Pathogenesis of chronic pancreatitis in the acute stage. Acute pancreatitis. Local complications of chronic pancreatitis

Delayed release and intraorganic activation of pancreatic enzymes - trypsin and lipase, which carry out autolysis of the parenchyma of the gland, reactive growth and cicatricial wrinkling of the connective tissue, which then leads to sclerosis of the organ, chronic circulatory disorders in the pancreas. In the teaching of the inflammatory process, the processes of autoaggression are of great importance. In chronic pancreatitis of infectious origin, the pathogen can penetrate into the pancreas from the lumen of the duodenum (for example, with dysbacteriosis) or from the biliary tract through the pancreatic ducts in an ascending way, which is facilitated by dyskinesia of the digestive tract, accompanied by duodeno- and choledocho-pancreatic reflux. Predispose to the occurrence of chronic pancreatitis spasms, inflammatory stenosis or tumor of the Vater nipple, which prevent the release of pancreatic juice into the duodenum, as well as insufficiency of the sphincter of Oddi, which facilitates the free entry of duodenal contents into the pancreatic duct, especially eneroxidase contained in intestinal juice, activating trypsin. The inflammatory process may be diffuse or limited to the area of ​​the head or tail of the pancreas. There are chronic edematous (interstitial), parenchymal, sclerosing and calculous pancreatitis.

In the case of the development of a pronounced exacerbation of CP against the background of the presence of gallbladder stones, there are indications for cholecystectomy.

Main mechanisms:

> Transfer of infection from the bile ducts to the pancreas through the common lymphatic tract.

> Difficulty in the outflow of pancreatic secretions and the development of hypertension in the pancreatic ducts (stones in the common bile duct).

> Biliary reflux into the pancreatic ducts.

Violation of liver function in hepatitis, cirrhosis leads to the production of pathologically altered bile containing a large amount of peroxides, free radicals, which, when released with bile into the pancreatic ducts, initiate protein precipitation in them, the formation of stones and the development of inflammation.

Diseases of the duodenum (DU) and major duodenal papilla (BD)

In the pathology of the duodenum, the development of pancreatitis is often associated with the reflux of the contents of the duodenum into the pancreatic ducts. Reflux occurs when:

> The presence of BDS deficiency (hypotension) - papillitis, diverticulitis, stone passage, dysmotility;

> Development of duodenal stasis (chronic duodenal obstruction);

> Combinations of these two states.

The development of chronic pancreatitis may be a complication of peptic ulcer

Ulcer penetration into the pancreas (secondary pancreatitis).

Alimentary factor

The use of fatty, fried, spicy foods, low protein content in the diet (for example, fibrosis and atrophy of the pancreas and its pronounced secretory insufficiency is observed in liver cirrhosis, malabsorption syndrome).

Genetically determined pancreatitis

Allocate the so-called hereditary pancreatitis - an autosomal dominant type of inheritance with incomplete penetrance. Pancreatitis in cystic fibrosis is also essentially hereditary.

Medicinal pancreatitis

Rarely seen. Pancreatodamaging factors include:

> Azathioprine;

> Estrogens;

> Glucocorticosteroids;

> Sulfonamides;

> Non-steroidal anti-inflammatory drugs (Brufen);

> Furosemide;

> Thiazide diuretics;

> Tetracycline;

> Indirect anticoagulants;

> Cimetidine;

> Metronidazole;

> Cholinesterase inhibitors.

Viral infection

In the genesis of chronic pancreatitis, the role of hepatitis B and C virus, Coxsackie virus, mumps virus is allowed.

Violation of the blood supply

Atherosclerosis, thrombosis, embolism, inflammatory changes in systemic vasculitis can lead to the development of ischemic pancreatitis.

Dysmetabolic pancreatitis

It is observed in diabetes mellitus (non-pancreatogenic variant), hyperparathyroidism, hemochromatosis, hyperlipidemia.

With hereditary hyperlipoproteinemia, pancreatitis manifests itself from childhood. Most often, chronic pancreatitis develops in patients with hyperchylomicronemia (I and V according to Friederiksen). In pathogenesis, the obstruction of the vessels of the gland by fatty particles, fatty infiltration of acinar cells, the appearance of free fatty acids resulting from the activation of TAG hydrolysis are important.

In hyperparathyroidism, secondary pancreatitis occurs in 10-19% of cases. Increases the calcium content in acinar cells (stimulation of enzyme secretion), activation of trypsinogen and pancreatic lipase (autolysis).

Idiopathic pancreatitis

The etiology remains undeciphered in 20-40% of patients. There are early idiopathic pancreatitis, with onset before the age of 35, and late.

Pathogenesis

Theory of M. Boger (1984)

Under the influence of etiological factors, dystrophic and then atrophic changes in the mucous membrane of the duodenum develop, a decrease in its regenerative abilities (impaired production of secretin and cholecystokinin-pancreozymin. Secretin regulates the volume of pancreatic juice, the amount of bicarbonates in it, reduces duodenal motility, motility of the stomach, intestines, reduces pressure in the duodenum and pancreatic ducts, relieves spasm of the sphincter of Oddi.

Under the influence of secretin deficiency:

> Increased pressure in the duodenum;

> Spasm of the sphincter of Oddi;

> Increased pressure in the pancreatic ducts;

> The volume of pancreatic juice decreases due to the liquid part;

> Decreased secretion of bicarbonates;

> Thickening of pancreatic juice and an increase in the concentration of protein in it;

> An increase in the viscosity of pancreatic juice, a decrease in the rate of its outflow, which is aggravated by spasm of the sphincter of Oddi.

The slowdown in the outflow of pancreatic juice, combined with an increase in its viscosity and protein content, leads to its precipitation, protein plugs are formed that clog various sections of the pancreatic ducts.

With a significant periodic increase in the secretory activity of the pancreas (alcohol, spicy food), an expansion of the ducts of the gland initially occurs; in the future, while maintaining secretory activity, the pancreatic secret enters the surrounding interstitial tissue,

causing swelling of the pancreas.

Under conditions of edema, as a result of mechanical compression and disturbance of trophism, atrophy of the acinar glands occurs with their replacement by connective tissue (nontryptic variant of chronic pancreatitis). In some cases, if there is a significant obstruction to outflow

pancreatic juice and increased secretory activity of the acinar glands, there is a rupture of the basement membrane of the acinar cells with the release of enzymes into the surrounding tissue (activation of proteases and limited self-digestion of the gland (tryptic recurrent form).

In the pathogenesis of chronic pancreatitis, the activation of the KKS is important,

coagulation and fibrinolytic systems (development of thrombosis, hemorrhage,

necrosis, impaired microcirculation).

The pathogenesis of chronic calcific pancreatitis

Chronic calcific pancreatitis accounts for 50-95% of all forms and is associated with alcohol consumption. Pathogenesis is associated with impaired formation of soluble protein-calcium associates. At the earliest stages of HCP formation, protein precipitates are detected in the pancreatic ducts. They are an insoluble fibrillar protein combined with the deposition of calcium carbonates. This protein has been isolated and named lipostatin. It is present in the pancreatic juice of healthy people. Its role is to maintain calcium in a soluble state, inhibiting nucleation, aggregation and the formation of insoluble crystals of calcium salts.

With HCP, the possibility of synthesizing the total pool of lipostatin decreases in conditions of increased demand for it.

Such conditions occur with increased protein hydrolysis in pancreatic juice, induction of polymerization of protein components, and increased secretion of calcium salts.

Classification

Classification according to A.L. Grebenev, 1982

I. By etiological grounds

1) Primary chronic pancreatitis (with the primary development of the inflammatory process in the pancreas);

2) Secondary chronic pancreatitis (against the background of other diseases of the digestive system);

II. According to morphological features

1) Edema form

2) Sclerotic-atrophic form

3) Fibrous (diffuse, diffuse-nodular form)

4) Pseudotumorous form

5) Calcifying form

III. According to the characteristics of the clinic

1) Polysymptomatic form (including chronic recurrent pancreatitis)

2) Painful form

3) Pseudotumor form

4) Dyspeptic form

5) Latent form

In each case, the phase of the disease is indicated:

1) Pancreatitis of mild severity (I stage of the disease - initial)

2) Pancreatitis of moderate course (II stage)

3) Severe pancreatitis (Stage III - terminal, cachetic).

At I Art. signs of violation of intra- and exocrine function are not expressed.

At II and III Art. there are signs of a violation of external and / or intrasecretory function (secondary diabetes mellitus).

Under III Art. persistent "pancreatogenic" diarrhea is observed,

polyhypovitaminosis, exhaustion.

Marseilles-Roman classification (1988)

I. Chronic pancreatitis calcifying. The most common form of the disease. The most common cause (alcohol). As a result of inflammation and changes in the structure of the smallest pancreatic ducts, the secretion thickens with the formation of plugs rich in protein and calcium. In this process, an important role is played by a decrease in the concentration of lithostatin (a protein that prevents stone formation).

II. Chronic obstructive pancreatitis. It is observed with pronounced narrowing of the main pancreatic duct or its large branches, or the nipple of Vater. Causes of development: alcohol, cholelithiasis, trauma, tumor, birth defects. The lesion develops distal to the site of duct obstruction. The epithelium at the site of duct obstruction was preserved. Occurs infrequently.

III. Chronic fibrous-indurative (parenchymal, inflammatory) pancreatitis. It is characterized by fibrosis, mononuclear cell infiltration, and exocrine tissue atrophy. Rare form. Intravenously Chronic cysts and pseudocysts of the pancreas.

Classification by Ivashkin V.G. and Khazanova A.I., 1990

I. By morphology

1) Interstitial-edematous

2) Parenchymal

3) Fibrosclerotic

4) Hyperplastic (pseudotumorous)

5) Cystic

II. by etiology

1) Biliary dependent

2) Alcoholic

3) Dysmetabolic (diabetes mellitus, hyperparathyroidism,

hyperlipidemia)

4) Infection (hepatitis B virus, CMV)

5) Medicinal

6) Idiopathic

III. According to clinical manifestations

1) Painful

2) Hyposecretory

3) Astheno-neurotic (hypochondriac)

4) Latent

5) Combined

Intravenously According to the nature of the clinical course

1) Rarely recurrent

2) Often recurrent

3) With persistent symptoms of chronic pancreatitis

Clinical picture, course options, complications, outcomes

The clinical picture is characterized by 3 main syndromes:

> Pain syndrome;

Pancreatitis is a severe disease of the pancreas, which is based on intraorganic activation of digestive enzymes produced by the gland and enzymatic tissue damage expressed to varying degrees (pancreatic necrosis), followed by the development of fibrosis, often spreading to surrounding tissues (parapancreatic fibrosis), and also complicated by secondary infection. Clinically, pancreatitis can occur in acute and chronic forms, often closely related.

Etiology.

The etiology of chronic pancreatitis is:

1. Alcohol, irritating the mucous membrane of 12 bp, not only enhances the production of secretin, pancreozymin, histamine, gastrin, and, consequently, the external secretion of the pancreas, but also causes a reflex spasm of the sphincter of Oddi, leading to intraductal hypertension. Prolonged alcohol use is accompanied by duodenitis with increasing atony of the sphincter, which leads to duodenopancreatic and biliarypancreatic reflux, especially during vomiting. The protein-vitamin insufficiency characteristic of chronic alcoholism is also important. Some authors believe that alcohol can also have a direct toxic effect on the pancreatic parenchyma. In addition, there is evidence that chronic alcohol intoxication changes the composition of pancreatic juice by increasing the amount of protein, lactoferrin and reducing bicarbonates and protease inhibitors, which contributes to the formation of calculi.

2. Diseases of the gallbladder and biliary tract, with the dominance of cholelithiasis, including the condition after cholecystectomy. The inflammatory-sclerotic process accompanying these diseases in the distal biliary tract leads to stenosis or insufficiency of the sphincter of Oddi. Spasm or stenosis of the sphincter leads to hypertension in the ductal system of the pancreas and, as a result, the release of pancreatic juice components into the parenchyma with the development of inflammatory and sclerotic changes in it. Bile reflux in this case is not of decisive importance, since CP also develops with a separate confluence of the choledochus and the Wirsungian duct in 12 p.k. The mucous membrane of the pancreatic ducts is normally resistant to the action of bile, and only with prolonged incubation of bile mixed with pancreatic secretions or bacterial cultures does bile acquire a damaging effect on the pancreas. In case of insufficiency of the major duodenal papilla, reflux of intestinal contents into the ducts of the pancreas occurs with the activation of proteolytic enzymes, which, in combination with hypertension, has a damaging effect on the parenchyma of the organ.

3. Injury to the pancreas, including intraoperative. In the development of postoperative pancreatitis, not only the direct effect on the gland tissue and its ducts is important, but also the devascularization of the pancreas,

4. Diseases of the gastrointestinal tract, especially 12 p.c.: edema in the region of Vater's nipple, which impedes the outflow of pancreatic secretions, duodenostasis, accompanied by duodenopancreatic reflux; diverticula 12 p.k., which can lead either to compression of the ducts with subsequent hypertension, or, if the duct opens into the diverticulum, to duodenopancreatic reflux. Duodenitis not only maintains the inflammation of Vater's nipple, but also causes secretory dysfunction of the pancreas due to a violation of the production of polypeptide hormones of the gastrointestinal tract. Ulcer penetration 12 p.k. or stomach in the pancreas often leads to a focal inflammatory process, and in some cases - to a typical chronic recurrent pancreatitis.

5. One-sided nutrition with carbohydrate and fatty foods with a lack of proteins leads to a sharp stimulation of external secretion, followed by a breakdown of regenerative processes in the pancreas. Of particular importance is the intake of alcohol with fatty foods.

6. Endocrinopathy and metabolic disorders:

Hyperparathyroidism leading to hypercalcemia and calcification of the pancreas/calcium promotes the conversion of trypsinogen to trypsin in the pancreatic ducts

Hyperlipidemia, which leads to fatty infiltration of pancreatic cells, damage to the vascular wall, the formation of blood clots, vascular microembolism;

7. Allergic factors. In the blood of a number of patients, antibodies to the pancreas are found; in some cases, there is marked eosinophilia (up to 30-40% or more). The literature describes cases of the appearance of pain crises when eating strawberries, and the development of CP against the background of bronchial asthma.

