1 GBOU VPO "Chelyabinsk State medical university Ministry of Health of the Russian Federation"
2 NUZ “Departmental hospital at the station. Zlatoust JSC Russian Railways
3 MBUZ OTKZ "City" clinical hospital No. 1"
Acute pancreatitis is a common emergency surgical pathology of the gastrointestinal tract, accompanied by a high mortality rate. However, a unified classification scheme that allows for the correct unification of approaches to the treatment of these patients in Russia has not yet become widespread. The paper presents a modern classification system, including points of the international classification Atlanta-92 of the third revision (2012), criteria for diagnosing “acute pancreatitis”, a modified Marshall scale for acute pancreatitis, morphological criteria for the severity of acute pancreatitis according to the Baltazar scale, clinical criteria for the severity of non-biliary pancreatitis according to Ranson scale and boundaries of zones of pancreatogenic aggression of retroperitoneal tissue. This classification system, diagnostic criteria and recommended prognostic integral scales are intended to unify the diagnosis and approaches to definitions, terminology, principles of stratification and treatment tactics for patients with this pathology.
classification
acute severe pancreatitis
acute pancreatitis
1. Bagnenko S.F. Acute pancreatitis (protocols, diagnosis and treatment) / S.F. Bagnenko, D.A. Blagovestnov, E.I. Galperin, T.G. Dyuzheva, M.D. Dibirov, M.I. Prudkov, M.I. Filimonov, A.V. Zhao [Electronic resource] - M. - 2014. - Access mode http://pancreonecrosis.ru/ostriy-pankreatit-protokoli-diag/ Date of access 10/12/2014.
2. Bukhvalov A.G. Possibilities of reducing the number of postoperative complications and deaths in purulent-destructive complications of non-biliary acute severe pancreatitis / A.G. Bukhvalov, N.M. Grekova, Yu.V. Lebedeva // Basic Research. - 2015. - No. 1 (part 1). - pp. 41–45.
3. Bukhvalov A.G. Cost-effectiveness of minimally invasive techniques for acute severe non-biliary pancreatitis / A.G. Bukhvalov, Yu.V. Lebedeva, N.M. Grekova, V.N. Bordunovsky, S.A. Bukhvalova // Contemporary issues science and education. – 2014. - No. 6. - P. 1177.
4. Vorobey A.V. International classification of acute pancreatitis (Atlanta, 1992) - current trends in revision / A.V. Vorobey, A.A. Litvin, V.M. Khokha // News of surgery. - 2010. - Volume 18, No. 10. - P. 149–159.
5. Dinerman G.V. Successful treatment of a patient with multiple intestinal fistulas / G.V. Dinerman, V.N. Bordunovsky, M.A. Drozhzhilov, Yu.I. Tokarev, N.M. Grekova // Surgery. Journal named after N.I. Pirogov. - 2003. - No. 11. - P. 44–45.
6. Ermolov A.S. / Diagnosis and treatment of acute pancreatitis / A.S. Ermolov, P.A. Ivanov, D.A. Blagovestnov, A.V. Grishin, V.G. Andreev –M.: Publishing house. House Vidar, 2013. - 384 p.
7. Krivoruchko I.A. Surgical treatment of pancreatic necrosis. / I.A. Krivoruchko, V.V. Boyko, Yu.V. Ivanova, M.S. Povelichenko // Current problems of surgical hepatology: Materials of the XX International. Congress of the Association of Surgeons-Hepatologists of the CIS Countries, Donetsk, September 18–20, 2013 – Donetsk, 2013. - pp. 189–190
8. Krokhin A.A. Assessment of the risk of formation of external pancreatic fistulas after surgical treatment of destructive pancreatitis / A.A. Krokhin, A.G. Bukhvalov, D.M. Smirnov // Current issues in surgery. Collection of scientific and practical works. Regional medical directorate provision at the South Ural Railway, State Budgetary Educational Institution of Higher Professional Education South Ural State Medical University of the Ministry of Health of the Russian Federation. - Chelyabinsk, 2014. - P. 52.
9. Mizgirev D.V. Complications and mortality in minimally invasive treatment of acute necrotizing pancreatitis / D.V. Mizgirev, B.L. Duberman, A.M. Epstein, V.V. Kremlev, S.V. Bobovnik, V.N. Pozdeev, E.V. Prudieva //Annals of surgical hepatology. - 2014. -T. 19, no. 2. - P. 66–71.
11. Balthazar E.J. Acute pancreatitis: assessment of severity with clinical and CT evaluation. / E.J. Balthazar // Radiology .- 2002. – V. 223.- R. 603–613
12. Banks P.A. Classification of acute pancreatitis-2012: revision of Atlanta classification and definitions by international consensus.// P.A. Banks, T.L. Bollen, C. Dervenis et al. Gut. - 2013. - 62. – R. 102–111
13. Bollen T.L. Dutch Acute Pancreatitis Study Group (2008) The Atlanta Classification of acute pancreatitis revisited. / T.L. Bollen, H.C. van Santvoort, M.G Besselink, M.S. van Leeuwen, K.D. Horvath, P.C. Freeny, H.G. Gooszen // Br. J Surg. - 1995. – R. 6–21.
14. Marshall J.C. Multiple organ dysfunction score: a reliable descriptor of complex clinical outcome /J.C. Marshall, D.J. Cook, N.V. Christou.//Crit. Care Med.– 1995.-V23.-R. 1638–1652.
15. Ranson J.H. Statistical methods for quantifying the severity of clinical acute pancreatitis. /J.H. Ranson, B.S. Pasternack //J Surg. Res. - 1977. - V. 22 - P. 79–91.
16. Tenner S. American College of Gastroenterology Guideline (ACG): Management of Acute Pancreatitis / S. Tenner, J. Baillie, J. De Witt, S. Swaroop // Am J Gastroenterol. - 2013. - V. 108. - R. 1400–1415
Acute pancreatitis (AP) is one of the most common emergency pathologies of the gastrointestinal tract. . Recent studies under the auspices of WHO have noted a constant increase in the annual incidence of AP, which ranges from 4.9 to 73.4 cases per 100,000 population. In Russia, the incidence of AP is 20-80 people per 100,000 population; in Russian hospitals, AP ranks 3rd among acute surgical diseases abdomen and accounts for 12.5% of all acute surgical abdominal pathology. Of all forms of acute pancreatitis, the most significant mortality rate is accompanied by acute severe pancreatitis (ASP), developing in 20-30%. The number of patients who develop infected pancreatic necrosis, late multiple organ failure and other severe purulent-destructive complications of acute pancreatitis - arrosive bleeding, duodenal fistula, small and large intestinal fistulas, pancreatic fistula - is increasing. At the same time, in the Russian Federation for the treatment of patients with infected pancreatic necrosis in intensive care units and intensive care At least 2 million rubles are spent within one month. .
For successful treatment For this severe pathology, it is important to develop unified approaches to treatment based on a single classification. However, in Russia the attitude towards the classification of OP is still ambiguous. In 2000, at the IX All-Russian Congress of Surgeons in Volgograd, V.S. Savelyev conducted a survey of surgeons from 18 regions of the Russian Federation regarding the classification of AP they used. The survey result was unexpected. 12% of surgeons did not use the classification in their work at all, 53% preferred the international Atlanta classification - 1992, the rest worked according to outdated classifications by V.S. Savelyev (1983) and S.A. Shalimova (1990).
