Pancreatic cysts clinical guidelines. Chronic pancreatitis with excretory insufficiency: what is it? Etiology and pathogenesis

Chronic pancreatitis is a progressive disease of the pancreas, accompanied by an increase in inflammatory and destructive changes in the structure of the organ. Pancreatitis occurring in a chronic form is listed under ICD 10 codes - K86.0 -K86.1

Chronic pancreatitis is a progressive disease of the pancreas, accompanied by an increase in inflammatory and destructive changes in the structure of the organ.

Stages

In medical practice, the most common classification of pancreatitis is based on the severity of organ damage. According to this principle, there are 3 stages of the process.

At stage 1 of the disease, there are no pronounced signs of impairment of internal and external secretory function. Manifestations of pathology occur periodically against the background of eating junk food. The duration of this stage of pancreatitis can be more than a year.

At stage 2 of pancreatitis, symptoms persist constantly. In this case, manifestations of a decrease in secretory function may be observed.

In medical practice, the most common classification of pancreatitis is based on the severity of organ damage; according to this principle, 3 stages of the process are distinguished.

At stage 3 of pancreatitis, critical damage to pancreatic tissue is observed. The intra- and exocrine function of the organ is disrupted. Severe complications often occur at this stage of the pathological process.

What does the pancreas look like in chronic pancreatitis?

With chronic pancreatitis, pathological changes in the structure of the organ increase gradually. Frequent relapses of inflammation lead to the death of parts of the gland tissue. During the period of remission, the affected areas become overgrown with fibrosis.

The connective tissue is not only unable to perform the function of healthy pancreatic cells, but also leads to deformation of the remaining healthy areas. All tissues of this organ are affected, including the islet epithelium of blood vessels, ducts, acini, nerves, etc.

With pancreatitis occurring in a chronic form, pathological changes in the structure of the organ increase gradually, frequent relapses of inflammation lead to the death of parts of the pancreatic tissue.

Due to the fact that the enzymes produced by the pancreas cannot be removed from the organ due to tract obstruction, pseudobrushes are formed that do not have an epithelial lining inside. Inside relatively recently formed formations of this type, tissues affected by necrosis with a small admixture of blood are often detected.

In especially severe cases, such pseudocysts may be damaged by pathogenic microflora.

When the pancreas is incised along the ducts, many small cystic formations filled with purulent contents are often discovered. Gradually, the functionality of the parenchyma and glandular tissue decreases.

Classification

Pathology can be primary or secondary. Depending on the etiology, pancreatitis is distinguished:

• infectious;
• alcoholic;
• dysmetabolic, etc.

Pancreatitis can be primary and secondary in nature, along the course it can be painful, latent and combined, and can be divided into types according to morphological characteristics.

Depending on the course, it can be painful, latent and combined. Based on morphological characteristics, the following species are distinguished:

• atrophic;
• cystic;
• fibrous, etc.

Depending on the preservation of the secretory and excretory functions, pancreatitis can occur either without such disorders or with intra- and exocrine insufficiency without exacerbation.

Pancreatitis with endo- and exocrine insufficiency has an unfavorable course.

Causes

The main reasons for the development of the chronic form of pancreatitis are alcohol abuse and the progression of gallstone disease. Due to the systematic consumption of alcoholic beverages, intoxication of the body with decay products is observed.

The main reasons for the development of the chronic form of pancreatitis are alcohol abuse and the progression of gallstone disease.

The development of cholelithiasis not only affects the possibility of normal outflow of bile, but also contributes to the addition of an infection that can spread to the pancreatic tissue, causing their inflammatory damage.

Pathology can develop after removal of the gallbladder due to progressive gallstone disease.

If a person abuses unhealthy food from a young age, this creates conditions for potential problems with the organ. In addition, factors contributing to the development of chronic pancreatitis are identified. These include:

• excess calcium in the blood;
• cystic fibrosis;
• diseases of the gastrointestinal tract;
• thyroid dysfunction;
• food poisoning;
• abdominal organ injuries;
• taking certain medications;
• gastrointestinal infections;
• obesity;
• circulatory disorders;
• endocrine diseases;
• frequent exposure to stressful situations.

If a person abuses unhealthy food from a young age, this creates conditions for potential problems with the organ.

The development of this pathology may be due to genetic abnormalities that are inherited. An idiopathic variant of the disease is also possible, which develops for no apparent reason.

Symptoms

In the early stages of the disease, when remission occurs, no signs of pathology are observed. At the same time, during an exacerbation, indirect symptoms may be present, including belching, short-term bowel movements and bad breath, which may indicate other diseases of the gastrointestinal tract.

Chronic pancreatitis may be indicated by the appearance of minor pain and heaviness after eating fatty and fried foods. However, already during this period, the appearance of a problem in the pancreas may be indicated by echo signs of the disease, including increased tissue density and foci of forming pseudocysts.

As pancreatitis progresses, patients experience attacks of dizziness and blood pressure increases.

During the period of exacerbation of pancreatitis at stages 2 and 3 of the disease, severe vomiting and diarrhea can cause dehydration in a matter of hours.

Patients with pancreatitis experience symptoms of discomfort in the back and shoulder blade, intense pain, characteristic rumbling sounds in the abdomen, etc.

As pancreatitis progresses, exacerbations become common. They are accompanied by severe symptoms. Patients complain of the following conditions:

• severe diarrhea;
• intense pain syndrome;
• discomfort in the back and shoulder blade;
• characteristic rumbling sounds in the stomach;
• bitterness in the mouth;
• constant burping;
• nausea;
• vomiting;
• increased body temperature;
• sudden weight loss;
• headache;
• skin itching;
• decreased appetite.

During the period of exacerbation at stages 2 and 3 of the disease, severe vomiting and diarrhea can cause dehydration in a matter of hours. Attacks of dizziness appear, blood pressure rises, and other signs of this condition are noted.

If the ducts are damaged due to the inflammatory process and swelling of the soft tissues, obstructive jaundice occurs.

Subsequently, as the disease goes into remission, the nature of the stool changes. Constipation may occur.

Diagnostics

If signs of pathology appear, the patient requires consultation with a gastroenterologist, who can perform an external examination, collect anamnesis and prescribe tests. Determining the nature of the damage to the gland requires performing studies such as:

• radiography;
• Pancreatoangioradiography.

An example of the formulation of a diagnosis in a patient’s chart may look like this: chronic pancreatitis, accompanied by pain, combined, stage 2.

If signs of pathology appear, the patient requires consultation with a gastroenterologist, who can perform an external examination, collect anamnesis and prescribe tests.

Ultrasound

With this form of pancreatitis, ultrasound reveals changes in the tissues of the gland, including:

• increase in duct up to 2 mm or more;
• notches on the borders of the organ;
• increase in organ size;
• pseudocysts;
• diffuse changes.

In the presence of atrophy, ultrasound can reveal a decrease in organ size.

Analyzes

Stool and blood tests are performed to confirm the diagnosis. When performing a coprogram in the stool of a person suffering from pancreatitis, excess fat caused by a lack of enzyme production is detected. A test is performed to determine the activity of enzymes in the blood, including lipase and amylase. Radioimmunoassay is performed to confirm trypsin and elastase activity.

In chronic pancreatitis, ultrasound reveals changes in the tissues of the pancreas; in the presence of atrophy, ultrasound can reveal a decrease in the size of the organ.

A test is performed to determine the activity of enzymes in the blood, including lipase and amylase.

When performing a coprogram in the stool of a person suffering from pancreatitis, excess fat caused by a lack of enzyme production is detected.

Treatment

Chronically persistent inflammation of pancreatic tissue requires complex therapy and patient compliance with recommendations issued by doctors. Medicines are selected to suppress inflammation and restore organ function. You must follow a special diet. In severe cases, surgery is required.

Drug therapy

For this form of pancreatitis, medications belonging to the following groups are prescribed:

• antienzyme;
• choleretic;
• antispasmodics;
• analgesics;
• proton pump inhibitors;
• H2 blockers;
• enzymes;
• antacids;
• antibiotics.

The use of medications can eliminate the inflammatory process, relieve spasms and relieve pain.

Medicines are selected taking into account the current condition. The use of medications can eliminate the inflammatory process, relieve spasms and relieve pain.

Diet

A person suffering from pancreatitis needs a complete, high-calorie and easily digestible diet. You should eat food 5-6 times a day. Portions should be small. Products are introduced into the diet gradually so as not to create an increased load on the pancreas.

Surgical

Surgical interventions for the chronic form of the disease are performed only when absolutely necessary. Stones are often excised to relieve duct obstruction. A sphincterotomy may be performed if there is evidence of blockage of the sphincter of Oddi. If necessary, sanitation of purulent foci and resection of areas of fibrosis that interfere with the functioning of healthy organs are performed. In addition, a complete or partial pancreatectomy may be performed.

Surgical interventions for the chronic form of the disease are performed only when absolutely necessary.

Nutrition

The diet should be balanced and include plenty of protein. Recommended foods and dishes for this disease include:

• boiled vegetables and fruits;
• puree soups;
• lean meat and fish;
• fermented milk food;
• porridge.

Fried, smoked, marinades, preservatives, semi-finished products and other harmful foods should be excluded from the diet. Fatty fish and meat are not allowed. You need to completely avoid carbonated and alcoholic drinks. If the patient adheres to the rules of a healthy diet starting from the first days of the onset of pathology, then complete recovery is possible.

You should eat food 5-6 times a day, portions should be small; if the patient adheres to the rules of a healthy diet starting from the first days of the onset of pathology, then full recovery is possible.

The diet of a patient with chronic pancreatitis should be balanced and include a lot of protein.

Fried, smoked, marinades, preservatives, semi-finished products and other harmful foods should be excluded from the diet.

Why is it dangerous?

The chronic form of pancreatitis gradually leads to the destruction of the pancreas. This contributes to disruption of the production of enzymes and hormones. In severe cases, pancreatitis not only makes the patient’s normal life impossible, but also causes premature death.

Risk factors

The patient’s reluctance to follow the specialist’s recommendations, which relate not only to taking medications, but also to giving up bad habits, increases the risk of an unfavorable outcome. Non-compliance with the diet worsens the prognosis.

Statistics for Russia

The development of the disease is often observed in young people. At the same time, the number of patients increases every year. Exact statistics for Russia have not been established, but according to available data, there are at least 50 patients per 10 thousand people.

Premature mortality due to progression of pancreatitis reaches 6-8%.

Complications

The pancreas is extremely important for the functioning of the entire body, therefore, against the background of pancreatitis, complications such as:

• disturbances in the outflow of bile;
• false aneurysms of arterial vessels in the gland;
• cysts in the organ;
• abscesses;
• diabetes.

Often the first manifestations of the pathology of pancreatitis are observed in people over 50 years of age.

Can it turn into cancer?

Chronically persistent inflammation of pancreatic tissue creates conditions for malignant cell degeneration.

Features in adults

Due to the characteristics of the body and the specificity of unfavorable factors in adults and children, the chronic type of pancreatitis can have significant differences in its course.

In men

Since men often ignore the first manifestations of the disease, trying to delay the period of giving up alcohol and other bad habits, their pancreatitis often occurs in an aggressive form.

Mortality cases in men from this disease are recorded more often than in women.

Specifics in women

In women, the chronic type of pancreatitis often occurs in a latent form. The process of destruction of the pancreas lasts for many years if there are no additional factors in the form of alcoholism or other pathologies that could spur the development of the disease.

Elena Malysheva. Symptoms and treatment of chronic pancreatitis

Chronic pancreatitis - symptoms, nutrition and treatment

In the elderly

Often the first manifestations of pathology are observed in people over 50 years of age. This is associated not only with maintaining an unhealthy lifestyle throughout the entire previous life, but also with age-related changes.

Reviews

Vladislav, 57 years old, Moscow

About 2 years ago I had an attack of pancreatitis. I went to the doctor and was diagnosed with a chronic form. The doctor prescribed a diet. Of the drugs I used only No-shpu and Pancreatin.

Grigory, 40 years old, Surgut

In my youth I drank a lot and had other bad habits, but about 5 years ago I felt the consequences of this. Acute inflammation of the gland turned chronic. Now I strictly follow a diet and have completely given up alcohol to prevent exacerbations. I take enzymes prescribed by the doctor and choleretic agents.

For many patients, a doctor’s entry in an outpatient chart is tantamount to a death sentence, in which the doctor adds “chronic” to the name of the disease in the medical history. There is nothing reassuring in such a formulation.

A specific property of chronic diseases is the fact that the disease lasts for years in the patient and requires constant treatment, which, unfortunately, only alleviates the symptoms and prevents the deterioration of the patient’s health, but does not cure completely. This type of disease is characterized by periods of remission and relapse. As a rule, the chronic form cannot be cured; a specialist prescribes restraining therapy. The statements also correspond to chronic inflammation of the pancreas. Before studying in detail the specifics of diagnosing and eliminating the disease, you will need to understand the terminology. Let's study the specifics of the disease.

Specifics of pancreatitis

Pancreatitis is an inflammatory disease that occurs in the human pancreas. The organ is located in the abdominal cavity and is equipped with two functions:

• Endocrine (internal). The gland produces hormones, the main of which is insulin. The hormone is important for regulating sugar levels in the body.
• Exocrine (external). The function is responsible for the production of pancreatic juice and delivery to the stomach in the required quantity. The juice contains enzymes that ensure the breakdown and absorption of proteins, carbohydrates and fats contained in the food consumed.

Treatment of chronic pancreatitis depends on the form of development (edematous, parenchymal, sclerosing, calculous).

The meaning of the disease is that the pancreatic duct stops supplying gastric juice, and the organ becomes inflamed. Juice production continues, and enzyme secretion disturbances are observed. Enzymes that have an alkaline structure normally begin to act when leaving the gland, keeping the organ tissues safe. In chronic pancreatitis, the process of enzyme activation is disrupted, and the substances begin to act within the organ.

The danger of the disease lies in the fact that the enzymes contained in the juice, which do not find a way out, directly corrode the inflamed internal organ. Chronic pancreatitis develops against the background of other chronic diseases of the digestive system. The disease develops into a chronic form from an acute one. Symptoms and treatment of the disease depend on the causes of inflammation.

Causes

The main cause of inflammation is considered to be disruption of the duct and stagnation of pancreatic juice. If previously doctors diagnosed “chronic pancreatitis” more often to older people, mainly women, now the disease affects different sex and age groups of the planet’s population. The increase in the incidence rate is associated with the incorrect lifestyle inherent in most people.

Risk group

The disease is more common among older people. With age, natural processes in the body slow down, including the work of the pancreas. A large percentage of inflammation occurs in people suffering from alcohol and drug addiction. Frequent drinking of alcohol causes exacerbation attacks. Repeated periodically, attacks can develop into a chronic form. Alcohol abuse causes exacerbation of chronic pancreatitis.

Close attention to health is paid to people who have a hereditary predisposition to the disease. Scientists suspect the occurrence of genetic mutations. Hereditary predisposition makes the pancreas vulnerable. Working in hazardous industries increases the risk of developing the disease. It is much easier to cure the disease if you eliminate the risks that provoke inflammation from your life.

Factors contributing to the disease

It is important for people who fall into these groups to understand that their risk of getting sick is much higher. Treatment of chronic pancreatitis is more difficult. It is imperative to avoid factors that provoke the development of the disease:

• Prolonged stress;
• Infections;
• Taking medications that cause intoxication of the body;
• Fasting, diets;
• Injuries;
• Eating junk food.