8. Hereditary factors. So it is known that in children whose parents suffer from CP, the likelihood of its development in an autosomal dominant manner is increased. The more frequent occurrence of CP in persons with 0(1) blood group is emphasized. In some cases, this is the cause of the so-called juvenile pancreatitis.

9. Malformations of the pancreatic-bilioduodenal zone: annular pancreas, accompanied by duodenostasis; additional pancreas with different variants of the course of the ducts that do not provide an outflow of secretions; enterogenic cysts of the pancreas.

10. Drugs: steroid hormones, estrogens, sulfonamides, methyldopa, tetracycline, sulfasalazine, metronidazole, a number of non-steroidal anti-inflammatory drugs, immunosuppressants, anticoagulants, cholinesterase inhibitors and others.

11. Nonspecific ulcerative colitis, Crohn's disease, hemochromatosis and a number of other diseases accompanied by sclerotic changes in the pancreas without clinical manifestation, which can be considered as a nonspecific tissue reaction to toxic or circulatory effects. Fibrosis of the pancreas in cirrhosis of the liver should probably be included in the same group.

Pathogenesis. It can be considered generally accepted that the basis of the pathogenesis of pancreatitis in the vast majority of patients is damage to the tissue of the gland by its own digestive enzymes. Normally, these enzymes are secreted in an inactive state (except for amylase and some fractions of lipase) and become active only after entering the duodenum. Most modern authors identify three main pathogenetic factors that contribute to the autoaggression of enzymes in the organ that secretes them:

1) obstruction of the outflow of secretion of the gland into the duodenum and intraductal hypertension;

2) abnormally high volume and enzymatic activity of pancreatic juice;

3) reflux into the ductal system of the pancreas of the contents of the duodenum and bile.

The mechanisms of pathological intraorganic activation of enzymes and damage to the gland tissue differ depending on the cause of pancreatitis. So it is known that alcohol, especially in large doses, sharply increases the volume and activity of pancreatic juice in a reflex and humoral way. To this is added the stimulating effect of the alimentary factor, since alcoholics eat irregularly, not so much eat as snack, taking a lot of fatty and spicy food. In addition, alcohol contributes to spasm of the sphincter of the hepatic-pancreatic ampulla (sphincter of Oddi), causes an increase in the viscosity of the pancreatic secretion, the formation of protein precipitates in it, which later transform into stones characteristic of the chronic form of the disease. All this complicates the outflow of secretion and leads to intraductal hypertension, which at a level exceeding 35-40 cm of water. Art., can cause damage to the epithelial cells of the ducts and acini and the release of cytokinases that trigger the mechanism of enzyme activation. Spasm of the sphincter of Oddi possibly leads to biliary-pancreatic reflux and intraductal activation of enzymes by bile acids. Do not exclude also the direct damaging effect of high concentrations of alcohol in the blood on the glandular cells.

In pancreatitis associated with diseases of the biliary tract, the main pathogenetic factor is a violation of the outflow of pancreatic juice into the duodenum, which is associated primarily with the presence of the mentioned "common channel", that is, the hepatic-pancreatic (vater) ampulla, through which bile calculi depart and where the main pancreatic duct usually empties. It is known that with a separate confluence of the bile and pancreatic ducts, as well as with a separate confluence into the duodenum of an additional duct communicating with the main pancreatic duct, biliary pancreatitis does not develop.

Passing through the ampulla of Vater, gallstones temporarily linger in it, causing spasm of the sphincter of Oddi and transient ductal hypertension, causing enzymatic damage to the gland tissue and, possibly, an attack of acute pancreatitis, in some cases occurring asymptomatically or masked by an attack of biliary colic. Repeated "pushing" of gallstones through the ampoule due to high pancreatic and biliary pressure can lead to trauma to the mucous membrane of the duodenal papilla and stenosing panpilitis, which makes it increasingly difficult for the passage of bile and pancreatic juice, as well as the repeated discharge of stones. Sometimes there is a persistent infringement of the gallstone in the ampoule, leading to obstructive jaundice and severe pancreatic necrosis.

An independent role in the pathogenesis of pancreatitis can also be played by diseases of the duodenum associated with duodenostasis and hypertension in its lumen and contributing to the reflux of duodenal contents into the pancreatic duct (including the "abductor loop syndrome" after resection of the stomach according to the Billroth type P). Some authors also point to the importance of duodenal diverticula, especially peripapillary ones, which can cause both spasm and (rarely) atony of the sphincter of Oddi.

Traumatic pancreatitis can be associated with both direct and indirect effects on the pancreas. In case of direct injury, mechanical damage to the gland leads to intraorganic activation of enzymes with the release of the already mentioned activators (cytokinases) from the dead cells and the subsequent development of enzymatic pancreatic necrosis in addition to the traumatic one. During endoscopic interventions on the major duodenal papilla (ERCP, EPST), the mucous membrane of the ampulla of Vater and the terminal section of the main pancreatic duct are often injured. As a result of trauma, hemorrhages and reactive edema, the outflow of pancreatic secretions may be difficult and ductal hypertension may develop. The walls of the duct may also be damaged from excessive pressure when a contrast agent is injected during ERCP.

With the indirect effect of accidental and surgical injuries on the pancreas (traumatic shock, blood loss, cardiac surgery with prolonged perfusion), damage to the glandular tissue with the release of activating cellular factors is mainly associated with microcirculatory disorders and corresponding hypoxia.

Attention should be paid to another important aspect of the pathogenesis of chronic pancreatitis, insufficiently covered in the literature. According to most clinicians, pancreatic necrosis is considered a defining feature of the most severe forms of acute destructive pancreatitis. However, damage and death (necrosis, necrosis) of the pancreatic tissue under the influence of intraorganic activation and autoaggression of digestive enzymes determines the occurrence and course of any, including chronic, forms of the disease in question.

In chronic pancreatitis, which is not a consequence of acute, there is also enzymatic damage, necrobiosis, necrosis and autolysis of pancreatocytes, occurring both gradually, under the influence of a long-acting factor, and sharply abruptly during exacerbations of the chronic process.

Pathological anatomy. In the process of development of pancreatitis in the tissue of the pancreas, connective tissue grows, resulting in the development of fibrosis and sclerosis. In the future, calcification develops, a violation of the patency of the pancreatic ducts.

In clinical practice, there are two main forms of the disease - acute and chronic pancreatitis.

Classification

More than 40 classifications of acute Pancreatitis have been proposed. The V All-Russian Congress of Surgeons in 1978 recommended using the following classification of acute Pancreatitis: 1) edematous Pancreatitis; 2) fatty pancreatic necrosis; 3) hemorrhagic pancreatic necrosis; 4) purulent Pancreatitis This classification, based on the morphological principle, does not reflect other aspects of the disease that are important for therapeutic tactics. For a more accurate assessment of the clinical course, it is necessary to distinguish three phases of the disease: 1) the phase of enzymatic toxemia; 2) phase of temporary remission; 3) phase of sequestration and purulent complications.

In the complicated course of Pancreatitis, it is necessary to assess the prevalence of peritonitis and the nature of the effusion in the peritoneal cavity. When the process spreads to the retroperitoneal tissue, the degree of damage to it should be determined. In addition, it is necessary to take into account the degree of damage to the pancreatic tissue, which can be limited, subtotal or total. With fatty pancreatic necrosis, foci of necrosis on the surface of the gland may be focal or confluent.

Story

In 1841, N. Tulp reported an abscess of the pancreas, discovered at autopsy of a patient who died with symptoms of an acute abdomen. Klebs (E. Klebs) in 1870 singled out acute Pancreatitis as a separate disease. Fitz (R. N. Fitz) in 1889 made a report that he recognized acute Pancreatitis during the life of the patient. This diagnosis was then confirmed by laparotomy and autopsy.

The first successful operation for acute pancreatitis was performed in 1890 by W. S. Halsted.

The first monographs on surgical diseases of the pancreas were published by A. V. Martynov in 1897, and then in 1898 by W. Korte, who for the first time successfully opened a pancreatic abscess and recommended active surgical tactics for pancreatic necrosis.

Statistics

Until the 1950s, acute pancreatitis was considered a rare disease, detected only during surgery or autopsy. According to V. M. Voskresensky (1951), from 1892 to 1941, only 200 patients with acute pancreatitis were described by domestic scientists. Since the mid-1950s, along with improved diagnosis of the disease, an increase in the incidence of acute pancreatitis has been noted. A. Nesterenko (1980), an increase in the number of patients with destructive forms of the disease is especially characteristic. Among acute surgical diseases of the abdominal organs, Pancreatitis ranks third in frequency after acute appendicitis and acute cholecystitis. According to G. N. Akzhigitov (1974), acute pancreatitis accounts for 0.47% of all somatic diseases and 11.8% of all surgical diseases. Among sick women there were 80.4%, men - 19.6%. In patients with pancreatic necrosis, the ratio of men and women is 1: 1. Men under the age of 40 suffer from Pancreatitis 2 times more often than women.

Etiology

Acute Pancreatitis is a polyetiological disease that occurs as a result of damage to pancreatic acinar cells, hypersecretion of pancreatic juice and difficulty in its outflow with the development of acute hypertension in the pancreatic ducts (pancreatic ducts), which can lead to activation of enzymes in the gland itself and the development of acute pancreatitis

Damage to acinar cells can occur with closed and open abdominal trauma, surgical interventions on the abdominal organs, acute circulatory disorders in the pancreas (ligation, thrombosis, embolism, vascular compression, and others), exogenous intoxications (alkalis, acids, etc.), severe allergic reactions, significant nutritional disorders and others.

The role of diseases of the bile ducts in the genesis of acute pancreatitis is generally recognized. Lancero (E. Lancereaux, 1899) hypothesized the development of acute pancreatitis due to bile reflux into the pancreatic duct.

Acute bile-pancreatic ductal hypertension and bile reflux into the pancreatic ducts easily occur in the presence of a common ampulla for the common bile duct and pancreatic duct in the event of a sudden blockade of the mouth of the large Vater papilla (duodenal papilla), for example, by a gallstone, and others. According to E. V. Smirnov et al. (1966), K. D. Toskin (1966) and others, in addition to biliary-pancreatic reflux (see full body of knowledge), duodenopancreatic reflux may also be the cause of acute pancreatitis. If in the first case, pancreatic enzymes are activated by bile (see the complete body of knowledge), then in the second case, enteropeptidase is their activator. Leakage of duodenal contents into the pancreatic ducts is possible with the gaping of the major duodenal papilla and an increase in intra-duodenal pressure.

Experimental studies by N. K. Permyakov and his co-workers (1973) showed that both excessive food intake, especially fats and carbohydrates, and its lack, especially proteins, lead to damage to the ultrastructures of acinar cells even in conditions of undisturbed outflow of pancreatic secretion and contribute to the development of primary -acinous form of pancreatitis (metabolic pancreatitis).

The role of the alimentary factor in the development of acute pancreatitis increases with the intake of an excess amount of juice food in conditions of violation of the outflow of pancreatic juice.

In the etiology of acute pancreatitis, in some cases, other factors can play a role: endocrine disorders (hyperparathyroidism, pregnancy, long-term treatment with corticosteroids, etc.), congenital or acquired disorders of fat metabolism (severe hyperlipemia), some infectious diseases (viral parotitis and viral hepatitis ).

Allergies are predisposing factors. Even Pancreatitis D. Solovoe in 1937 explained the origin of pancreatic necrosis by hyperergic inflammation of the vessels of the pancreas.

Subsequently, it was proved that by sensitizing animals with foreign proteins or bacterial toxins, acute pancreatitis in all phases can be reproduced.

MN Molodenkov (1964) caused acute pancreatitis by ligating the pancreatic ducts after sensitization of rabbits by four subcutaneous injections of normal horse serum.

V. V. Chaplinsky and A. I. Gnatyshak (1972) reproduced acute pancreatitis in dogs by sensitizing the body with a foreign protein and introducing, against this background, resolving exogenous (food) and endogenous (metabolite) allergens. However, the numerous patterns of allergic pancreatitis are far from identical to the similar disease in humans.

According to V. I. Filin et al. (1973), G. N. Akzhigitov (1974), in patients admitted to surgical hospitals, diseases of the bile ducts and other digestive organs, diseases of the cardiovascular system most often contribute to the development of acute pancreatitis of non-traumatic origin. systems, nutritional disorders, alcohol abuse and others.

Pathogenesis

The most widespread enzymatic theory of the pathogenesis of acute pancreatitis

Activation of the pancreas' own enzymes (trypsin, chymotrypsin, elastase, lipase, phospholipase, and others) under conditions of increased function, difficult outflow of pancreatic secretion and subsequent enzymatic damage to the gland tissue in the form of edema and necrosis (fatty, hemorrhagic, mixed) are the most characteristic link in pathogenesis of acute pancreatitis

This process in the pancreas proceeds as a chain reaction and usually begins with the release of cytokinase from the damaged cells of the parenchyma of the gland. Under the action of cytokinase, trypsinogen is converted to trypsin (see full body of knowledge). Pancreatic kallikrein, activated by trypsin, acting on kininogen, forms a highly active peptide - kallidin, which quickly turns into bradykinin (see the full body of knowledge: Mediators of allergic reactions). Bradykinin can also be formed directly from kininogen. Under the action of trypsin, histamine (see the complete body of knowledge) and serotonin (see the full body of knowledge) are released from various cells of the pancreas. Through the lymphatic and circulatory pathways, pancreatic enzymes enter the general bloodstream. In the blood, trypsin activates the Hageman factor (see the full body of knowledge: Blood coagulation system) and plasminogen, and thereby affects the processes of hemocoagulation and fibrinolysis.

The initial pathological changes in the pancreas and other organs are manifested by pronounced vascular changes: narrowing and then dilatation of blood vessels, a sharp increase in the permeability of the vascular wall, slowing blood flow, the release of the liquid part of the blood and even formed elements from the lumen of the vessels into the surrounding tissues. There are serous, serous-hemorrhagic, hemorrhagic edema and even massive hemorrhages in the gland, retroperitoneal tissue.

In conditions of disturbed local blood circulation, tissue metabolism and direct action on the cells of enzymes, foci of necrosis of the pancreatic parenchyma and the surrounding adipose tissue appear. This is facilitated by thrombus formation, which is most characteristic of hemorrhagic forms. Pancreatitis Lipases are released from destroyed cells (see full body of knowledge). The latter, especially phospholipase A, hydrolyze fats and phospholipids, causing fatty necrosis of the pancreas, and spreading through the blood and lymph flow, cause steatonecrosis of distant organs.