The international community of pancreatological surgeons is constantly working on issues of a unified strategy in the diagnosis and treatment of AP. An international group of 40 experts from 15 international and national associations of pancreatic surgeons in 1992 prepared and reported at the International Congress on September 11-13, 1992 in Atlanta (USA) the first substantiated classification system for OP. Over the past more than 20 years, some important points classifications were revised by international groups of leading pancreatologists in the world in accordance with the deepening of knowledge about the pathophysiology, morphology, course of AP, as well as taking into account the emergence of new diagnostic capabilities. In 2007, on the initiative of M.G. Sarr (USA) once again created an international working group on the 3rd revision of the classification of AP Atlanta 1992. For 5 years, experts studied international experience in the diagnosis and treatment of AP in large-scale studies, and in 2013 the text of the third was published and recommended for use revision of the OP classification - 2012.
Below we present the most significant, in our opinion, criteria for a practicing physician, classification points and prognostic scales recommended by an international working group for use in widespread practice.
Diagnostic criteria
The diagnosis of “acute pancreatitis” is made when at least two of the three signs listed below are detected:
1) abdominal pain characteristic of acute pancreatitis;
2) increase in the level of serum lipase or serum amylase by 3 times in relation to upper limit norms;
3) detection characteristic features with ultrasound and contrast-enhanced CT, MRI.
The time of onset of the disease is considered to be the moment when typical abdominal pain appears.
Pancreatic necrosis is diagnosed in the presence of a diffuse or focal area of non-viable pancreatic parenchyma (PG) more than 3 cm in diameter or occupying more than 30% of the pancreas (according to radiological diagnostic methods).
Items of the international classification Atlanta-92 third revision (2012)
Section A. By type of acute pancreatitis
1. Interstitial edematous acute pancreatitis
2. Necrotizing acute pancreatitis
Section B. According to the clinical picture and severity
|
Moderate severity |
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|
|
|
Modified Marshall Scale for Acute Pancreatitis
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Organ systems |
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Respiratory system(PaO2/FiO2) |
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(plasma creatinine, μmol/l) (plasma creatinine mg/dl) |
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Cardiovascular system (BP mm/Hg) without inotropic support |
increases during infusion |
does not increase during infusion |
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Acute mild pancreatitis is characterized by rapid positive effect from infusion therapy usually within 3-7 days. Does not require a stay in the ICU, there is no need for surgical treatment. Frequency: 80-85% of patients with AP. Morphologically it corresponds to interstitial edematous pancreatitis; microscopic necrosis of the pancreatic parenchyma is rare.
Acute pancreatitis of moderate severity is characterized by transient organ dysfunction, which can be relieved with appropriate infusion therapy within 48 hours. Morphologically, there are local or diffuse areas of non-viable pancreatic parenchyma of varying extent and location, necrosis of peripancreatic tissues of varying extent and location. Moderate AP can occur with or without complications of acute pancreatitis.
Severe acute pancreatitis is accompanied by permanent or progressive organ dysfunction, which is not relieved by infusion therapy for more than 48 hours. Morphologically, there is necrosis of the pancreatic parenchyma and/or peripancreatic tissues of varying prevalence and localization, sterile or infected; the formation of acute fluid accumulations and other local complications of acute pancreatitis. Severe pancreatitis occurs in 15-20% of patients.
Section B. Phases of acute pancreatitis
1. Early phase - 1-2 weeks from the onset of the disease. It is characterized by activation of the cytokine cascade due to severe inflammation in the pancreas. Clinically, SIRS manifests itself c high risk development of organ failure and pancreatogenic shock.
2. Late phase - after the first or second weeks of the disease. Develops only in patients with acute pancreatitis moderate severity and severe AP, is characterized by the development of local complications, often purulent, leading to transient or permanent organ failure.
Section D. Complications of acute pancreatitis
|
Local complications of acute pancreatitis |
Extrapancreatic manifestations and systemic complications |
|
1. Acute fluid collections 2. Acute pancreatic necrosis, undemarcated - sterile / infected 3. Acute peripancreatic necrosis is not delimited - sterile or infected 4. Acute, limited pancreatic necrosis - sterile or infected. 5. Acute, limited peripancreatic necrosis (extrapancreatic necrosis) - sterile or infected 6. Pancreatic pseudocyst (sterile or infected) |
1. Cholecystolithiasis. 2. Choledocholithiasis. 3. Dilation of the extrahepatic bile ducts. 4. Portal vein thrombosis. 5. Varicose veins veins of the esophagus and stomach. 6. Arterial pseudoaneurysm. 7. Hydrothorax. 9. Spread of inflammation to the stomach, duodenum, colon, kidney. 10. Necrosis of the wall colon |
Morphological criteria for the severity of AP according to the Balthazar scale
Scores for the severity of pancreatitis and the extent of necrosis are summed up. The maximum severity is 10 points, the minimum is 0 points.
Clinical criteria for severity of AP for non-biliary pancreatitis
Ranson scale
The presence of each characteristic is scored 1 point, the absence - 0 points, all points are summed up. The prognostic value of the scale is as follows: if there are 2 or less points, mortality is less than 1% (mild severity of pancreatitis), from 3 to 5 points - mortality is up to 15% ( average degree severity of pancreatitis), from 6 to 8 points - mortality up to 40% and 9 or more points - mortality up to 100% (6 or more points - severe pancreatitis).
For the right choice access and volume of surgery, a standardized assessment of the location of the lesion in the retroperitoneal tissue is necessary. For these purposes, we find the following scheme most convenient, highlighting zones of pancreatogenic aggression
Peripancreatic fiber. Fiber located around the pancreas and directly adjacent to its surface. Its main part can be adequately drained through a bursoomentostomy.
S1 - left upper quadrant of the retroperitoneum. Fiber located to the left of the spine and above the mesentery of the colon. It is often involved in the process together with the parapancreatic, and its drainage requires extraperitoneal contraperture in the left lumbar region.
S2 - left lower quadrant of the retroperitoneum. Fiber located to the left of the spine and below the mesentery of the colon. As a rule, it is a consequence of the progression of pancreatogenic aggression from S1, and for its adequate drainage, in addition to bursoomentostomy and making an incision in the left lumbar region, extraperitoneal division of all retroperitoneal tissue to the left of the spine and extraperitoneal contraperture in the left iliac region are necessary.
D1 - right upper quadrant of the retroperitoneum. Fiber located to the right of the spine and above the mesentery of the colon. A significant part of it is difficult to reach from the lumen of the omental bursa; for its drainage, an upper transrectal subhepatic approach through the abdominal cavity is used with elements of mobilization of the duodenum according to Kocher and an extraperitoneal contraperture in the right lumbar region.
D2 - right lower quadrant of the retroperitoneum. Fiber located to the right of the spine and below the mesentery of the colon. As a rule, it is a consequence of the progression of pancreatogenic aggression from D1, and for its adequate drainage, extraperitoneal separation of all retroperitoneal tissue to the right of the spine and extraperitoneal counter-opening in the right iliac region are additionally required.
Thus, the lack of standardized approaches to diagnostic and treatment algorithms plays a role in the continued high overall and postoperative mortality in severe AP. To overcome this situation, it is critically necessary to introduce scientifically based modern classification schemes into widespread surgical practice.