Chronic pancreatitis of the pancreas often develops against the background of other chronic diseases: gastritis, stomach ulcers, inflammation of the gallbladder and others. Cholecystitis is especially dangerous.

Symptoms of the disease

Chronic pancreatitis is a disease that lasts for many years. Characterized by periods of exacerbation and remission. In the early stages, it is difficult to determine the diagnosis. Patients refer to general malaise and do not seek help from a doctor. Signs of chronic pancreatitis are easier to detect during exacerbation of the disease. Then the symptoms are similar to the clinical picture of the acute form.

1. Weight loss. The patient loses weight for no apparent reason, and regaining body weight is difficult.
2. Pain in the epigastric region and in the left upper part of the abdominal cavity. With chronic pancreatitis, the pain is dull and aching.
3. Natural digestive processes are disrupted. The patient experiences nausea, often accompanied by vomiting, heartburn, and heaviness.

Exacerbation of chronic pancreatitis is characterized by increased symptoms. During exacerbations, symptoms are easier to notice. A characteristic sign is a violation of the stool. Due to the lack of sufficient juice, food is not broken down sufficiently. The stool becomes foul-smelling and becomes greasy.

In chronic pancreatitis, a violation of the endocrine function of the internal organ is detected. Because of this, the body produces insufficient amounts of hormones, including insulin. Lack of insulin in the body leads to diabetes.

Diagnosis and treatment

If symptoms of chronic pancreatitis are detected, you should immediately consult a doctor. It is important to understand the seriousness of the disease. If you delay treatment, irreversible consequences are possible that will lead to death. In addition, against the background of this disease, others arise that are no less dangerous. And therapy for one disease is tolerated much easier by the body than for several at the same time.

Appointment with a specialist

If you suspect inflammation, first consult a therapist. The doctor collects anamnesis and draws up a general clinical picture. When a therapist diagnoses “chronic pancreatitis,” the symptoms and complaints expressed by the patient are confirmed by additional studies. The observed symptoms are recognized as characteristic of most diseases of the digestive system. This is where the difficulty of making a diagnosis lies. Therefore, the diagnosis of chronic pancreatitis requires careful research. Diagnosis stages:

1. Taking anamnesis, listening to complaints;
2. Visual examination of the patient;
3. Palpation (palpation) to determine the boundaries of internal organs;
4. Laboratory research;
5. Instrumental research.

The last two stages are considered decisive for the diagnosis of chronic pancreatitis. Therefore, let's look at them in more detail. Laboratory diagnostics includes examination of the patient's blood, urine and stool. Laboratory diagnostics are most effective if studies are carried out when chronic pancreatitis is in the acute stage. This study aims to determine the levels of enzymes in the human body, especially amylase. In chronic pancreatitis, the level of this enzyme increases significantly 2-3 hours after the onset of an exacerbation. The level of lipase in the body increases and remains elevated for a period of up to two weeks.

A considerable amount of information is provided by a general and biochemical blood test. In patients diagnosed with chronic pancreatitis, there is an increase in the level of leukocytes. This is typical for every inflammatory process. Biochemical analysis registers a decrease in proteins in the blood. The amount of fat in feces is also recognized as an important indicator in diagnosing the disease.

There are several signs that help diagnose chronic pancreatitis:

1. The pulsation of the aorta under the sternum is difficult to palpate;
2. Formation of bruises in some areas of the abdominal cavity;
3. When tapping the pancreas area, painful sensations occur;
4. Pain when palpating the area between the spine and ribs on the left.

Diagnosis and treatment of the disease is determined with greater accuracy through the use of medical equipment. The equipment is widely used in instrumental diagnostic methods.

Instrumental diagnostics

Chronic pancreatitis is often diagnosed using instrumental diagnostic methods. The most common method is ultrasound examination. This method of visualizing internal organs helps determine the size and structure of organ tissue.

Echo signs of chronic inflammation during ultrasound examination:

• Uneven contour of the organ;
• Presence of cysts;
• Increased echogenicity of the gland;
• Presence of stones in the duct;
• Dilation of the duct in uneven lobes.

The radiography method is prescribed to the patient by the attending physician to determine the presence of stones in the pancreas and ducts. Computed tomography helps to obtain information about tissue necrosis of an internal organ and identifies tumors and cysts.

Endoscopy is a method of visual examination of an organ using a video camera. This is a surprisingly informative method. Using a digital endoscope, you can get an extremely clear image of the internal organs and assess their condition. In chronic pancreatitis, endoscopy allows one to study the effect of inflammation on other internal organs.

Specifics of treatment

A doctor who studies inflammation of the pancreas specializes in gastroenterology. Therefore, with the question “how to treat the pancreas,” they turn to a gastroenterologist. Many methods have been developed to treat the disease. The choice depends on the specifics and form of the disease. The main goal of the prescribed treatment is to reduce the risk of complications. Therefore, therapy is aimed at relieving pain and preventing exacerbations. The treatment method also depends on the stage of the disease.

During an exacerbation, the pain syndrome is relieved first. During exacerbations, treatment of pancreatitis is best done while in a hospital, under the constant supervision of doctors. In the first days, patients are recommended to fast; only certain liquids are allowed to be consumed. When the exacerbation passes, the intensity of treatment is reduced and replacement therapy is prescribed for further treatment of the patient. The point is to take enzyme preparations. Pain syndrome is reduced with the help of antispasmodics. Additionally, the doctor prescribes medications that reduce gastric secretion.

In addition to drug treatment, therapy includes adherence to certain nutritional rules. The patient now needs to follow a diet and visit a gastroenterologist for life.

Diet for patients with pancreatitis

A patient diagnosed with chronic pancreatitis continues treatment throughout his life. This concerns a special diet that will need to be followed to avoid complications. In the first few days of the acute form, experts do not recommend eating food. Nutrients are introduced into the body through a tube. You are allowed to drink only still mineral water and rosehip decoction on your own. Further, it is allowed to eat jelly-like foods and foods that will not cause the secretion of pancreatic juice.

When the exacerbation passes, the patient is allowed to begin taking carbohydrate products of a uniform consistency. These are porridges, pureed soups and the like. Ten days after the attack, the patient is advised to consume fermented milk products and steamed lean meat.

Chronic pancreatitis will require adherence to nutritional rules throughout life. The patient will have to avoid eating fatty, spicy, fried foods. Completely exclude alcohol, mushrooms, baked goods and sweets. It is also important to consider the way you eat. You need to use small portions. This will help avoid unnecessary stress on the pancreas. Compliance with diet and nutritional rules, coupled with therapy prescribed by a doctor, is the answer to the question of how to treat chronic pancreatitis.

A healthy diet and stopping smoking and drinking alcohol are recognized as important ways to prevent pancreatic diseases. Remember this to exclude yourself from the risk group. Chronic pancreatitis is difficult to treat, requiring both moral and material costs. It is easier to avoid the occurrence of disease if you follow the rules of a healthy lifestyle.

In addition, prevention will help avoid other dangerous diseases. Therefore, healthy people, before wondering how to treat the disease, should study in more detail the methods of preventing pancreatitis.

In the structure of diseases of the digestive system, a share of 5.1 to 9% belongs to chronic pancreatitis (CP). With these ailments, the pancreas is affected and an inflammatory process begins. As a result, degenerative changes occur in the organ. Initially, the pathological process may occur in the tail of the pancreas, its head or middle part. The outcome of the disease is damage to the entire organ. Some people who suffer from chronic pancreatitis eventually die. The mortality rate in the world averages about 11%.

More about the disease

So, what is chronic pancreatitis? Experts use this term to designate a whole group of pancreatic diseases. All diseases are characterized by the following features:

• phase-progressive course with episodes of acute pancreatitis;
• focal, segmental or diffuse damage to the pancreatic parenchyma with subsequent replacement with connective tissue;
• changes in the duct system of the organ;
• formation of cysts, pseudocysts, stones and calcifications;
• development of endocrine and exocrine insufficiency.

The fact that there are different types of disease is evidenced by the International Statistical Classification, Tenth Revision. Chronic pancreatitis ICD-10 is divided into:

• CP of alcoholic etiology (code K86.0);
• other CP - infectious, recurring, relapsing, unspecified etiology (code K86.1).

The most common causes of chronic pancreatitis

Most often, the disease occurs due to alcohol abuse over a long period of time. In men, chronic pancreatitis of the pancreas can develop if they drink for more than 15 years. In women, the likelihood of developing the disease increases with alcohol abuse for more than 10 years.

Alcohol is not the only factor contributing to the development of chronic pancreatitis. The cause of the disease may be smoking. Substances that enter the lungs with smoke penetrate the blood and spread throughout the body, having a negative effect on all internal organs, including the pancreas.

Other causes of the disease

Other factors causing chronic pancreatitis (ICD-10 code - 86.0 and 86.1) include:

• abuse of fatty foods, long-term protein-free diet;
• various diseases of the gastrointestinal tract (neoplasms, cholecystitis, etc.);
• overweight, obesity;
• taking certain medications (Azathioprine, Furosemide, Prednisolone, synthetic estrogens, Erythromycin, Ampicillin, etc.);
• infection with viruses (cytomegalovirus, hepatitis B, C, etc.).

Studies conducted in recent years have shown that there is hereditary chronic pancreatitis of the pancreas. This is an autosomal dominant disease with incomplete penetrance (with different frequencies of gene expression in the phenotype of carriers). In sick people, hereditary chronic pancreatitis manifests itself quite early. However, the final stage occurs later than in other forms of the disease.

Forms of pancreatitis

There are different classifications of the disease. One of them is a list of the following forms of chronic pancreatitis:

1. Recurrent. It occurs in 55-60% of cases. With this form, periods of remission are replaced by exacerbations of the pathological process.
2. Constant pain. This form is found much less frequently (in 20% of cases). With it, patients complain of constant pain, localized in the upper abdomen and radiating to the back.
3. Pseudotumor (icteric). The incidence of this form of chronic pancreatitis is 10%. The pathological process is characterized by the development of inflammation in the head of the pancreas and compression of the common bile duct.
4. Painless (latent). The form is detected in 5-6% of cases. The pain associated with the disease is mild or not felt at all. Dyspeptic disorders periodically occur due to impaired functioning of the pancreas.
5. Sclerosing. With this form, pain occurs in the upper abdomen. They intensify after meals. The pain is accompanied by nausea, loose stools, and weight loss. When performing an ultrasound examination, specialists notice a decrease in size and thickening of the pancreas.

According to the Marseille-Roman classification, there are such forms of pancreatitis as calcific, obstructive, parenchymal and fibrosis. With the first of them, uneven lobular lesions of the pancreas are observed. Pseudocysts, cysts, calcifications, and stones appear in the ducts. What is chronic pancreatitis in obstructive form? With this type of disease, the internal organ is affected evenly. Stones do not form, and obstruction of the main pancreatic duct is observed. In the parenchymal form, foci of inflammation develop in the parenchyma. Calcifications are not formed, the ductal system is not affected. Fibrosis is characterized by the replacement of the parenchyma of an internal organ with connective tissue. Because of this process, exo- and endocrine insufficiency progresses.

Symptoms of the disease

Speaking about what chronic pancreatitis is, it is worth considering the signs of this disease. In the early stages, during periods of exacerbation, attacks are observed. They are characterized by pain in the epigastric region. In most cases they radiate posteriorly. Girdle pain is much less common. In people suffering from chronic pancreatitis, attacks occur due to the impact of provoking factors on the body. These include eating fatty foods, alcoholic and carbonated drinks.

The disease is also characterized by dyspeptic syndrome. Approximately 56% of sick people report nausea and vomiting. In 33% of cases, weight loss is observed, in 29% - flatulence, in 27% - loss of appetite. The disease may also cause symptoms such as general weakness, fatigue, and decreased ability to work.

The course of chronic pancreatitis

Experts distinguish 4 stages in the development of the disease:

1. Preclinical stage. At this stage, sick people do not notice the symptoms of chronic pancreatitis. The disease is often detected incidentally during an ultrasound or computed tomography scan of the abdominal organs.
2. The stage of initial manifestations in the development of such a disease as chronic pancreatitis. At this time, adults begin to suffer from the first symptoms of the disease. The duration of the stage can be several years. In some cases, the disease progresses very quickly.
3. Stage of development of permanent clinical symptoms. Patients develop signs of endocrine and exocrine insufficiency. People eat very little and complain of stomach pain.
4. Final stage. The pain becomes less pronounced. People are losing weight noticeably. At the final stage, various complications of chronic pancreatitis arise due to pancreatic atrophy, endocrine and exocrine insufficiency. One of them is cancer of the named internal organ.

Depending on the characteristics of the development of chronic pancreatitis, mild, moderate and severe forms of the disease are distinguished. With a mild course, periods of exacerbation occur rarely (1-2 times a year). The pain is moderate. The functions of the pancreas are not impaired.

What is moderate chronic pancreatitis? This is a disease in which there are 3-4 exacerbations per year. They last longer than with mild pancreatitis. In sick people, body weight decreases. The exocrine function of the pancreas is moderately reduced, and pancreatic hyperenzymemia is observed.

In severe cases of the disease, exacerbations are frequent and prolonged. The pain is accompanied by severe dyspeptic syndrome.

Treatment of the disease: goals and necessary measures

For chronic pancreatitis, therapy is prescribed to achieve the following goals:

• reduction of clinical manifestations of the disease;
• prevention of relapses;
• reducing the likelihood of complications of the disease.

Specialists prescribe non-drug treatment and drug therapy to their patients. If necessary, surgical intervention is performed. Treatment of chronic pancreatitis in adults can be carried out both at home and in the hospital. The indication for hospitalization is the transition of the disease to the acute stage, because it is during this period that the patient’s life is threatened and the need for parenteral administration of drugs arises.

Non-drug treatment

Nutrition plays an important role in the treatment of chronic pancreatitis. In case of severe exacerbations, fasting days (1-3 or more) and abundant alkaline drinking are indicated. According to indications, parenteral or enteral (introduction of nutrients into the colon using a special tube) nutrition is prescribed. Thanks to this measure, it is possible to stop the secretion of the pancreas, intoxication decreases and the pain syndrome becomes weaker.

After normalization of the condition, sick people are transferred to oral nutrition. Meals should be frequent and divided. The daily menu consists of slimy soups, vegetable purees, and liquid pureed milk porridges. Drinks allowed are compotes, jelly, weak tea, mineral water, and rosehip decoction.

The following products are necessarily excluded:

• causing flatulence;
• containing coarse fiber;
• stimulating the production of digestive juices;
• rich in extractive substances.

With chronic pancreatitis, is it possible to eat fish and meat broths, mushroom and strong vegetable broths, canned food, smoked meats, sausages, fatty fish and meats, fried foods, raw vegetables and fruits, baked goods, confectionery, black bread? All these products are prohibited during exacerbation of the disease, so they should be abandoned. You also need to remove spices, ice cream, and alcohol from your menu.

During remissions, the diet changes slightly. People diagnosed with chronic pancreatitis of the pancreas are allowed to eat pasta, raw vegetables and fruits, soft, mild cheeses, and baked fish. Puree soups can be replaced with regular vegetarian ones (cabbage should be excluded from the ingredients). Porridges can be crumbly or thicker.

Pharmacotherapy of chronic pancreatitis

The goal of drug therapy at the first stage is to ensure functional rest of the pancreas. This is achieved through:

1. Taking large doses of modern multienzyme drugs. Such medications include Mezim-Forte, Creon, and Pancitrate.
2. Maximum inhibition of acidic gastric secretion using histamine H2 receptor blockers (Ranitidine, Famotidine) or proton pump inhibitors (Omeprazole, Esomeprazole). The drugs are administered parenterally or taken orally.
3. Administration of Octreotide or Sandostatin. These drugs are synthetic analogs of the hormone somatostatin. Thanks to them, hypertension in the pancreatic ductal system is reduced, and due to this, pain is weakened and relieved.