General changes in the body are caused at the beginning by enzymatic (enzymatic), and then tissue (from foci of necrosis) intoxication. Due to the generalized effect of vasoactive substances on the vascular bed, significant circulatory disorders occur very quickly at all levels: tissue, organ and systemic. Circulatory disorders in the internal organs (heart, lungs, liver, and others) lead to dystrophic, necrobiotic, and even obvious necrotic changes in them, after which secondary inflammation develops.

Significant exudation in the tissue and cavity, deep functional and morphological changes in internal organs and other causes cause pronounced disturbances in water-electrolyte, carbohydrate, protein and fat metabolism.

pathological anatomy

Pathologically, acute pancreatitis is based on primary destructive changes in acini caused by intraorganic (intracellular) activation of digestive enzymes produced by the pancreas. Developing enzymatic autolysis of acinar cells is accompanied by the formation of foci of necrosis and aseptic (abacterial) inflammation. Therefore, the assignment of acute pancreatitis to the group of inflammatory processes is very conditional; the term "pancreatic necrosis" more accurately reflects the essence of the pathological process. Inf. inflammation of the gland, as a rule, is a complication of pancreatic necrosis; it develops in the late stages of the disease due to microbial infection of necrosis foci. Only occasionally purulent Pancreatitis can be observed with septicopyemia as a concomitant lesion due to metastasis of a purulent infection.

There is no generally accepted pathoanatomical classification for pancreatitis. Most pathologists distinguish between necrotic and hemorrhagic-interstitial forms of acute pancreatitis, acute serous, and acute purulent pancreatitis

Acute serous Pancreatitis (acute edema of the pancreas) most often undergoes regression and only sometimes becomes destructive. However, with the lightning-fast development of the disease, death can occur from enzyme shock in the first three days, when the destruction of the gland has not yet occurred. These cases are difficult for pathoanatomical diagnosis, since macroscopic changes in the pancreas (edema) do not correspond to the severity of the clinical course. Only a few fatty necroses (see the full body of knowledge) found in the surrounding cellulose can testify to the defeat of the gland (color figure 1). Microscopically, in the gland itself, as a rule, changes are found that correspond to diffuse focal Pancreatitis (color figure 2). A similar course Pancreatitis is observed, as a rule, in chronic alcoholism.

Pathological changes in the gland in hemorrhagic-necrotic pancreatitis (pancreatic necrosis) depend on the extent of the lesion and the duration of the disease. Macroscopically, in the initial phases (1-3 days), the gland is significantly enlarged in volume (color figure 3), compacted, the cut surface has a homogeneous gelatinous appearance, the lobular structure of its structure is erased, but clear foci of necrosis are not yet visible. Only under the parietal peritoneum covering the pancreas (the so-called capsule), in the lesser and greater omentums, the capsule of the kidneys, the mesentery of the intestine, one can detect scattered small yellow foci of fat necrosis in combination with serous and serous-hemorrhagic effusion in the peritoneal cavity (color figure 4 ).

The macroscopic view of the pancreas within 3-7 days from the onset of the disease depends on the prevalence of pancreatic necrosis. According to the scale of the lesion, pancreatic necrosis can be divided into three groups: diffuse-focal, large-focal, subtotal (total).

With diffuse focal pancreatic necrosis in these terms, foci of necrosis with a diameter of 0.2-1 centimeters of yellow or reddish color are clearly delimited from the preserved parenchyma of the gland. Microscopically, progressive sclerosis of necrotic areas, gradual decay of leukocytes and a change in the cellular composition of the inflammatory infiltrate with lymphoplasmic and histiocytic elements are noted.

Foci of fatty necrosis of the surrounding tissue are either absent or present in small quantities. The pancreatic capsule is not destroyed.

In the affected areas, proliferation of small ducts is found, which never ends with the regeneration of acini. The outcome of this form of pancreatic necrosis is diffuse focal fibrosis and pancreatic lipomatosis.

In the large-focal form of Pancreatitis, one or more foci of necrosis 2 × 3–3 × 4 centimeters in size are formed, which, unlike a heart attack, have irregular outlines. The foci of necrosis, as a rule, are yellow in color and capture the capsule of the gland. Their evolution, as well as the outcomes of the disease, depend on the depth of the lesion and localization (head, body, tail of the gland). Necrosis of the tail of the gland is most often replaced by fibrous tissue. With necrosis of the body and head of the gland, the outcome of the disease is determined by the degree of secondary lesions of the walls of blood vessels and large ducts. Large foci of necrosis of this localization often undergo diffuse fusion and sequestration with the formation of an abscess (intraorganic, omental sac) or a false cyst (see the full body of knowledge: Pancreas).

The cavity of the cyst (color figure 5), as a rule, is connected with the ducts of the gland, through which there is a constant discharge of the secret.

In progressive variants of acute pancreatitis, the initial stage of serous edema of the pancreas is replaced very early by the stage of hemorrhagic necrosis with significant hemorrhage (color figure 7) in the tissue or without it. This is followed by the stage of melting and sequestration of necrotic foci of the pancreas and retroperitoneal fat. In the last stage, suppuration often occurs, which initially has an aseptic character. The reverse development of the second stage and its transition to the third can be carried out through the formation of a massive inflammatory infiltrate in the gland zone, in which not only the gland, but also the para-pancreatic retroperitoneal tissue, and neighboring organs (stomach, duodenum, spleen and other).

In most cases, the development of acute pancreatitis stops at the stage of edema or necrosis, without passing into the stage of sequestration.

If edema and necrosis of the pancreas and retroperitoneal tissue in acute pancreatitis usually develop in the coming hours of the disease, then the melting of necrotic foci begins no earlier than the 3-5th day, and sequestration - after 2-3 weeks and later from the onset of the disease.

Sometimes purulent inflammation of the gland acquires a diffuse character. In this case, leukocyte infiltrates spread in the stroma of the gland as a phlegmon (phlegmonous pancreatitis), which usually indicates the addition of an infection.

The walls of the abscess of the stuffing box are formed due to the organs that form this cavity; their serous membranes undergo fibrosis. Sclerotic processes can be so intense that all the hollow organs of the upper half of the abdominal cavity are soldered into one conglomerate, which makes laparotomy difficult. This conglomerate is sometimes mistaken for a tumor. The contents of the abscess are usually tissue detritus, pus, and pancreatic secretions. Further evolution of the abscess proceeds in the following main variants: the formation of a false cyst, erosion of the walls of adjacent organs (stomach, duodenum, transverse colon) with the formation of an internal fistula, erosion of a large arterial trunk with bleeding into the gastrointestinal tract, a breakthrough into the free peritoneal cavity with development purulent peritonitis (cm).

The severity of the course of macrofocal acute pancreatitis also depends on the extent of fat necrosis. In severe extraorganic lesions, melting of the retroperitoneal tissue is observed, followed by the formation of para-pancreatic phlegmon, which then spreads through the retroperitoneal space.

Subtotal (total) form Pancreatitis usually has the character of hemorrhagic necrosis and ends with melting and sequestration of the gland with the development of the complications described above.

Microscopically, already in the early phases of the development of pancreatic necrosis, in addition to interstitial edema, multiple foci of fatty necrosis and necrosis of the acini, located mainly along the periphery of the pancreatic lobules, are found. In the foci of necrosis, thrombosis of capillaries, venules and parietal thrombosis of larger veins are naturally detected (color figure 6). Disorders of hemocirculation in the intraorgan veins are accompanied by extensive hemorrhages and hemorrhagic impregnation of the parenchyma of the gland. The degree of damage to the venous bed, apparently, mainly determines both the hemorrhagic nature of necrosis and its extent.

Violations of the permeability of capillaries in the first 1-2 hours after the destruction of the acini are accompanied by diapedesis of leukocytes. At the same time, a large number of mast cells (labrocytes) appear in the edematous stroma, which are associated with the production of biologically active substances that are important in the development of an inflammatory reaction (see the full body of knowledge: Inflammation). After 1-2 days, a demarcation shaft appears around the foci of necrosis (color figure 8), consisting of leukocytes and nuclear detritus. Subsequently, histiocytes and lymphoplasmic cell elements are detected in it. A feature of the evolution of pancreatic necrosis is the rapid activation of fibroblasts, accompanied by intensive formation of collagen with the formation of connective tissue capsules and fibrosis fields (color figure 9-13).

When a cyst or abscess is formed, microscopically, their walls are represented by hyalinized fibrous tissue with diffuse focal infiltrates consisting of lymphocytes, plasma cells, and histiocytes. The inner shell of the abscess is usually covered with necrotic plaque and fibrin with leukocyte detritus and isolated intact leukocytes.

Electron microscopic studies of the pancreas, performed on various models of experimental Pancreatitis, reveal the initial phases of damage to acinar cells. Progressive autolysis of acini is usually preceded by partial necrosis of acinar cells with the formation of a large number of autophagosomes and accumulation of numerous lipid vacuoles in the cytoplasm. These changes are accompanied by a significant restructuring of the function of acinar cells, which is manifested by a change in the merocrine type of secretion normal for the gland to apocrine and micro-holocrine, which are characterized by sequestration of the apical sections of the cytoplasm along with secretion granules. There is also a peculiar relocation of zymogen granules, containing the entire set of synthesized digestive enzymes, to the basal sections of the cytoplasm of acinar cells. At the same time, any destruction of the basement membrane inevitably leads to a paradoxical release of secretory granules not into the lumen of the tubule, but into the interstitium, from where they can be resorbed into the blood and lymphatic channels. Concomitant damage to the capillary endothelium and intense edema of the stroma contribute to secretion resorption. The described changes are accompanied by rapid activation of the kallikrein-trypsin system and phospholipase A, which leads to progressive autolysis with the formation of foci of aseptic necrosis.

Clinical picture

Severe pain in the upper abdomen of a girdle character is the leading and most constant symptom of acute pancreatitis. In some cases, pain radiates behind the sternum and into the region of the heart. The intensity of pain is associated with irritation of the receptors, increased pressure in the common bile duct and pancreatic ducts, and chemical exposure to trypsin.

Due to sharp pains, patients are restless and constantly change position without getting relief. Pain is especially pronounced with temorragic pancreatic necrosis, although severe pain can also be observed during the edematous phase of Pancreatitis. With the onset of necrosis of nerve endings, the intensity of pain decreases, therefore, it is not always possible to judge the degree of damage to the pancreas by the intensity of pain.

Nausea and vomiting are the second leading symptom of acute pancreatitis. Vomiting is often painful, indomitable, not bringing relief. Usually, its first portions contain food masses, the last - bile and mucous contents of the stomach. With destructive pancreatitis, sometimes due to the occurrence of acute stomach ulcers, an admixture of blood appears in the vomit (the color of coffee grounds).

The skin and mucous membranes in acute pancreatitis are often pale, sometimes with a cyanotic tint. In severe forms of the disease, the skin is cold, covered with sticky sweat. Quite often, acute pancreatitis is accompanied by obstructive jaundice (see full body of knowledge), due to obstruction of the common bile duct by gallstones or compression of its inflammatory infiltrate in the head of the pancreas.

Described pathognomonic signs in destructive Pancreatitis - areas of cyanosis of the skin or subcutaneous hemorrhages around the navel, on the lateral areas of the abdomen, anterior abdominal wall, face.

Body temperature, in the first hours of the disease, is normal or low, with the addition of inflammation, it rises. High temperature, which does not tend to decrease, is often a sign of destructive pancreatitis, and a late increase in hectic temperature is a sign of purulent complications (retroperitoneal phlegmon, abscess formation).

At the beginning of the disease, bradycardia is often observed, later, with an increase in intoxication, the pulse rate usually gradually increases. In the edematous form of acute pancreatitis, arterial hypertension is possible, and in the destructive form, hypotension and even collapse (see full body of knowledge).

Complications

Two groups of complications of acute pancreatitis can be distinguished: local complications associated with damage to the pancreas, and complications caused by the general effect of the disease on the body.

General complications: hepatic-renal failure, sepsis, obstructive jaundice, psychosis, diabetes mellitus.

Local complications: peritonitis (limited, widespread); retroperitoneal phlegmon, abscesses of the abdominal cavity, omental bag; necrosis of the wall of the stomach, transverse colon; pancreatic fistulas internal and external; false cyst of the pancreas; arrosive bleeding.

With edematous pancreatitis, complications are rare. With destructive pancreatitis, they occur in almost every patient.

Liver failure (see the complete body of knowledge) and kidney failure (see the full body of knowledge) are caused by intoxication of enzymatic and inflammatory origin, hemodynamic disturbances, hypoxia and previous violations of the functional state of the liver and kidneys.

Acute mental disorders are caused by intoxication and more often develop in people who have abused alcohol. Diabetes mellitus (see the complete body of knowledge: Diabetes mellitus) usually occurs with destructive Pancreatitis and the destruction of all or almost all of the islet apparatus of the pancreas, and in patients with latent diabetes, it can also occur with edematous Pancreatitis.

Diagnosis

Physical research. The tongue in acute pancreatitis is usually dry, coated with a white or brown coating. On palpation in the first hours of the disease, the abdomen is sharply painful in the epigastric region, but relatively soft in all departments. Gradually, with the development of paresis of the gastrointestinal tract, the abdomen increases in size and does not participate in the act of breathing. Initially, swelling of the abdominal wall is noted locally in the epigastric region (Bode's symptom), then it spreads to the underlying regions. Peristalsis is sharply weakened or not audible, gases do not go away.

Rigidity of the anterior abdominal wall in the epigastric region, determined in the projection of the pancreas (Kerte's symptom), is found in almost 60% of cases. Acute pancreatitis may be accompanied by tension of the abdominal wall, sometimes to a board-like character. The Shchetkin-Blumberg symptom is less common than the rigidity of the anterior abdominal wall. Mayo-Robson's symptom (pain in the costovertebral angle) is noted on the left when the caudal pancreas is involved in the process and on the right when its head is affected.