Reviewers:
Garbuzenko D.V., Doctor of Medical Sciences, Professor of the Department of Faculty Surgery of the State Budgetary Educational Institution of Higher Professional Education "Southern State Medical University of the Ministry of Health of Russia", Chelyabinsk;
Plotkin L.L., Doctor of Medical Sciences, Professor of the Department of Faculty Surgery of the State Budgetary Educational Institution of Higher Professional Education "Southern State Medical University of the Ministry of Health of Russia", Chelyabinsk.
We bring to your attention magazines published by the publishing house "Academy of Natural Sciences"
Chronic pancreatitis is the most common and serious illness digestive system organism, characterized by irreversible pathological changes in the functioning of the pancreas and accompanied by constant or recurrent pain. In the process of diagnosing and treating a disease, it is important to know what classification chronic pancreatitis taken into account in this case.
This disease causes a huge number of pathological complications that develop against the background of exacerbation of processes that disrupt the normal functioning of the pancreas. The pancreas produces special digestive enzymes that pass through the duct into the intestines. With pancreatitis, the organ becomes inflamed, which causes blockage of the excretory duct. When food enters the stomach and then the intestines, the pancreas begins to produce digestive enzymes. They cannot pass through the duct and accumulate, which leads to digestion from within the pancreas itself and the appearance of pain. As a result of this process, a complication such as pancreatic necrosis may occur. It represents the death of tissue of part of an organ or the entire pancreas due to self-digestion by its own enzymes.
Due to the peculiarities of the location of the pancreas in the human body, when diagnosing this disease and carrying out medical examination Difficulties often arise. Therefore, timely identification of the clinical picture of the disease can significantly facilitate the treatment process.
Acute pancreatitis is an inflammation localized in the pancreas. At the same time, the functioning of other tissues and organ systems is disrupted.
Symptoms of acute pancreatitis: pain; nausea and hiccups; pale facial skin; increase in temperature; low or high blood pressure; unstable stool accompanied by constipation or diarrhea; shortness of breath and bloating.
According to the etiological characteristics, chronic pancreatitis, the classification of which takes into account many characteristics, is primary and secondary. It is this division that is decisive when prescribing a course of treatment and underlies any classification of pancreatitis.
With primary pancreatitis, inflammation occurs immediately in the pancreas itself, and the symptoms that appear are signs of this particular disease. Sometimes accompanied by other diseases, usually related to the digestive system. If the disease is by its nature a secondary factor, then the symptoms may be mild or not expressed at all. This is due to the fact that chronic pancreatitis in in this case is concomitant disease against the background of another disease, the symptoms of which may fully manifest themselves.
This division is of great importance in medical practice when determining treatment methods. In case of secondary pancreatitis, it is important to begin treatment of the underlying disease, without which it is impossible to improve the concomitant disease. Exacerbation of chronic pancreatitis, the symptoms of which may not appear, also requires therapeutic intervention.
There are various options classifications of pancreatitis. Domestic and foreign experience indicates that such diversity in an attempt to structure signs and symptoms of this disease leads only to difficulties in developing ideas about the etiology, symptoms, clinical features, detection methods and methods of treating the disease.
In modern therapeutic practice, there is no single generally accepted classification of this disease. In 1980, A.S. Loginov’s classification was developed, which for a long time enjoyed enormous popularity. In modern practice in scientific research circles, the Marseille-Roman classification, adopted in 1989 by European countries, is used. However, this model is limited in its use in medicine, since a detailed study of the functional morphology of the pancreas is required.
As an alternative, another classification model of pancreatitis was considered, created in 1987 by doctor A.I. Khazanov, on the basis of which five clinical types of the disease are distinguished. This model is practice-oriented and most suitable for medical practice. Its structure is an attempt to take into account the morphological type of chronic pancreatitis after ultrasound.
In foreign medicine, the Cambridge classification is accepted as the working version. The International Classification of Acute Pancreatitis is very popular.
Particular attention should be paid to the classification schemes proposed by domestic scientists Ya.S. Zimmerman, V.T. Ivashkin in collaboration with others
specialists. Also interesting is the Zurich classification, which considers the features of the occurrence of the disease against the background alcohol addiction.
According to the classification proposed by one of the leading domestic gastroenterologists Ya.S. Zimmerman, pancreatitis can be characterized by different sides- focusing on the criterion that is taken as a basis.
From the point of view of etiology, pancreatitis occurs:
– alcoholic (against the background of alcohol dependence);
– idiopathic (fatty degeneration of the pancreas or cessation of excretory function);
– with kwashiorkor (severe dystrophy due to acute protein deficiency);
– hereditary or “family” (gene mutation of pancreatic enzymes);
– medicinal (use of certain medicines for a long time);
– ischemic (insufficient blood supply to the pancreas); secondary, which occurs against the background various diseases:
– liver cirrhosis and chronic hepatitis in active form;
– gastro-duodenal pathology (peptic ulcer of the digestive system);
– biliary pathology (cholepancreatitis);
– mumps (mumps) in all clinical manifestations;
– cystic fibrosis (hereditary disease of the respiratory system and exocrine glands);
– hyperparathyroidism (damage to the parathyroid glands);
– hemochromatosis (disorder of iron metabolism in the body);
– Crohn’s disease (inflammation of the gastrointestinal tract);
– ulcerative colitis (a complication associated with an inflammatory disease of the colon mucosa).
Considering the clinical manifestations of the disease, Professor Zimmerman notes:
– recurrent pain (occurs periodically, during periods of exacerbation);
– constant moderate pain (monotonic pain);
– cholestasis (stagnation of bile);
– chronic duodenal obstruction (dysfunction of the duodenum);
According to the morphological nature, pancreatitis is divided into:
According to the functional picture of the disease, pancreatitis can be of several types:
– hypersecretory type (superficial, diagnosed in the early stages of the disease);
– hyposecretory type (decreased amount of pancreatic enzymes):
compensated or decompensated
– obstructive type (difficulty in the outflow of pancreatic juice);
– ductular type (decrease in the volume of pancreatic juice with the usual amount of pancreatic enzymes);
– hyperinsulinism (excessive production of the hormone insulin in the islet cells of the pancreas);
– hypofunction of the insular apparatus (the occurrence of diabetes mellitus).
Depending on the severity of the course and the degree of complexity of the clinical picture, the scientist proposes to classify diseases as:
Proposed by Academician of the Russian Academy of Medical Sciences, Professor V.T. Ivashkin’s classification model of chronic pancreatitis is based on criteria such as:
– etiology of chronic pancreatitis (alcoholic, biliary-dependent, dysmetabolic);
– morphological characteristics(parenchymatous, fibrous-sclerotic, hyperplastic, cystic, interstitial-edematous);
– clinical manifestations of chronic pancreatitis (painful, asthenoneurotic, hyposecretory, latent, combined);
- character clinical course pancreatitis (rarely or often recurrent, persistent).
The Zurich classification, which primarily characterizes the characteristics of the course of the disease against the background of alcohol dependence, may also be applicable to
to other forms of the disease. This classification of pancreatitis is not widely used due to its complexity. And the fact that it does not focus on many etiological factors of chronic pancreatitis limits its use in medical practice. Alcoholic pancreatitis is diagnosed by one or more signs:
The diagnosis of “Chronic pancreatitis” is likely if the following diagnostic symptoms appear:
Among the etiological factors, alcoholic and non-alcoholic chronic pancreatitis are primarily distinguished. In the case of a non-alcoholic nature of the disease, we can talk about such types of pancreatitis as:
Exacerbations associated with changes in the functioning of the pancreas can be diagnosed on different clinical stages. On early stage the disease is expressed in the form of repeated attacks of acute pancreatitis without any obvious signs complications in the functioning of the pancreas. Late stage the development of pancreatitis has pronounced symptoms of a probable or definite type.