If therapeutic measures aimed at reducing pancreatic secretion do not have an analgesic effect, doctors prescribe non-narcotic or narcotic analgesics. “Analgin”, “Ketoprofen”, “Paracetamol” - any drug for chronic pancreatitis can be prescribed by a doctor from the first group of drugs. Among the drugs related to narcotic analgesics, Promedol, Tramal, Fortral can be selected.

Treatment of chronic pancreatitis in adults may also include enzyme replacement therapy. Indications for its use are excretion of more than 15 g of fat per day in feces, diarrhea, rapid loss of body weight. Multienzyme drugs are “Abomin”, “Forte-N”, “Creon”, “Pancreatin”, “Festal”, “Pankreoflat”, “Digestal”, “Wobenzym”.

Surgical treatment of the disease

In some cases, chronic pancreatitis requires surgery. The indications are:

• pain that is not relieved with medications and diet;
• the presence of abscesses and cysts in the pancreas;
• obstruction of the bile ducts, which cannot be resolved using the endoscopic method;
• duodenal stenosis;
• fistulas in the pancreas with the development of pleural effusion or ascites;
• suspected cancer, not confirmed cytologically or histologically.

“Chronic pancreatitis, symptoms and treatment in adults” is an important medical topic that requires attention. This is an insidious disease, a progressive and irreversible process. However, treatment is still necessary. It allows you to prolong the life of sick people, relieves the unpleasant symptoms characteristic of chronic pancreatitis. For example, if you follow the recommendations on diet, abstinence from alcohol, and proper drug therapy, patients live up to 10 years. Half of those who do not seek medical help and continue to drink alcohol, smoke, and eat poorly die before this time.

The most dangerous of the pathological processes that occur in the pancreas is chronic pancreatitis, which develops over a long period of time.

It affects the functioning of adjacent organs and also provokes dangerous complications.

This is a long-term inflammatory disease of the pancreas, which manifests itself with irreversible changes that cause pain or persistent deterioration in function.

The disease in question requires following a special diet, drug treatment, and in some situations, surgical intervention.

Since the chronic form of pancreatitis has various causes and differs in the degree of poisoning, pathology therapy involves immediately calling an ambulance and sending the patient to the hospital for further examination.

The diagnosis is made taking into account attacks of abdominal pain, manifestations of insufficiency of pancreatic exocrine function in a patient who constantly drinks alcohol.

In contrast to acute pancreatitis, in chronic pancreatitis there is rarely an increase in the content of enzymes in the bloodstream or urine, so when this happens, it is possible to suggest the formation of a pseudocyst or pancreatic ascites.

The choice of imaging methods is based on the availability of the technique, the presence of the necessary skills among specialists and the invasiveness of the diagnostic method.

• Radiography. In 1/3 of situations, this procedure helps to identify pancreatic calcification or stones inside the duct. This will make it possible to eliminate the need for subsequent diagnostics to confirm the disease. The degree of certainty of evidence is 4. The level of strength of recommendations is C.
• Transabdominal ultrasound. This diagnostic measure lacks sensitivity and specificity. Infrequently provides information that is sufficient to identify pathology. Its main purpose will be to eliminate other factors of pain in the abdominal cavity. The degree of credibility of recommendations is A.
• CT scan with contrast agent injection. Today it is considered the method of choice for the initial diagnosis of the disease. The most effective method for determining the location of pancreatic stones. The strength of the recommendations is B.
• Endoscopic ultrasound. The method is minimally invasive. Used for medicinal purposes. It is considered the most proven method for visualizing changes in the parenchyma and ducts of the pancreas at the initial stage of chronic pancreatitis.
• ERCP. High probability of detecting the disease in question.

Lead tactics

The tactics for managing a patient with this pathology are based on the following components:

• Establishing a diagnosis of chronic pancreatitis;
• An attempt to identify the origin of the disease;
• Establishing the stage;
• Diagnosis of pancreatitis;
• Development of a therapeutic regimen;
• Prognosis based on the current situation and the chosen treatment regimen.

Conservative treatment

Conservative therapy for patients with the disease in question is aimed at relieving symptoms and preventing the occurrence of adverse consequences; the following tasks are highlighted:

• refusal to use alcoholic beverages and tobacco smoking;
• identifying provoking factors of pain in the abdominal cavity and reducing their intensity;
• therapy for insufficiency of pancreatic exocrine function;
• detection and treatment of endocrine insufficiency in the initial stages before the formation of adverse consequences;
• nutritional support.

Behavior change

Complete exclusion from drinking alcoholic beverages is recommended to reduce the incidence of dangerous consequences and deaths.

It is extremely difficult to identify the role of tobacco smoking with excessive consumption of alcoholic beverages as a provoking factor that affects the course of chronic pancreatitis, since it often accompanies excessive alcohol consumption.

However, refusing to drink alcohol does not slow down the progression of the pathological process in all cases.

In such a situation, patients with the disease in question are recommended to quit smoking. Level of credibility of recommendations C.

Relief of abdominal pain

Often pain is caused by pseudocysts, duodenal stenosis, and severe duct obstruction.

In a situation where clinical diagnosis confirms the presence of an unpleasant pathology and substantiates the relationship with abdominal pain, endoscopic and surgical treatment methods are required at the initial stage of therapy.

Typically, such cases are discussed collectively by specialists from various fields to develop an optimal treatment regimen.

The duration of continuous treatment with paracetamol is no more than 3 months with monitoring of the patient’s well-being and blood counts. Strength of recommendations - C.

Treatment of exocrine pancreatic insufficiency

Impaired digestibility of fats and proteins manifests itself only when the functioning of the pancreas deteriorates by more than 90%.

Surgery on this organ can provoke the formation of exocrine insufficiency and the implementation of enzyme replacement treatment.

Proper and timely therapy makes it possible to prevent dangerous consequences and reduce mortality due to malnutrition.

The purpose of replacement treatment will be to improve the patient’s ability to consume, process and assimilate a certain amount of basic food components.

Laboratory signs for such therapy:

• steatorrhea;
• chronic diarrhea;
• nutritional deficiency;
• pancreatic necrosis, severe form of chronic pancreatitis;
• undergone surgery on the pancreas with impaired passage of food;
• condition after surgery on this organ with manifestations of exocrine insufficiency.

Prescription of enzyme replacement treatment of the pancreas is recommended for patients with chronic pancreatitis and insufficiency of exocrine function, as it helps improve the processing and absorption of fats.

Treatment of endocrine insufficiency of the pancreas

Dietary nutrition for pancreatogenic diabetes mellitus requires correction of malabsorption. Fractional meals are used in preventive measures for hypoglycemia.

If insulin treatment is prescribed, the target glucose level corresponds to that for type 1 diabetes mellitus.

It is necessary to teach the patient to prevent severe hypoglycemia, to focus on avoiding alcoholic beverages, to increase physical activity, and to eat small meals.

When treating diabetes mellitus with chronic pancreatitis, it is recommended to monitor the glucose level in the bloodstream in order to prevent adverse consequences. Convincingness of recommendations -V.

Surgery

In case of complex pathological process, in some situations with intractable pain in the abdominal cavity, endoscopic or surgical therapy is prescribed.

The decision is made by doctors who specialize in the treatment of pancreatic diseases.

In the normal course of the pathology, invasive intervention is aimed at correcting changes in the ducts of a given organ and inflammation of the parenchyma.

The decision to carry out an operation must be balanced, taking into account all the risks of adverse consequences.

It is necessary to exclude other factors of pain in the gastrointestinal tract. Such treatment will be necessary if there is no adequate relief of discomfort within 3 months of conservative therapy, as well as if there is a significant deterioration in the quality of life.

Endoscopic treatment

There are no studies evaluating the effect of endoscopic therapy on pancreatic function in patients.

Treatment for pseudocysts is not prescribed regardless of their size. Drainage may be more appropriate than surgical intervention, as it has a better benefit/risk profile.

Prevention and follow-up

Preventive measures for chronic pancreatitis are based on extrapolation of research data, according to the results of which it is possible to suggest that eliminating the consumption of alcoholic beverages and smoking is the reason that reduces the likelihood of progression of the disease in question.

It is likely that more significant provoking factors for exacerbation of chronic pancreatitis will be obesity, overeating and hypokinesia after eating, and a constant lack of antioxidants in food products.

However, it should be remembered that some patients scrupulously adhere to a strict diet in order to prevent a re-attack of the disease.

As a result, they can become nutritionally deficient. Based on the above, based on the results of various studies, the following lifestyle changes are recommended to prevent the disease in question:

• articulate meals (up to 6 times a day, in small portions with even distribution of fatty foods), avoidance of overeating;
• taking various foods with a low concentration of fats and cholesterol (unrefined vegetable fats are limited only to those patients who are overweight);
• drawing up a menu with the required amount of dietary fiber, which is contained in grains, vegetables and fruits;
• maintaining a balance between the food eaten and physical activity (in order to stabilize body weight to achieve optimal weight, taking into account age indicators).

For the purpose of effective primary prevention of chronic pancreatitis, it would be optimal to conduct a total dispensary control of the population for the timely detection of the disease of the bile ducts in question, hyperlipidemia.

However, today this idea has no practical implementation on the planet, since it requires significant material investments.

The validity of such tactics can be confirmed by pharmacoeconomic diagnostics.

However, such studies are unlikely due to the relatively low incidence rates of chronic pancreatitis.

These instructions are a comprehensive practical guide to eliminating the disease in question.

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Acute pancreatitis (K85)

Surgery

general information

Short description

Russian Society of Surgeons
Association of Hepatopancreatobiliary Surgeons of the CIS Countries

ICD 10: K85.0 /K85.1/ K85.2 /K85.3/ K85.8 /K85.9

Year of approval (revision frequency): 2015 (reviewed every 5 years)
ID: KR326

Definition
Acute pancreatitis(OP) is an initially aseptic inflammation of the pancreas, which can damage surrounding tissues and distant organs, as well as systems.

Coding according to ICD 10
Acute pancreatitis (K85):
. pancreatic abscess;
. acute and infectious necrosis of the pancreas;
. pancreatitis:
o acute (recurrent);
o hemorrhagic;
o subacute;
o purulent;
o NOS.

K85.0 - Ideopathic acute pancreatitis;
K85.1 - Biliary acute pancreatitis:
. gallstone panreatitis;
K85.2 - Alcoholic acute pancreatitis;
K85.3 - Drug-induced acute pancreatitis;
K85.8 - Other types of acute pancreatitis;
K85.9 - Acute pancreatitis, unspecified

Classification

The classification of acute pancreatitis of the Russian Society of Surgeons (2014) was developed taking into account the Atlanta-92 classification and its modifications proposed in Cochin in 2011 (International Association of Pancreatology) and the International Working Group on the Classification of Acute Pancreatitis (Acute Pancreatitis Classification). Working Group) in 2012
1. Mild acute pancreatitis. Pancreatic necrosis does not form in this form of acute pancreatitis (edematous pancreatitis) and organ failure does not develop.
2. Moderate acute pancreatitis. It is characterized by the presence of either one of the local manifestations of the disease: peripancreatic infiltrate, pseudocyst, localized infected pancreatic necrosis (abscess), or/and the development of general manifestations in the form of transient organ failure (no more than 48 hours).
3. Severe acute pancreatitis. It is characterized by the presence of either unbounded infected pancreatic necrosis (purulent-necrotic parapancreatitis), or/and the development of persistent organ failure (more than 48 hours).
The diagnosis of mild, moderate or severe acute pancreatitis is established based on the completed case of the disease.

Etiology and pathogenesis

The following etiological forms of acute pancreatitis are distinguished:
1. Acute alcoholic-alimentary pancreatitis - 55%.
2. Acute biliary pancreatitis (occurs due to bile reflux into the pancreatic ducts during biliary hypertension, which usually occurs due to cholelithiasis, sometimes from other causes: diverticulum, papillitis, opisthorchiasis, etc.) - 35%.
3. Acute traumatic pancreatitis (due to trauma to the pancreas, including in the operating room or after ERCP) 2 - 4%.
4. Other etiological forms of the cause: autoimmune processes, vascular insufficiency, vasculitis, drugs (hypothiazide, steroid and non-steroidal hormones, mercaptopurine), infectious diseases (viral mumps, hepatitis, cytomegalovirus), allergic factors (varnishes, paints, odors of building materials, anaphylactic shock), dyshormonal processes during pregnancy and menopause, diseases of nearby organs (gastroduodenitis, penetrating ulcer, tumors of the hepatopancreatoduodenal region) - 6 - 8%.

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

Primary factors of aggression:

a) pancreatic enzymes: trypsin, chymotrypsin - cause proteolysis of tissue proteins;

b) phospholipase A2 destroys cell membranes;

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

d) elastase destroys the vascular wall and interstitial connective tissue structures, which leads to necrosis.

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

Tertiary factors. Macrophages, mononuclear cells, neutrophils against the background of microcirculation disorders, SVR, hypoxia produce cytokines (interleukin 1,6 and 8, tumor necrosis factor, platelet activating factor, prostaglandins, thromboxane, leukotrienes, nitric oxide, suppression of the immune status.

Factors of aggression of the fourth order. Cytokines, enzymes, metabolites of various nature, formed in the pancreas, fatty tissue, intestinal wall, abdominal cavity, increase the permeability of the intestinal wall, translocation of the intestinal flora occurs, promote the entry of toxins into the portal and systemic bloodstream and lymphatic bed with damage to target organs: liver, lungs , kidneys, heart, brain, intestines, mucous membranes of the stomach and intestines.

Factors of aggression and organ dysfunction create a syndrome of “mutual burden.”

Phases of acute pancreatitis. Edematous (interstitial) pancreatitis in frequency occupies 80-85% of the structure of the disease. It is characterized by a mild degree of severity of the disease and the rare development of local complications or systemic disorders; it does not have a phase course.

Necrotizing pancreatitis (pancreatic necrosis) occurs in 15-20% of patients, clinically always manifests as a moderate or severe degree of the disease, and has a phased course of the disease with two peaks of mortality - early and late. After the early phase, which usually lasts for the first two weeks, there is a second or late phase, which can last for a period of 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 diagnostic and treatment algorithm.

Phase I - early, in turn is divided into two periods:

Phase IA is usually the first week of the disease. During this period, foci of necrosis form in the pancreatic parenchyma or surrounding tissue of varying volumes and endotoxemia develops. Endotoxicosis manifests itself as mild or profound systemic disorders in the form of organ (multiple organ) failure. The maximum period for the formation of necrosis in the pancreas is usually three days, after which it does not progress further. However, with severe pancreatitis, the period of its formation is much shorter (usually 24-36 hours). Enzymatic effusion accumulates in the abdominal cavity (enzymatic peritonitis and parapancreatitis), which is one of the sources of endotoxicosis. The average severity of the disease is manifested by transient dysfunction of individual organs or systems. In severe forms of the disease, the clinical picture may be dominated by organ (multiple organ) failure: cardiovascular, respiratory, renal, hepatic, etc.

Phase IB is usually the second week of the disease. It is characterized by the body’s reaction to formed foci of necrosis (both in the pancreas and in parapancreatic tissue). Clinically, the phenomena of resorptive fever prevail, and a peripancreatic infiltrate is formed.