Other symptoms are also described in acute Pancreatitis, which have a certain diagnostic value: Voskresensky's symptom (disappearance of aortic pulsation in the epigastric region), Razdolsky's (pain on percussion over the pancreas), Kacha (hyperesthesia along the paravertebral line on the left, respectively, segments Th VII-IX), Makhova (hyperesthesia above the navel) and others

Laboratory research methods. Hematological changes usually occur in destructive forms of the disease. In some patients, hypochromic anemia is detected, although, according to V. V. Chaplinsky, V. M. Lashchevker (1978) and others, with severe dehydration, erythrocytosis may be noted in the first two days. Leukocytosis is found in approximately 60% of patients. Neutrophilic shift to the left due to an increase in immature forms, lymphopenia, aneosinophilia, and acceleration of ESR are also characteristic. Of the pancreatic enzymes (amylase, lipase, trypsin), the determination of urine amylase is of practical importance (see the full body of knowledge: Wolgemuth method). An increase in its activity, reaching 8192-32768 units (according to the Wolgemuth method, in which normal values ​​do not exceed 16-128 units), is noted in more than 70% of patients. However, low activity of the enzyme does not exclude the diagnosis of acute pancreatitis. It may be due to sclerotic changes or necrosis of acinar cells, renal failure, early or, conversely, late admission of the patient. In severe acute pancreatitis, serum amylase should be determined, since in a number of patients urine amylase can be normal, and in the blood it can be sharply increased and reach 400-500 units (according to the Smith-Row method, in which normal values ​​do not exceed 100-120 units ). Trypsin activity usually increases, while the activity of its inhibitor decreases. Determination of lipase activity due to its significant fluctuations in the norm has less diagnostic value. According to A. A. Shelagurov (1970), an increase in the activity of pancreatic enzymes in the blood is found in 82.5-97.2% of patients. It is important to dynamically study the activity of enzymes.

In the diagnosis of acute pancreatitis, the level of bilirubin in the blood is also important, which can increase with an increase in the head of the pancreas.

Determination of the concentration of potassium, sodium, calcium ions in the blood, as well as sugar, total protein and protein fractions, makes it possible to assess the severity of the patient's condition and the degree of disturbance of the corresponding types of metabolism.

Changes in the blood coagulation system also depend on the form of the disease. With edematous form and fatty pancreatic necrosis, as a rule, hypercoagulation is observed, with hemorrhagic Pancreatitis, hypocoagulation. Hyperfibrinogenemia and an increase in C-reactive protein are almost always noted. According to V. S. Savelyev et al. (1973), G. A. Buromskaya et al. (1979), changes in the kallikrein-kinin system are characterized by a decrease in the level of kininogen, prekallikrein, a kallikrein inhibitor, which is most pronounced in destructive pancreatitis

Changes in the indicators of daily and hourly diuresis to a certain extent depend on the severity of the pancreatic lesion. A sharp decrease in daily and hourly diuresis, anuria are usually observed with pancreatic necrosis. In patients with acute pancreatitis, proteinuria, microhematuria, and cylindruria are also detected.

X-ray diagnostics. A survey X-ray examination of the chest and abdomen reveals a high position of the left half of the diaphragm, limitation of its mobility, accumulation of fluid in the left pleural cavity, pneumatosis of the stomach and duodenum, paresis of individual loops of the jejunum.

In a contrast X-ray examination of the gastrointestinal tract, due to an increase in the pancreas and edema of the lesser omentum and retroperitoneal tissue, an anterior displacement of the stomach, expansion of the duodenum, straightening of the medial contour of its vertical part, and an increase in the so-called gastrocolic distance.

Computed tomography (see the full body of knowledge: Computed tomography) detects an increase in the pancreas. With the edematous form of acute pancreatitis, its shadow has clear contours. With hemorrhagic, necrotic and purulent pancreatitis, the outlines of the gland disappear, and its shadow becomes intense and heterogeneous; sometimes cavities of abscesses are distinguishable.

With celiacography (see full body of knowledge), increased blood supply to the vessels of the pancreas, an increase in its volume, lengthening of the parenchymal phase with heterogeneity of the shadow of the gland is determined. In pancreatic necrosis, V. I. Prokubovsky (1975) noted a weakening or disappearance of the shadow of the intraorganic vessels of the pancreas, pushing the gastroduodenal artery to the right, angular deformity and pushing up the common hepatic artery.

Special research methods. Ultrasound diagnostics (see the full body of knowledge) allows you to distinguish between the boundaries and structure of the pancreas (focal and diffuse changes). With interstitial pancreatitis, an increase in the size of the organ is detected, its clear delimitation from the surrounding tissues is preserved, and a transmission pulsation appears from the aorta. With destructive pancreatitis, the pancreas loses its homogeneity, its contours merge with the surrounding background, and unstructured areas are found. With the development of a pseudocyst, a homogeneous formation with a well-defined capsule is determined, pushing back neighboring organs. If there is an effusion in the abdominal cavity, echolocation can determine it already in the amount of 200 milliliters.

During gastroscopy (see the full body of knowledge) and duodenoscopy (see the full body of knowledge), usually performed in difficult diagnostic cases, the following signs of acute pancreatitis can be detected: a) pushing back the back wall of the body and the pylorus; b) hyperemia, edema, mucus and erosion in the area of ​​displacement, and sometimes signs of diffuse gastritis; c) reversal of the duodenal loop, duodenitis, papillitis. Displacement of the posterior wall of the stomach in combination with pronounced inflammatory changes are signs of an abscess of the omental sac.

Of great importance in the diagnosis of acute pancreatitis is laparoscopy (see the full body of knowledge: Peritoneoscopy), which allows you to reliably diagnose the most severe form of the disease - pancreatic necrosis.

Laparoscopic signs of pancreatic necrosis are plaques of focal necrosis of adipose tissue found on the greater and lesser omentums, gastrocolic ligament, sometimes on the peritoneum of the anterior abdominal wall, round ligament of the liver, mesentery of the transverse colon and small intestine.

The second sign of pancreatic necrosis is the presence of exudate in the peritoneal cavity. With fatty pancreatic necrosis, it has a serous character. The amount of exudate is different - from 10-15 milliliters to several liters. Proof of the pancreatogenic nature of such peritonitis is a sharp increase in the activity of pancreatic enzymes in the exudate. The study of the activity of trypsin and lipase in the exudate is of lesser importance.

A frequent sign of pancreatic necrosis is serous impregnation of fatty tissue (the so-called vitreous edema).

Hemorrhagic pancreatic necrosis is characterized by the presence of red exudate - from brownish-brown to clearly hemorrhagic. Occasionally, foci of hemorrhage in the gastrocolic ligament or greater omentum are seen.

Unlike pancreatic necrosis, edematous Pancreatitis usually does not have characteristic laparoscopic findings, since the pathological process, as a rule, does not go beyond the omental sac. However, in some cases, a serous effusion with high enzyme activity is found in the abdominal cavity.

Differential diagnosis of acute pancreatitis is carried out with acute cholecystitis (see the full body of knowledge), cholecystopancreatitis (see the full body of knowledge), perforated ulcer of the stomach and duodenum (see the full body of knowledge: Peptic ulcer), acute appendicitis (see the full body of knowledge), acute intestinal obstruction (see the full body of knowledge: Intestinal obstruction), intestinal infarction (see the full body of knowledge), acute gastritis (see the full body of knowledge), food poisoning (see the full body of knowledge: Food poisoning), myocardial infarction (see the full body of knowledge).

Differentiation of edematous and destructive forms of pancreatitis subject to different treatment remains difficult. Both edematous and destructive forms of pancreatitis often begin in the same way. However, within a few hours after intensive therapy, clinical manifestations in edematous Pancreatitis subside, the patient's condition improves. Symptoms of destructive Pancreatitis, despite ongoing therapy, persist for a long time, the patient's condition improves slightly. With the progression of the process, it worsens: tachycardia increases, intoxication and peritoneal phenomena increase. With total pancreatic necrosis, a severe clinical picture develops from the first hours of the disease (pointed facial features, frequent small pulse, oliguria).

In difficult-to-diagnose cases, laparoscopy and other instrumental research methods become necessary.

Criteria have been developed to guide the differential diagnosis of various forms of pancreatitis (table).

Treatment

In a serious condition of the patient, therapeutic measures should be started even at the pre-hospital stage. They should be aimed at combating a pronounced pain syndrome and arterial hypotension, that is, include elements of infusion therapy (polyglucin, gemodez and others), as well as the use of cardiac glycosides, analeptics that stimulate breathing, analgesics, except for narcotic ones.

Hospitalization of patients with acute pancreatitis should be carried out only in a surgical hospital. The nature of the therapeutic measures carried out in the hospital depends on the severity of the clinical, the picture of the disease, the severity of the patient's condition, the data of laboratory and instrumental research methods.

Treatment of the edematous form of acute pancreatitis, in most cases not accompanied by severe intoxication, should be comprehensive. First of all, it is aimed at creating a functional rest of the pancreas, which is provided by hunger (3-5 days), the appointment of ice on the epigastric region, the intake of alkaline solutions, transnasal drainage of the stomach and duodenum, suppression of the enzymatic activity of the gland, for which anticholinergics (atropine) are prescribed. , scopolamine, platifillin), pyrimidine derivatives (methyluracil, pentoxyl).

Prevention and elimination of the phenomena of biliary and pancreatic hypertension are achieved with the help of antispasmodics (nitroglycerin, papaverine, no-shpy, aminophylline), intravenous administration of novocaine.

The elimination of pain and various neuroreflex disorders is achieved by the appointment of analgesics, antispasmodics, ganglioblockers (pentamine, benzohexonium, etc.), as well as perirenal blockade (see the full body of knowledge: Novocaine blockade) or blockade of the round ligament of the liver.

To reduce the permeability of the vascular wall, antihistamines are prescribed (diphenhydramine, pipolfen, etc.). Treatment of patients in serious condition with severe toxemia, which is characteristic, as a rule, for destructive forms of acute pancreatitis, should be carried out in the intensive care unit or intensive care unit together with a surgeon, resuscitator, therapist.

Therapeutic measures taken in severe forms of the disease should be aimed at blocking the enzyme-forming function of the pancreas, removing pancreatic enzymes and intensive detoxification of the body, and preventing purulent complications.

Blockade of the excretory function of the pancreas can be carried out by the appointment of hunger, atropine and local cold. In severe cases of the disease, local hypothermia of the gland or the introduction of cytostatics are more effective.

Cooling of the pancreas is carried out by local gastric hypothermia (see the full body of knowledge: Artificial hypothermia, local) using long-term gastric lavage with cold water (open method) or special cooling devices AGZH-1 and others (closed method). Hypothermia can significantly suppress the excretory function of gland cells. However, the duration of the procedure (4-6 hours), the frequent occurrence of complications from the lungs, severe acid-base balance disorders due to loss of gastric juice in the open method limit the use of hypothermia in clinical practice, especially in elderly and senile patients.

Since the beginning of the 70s, various cytostatics (5-fluorouracil, cyclophosphamide, ftorafur) have been increasingly used for the treatment of acute pancreatitis. The most effective use of cytostatics is with regional administration into the celiac trunk after its catheterization according to Seldinger-Edman, which makes it possible to reduce the dose of the administered drug, while significantly increasing its concentration in the tissues of the pancreas.

According to Johnson (R. M. Johnson, 1972), A. A. Karelin and co-authors (1980), the mechanism of therapeutic action of cytostatics in acute Pancreatitis is to inhibit the excretory function of pancreatic cells. Experimental studies by Yu. A. Nesterenko and colleagues (1979) found that intra-arterial administration of fluorouracil at a dose of 5 milligrams per 1 kilogram of weight causes a decrease in external pancreatic secretion by 91% and is the optimal therapeutic dose. With intravenous administration, this dose can be increased by 2-3 times. The use of cytostatics is indicated for destructive pancreatitis. Their use in patients with total pancreatic necrosis, purulent complications of pancreatitis and renal and hepatic insufficiency is inappropriate.

Excretion of pancreatic enzymes and detoxification of the body is carried out using the methods of intravenous or intra-arterial administration of diuretics (for forced diuresis), peritoneal dialysis and drainage of the thoracic lymphatic duct.

With forced diuresis, pancreatic enzymes, components of the kinin system, as well as some cellular decay products are excreted by the kidneys. Forced diuresis technique includes water load, administration of diuretics, correction of electrolyte and protein balance. The main components of the injected fluid can be 5-10% glucose solution, Ringer's solution, reopoliglyukin, saline solution. With the intravenous method, 5-6 liters of fluid are administered daily for 3-10 days. Forcing diuresis is carried out by administering diuretic drugs (Lasix, mannitol) after infusion every 2 liters of fluid and achieving a daily diuresis of 3½-4 liters.

According to G. A. Buromskaya et al. (1980), intra-arterial administration of diuretics more effectively eliminates extra and intracellular hydration, does not increase central venous pressure, and does not cause hypervolemia. At the same time, this method removes toxic products directly from the cells of the pancreas, which leads to a more pronounced detoxification effect. The volume of injected intra-arterial fluid depends on intoxication and the degree of dehydration of the patient and averages 4-5 liters per day. The duration of intra-arterial fluid administration is usually 3-4 days. When carrying out forced diuresis, it is necessary to control central venous pressure, hematocrit, average erythrocyte diameter, indicators of circulating blood volume, acid-base balance, and electrolyte levels.

An important role in the fight against enzymatic toxemia is played by anti-enzymatic drugs (trasilol, contrical, tzalol, pantrypin, gordox and others). They must be administered in large doses over 3-5 days.

Drainage of the thoracic lymphatic duct (see Thoracic duct) is carried out with destructive forms of pancreatitis in order to remove pancreatic enzymes from the body.

The amount of lymph removed depends on the degree of intoxication and the possibilities of replacement therapy. Lymph, purified from toxic products and pancreatic enzymes by filtering through ion-exchange columns (see the full body of knowledge: Lymphosorption), is reinfused into a vein. According to V. M. Buyanov and colleagues (1979), a promising method of detoxification of the body in acute pancreatitis is intravenous fluid lymphostimulation.

Peritoneal dialysis is indicated when a large amount of serous or hemorrhagic effusion is found in the abdominal cavity during laparoscopy or laparotomy. Depending on the function of the drains and the condition of the patient, dialysis is continued for 2-4 days.