Any classification of pancreatitis created by scientists and medical practitioners characterizes the features of the course of chronic pancreatitis, considering this
process from different sides. However, each of them uses different criteria as a basis. Hence, with a sufficiently detailed and thoroughly developed system for analyzing the disease, it may be impossible to apply it in practice. The creators of a variety of classifications sought to take into account the diversity of morphological criteria and etiological signs of the manifestation of the disease, significantly complicating the classification schemes.
In modern medical practice, from the entire variety of classification models, those that allow not only visual diagnosis clinical picture diseases, but also take into account the stages of development of acute pancreatitis and the possibility of changing the morphological picture of the disease.
Classifications and types of pancreatitis - common types and subforms of the disease, which are used in medical practice to make a diagnosis. Pancreatitis is a disease inflammatory in nature, which affects the pancreas. In medical practice, it is most often discovered that the disease is formed under the influence of abuse bad habits and poor nutrition.
Clinicians identify forms of development of pancreatitis that are used in practice:
Each type has its own symptoms, indicators and treatment principles.
At the first International Conference in Marseille, participants identified 5 main types of pathology. When compiling the classification, scientists relied on the degree of organ damage. As a result, the following varieties were developed:
The classification of acute pancreatitis has several varieties. Clinicians divide the disease according to certain characteristics.
According to the severity of the pathology, they are distinguished:
Based on the scale and nature of damage to the gland, 5 types of pancreatitis have been identified:
Also, to determine the exact disease, doctors developed a causal classification. Acute pancreatitis is divided into food, biliary, gastrogenic, ischemic, infectious, toxic-allergic, congenital and traumatic.
To quickly determine the severity of an acute type of pathology, doctors identify clinical forms diseases:
The chronic type of the disease is much more common. It is characterized specific symptoms, which can fade away and reappear. Clinicians distinguish several types of the disease according to different criteria. Classification of chronic pancreatitis according to morphological characteristics:
Chronic disease is divided into 2 stages - and remission. Based on the frequency of repeated inflammation, clinicians have identified the following types of chronic pancreatitis:
Chronic pancreatitis is characterized in practice by various symptoms, under the influence of which another systematization of types has been created. Depending on the dominant symptom, the following diseases are distinguished:
Acute and chronic pancreatitis have certain causes that form the disease. Therefore, according to etiological factor The classification of these two types of illness is a little similar:
The classification of chronic pancreatitis is also based on the form of complications. According to this principle, doctors distinguish 5 forms of the disease:
As a result of the development of the disease and the manifestation of new causes of the disease, the types of pancreatitis that were identified by scientist Ivashkin are considered obsolete based on etiology. The doctor proposed a complete classification of the disease, which was divided according to many factors and allowed doctors to make an accurate diagnosis.
The form of development of the disease varies. In this regard, the doctor identified a separate section of the classification for the types of pancreatitis by structure:
Based on the signs of the disease, the following were identified:
According to the severity of the disease:
Due to the manifestation of pathology:
Types of pathology associated with complications:
Based on the etiology, Dr. Zimmerman identified two types of the disease - primary and secondary, in which more precise reasons for the formation of the pathology were identified:
Primary reasons:
Secondary causes:
Chronic and acute pancreatitis has special clinical manifestations, so the doctor identified the following types:
Painful option:
According to morphological indicator:
The functionality of the organ also influenced classification. Therefore, the following types are distinguished:
The disease can occur in three different stages:
The disease is characterized by certain complications, which also served as the reason for the formation of the classification:
In their work, clinicians use only a few of the most common classifications of the disease.
Similar materials
Pancreatitis is an inflammatory process localized in the pancreas. It can occur both acutely and chronically. It is precisely because of the presence of inflammation that the question arises: can the temperature rise? In this case, clinicians do not give a definite answer, since everything depends on the clinical picture and anamnesis.
Acute pancreatitis is a disease of the pancreas that occurs as a result of autolysis of pancreatic tissue by lipolytic and activated proteolytic enzymes, manifested by a wide range of changes - from edema to focal or extensive hemorrhagic necrosis. In most cases (about 90%), slight tissue autolysis is observed, accompanied only by swelling of the pancreas and moderate pain. In severe cases, fatty or hemorrhagic tissue necrosis occurs with severe metabolic disturbances, hypotension, fluid sequestration, multiple organ failure and fatal. After acute pancreatitis, pancreatic functions usually return to normal. In chronic pancreatitis, residual effects persist with impaired pancreatic function and periodic exacerbation.
Among emergency surgical diseases of the abdominal organs, acute pancreatitis ranks 3rd in frequency, second only to acute appendicitis and acute cholecystitis. People of mature age (30-60 years) become ill more often, women - 2 times more often than men.
Etiology and pathogenesis. The pathogenesis of acute pancreatitis is not well understood. The main etiological factor is autolysis of the pancreatic parenchyma, which usually occurs against the background of hyperstimulation of exocrine function, partial obstruction of the ampulla of the major duodenal papilla, increased pressure in the Wirsung duct, and bile reflux in the Wirsung duct. Acutely developing intraductal hypertension causes damage and increased permeability of the walls of the terminal ducts. Conditions are created for the activation of enzymes, their release beyond the ducts, infiltration of the parenchyma and autolysis of pancreatic tissue.
In patients cholelithiasis temporary obstruction of bile outflow leads to increased pressure and reflux into the pancreatic duct. These changes are associated with the migration of small stones or sand (microlithiasis). A favorable condition for biliary hypertension is the presence of a common channel (ampule) for the outflow of bile and pancreatic juice. This theory can be supported by the fact that the common channel (ampule), according to cholangiography, is observed in almost 90% of people with pancreatitis. , and in persons with cholelithiasis who did not have a history of episodes of pancreatitis - only 20-30%.
Acute pancreatitis is often caused by excessive alcohol consumption and fatty foods. It is known that alcohol increases the tone and resistance of the sphincter of Oddi. This can cause difficulty in the outflow of exocrine pancreatic secretions and increased pressure in the small ducts. Experimental studies have proven that enteral administration of alcohol increases pressure in the pancreatic ducts and increases the permeability of the walls of small ducts for macromolecules of pancreatic juice. There are reports that large protein molecules can cause obstruction of pancreatic juice flow. Alcohol increases the secretion of gastric juice and the production of hydrochloric acid, which stimulates the production of secretin, causing exocrine hypersecretion of the pancreas, creating the preconditions for increased pressure in the ducts. Thus, conditions are created for the penetration of enzymes into the parenchyma, activation of proteolytic enzymes and autolysis of pancreatic cells.
Depending on the cause of intraductal hypertension, biliary and alcoholic pancreatitis are distinguished. These types of pancreatitis account for 90% of all pancreatitis. Each of them has certain features in the clinical course and outcome of the disease. More rare causes of the development of acute pancreatitis include open and closed abdominal injuries, intraoperative damage to gland tissue, atherosclerotic occlusion of the visceral branches of the abdominal aorta, portal hypertension, and certain medications (corticosteroids, estrogen contraceptives and tetracycline antibiotics).