Phase II - late, sequestration phase (starts, as a rule, from the 3rd week of the disease, can last several months). Sequesters in the pancreas and retroperitoneal tissue usually begin to form from the 14th day from the onset of the disease. When large large fragments of necrotic pancreatic tissue are rejected, depressurization of its ductal system and the formation of an internal pancreatic fistula can occur. The configuration of pancreatic necrosis (localization, depth, relationship to the main pancreatic duct, etc.) and the volume of remaining viable pancreatic parenchyma determine the number, scale and rate of spread of fluid formation in the retroperitoneal space, the risk of infection and the development of other complications. There are two possible options for the course of this phase:

Aseptic sequestration - sterile pancreatic necrosis is characterized by the formation of an isolated accumulation of fluid in the pancreas and postnecrotic 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, which can be limited (abscess) or not limited (purulent-necrotizing parapancreatitis). With the progression of purulent complications, infected pancreatic necrosis may have its own complications (purulent-necrotic leaks, abscesses of the retroperitoneal space and abdominal cavity, purulent peritonitis, arrosive and gastrointestinal bleeding, digestive fistulas, sepsis, etc.) with the development of endotoxicosis of infectious origin, organ (multiple organ) failure.

Epidemiology

Currently, the prevalence of acute pancreatitis is 32-389 people per 1 million population, mortality from this disease ranges from 6 to 12 people per 1 million population. At the present stage, there have been significant changes in the statistics on the frequency of diseases in large metropolitan areas, passing through ambulances under the brand of “acute abdomen”: for the period from 2000. until 2009 acute pancreatitis confidently took first place. In recent years, the number of patients with acute pancreatitis has decreased, however, despite the decrease in the total number of patients, the share of AP in the structure of diseases of the “acute abdomen” remains at a fairly high level (25%-35%), takes second place and is second only to acute appendicitis. During this period, there was a tendency towards a decrease in overall mortality in acute pancreatitis from 4.0%-4.5% to 2.5%-3.5%, however, postoperative mortality remains at a fairly high level (20%-25%).

Diagnostics

Diagnosis of AP is an emergency measure. Patients with suspected AP are subject to emergency hospitalization in the surgical department of a multidisciplinary hospital.

Complaints and anamnesis
The basis for the diagnosis of acute pancreatitis during the initial examination of the patient is the classic triad of symptoms - severe epigastric pain radiating to the back or encircling in nature, repeated vomiting and muscle tension in the upper abdomen. Most often, the appearance of symptoms is preceded by a heavy intake of food or alcohol, or the presence of gallstones. Typical pain syndrome always occurs with acute pancreatitis. Usually it is intense, persistent, and is not relieved by antispasmodics and analgesics. The onset of acute pancreatitis should be determined by the time of onset of abdominal pain syndrome, and not by the time the patient was admitted to the hospital. The moment of onset of the disease can be identified by carefully collecting anamnesis. In case of severe pain, injection of antispasmodic and non-steroidal anti-inflammatory drugs is acceptable. When transferring a patient from one hospital to another (for example, from a central district hospital to a regional hospital), the onset of the disease should be considered the time of onset of pain when initially seeking medical help.
Clinical manifestations of acute pancreatitis depend on the morphological form, phase of the disease, the 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 AP, so it is advisable to consider the diagnosis of AP in the corresponding phases of the disease.

Primary protocol for diagnosis and tactics for acute pancreatitis in phase IA of the disease. As a rule, it is carried out in the emergency department or emergency department.
To establish the diagnosis of acute pancreatitis (after excluding other surgical pathologies) recommended use a combination of at least two of the following identified characteristics:
a) typical clinical picture (intense girdling pain that cannot be controlled by antispasmodics, uncontrollable vomiting, bloating; consumption of alcohol, spicy food, or a history of cholelithiasis, etc.);
b) characteristic signs according to ultrasound: increased size, decreased echogenicity, blurred contours of the pancreas; the presence of free fluid in the abdominal cavity;
c) hyperenzymemia (hyperamylasemia or hyperlipasemia), exceeding the upper limit of normal by three times or more.

Comments: If the diagnosis of acute pancreatitis is established on the basis of methods a), b) and c), then performing multispiral computed tomographic angiography (MSCT) or magnetic resonance imaging (MRI) to make a diagnosis of acute pancreatitis Not recommended.
Convincing level of recommendation is “B”.

To assess the severity of AP and prognosis of disease development recommended application of the scale of criteria for primary express assessment of the severity of acute pancreatitis (St. Petersburg Research Institute of Emergency Medicine named after I.I. Dzhanelidze - 2006):
- peritoneal syndrome;
- oliguria (less than 250 ml in the last 12 hours);
- skin symptoms (facial hyperemia, marbling, cyanosis);
- systolic blood pressure less than 100 mm Hg;
- encephalopathy;
- hemoglobin level more than 160 g/l;
- leukocyte count more than 14 x10 9 /l;
- blood glucose level more than 10 mmol/l;
- urea level more than 12 mmol/l;
- metabolic disorders according to ECG data;
- cherry or brown-black color of enzymatic exudate obtained during laparoscopy (laparocentesis);
- detection during laparoscopy of widespread enzymatic parapancreatitis, extending beyond the boundaries of the omental bursa and spreading along the flanks;
- the presence of widespread steatonecrosis detected during laparoscopy;
lack of effect from basic therapy.
Comments: Scale rating:
· If a particular patient has at least 5 of the listed signs, then with a 95% probability he has a severe form of AP.
· If there are 2-4 signs - moderate OP.
· If there is no sign or there is at most one of these is a mild form of AP.
The most important thing is the early detection of severe pancreatitis, the results of treatment of which are largely determined by the timing of its onset. The presence of at least two signs listed in the rapid assessment scale allows one to diagnose moderate-to-severe (severe) AP, which is subject to mandatory referral to the intensive care unit. For the remaining patients (mild AP), hospitalization in the surgical department is indicated.

· To assess organ and multiple organ dysfunctions recommended use the SOFA scale. If it is impossible to use multiparameter scales to determine the severity of AP recommended application of clinical and laboratory criteria: signs of systemic inflammatory response syndrome (SIRS); hypocalcemia< 1,2 ммоль/л, гемоконцентрация: гемоглобин крови >160 g/l or hematocrit > 40 units, hyperglycemia > 10 mmol/l; C - reactive protein > 120 mg/l; shock (systolic blood pressure< 90 мм.рт.ст.) дыхательная недостаточность (РО2<60мм.рт.ст.); почечная недостаточность (олиго-анурия, креатинин >177 µmol/l); liver failure (hyperfermentemia); cerebral insufficiency (delirium, stupor, coma); gastrointestinal bleeding (more than 500 ml/day); coagulopathy (platelet< 100 х 10 9 /л, фибриноген < 1,0г/л). Convincing level of recommendation is “B”.

· Intense pain syndrome, not relieved by narcotic analgesics, rapidly progressing jaundice, absence of bile in the duodenum during FGDS, signs of biliary hypertension according to ultrasound data indicate the presence of an impacted stone in the major duodenal papilla (MDP). In this case, the patient recommended urgent (12-24 hours) restoration of the passage of bile and pancreatic juice, the optimal method of which is EPST with lithoextraction, after which, if possible, it is advisable to drain the main pancreatic duct. In case of an impacted stone of the obstructive stone and in acute pancreatitis of the EPST, it is undesirable and dangerous to perform contrasting of the ducts. Convincing level of recommendation is “C”.
· CT scan. Recommended performing early MSCT (MRI) in the following cases:
- Uncertainty of diagnosis and differential diagnosis with other diseases.
- The need to confirm the severity based on identified clinical prognostic signs of severe AP.
- Lack of effect from conservative treatment.
Convincing level of recommendation is “C”.

· For the diagnosis of pancreatic necrosis in the optimal time (and assessment of the entire volume of pathological changes in the chest, abdominal cavity and retroperitoneal tissue) recommended performing MSCT (MRI) on days 4–14 of the disease. Convincing level of recommendation is “B”.

· Follow-up MSCT (MRI) recommended perform when the disease progresses, in the absence of effect from treatment and to clarify the localization of foci of suppuration before performing drainage interventions. Convincing level of recommendation is “C”.
Comments: The use of the Balthazar CT severity index of pancreatitis in clinical practice is not a mandatory diagnostic test. It is advisable to use it to predict the severity of the disease.

Protocol for diagnosis and monitoring of peripancreatic infiltrate in phase IB of the disease.
The second week of the disease is characterized by the onset of a period of aseptic inflammatory reaction to foci of necrosis in the pancreas and surrounding tissue, which is clinically expressed by the appearance of an infiltrate in the epigastric region (local component) and resorptive fever (systemic component of inflammation). Peripancreatic infiltrate (PI) and resorptive fever are natural signs of severe or moderate pancreatitis, while in mild pancreatitis these signs are not detected.
In addition to clinical signs (peripancreatic infiltrate and fever) in the second week of the early phase of AP recommended define:
- Laboratory indicators of systemic inflammatory response syndrome: leukocytosis with a shift to the left, lymphopenia, increased ESR, increased concentration of fibrinogen, C-reactive protein, etc.;
- Ultrasound signs of PI (continued increase in the size of the pancreas, blurred contours and the appearance of fluid in the peripancreatic tissue). D".
To monitor peripancreatic infiltrate recommended carry out a dynamic study of clinical and laboratory parameters and repeated ultrasounds (at least 2 studies in the second week of the disease). Recommendation Conviction Level "D".
At the end of the second week of illness recommended performing a computed tomography scan of the pancreas, Convincing level of recommendation is “C”.
Comments: By this time, the vast majority of patients experience one of three possible outcomesPhase IB:
- Resorption, in which there is a reduction in local and general manifestations of the acute inflammatory reaction.
- Aseptic sequestration of pancreatic necrosis with a possible subsequent outcome in a pancreatic pseudocyst: preservation of the size of the PI with normalization of health and subsidence of the systemic inflammatory response syndrome (SIRS) against the background of persistent hyperamylasemia.
- Septic sequestration (development of purulent complications).

Protocol for diagnosis and monitoring of pancreatic pseudocysts in phase II of the disease (in the phase of aseptic sequestration).
The clinical form of acute pancreatitis in the aseptic sequestration phase is a postnecrotic pancreatic pseudocyst, the formation period of which ranges from 4 weeks and on average up to 6 months.
· In the phase of aseptic sequestration recommended Use the following criteria to verify a pancreatic cyst:
- Subsidence of the systemic inflammatory response syndrome against the background of persistent hyperamylasemia. Recommendation Conviction Level "D".
- An increase in the size of the fluid accumulation in the parapancreatic tissue by the 5th week of the disease and the appearance of a wall according to ultrasound and CT. Convincing level of recommendation is “C”.
- If there are no complications (see below), the patient can be discharged for outpatient treatment. The size of the cyst must be monitored by ultrasound (once every 2-4 weeks). Recommendation Conviction Level "D".
Comments:If during aseptic sequestration the pancreatic ductal system is not opened, then cyst formation does not occur. In this case, as a rule, there is resorption of the peripancreatic infiltrate (reduction of fluid accumulation in the pancreas) within a period of up to 4 weeks. This period is sick recommended carried out under dynamic medical supervision (permissible on an outpatient basis).

Protocol for the diagnosis of purulent complications of acute pancreatitis in phase II of the disease (in the phase of septic sequestration).
Infection of the focus of pancreatogenic destruction occurs, on average, at the end of the 2nd - beginning of the 3rd week from the onset of the disease. However, with late admission of the patient, inadequate treatment, or after too early and hasty surgery, infection of areas of pancreatic necrosis and purulent-destructive complications may develop earlier, bypassing the period of aseptic destruction (“crossover phases”). The clinical form of acute pancreatitis in the phase of septic sequestration (the third week from the onset of the disease or more) is infected pancreatic necrosis: limited - pancreatic abscess (PA) or not limited - purulent-necrotic parapancreatitis (NPP) of varying degrees of prevalence. An important point is the timely diagnosis of infection and verification of clinical and morphological forms of pancreatogenic infection.
To verify pancreatic abscess or purulent-necrotic parapancreatitis recommended use:
1). Clinical and laboratory manifestations of a purulent focus:
- Progression of clinical and laboratory indicators of acute inflammation in the third week of AP. Convincing level of recommendation is “C”.
- Markers of acute inflammation (increased fibrinogen by 2 times or more, high “C”-reactive protein, procalcitonin, etc.). Convincing level of recommendation is “C”.
2). MSCT, MRI, ultrasound (increase in the process of observation of fluid formations, identification of devitalized tissues and/or the presence of gas bubbles). Convincing level of recommendation is “B”.
3). Positive results of bacterioscopy and bacterial culture of the aspirate obtained by fine-needle puncture. Convincing level of recommendation is “B”.
Comments: In the case where the methods of paragraphs 2 and 3 fail to identify signs of infection, recommended The decision about the presence of purulent complications in patients and indications for surgical treatment is made on the basis of the laboratory and clinical minimum (clause 1.1).

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Treatment

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

Conservative treatment
Early ( I ) phase

I And the phase of the disease.
As the optimal treatment for AP in phase IA recommended intensive conservative therapy.
Recommendation Conviction Level "A".
Comments: Surgical intervention in the form of laparotomy is indicated only in the event of the development of surgical complications that cannot be eliminated with minimally invasive technologies.

I. Protocol for the treatment of mild acute pancreatitis.
1) Hospitalization of patients with mild AP is carried out in the surgical department.
For the treatment of mild pancreatitis recommended carrying out a basic treatment complex:
- hunger;
- probing and aspiration of gastric contents;
- local hypothermia (cold on the stomach);
- analgesics;
- antispasmodics;
- infusion therapy in a volume of up to 40 ml per 1 kg of patient’s body weight with forced diuresis for 24-48 hours.
· It is advisable to enhance basic therapy with inhibitors of pancreatic secretion. Convincing level of recommendation is “C”.
2) If there is no effect from the basic therapy (item 1) within 6 hours and the presence of at least one more sign of the express assessment scale (protocol I.2), moderate-to-severe (severe) pancreatitis should be stated.
· For moderate-to-severe (severe) pancreatitis, treatment of the patient recommended carry out to the intensive care unit in accordance with protocols III, IV. Convincing level of recommendation is “C”.

II. Intensive care protocol for moderate acute pancreatitis
The main type of treatment is conservative therapy. The above basic treatment complex for moderate-severe AP recommended supplemented with a specialized treatment complex (see below). The effectiveness of the latter is maximum when treatment is started early (the first 24 hours from the onset of the disease). Upon admission, patients with moderate AP must be hospitalized in the intensive care unit (ICU). To eliminate diagnostic errors, it is advisable for the duty service to observe patients with moderate AP during the day in the ICU. In the absence of signs of organ failure and progression of the disease during the day, patients with moderate AP can be transferred to the surgical department. Subject to the appearance of signs of organ dysfunction or failure in patients with moderate AP who are in the surgical department, which indicates the progression of the disease - hypotension (BP<100мм.рт.ст.), дыхательной недостаточности (ЧД>30 per minute), delirium, etc. (see protocol I.2, I.3), - the latter must be transferred to the ICU.
Convincing level of recommendation is “C”.