Prevention and treatment of thromboembolic complications is carried out under the control of lastogram and coagulogram thrombosis indicators. In case of destructive Pancreatitis, already in the first hours of the disease, in the presence of high fibrinolytic activity and hypertrypsinemia, in order to prevent widespread intravascular coagulation, it is advisable, in addition to antienzymes, to administer heparin, low molecular weight solutions (5% glucose solution, hemodez, reopoliglyukin, polyvinol, neocompensan, etc.).

Correction of electrolyte metabolism is carried out by introducing isotonic or 10% sodium chloride solution, 10% potassium chloride solution, 1% calcium chloride solution, Ringer-Locke solution and others. If carbohydrate metabolism is disturbed, the necessary doses of glucose and insulin are administered. In order to correct protein metabolism, blood, plasma, aminone, and albumin are transfused.

To prevent purulent complications, especially in the phase of melting and sequestration of necrotic foci in the pancreas, broad-spectrum antibiotics (kanamycin, gentamicin, monomycin, tseporin and others) are used.

According to VS Savelyev (1977), the most effective introduction of antibiotics into the celiac trunk.

With necrotic forms of pancreatitis, it is also necessary to stimulate reparative processes in the pancreas and other organs. For this, pentoxyl, methyluracil, anabolic hormones are prescribed.

All operations in acute pancreatitis should be divided into three groups: 1) emergency and urgent, performed in the first hours and days of the disease; 2) delayed, which are produced in the phase of melting and sequestration of necrotic foci of the pancreas and retroperitoneal tissue, after 10-14 days and later from the onset of the disease; 3) planned, performed during the period of complete cessation of acute inflammation in the pancreas, 4-6 weeks after the onset of the attack, after the completion of the examination of the patient (these operations are designed to prevent the recurrence of acute pancreatitis).

Indications for emergency and urgent operations: diffuse enzymatic peritonitis; acute pancreatitis caused by choledocholithiasis (obstruction of the major duodenal papilla).

In case of emergency and urgent operations after laparotomy through the upper median incision (see the full body of knowledge: Laparotomy), an audit of the abdominal cavity is performed, finding out the state of the pancreas, retroperitoneal tissue, parietal peritoneum and biliary tract.

With edematous pancreatitis, a serous or bilious effusion is sometimes found in the abdominal cavity. The pancreas is enlarged in volume, dense to the touch, petechial hemorrhages are visible on its pale or matte surface. With hemorrhagic pancreatic necrosis, a bloody effusion is found, often with a putrid odor, often with an admixture of bile, with purulent Pancreatitis, a cloudy effusion with fibrin. The pancreas at an early stage of hemorrhagic pancreatic necrosis is enlarged, its surface is covered with multiple hemorrhages. With total pancreatic necrosis, it is brown or black, on the greater and lesser omentum, parietal peritoneum, mesentery of the small and large intestines and other organs, foci of steato-necrosis are often visible.

Exudate with an admixture of bile, impregnation of the hepatoduodenal ligament, an increase in the size of the gallbladder, and an expansion of the common bile duct indicate Pancreatitis complicated by biliary hypertension.

In case of edematous Pancreatitis, after removal of the effusion, the abdominal cavity is usually sutured tightly after the gland has been injected with a solution of novocaine with antibiotics and antienzymatic drugs.

With severe hemorrhagic or biliary imbibition of the retroperitoneal tissue, a wide opening of the retroperitoneal space around the gland and in the lateral canals of the abdomen (colonic sulci) is performed. The operation is completed by drainage of the omental sac, sometimes in combination with omentopancreatopexy, or by drainage of the peritoneal cavity followed by peritoneal dialysis.

With extensive hemorrhagic pancreatic necrosis, A. A. Shalimov with employees (1978), V. I. Filin with employees (1979), Hollender (L. F. Hollender, 1976) and others perform pancreatic resection, most often left-sided.

In acute pancreatitis occurring with jaundice caused by choledocholithiasis, choledochotomy is performed (see the complete body of knowledge), stones are removed, ending the operation with external drainage of the common bile duct (see the full body of knowledge: Drainage). With wedged stones of the major duodenal papilla, plastic surgery of the major duodenal papilla is performed - transduodenal papillosphincteroplasty (see the full body of knowledge: Vater's nipple).

In the phase of melting and sequestration of necrotic foci of the pancreas, necrectomy and sequestrectomy are performed.

Necrectomy is possible no earlier than 2 weeks from the onset of the disease, since the zone of necrosis of the gland is clearly defined no earlier than the 10th day from the moment of an attack of acute Pancreatitis th weeks from the onset of the disease.

The operation in the phase of melting and sequestration consists in a wide opening of the omental sac through the gastrocolic ligament, revision of the gland and retroperitoneal tissue, removal of necrotic tissues, drainage and tamponade of the omental sac and retroperitoneal space. After the operation, active aspiration of the purulent discharge is carried out through the drains.

Planned operations are mainly aimed at sanitation of the gallbladder and ducts (cholecystectomy, choledocholithotomy, choledochoduodenostomy, and others) and treatment of diseases of other digestive organs that cause recurrence of acute pancreatitis (gastric ulcer, duodenal ulcer, duodenal diverticula, duodenostasis, and others).

In the postoperative period, complex conservative treatment of acute pancreatitis is continued.

Swabs from the stuffing bag are changed on the 7-8th day, trying to form a wide wound channel, which is periodically washed with antiseptic solutions (furatsilina, rivanol, iodinol).

In the sequestration phase, arrosive bleeding may occur. Sometimes they can be caused by disorders of the blood coagulation system. With profuse bleeding, sheathing and ligation of vessels in the wound or throughout, or their embolization, tamponade or resection of the pancreas, is performed. With fibrinolytic bleeding, direct blood transfusions are indicated (see the full body of knowledge: Blood transfusion) and the introduction of fibrinolysis inhibitors - γ-aminocaproic acid, antienzymes and others

Fistulas of the pancreas occur as a result of its ongoing purulent destruction or after surgery for pancreatic necrosis. In most cases, with conservative treatment, especially with the use of radiotherapy, fistulas heal within a few weeks or months. If the amount of discharge from the fistula does not decrease within 2-3 months, surgical treatment is indicated.

A false cyst of the pancreas is also formed due to local necrosis of the organ. At the same time, the secretion of pancreatic juice continues through the destroyed excretory ducts into the focus of destruction, which is delimited by the newly formed connective tissue, which gradually forms the wall of the cyst. Pseudocyst of the pancreas can fester, perforate or, squeezing neighboring organs, cause intestinal obstruction, the common bile duct. The method of choice in the surgical treatment of postnecrotic pseudocysts is pancreatocystoentero and pancreatocystogastroanastomosis. At a distal arrangement of a cyst the resection of a pancreas is shown; with suppuration, cysts produce marsupialization (see the full body of knowledge).

Prevention

Expedient prophylactic medical examination of patients who have undergone acute pancreatitis Considering the important role of biliary tract diseases in the occurrence of acute pancreatitis, their sanitation is an effective measure to prevent the recurrence of the disease. It is also necessary to follow a diet and avoid alcohol abuse. During the period of remission, sanitary chickens are recommended. treatment in sanatoriums of the gastrointestinal profile (Borjomi, Zheleznovodsk, Truskavets, Krainka, Karlovy Vary).

Features of acute pancreatitis in the elderly and senile age

Patients of elderly and senile age account for more than 25% of patients with acute pancreatitis This is primarily due to the increase in the number of people of this age among the population. Of no small importance are also age-related changes in the pancreas, in particular, such as deformation of the ducts with obliteration and expansion of them, desolation of the circulatory capillary network, fibrosis of the interlobular septa, etc. Contribute to the more frequent development of acute Pancreatitis and functional disorders of the digestive organs, characteristic of this age , as well as common diseases of the hepatic and bile ducts, stomach, duodenum and large intestine, cardiovascular system.

Along with the usual pathomorphological picture of the disease in patients of this age group, pancreatic apoplexy or massive fatty necrosis with stromal lipomatosis of the gland is often observed.

Clinical manifestations of acute pancreatitis in this group of patients are characterized by a number of features. Due to the frequent presence of various concomitant diseases, even mild forms of acute pancreatitis often occur with a pronounced dysfunction of vital organs and systems. Therefore, the course of the disease is often accompanied by the development of acute cardiovascular, respiratory, hepatic and renal insufficiency, various types of encephalopathies and impaired endocrine function of the pancreas. This is manifested by jaundice, oligo and anuria, hypo or hyperglycemia. At the same time, slight pain on palpation in the epigastric region and pronounced paresis of the gastrointestinal tract are characteristic. Comprehensive conservative treatment of acute pancreatitis in elderly and senile patients must necessarily include measures for the treatment of concomitant diseases, primarily of the cardiovascular and respiratory systems, prevention and treatment of hepatic and renal failure, carbohydrate metabolism disorders. In this regard, the treatment of such patients is carried out in the intensive care unit or intensive care unit.

Features of acute pancreatitis in children

Acute pancreatitis is rare in children. The etiology of the disease is very diverse (some infectious diseases, allergic conditions, etc.). In most cases, etiological factors remain unclear; in this regard, in children, sudden onset of acute pancreatitis is usually called idiopathic.

The disease often begins with a general malaise of the child, refusal of food and outdoor games. Developing then clinical, the picture to a certain extent depends on the form of acute pancreatitis

Acute pancreatic edema in children (especially in the younger age group) is relatively mild, the symptoms are less pronounced than in adults, and are often regarded by pediatricians as "intoxication of unknown etiology." The ongoing symptomatic treatment leads to a rapid improvement in the general condition. Only a special examination allows you to make the correct diagnosis. In older children, the disease begins with acute pain in the abdomen, diffuse at first, and then localized in the epigastric region or wearing a girdle. Less often there is a gradual increase in pain. At the same time, repeated vomiting, profuse salivation appear. The child takes a forced position, often on the left side. The body temperature is normal or subfebrile, the tongue is moist, moderately coated with white coating. The pulse is of satisfactory filling, rhythmic, quickened, blood pressure is normal or slightly lowered. On examination, pallor of the skin is noted. The abdomen is of the correct form, not swollen, participates in the act of breathing. Palpation of the anterior abdominal wall is painless, the abdomen is soft. Such a discrepancy between severe pain in the abdomen and the absence of objective data indicating the presence of an acute disease of the abdominal organs is characteristic of the edematous form of acute Pancreatitis Moderate leukocytosis is noted in the blood, without a significant change in the formula. The most informative and early diagnostic sign is an increase in the activity of amylase in the blood. Somewhat later, the content of amylase in the urine increases. As a rule, moderate hyperglycemia is observed.

Hemorrhagic and fatty necrosis is accompanied by severe symptoms and a severe course. In young children, the disease is manifested by rapidly increasing anxiety. The child screams and rushes about in pain, takes a forced position. Gradually, restlessness is replaced by adynamia. Older children usually indicate the localization of pain in the upper abdomen, their surrounding nature, irradiation to the supraclavicular region, shoulder blade. There is repeated vomiting, exhausting the child. The general condition progressively worsens. The skin is pale, with a cyanotic tint. Exsicosis, severe intoxication develop. Tongue dry, lined. The pulse is frequent, sometimes weak filling, blood pressure gradually decreases. Body temperature is usually subfebrile, in rare cases it rises to 38-39 °.

With purulent Pancreatitis at the onset of the disease, the discrepancy between the subjective signs of an acute abdomen and the absence or low severity of objective data is even more pronounced. The child's abdomen is actively involved in the act of breathing. Percussion and palpation are slightly painful. The tension of the muscles of the anterior abdominal wall is weakly expressed. Then intestinal paresis develops, pain on palpation intensifies, symptoms of peritoneal irritation appear. Body temperature rises, significant leukocytosis is characteristic. There is a violation of the water-electrolyte balance, the amount of sugar in the blood rises. Sharply increases the concentration of amylase in the blood and urine. A decrease in its level is a poor prognostic sign.

Sometimes in young children, severe hemorrhagic or fat necrosis manifests itself clinically, a picture of acute progressive ascites.

Radiological research at children, as a rule, is a little informative.

In older children, with reasonable suspicion of pancreatic necrosis, laparoscopy can be used.

Differential diagnosis of acute pancreatitis in children is carried out with acute appendicitis, intestinal obstruction and perforation of hollow organs.

Treatment of acute pancreatitis in children is predominantly conservative. After the diagnosis is established, all children are prescribed a set of therapeutic measures aimed at combating pain, intoxication and secondary infection. An important task is to create a functional dormancy of the pancreas, blockade of its enzyme-forming function, and combat water and electrolyte imbalance.

Complex conservative treatment in children with acute pancreatitis, diagnosed in the early stages (1-2 days), usually leads to recovery.

With clear clinical signs of purulent Pancreatitis or peritonitis, surgery is indicated. In preschool children, the complexity of differential diagnosis often leads to the need to recognize acute pancreatitis during laparotomy performed for suspected acute appendicitis or other disease. Surgical treatment is carried out according to the same principles as in adults.

All children who have had acute pancreatitis need long-term (up to 2 years) dispensary observation with a surgeon and an endocrinologist.

Chronic pancreatitis

Chronic Pancreatitis is common - according to sectional data, from 0.18 to 6% of cases. However, in clinical practice, this disease seems to be even more common, but not always diagnosed. Usually chronic pancreatitis is detected in middle and old age, somewhat more often in women than in men. Chronic pancreatitis is rare in children.

There are primary chronic Pancreatitis, in which the inflammatory process is localized from the very beginning in the pancreas, and the so-called secondary, or concomitant, Pancreatitis, which gradually develops against the background of other diseases of the gastrointestinal tract, for example, peptic ulcer, gastritis, cholecystitis and others.

Etiology and pathogenesis

The etiology of primary chronic pancreatitis is varied. Severe or protracted acute Pancreatitis can become chronic. But more often, chronic Pancreatitis occurs gradually under the influence of such factors as unsystematic irregular nutrition, frequent consumption of spicy and fatty foods, chronic alcoholism, especially in combination with a deficiency in the diet of proteins and vitamins. According to Benson (J. A. Benson), in the US chronic recurrent Pancreatitis in 75% of cases occurs in patients suffering from chronic alcoholism. Penetration of a stomach or duodenal ulcer into the pancreas can also lead to the development of a chronic inflammatory process in it. Other etiological factors include chronic circulatory disorders and atherosclerotic lesions of the pancreatic vessels, infectious diseases, and exogenous intoxications. Sometimes Pancreatitis occurs after operations on the biliary tract or stomach. A more rare cause is damage to the pancreas with periarteritis nodosa, thrombocytopenic purpura, hemochromatosis, hyperlipemia. In some cases, according to some researchers, in 10-15% the cause of chronic pancreatitis remains unclear. Predisposing factors in the occurrence of chronic pancreatitis are also obstacles to the release of pancreatic juice into the duodenum, caused by spasm or stenosis of the ampulla of the sphincter of Oddi, as well as its insufficiency, which facilitates the entry of duodenal contents into the pancreatic duct.

