic tissue detach, depressurization of its duct system and the formation of an internal pancreatic fistula can occur. The configuration of pancreatic necrosis (localization, depth, relation to the main pancreatic duct, etc.) and the volume of the remaining viable pancreatic parenchyma determine: the number, scale, and rate of spread of fluid collections in the retroperitoneal space, as well as the risk of infection and other complications. Two variants of the course of this phase are possible:

• aseptic sequestration — sterile pancreatic necrosis is characterized by the formation of an isolated fluid collection in the area of the pancreas and post-necrotic pancreatic pseudocysts;

• septic sequestration occurs when necrosis of the pancreatic parenchyma and parapancreatic tissue becomes infected, with the further development of purulent complications. The clinical form of this phase of the disease is infected pancreatic necrosis (purulent-necrotic parapancreatitis). With the progression of purulent complications, infected pancreatic necrosis can have its own complications (purulent-necrotic tracts, retroperitoneal and abdominal abscesses, purulent peritonitis, erosive and gastrointestinal bleeding, digestive fistulas, sepsis, etc.) with the development of endotoxemia of infectious origin and organ (multiple organ) failure [2,10–14].

1.3 Epidemiology of the Disease or Condition

In the Russian Federation, according to official statistics (Federal Statistical Observation Form No. 14), 169,091 patients with acute pancreatitis (K85) were discharged after inpatient treatment in 2023, which is 8.9% higher than the previous year's figure. A total of 5,809 patients died in the hospital (3.3% of the total number of treated patients). Inpatient mortality in the previous three years was 4.26%, 4.04%, and 3.50%, respectively.

The postoperative mortality rate (19.30%) remained at the level of the previous three years, as did the surgical activity rate (9.59%) [9].

1.4 Features of Coding the Disease or Condition

Acute pancreatitis (K85):

K85.0 — Acute idiopathic pancreatitis;

K85.1 — Acute biliary pancreatitis;

K85.2 — Acute alcoholic pancreatitis;

K85.3 — Acute drug-induced pancreatitis;

K85.8 — Other acute pancreatitis;

K85.9 — Acute pancreatitis, unspecified

1.5 Classification of the disease or condition

The classification of acute pancreatitis by the Russian Society of Surgeons (2014) was developed taking into account the Atlanta-92 classification and its modifications proposed in Kochi in 2011 (International Association of Pancreatology) and the Acute Pancreatitis Classification Working Group in 2012.

Mild acute pancreatitis. Pancreatic necrosis does not form in this form of acute pancreatitis (edematous pancreatitis), and organ failure does not develop.

Moderately severe acute pancreatitis. Characterized by the presence of at least one of the local manifestations of the disease: acute peripancreatic fluid collection, acute necrotic collection, peripancreatic infiltrate, pancreatic pseudocyst, walled-off necrosis, and/or the development of general manifestations in the form of transient organ failure (no more than 48 hours).

Severe acute pancreatitis. Characterized by the presence of infected pancreatic necrosis (purulent-necrotic parapancreatitis) and/or the development of persistent organ failure (more than 48 hours).

The diagnosis of mild, moderately severe, or severe acute pancreatitis is established based on a completed case of the disease [1,2,5–8,12,14,16–19,20–22].

1.6 Clinical presentation of the disease or condition

Clinical manifestations of acute pancreatitis depend on the morphological form, phase of the disease, severity of the systemic inflammatory response syndrome, and the development of organ (multiple organ) failure. Each phase of the disease corresponds to a specific clinical and morphological form of acute pancreatitis, so it is advisable to consider the diagnostics and treatment of acute pancreatitis within the respective phases of the disease (see 1.2 Etiology and Pathogenesis).

2. Diagnostics, medical indications and contraindications for diagnostic methods

Diagnostic criteria

The diagnosis of acute pancreatitis is established based on the following data:

— clinical data (intense, unremitting girdle pain, indomitable vomiting, abdominal distension; history of alcohol consumption, spicy food, or presence of cholelithiasis);

— laboratory data (hyperamylasemia or hyperlipasemia exceeding the upper limit of normal by three times or more);

— instrumental data (characteristic ultrasound signs: enlargement, decreased echogenicity, blurred contours of the pancreas; presence of free fluid in the abdominal cavity).

2.1 Complaints and Anamnesis

• For preliminary diagnosis of acute pancreatitis, it is recommended to determine the triad of symptoms identified during the initial patient examination: severe epigastric pain radiating to the back or of a girdle character, repeated vomiting, and muscle defense in the upper half of the abdomen [2,5,10,15,23].

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

Commentary. Most often, the appearance of symptoms is preceded by a heavy meal or alcohol intake, or the presence of cholelithiasis. Typical pain is always present in acute pancreatitis. Usually, it is intense, persistent, and not relieved by antispasmodics and analgesics. The onset of acute pancreatitis should be determined by the time of appearance of abdominal pain, rather than the time of the patient's admission to the hospital.

2.2 Physical Examination

Patients with acute pancreatitis are generally restless. In the early stages of the disease, body temperature is subfebrile; as the process progresses, hectic fever may be observed. Tachycardia is noted. Blood pressure levels are within normal limits at the beginning of the disease, with a subsequent tendency toward hypotension. On physical examination: the abdomen participates in respiration, distended; skin and mucous membranes are mostly pale, jaundice and scleral icterus, cyanosis of the face and extremities may be observed (purple spots on the face — Mondor's sign, cyanotic spots on the flanks — Grey Turner's sign, periumbilical cyanosis — Cullen's sign). In the late stages of the disease, cyanosis may be replaced by bright hyperemia of the skin, especially the face. These signs are based on rapidly progressive hemodynamic and microcirculatory disorders. The tongue is dry and coated. Palpation reveals pain in the epigastric region, rarely combined with tension of the anterior abdominal wall muscles and Shchetkin-Blumberg sign; Voskresensky's sign (absence of abdominal aorta pulsation due to pancreatic enlargement and retroperitoneal edema), Mayo-Robson sign (pronounced tenderness upon palpation of the lumbar region, especially the left costovertebral angle), Korte's sign (transverse painful resistance of the anterior abdominal wall in the projection of the pancreas). Percussion reveals: pronounced tympanitis due to paresis of the transverse colon; dullness in dependent areas of the abdomen in the presence of effusion in the abdominal cavity. Auscultation reveals weakened or absent bowel sounds as a manifestation of dynamic intestinal obstruction [2,10,15,24].

2.3 Laboratory Diagnostics

• All patients with suspected AP are recommended to undergo the following laboratory tests: complete blood count and urinalysis, general clinical blood biochemistry with determination of total protein, total bilirubin and its fractions (determination of free and bound bilirubin levels in the blood), determination of aspartate aminotransferase, alanine aminotransferase, and amylase activity in the blood, and determination of blood urea, creatinine, and glucose levels [5, 10, 15, 24 – 28].

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

• In moderate/severe AP, recommended laboratory tests include: a coagulogram (exploratory hemostasis assay) determining the international normalized ratio (INR), prothrombin time (PT) in blood or plasma, activated partial thromboplastin time (APTT), serum C-reactive protein (CRP) assay, and serum lipase activity determination to assess vital functions [5, 10, 15, 24 – 28]. In children, due to the rapid development of water-electrolyte disturbances, it is additionally recommended to determine acid-base balance parameters and major electrolytes (blood sodium, potassium, and chloride levels) to assess homeostasis systems [1, 2, 3, 93 – 95].