Specialized treatment:
· Recommended the use of pancreatic secretion inhibitors (the optimal period is the first three days of the disease). Recommendation Conviction Level "D».
· Recommended active rheological therapy. Recommendation Conviction Level "D».
· Recommended infusion therapy with a total of at least 40 ml of appropriate infusion agents per 1 kg of body weight with forced diuresis in the presence of organ dysfunction (in the absence of contraindications). Convincing level of recommendation is “C”.
· Recommended antioxidant and antihypoxic therapy. Recommendation Conviction Level "D».
· Recommended evacuation of toxic exudates according to indications (see standard V). For enzymatic peritonitis - sanitation laparoscopy. Percutaneous drainage of the abdominal cavity under ultrasound guidance or laparocentesis is acceptable. Recommendation Conviction Level "D».
· Not recommended use of antibiotics for prophylactic purposes. Convincing level of recommendation is “B”.

III. Intensive care protocol for severe acute pancreatitis
The main type of treatment is intensive therapy. The above basic treatment complex for severe AP is not effective enough, recommended it should be supplemented with a specialized treatment complex (see below). The effectiveness of the latter is maximum when treatment is started early (the first 12 hours from the onset of the disease). Upon admission, patients with severe AP should be hospitalized in the intensive care unit. The treatment and diagnostic complex for patients with severe AP must be carried out in an ICU; after relieving the symptoms of organ failure and stabilizing the condition (relieving delirium, hemodynamic disorders, respiratory activity, etc.), it is possible to transfer the patients to the surgical department. Convincing level of recommendation is “C”.

Specialized treatmente:
The following are added to Protocols II and III:
· Recommended use of extracorporeal detoxification methods:
- a) plasmapheresis;
- b) hemofiltration
Recommendation Conviction Level "D".
· Recommended nasogastric intubation for decompression and, if possible, nasogastrointestinal intubation for early enteral support. Recommendation Conviction Level "D".
· Recommended correction of hypovolemic disorders. Convincing level of recommendation is “C”.
· Recommended performing an epidural block. Recommendation Conviction Level "D".
· Not recommended use of antibiotics for prophylactic purposes in the first three days of the disease. Convincing level of recommendation is “C”.
· Recommended prescription of disaggregant antithrombotic therapy. Recommendation Conviction Level "D".

Protocol for the treatment of acute pancreatitis in I In the disease phase, i.e. treatment of peripancreatic infiltrate
In the vast majority of patients, treatment of peripancreatic infiltrate is conservative. Laparotomy in the second week of AP is performed only for surgical complications (destructive cholecystitis, gastrointestinal bleeding, acute intestinal obstruction, etc.) that cannot be eliminated with minimally invasive technologies.

Composition of the treatment complex:
· Recommended continuation of basic infusion-transfusion therapy aimed at replenishing water-electrolyte, energy and protein losses according to indications. Convincing level of recommendation is “C”.
· Recommended therapeutic nutrition: table No. 5 for moderate-severe AP; nutritional support (oral, enteral or parenteral) for severe AP. Convincing level of recommendation is “C”.
· Recommended systemic antibiotic prophylaxis (cephalosporins of III-IV generations or fluoroquinolones of II-III generations in combination with metronidazole, reserve drugs - carbapenems). Convincing level of recommendation is “C”.
· Recommended immunotherapy (correction of cellular and humoral immunity is desirable). Recommendation Conviction Level "D».

Late ( II ) phase (sequestration)

Protocol for the treatment of acute pancreatitis in the aseptic sequestration phase, i.e. treatment of pancreatic pseudocyst
· Not recommended to operate on small pancreatic pseudocysts (less than 5 cm). Convincing level of recommendation is “C”. Comments: Small pancreatic pseudocysts (less than 5 cm) are subject to dynamic observation by a surgeon.
Large pancreatic pseudocysts (more than 5cm) recommended operate as planned in the absence of complications. Convincing level of recommendation is “C”.
Comments: The operation of choice for an immature (unformed) pseudocyst (less than 6 months) is external drainage. A mature (formed) pseudocyst (more than 6 months) is subject to surgical treatment as planned.
Complications of pancreatic pseudocyst:
1. Infection.
2. Bleeding into the cyst cavity.
3. Perforation of the cyst with a breakthrough into the free abdominal cavity with the development of peritonitis.
4. Compression of neighboring organs with the development of obstructive jaundice, gastric stenosis, intestinal obstruction, etc.

Surgery

Early ( I ) phase

Protocols for the treatment of acute pancreatitis in I And the phase of the disease
Laparoscopic surgery protocol
· Perform laparoscopy recommended:
- patients with peritoneal syndrome, including those with ultrasound signs of free fluid in the abdominal cavity. Convincing level of recommendation is “C”. ;
- if necessary, differential diagnosis with other diseases of the abdominal organs. Recommendation Conviction Level "C».
Comments: The objectives of laparoscopic surgery can be diagnostic, prognostic and therapeutic.
· Recommended performing percutaneous drainage of the abdominal cavity under ultrasound guidance or laparocentesis. Convincing level of recommendation is “C”.
Objectives of laparoscopic surgery:
a) confirmation of the diagnosis of acute pancreatitis (and, accordingly, exclusion of other diseases of the abdominal cavity, primarily acute surgical pathology - mesenteric thrombosis, etc.); Signs of OP include:
- the presence of edema of the root of the mesentery of the transverse colon;
- presence of effusion with high amylase activity (2-3 times higher than blood amylase activity);
- presence of steatonecrosis;
b) identifying signs of severe pancreatitis:
- hemorrhagic nature of the enzymatic effusion (pink, raspberry, cherry, brown);
- widespread foci of steatonecrosis;
- extensive hemorrhagic permeation of the retroperitoneal tissue, extending beyond the pancreas;
Verification of serous (“vitreous”) edema in the first hours of the disease (especially against the background of the patient’s severe general condition) does not exclude the presence of severe pancreatitis, since laparoscopy in the early stages may not reveal signs of severe pancreatitis, i.e. the disease may further progress.
c) therapeutic tasks:
· removal of peritoneal exudate and drainage of the abdominal cavity.

Late ( II ) phase (sequestration)

Protocol for the treatment of acute pancreatitis in the phase of septic sequestration, i.e. treatment of purulent complications
· For purulent complications of AP recommended surgical intervention, the purpose of which is the rehabilitation of the affected retroperitoneal tissue. Recommendation level “A”
Comments: The intervention includes opening, sanitation and drainage of the affected retroperitoneal tissue. The main method of sanitation of purulent-necrotic foci is necrosequestrectomy, which can be either single-stage or multi-stage, and is achieved using both minimally invasive and traditional methods.
· When deciding on primary drainage of a pancreatic abscess or purulent-necrotic parapancreatitis recommended give preference to minimally invasive interventions (ultrasound-guided drainage, retroperitoneoscopy, minilaparotomy using the Mini-Assistant kit, etc.). Convincing level of recommendation is “B”.
Comments: If minimally invasive drainage is ineffective, the operation of choice is sanitary laparotomy with necrosequestrectomy. Drainage is preferably performed via extraperitoneal approaches. The optimal timing for performing the first sanitary laparotomy with necrosequestrectomy is 4-5 weeks of illness. If complications develop that cannot be treated with minimally invasive interventions, it is necessary to perform open surgery, including through a mini-access.
After surgery, most patients develop an external pancreatic fistula, which, after stopping the inflammatory process, is treated conservatively and closes on its own in an average of 2-4 months.
· For persistent pancreatic fistula that does not close for more than 6 months, recommended surgical treatment as planned. Convincing level of recommendation is “C”.
Comments: As a rule, a pancreatic fistula in this case is associated with the large ducts of the pancreas.
In the postoperative period, complex therapy is indicated:
· Recommended parenteral or enteral nutritional support (through a tube inserted into the small intestine through the ligament of Treitz) if oral nutrition is not possible. Convincing level of recommendation is “B”.
· Recommended systemic antibiotic therapy in combination with the prevention of dysbacteriosis and other complications. Recommendation Conviction Level "B».
Comments:The choice of antibacterial drug depends on the sensitivity of the isolated microorganisms.
· Recommended Immunocorrection, the options of which are determined individually depending on clinical and laboratory parameters. Recommendation Conviction Level "D».

Criteria for assessing the quality of medical care

№	Quality criteria	Level of evidence	Recommendation Conviction Level
1	Examination by a surgeon was performed no later than 1 hour from the moment of admission to the hospital	WITH	2+
2	Performing MSCT (MRI) to determine pancreatic necrosis	IN	1+
3	Hospitalization of a patient in the ICU when organ failure is detected	IN	1+
4	The use of conservative therapy as the optimal type of treatment in the early (I) phase of the disease	A	1++
5	Use of laparoscopy, ultrasound-guided percutaneous drainage of the abdominal cavity or laparocentesis in phase IA of the disease in the presence of peritoneal syndrome or for differential diagnosis with other diseases	WITH	2++
6	The use of surgical intervention in the development of purulent complications in the late (II) phase of the disease (minimally invasive or traditional laparotomy)	A	1++
7	The use of minimally invasive interventions (ultrasound-guided drainage, retroperitoneoscopy, minilaparotomy using the Mini-Assistant kit, etc.) when deciding on primary drainage of a pancreatic abscess or purulent-necrotic parapancreatitis	IN	2++
8	A study of effusion from the abdominal cavity was performed to determine the level of amylase in phase IA of the disease	WITH	2+
9	A bacteriological examination of the contents obtained during a fine-needle puncture or after performing a sanitizing operation was performed	IN	1+
10	The severity of AP was assessed on the SOFA scale more than 2 points or signs of organ failure: renal failure: creatinine >171 μ mol/L (>2.0 mg/dL) < 300 mmHg (<40 kPa).	IN	1+
11	Establishing a diagnosis of “acute pancreatitis” no later than 1 hour after receiving ultrasound data and blood enzymes	IN	1+

Information

Sources and literature

1. Clinical recommendations of the Russian Society of Surgeons
   1. 1. Bradley E.L. 3rd. A clinically based classification system for acute pancreatitis. Summary of the international symposium on acute pancreatitis, Atlanta, 1992 // Arch. Surg. – Vol. 128, 1993; R. 586-590. 2. Tolstoy A.D., Sopiya R.A., Krasnorogov V.B., Vashetko R.V., Goltsov V.R., Andreev M.I. Destructive pancreatitis and parapancreatitis. - St. Petersburg, “Hippocrates”, 1999, - 128 p. 3. Uhl W., Warshaw A., Imrie C. IAP guidelines for the surgical management of acute pancreatitis // Pancreatology. 2002. Vol. 2. P. 565–573. 4. Bagnenko S.F., Tolstoy A.D., Krasnogorov V.B. and others. Acute pancreatitis (Diagnosis and treatment protocols) // Annals of Surgical Hepatology. – 2006, T.11, No. 1. – P. 60 – 66 5. Banks P.A., Freeman M.L. Practice Guidelines in Acute Pancreatitis // Am J Gastroenterol 2006;101:2379–2400. 6. Savelyev V.S., Filimonov M.I., Burnevich S.Z. Acute pancreatitis. / National Guide to Surgery. – 2009, vol.2. - With. 196 – 229. 7. Dellinger E.P., Forsmark C.E., Layer P., Levy P., Maravi-Poma E., Petrov M.S., Shimosegawa T., Siriwardena A.K., Uomo G., Whitcomb D.C., Windsor J.A. Determinant_based classification of acute pancreatitis severity: an international multidisciplinary consultation. Ann. Surg. 2012; 256(6):875–880. 8. Banks P.A., Bollen T.L., Dervenis C., Gooszen H.G., Johnson C.D., Sarr M.G., Tsiotos G.G., Vege S.S. Acute Pancreatitis Classification Working Group. Classification of acute pancreatitis 2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013; 62(1):102–111. 9. Tolstoy A.D. Parapancreatitis (etiology, pathogenesis, diagnosis, treatment). / A.D. Tolstoy, V.P. Panov, V.B. Krasnorogov and others // – St. Petersburg, 2003. – 256 p. 10. Kubyshkin, V.A. Acute pancreatitis // Pacific Medical Journal. – 2009., No. 2. – P. 48-52. 11. Bagnenko S.F. Surgical pancreatology / Bagnenko S.F., Kurygin A.A., Sinenchenko G.I. – St. Petersburg: Rech, 2009. – 608 p. 12. Ermolov A.S., Ivanov P.A., Blagovestnov D.A. and others. Diagnosis and treatment of acute pancreatitis. – M., “VIDR”, 2013. – 382 p. 13. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Working Group IAP/APA (International Association of Pancreatology /American Pancreatic Association) Acute Pancreatitis Guidelines // Pancreatology - No. 13,2013; R. 1-15. 14. Zatevakhin I.I., Tsitsiashvili M.Sh., Budurova M.D., Altunin A.I. Pancreatic necrosis. – M., 2007 – 223 p. 15. Prudkov M.I. Clinical recommendations for the provision of medical care to the population of the Ural Federal District. – Ekaterinburg, 2013. – pp. 23 – 29. 16. Protocols for examination and treatment of patients with acute pancreatitis. Methodological recommendations edited by Yu.L. Shevchenko. – M., 2010 – 21 p. 17. Dibirov M.D., Yuanov A.A. Pancreatic necrosis. Diagnostic and treatment protocol. Educational and methodological manual. – Moscow, 2012. – 366 p. 18. Polushin Yu.S., Sukhovetsky A.V., Surkov M.V., Pashchenko O.V., Shirokov D.M. Acute postoperative pancreatitis. – St. Petersburg: Foliant, 2003. – 160 p. 19. Savelyev V.S., Gelfand B.R., Filimonov M.I. and others. Destructive pancreatitis. Evidence-based methods of diagnosis and treatment. Guidelines. – M., 2008. – 11 p. 20. Dyuzheva T.G., Dzhus E.V., Ramishvili V.Sh., Shefer A.V., Platonova L.V., Galperin E.I. Early CT signs of predicting various forms of parapancreatic necrosis. // Annals of surgical hepatology. – 2009., T. 14. No. 4. – P. 54-63. 21. Dyuzheva T.G., Dzhus E.V., Shefer A.V., Akhaladze G.G., Chevokin A.Yu., Kotovsky A.E., Platonova L.V., Galperin E.I. Configuration of pancreatic necrosis and differentiated treatment of acute pancreatitis. // Annals of surgical hepatology. – 2013., T.18, No. 1. – pp. 92-102. 22. Dyuzheva T.G., Ternovoy S.K., Dzhus E.V., Shefer A.V., Galperin E.I. Multislice computed tomography in the diagnosis of acute pancreatitis and local parapancreatic complications. // Medical visualization. – 2011., No. 4. – P. 137-139. 23. Ruedi F. Thoeni. The Revised Atlanta Classification of Acute Pancreatitis: Its Importance for the Radiologist and Its Effecton Treatment. Radiology. 2012. V. 262. No. 3. P. 751-763. 24. Bagnenko S.F., Savello V.E., Goltsov V.R. Radiation diagnostics of pancreatic diseases: acute pancreatitis / Radiation diagnostics and therapy in gastroenterology: national guidelines (chief editor of the volume G.G. Karmazanovsky). – M.: GEOTAR-Media, 2014. – P. 349-365. 25. Danilov M.V. Pancreatitis: basic principles of diagnosis and treatment. // RMJ. – 2001. – T. 9 – P.13 – 14. 26. Beger H.G. Severe acute pancreatitis: Clinical course and management / Beger H.G., Rau B.M. // World J Gastroenterol. 2007;13(38): P. 5043-5051 27. Freeman M.L., Werner J., van Santvoort H.C., Baron T.H., Besselink M.G., Windsor J.A., Horvath K.D., van Sonnenberg E., Bollen T.L., Vege S.S. Interventions for Necrotizing Pancreatitis. Summary of Multidisciplinary Consensus Conference. Pancreas. 2012; 41(8):1176–1194. 28. Savelyev V.S., Filimonov M.I., Burnevich S.Z. Pancreatic necrosis. – M., MIA, 2008 – 264 p. 29. Goltsov V.R., Savello V.E., Bakunov A. M. et al. Purulent-necrotic parapancreatitis: evolution of views on treatment tactics // Annals of Surgical Hepatology - 2015, T. 20, No. 3 - P. 75-83. 30. Andreev A.V., Ivshin V.G., Goltsov V.R. Treatment of infected pancreatic necrosis using minimally invasive interventions // Annals of Surgical Hepatology. – 2015, T. 20, No. 3 – P. 110-116. 31. Shabunin A.V., Lukin A.Yu., Shikov D.V. Optimal treatment of acute pancreatitis depending on the “model” of pancreatic necrosis. Annals of surgical hepatology. 2013. T. 18. 3. pp. 70-78. 32. Ivshin V.G., Ivshin M.V. Percutaneous treatment of patients with pancreatic necrosis and widespread parapancreatitis. – Tula: Grif and K, 2013. – 128 p.