One of the leading mechanisms for the development of a chronic inflammatory process in the pancreas is a delay in the release and intraorgan activation of pancreatic enzymes, primarily trypsin and lipase (phospholipase A), which autolyze the parenchyma of the gland. Activation of elastase and some other enzymes leads to damage to the vessels of the pancreas. The action of kinins on the smallest vessels leads to the development of edema. The hydrophilic effect of decay products in the foci of necrosis of the pancreatic tissue also contributes to edema, and subsequently to the formation of false cysts. In the development, especially the progression of a chronic inflammatory process, the processes of autoaggression are of great importance.

In chronic gastritis (see the complete body of knowledge) and duodenitis (see the full body of knowledge), the production of polypeptide hormones by enterochromaffin cells of the mucous membrane of the stomach and duodenum, which are involved in the regulation of pancreatic secretion, is disrupted.

In chronic Pancreatitis of infectious origin, the pathogen can penetrate into the pancreas from the duodenum (for example, with dysbacteriosis, enteritis) or from the biliary tract (with cholecystitis, cholangitis) through the pancreatic ducts in an ascending way, which is facilitated by dyskinesia of the gastrointestinal tract, accompanied by duodenopancreatic and choledochopancreatic reflux.

pathological anatomy

Pathologically, chronic pancreatitis is subdivided into chronic recurrent pancreatitis and chronic sclerosing pancreatitis.

Chronic recurrent pancreatitis is essentially a prolonged variant of acute small-focal pancreatic necrosis, since every relapse of the disease is accompanied by the formation of fresh foci of necrosis of the pancreatic parenchyma and surrounding fatty tissue.

Macroscopically, during the period of exacerbation of iron, it appears somewhat enlarged in volume and diffusely compacted. Microscopically, fresh and organizing foci of necrosis of the parenchyma and adipose tissue are found in it, alternating with cicatricial fields, foci of calcification, and small pseudocysts devoid of epithelial lining. There is also a significant deformation and expansion of the lumen of the excretory ducts, containing a compacted secret and often microliths. In some cases, diffuse-focal calcification of the interstitium is observed, and then they speak of chronic calcifying Pancreatitis

Inflammatory infiltration from leukocytes is observed only in the foci of fresh necrosis of the parenchyma. It gradually subsides as the destruction foci are organized, giving way to diffuse-focal infiltrates from lymphoid, plasma cells and histiocytes. Many researchers consider these infiltrates to be manifestations of a delayed-type autoimmune reaction that occurs in response to constant antigenic exposure from foci of acini destruction.

Chronic sclerosing pancreatitis is characterized by diffuse compaction and a decrease in the size of the pancreas. The tissue of the gland acquires a stony density and macroscopically resembles a tumor. Microscopically detect diffuse focal and segmental sclerosis with progressive growth of connective tissue around the ducts, lobules and inside the acini. The cause of sclerosis is the constant loss of the parenchyma, proceeding as necrosis or atrophy of individual acini and groups of acini. In advanced cases, against the background of diffuse fibrosis, small islands of atrophic parenchyma are hardly detected. Along with this, there is a pronounced proliferation of the ductal epithelium with the formation of adenomatous structures, which are sometimes difficult to differentiate from adenocarcinoma. In the gaps of the dilated excretory ducts, a thickened secretion, crystalline deposits of lime, and microlites are constantly found. In the circumference of the ducts, a large number of hyperplastic pancreatic islets (Langerhans) are found. Neoplasms of acini do not occur, necrosis of the parenchyma of the gland is replaced by a scar.

As in the recurrent form of Pancreatitis, among the fields of fibrous tissue, one can detect lymphoplasmacytic infiltrates, which are a reflection of autoimmune processes. At the same time, morphologically, not necrotic, but dystrophic-atrophic changes in acini with their slow replacement by connective tissue predominate in the pancreas.

In all variants of chronic pancreatitis, the same complications are observed. The most common cicatricial stricture of the pancreatic duct, as well as blockage of its stone or adenomatous polyp. In this case, obstruction of the common bile duct with the development of obstructive jaundice is possible. Sometimes there is thrombosis of the splenic vein. Often, against the background of chronic pancreatitis, diabetes mellitus develops, although, unlike acini, the islets of Langerhans regenerate well, and they can always be found among the scar tissue.

Clinical picture

The clinical picture of chronic pancreatitis is very variable, but in most cases includes the following symptoms: pain in the epigastric region and left hypochondrium; dyspeptic phenomena; the so-called pancreatogenic diarrhea; weight loss, hypoproteinemia, symptoms of polyhypovitaminosis; signs of diabetes.

The pain is localized in the epigastric region on the right (with the predominant localization of the process in the region of the head of the pancreas); when involved in the inflammatory process of her body, pain is observed in the epigastric region; with the defeat of her tail - in the left hypochondrium. Often, the pain radiates to the back (at the level of the X-XII thoracic vertebrae) or has a girdle character, intensifies when the patient is lying on his back and may weaken in the sitting position, especially with a slight forward lean. The pain can also radiate to the region of the heart, simulating angina pectoris, to the left shoulder blade, left shoulder, and sometimes to the left iliac region. The intensity and nature of the pains are different; they can be constant (pressing, aching), appear some time after eating (as with peptic ulcer), especially after eating fatty or spicy foods, or be paroxysmal like pancreatic colic.

Dyspeptic symptoms (pancreatic dyspepsia) are common, especially during an exacerbation of the disease or a severe course of the disease. Many patients also note loss of appetite, aversion to fatty foods. At the same time, with the development of diabetes, patients may feel severe hunger and thirst. Often observed increased salivation, belching, nausea, vomiting, flatulence. Stools in mild cases are normal, in more severe cases there is a tendency to diarrhea or alternation of constipation and diarrhea. However, in typical advanced cases of chronic pancreatitis (in the presence of obvious signs of exocrine pancreatic insufficiency), pancreatic diarrhea is more characteristic with the release of profuse, mushy, fetid, greasy feces.

Due to the development of exocrine pancreatic insufficiency and violations of the processes of digestion and absorption in the intestine, weight loss increases. It is facilitated by the loss of appetite usually observed in patients, as well as the addition of diabetes mellitus.

In severe forms of the disease, depression, hypochondria and other mental disorders are possible. In alcoholic pancreatitis, mental disorders may be due to the prolonged effect of alcohol on the central nervous system.

The course of the disease is usually protracted. There are 5 forms of the disease: 1) recurrent form, characterized by distinct periods of remission and exacerbations of the process; 2) pain form, proceeding with constant pain, dominating the clinical picture; 3) pseudotumor form; 4) latent (painless) form; 5) sclerosing form, which is characterized by early onset and progressive signs of pancreatic insufficiency. In the latter form, obstructive jaundice is sometimes observed due to compression of the common bile duct by the sclerotic head of the pancreas. T. G. Reneva et al. (1978) distinguishes 3 forms of chronic pancreatitis: mild, moderate and severe. The latter proceeds with persistent diarrhea, dystrophic disorders, and increasing exhaustion.

Diagnosis

Physical research. Palpation of the abdomen in patients with chronic pancreatitis is usually characterized by pain in the epigastric region and the left hypochondrium. A number of researchers described pain points and zones, pain in which is especially characteristic. So, with damage to the head of the pancreas, pain can be noted with pressure at the so-called pancreatic point of Desjardins, located in the projection area on the anterior abdominal wall of the distal pancreatic duct (approximately at a distance of 5-7 centimeters from the navel along the line connecting the navel with the right axillary depression), or in the wider choledocho-pancreatic zone of Chauffard, located between the above line, the anterior median line of the body and the perpendicular, lowered to the last line from the Desjardins point. Often there is pain in the point in the costovertebral angle (Mayo-Robson symptom). Sometimes there is a zone of skin hyperesthesia corresponding to the zone of innervation of the 8th - 10th thoracic segment on the left (Kach's symptom) and some atrophy of the subcutaneous tissue in the projection of the pancreas on the anterior abdominal wall, described by A. A. Shelagurov (1970). It is very rare to palpate an enlarged and compacted pancreas in chronic pancreatitis.

Auscultation of the epigastric region during full expiration may have some diagnostic value: sometimes a systolic murmur is heard, which occurs due to compression of the abdominal part of the aorta by an enlarged and compacted pancreas.

Laboratory research methods often reveal in patients with chronic pancreatitis moderate hypochromic anemia, accelerated ESR, neutrophilic leukocytosis, dysproteinemia due to an increased content of globulins, increased activity of transaminases and aldolase in the blood serum. When the islet apparatus of the pancreas is damaged, hyperglycemia is detected (see the full body of knowledge) and glycosuria (see the full body of knowledge), however, to identify mild degrees of carbohydrate metabolism disorders, it is necessary to study the sugar curve with a double load of glucose (see the full body of knowledge: Carbohydrates, methods of determination) . In case of violations of the exocrine function of the pancreas, more or less pronounced hypoproteinemia is usually detected; in more severe cases - a violation of electrolyte metabolism, in particular hyponatremia (see full body of knowledge). The determination of the content of pancreatic enzymes in the duodenal contents, as well as in the blood and urine, allows us to assess the functional state of the organ. In the duodenal contents obtained using a two-channel probe (see the full body of knowledge: Duodenal sounding), before and after stimulation of the pancreas with secretin and pancreozymin, the total amount of juice, its bicarbonate alkalinity, the content of trypsin, lipase and amylase are determined; in the blood - the content of amylase, lipase, antitrypsin; in urine - amylase. Simultaneous study of the content of pancreatic enzymes in duodenal juice, blood, and amylasuria allows much more accurate reflection of the state of the exocrine function of the pancreas in patients with chronic pancreatitis than the separate conduct of these studies on different days.

Hyperamilasuria, sometimes reaching 2048-4096 units (according to Wolgemut) in chronic Pancreatitis, is detected more often than hyperamylasemia, however, an increase in urine amylase (up to 256-512 units) is sometimes observed in other diseases of the abdominal organs.

The content of enzymes in the blood and urine increases during an exacerbation of pancreatitis, as well as with obstacles to the outflow of pancreatic juice (inflammatory edema of the head of the gland and compression of the ducts, cicatricial stenosis of the major duodenal papilla, and others). In the duodenal contents, the concentration of enzymes and the total volume of juice in the initial period of the disease may be slightly increased, but with a pronounced atrophic-sclerotic process in the gland, these indicators decrease.

A scatological study (see the full body of knowledge: Cal) reveals an increased content of undigested food in the feces (steatorrhea, creatorrhea, amylorrhea, cytarinorrhea). According to Oste (W. J. Austad, 1979), persistent steatorrhea in chronic II. appears when the external secretion of the pancreas is reduced by at least 90%.

X-ray diagnostics. An x-ray examination of the gastrointestinal tract reveals, in the case of an enlarged pancreas, an upward and anterior displacement of the stomach, an expansion of the duodenal loop and a flattening of the medial contour of the descending part of the duodenum (Figure 1). With the help of relaxation duodenography (see the full body of knowledge: Relaxation duodenography), short rigid areas, a number of pointed depressions in the form of needles (spicules), depressions along the edges of the major duodenal papilla can be detected on this contour. Pancreatic scans also show stones or deposits of calcium salts (Figure 2), and computed tomograms reveal an enlarged and deformed pancreatic duct. With cholegraphy (see the full body of knowledge), sometimes a narrowing of the distal common bile duct is found.

Of great importance in the diagnosis of chronic pancreatitis is endoscopic retrograde cholangiopancreatography (see the full body of knowledge: Retrograde pancreatocholangiography). At the beginning of the disease, the pancreatic ducts are not changed or there is a deformation of the small excretory ducts of the pancreas. In the future, these ducts narrow, some of them are obliterated, and in others, small cyst-like extensions can be determined. The lumen of the pancreatic duct becomes uneven, irregularities and pressures appear on its walls. In the case of the formation of abscesses and pseudocysts, the contrast agent from the destroyed ducts penetrates into the parenchyma of the gland and outlines the cavities in it, making it possible to clarify their position and size. In contrast to pseudocysts, necrotic masses can be detected in abscesses.

With celiacography, two forms of chronic pancreatitis can be distinguished. For the first form, an increase in the pancreas, its hypervascularization and inhomogeneous contrasting in the parenchymal phase are typical (Figure 3). The second form is more characteristic of Pancreatitis with severe fibrotic changes in the pancreas. It is characterized by displacement and narrowing of blood vessels and depletion of the vascular pattern. The parenchymal phase is absent or weakened. In all forms of Tileni Arnesjo (H. Tylen, V. Arnesjo, 1973), stenoses of large arteries outside the pancreas were observed - own hepatic, gastroduodenal, splenic. The contours of the narrowed areas remained smooth, while in pancreatic cancer they had a "corroded" character. Pseudocysts appear as rounded avascular masses displacing adjacent arterial branches. During the operation and in the postoperative period (if a drainage catheter is left in the pancreatic ducts or cyst cavity), pancreatography can be performed to clarify the condition of the ducts (see full body of knowledge). If an external or internal fistula of the pancreas has formed after surgery for a cyst, it is advisable to perform fistulography (see full body of knowledge), which allows you to characterize the fistulous tract and the residual cavity of the cyst (Figure 4).

Radioisotope scanning of the pancreas with selenium-75 labeled methionine also has a certain diagnostic value.

Sonography allows you to identify the presence, nature and extent of morphological changes in the pancreas.

Differential diagnosis is often very difficult. Chronic Pancreatitis must be differentiated primarily from a tumor of the pancreas (see full body of knowledge); at the same time, methods of instrumental diagnostics are of great importance: celiacography, endoscopic retrograde cholangiopancreatography, computed tomography, echography and radioisotope scanning of the pancreas.

Differential diagnosis is also carried out with cholelithiasis (see full body of knowledge), peptic ulcer of the stomach and duodenum, chronic enteritis and others.