Necrosis of pancreatic cells and tissue surrounding the pancreatic lobules occurs at the very beginning of the process under the influence of lipase. Lipase penetrates into the cell, hydrolyzes intracellular triglycerides to form fatty acids. In damaged gland cells, intracellular acidosis develops with a pH shift to 3.5-4.5. Under conditions of acidosis, inactive trypsinogen is transformed into active trypsin, which activates phospholipase A, releases and activates lysosomal enzymes (elastase, collagenase, chymotrypsin, etc.). The content of phospholipase A and lysolecithin in pancreatic tissue during acute pancreatitis increases significantly. This indicates its role in the autolysis of gland tissue. Under the influence of lipolytic, activated proteolytic enzymes, microscopic or macroscopically noticeable foci of fat necrosis of the pancreatic parenchyma appear. Against this background, elastase lyses the walls of venules and interlobular connective tissue septa. As a result, extensive hemorrhages occur, and fatty pancreatic necrosis transforms into hemorrhagic. Thus, the proteolytic and lipolytic phases of the development of acute destructive pancreatitis are interrelated with each other.
Leukocytes rush to the foci of primary necrosis. The accumulation of leukocytes around foci of necrosis means the development of a protective inflammatory reaction, accompanied by hyperemia and edema. To delimit foci of necrosis and eliminate necrotic tissue, macrophages, leukocytes, lymphocytes, endothelial cells secrete pro-inflammatory (IL-1; IL-6; IL-8) and anti-inflammatory (IL-4; IL-10, etc.) interleukins, reactive oxygen radicals . As a result of this reaction, small foci of necrosis are delimited, undergo lysis, followed by elimination of decay products. These processes cause a moderate local reaction to inflammation in the body.
With extensive necrosis, macrophages, neutrophil leukocytes, and lymphocytes are overstimulated, the production of interleukins and oxygen radicals increases, and goes beyond the control of the immune system. The ratio of pro- and anti-inflammatory interleukins changes. They damage not only gland tissue, but also other organs. Tissue necrosis is caused not so much by interleukins themselves, but by reactive oxygen radicals, nitric oxide (NO) and the most aggressive peroxynitrile (ONOO). Interleukins only prepare the ground for this: they reduce the tone of venous capillaries, increase their permeability, and cause capillary thrombosis. Changes in the microvasculature are caused predominantly by nitric oxide. The inflammatory reaction progresses, the necrosis zone expands. The local reaction to inflammation turns into a systemic one, and Systemic Inflammatory Respons Syndrome develops. The severity of the patient's condition correlates with the high levels of IL-6 and IL-8 in the blood. With an increased concentration in the blood, multiple organ dysfunction and failure can be predicted with a high degree of probability.
Changes in the microvasculature lead to the movement of a significant part of the body fluid into the interstitial space. Dehydration occurs, BCC decreases, water-electrolyte imbalances and acid-base imbalance occur. Against the background of increased concentrations of interleukins and hyperenzyme, foci of necrosis appear on the omentum and peritoneum. Effusion in abdominal cavity contains amylase and other pancreatic enzymes in high concentration. Toxic products circulating in the blood have a direct toxic effect on the heart, kidneys, liver, and central nervous system. The severity of the systemic response to inflammation syndrome increases in accordance with increasing ischemia, increasing concentrations of NO, cytokines, hypoxia and dystrophy in vital organs. Intoxication in combination with hypovolemia quickly leads to the development of shock. Disseminated intravascular coagulation (DIC) and multiple organ failure occur.
Subsequently, after 10-15 days, the phase of sequestration and melting of dead areas begins. Sequesters and the liquid accumulated near them may remain aseptic for some time. Infection and suppuration with the formation of parapancreatic and retroperitoneal abscesses occur due to the translocation of bacteria from the lumen of the paralyzed intestine, which occurs in response to pathological changes in the pancreas and retroperitoneal tissue. In the late period, false pancreatic cysts form in the area of necrosis.
Classification. Based on the nature of changes in the pancreas, the following are distinguished: 1) edematous or interstitial pancreatitis; 2) fatty pancreatic necrosis and 3) hemorrhagic pancreatic necrosis.
The edematous or abortive form of pancreatitis develops against the background of minor, microscopic damage to pancreatic cells. The edema phase can turn into a necrosis phase within 1-2 days. With progressive pancreatitis, fatty pancreatic necrosis develops, which, as hemorrhages develop, turns into hemorrhagic with the formation of extensive edema in the retroperitoneal tissue and the appearance of hemorrhagic effusion in the abdominal cavity (pancreatogenic aseptic peritonitis). In some cases, mixed forms of pancreatitis are observed: hemorrhagic pancreatitis with foci of fatty necrosis and fatty pancreatic necrosis with hemorrhages (Fig. 14.2).
Depending on the extent of the process, focal, subtotal and total pancreatic necrosis are distinguished.
According to the clinical course, the disease is divided into abortive and progressive. According to the phases of the course of severe forms of acute pancreatitis, a period of hemodynamic disturbances is distinguished - pancreatogenic shock, functional failure (dysfunction) internal organs and a period of purulent complications that occurs after 10-15 days.
Rice. 14.2. Acute mixed - fatty and hemorrhagic pancreatitis.
Pathological picture. In the edematous form of pancreatitis, microscopic foci of necrosis are detected. Due to swelling, the pancreas increases in volume. In most patients, the development of the pathological process stops at this stage.
With progressive pancreatitis, macroscopically noticeable fat necrosis develops. The pancreas in these cases becomes dense and has a motley appearance on the section due to multiple foci of necrosis. The cellular elements in these foci do not differentiate; leukocyte infiltration of tissues and perifocal aseptic inflammation are observed around them. In areas of fat necrosis of the omentum, parietal and visceral peritoneum, in preperitoneal and subcutaneous fatty tissue, pleura, and pericardium, clumps of calcium soaps (crystals of fatty acids) are formed. They have a cloudy whitish color (stearic plaques). The binding of calcium in foci of necrosis leads to a decrease in its concentration in the blood. There is a direct relationship between calcium concentration, the prevalence of fat necrosis and the severity of the patient's condition.
There is a dense infiltrate around the pancreas, which often involves the stomach, omentum, mesentery of the transverse colon, and retroperitoneal tissue. In the abdominal cavity there is usually a cloudy serous exudate, in the pleural cavities there is sympathetic pleurisy with a small amount of serous effusion.
With hemorrhagic pancreatic necrosis, the pancreas is enlarged, dense, with foci of hemorrhage around small vessels; due to the abundance of hemorrhages, it becomes purple-black. The section reveals alternating foci of dark red necrosis with areas of fat necrosis and unchanged parenchyma, and hemorrhagic exudate in the abdominal cavity. The visceral and parietal peritoneum are dull (aseptic peritonitis). The small and large intestines are distended with gas and fluid accumulated in the lumen. With such changes, the protective barrier of the mucous membrane is disrupted. The intestinal walls become permeable to bacteria and endotoxins, which leads to the transformation of aseptic peritonitis into widespread purulent one. Subsequently, as the disease progresses, extensive areas of pancreatic necrosis appear.