Information

Keywords
. Acute pancreatitis
. acute alcohol-nutritional pancreatitis
. acute biliary pancreatitis
. acute traumatic pancreatitis
. edematous pancreatitis
. necrotizing pancreatitis
. pancreatic necrosis
. sterile pancreatic necrosis
. infected pancreatic necrosis
. peripancreatic infiltrate
. pancreatic pseudocyst

List of abbreviations
BP - blood pressure
MDP - major duodenal papilla
NOS - not otherwise specified
BT - basic therapy
GNPP - purulent-necrotizing parapancreatitis
GO - purulent complications
DN - respiratory failure
Duodenum - duodenum
D-5 - diet No. 5
CT - computed tomography
LAP - mild acute pancreatitis
MSCT - multislice computed tomographic angiography
MRI - magnetic resonance imaging
OH - organ failure
AP - acute pancreatitis
ICU - intensive care unit
PA - pancreatic abscess
Pancreas - pancreas
PI - peripancreatic infiltrate
PPC - pancreatic pseudocyst
PN - renal failure
MON - multiple organ failure
SOP - moderate acute pancreatitis
ESR - erythrocyte sedimentation rate
SIRS - systemic inflammatory response syndrome
SIRS - systemic inflammatory response syndrome
CHF - cardiovascular failure
TOP - severe acute pancreatitis
Ultrasound - ultrasound examination
FGDS - fibrogastroduodenoscopy
C/O - surgical department
CHO - frequency of purulent complications
RR - respiratory rate
EPST - endoscopic papillosphincterotomy
ERCP-endoscopic retrograde cholangiopancreatography

Terms and Definitions
Purulent complications(pancreatic abscess or purulent-necrotizing parapancreatitis) are determined if at least one of the following signs is present:
- air bubbles in the area of ​​pancreatic necrosis, identified by computed tomography;
- positive bacterial culture of the aspirate obtained by fine-needle puncture;
- positive bacterial culture of the discharge obtained during the sanitizing operation.

Infected pancreatic necrosis (“infected pancreatic necrosis")- bacterially seeded necrosis of pancreatic tissue and retroperitoneal tissue with purulent melting and sequestration. Infected pancreatic necrosis that is not distinguished from healthy tissue is called purulent-necrotic parapancreatitis. Infected pancreatic necrosis, which is demarcated from healthy tissues, should be regarded as pancreatic abscess.

Necrotizing pancreatitis (nancronecrosis, "pancreaticnecrosis")- diffuse or focal zones of non-viable parenchyma of the subgastric gland, which, as a rule, are combined with necrosis of retroperitoneal fatty tissue.

Organ failure (“oorgan failure")- determined by the worst performance of one of 3 organ systems (cardiovascular, renal and respiratory) over a 24-hour period without previous organ dysfunction. The determination is made according to the corresponding indicators of the SOFA (Sepsis-related Organ Failure Assessment) scale: exceeding the threshold of 2 points is the basis for diagnosing organ failure:
Cardiovascular failure: need for inotropic drugs
renal failure: creatinine >171 μ mol/L (>2.0 mg/dL)
· respiratory failure: Pa02/Fi02< 300 mmHg (<40 kPa).

Edematous pancreatitis (“iinterstitial oedematous pancreatitis")- characterized by diffuse (or sometimes local) enlargement of the pancreas due to inflammatory edema.

Peripancreatic infiltrate (“acutefluid collection", "acute necrotic collection") is an exudative-proliferative inflammatory process in the pancreas and surrounding tissues, which is accompanied by an acute accumulation of fluid (with or without pancreatic necrosis), located inside or near the pancreas and without walls of granulation or fibrous tissue. Occurs in the IB phase of acute pancreatitis, has the following outcomes: complete resolution and resorption (usually by the 4th week of the disease), formation of a pancreatic pseudocyst, development of purulent complications.

Persistent organ failure (“ppersistent organ failure")- failure of one organ system for 48 hours or more.

Multiple organ failure (“multiple organ failure")- failure of two or more organ systems.

Pancreatic pseudocyst (“acutepseudocyst") is an accumulation of fluid (with or without sequesters), delimited by fibrous or granulation tissue, occurring after an attack of acute pancreatitis. Occurs 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 infiltration. The contents of the cyst may be aseptic and infected. Bacterial contamination of the cyst contents often does not have clinical manifestations, but the likelihood of infection is always higher in the presence of sequestration. An infected cyst is more correctly called a pancreatic abscess.

Sterile pancreatic necrosis (“sterile pancreatic necrosis")- pancreatic necrosis, which does not contain pathogenic microflora and is not accompanied by the development of purulent complications.

Transient organ failure (“tearly organ failure")- failure of one organ system for less than 48 hours.

Appendix A1. Composition of the working group
1. Academician of the Russian Academy of Sciences, professor Kubyshkin Valery Alekseevich(Moscow)
2. Academician of the Russian Academy of Sciences, professor Zatevakhin Igor Ivanovich(Moscow),
3. Academician of the Russian Academy of Sciences, professor Bagnenko Sergey Fedorovich(Saint Petersburg)
4. Doctor of Medical Sciences, Professor Blagovestnov Dmitry Alekseevich(Moscow),
5. Doctor of Medical Sciences, Professor Vishnevsky Vladimir Alexandrovich(Moscow),
6. Doctor of Medical Sciences, Professor Galperin Eduard Izrailevich(Moscow),
7. Academician of the Russian Academy of Sciences, professor Gelfand Boris Romanovich(Moscow),
8. Doctor of Medical Sciences, Professor Goltsov Valery Remirovich(Saint Petersburg)
9. Doctor of Medical Sciences, Professor Danilov Mikhail Viktorovich(Moscow),
10. Doctor of Medical Sciences, Professor Dibirov Magomed Dibirovich(Moscow),
11. Doctor of Medical Sciences, Professor Dyuzheva Tatyana Gennadievna(Moscow),
12. Doctor of Medical Sciences, Professor Ivshin Vladislav Gennadievich(Tula),
13. Doctor of Medical Sciences, Professor Korolev Mikhail Pavlovich(Saint Petersburg),
14. Academician of the Russian Academy of Medical Sciences, professor Maistrenko Nikolay Anatolievich(Saint Petersburg),
15. Corresponding Member of the Russian Academy of Sciences, Professor Polushin Yuri Sergeevich(Saint Petersburg),
16. Doctor of Medical Sciences, Professor Prudkov Mikhail Iosifovich(Ekaterinburg),
17. Doctor of Medical Sciences, Professor Filimonov Mikhail Ivanovich(Moscow),
18. Doctor of Medical Sciences, Professor Tsitsiashvili Mikhail Shalvovich(Moscow),
19. Doctor of Medical Sciences, Professor Shabunin Alexey Vasilievich(Moscow).
None of the members of the working group, when developing these clinical guidelines, had a conflict of interest, namely, a personal interest in receiving personally or through a company representative a material benefit or other advantage that would or could affect 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 different regions of the country (Moscow, St. Petersburg, Yekaterinburg, Samara), who were already working on regional protocols for providing medical care for AP, was asked to develop a draft clinical guidelines. As a result of a preliminary interactive discussion, it was decided to take as a basis the “Protocols for the diagnosis and treatment of acute pancreatitis” developed in St. Petersburg. For a more detailed discussion of this version of clinical recommendations, October 30, 2014. In St. Petersburg, a Round Table and a joint meeting of the Russian Society of Surgeons and the Association of Hepatopancreatobiliary Surgeons of the CIS Countries were organized. The country's leading experts on this issue were included in the expert group to discuss clinical guidelines for acute pancreatitis. During the Round Table, an on-line broadcast of the meeting was organized on the Internet. After accepting the draft clinical guidelines as a basis, the expert group edited the adopted document within two months through interactive discussion. At the second stage - free discussion on the Internet - the latest edition of clinical recommendations was published on the website of the Russian Society of Surgeons and was there for a year. At the third stage - approval - clinical recommendations for acute pancreatitis were publicly approved at the XII Congress of Russian Surgeons in Rostov-on-Don on October 8, 2015, which was held by the Russian Society of Surgeons.
Target audience of these clinical recommendations:
· Specialists in the specialty "Surgery"
· Table P1. Levels of Evidence
· Table P2. Recommendation Conviction Level
· The procedure for updating clinical recommendations - once every 5 years

Table P1.Levels of Evidence

Levels of Evidence	Description	Levels of Evidence
1++	High-quality meta-analyses, systematic reviews of randomized controlled trials (RCTs), or RCTs with very low risk of bias	1++
1+	Well-conducted meta-analyses, systematic ones, or RCTs with low risk of bias	1+
1-	Meta-analyses, systematic, or RCTs with a high risk of bias	1-
2++	High-quality systematic reviews of case-control or cohort studies. High-quality reviews of case-control or cohort studies with very low risk of confounding effects or bias and moderate probability of causality	2++
2+	Well-conducted case-control or cohort studies with moderate risk of confounding effects or bias and moderate probability of causality	2+
2-	Case-control or cohort studies with a high risk of confounding effects or bias and a moderate probability of causality	2-
3	Non-analytical studies (for example: case reports, case series)	3
4	Expert opinions	4

Note: RCT - randomized clinical trials

Force	Description
A	At least one meta-analysis, systematic review, or RCT rated 1++, directly applicable to the target population and demonstrating robustness of the results, or a body of evidence including results from studies rated 1+, directly applicable to the target population and demonstrating overall sustainability of results
IN	A body of evidence that includes results from studies rated 2++ that are directly applicable to the target population and demonstrate general robustness of the results, or evidence extrapolated from studies rated 1++ or 1+
WITH	A body of evidence that includes results from studies rated 2+ that are directly applicable to the target population and demonstrate general robustness of the results, or evidence extrapolated from studies rated 2++
D	Level 3 or 4 evidence or extrapolated evidence from studies rated 2+

The level of conviction of the recommendation (A-D), levels of evidence (1++, 1+, 1-, 2++, 2+, 2-, 3, 4) are given when presenting the text of clinical recommendations (protocols).

Appendix A3. Related documents

These clinical recommendations were developed taking into account the following regulatory documents:
1. Order of the Ministry of Health of the Russian Federation dated November 15, 2012 No. 922n “On approval of the Procedure for providing medical care to the adult population in the field of surgery”;
2. Order of the Ministry of Health of Russia dated July 15, 2016 N 520n “On approval of criteria for assessing the quality of medical care”

Appendix B. Patient management algorithm

ACUTE PANCREATITIS

Appendix G1

SOFA scale

Indicators	Grade
	0	1	3	4	5
PaO2/FiO2	>400	300-399	200-299	100-199	<100
Platelet count in ml	>150000	100000-149000	50000 - 99999	20000-49999	<20000
Serum bilirubin	<20	20-32	33-101	102-204	>204
Mean arterial pressure	>70 mmHg Art.	<70 мм рт. ст. без использования вазопрессоров	Use of any dose of dobutamine. Dopamine< 5 мкг/кг в минуту	Dopamine 5-15 mcg/kg per minute. Adrenalin< 0.1 мкг/кг в минуту. Норадреналин < 0.1 мкг/кг в минуту.	Dopamine > 15 mcg/kg per minute. Epinephrine > 0.1 mcg/kg per minute. Norepinephrine > 0.1 mcg/kg per minute.
Glasgow Coma Severity Score	15	13-14	10-12	6-9	3-5
Serum creatinine or diuresis	Serum creatinine< 100 мкмоль/л	Serum creatinine 100 - 170 µmol/l	Serum creatinine 171 - 299 µmol/l	Serum creatinine 300 - 400 µmol/l. Daily diuresis 200 - 499 ml	Serum creatinine > 440 µmol/l. Daily diuresis< 200 мл

Explanations on the use of the SOFA scale:
1. PaO2 in mm. rt. Art. FiO2 from 0.21 to 1.00.
2. Adrenergic drugs were used for at least 1 hour. Dosage - in mcg/kg per minute.
3. 0 - the most optimal parameter, 4 - the most anomalous parameter.
4. Information should be collected and assessed once a day during the entire time the patient is in the intensive care unit.
5. Average (systemic) blood pressure is calculated using the formula: SBP = (BPsyst + BPdiast) / 3.
6. SOFA index is equal to the sum of all six indicators.

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Protocols for diagnosis and treatment of acute pancreatitis

Acute pancreatitis (AP) characterized by the development of pancreatic edema (edematous pancreatitis) or primary aseptic pancreatic necrosis (destructive pancreatitis) followed by an inflammatory reaction. Acute destructive pancreatitis has a phase course, and each phase corresponds to a specific clinical form.

Phase I – enzymatic , the first five days of the disease, during this period the formation of pancreatic necrosis of varying extent, the development of endotoxemia (the average duration of hyperenzymemia is 5 days), and in some patients, multiple organ failure and endotoxin shock. The maximum period for the formation of pancreatic necrosis is three days, after this period it does not progress further. However, with severe pancreatitis, the period of formation of pancreatic necrosis is much shorter (24-36 hours). It is advisable to distinguish two clinical forms: severe and non-severe AP.

Severe acute pancreatitis. The incidence is 5%, mortality is 50-60%. The morphological substrate of severe AP is widespread pancreatic necrosis (large focal and total-subtotal), which corresponds to severe endotoxicosis.

Mild acute pancreatitis. The incidence is 95%, mortality is 2-3%. Pancreatic necrosis in this form of acute pancreatitis either does not form (swelling of the pancreas) or is limited in nature and does not spread widely (focal pancreatic necrosis - up to 1.0 cm). Mild AP is accompanied by endotoxemia, the severity of which does not reach a severe degree.

Phase II – reactive (2nd week of the disease), is characterized by the body’s reaction to the formed foci of necrosis (both in the pancreas and in the parapancreatic tissue). The clinical form of this phase is peripancreatic infiltrate.

Phase III – melting and sequestration (starts from the 3rd week of the disease, can last several months). Sequesters in the pancreas and retroperitoneal tissue begin to form from the 14th day from the onset of the disease. There are two possible options for the course of this phase:

aseptic melting and sequestration – sterile pancreatic necrosis; characterized by the formation of postnecrotic cysts and fistulas;

septic meltdown and sequestration– infected pancreatic necrosis and necrosis of parapancreatic tissue with further development of purulent complications. The clinical form of this phase of the disease is purulent-necrotic parapancreatitis and its own complications (purulent-necrotic leaks, abscesses of the retroperitoneal space and abdominal cavity, purulent omentobursitis, purulent peritonitis, arrosive and gastrointestinal bleeding, digestive fistulas, sepsis, etc.) .