Rice. 1. Micropreparation of fiber in acute pancreatitis: the focus of fat necrosis is indicated by arrows; staining with hematoxylin-eosin; × 80. Rice. 2. Macropreparation of the pancreas in diffuse focal pancreatitis: small foci of fat necrosis. Rice. 3. Macropreparation of the pancreas with total hemorrhagic pancreatic necrosis: an increase in size and hemorrhagic impregnation of the gland tissue. Rice. 4. Macropreparation of a normal pancreas (given for comparison). Rice. 5. The opened cavity of a false cyst of the pancreas, formed as a result of hemorrhagic pancreatic necrosis. Rice. 6. Micropreparation of the pancreas in acute pancreatitis: the arrow indicates the thrombus in the lumen of the vein; Mallory stain; × 80. Rice. 7. Micropreparation of the pancreas in hemorrhagic pancreatic necrosis: extensive hemorrhages (indicated by arrows) in the gland tissue; Mallory stain; × 80.

Rice. 8. Micropreparation of the pancreas in pancreatic necrosis: the zone of necrosis (1) is delimited by leukocyte infiltrate (2) and granulation shaft (3); staining with hematoxylin-eosin; × 80. Rice. 9. Micropreparation of the pancreas in chronic pancreatitis; a fresh focus of necrosis (1) against the background of fibrosis (2) of the gland; staining with hematoxylin-eosin; × 80. Rice. 10. Micropreparation of the pancreas in chronic recurrent pancreatitis: a calculus is visible in the dilated duct (1), the gland tissue is permeated with connective tissue strands (2); staining with hematoxylin-eosin; × 80. Micropreparations of the pancreas in chronic sclerosing pancreatitis (Fig. 11 - 13). Rice. 11. Against the background of sclerosis (1) and lipomatosis (2), individual acini (3) and lymphoid follicles (4), as well as dilated ducts (5) are visible; coloring according to Van Gieson, × 80. Rice. 12. Among the fibrous tissue (1) there are many islets of Langerhans (2), an enlarged duct (3) with papillomatous proliferation of the epithelium; hematoxylin-eosin staining, × 80. Rice. 13. In the circumference of individual acini (1), proliferating ducts (2) are visible, forming adenomatous foci; staining with hematoxylin-eosin; × 36.

Treatment

Conservative treatment is carried out in the initial stages of the disease and in the absence of complications. In the period of severe exacerbation, inpatient treatment is indicated, as in acute pancreatitis.

Conservative treatment of chronic pancreatitis is aimed at creating the most favorable conditions for the functioning of the pancreas and eliminating factors that support the inflammatory process, to combat pain, compensate for violations of external and intrasecretory pancreatic insufficiency.

The patient's nutrition should be fractional, 5-6 times a day, in small portions. Exclude alcohol, marinades, fried, fatty and spicy foods, strong broths that have a stimulating effect on the pancreas. The diet should contain up to 150 grams of protein, of which 60-70 g of animal origin (lean meats, fish, low-fat cottage cheese, mild cheese). The content of fats in the diet is limited to 80-70 grams per day, mainly due to coarse fats of animal origin (pork, lamb). With significant steatorrhea, the fat content in the diet is reduced to 50 grams. The amount of carbohydrates is also limited, especially mono and disaccharides; with the development of diabetes, they are completely excluded. All food is given in a warm form, since cold dishes can increase intestinal dyskinesia, cause spasm of the sphincter of Oddi.

Of the drugs, pyrimidine derivatives (pentoxyl, methyluracil) are prescribed for 3-4 weeks. With severe pain, pararenal, paravertebral, celiac novocaine blockade, non-narcotic analgesics, reflexology are indicated; in especially severe cases - narcotic analgesics in combination with anticholinergic and antispasmodic drugs.

In exocrine pancreatic insufficiency, for the purpose of replacement therapy, enzyme preparations are prescribed: pancreatin, abomin, cholenzim, panzinorm, festal, vitohepat and others, as well as vitamin preparations: riboflavin (B 2), pyridoxine (B 6), cyanocobalamin (B 12), calcium pangamate (B 15), retinol (A), nicotinic and ascorbic acids. Anabolic hormones (methandrostenolone, retabolil), glutamic acid, cocarboxylase are also prescribed. In the fight against increasing dysproteinemia, it is advisable to use protein blood products (amino blood, casein hydrolyzate, etc.). Intrasecretory pancreatic insufficiency requires an appropriate diet and therapeutic measures.

After the removal of acute phenomena and in order to prevent exacerbation in remission, spa treatment is recommended in gastroenterological sanatoriums (Borjomi, Essentuki, Zheleznovodsk, Pyatigorsk, Karlovi Vari).

Operative treatment. Indications: cysts and long-term non-healing external fistulas of the pancreas; calculi of the ducts of the gland; stenosis of the pancreatic duct with a violation of the outflow of pancreatic juice; indurative (pseudotumor) Pancreatitis, especially in the presence of jaundice; persistent pain syndrome, not amenable to conservative measures.

The type of surgical intervention on the pancreas in chronic pancreatitis depends on the nature of the lesion of its parenchyma and ducts, in particular on the level and extent of their obstruction and the reasons that led to it. The most important task of the operation is to create conditions that exclude the development of intraductal pancreatic hypertension.

With obturating (gallstone) and stenosing lesions of the major duodenal papilla, the operation of choice is transduodenal papillosphincterotomy (plasty). In the presence of simultaneous stenosis of the mouth of the pancreatic duct or its blockage with a stone, a virzungotomy (plastic) is also performed.

With widespread stricture of the pancreatic duct in the region of the head and expansion of the duct like a "chain of lakes" at the level of the body and tail of the gland, pancreatojejunostomy is indicated. At the same time, all cavities and pockets of the pancreatic duct and its branches are opened as much as possible, and they are freed from stones and putty-like mass. The small intestine is anastomosed with the entire longitudinally dissected tissue of the gland.

When chronic pancreatitis is combined with a parapancreatic cyst, into the cavity of which the fistula of the pancreatic duct opens, a pancreatocystojejunostomy is performed.

In case of large-focal polycystic or calculous Pancreatitis, combined with obstruction of the pancreatic duct in the zone of the greatest damage to the gland, its resection is indicated. If such changes are localized in the tail and the adjacent part of the body of the gland, a left-sided resection of the gland is performed, and if localized in the head, a pancreatoduodenal resection is performed (see full code of knowledge: Pancreatoduodenectomy).

Recurrent pancreatitis can be complicated by focal polycystic gland and pancreatic fistula. When these changes are located in the tail or body of the gland, a left-sided resection of the pancreas is performed.

With recurrent chronic pancreatitis with significant damage to the gland tissue in the tail and body, in some cases, a left-sided subtotal resection of the gland can be performed. Various operations on the higher nervous system (splanchnicotomy, neurotomy) did not justify themselves.

Since the late 1970s, intraoperative occlusion of the pancreatic ducts with alloplastic material has been used in clinical practice, which leads to inhibition of its external secretion.

Operations on the pancreas in chronic pancreatitis may be complicated by pancreatic necrosis, peritonitis, bleeding, and others. In the postoperative period, the complex of ongoing conservative measures must necessarily include the prophylactic administration of antienzymatic drugs, cytostatics.

Prevention

Prevention consists in the timely treatment of diseases that contribute to the occurrence of chronic pancreatitis, the elimination of the possibility of chronic intoxication, primarily alcohol abuse, and the provision of a balanced diet. In this regard, it is advisable to conduct a medical examination of patients with chronic pancreatitis.

Features of chronic pancreatitis in the elderly and senile age

Various forms of chronic pancreatitis in the elderly and senile age are more common than in earlier age groups. However, it is usually combined with various diseases of other organs of the gastrointestinal tract (chronic gastritis, cholecystitis, colitis, and so on). According to A. A. Shelagurov (1970) and others, with age in the pathogenesis of Pancreatitis, progressive atherosclerotic lesions of the vessels of the pancreas, as well as a decrease in its compensatory capabilities due to physiological aging, atrophic and sclerotic processes in the pancreas, a decrease in its excretory and endocrine functions.

Clinical, the picture of chronic pancreatitis in the elderly is polymorphic; sometimes concomitant diseases obscure the clinic of the disease. However, a comparative study of the course of the pain form of chronic pancreatitis reveals that the disease often takes a chronic course from the very beginning. Pain attacks in older people are usually less intense. They occur with errors in the diet, especially after exercise. With a long course of the disease, significant weight loss is noted, more often than in young people, dyspeptic disorders occur. The exocrine function of the pancreas decreases in old age, which makes it difficult to use the data of its study for the diagnosis of the disease.

Treatment of chronic pancreatitis in the elderly has its own characteristics. When prescribing a diet, one should take into account the concomitant diseases often present in such patients (atherosclerosis, coronary heart disease, hypertension, and others). Due to the age-related decrease in the exocrine function of the pancreas, aggravated by chronic pancreatitis, such patients are shown longer treatment with pancreatic enzymatic preparations (pancreatin, panzinorm, festal, etc.). Surgical treatment of chronic pancreatitis in this group of patients is used only for intractable jaundice caused by compression of the common bile duct. duct with an enlarged head of the gland, long-term non-healing external fistulas of the gland, as well as suppuration of the cyst.

Experimental pancreatitis

For the first time, acute pancreatitis was obtained by C. Bernard in 1856 by retrograde injection of olive oil into the pancreatic duct, and chronic pancreatitis by I. Pavlov in 1877 by ligation of the pancreatic duct of a dog. These experiments marked the beginning of the search for various models of experimental pancreatitis.

The most suitable animals for: Pancreatitis reproduction are dogs due to the similarity of the anatomical structure of their excretory ducts with those of humans. At the same time, white rats are a convenient object for studying the effectiveness of the treatment of experimental pancreatitis. There are at least 100 models of Pancreatitis, which can be conditionally systematized as follows.

Obstructive-hypertensive Pancreatitis caused by a temporary or permanent increase in pressure in the pancreatic duct system by ligation or retrograde administration of various substances (bile, natural or synthetic bile acids, trypsin, lipase, elastase, enterokinase or a mixture of the latter with bile or blood, etc. ). In addition to increasing intraductal pressure at the time of administration, these substances activate pancreatic enzymes or stimulate the gland's own secretion of the parenchyma. The works of I. Pavlov's Pancreatitis proved that ligation of the pancreatic duct does not cause Pancreatitis, but is accompanied by a gradual atrophy of the exocrine parenchyma. If, against this background, secretion is stimulated, then Pancreatitis, as a rule, develops. Pancreatitis models, caused by dosed or prolonged duodenal hypertension, which contributes to the throwing of intestinal contents into the pancreatic ducts, should be attributed to the same group.

Intoxication-metabolic Pancreatitis is caused by a number of pharmacological and chemical agents or a deficiency of amino acids in the diet. The most widespread models are acute and chronic pancreatitis, caused by the introduction of ethionine into the pancreatic parenchyma or intraperitoneally, as well as by enteral administration of alcohol on the background of protein-deficient nutrition.

Allergic Models Pancreatitis is created by sensitizing animals with horse serum or meningococcal endotoxin. A permissive dose of the agent is injected into one of the pancreatoduodenal arteries or into the gland tissue. This group also includes the so-called paraallergic models Pancreatitis, created by sensitizing rabbits or dogs with horse serum according to the generally accepted method, however, ligation of the duct or drug stimulation of gland secretion is used as a resolving factor. Acute and chronic pancreatitis is also caused by pancreatotoxic serum.

Ischemic (hypoxic) models Pancreatitis is caused by ligation of the splenic vein or intraorgan vessels. The same effect is achieved by embolization of the arterial bed with a fat emulsion. However, without additional stimulation of secretion or exposure to other damaging agents, a convincing model of Pancreatitis, as a rule, cannot be obtained.

Neurogenic models Pancreatitis is obtained by disrupting the innervation of the pancreas or electrical stimulation of sympathetic and parasympathetic nerve trunks with the simultaneous introduction of damaging agents into the ducts of the gland.

The most effective models of experimental pancreatitis are combined methods that combine hypertension of the gland ducts and activation of its enzymes against the background of increased secretion or ischemia of the organ.

In all models of experimental pancreatitis, the disease is based on enzymatic autolysis (see the full body of knowledge), which develops as a result of a violation of the synthesis and release of enzymes, focal focal or widespread pancreonecrosis with a secondary inflammatory reaction, accompanied by vein thrombosis, as well as microvasculature and hemorrhages in the parenchyma of the gland.

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The development of chronic pancreatitis is a fairly common pathological disease characterized by the development of an inflammatory process in the pancreatic cavity and a decrease in its functionality. The clinic of manifestation of this disease is quite diverse, depending on the degree of damage to the gland and the period of pathology. Pain in chronic pancreatitis begins to manifest during the progressive stage of the disease, along with the development of atrophic processes in the glandular tissues, as well as fibrous lesions and replacement of pancreatic cells with epithelial structures. In the materials of the presented review, we will take a closer look at where it hurts locally in pancreatitis, the causes that contribute to the onset of pain, diagnostic methods, and we will also tell you how to relieve pain in chronic pancreatitis and what methods of treatment and prevention exist.

Pain in chronic pancreatitis

Pain in pancreatic lesions of the pancreas is one of the main and significant symptomatic signs of this disease that occurs in the epigastric region.

Soreness can radiate to the area of ​​the cardiovascular system of organs, to the area of ​​the left half of the body and the area of ​​the left shoulder, simulating angina attacks and accompanied by a headache. With the development of an inflammatory process in the area of ​​​​the head of the gland, the pain radiates to the right hypochondrium, if the body of the organ is damaged, to the epigastric part, and if the caudal part of the gland is affected, the pain is localized in the area of ​​the hypochondrium on the left side. If the inflammatory process covers the entire cavity of the gland, then the pain acquires a shingling character of development.

A decrease in the intensity of the manifestation of pain occurs at the moment of taking a position, sitting with a slightly inclined torso forward and knees pulled up to the chest. The pain becomes sharper and sharper if the patient lies on his back.

Soreness in the abdominal area appears, both during periods of exacerbation of a chronic disease, and during a period of stable remission. The nature of the pain can also be different, as sharp and cutting pains, as well as aching and dull. The intensity of pathogenesis depends on the provoking factor.