In the stage of complications, foci of necrosis and exudate become infected, peritonitis, abscesses or phlegmon of the retroperitoneal tissue, and peritoneal sepsis develop. Later, one or more false cysts form. Infected cysts contain a turbid brown liquid and remnants of unmelted dead tissue. With the ongoing purulent process in the parapancreatic retroperitoneal tissue, “necrosis tracks” are formed in the form of purulent streaks, spreading to adipose tissue at the root of the mesentery of the transverse colon and lateral canals. In those who died within 7 days from the onset of the disease, congestive plethora and pulmonary edema, and degeneration of parenchymal organs predominated. In 77% of those who died after the specified period, purulent complications predominated.
Clinical picture and diagnosis. Clinical symptoms of acute pancreatitis depend on the morphological form, period of development and severity of the systemic response to inflammation syndrome. In the initial period of the disease (1-3 days), both with the edematous (abortive) form of pancreatitis and with progressive pancreatitis, patients complain of sharp, constant pain in the epigastric region, radiating to the back (girdling pain), nausea, and repeated vomiting.
The pain can be localized in the right or left quadrant of the abdomen. There is no clear connection between pain and the localization of the process in the pancreas. Sometimes the pain spreads throughout the abdomen. With alcoholic pancreatitis, pain occurs 12-48 hours after intoxication. With biliary pancreatitis (cholecystopancreatitis), pain occurs after a heavy meal. In rare cases, acute pancreatitis occurs without pain, but with a pronounced systemic reaction syndrome, manifested by hypotension, hypoxia, tachycardia, respiratory failure, impaired consciousness. With this course of the disease, acute pancreatitis can be diagnosed using ultrasound, computed tomography, and laboratory tests.
IN early dates from the onset of the disease, objective data are very scarce, especially in the edematous form: pallor skin, slight yellowness of the sclera (with biliary pancreatitis), mild cyanosis. The pulse may be normal or accelerated, the body temperature is normal. After infection of foci of necrosis, it increases, as with any purulent process.
The abdomen is usually soft, all parts participate in the act of breathing, and sometimes some bloating is noted. Shchetkin-Blumberg's symptom is negative. In approximately 1-2% of seriously ill patients, bluish, sometimes with a yellowish tinge spots (Gray Turner's symptom) and traces of resorption of hemorrhages in the pancreas and retroperitoneal tissue appear on the left side wall of the abdomen, indicating hemorrhagic pancreatitis. The same spots can be observed in the navel area (Cullen's sign). Percussion reveals high tympanitis over the entire surface of the abdomen - intestinal paresis occurs due to irritation or phlegmon of the retroperitoneal tissue or concomitant peritonitis. When a significant amount of exudate accumulates in the abdominal cavity, there is a dullness of percussion sound in the sloping parts of the abdomen, which is more easily detected when the patient is positioned on his side.
When palpating the abdomen, pain in the epigastric region is noted. There is no tension in the abdominal muscles in the initial period of development of pancreatitis. Only sometimes resistance and pain are noted in the epigastrium in the area where the pancreas is located (Kerte's symptom). Palpation in the left costovertebral angle (projection of the tail of the pancreas) is often painful (Mayo-Robson sign). With fatty necrosis of the pancreas, an inflammatory infiltrate forms early. It can be determined by palpation of the epigastric region. Due to paresis and swelling of the transverse colon or the presence of infiltration, it is not possible to clearly determine the pulsation abdominal aorta(Voskresensky symptom). Peristaltic sounds are already weakened at the very beginning of the development of pancreatitis, disappearing as the pathological process progresses and peritonitis appears. Percussion and auscultation of the chest in a number of patients reveals a sympathetic effusion in the left pleural cavity.
With very severe pancreatitis, a systemic response syndrome to inflammation develops, the functions of vital organs are disrupted, respiratory failure occurs, manifested by an increase in respiratory rate, adult respiratory distress syndrome (interstitial pulmonary edema, accumulation of transudate in the pleural cavities), cardiovascular failure (hypotension , frequent thread-like pulse, cyanosis of the skin and mucous membranes, decrease in blood volume, central venous pressure, minute and stroke volume of the heart, signs of myocardial ischemia on the ECG), liver, kidney and gastrointestinal failure (dynamic intestinal obstruction, hemorrhagic gastritis). Most patients experience a mental disorder: agitation, confusion, the degree of disturbance of which should be determined using Glasgow scale scores.
Functional liver disorders are usually manifested by a icteric discoloration of the skin. With persistent obstruction of the common bile duct, obstructive jaundice occurs with increased levels of bilirubin, transaminases, and enlarged liver. Acute pancreatitis is characterized by an increase in amylase and lipase in the blood serum. The concentration of amylase (diastase) in the urine and in the exudate of the abdominal and pleural cavities increases significantly. With total pancreatic necrosis, the amylase level decreases. A more specific test for the early diagnosis of pancreatitis is the determination of trypsin in the blood serum, α-chymotrypsin, elastase, carboxypeptidase, and especially phospholipase A, which plays a key role in the development of pancreatic necrosis. However, the complexity of their definition hinders the widespread use of these methods.
The acid-base state undergoes a shift to acidosis, against the background of which the flow of intracellular potassium into the blood increases while its excretion by the kidneys decreases. Hyperkalemia, which is dangerous for the body, develops. A decrease in calcium content in the blood indicates the progression of fat necrosis, the binding of calcium by fatty acids released as a result of the action of lipase on fatty tissue in foci of necrosis. Small foci of steatonecrosis occur on the omentum, parietal and visceral peritoneum (“stearin spots”). Calcium levels below 2 mmol/l (normal 2.10-2.65 mmol/l, or 8.4-10.6 mg/dl) are an unfavorable prognostic indicator.
Diagnosis of acute pancreatitis is based on medical history (the appearance of sharp abdominal pain after a heavy meal, drinking alcohol or exacerbation of chronic calculous cholecystitis), data from physical, instrumental and laboratory studies.
Ultrasound examination. Ultrasound provides significant assistance in diagnosis, making it possible to establish etiological factors (cholecysto- and choledocholithiasis), identify swelling and enlargement of the pancreas, accumulation of gas and liquid in distended intestinal loops. Signs of pancreatic edema are an increase in its volume, a decrease in the echogenicity of the pancreatic tissue and
reducing the degree of signal reflection. With necrosis of the pancreas, vaguely limited areas of reduced echogenicity or complete absence of an echo signal are detected. Spread of necrosis beyond the pancreas (“necrosis tracks”), as well as abscesses and false
cysts can be visualized with great accuracy using ultrasound (Fig. 14.3; 14.4; 14.5). Unfortunately, the capabilities of ultrasound are often limited due to the location in front of the pancreas of the intestine, swollen with gas and liquid, covering the gland.
Computed tomography is a more accurate method for diagnosing acute pancreatitis compared to ultrasound. There are no obstacles to carrying it out. The reliability of diagnosis increases with intravenous or oral enhancement with contrast material. Enhanced computed tomography can more clearly identify diffuse or local enlargement of the gland, edema, foci of necrosis, fluid accumulation, changes in peripancreatic tissue, “paths of necrosis” outside the pancreas, as well as complications in the form of abscesses and cysts.
Magnetic resonance imaging is a more advanced diagnostic method. It provides information similar to that obtained from a computed tomography scan.