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

2.4 Instrumental Diagnostics

• All patients with suspected AP are recommended to undergo abdominal ultrasound (US) for diagnostic purposes [12, 14, 16 – 19, 29 – 31].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. Characteristic ultrasound features of AP include: enlargement, decreased echogenicity, and blurred contours of the pancreas; presence of fluid in the omental bursa and free fluid in the abdominal cavity. In addition to the above features, an ultrasound criterion for AP in children is dilation of the Wirsung duct. A pancreatic duct diameter greater than 1.5 mm in children aged 1 to 6 years, greater than 1.9 mm at ages 7 to 12, or greater than 2.2 mm at ages 13 to 18 is typically associated with AP [1, 95, 96].

• All patients with suspected AP are recommended to undergo computed tomography (CT) or magnetic resonance imaging (MRI) of the abdominal cavity with intravenous bolus contrast enhancement (in the absence of contraindications) early on (24–96 hours from disease onset) if the diagnosis is unclear or for differential diagnosis with other conditions, when it is necessary to confirm severity based on clinical prognostic signs of severe AP, or if conservative treatment fails [14].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. Morphological manifestations of pancreatic necrosis are usually detected via imaging methods at later stages; therefore, routine early CT and MRI for all patients with AP is unjustified.

When evaluating CT in patients with severe pancreatitis, it is advisable to consider the configuration of pancreatic necrosis and the extent of parapancreatitis. Necrosis configuration refers to the mutual arrangement of deep transverse necrosis and viable pancreatic parenchyma. Deep transverse necrosis (greater than 50% in the sagittal plane) with viable pancreas located distal to the necrosis (configuration type 1) indicates a high probability of pancreatic duct injury and the development of extensive parapancreatitis. The absence of viable parenchyma distal to deep transverse necrosis (configuration type 2) allows for a more favorable prognosis.

To predict necrosis and its configuration on days 1–2 of the disease, perfusion CT may be performed where available.

MRI should be performed when a patient has contraindications to CT, such as contrast agent intolerance or renal failure. The morphological imaging features of acute pancreatitis on CT and MRI are similar. Diagnostic MRI is advisable in patients with biliary pancreatitis who present with elevated liver enzymes while the common bile duct is either inadequately visualized or considered normal on ultrasound, provided technical capabilities exist. The advent of endoscopic ultrasonography (EUS) has significantly expanded the options for identifying the etiology of AP. MRI and EUS can serve as alternatives to ERCP when choledocholithiasis is suspected in patients with biliary pancreatitis [12, 14, 16 – 19, 32 – 39].

• All patients with AP are recommended to undergo abdominal CT/MRI with intravenous bolus contrast enhancement (in the absence of contraindications) to determine the localization of pathological foci when planning surgical intervention, no later than 12 hours prior to the procedure [14, 29, 40].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

• All patients with AP are recommended to undergo subsequent abdominal CT/MRI scans with intravenous bolus contrast enhancement (in the absence of contraindications) in case of disease progression, lack of treatment response, and to refine the localization of suppurative foci prior to drainage procedures, at a frequency of at least every 7–10 days [11, 14, 29, 40 – 42].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. The use of Balthazar's CT severity index for pancreatitis in clinical practice is not a mandatory diagnostic test. It is preferably used to predict disease severity.

2.4.1 Features of diagnosing acute pancreatitis in phase IA of the disease

• To establish a diagnosis of acute pancreatitis (after ruling out other surgical conditions), it is recommended to use a combination of at least two of the following findings: typical clinical presentation, characteristic ultrasound features, and hyperenzymemia [4, 11, 14, 24].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. Hyperenzymemia refers to hyperamylasemia or hyperlipasemia exceeding the upper limit of normal by three times or more.

• To assess organ and multiple-organ dysfunction in patients with AP, it is recommended to use the SOFA scale (see Appendix G2) [6, 7, 14, 43 – 45].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. Early identification of severe pancreatitis is paramount, as treatment outcomes largely depend on how early therapy is initiated. To assess the severity of AP and predict disease progression, it is advisable to use the 2006 rapid initial severity scoring scale for acute pancreatitis by the St. Petersburg I.I. Dzhanelidze Research Institute of Emergency Medicine (see Appendix G1). The presence of at least two criteria listed in the rapid assessment scale indicates moderately severe (severe) AP, which requires mandatory transfer to the ICU. Other patients (mild AP) are indicated for admission to the surgical department or the inpatient emergency department.

2.4.2 Features of diagnosing acute pancreatitis in phase IB of the disease

• Patients in phase IB of AP are recommended to undergo diagnosis and monitoring of peripancreatic infiltration via abdominal and retroperitoneal CT/MRI with intravenous bolus contrast enhancement (in the absence of contraindications) to determine the dynamics of the inflammatory process (the outcome of phase IB) [11, 14, 29, 40 – 42].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. The second week of the disease is characterized by the onset of an aseptic inflammatory response to foci of necrosis in the pancreas and surrounding adipose tissue, clinically manifested by an infiltrate in the epigastric region (local component) and resorptive fever (systemic inflammatory component). Peripancreatic infiltrate (PI) and resorptive fever are regular signs of severe or moderately severe pancreatitis, whereas they are absent in mild pancreatitis. Laboratory markers of systemic inflammatory response syndrome (SIRS) include leukocytosis with a left shift, lymphopenia, elevated ESR, increased concentrations of fibrinogen, CRP, etc. Ultrasound signs of PI include persistent pancreatic enlargement, blurred contours, and fluid accumulation in the parapancreatic adipose tissue. Monitoring PI requires serial assessments of clinical and laboratory parameters along with repeat ultrasound scans (at least twice during the second week of the disease).

At the end of the second week of the disease, it is advisable to perform a CT (MRI) scan of the pancreatic region. By this time, the vast majority of patients exhibit one of three possible outcomes of phase IB:

- Resolution, characterized by a reduction in local and systemic manifestations of the acute inflammatory reaction.

- Aseptic sequestration of pancreatic necrosis with a potential subsequent outcome into walled-off pancreatic necrosis (WOPN): persistence of PI dimensions while general well-being normalizes and systemic inflammatory response syndrome (SIRS) subsides against the background of persistent hyperamylasemia.

- Septic sequestration (development of purulent complications).

2.4.3 Diagnostic features of pancreatic pseudocyst in phase II of the disease (phase of aseptic sequestration)

• In patients with AP who develop a post-necrotic pancreatic pseudocyst, abdominal ultrasound (cyst monitoring) is recommended every 2–4 weeks to timely detect potential complications and monitor its size [46].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. The clinical form of acute pancreatitis in the phase of aseptic sequestration is a post-necrotic pancreatic pseudocyst, with a formation period ranging from 4 weeks up to 6 months on average. In the absence of complications (infection, bleeding into the cyst cavity, cyst perforation with rupture into the free abdominal cavity leading to peritonitis, compression of adjacent organs leading to obstructive jaundice, gastric stenosis, intestinal obstruction, etc.), the patient can be discharged for outpatient treatment. The size of the cyst must be monitored via ultrasound (every 2–4 weeks). If aseptic sequestration does not involve the opening of the pancreatic duct system, cyst formation does not occur. In this case, resorption of the peripancreatic infiltrate (reduction of fluid collection in the pancreatic region) is typically observed within up to 4 weeks. During this period, the patient requires dynamic medical supervision (outpatient setting is acceptable).

2.4.4 Diagnostic features of purulent complications of acute pancreatitis in phase II of the disease (phase of septic sequestration)

Infection of the pancreatogenic destruction focus occurs, on average, by the end of the 2nd to the beginning of the 3rd week from the onset of the disease. However, in cases of late presentation, inadequate treatment, or excessively early and hasty surgery, infection of pancreatic necrosis zones and purulent-destructive complications may develop earlier, bypassing the period of aseptic destruction ("phase crossover"). The clinical form of acute pancreatitis in the septic sequestration phase (third week from disease onset and later) is infected pancreatic necrosis. An important aspect is the timely diagnosis of infection and verification of the clinical and morphological forms of pancreatogenic infection. The clinical and laboratory manifestations of a purulent focus imply the progression of clinical and laboratory indicators of acute inflammation in the third week of AP and the detection of acute inflammation markers (fibrinogen elevation by 2 times or more, high CRP, procalcitonin, etc.). Diagnostic imaging methods (CT, MRI, ultrasound) reveal: an increase in fluid collections during observation, devitalized tissues, and/or the presence of gas bubbles.