Patients diagnosed with acute pancreatitis should, if possible, be sent to multidisciplinary hospitals.

Modern pancreatology is a dynamically developing branch of gastroenterology, which is naturally reflected in the growing number of national (including Russia) consensus documents (guidelines) on the diagnosis and treatment of chronic pancreatitis (CP), characterized by the presence of contradictory or ambiguous recommendations. To level out such inconsistencies, for the first time it was decided to create the first European clinical protocol, compiled in compliance with the principles of evidence-based medicine and containing scientifically based recommendations on key aspects of the conservative and surgical treatment of CP. Systematic reviews of the scientific literature were conducted using predefined clinical questions by 12 interdisciplinary expert working groups (EWGs). Various ERGs considered the etiology of CP, instrumental diagnosis of CP using imaging methods, diagnosis of exocrine pancreatic insufficiency (PIN), surgical, drug and endoscopic treatment of CP, as well as issues of treatment of pancreatic pseudocysts, pancreatic pain, malnutrition and nutrition, pancreatogenic diabetes mellitus, The natural history of the disease and quality of life in CP were assessed. Coverage of the main provisions of this consensus, which are more in demand among gastroenterologists, their analysis and the need for adaptation to Russian clinical practice were the goals of writing this article.

Keywords: chronic pancreatitis, exocrine pancreatic insufficiency, diagnosis, treatment, pancreatin preparations.

For quotation: Bordin D.S., Kucheryavyi Yu.A. Key positions of pan-European clinical recommendations for the diagnosis and treatment of chronic pancreatitis in the focus of a gastroenterologist // RMZh. 2017. No. 10. pp. 730-737

The key points of the pan-European clinical guidelines for the diagnosis and treatment of chronic pancreatitis in the focus of gastroenterologist
Bordin D.S. 1 , 2 , Kucheryavy Yu.A. 3

1 Moscow Clinical Scientific And Practical Center named after A.S. Loginov
2 Tver State Medical University
3 Moscow State Medical Dental University named after A.I. Evdokimov

Modern pancreatology is a dynamically developing branch of gastroenterology, that naturally results in a growing number of national (including Russia) guidelines for the diagnosis and treatment of chronic pancreatitis (CP), characterized by conflicting or ambiguous recommendations. To compensate such inconsistencies there was taken a decision to make the first European clinical protocol, compiled with observation of the principles of the evidence-based medicine and containing scientifically grounded recommendations on key aspects of conservative and surgical treatment of CP. Twelve interdisciplinary expert working groups (EWG) made systematic literature reviews on the pre-formulated clinical questions. Various ERGs considered the CP etiology, CP diagnostics tools using imaging techniques, diagnosis of pancreatic exocrine insufficiency, surgical, medical and endoscopic treatment, as well as issues of treatment of pancreatic pseudocysts, pancreatic pain, malnutrition and nutrition, pancreatogenic diabetes, natural history of disease and quality of life at CP. The aims of writing this article were the coverage of the main provisions of this consensus, which are in demand among gastroenterologists, their analysis and the need to adapt them to Russian clinical practice.

Key words: chronic pancreatitis, pancreatic exocrine insufficiency, diagnosis, treatment, pancreatin preparations.
For citation: Bordin D.S., Kucheryavy Yu.A. The key points of the pan-European clinical guidelines for the diagnosis and treatment of chronic pancreatitis in the focus of gastroenterologist // RMJ. 2017. No. 10. P. 730–737.

The key positions of pan-European clinical guidelines for the diagnosis and treatment of chronic pancreatitis are presented.

Introduction

Recent years have been marked by a rethinking of our understanding of chronic pancreatitis (CP), which is due to breakthroughs in diagnosis and discoveries in the genetics and pathophysiology of the disease. The pool of randomized clinical trials (RCTs) in patients with CP has also naturally been updated. This trend was picked up by regional gastroenterological and pancreatological associations (including Russia) with the aim of creating a large number of national consensus documents (guidelines) for the diagnosis and treatment of CP. In general, such clinical recommendations are similar in essence, but noteworthy are the variations in the number of provisions and approaches to achieving consensus, and the presence of contradictory or ambiguous decisions. To level out such inconsistencies, for the first time it was decided that it was necessary to create international clinical guidelines for the diagnosis and treatment of CP. A working group on the “Unification of principles for the diagnosis and treatment of CP in Europe” (HaPanEU) was established in collaboration with the United European Gastroenterology (UEG), the result of which was the first European clinical protocol compiled in compliance with the principles of evidence-based medicine, published in March 2017. Twelve interdisciplinary expert working groups (EWGs) performed systematic reviews of the scientific literature to answer 101 predefined clinical questions. Thus, ERG 1 considered the issues of the etiology of CP, ERG 2 and 3 - issues of instrumental diagnosis of CP using imaging methods, ERG 4 - issues of diagnosing exocrine pancreatic insufficiency (EPI), ERG 5, 6 and 7 - issues of surgical, drug and endoscopic treatment HP respectively; ERG 8, 9 and 10 – issues of treatment of pancreatic pseudocysts (PZ), pancreatic pain, malnutrition and nutrition, ERG 11 – issues of pancreatogenic diabetes mellitus, ERG 12 – natural course of the disease and quality of life in CP. Recommendations were classified using the Recommendation Assessment, Development and Review system, and responses were assessed by the entire EWG using the online Delphi method. The EWGs presented their recommendations at the annual meeting of the Joint European Association of Gastroenterology in 2015. At this one-day interactive conference, relevant comments were made and each recommendation was agreed upon by a plenary vote (Test and Evaluation Authority). After a final round of revisions based on these comments, a draft document was produced and sent to external reviewers. The vote count classified 70% as “strong” and the plenary vote found “high agreement” on 99 (98%) recommendations. Thus, the proposed HaPanEU / United European Gastroenterological Association 2016 clinical protocol contains evidence-based recommendations on key aspects of conservative and surgical treatment of CP, compiled on the basis of modern scientific data, which dictates the need for their analysis and adaptation to Russian clinical practice. This is the purpose of this article, created to help practicing physicians in their work. Since it is impossible to reflect in one article all the information processed and reported by the ERG, below are discussed those questions and statements that are most relevant in the work of a gastroenterologist, therapist, and general practitioner. For each clinical question, criteria for evidence and applicability of scientific evidence were proposed:
1. Recommendation: degree of conviction of the recommendation according to the GRADE system (1 – high, 2 – low).
2. Quality of the evidence base (A – high, B – average, C – low).
3. Level of consensus of the decision (high/low) during plenary voting.

Etiology of CP (ERG 1)

Question 1-1. What needs to be done to determine the etiology of CP in adult patients?
Statement 1-1. In patients with CP, a complete and detailed history, laboratory tests, and imaging studies should be obtained (GRADE 2C, high agreement).
Comments. CP is an inflammatory disease of the pancreas with, as a rule, a long history, which leads to the replacement of the gland's own tissue with fibrous tissue, the development of endocrine and/or exocrine insufficiency of the pancreas. Patients with CP have an increased risk of developing pancreatic cancer. The most common risk factor for CP is alcohol abuse, and the risk increases exponentially, and the specific type of alcohol consumed does not matter. The amount and duration of alcohol consumption required for the development of CP have not yet been clearly established. Some authors talk about alcohol consumption at a level of at least 80 g/day for at least 6 years. Smoking is an independent risk factor for CP and leads to the progression of CP, so all patients should be advised to quit smoking.
Genetic factors also contribute to the development of CP. The most important genetic risk factors are changes in the genes for cationic trypsinogen (PRSS1), serine protease inhibitor Casal-1 (SPINK1), and carboxypeptidase A1 (CPA1). Other genes that indicate genetic susceptibility include cystic fibrosis transmembrane conductance regulator (CFTR), chymotrypsinogen C (CTRC) and carboxylestrolipase (CEL).
To diagnose CP and attempt to determine the etiology, it is necessary to collect a complete history of life and disease, conduct a clinical examination, including imaging studies and functional tests. The etiology of CP is determined after a thorough examination of the patient, taking into account all known risk factors, including assessment of alcohol history and smoking history, determination of latent commitment to alcohol (for example, using the AUDIT questionnaire), as well as using a screening block of laboratory parameters ( triglyceride level, ionized calcium level to exclude primary hyperparathyroidism; level of carbohydrate-deficient transferrin/phosphatidylethanol) in the blood and family history.
In accordance with current consensus recommendations, autoimmune pancreatitis (AIP) should be excluded, including when no other etiology can be identified. Signs of AIP include elevated levels of serum immunoglobulin IgG4, the presence of autoantibodies to lactoferrin and carbonic anhydrase, as well as typical signs of AIP using imaging techniques.
Cholecystolithiasis and/or choledocholithiasis in themselves are not considered risk factors for the development of CP. Whether anatomical abnormalities, such as pancreas divisum, increase the risk of CP is still a matter of debate; however, in the presence of additional risk factors, a split pancreas can lead to the development of CP. If the etiological factor cannot be identified, genetic screening for variants in susceptibility genes can be suggested.
Recent clinical guidelines have classified CP into various forms (calcific, obstructive, autoimmune and sulcal). groove pancreatitis)). This classification is based on clinical signs, morphological characteristics and response to treatment. In calcific CP, for example, there is perilobular fibrosis and destruction of the acinar apparatus with inflammatory cell infiltration. Obstructive CP develops as a secondary process due to the destruction of part of the pancreas with the development of block and distal dilatation of the pancreatic duct, subsequent atrophy of acinar cells and fibrosis. The characteristics of AIP are discussed in detail below. Finally, sulcal pancreatitis affects the groove between the head of the pancreas, the duodenum and the bile duct.
Question 1-4. Should the diagnosis of AIP be excluded in all patients with pancreatitis?
Statement 1-4. If the etiology of CP cannot be established in a patient, then the diagnosis of AIP should be excluded (GRADE 2C, high agreement).
Comments. AIP is a rare form of the disease, accounting for up to 5% of all CP with gender differences in favor of men (2:1 ratio). Approximately 5% of patients with suspected pancreatic cancer are eventually diagnosed with AIP. Conditionally specific for AIP are recurrent abdominal pain and obstructive jaundice in approximately 50% of patients. There are 2 types of AIP. In AIP type 1, the serum level of IgG4 is elevated in most cases, and the histological picture corresponds to lymphoplasmacytic sclerosing pancreatitis (LPSP) with obliterative phlebitis and periductular fibrosis. In type 2 AIP, serum IgG4 levels remain within the normal range, and histological findings include idiopathic ductal-concentric pancreatitis (IDCP) and granulocytic epithelial lesions. If AIP type 1 is often combined with a wide range of IgG4-associated diseases, then AIP type 2 may be accompanied by ulcerative colitis. An important feature of AIP is a good response to immunosuppressive therapy, the timely administration of which can help normalize the exocrine and endocrine functions of the pancreas. However, making the diagnosis of AIP remains challenging because patients with this disease often present with atypical symptoms. Thus, AIP may underlie any inflammation of the pancreas, therefore, it is necessary to perform a comprehensive diagnosis.

Classification

Question 1-5. Is there a recommended classification system that should be used when determining the etiology of a disease?
Statement 1-5. There is no optimal classification system for CP with etiology; existing classification systems need to be studied in RCTs with morbidity and mortality endpoints. Only in this way will it be possible to recommend in the future the most valid classification system for CP (GRADE 2C, high agreement).
Comments. Classification systems are of great importance for determining patient management strategies, since treatment strategy cannot be based solely on the type and extent of morphological changes in the pancreas, but must include the results of clinical, functional and imaging studies. To date, a generally accepted classification system has not been created. The most well-known classifications are:
1. Manchester classification.
2. ABC classification.
3. M-ANNHEIM classification.
4. TIGAR-O classification.
5. Rosemont classification.
The Manchester classification uses imaging techniques and clinical features of CP. The severity of the disease largely depends on the presence of exocrine and/or endocrine insufficiency or the presence of complications, while the results of imaging studies are of secondary importance. The ABC classification is based on the same provisions as the Manchester classification. The Rosemont classification was developed for the diagnosis of CP using endo-ultrasound. The M-ANNHEIM classification system combines the degree, severity and clinical characteristics of CP, and takes into account the disease severity index. The TIGAR-O classification includes 6 etiological groups of CP: toxic-metabolic, idiopathic, genetic, autoimmune, obstructive CP and recurrent acute pancreatitis. Thus, the factor of the etiology of CP is taken into account only in the TIGAR-O and M-ANNHEIM classifications.

Clinical course of CP

Question 1-6. Can CP progress in different ways?
Statement 1-6. Depending on the etiology, CP is characterized by different clinical course and long-term complications (GRADE 1B, high agreement).
Comments. The course of CP and the risk of developing pancreatic cancer vary significantly between different etiological groups. Calcification, exocrine and endocrine insufficiency develop in patients with alcoholic and hereditary CP after a shorter period of time than in other etiologies. Quitting alcohol consumption can reduce the rate of disease progression and reduce pancreatic pain. Smoking is recognized as an independent risk factor for the development of CP and pancreatic calcification. In patients with early onset CP (<20 лет), особенно наследственной этиологии, риск рака ПЖ значительно увеличивается, и отказ от курения может снизить риск в этой группе . При наследственном ХП риск развития аденокарциномы ПЖ возрастает в 69 раз, в то время как при другой этиологии – в 13 раз . Риск развития аденокарциномы ПЖ не связан с генотипом , ранний дебют заболевания у этих пациентов и более продолжительное течение болезни являются основными причинами повышенного риска развития рака ПЖ. Комбинация различных генетических факторов риска или прочих факторов риска, например, pancreas divisum with genetic mutations may increase the risk of developing CP. Therefore, the correct determination of the etiology of the disease by the doctor is important.