X-ray examination reveals pathological changes in the abdominal cavity in most patients: isolated dilatation of the transverse colon, segments of the jejunum and duodenum adjacent to the pancreas, sometimes radiopaque stones in the bile ducts, in the pancreatic duct or calcium deposits in its parenchyma (mainly with alcoholic pancreatitis). With large processes in the pancreas (false cysts, inflammatory infiltrates, abscesses), a change in the location (pushing to the sides) of the stomach and duodenum is observed. X-ray examination reveals signs of paralytic intestinal obstruction, effusion in the pleural cavity, discoid atelectasis of the basal parts of the lungs, often accompanying acute pancreatitis. Examination of the stomach and intestines with a contrast agent in the acute period of the disease is contraindicated.
Esophagogastroduodenoscopy is performed for gastrointestinal bleeding from acute erosions and ulcers, which are complications of acute (most often destructive) pancreatitis. Retrograde pancreatic cholangiography in acute pancreatitis is contraindicated, since this procedure further increases the pressure in the main pancreatic duct.
Laparoscopy is indicated for unclear diagnosis, if laparoscopic installation of drains is necessary for the treatment of acute pancreatitis. Laparoscopy allows you to see foci of steatonecrosis (stearin spots), inflammatory changes in the peritoneum, gall bladder, penetrate into the cavity of the lesser omentum and examine the pancreas, install drains for the outflow of exudate and rinsing the cavity of the lesser omentum. If it is not possible to use laparoscopy to take peritoneal exudate and perform diagnostic lavage, a so-called “groping” catheter can be inserted into the abdominal cavity through a puncture in the abdominal wall (laparocentesis).
Electrocardiography is necessary in all cases, both for differential diagnosis with acute myocardial infarction, and for assessing the state of cardiac activity during the development of the disease.
To assess the condition of patients and to predict the outcome of the disease, a number of tests and criteria based on indicators of impairment of physiological functions and laboratory data have been proposed. Even just determining the amount of fluid sequestered (the amount of fluid administered minus the amount of urine excreted) is important in determining the severity of the disease. If fluid sequestration exceeding 2 liters per day persists for 2 days, then there is reason to consider pancreatitis severe, life-threatening. If this indicator is less, then pancreatitis can be considered moderate or mild. Renson criteria are often used to predict and assess the severity of acute pancreatitis. Such criteria at the onset of the disease are age (over 55 years), leukocytosis over 16,000, blood glucose over 200 mg%, transaminase (ACT) over 250, serum lactate dehydrogenase over 350 i.u./l. The criteria that develop within 24 hours are: a decrease in hematocrit by more than 10%, an increase in blood urea by more than 8 mg%, a decrease in calcium to a level of less than 8 mg/l, arterial blood p02 less than 60 mm Hg, deficiency bases over 4 mEq/L, detectable fluid sequestration over 600 ml. Morbidity and mortality correlate with the number of identified criteria. The probability of death in the presence of 0-2 criteria is 2%, with 3-4 criteria - 15%, with 5-6 criteria - 40% and with 7-8 criteria - up to 100% . More complex, but more universal is the APACNE-P scale (acronym for Acute Physiology Assessment and Chronic Health Evaluation). The patient's condition is assessed based on the severity of physiological dysfunctions, chronic diseases, and the patient's age. The identified scores make it possible to objectively and clearly determine the severity of the disease, the effectiveness of the treatment measures, and compare the advantages and disadvantages of different treatment methods in groups of patients comparable in severity.
Differential diagnosis. Differential diagnosis must be carried out primarily with thrombosis of the mesenteric vessels, since with this disease sudden sharp pains, a state of shock with a soft abdomen and normal body temperature may resemble acute pancreatitis. Paralytic ileus and peritonitis occur in both diseases. If the diagnosis is unclear, it is advisable to perform upper mesentericography.
According to clinical data, myocardial infarction is difficult to differentiate from acute pancreatitis, since in the acute phase of pancreatitis, ECG changes characteristic of myocardial infarction sometimes occur. In both intestinal mesenteric infarction and myocardial infarction, ultrasound helps differentiate these diseases. Acute cholecystitis and its complications can be relatively easily distinguished by the typical clinical picture and ultrasound symptoms. Acute pancreatitis must be differentiated from perforated gastric and duodenal ulcers, strangulating small intestinal obstruction, dissecting aortic aneurysm, and renal colic.
Complications. Acute pancreatitis can be accompanied by numerous complications. The most severe of them are:
hypovolemic shock;
multiple organ failure, including acute renal failure, resulting from the progression of the systemic response syndrome to inflammation and the development of shock;
pleuropulmonary complications, manifested by respiratory failure due to the development of shock lung, exudative pleurisy, atelectasis of the basal parts of the lungs, high position of the diaphragm;
liver failure (from mild jaundice to severe acute toxic hepatitis, developing as a result of shock and the influence of toxic enzymes and protein substances); the disease contributes to this biliary tract and accompanying cholangitis;
pancreatic abscesses and extrapancreatic abscesses in the retroperitoneal tissue, the appearance of which is caused by an infection that easily develops in foci of necrosis;
external pancreatic fistulas often form at the site of drainage or a postoperative wound; internal fistulas usually open into the stomach, duodenum, small and large intestine;
widespread purulent peritonitis occurs when a parapancreatic abscess breaks into the free abdominal cavity or translocation of bacteria from the intestine into the free abdominal cavity, aseptic pancreatogenic peritonitis becomes purulent;
bleeding resulting from vascular arrosion (blood from the abdominal cavity is released through a wound or through a drainage channel).
Internal bleeding is most often a consequence of erosive gastritis, stress ulcers, Mallory-Weiss syndrome, and also due to disturbances in the hemostatic system (consumptive coagulopathy).
Late complications of pancreatic necrosis include pseudocysts. Necrotic pancreatic tissue with extensive necrosis does not completely resolve. It is encapsulated and turns into a postnecrotic pseudocyst due to the formation of a connective tissue capsule around the focus of necrosis. The contents of the cyst may be sterile or purulent. Sometimes spontaneous resorption of cysts occurs (most often when it communicates with the excretory ducts of the pancreas).
International classifications of pancreatitis
The lack of a classification suitable for clinical use was the reason for the convening of the first international conference in Marseille (1963), initiated by Sarles H. The result of the work of an international group of pancreatology experts was the first international classification, which includes mainly clinical categories. It was distinguished by its simplicity and received wide recognition abroad. Only 20 years later, due to the further deepening of ideas about acute pancreatitis, the need arose to revise it at international conferences in Cambridge in 1983 and again in Marseille in 1984.
International Marseille (1963) classification of pancreatitis
In accordance with the agreements adopted at this conference, 4 forms of pancreatitis are considered: acute, recurrent, chronic recurrent and chronic.
Table 1. Division of forms of pancreatitis in accordance with decisions of international conferences
|
Marseille, 1963 |
Cambridge, 1984 |
|
Acute pancreatitis Recurrent pancreatitis Chronic recurrent pancreatitis Chronic pancreatitis |
Acute pancreatitis Chronic pancreatitis |
|
Marseille, 1984 |
Atlanta, 1992 |
Acute pancreatitis Chronic pancreatitis |
Acute pancreatitis easy heavy |
International classifications differ not only in the categorization of the spectrum of forms of pancreatitis, but also in their definitions, given in Table 2.
At the Cambridge conference, the main attention of the participants was focused on the characterization of the anatomical structures of the pancreas in chronic damage to this organ, methods of their identification and objective assessment, and the use of the obtained data to categorize the pathological condition.