• When patients in phase II of AP show no signs of infection according to diagnostic imaging and pancreatic puncture followed by bacteriological examination, further treatment strategy is recommended to be determined by a medical concilium consisting of a surgeon/pediatric surgeon and an anesthesiologist-intensivist based on laboratory and clinical data (progression of organ dysfunction) and instrumental examination methods [2,11,24,46,47].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

• Following fine-needle aspiration or debridement surgery in patients with AP in the septic sequestration phase, bacteriological examination of peritoneal fluid for aerobic and facultatively anaerobic opportunistic microorganisms is recommended in order to select appropriate antibacterial therapy [3,12,14,47].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

2.5 Other Procedures

Other diagnostic examinations are not required.

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

Since each phase of the disease corresponds to a specific clinical and morphological form of AP, it is most appropriate to consider the treatment strategy for AP within the corresponding disease phases.

3.1. Conservative management

Early (I) phase

Treatment protocols for acute pancreatitis in phase IA

• Conservative therapy is recommended as the optimal treatment modality for AP in phase IA [2–4,10,11,14,25,48–50].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. Therapy should be tailored based on the form of AP (mild, moderately severe, severe). All patients with a confirmed diagnosis of mild AP must be hospitalized in a surgical department or short-stay beds of the emergency department. The therapeutic and diagnostic management for patients with moderately severe/severe AP must be carried out in an ICU; after the resolution of organ failure and stabilization of the condition (relief of delirium, hemodynamic and respiratory disorders, etc.), transfer of patients to a surgical department is possible.

• To treat functional gastrointestinal disorders and provide detoxification, a basic treatment complex is recommended for all patients with mild AP [2,11,15,47,51].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. The basic complex includes: fasting for 24 hours, medications to treat functional gastrointestinal disorders, infusion therapy (sodium chloride** 0.9% solution) in volumes according to the instructions for use for 24–48 hours, antisecretory therapy (proton pump inhibitors) (prescribed to treat existing, typically comorbid conditions—acute esophagitis, acute gastroduodenitis, acute gastric ulcer, duodenal ulcer). If there is no response to the ongoing basic therapy within 6 hours and at least one additional sign from the rapid assessment scale (see Appendix G1) is present, moderately severe (severe) pancreatitis should be diagnosed, and the patient transferred to the ICU.

• In all patients with mild and moderately severe AP, after the relief of pain syndrome and gastric dyspepsia (nausea, vomiting), as well as hyperfermentemia (serum amylase less than 3 upper limits of normal), a gentle natural diet with mechanical and chemical sparing is recommended [101,102].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. To ensure maximum mechanical and chemical sparing of the exocrine function of the pancreas and to increase the biological value of the diet, the prescription of balanced ready-to-use enteral nutrition formulas via sipping is recommended (oral intake of liquid nutrient mixtures through a straw or in very small sips, slowly, 100–200 ml per hour).

• When patients with AP develop signs of organ dysfunction or failure, continuous monitoring of vital functions in the ICU is recommended [4,12,43–45].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. High-volume infusion therapy, the need for timely diagnosis and correction of gas exchange disorders and other organ dysfunctions in moderately severe/severe pancreatitis, and the high probability of complications necessitate the hospitalization of patients in the intensive care unit (ICU). The heterogeneity of ICU capabilities and equipment complicates the establishment of a standardized approach to the scope of monitoring. Universal markers that could be used to determine disease severity are currently lacking. To assess the severity of the patient's condition, it is advisable to use the SOFA (Sequential Organ Failure Assessment) scale (Appendix G2). Its application is a mandatory criterion enabling the medical organization upon completion of patient care to recoup expenses incurred during treatment using the CSG st04.006 "Pancreatitis with organ dysfunction syndrome". The use of the SOFA scale does not exclude the application of other scales to determine disease severity, the patient's condition, and the choice of management algorithm.

• Early infusion therapy (solutions affecting water-electrolyte balance – sodium chloride** 0.9% solution, Potassium chloride + Calcium chloride + Magnesium chloride + Sodium acetate + Sodium chloride + Malic acid**, meglumine sodium succinate**) is recommended for all patients in phase I of AP with a moderately severe and severe course to eliminate dehydration and provide detoxification [14,57–61].

GPP CLOE 5Grade of Recommendation C (Level of Evidence - 5)

Comment. It is hypothesized that a preventive microcirculation support strategy using volume infusion therapy is one of the factors reducing mortality from acute pancreatitis by preventing the development of pancreatic necrosis. However, data on the required infusion volume for the prevention of necrotic complications are contradictory. The volume and rate of infusion during the first 12–24 hours are adjusted based on the need to restore hemodynamics and diuresis. The estimated initial volume of fluid loading is 30–40 ml/kg of body weight, but it can be adjusted depending on age, the presence of cardiovascular and/or renal dysfunction, and the severity of initial dehydration. Hematocrit, lactate (lactic acid), urea, and creatinine levels can be considered as laboratory markers of volemia and adequate tissue perfusion; therefore, it is advisable to monitor them dynamically. Randomized trials have not shown a significant advantage of Potassium chloride + Calcium chloride + Sodium chloride** compared to 0.9% sodium chloride solution**. However, it should be borne in mind that the infusion of large volumes of these solutions carries the risk of developing hyperchloremic acidosis, which may exacerbate renal dysfunction. It is advisable to monitor and, if necessary, correct blood potassium and chloride levels. The benefits of goal-directed fluid therapy in acute pancreatitis (reducing heart rate below 120 bpm, achieving a mean arterial pressure of 65–85 mm Hg, restoring diuresis to 0.5–1 ml/kg/h) remain unproven [1, 5].

When administering infusion therapy in children, it is advisable to use polyionic solutions: Potassium chloride + Sodium acetate + Sodium chloride**, Potassium chloride + Calcium chloride + Sodium chloride + Sodium lactate solution** or Potassium chloride + Magnesium chloride + Sodium acetate + Sodium glucose + Sodium chloride. It is also necessary to include dextrose solutions** (5%, 10%); this is due to the high risk of hypoglycemia, ketosis, and dehydration, especially in young children. In the presence of concomitant hyperglycemia, dextrose solutions** are not infused. If severe hypoproteinemia develops, transfusion of solutions or albumin** is indicated [94-97].

• In patients with AP, the use of nonsteroidal anti-inflammatory drugs (nonsteroidal anti-inflammatory and antirheumatic drugs) for pain relief is not recommended in acute kidney injury [4, 5, 12, 16–18, 62].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. Pain is one of the main symptoms of AP, and its relief is a priority task in complex therapy. Currently, there are no data limiting the use of specific analgesics in AP. In the presence of pain, all patients are prescribed analgesics to improve quality of life, especially in the first 24 hours of hospitalization. If nonsteroidal anti-inflammatory drugs (nonsteroidal anti-inflammatory and antirheumatic drugs) are ineffective or contraindicated, opioids/opioid analgesics (morphine**) may be used in accordance with the instructions. In children, tramadol** is preferred: older than 1 year, intravenously or intramuscularly, in a single dose of 1–2 mg/kg. If tramadol** is ineffective, the use of morphine** is indicated. Currently, there is no evidence indicating a negative impact of opioids on disease outcomes [1, 96].