Diagnostics

Question 2-1. What is the best imaging modality for making the diagnosis of CP?
Statement 2-1. Endo-ultrasound, MRI and CT are considered the best imaging modalities for diagnosing CP (GRADE 1C, high agreement).
Comments. The most common methods of imaging the pancreas are ultrasound, endo-ultrasound, MRI, CT and ERCP. A meta-analysis aimed at obtaining pooled estimates of the sensitivity and specificity of various imaging modalities used to evaluate CP (42 studies, 3392 patients) showed that endo-ultrasound, ERCP, MRI and CT have comparable high diagnostic accuracy in the initial diagnosis of CP. Endo-ultrasound and ERCP are superior to other imaging methods, and ultrasound is considered the least accurate method. ERCP today is not considered as a diagnostic test for CP due to significant invasiveness, local inaccessibility, and high cost. The results of the meta-analysis are consistent with previously published German clinical practice guidelines S3.
Question 2-2. Which method is most suitable for detecting pancreatic calcifications?
Statement 2-2. CT is the most appropriate method for detecting pancreatic calcifications, and non-contrast-enhanced CT is preferred for detecting microcalcifications (GRADE 2C, high agreement).
Comments. Pancreatic calcification is a common finding in patients with CP. It is estimated that 90% of patients will develop calcification during long-term follow-up, especially in patients with alcoholic CP. Imaging with portal phase CT with bolus contrast enhancement has moderate sensitivity and very high specificity (approaching 100%) for detecting intraductal stones. However, small calcifications may appear in the shadow of the contrasted pancreatic parenchyma; thus, non-contrast phase CT may be a necessary adjunct to portal phase CT with bolus contrast enhancement to visualize calcifications missed in the later phase.
Question 2-3. To make a diagnosis of CP, is it sufficient to perform an MRI/MRCP study to assess the unevenness of the contour of the main pancreatic duct (MPD), its pathologically altered lateral branches, strictures and dilations?
Statement 2-3. The presence of signs typical of CP on MRI/MRCP is considered sufficient to establish a diagnosis; however, MRI/MRCP findings within the normal range do not always exclude the presence of mild forms of the disease (GRADE 1C, high agreement).
Comments. MRCP relies heavily on T2-weighted images to detect ductal narrowing, dilatation, and filling defects in CP with moderate to high accuracy comparable to ERCP. However, in mild CP, MRCP is characterized by relatively low sensitivity, inferior to ERCP in detecting subtle changes in the MLP and its side branches.
Question 2-4. What are the advantages of intravenous (IV) administration of secretin during MRCP for the diagnosis of CP?
Statement 2-4. The use of secretin increases the diagnostic potential of MRCP in the evaluation of patients with confirmed/suspected CP (GRADE 1C, high agreement).
Comments. IV administration of secretin stimulates the exocrine function of the pancreas and increases the excretion of secretions by the pancreatic ductal system, which provides the following benefits:
1. Better visualization of the MLP and pathologically altered side branches compared to those with MRCP without stimulation, which ensures an increase in the sensitivity of diagnosing CP from 77% to 89%.
2. The ability to perform a quantitative assessment of exocrine pancreatic function, which correlates with the severity of pancreatitis.
3. The theoretical possibility of diagnosing intraductal papillary mucinous tumor of the pancreas, which should be proven in specially designed studies.
Question 2-6. What is the role of abdominal ultrasound in suspected CP?
Statement 2-6. Abdominal ultrasound can only be used to diagnose more severe CP (GRADE 1A, high agreement).
Comments. Abdominal ultrasound is usually the first imaging modality used in patients with abdominal pain and suspected CP. Ultrasound is widely available in most institutions, including for repeat examinations without the risks associated with other imaging modalities (x-rays and/or contrast agents). The sensitivity and specificity of ultrasound (67% / 98%) is lower than that of CT (75% / 91%) and endo-ultrasound (82% / 91%), respectively, which is determined by the dependence of ultrasound results on the experience and knowledge of the diagnostician, and also difficult visualization of the pancreas in obese patients, with flatulence, etc.
Question 2-7. What is the role of abdominal ultrasound in confirmed CP?
Statement 2-7. Ultrasound can be prescribed to patients with suspected complications of CP (GRADE 2C, high agreement).
Comments. Ultrasound can be used to visualize complications of CP, such as fluid collections, pseudocysts, exacerbation of CP, and pseudoaneurysms. There are no RCTs comparing ultrasound with other imaging modalities. Ultrasound can also be used for diagnostic and therapeutic interventions on the pancreas under ultrasound guidance (biopsy, drainage).
Question 2-8. What are the indications for contrast-enhanced endo-ultrasound?
Statement 2-8. Endo-ultrasound with contrast may improve diagnostic accuracy in patients with CP with cystic and solid lesions in the pancreas (GRADE 1C, high agreement).
Comments. Contrast enhances accuracy in the description of focal lesions of the pancreas, but there are no RCTs evaluating contrast in endo-ultrasound in patients with CP. Standard B-mode ultrasound does not differentiate pseudotumorous CP from pancreatic cancer. On contrast, ductal adenocarcinoma is usually hypoechoic in the arterial phase due to its low vascularity, whereas focal CP usually demonstrates contrast enhancement similar to that seen in the surrounding pancreatic parenchyma. In CP with a long history, heterogeneous hypovascularization due to fibrosis may be observed, which significantly complicates the differential diagnosis with pancreatic cancer.
Question 2-9. What is the role of endo-ultrasound in patients with suspected CP?
Statement 2-9. Endo-ultrasound is the most sensitive imaging modality for diagnosing early CP, and its specificity increases with the number of diagnostic criteria (GRADE 1B, high agreement).
Comments. Endo-ultrasound is the most sensitive imaging method for diagnosing CP. Certain criteria for CP have been developed, divided into parenchymal and ductal. To make a diagnosis of CP, a threshold sum of 3–4 criteria is most often used. Recognizing that not all criteria are equally important, the Rosemont classification proposes specific diagnostic criteria for endo-ultrasound, indicating their specific validity. Compared with histological examination as the gold standard, the sensitivity of endo-ultrasound exceeds 80% and the specificity reaches 100%.

Diagnosis of EPI

Question 3-2. What are the clinical consequences of varying degrees of pancreatic failure?
Statement 3-2. Taking into account the large reserve capacity of the pancreas, “mild” and “moderate” EPI can be compensated by the body itself, and obvious steatorrhea occurs already when the secretion of pancreatic lipase decreases to<10% от нормы («тяжелая»/«декомпенсированная» недостаточность). Однако пациенты с «компенсированной» ВНПЖ также имеют повышенный риск мальнутриции (в частности, жирорастворимых витаминов с соответствующими клиническими последствиями) (GRADE 1В, высокая согласованность).
Comments. Patients with steatorrhea typically complain of weight loss and more frequent bowel movements during the day with fatty, large stools that are difficult to flush down the toilet (mostly occurring after high-fat meals). By reducing fat in the diet, steatorrhea may be absent. Clinical symptoms and signs of impaired absorption of fat-soluble vitamins include: vitamin K deficiency - ecchymosis; vitamin E deficiency – ataxia, peripheral neuropathy; vitamin A deficiency – visual impairment, xerophthalmia; Vitamin D deficiency – muscle contractions or spasms, osteomalacia and osteoporosis. In addition, the clinical consequences of EPI may include hyperoxaluria, oxalate stones in the urinary tract, renal failure, and impairment of cognitive function and hence performance. Decreased absorption of fat-soluble vitamins is also possible in the absence of steatorrhea in patients with mild to moderate EPI.
Question 3-5. Is it possible to diagnose or exclude EPI using various imaging methods (morphological studies)?
Statement 3-5.1. CP symptoms (morphological changes) and functional impairment usually develop in parallel, although not always (GRADE 1B, high agreement).
Comments. In most patients with CP, there is an association between the severity of morphological and functional changes, but in 25% of patients there is a discrepancy between them.
Question 3-6. What analysis/research is indicated for diagnosing EPI in clinical practice?
Statement 3-6. In a clinical setting, it is necessary to conduct a non-invasive functional study of the pancreas. The fecal elastase-1 (FE-1) test is widely available, and the 13C-mixed triglyceride breath test (13C-MTG-DT) appears to be an alternative screening option. The use of MRCP with secretin can also be used as a method of diagnosing EPI, but it provides only semi-quantitative data (Grade 1B, agreement was not indicated by the authors in the original publication, but in the opinion of the authors of this publication, the agreement should be of a high level due to the large number of evidence-based relevant studies ).
Comments. Determination of FE-1 (elastase test) is a very simple and widely available test for indirect and non-invasive assessment of pancreatic secretion. Unfortunately, the elastase test does not rule out mild to moderate EPI. The threshold value of PE-1 indicating EPI is less than 200 μg/g. The possibility of false-positive results due to stool dilution should be taken into account and a monoclonal test should be used in clinical practice.
Fat absorption coefficient (FAC) is considered the gold standard for diagnosing steatorrhea in severe EPI and is the only test approved by the US Food and Drug Administration (FDA) and the European Medicines Agency (EMA) for the diagnosis and monitoring of fat replacement. enzyme therapy in clinical trials. The CAF test requires patients to follow a strict diet containing 100 g of fat per day for 5 days and collect all stool for the last 3 days of that 5-day period. KAJ indicator< 93% считается патологическим. К недостаткам метода относятся применимость только при тяжелой ВНПЖ, низкая специфичность (ложноположительные результаты при множестве причин вторичной панкреатической недостаточности или непанкреатической мальабсорбции), низкая доступность, трудоемкость, сложности логистики. Поэтому в некоторых европейских странах он больше не используется.
13C-GH-DT is an alternative to the QAF test, both for diagnosing EPI and for assessing the effectiveness of pancreatin therapy in clinical practice, and new modifications of the test can detect mild and moderate EPI. However, this test also has limitations regarding specificity (false-positive results for non-pancreatic fat malabsorption) and is not yet widely available. The test is only commercialized in some European countries. In Russia, this test is also not available due to the lack of substrate (13C-labeled triglycerides).
Only direct tests requiring collection of duodenal juice in response to hormonal stimulation (secretin and/or cholecystokinin) can quantify pancreatic exocrine secretion and reliably determine the presence of mild to moderate EPI. Based on this, they were adopted as a standard. Previously, these tests were performed by inserting a nasoduodenal tube, although endoscopic versions of the procedure have been developed and are now preferred in the United States and some European countries. However, regardless of which specific method is used to collect duodenal juice, the examination itself is invasive, time-consuming and expensive, and can only be performed in specialized centers.
Question 3-7. Is a functional study of the pancreas always required when diagnosing CP?
Statement 3-7. To diagnose CP, a functional study is required (GRADE 2B, high agreement).
Comments. The diagnosis of CP is based on a combination of clinical, histological, imaging and functional criteria. Proof of exocrine dysfunction using functional studies is especially indicated in the case of diagnostics in patients with CP with inconclusive morphological data. Additionally, exocrine function is taken into account in some diagnostic and classification systems.
Question 3-8. Should a functional study of the pancreas be performed after diagnosing CP?
Statement 3-8. Every patient newly diagnosed with CP should be screened for EPI (GRADE 1A, high agreement).
Comments. Even with convincing morphological signs of CP, clinical symptoms of EPI do not always appear at the time of diagnosis, and the absence of symptoms does not reliably exclude exocrine insufficiency.
Question 3-10. Should pancreatic function testing be performed to monitor pancreatin enzyme replacement therapy (ERRT)?
Statement 3-10. To assess the effectiveness of PPTP, in most cases it is enough to ensure normalization of nutritional status and improvement of clinical symptoms. If symptoms of EPI persist even despite adequate PTSD, a functional test (13C-GH-DT or QAF test) is recommended to assess the effectiveness of treatment (GRADE 2B, high agreement).
Comments. Typically, when patients with EPI are treated with adequate EPTA, rapid improvement in clinical symptoms and an increase in weight/body mass index are observed. The effect of treatment should also be assessed by determining indicators of nutritional status in the blood serum over time, since the absence of symptoms does not exclude the presence of latent EPI.
Question 3-12. What parameters in the blood allow you to determine malnutrition?
Statement 3-12. Tests should be performed for proven markers of malnutrition: prealbumin, retinol binding protein, 25-OH cholecalciferol (vitamin D), and minerals/trace elements (including serum iron, zinc, and magnesium) (GRADE 2C, high agreement).
Comments. Malnutrition (exhaustion) caused by EPI is no different from malnutrition due to other causes, which determines the absence of strictly specific markers of pancreatogenic malnutrition.

Drug treatment of exocrine pancreatic insufficiency (ERG 6)

Question 4-2.1. What are the indications for PPTP in CP?
Statement 4-2.1. SFTP is indicated for patients with CP and EPI in the presence of clinical symptoms or laboratory signs of malabsorption. An appropriate nutritional assessment (GRADE 1A, high agreement) is recommended to identify signs of malnutrition.
Comments. EPI in CP is clearly associated with biochemical markers of malnutrition (emaciation). The classic indication for PETP is steatorrhea with fecal fat excretion > 15 g/day. However, quantification of fats in feces is often not carried out. Therefore, indications for FTRT are also pathological results of a functional study of the pancreas in combination with clinical signs of malabsorption or anthropometric and (or) biochemical signs of malnutrition. These symptoms include weight loss, diarrhea, severe flatulence, and abdominal pain. Low values ​​of the most common markers of nutritional deficiency (fat-soluble vitamins, prealbumin, retinol-binding protein and magnesium) are also an indication for the use of EFT. In uncertain situations, it is allowed to prescribe ZFTP for 4–6 weeks as a trial experimental pharmacotherapy regimen.
Question 4-2.2. Which enzyme preparations are considered preferable?
Statement 4-2.2. The drugs of choice for EPI are microencapsulated pancreatin preparations in an enteric coating, size up to 2 mm. Micro or mini tablets measuring 2.2–2.5 mm may also be effective, although there is much less scientific evidence on this. Comparative RCTs various There are no enzyme preparations (GRADE 1B, high agreement).
Comments. The effectiveness of pancreatic enzyme preparations depends on a number of factors: a) connection with food intake; b) synchronized evacuation along with food; c) adequate segregation in the duodenum; d) rapid release of enzymes in the duodenum.
Effective pancreatin preparations are presented in a dosage form in the form of pH-sensitive microspheres/microtablets with an enteric coating, which protects enzymes from gastric acid and allows them to quickly release pancreatin at pH 5.5 in the duodenum. Enteric-coated drugs have demonstrated higher efficacy than conventional non-enteric-coated drugs. A recent Cochrane review assessing the effectiveness of pancreatin in cystic fibrosis with EPPI demonstrated superior efficacy of microencapsulated formulations compared with enteric-coated tablets.
Question 4-2.3. How should you take pancreatin preparations?
Statement 4-2.3. Oral pancreatin preparations should be distributed evenly throughout the day at all main and additional meals (GRADE 1A, high consistency).
Comments. The effectiveness of pancreatic enzymes depends on the adequacy of mixing pancreatin microparticles with chyme, which determines the need to take the drug with meals. If you need to take more than 1 capsule per meal, it is reasonable to divide the entire dose into fractions throughout the meal.
Question 4-2.4. What is the optimal dose of pancreatin for EPI on the background of CP?
Statement 4-2.4. The recommended minimum dose of lipase for initial therapy is 40-50 thousand units with main meals and half this dose with intermediate meals (GRADE 1A, high agreement).
Comments. The recommended initial dose is about 10% of the dose of lipase physiologically secreted in the duodenum after a normal meal, i.e., to digest normal food, a minimum lipase activity of 90,000 units is required, which is achieved by summing up endogenously secreted enzymes and exogenously (orally) supplied enzymes.
Question 4-2.5. How to evaluate the effectiveness of RFTP?
Statement 4-2.5. The effectiveness of FTP can be objectively judged by the relief of symptoms associated with maldigestion (steatorrhea, weight loss, flatulence) and the normalization of the nutritional status of patients. In patients who have not sufficiently responded to treatment, the use of pancreatic function tests (FA or 13C-GH-DT analysis) in the setting of FTRT may be useful (GRADE 1B, high agreement).
Comments. Although resolution of clinical signs of malabsorption is generally considered the most important criterion for the success of EFT, which is associated with improved quality of life, more recent studies have demonstrated that relief of symptoms is not always combined with normalization of nutritional status. A recent review confirms that the optimal way to assess the effectiveness of EFT is to normalize parameters of nutritional status, both anthropometric and biochemical.
The lack of a full effect of ZFTP may be due to secondary mechanisms. The success of PPTP cannot be assessed by the concentration of PE-1, since in this case only the concentration of the natural human enzyme is measured, and not the therapeutically administered enzyme contained in pancreatin. Fecal chymotrypsin excretion testing does not provide information about the effects of TFTP on digestion and nutrient absorption; however, it can be used to test compliance (low values ​​indicate incorrect drug administration). Only 13C-GH-DT allows effective assessment of fat absorption and is suitable for monitoring the effectiveness of PETP.
Question 4-2.6. What should be done if the clinical response is unsatisfactory?
Statement 4-2.6. If the clinical response to EFT is unsatisfactory, the dose of enzymes should be increased (double or triple) or a proton pump inhibitor (PPI) should be added to therapy. If these therapeutic strategies are unsuccessful, another cause of the digestive disorder should be sought (GRADE 2B, high agreement).