Participants at the Cambridge conference were unable to formulate a definition of the intermediate - recurrent form, but noted that acute pancreatitis can recur and that exacerbations may occur in a patient with chronic pancreatitis.
Cambridge and Marcel (1984) formulated clinical descriptions of acute pancreatitis that were similar in content. In Cambridge, the definition of severe AP included the concept of “system failure” - “insufficiency of organ systems”. None of these conferences produced definitions of complications of acute pancreatitis that meet the needs of clinical practice.
In 1988, Glazer G. formulated the main problems and classifications of OP:
Morphological changes do not always provide a reliable indication of the likely outcome;
Macroscopic or radiological semiotics of pancreatic lesions do not always correspond to histological changes and bacteriological data;
Objective criteria for distinguishing between “mild” and “severe” AP, reflecting “systemic disorders,” lack precision and gradation of the intensity of these disorders, both in general and systemically;
Definitions of local complications use the poorly defined terms “abscess” and “infected fluid collections.”
At the same time, the Marseille and Cambridge conferences marked a “change of milestones” in pancreatology and, above all, in the classifications of acute and chronic pancreatitis. To replace the multi-colored “kaleidoscope” of terms, weighted, criteria-defined categories agreed upon by international groups of experts were proposed, which predetermine the choice of approach to the treatment of these diseases.
It should be recognized that these classifications are still far from perfect and are not sufficiently familiar to domestic authors, which is facilitated by insufficient information about them in the pancreatological literature in Russian.
An attempt to eliminate these shortcomings was made by Glazer G. in the modern clinical and morphological classifications, consistent with the principles used by international expert groups.
An analysis of the classifications of acute pancreatitis shows that the most controversial point in them is the definition of purulent forms. To characterize them, 12 terms are used. The confusion is aggravated by the addition of the terms “primary” and “secondary”, attempts to take into account the morphological and topographic-anatomical variants of infectious pathology of the pancreas, the severity of the clinical course in the early stages of the disease, the size and location of abscesses, and the identification of groups with different routes of infection into the pathological focus. On the other hand, the terminological “kaleidoscope” is due to changes in the properties of the pathology, an increase in its frequency, diversity and severity, depending on the nature of treatment in the early stages of the disease.
Table 2. Definitions of forms of pancreatitis in accordance with decisions of international conferences
|
INTERNATIONAL CLASSIFICATIONS OF PANCREATITIS |
|
Marseille, 1963 |
|
For two acute forms on the part of the pancreas, complete restoration of structure and function is expected. Chronicity of pancreatitis after them is unlikely, although not excluded. For two chronic forms There are persistent changes in the structure of the pancreas, but exacerbations are possible. Chronic pancreatitis can develop from a chronic recurrent form, less often from an acute or primary form.v Main disadvantage This classification requires information about the histological structure of the pancreas, which, as a rule, is missing. |
|
Cambridge, 1984 |
Acute pancreatitis – acute condition, typically manifested by abdominal pain, usually accompanied by an increase in the activity of pancreatic enzymes in the blood and urine. Chronic pancreatitis– an ongoing inflammatory disease of the pancreas, characterized by irreversible morphological changes and typically causing pain and/or permanent loss of function. |
|
Marseille, 1984 |
Acute pancreatitis Chronic pancreatitis - Clearly delineated morphological form chronic pancreatitis is obstructive chronic pancreatitis, characterized by expansion of the ductal system above the occlusion (tumor, scars), diffuse atrophy of the acinar parenchyma and the same type of diffuse fibrosis. Stones are not typical. With this pathology, functional changes regress with the elimination of obstruction, while in other forms of chronic pancreatitis they are irreversible morphological changes lead to a progressive or permanent decrease in the exocrine and intrasecretory function of the pancreas. |
|
Atlanta, 1992 |
Acute pancreatitis – acute inflammatory process in the pancreas with various involvement of other regional tissues and distant organ systems. Easy– accompanied by minimal dysfunction organs and a smooth recovery. The main pathological phenomenon is interstitial edema of the pancreas. Heavy– accompanied by dysfunction of organs and/or local complications (necrosis with infection, false cysts or abscess. Most often it is a manifestation of the development of pancreatic necrosis, although patients with edematous AP may have a clinical picture of severe AP. |
No less number of “synonyms” (18) are found when describing “hemorrhagic pancreatitis”.
The inaccuracy of nosological definitions of the forms and complications of acute pancreatitis, which hinders the development of methods for their treatment, became the subject of consideration at an international conference in Atlanta (1992) (Tables 1 and 2). The conference decision recommended distinguishing between two forms of infectious complications in AP:
"Infected necrosis"- subject to colliquation and/or suppuration, bacterially seeded infiltrated necrotic mass of the pancreas and/or retroperitoneal tissue, not demarcated from healthy tissues.”
"Pancreatic abscess"- a limited intra-abdominal accumulation of pus, usually near the pancreas, not containing necrotic tissue or containing it in small quantities and arising as a complication of acute pancreatitis.”
It should be noted that, by definition and characteristics established in subsequent studies, the term “infected necrosis” is much closer to the term “purulent-necrotizing pancreatitis”, widely used in the domestic literature since the early 70s, than to the more popular term in the West "pancreatic abscess".
Atlanta conference participants also approved definitions for “acute pancreatitis,” “severe acute pancreatitis,” “mild acute pancreatitis,” “acute fluid collections,” “pancreatic necrosis,” and “acute pseudocyst.” It is not recommended to use terms that can be ambiguous, such as “phlegmon” and “hemorrhagic”. In the domestic literature, we did not find publications introducing these definitions, and therefore we present them based on the materials “United Kingdom guidelines for the management of acute pancreatitis” published by Glazer G. and Mann D.V. 1998 on behalf of a working group of the British Society of Gastroenterology.
« Acute pancreatitis- acute inflammatory process of the pancreas with varied involvement of other regional tissues or distant organ systems.”
« Severe acute pancreatitis- accompanied by organ failure and/or local complications such as necrosis (with infection), false cyst or abscess. Most often this is a consequence of the development of pancreatic necrosis, although patients with edematous pancreatitis may have clinical signs serious illness."
« Mild acute pancreatitis- associated with minimal organ dysfunction and unimpeded recovery. The predominant manifestation pathological process is interstitial edema of the (pancreas).
« Acute fluid collections- occur in the early stages of acute pancreatitis, are located in and around the pancreas and never have walls of granulation or fibrous tissue.”
« Pancreatic necrosis- diffuse or focal zone(s) of non-viable pancreatic parenchyma, which, as a rule, is combined with necrosis of peripancreatic fatty tissue.”
« Acute pseudocyst- an accumulation of pancreatic juice surrounded by a wall of fibrous or granulation tissue that occurs after an attack of acute pancreatitis. The formation of a false cyst continues for 4 or more weeks from the onset of acute pancreatitis.”
The practical significance of the decisions of the Atlanta conference is that the given definitions relate to pathological conditions that are the “nodal points” of therapeutic, tactical and diagnostic algorithms. “Definitions” include only the most important - distinctive properties of the concept - its discriminants, which diagnostic methods are aimed at identifying.
This international classification allows the formation of more homogeneous groups in controlled studies, a clearer assessment of the results of the use of treatment and preventive measures, and the development of methods for predicting, treating and preventing complications.