• Mechanical ventilation is recommended for patients with AP if, despite oxygen inhalation and/or the use of other respiratory support methods (high-flow nasal cannula oxygen therapy, non-invasive positive pressure ventilation (A16.09.011.006)), it is not possible to prevent worsening tachypnea and hypoxemia. Both non-invasive and invasive mechanical ventilation can be used. Invasive mechanical ventilation, however, is preferable when the patient's ability to cough up bronchial secretions is reduced, psychological contact with the patient is absent, and/or respiratory muscle weakness is progressing [64, 65].

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

Comment. No specific respiratory support strategy, including mechanical ventilation, has been developed for acute pancreatitis. Tachypnea and dyspnea in these patients may be caused not only by hypoxia but also by other factors. They can occur in pain syndrome, intra-abdominal hypertension, and pleural effusion, despite normal arterial blood oxygen levels. Increased systemic vascular permeability can provoke the development of pulmonary edema during infusion therapy. Therefore, approaches to resolving respiratory disorders must take into account their multifactorial nature. In the case of invasive mechanical ventilation, it is advisable to use a protective ventilation strategy. When acute respiratory distress syndrome develops, approaches to mechanical ventilation are the same as when it develops due to other causes.

In addition to organ and nutritional support, patients with acute pancreatitis do not require any other specific drug therapy, including antisecretory and antiprotease therapy. Despite numerous studies, none has proven the efficacy of any antisecretory and antiprotease drug therapy [66,67]. Nevertheless, the use of somatostatin and its analogues (octreotide**) is justified in pediatric practice.

• The use of prophylactic antibiotics in the treatment of patients with AP is not recommended, as current research data have not shown a significant effect on reducing disease severity and mortality [62, 68–72].

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

• Routine prophylactic use of systemic antifungals in patients with infected pancreatitis is not recommended, although Candida spp. are frequently found in patients with infected pancreatic necrosis [100].

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

Comment. Opinions on the use and efficacy of prophylactic antibiotic therapy in acute pancreatitis to prevent infectious complications (in patients without clinical signs of infection) have always been controversial. Some studies indicate that early administration of antibiotics can prevent infectious complications in patients with sterile pancreatic necrosis. However, subsequent, more rigorous studies failed to confirm this benefit. Currently, the results of numerous studies have shown that early administration of antibiotic therapy in patients with acute pancreatitis is not associated with a significant reduction in disease severity and mortality. Thus, prophylactic antibiotic therapy is no longer routinely indicated for the treatment of all patients with acute pancreatitis. Antibacterial drugs are prescribed only for extrapancreatic infection (pneumonia, urinary tract infection, etc.), strong suspicion of cholangitis, confirmed cholecystitis, or suspected infected pancreatic necrosis. Extrapancreatic infection is treated according to existing guidelines. The onset of infectious complications in acute pancreatitis is variable and unpredictable, most commonly occurring in the second to fourth week of the disease. Despite their high significance, clinical signs are still not recognized as sufficiently specific.

• For empirical antibiotic therapy of infected acute pancreatitis, it is recommended to use antibacterial drugs (systemic antibacterial drugs) capable of penetrating necrotic zones, combining agents active against both aerobic and anaerobic microorganisms, as well as Gram-positive and Gram-negative flora [73, 74].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comments: Technologies that allow the removal of intoxication-inducing factors from the blood in acute pancreatitis (such as hemofiltration, etc.) are not mandatory for inclusion in the treatment protocol. Extracorporeal blood purification is performed using various technologies (hemofiltration, hemoadsorption, plasma exchange, plasma filtration, etc.) that enable the removal of endotoxins, cytokines, and other substances. However, despite many years of experience with their use in acute pancreatitis and sepsis, evidence regarding their efficacy or inefficacy is very low, although some studies present promising results. Further research is required to clarify the role of blood purification methods in this pathology. Renal replacement therapy is performed not only according to traditional indications for the development of acute kidney injury (taking into account potassium and nitrogen waste levels), but also when necessary to correct fluid balance [73-75].

• In patients with severe AP, it is recommended to place a nasogastric tube for decompression and, if possible, a nasointestinal tube for early enteral nutritional support [52 – 54, 76].

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

Comment. In severe AP, which is typically accompanied by intestinal paresis and gastrostasis, prolonged nasogastric decompression should be performed until they resolve and marked amylasemia decreases (serum amylase less than 3 times the upper limit of normal). Tube feeding with specialized balanced isocaloric enteral nutrition formulas ("Nutrien standard", "Isorus standard", "Fresubin original", "Nutrison standard", "Nutricomp standard") can be administered in gradually increasing volumes (monitoring tolerance and the residual volume of intestinal contents obtained every 3-4 hours). Administration of nutritional formulas via a nasogastric tube is possible after the resolution of intestinal paresis and gastroparesis, as well as hyperamylasemia (serum amylase less than 3 times the upper limit of normal).

Enteral support implies: decompression of the intestinal pacemaker (interstitial cell of Cajal), enterosorption, early intestinal decontamination, and enteroprotection with fluid administration and the prescription of minimal enteral nutrition in a volume of no more than 300 ml of an isocaloric nutritional formula ("Nutrien standard", "Isorus standard", "Fresubin original", "Nutrison standard", "Nutricomp standard") at an administration rate of 30 ml/hour. In cases of pronounced intestinal paresis, intraluminal administration of solutions is best performed in a lavage mode.

• If tube feeding cannot be implemented for 3-5 days in the minimum required volume (1500 kcal and 60 g of protein, 2-3 g/kg for children), it is recommended to prescribe supplementary, and if necessary, total parenteral nutrition (parenteral nutrition solutions) with its gradual withdrawal as the patient's ability to receive adequate substrate supply via the gastrointestinal tract in optimal volume is restored [77 – 84].

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

Comment. The optimal volume of adequate substrate supply is considered to be: energy 25-30 kcal/kg, protein 1.3-1.5 g/kg calculated for ideal body weight. For children, these figures are 45-55 kcal/kg and 1.5-4 g/kg, respectively, depending on age. Upon restoration of the motor-evacuatory function of the gastrointestinal tract and the absence of hyperamylasemia, removal of tubes and switching to a sparing diet combined with oral consumption of balanced nutritional formulas via sipping is possible. [2,93,94]

3.2. Surgical treatment

Early (I) phase

• In patients with peritoneal syndrome, including the presence of free fluid in the abdominal cavity according to ultrasound data, as well as when differential diagnosis with other abdominal cavity diseases is required, it is recommended to perform diagnostic laparoscopy or ultrasound-guided percutaneous drainage of the abdominal cavity (A16.30.007.001), or paracentesis [2,5,10,11,13,15,24,25,47,51].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. The objectives of laparoscopy can be diagnostic, prognostic, and therapeutic. Confirmation of the diagnosis of acute pancreatitis (and, accordingly, exclusion of other abdominal diseases, primarily acute surgical pathology such as mesenteric thrombosis, etc.): presence of edema at the root of the transverse mesocolon (during laparoscopy); presence of effusion with high amylase activity (2-3 times exceeding blood amylase activity); presence of steatonecrosis (during laparoscopy). Detection of signs of severe pancreatitis: hemorrhagic nature of the enzymatic effusion (pink, crimson, cherry-colored, brown); widespread foci of steatonecrosis and extensive hemorrhagic infiltration of the retroperitoneal tissue extending beyond the pancreas zone (during laparoscopy). Verification of serous ("glassy") edema during laparoscopy in the first hours of the disease (especially against the background of a severe general condition of the patient) does not exclude the presence of severe pancreatitis, since signs of severe pancreatitis may not be detected during early laparoscopy, i.e., the disease may subsequently progress. Therapeutic objectives: removal of peritoneal exudate, drainage of the abdominal cavity, and decompression of the retroperitoneal tissue in enzymatic cellulitis.

Enzymatic cellulitis is an aseptic lesion of the retroperitoneal fat in sterile pancreatic necrosis, caused by spread of enzymatic effusion into the retroperitoneal fat with its destruction during phase 1A of the disease. CT with intravenous contrast is most informative for diagnosing enzymatic cellulitis, with verification accuracy for retroperitoneal fat involvement ranging from 70 to 80% depending on the affected area. Laparoscopy reveals hemorrhagic effusion in the abdominal cavity with hemorrhagic infiltration of the retroperitoneal fat, separately involving the left, right, or both lateral canals. In this situation, laparoscopic drainage of the abdominal cavity should be supplemented with decompression of the retroperitoneal fat of the right and left paracolic spaces by incising the peritoneum along the lateral canals. Peritoneal incision is performed using a coagulation hook from the subhepatic space to the pelvic inlet on the right, and from the splenic flexure of the colon to the pelvic inlet on the left. This method should be applied within the first three to four days from disease onset, when the process is still sterile [32,33,34].

• If an impacted stone of the major duodenal papilla (MDP) is present, the patient is recommended urgent (6-24 hours) restoration of bile and pancreatic juice passage, the optimal method for which is endoscopic retrograde papillosphincterotomy with lithoextraction (ERPS), after which, if facilities are available, drainage of the main pancreatic duct is desirable. In cases of an impacted MDP stone and acute pancreatitis, it is undesirable and dangerous to perform duct contrast enhancement. If ERPS cannot be performed, measures should be taken to evacuate the patient to the next level of medical care, and decompression of the biliary tract is permissible to reduce intraductal hypertension [10,11,23-25,47,85-89].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. Intense pain syndrome not relieved by opioids, rapidly progressive jaundice, absence of bile in the duodenum during upper endoscopy, and signs of biliary hypertension according to ultrasound data indicate the presence of an impacted stone of the major duodenal papilla.

• In AP patients with asymptomatic acute fluid/necrotic collections (AFC/ANC) (absence of pain syndrome, compression of adjacent organs, blood vessels, obstructive jaundice, gastric stenosis, intestinal obstruction, signs of infection confirmed by clinical, laboratory, and instrumental data), it is not recommended to perform surgical interventions regardless of their size and location [14,16,90-92].

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

Comment. With an uncomplicated course of AFC/ANC, conservative treatment achieves their involution and resolution in 60-70% of observations.

• In patients with complicated forms of acute fluid/necrotic collections, surgical treatment is recommended, preferably using minimally invasive technologies: percutaneous, transgastric, and transduodenal punctures and drainage under endoscopic ultrasound (EUS) guidance, retroperitoneoscopy, minilaparotomy using a small-incision instrument set, etc. (ultrasound-guided drainage of the abdominal cavity and retroperitoneal space, ultrasound-guided drainage of a retroperitoneal abscess) or via laparoscopy (laparoscopic drainage of the abdominal cavity; laparoscopic drainage of the retroperitoneal space) [12,14,16-19].

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

Comment. To eliminate the communication between acute fluid collections/acute necrotic collections and the main pancreatic duct in type 1 necrosis configuration, it is advisable to perform endoscopic transpapillary drainage/stenting of the main pancreatic duct, preferably placing the drain beyond the zone of deep transverse necrosis. For progressive acute fluid collections/acute necrotic collections of the parapancreatic tissue, drainage should be performed using minimally invasive technologies [32-34].

• In patients with complicated forms of acute fluid/necrotic collections in whom minimally invasive interventions are ineffective, treatment from open approaches (including minilaparotomic and extraperitoneal approaches), as well as video-assisted retroperitoneal debridement without gas insufflation (VARD technique) (retroperitoneal drainage, abdominal organ necrosectomy) is recommended [14,16-19].

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

• Conservative treatment is recommended for children with sterile pancreatic necrosis. Surgical treatment is indicated only upon the development of infected pancreatic necrosis. The principles of surgical treatment for infected pancreatic necrosis in children include an organ-sparing approach involving pancreatic necrosectomy (A16.30.044), minimization of intraoperative blood loss, and the most complete removal of tissue detritus and inflammatory exudate. The removal of freely lying necrotic substrates within necrotic tissues is the most effective and safe manipulation in infected pancreatic necrosis [1,4,97].

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

• Drainage of an acute fluid collection is recommended in children with a high rate of fluid accumulation and high amylase activity, which indicates pancreatic destruction [1,93,96].

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

Late (II) phase (sequestration phase)

• Surgical treatment is recommended on an elective basis for large pancreatic pseudocysts (greater than 5 cm) in the absence of complications [2,5,11,24,46].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. The procedure of choice for an immature (unformed) pancreatic pseudocyst (< 6 months) is external drainage (abdominal cyst drainage). A mature (formed) pancreatic pseudocyst (> 6 months) is subject to elective surgical treatment. Complications of pancreatic pseudocysts include infection, bleeding into the cyst cavity, cyst perforation into the free peritoneal cavity leading to peritonitis, and compression of neighboring organs leading to obstructive jaundice, gastric outlet obstruction, intestinal obstruction, etc.

• In the event of purulent complications in patients with acute pancreatitis, surgical intervention (retroperitoneal drainage, abdominal organ necrosectomy) is recommended with the aim of debriding the affected retroperitoneal tissue [2-4,11,12,14,25,49,50].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

• In phase II of acute pancreatitis, sequestrectomy is recommended after assessing indications, determining the optimal surgical method and access, as well as the scope of the operation. It is recommended to use the typing technology for purulent-destructive complications of pancreatic necrosis, which allows determining the involvement of retroperitoneal tissue spaces and selecting the optimal surgical access (Appendix G3) [2,4,11,14,48,51].

GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)

Comment. The intervention involves opening, debriding, and draining the affected retroperitoneal tissue. The main method for debriding purulent-necrotic foci is sequestrectomy, which can be either single-stage or multi-stage, and is achieved using both minimally invasive and traditional methods.

• When indications for surgical intervention are present, and when addressing the issue of primary drainage of purulent-necrotic parapancreatitis, it is recommended to resort to minimally invasive interventions whenever possible (ultrasound-guided drainage (retroperitoneal drainage; abdominal cyst drainage), retroperitoneoscopy, minilaparotomy using a special instrument set, etc.) [2,4,11,14,48,51].

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

Comment. If minimally invasive drainage is ineffective, the procedure of choice is debridement laparotomy with sequestrectomy. Drainage is preferably performed via extraperitoneal approaches. The optimal timing for performing the first debridement laparotomy/lumbotomy with sequestrectomy is 4–5 weeks of the disease. If complications develop that cannot be managed with minimally invasive interventions, open surgery must be performed, including through a mini-approach. When hemorrhagic complications develop from the pancreatic zone, preference should be given to endovascular methods of hemostasis.

• In the presence of a persistent pancreatic fistula that does not close within more than 6 months, elective surgical treatment is recommended [2,24,46].

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

Comment. Following surgery, the majority of patients develop an external pancreatic fistula, which, after the inflammatory process subsides, is treated conservatively and closes spontaneously within an average of 2–4 months. A persistent pancreatic fistula is usually associated with large pancreatic ducts and in most cases requires elective surgical intervention.

Abdominal compartment syndrome

Caused by the consequences of the pancreatic inflammatory process, which induces edema of the peritoneum covering internal organs and the retroperitoneal space, fluid accumulation within them, and, in a number of patients, is associated with aggressive hydration therapy. Widespread involvement of the retroperitoneal tissue, more so than the presence of peritoneal effusion, determines persistent intra-abdominal hypertension [5,9,10,15,24,25].

• In all patients with severe acute pancreatitis presenting with high intra-abdominal pressure and the development of abdominal compartment syndrome (ACS) (in conjunction with existing clinical signs), treatment utilizing both conservative measures (adequate analgesia, elimination of hyperhydration) and surgical interventions (placement of a nasointestinal tube, ultrasound-guided drainage of the abdominal cavity and retroperitoneal space) is recommended [5,9,10,14,15,24,25].

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

Comment. The duration of exposure to high intra-abdominal pressure (IAP) is a more important prognostic factor than the mere fact of its occurrence. Timely reduction of IAP leads to the reversal of organ and systemic dysfunctions. Conservative treatment of ACS is primarily beneficial in grade I IAP (intra-abdominal pressure of 12–15 mm Hg) and grade II IAP (intra-abdominal pressure of 16–20 mm Hg) and can be a simple first step toward reducing IAP in these patients.

• In intra-abdominal hypertension, deep sedation and neuromuscular blockade are recommended when other measures are ineffective (adequate analgesia, elimination of hyperhydration, removal of peritoneal effusion) [5,9,10,14,15,24,25].

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

Comment. Intra-abdominal hypertension is a consequence of intestinal paresis and the inflammatory process in the pancreas, which causes increased systemic vascular permeability, peritoneal edema, and retroperitoneal edema. Aggressive hydration therapy may contribute to worsening edema. Excessive sedation may also increase bowel dysfunction with a subsequent increase in intra-abdominal pressure.

4. Medical Rehabilitation and Sanatorium-Resort Treatment

• Medical rehabilitation is recommended for all patients with acute pancreatitis; the choice of the optimal rehabilitation method depends on each specific case of acute pancreatitis [98,99].

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

• Rehabilitation measures are recommended to be initiated as early as possible from the onset of the disease [98,99].

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

Comment. Medical rehabilitation for acute pancreatitis should begin as early as possible and be carried out concurrently with treatment. Rehabilitation is performed 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).

If functional insufficiency develops after the completion of surgical treatment or conservative therapy (at the end of the first stage of rehabilitation), the patient may be referred to the second or third stage of rehabilitation based on an assessment of their self-care ability and rehabilitation potential.

Rehabilitation is organized by a multidisciplinary rehabilitation team, which includes: a rehabilitation physician (coordinator of the rehabilitation team), physical 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 the surgeon and an anesthesiologist-intensivist (if the patient is in the ICU). Other specialists may be involved as needed.

The most common rehabilitation problems in patients with acute pancreatitis include:

• ICU-acquired weakness (ICS),

• Immobilization syndrome and motor deprivation,

• Malnutrition,

• Communicative and sensory deprivation,

• Psychological attitudes toward death or illness,

• Pain,

• Stress.

A prolonged stay in the ICU or hospital for severe acute pancreatitis can lead to motor deficit (loss of the ability to walk), muscle atrophy, pressure ulcers, cachexia, and other problems that may result not only in functional impairment but also in 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 evidence of the superiority of specific physiotherapy methods in acute pancreatitis; physiotherapy may be considered as an alternative and complementary technique to supplement basic surgical care, conservative therapy, and rehabilitation.

Patients presenting with pain syndrome should be provided with pain management measures. In the absence of specific contraindications, a multimodal analgesic regimen is recommended (organized jointly with a medical psychologist and occupational therapist), including narcotic analgesics (opioid analgesics), nonsteroidal anti-inflammatory drugs (nonsteroidal anti-inflammatory and antirheumatic drugs), and paracetamol**.

For patients with acute pancreatitis, the ward or ICU environment should be arranged to minimize negative impacts on the patient, reduce stress and suffering, which is managed by an occupational therapist.

A patient with severe pancreatitis must be positioned to prevent pressure ulcers and the development of contractures.

Physiotherapy (given the lack of evidence of efficacy – see above):

• General ultraviolet irradiation (UVI) according to the standard schedule combined with drug electrophoresis for pancreatic diseases, every other day. A course of treatment consists of 15–20 irradiations.

• Abdominal UVI, 2–3 biodoses, every 2–3 days. A course of treatment consists of 5–6 procedures; Sollux lamp to the abdomen, procedure duration 10 min, daily:

• Abdominal inductothermy, dose 200 mA, procedure duration 15–20 min, every other day. Course of treatment – 10–15 procedures; 5) paraffin-ozokerite applications to the abdomen (temperature 48–50°C, procedure duration 20–30 minutes, every other day, or:

• Mud applications to the abdomen (temperature 40–42°C), procedure duration 15 min, every other day:

• Iodine drug electrophoresis to the abdomen, procedure duration 20 min, every other day.

5. Prevention and Dispensary Observation

• As prevention of acute pancreatitis, timely treatment of cholelithiasis, extrahepatic biliary tract, and pancreatic diseases, as well as regular follow-up (dispensary observation) by a gastroenterologist, general practitioner/pediatrician, and surgeon/pediatric surgeon is recommended [5,11].

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

6. Organization of Medical Care

Stages of Medical Care Delivery

1. Medical evacuation of patients with acute pancreatitis to medical organizations is carried out based on a three-tier system of specialized emergency and urgent medical care established in a constituent entity of the Russian Federation, in order to provide differentiated volumes of medical examination and treatment depending on the severity of acute pancreatitis, the degree of risk of complications, taking into account the structure, bed capacity, level of equipment, and availability of qualified personnel in said medical organizations.

Depending on bed capacity, equipment, and staffing, medical organizations providing specialized, including high-tech, emergency and urgent medical care to patients with acute pancreatitis are divided into three groups regarding the feasibility of providing this care within the three-tier system of specialized emergency and urgent medical care:

a) first tier – district medical organizations for the provision of specialized emergency and urgent medical care;

b) second tier – interdistrict medical organizations for the provision of specialized emergency and urgent medical care;

c) third tier – regional medical organizations for the provision of specialized, including high-tech, emergency and urgent medical care.

2. When providing ambulance, including specialized ambulance care outside a medical organization, emergency medical teams carry out medical evacuation of patients with acute pancreatitis to first-tier medical organizations if the following triad of symptoms is identified during the initial patient examination:

— severe epigastric pain radiating to the back or girdle-like in character;

— repeated vomiting;

— muscle guarding in the upper abdomen.

Upon the additional identification of at least two of the symptoms listed below, emergency medical teams carry out medical evacuation of patients with acute pancreatitis to second-tier medical organizations:

— peritoneal signs;

— oliguria (less than 250 ml over the last 12 hours from the moment of patient examination by the ambulance team);

— skin symptoms (facial hyperemia, livedo reticularis, cyanosis);

— systolic blood pressure less than 100 mmHg;

— encephalopathy.

3. The criterion for the provision of specialized medical care in first-tier medical organizations is the presence of mild acute pancreatitis. With this form of acute pancreatitis, pancreatic necrosis does not form (edematous pancreatitis), and organ failure does not develop.

The criterion for the provision of specialized medical care in second-tier medical organizations is the presence of moderately severe acute pancreatitis, which is characterized by either one of the local manifestations of the disease: acute peripancreatic fluid collection, acute necrotic collection, peripancreatic infiltrate, walled-off pancreatic necrosis, encapsulated necrosis, - and/or the development of general manifestations in the form of transient organ failure (no more than 48 hours).

The criterion for the provision of specialized, including high-tech, medical care in third-tier medical organizations is the presence of severe acute pancreatitis, which is characterized by either infected pancreatic necrosis (purulent-necrotic parapancreatitis), and/or the development of persistent organ failure (more than 48 hours).

Medical evacuation of patients with acute pancreatitis from first-tier medical organizations lacking the capability to provide necessary specialized care to second- or third-tier medical organizations, as well as from second-tier medical organizations lacking this capability to third-tier medical organizations, is carried out in accordance with the criteria set forth in this clause by specialized emergency anesthesiology-resuscitation ambulance teams, air medical ambulance teams, or emergency consultative ambulance teams.

Indications for Hospitalization in a Medical Organization

• Acute pancreatitis is an absolute indication for emergency hospitalization in a specialized inpatient department of a tier 1–3 medical organization.

Criteria for discharging a patient from a medical organization

• Satisfactory general condition and well-being of the patient, normalization of body temperature, normalization of laboratory parameters.

7. Additional Information

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

• Purulent-necrotic and other complications of acute pancreatitis (sepsis, digestive fistulas, erosive and gastrointestinal bleeding, etc.);

• Other acute surgical conditions (acute appendicitis, hollow organ perforation, acute intestinal ischemia, mesenteric thrombosis, incarcerated hernia, acute intestinal obstruction, gastrointestinal bleeding, and others);

• Fulminant course of the disease;

• Hypersensitivity to immunoglobulins and other blood products;

• Polyvalent allergy (including a history of allergic reactions to the administration of horse serum (anti-diphtheria, anti-tetanus, etc.);

• Infectious and parasitic diseases and/or suspected infectious/parasitic diseases (foodborne toxicoinfection, dysentery, viral hepatitis, influenza, malaria, brucellosis, pseudotuberculosis, yersinosis, etc.);

• History of leukemia, oncological diseases, tuberculosis, or positive reactions for HIV infection, hepatitis B and C, syphilis);

• Severe congenital defects confirmed by history and/or objective 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 the bigeminy/trigeminy type, ventricular tachycardia, complete left bundle branch block, trifascicular block, ventricular fibrillation, sinoatrial block greater than grade I, atrioventricular block grade II–III, Frederique syndrome);

• Chronic heart failure grade 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, rheumatism, and others);

• Type I and type II diabetes mellitus;

• Obesity with a body mass index greater than 40; Acute renal failure;

• Chronic renal failure with a glomerular filtration rate of less than 30 ml/min; Peptic ulcer of the stomach and duodenum 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.

Criteria for Evaluating the Quality of Medical Care

References

Appendix A1. Working Group Composition

• Academician of the Russian Academy of Sciences, Professor Igor I. Zatevakhin (Moscow),

• Academician of the Russian Academy of Sciences, Professor Amiran Sh. Revishvili (Moscow),

• Academician of the Russian Academy of Sciences, Professor Sergey F. Bagnenko (Saint Petersburg),

• Academician of the Russian Academy of Sciences, Professor Yury S. Polushin (Saint Petersburg),

• Academician of the Russian Academy of Sciences, Professor Nikolay A. Maystrenko (Saint Petersburg),

• Academician of the Russian Academy of Sciences, Professor Igor E. Khatkov (Moscow),

• Academician of the Russian Academy of Sciences, Professor Alexey V. Shabunin (Moscow),

• Corresponding Member of the Russian Academy of Sciences, Professor Sergey S. Petrikov (Moscow),

• Corresponding Member of the Russian Academy of Sciences, Professor Alexander Yu. Razumovsky (Moscow),

• Doctor of Medical Sciences, Professor Sergey S. Bagnenko (Saint Petersburg),

• Doctor of Medical Sciences, Professor Vladimir V. Bedin (Moscow),

• Doctor of Medical Sciences, Professor Eduard I. Galperin (Moscow),

• Doctor of Medical Sciences, Professor Valery R. Goltsov (Saint Petersburg),

• Doctor of Medical Sciences, Professor Vladimir V. Darvin (Surgut),

• Doctor of Medical Sciences, Professor Andrey E. Demko (Saint Petersburg),

• Doctor of Medical Sciences, Professor Magomed D. Dibirov (Moscow),

• Doctor of Medical Sciences, Professor Tatyana G. Dyuzheva (Moscow),

• Doctor of Medical Sciences, Professor Vyacheslav I. Egorov (Moscow),

• Doctor of Medical Sciences, Professor Mikhail P. Korolev (Saint Petersburg),

• Doctor of Medical Sciences, Professor Nikolay Yu. Kokhanenko (Saint Petersburg),

• Doctor of Medical Sciences, Professor Andrey G. Kriger (Moscow),

• Doctor of Medical Sciences, Professor Alexander L. Levit (Yekaterinburg),

• Doctor of Medical Sciences, Professor Valery M. Luft (Saint Petersburg),

• Doctor of Medical Sciences, Professor Igor V. Molchanov (Moscow),

• Doctor of Medical Sciences, Professor Igor P. Parfenov (Moscow),

• Doctor of Medical Sciences, Professor Mikhail I. Prudkov (Yekaterinburg),

• Doctor of Medical Sciences, Professor Vladimir A. Rudnov (Yekaterinburg),

• Doctor of Medical Sciences, Professor Viktor E. Savello (Saint Petersburg),

• Doctor of Medical Sciences, Professor Andrey P. Stepanchenko (Moscow),

• Doctor of Medical Sciences, Professor Viktor V. Tsvirkun (Moscow),

• Doctor of Medical Sciences, Professor Mikhail Sh. Tsitsiashvili (Moscow),

• Doctor of Medical Sciences, Professor Andrey Yu. Korolkov (Saint Petersburg),

• Doctor of Medical Sciences, Vladimir E. Olovyanniy (Moscow),

• Doctor of Medical Sciences, Professor Ruben G. Avanesyan (Saint Petersburg),

• Doctor of Medical Sciences, Professor Irina V. Shlyk (Saint Petersburg),

• Candidate of Medical Sciences Maxim A. Golovanev (Moscow),

• Candidate of Medical Sciences Vladimir I. Kulagin (Saint Petersburg),

• Doctor of Medical Sciences Denis N. Protsenko (Moscow),

• Candidate of Medical Sciences Dmitry N. Popov (Saint Petersburg),

• Candidate of Medical Sciences Maria A. Anischenko (Moscow)

None of the members of the working group had a conflict of interest during the development of these clinical guidelines, specifically, no personal interest in receiving material gain or other advantage, either personally or through a company representative, that would or could influence the proper performance of their professional duties.

Appendix A2. Methodology for Developing Clinical Guidelines

The development of these clinical guidelines included three stages. At the first preparatory stage, a group of scientists from various regions of the country (Moscow, Saint Petersburg, Yekaterinburg, Samara), who had already been working under regional care protocols for acute pancreatitis (AP), was invited to draft the clinical guidelines. As a result of preliminary interactive discussions, it was decided to base them on the "Protocols for Diagnosis and Treatment of Acute Pancreatitis" developed in Saint Petersburg. For a more detailed discussion of this draft, a Round Table and a joint meeting of the Russian Society of Surgeons and the CIS Association of Hepatopancreatobiliary Surgeons were organized in Saint Petersburg on October 30, 2014. The expert group for discussing the clinical guidelines on acute pancreatitis included the country's leading specialists in this field. During the Round Table, an online broadcast of the meeting was organized on the Internet. After the draft clinical guidelines were adopted as a basis, the expert group edited the document over two months through interactive discussion. At the second stage—open internet discussion—the latest version of the clinical guidelines was published on the website of the Russian Society of Surgeons and remained there for a year. At the third stage—approval—the clinical guidelines for acute pancreatitis were publicly endorsed at the XII Congress of Surgeons of Russia in Rostov-on-Don on October 8, 2015, organized by the Russian Society of Surgeons.

On June 21, 2019, a working meeting was held in Saint Petersburg to introduce amendments to the national clinical guidelines for acute pancreatitis adopted on October 8, 2015, at the XII Congress of Surgeons of Russia (RSS) in Rostov-on-Don. The meeting took place at the First Saint Petersburg State Medical University named after Acad. I.P. Pavlov. Under the leadership of RSS President, Academician of the RAS I.I. Zatevakhin, Academician of the RAS S.F. Bagnenko, and with the participation of the Chief Surgeon of the Russian Federation, Academician of the RAS A.Sh. Revishvili, leading pancreatic surgeons, intensivists, and diagnostic radiologists of the country gathered (40 experts in total). The discussion of the national clinical guidelines for acute pancreatitis lasted for 6 hours in real time, including via an online broadcast with leading specialists from the A.V. Vishnevsky Institute of Surgery in Moscow. As a result of a heated discussion, the previous guidelines were retained as a basis, a consensus was reached on introducing amendments to the 2015 National Clinical Guidelines, and it was decided to incorporate these changes into the new version. After the draft guidelines were accepted as a basis, the expert group edited the adopted document over two months through interactive discussion.

Target audience of these clinical guidelines

• surgeons,

• anesthesiologists and intensivists,

• endoscopists,

• radiologists.

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 regarding 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.

Table A2.1. Scale for grading levels of evidence (LE) for diagnostic methods (diagnostic interventions)

Table A2.2. Scale for grading levels of evidence (LE) for prevention, treatment, and medical rehabilitation methods, including those based on natural therapeutic factors (preventive, therapeutic, and rehabilitative interventions)

Table A2.3. Scale for grading grades of recommendation (GR) for prevention, diagnostic, treatment, and medical rehabilitation methods, including those based on natural therapeutic factors (preventive, diagnostic, therapeutic, and rehabilitative interventions)

Appendix A3. Reference Materials

These clinical guidelines were developed taking into account the following regulatory legal documents:

• Order of the Ministry of Health of the Russian Federation No. 922n dated November 15, 2012, "On Approval of the Procedure for Providing Medical Care to Adult Patients in the Profile of 'Surgery';"

• Order of the Russian Ministry of Health No. 203n dated May 10, 2017, "On Approval of Criteria for Assessing the Quality of Medical Care";

• Order of the Russian Ministry of Health No. 231n dated March 19, 2021, "On Approval of the Procedure for Monitoring the Volume, Timeliness, Quality, and Conditions of Provision of Medical Care under Compulsory Medical Insurance to Insured Persons, as Well as Its Financial Provision" (as amended)

• Letter of the Federal Compulsory Medical Insurance Fund No. 6545/30-5 dated December 30, 2014, "On Targeted Quality Appraisals of Medical Care";

• Order of the Russian Ministry of Health No. 103n dated February 28, 2019, "On Approval of the Procedure and Timelines for the Development and Revision of Clinical Practice Guidelines, Their Standard Template, and Requirements for Their Structure, Composition, and Scientific Validity of Information Included Therein."

Appendix B. Physician Action Algorithms

Appendix C. Patient Information

The patient must adhere to relatively simple and manageable restrictions. They are quite straightforward to follow, especially considering that ignoring them is fraught with rather unpleasant and undesirable consequences.

Meals at home should be pureed and gruel-like. Milk and milk kissels, thin porridges (preferably made with water), chicken and vegetable broth, and vegetable purees are permitted. Dietary nutrition is prescribed to the patient for the first 2–3 months. The diet affects the composition of the intestinal microflora and the activity of its functions. It is necessary to follow these principles:

• frequent and fractional meals; simultaneous consumption of large portions of food is contraindicated;

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

• adequate nutrition providing the body with a full range of nutrients, vitamins, and minerals, since stimulation and strengthening of the immunity are required during the recovery period;

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

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. To restore normal microflora, dairy and fermented milk products and abundant drinking are beneficial for the body. It is better to give up bread and bakery products; a great alternative to them can be crispbreads, which contain a minimum of fiber and carbohydrates. Vegetables (carrots, beets) and bananas are well-perceived by the body, while citrus fruits are best avoided. At the same time, for immunization, the body needs vitamin C, which can be sourced from other food products or consumed in tablet form, as well as other vitamins and multivitamin-mineral complexes. The end of the diet should not be abrupt. It is recommended to gradually expand the diet.

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

Appendix G1. Scale of criteria for primary rapid assessment of acute pancreatitis severity

(St. Petersburg I.I. Dzhanelidze Research Institute of Emergency Medicine - 2006):

Russian title: Scale of criteria for primary express assessment of the severity of acute pancreatitis

Source (official website of the developers, validation publication):

https://elibrary.ru/item.asp?id=11744367

Type (underline):

- rating scale

- index

- questionnaire

Purpose: primary assessment of the severity of acute pancreatitis

Content:

• peritoneal syndrome;

• oliguria (less than 250 ml over the last 12 hours);

• skin symptoms (facial hyperemia, mottling, cyanosis);

• systolic blood pressure less than 100 mm Hg; encephalopathy;

• hemoglobin level greater than 160 g/l; leukocyte count greater than 14×10⁹/l;

• blood glucose level greater than 10 mmol/l;

• urea level greater than 12 mmol/l;

• metabolic disorders according to ECG data;

• cherry or brownish-black color of the enzymatic exudate obtained during laparoscopy (paracentesis);

• detection during laparoscopy of widespread enzymatic parapankreatitis extending beyond the boundaries of the lesser sac and spreading along the flanks;

• presence of widespread fat necrosis detected during laparoscopy; lack of response to basic therapy.

Key (interpretation):

If a particular patient has at least 5 signs out of the listed ones, they have a severe form of acute pancreatitis with a 95% probability.

If there are 2–4 signs – moderately severe acute pancreatitis.

If there are no signs or a maximum of one of them – mild acute pancreatitis.

Appendix G2. SOFA score

Original name: Sequential Organ Failure Assessment (SOFA)

Russian name: SOFA scale

Source (official website of the developers, validation publication):

https://pubmed.ncbi.nlm.nih.gov/29443733/

Tee Y.S., Fang H.Y., Kuo I.M., Lin Y.S., Huang S.F., Yu M.C. Serial evaluation of the SOFA score is reliable for predicting mortality in acute severe pancreatitis. Medicine (Baltimore). 2018 Feb; 97(7):e9654. doi: 10.1097/MD.0000000000009654.

Type (underline):

- rating scale

- index

- questionnaire

Purpose: determination of organ failure

Content:

Key (interpretation):

PaO2 in mmHg, FiO2 from 0.21 to 1.00.

Adrenergic agents used for at least 1 hour. Dosage in µg/kg/min.

0 – optimal parameter, 4 – most abnormal parameter.

Data must be collected and evaluated once daily throughout the patient's stay in the intensive care unit.

Mean arterial pressure (MAP) is calculated as: MAP = (SBP + 2DBP) / 3. The SOFA score is the sum of all six parameters.

Appendix G3. Types of infected pancreatic necrosis in the sequestration phase

(St. Petersburg Dzhanelidze Research Institute of Emergency Medicine – 1990):

Russian title: types of infected pancreatic necrotizing pancreatitis in the sequestration phase

Source (official website of the developers, validation publication):

Tolstoy A.D., Sopiya R.A., Krasnogorov V.B., Vashetko R.V., Goltsov V.R., Andreev M.I. Destructive pancreatitis and parapancreatitis. - St. Petersburg, "Hippocrates", 1999, - 128 p.

Type (underline):

- rating scale

- score

- questionnaire

Purpose: assessment of the types of infected pancreatic necrotizing pancreatitis in the sequestration phase

Content:

• Type I – spread of changes within the retroperitoneal (parapancreatic) cellular space proper;

• Type IIa – spread of changes in the parapancreatic and left paracolic cellular spaces;

• Type IIb – spread of changes in the parapancreatic, left paracolic, and left perirenal spaces;

• Type IIIa – spread of changes in the parapancreatic and right paracolic cellular spaces;

• Type IIIb – spread of changes in the parapancreatic, right paracolic, and right perirenal cellular spaces;

• Type IV – spread of changes in the parapancreatic, paracolic, perirenal spaces, as well as cellular spaces along the ureters and great vessels.