Causes of pain in pancreatitis

The reasons contributing to the development of painful symptoms, in fact, are not so many. Consider the most common of them:

1. Acute inflammatory process in the parenchyma zone.
2. Systematic malnutrition of the patient, characterized by untimely consumption of foods with a high percentage of fat, spiciness or salt and spices.
3. Pathological processes in the gastrointestinal tract, among which cholecystitis is noted, as well as the development of obstructive pathologies in the gallbladder cavity.
4. Alcohol abuse.
5. Long-term treatment with certain groups of drugs.
6. Traumatization of the abdominal cavity of a different nature.
7. hereditary factor.

It is also worth noting that the female half of the population is twice as likely to be affected by a chronic form of pancreatic pathology.

Diagnosis of pain in chronic pancreatitis

Diagnostics consists in carrying out the following activities:

• palpation examination of the patient's abdominal cavity;
• delivery of general blood tests, feces and urine;
• conducting a biochemical study of the patient's blood;
• ultrasound and radiographic examination of the entire peritoneal cavity;
• CT or MRI with endoscopic retrograde cholangiopancreatography.

pain clinic

Pain plays a leading role in the clinical manifestations of chronic pancreatitis. Indicators such as its intensity and severity of manifestation contribute to the division of painful sensations into sphincter and capsular pain.

Sphincter pains have a paroxysmal manifestation and are formed against the background of a spasm in the region of the Wirsung duct or the sphincter of Oddi. As a rule, the pancreas begins to hurt after a violation of the diet, when eating fried foods, foods with a high percentage of fat or mushrooms. Pretty quick relief of pain is achieved by taking drugs with an antispasmodic spectrum of action.

Capsular pain occurs against the background of stretching of the capsule, a progressive stage of pancreatic edema, or the onset of progression of sclerotic processes. Such painful symptoms have a permanent course. Increased pain occurs after a violation of the dietary diet and the use of alcoholic beverages. They can decrease when taking a position, sitting with a slight inclination forward.

In most cases, it hurts the patient exactly in the place where the lesion is localized, but do not forget that such symptoms of pain in chronic pancreatitis can also have a combined manifestation with irradiation to various parts of the body, from different sides of the hypochondrium to the lower back and inguinal areas. They can be removed through the use of analgesic and diuretic medications.

Local mechanisms of pain in chronic pancreatitis

The development of inflammatory processes, pathological violations of the structural structure of the membranes of the gland, as well as blockage of the pancreatic ducts leads to the appearance of painful symptoms.

The pathogenesis of tumor-like neoplasms and scars blocks the normal outflow of pancreatic juice, which leads to an increase in pressure in the cavity of the ducts and disruption of the processes of blood supply to the tissue structures of the gland.

The inflammatory process contributes to an increase in the surface of nerve endings and damage to their membranes, which causes unbearable pain.

How to relieve pain in exacerbated or chronic pancreatitis?

The occurrence of severe pain in pancreatic lesions of the pancreas can cause the development of pain shock. To normalize the patient's condition, it is necessary to properly provide first aid, and then deliver the patient to a medical facility for basic treatment of the pathology.

It is important to remember that improper treatment of pain syndrome can be fatal, so before using any medication, you should consult your doctor.

As a first aid at home or at work, it is recommended to apply cold to the site of pain and take one of such drugs as Drotaverine, No-shpa, Spasmalgon or Maksigan.

The main treatment for pain during exacerbation of pancreatic pathology is as follows:

• visit doctor;
• ensuring complete rest at the time of the attack;
• conducting drug therapy;
• appointment of antienzymatic therapy;
• then drugs with pancreatic enzymes are taken;
• normalization of acid-base balance in the affected organ;
• carrying out vitamin therapy;
• the use of folk remedies;
• diet therapy;
• surgical intervention;
• treatment in a sanatorium.

It is necessary to treat pancreatic pathology of the gland only in a hospital setting.

Drug therapy

To reduce and subsequently relieve pain, the following medications are prescribed:

• drugs with an antispasmodic spectrum of action: No-shpa, Drotaverin, Spazmalgon, Spareks;
• m-anticholinergic drugs: Metopine, Atropine or Gastocepin;
• H2 blockers prescribed for persistent painful symptoms: Famotidine or Ranitidine.

Anti-Enzyme Therapy

Carrying out antifermental therapy helps to prevent destructive processes in the pancreatic cavity. Appointed:

• drugs of cytostatic action: Gordoks, Patripin, Amidopyrin, etc.;
• drugs that block the activity of the proton pump: Omeprazole, Omez, Rabelok, Nexium.

With the development of the edematous form of the pathology, Asparkam is also prescribed.

vitamin therapy

It consists in prescribing the use of a vitamin complex, which includes vitamins of the following groups: A, B, E, C, D, K.

Lipoic acid and cocarboxylase are also prescribed.

Folk remedies

The use of traditional medicine helps to normalize the functionality of the pancreas and maintain it during a period of stable remission at home. The most effective are infusions, teas and decoctions from such medicinal herbs as calendula, chamomile, immortelle, milk thistle, bitter wormwood, dill, parsley and peppermint.

diet therapy

Compliance with the diet is the key to successful treatment of pancreatic pathology. During the period of exacerbation of the disease during the first 2-3 days, a complete hunger strike is necessary, only fractional alkaline drinking is allowed.

Food for pancreatic pathology should be saturated with proteins and vitamins, and foods with a high content of fats and carbohydrates should be reduced to a minimum.

You can eat the following types of food:

• vegetarian soups;
• lean varieties of meat and fish in boiled form;
• pasta and cereals;
• vegetable and fruit crops in baked form;
• vegetable purees;
• natural juices, compote, weak tea drink, decoctions with wild rose;
• and for dessert, you can have a little honey, jam and jelly.

You need to eat fractionally, at least 5 times a day with small proportions.

Pain prevention

To prevent recurrence of the formation of pain, the following recommendations must be observed:

• adherence to the prescribed diet;
• giving up alcohol and smoking;
• observe fractional and portioned nutrition;
• avoid stressful situations.

Compliance with the rules of a healthy lifestyle has never harmed anyone. Therefore, in order to stop the progression of destructive processes inside the body, it is necessary to treat your health with the utmost responsibility and timely apply for qualified assistance in case of any violations and malfunctions in the performance of the whole organism.

Bibliography

1. Toporkov A.S. The effectiveness of selective myotropic antispasmodics for the relief of abdominal pain. Breast cancer, section "Diseases of the digestive system" 2011 No. 28. pp. 1752–1761.
2. Gubergrits N.B. Chronic abdominal pain. Pancreatic pain: how to help the patient. M.: ID Medpraktika, 2005, p.176.
3. Kostyuchenko A.L., Filin V.I. Urgent Pancreatology: A Handbook for Physicians, 2nd Edition, Revised and Expanded. SPb. Dean Publishing House, 2000
4. Belousova L.N., Baryshnikova N.V., Pavlova E.Yu. Peculiarities of action of various antispasmodics: analysis of PEGEG data. Pharmateka. Gastroenterology. 2014 No. 14 pp. 70–75.
5. Belousova E.A. Antispasmodics in gastroenterology: comparative characteristics and indications for use. Pharmateka 2002 No. 9, pp. 40–46.
6. Zhukova E.H. Comparative evaluation of various diagnostic criteria in exacerbation of chronic pancreatitis. Russian Gastroenterological Journal 1998 No. 1.

- inflammation of the pancreas. Symptoms of acute pancreatitis: acute, unbearable pain in the abdomen. Depending on which part of the gland is inflamed, localization of pain is possible in the right or left hypochondrium, in the epigastric region, the pain can be girdle. Chronic pancreatitis is accompanied by loss of appetite, indigestion, acute pain (as in the acute form) that occurs after eating fatty, spicy foods or alcohol.

General information

Pancreatitis is a disease characterized by the development of inflammation in the tissue of the pancreas. According to the nature of the course, pancreatitis is divided into acute and chronic. Acute pancreatitis ranks third among acute abdominal diseases requiring treatment in a surgical hospital. The first and second places are occupied by acute appendicitis and cholecystitis.

According to world statistics, from 200 to 800 people out of a million fall ill with acute pancreatitis every year. This disease is more common in men. The age of patients varies widely and depends on the causes of pancreatitis. Acute pancreatitis on the background of alcohol abuse occurs on average at the age of about 39 years, and in pancreatitis associated with gallstone disease, the average age of patients is 69 years.

Causes

Pathogenesis

In the development of acute inflammation of the pancreas, according to the most common theory, the main factor is cell damage by prematurely activated enzymes. Under normal conditions, digestive enzymes are produced by the pancreas in an inactive form and are activated already in the digestive tract. Under the influence of external and internal pathological factors, the production mechanism is disrupted, enzymes are activated in the pancreas and begin digestion of its tissue. The result is inflammation, tissue edema develops, and the vessels of the parenchyma of the gland are affected.

The pathological process in acute pancreatitis can spread to nearby tissues: retroperitoneal tissue, omental bag, peritoneum, omentum, mesentery of the intestine and ligaments of the liver and duodenum. A severe form of acute pancreatitis contributes to a sharp increase in the level of various biologically active substances in the blood, which leads to pronounced general disorders of life: secondary inflammation and degenerative disorders in tissues and organs - lungs, liver, kidneys, heart.

Classification

Acute pancreatitis is classified according to severity:

1. mild form proceeds with minimal damage to organs and systems, is expressed mainly by interstitial edema of the gland, is easily amenable to therapy and has a favorable prognosis for a quick recovery;
2. severe form acute pancreatitis is characterized by the development of pronounced disorders in organs and tissues, or local complications (tissue necrosis, infection, cysts, abscesses).

Severe acute pancreatitis may be accompanied by:

• acute accumulation of fluid inside the gland or in the peripancreatic space, which may not have granulation or fibrous walls;
• pancreatic necrosis with possible tissue infection (a limited or diffuse zone of dying parenchyma and peripancreatic tissues occurs, with the addition of infection and the development of purulent pancreatitis, the likelihood of death increases);
• acute false cyst (accumulation of pancreatic juice surrounded by fibrous walls, or granulations that occurs after an attack of acute pancreatitis, is formed within 4 or more weeks);
• pancreatic abscess (accumulation of pus in the pancreas or nearby tissues).

Symptoms of acute pancreatitis

Typical symptoms of acute pancreatitis.

• Pain syndrome. The pain can be localized in the epigastrium, left hypochondrium, be girdle in nature, radiate under the left shoulder blade. The pain is of a pronounced permanent nature, in the supine position it intensifies. Increased pain occurs after eating, especially fatty, spicy, fried, alcohol.
• Nausea, vomiting. Vomiting may be indomitable, contains bile, does not bring relief.
• Increase in body temperature.
• Moderately pronounced yellowness of the sclera. Rarely - mild jaundice of the skin.

In addition, acute pancreatitis may be accompanied by dyspeptic symptoms (flatulence, heartburn), skin manifestations (bluish spots on the body, hemorrhages in the navel).

Complications

The danger of acute pancreatitis lies in the high likelihood of developing severe complications. When the inflamed tissue of the gland is infected with bacteria that live in the small intestine, necrosis of the gland sites and the occurrence of abscesses are possible. This condition without timely treatment (up to surgery) can be fatal.

In severe pancreatitis, a state of shock may develop and, as a result, multiple organ failure. After the development of acute pancreatitis, pseudocysts (accumulations of fluid in the parenchyma) can begin to form in the gland tissue, which destroy the structure of the gland and bile ducts. When a pseudocyst ruptures and its contents leak out, ascites occurs.

Diagnostics

Diagnosis of pancreatitis by gastroenterologists is carried out on the basis of complaints, physical examination, identification of characteristic symptoms. When measuring blood pressure and pulse, hypotension and tachycardia are often noted. To confirm the diagnosis, laboratory tests of blood and urine, MSCT and ultrasound of the abdominal organs, MRI of the pancreas serve.

• Biochemistry of blood. In the study of blood in the general analysis, signs of inflammation are noted (ESR accelerated, the content of leukocytes is increased), in the biochemical blood test, an increase in the activity of pancreatic enzymes (amylase, lipase) is detected, hyperglycemia and hypocalcemia are possible. There may be bilirubinemia and increased activity of liver enzymes.
• Biochemistry of urine. Determine the concentration of enzymes in the urine. When diagnosing acute pancreatitis, a biochemical analysis of urine is taken and urine amylase activity is determined.
• Instrumental methods. Visual examination of the pancreas and nearby organs (ultrasound, CT, MRI) can reveal pathological changes in the parenchyma, an increase in the volume of the organ, detect abscesses, cysts, and the presence of stones in the bile ducts.

Differential diagnosis of acute pancreatitis is carried out with:

• acute appendicitis and acute cholecystitis;
• perforations of hollow organs (perforated ulcers of the stomach and intestines);
• acute intestinal obstruction;
• acute gastrointestinal bleeding (bleeding ulcer of the stomach and 12p. intestines, bleeding from varicose veins of the esophagus, intestinal bleeding);
• acute ischemic abdominal syndrome.

Treatment of acute pancreatitis

In acute pancreatitis, hospitalization is indicated. All patients were prescribed bed rest. The main goals of therapy are to relieve pain, reduce the load on the pancreas, and stimulate the mechanisms of its self-healing.

Therapeutic measures:

• novocaine blockade and antispasmodics to relieve severe pain;
• hunger, ice on the gland projection area (creating local hypothermia to reduce its functional activity), parenteral nutrition is carried out, gastric contents are aspirated, antacids and proton pump inhibitors are prescribed;
• pancreatic enzyme deactivators (proteolysis inhibitors);
• necessary correction of homeostasis (water-electrolyte, acid-base, protein balance) with the help of infusion of saline and protein solutions;
• detoxification therapy;
• antibiotic therapy (broad-spectrum drugs in high dosages) as a prophylaxis of infectious complications.

Surgery

Surgical tactics is indicated in case of detection of:

• stones in the bile ducts;
• accumulations of fluid in or around the gland;
• areas of pancreatic necrosis, cysts, abscesses.

Operations performed in acute pancreatitis with the formation of cysts or abscesses include: endoscopic drainage, cyst marsupialization, cystogastrostomy, etc. When areas of necrosis are formed, depending on their size, necrectomy or resection of the pancreas is performed. The presence of stones is an indication for operations on the pancreatic duct.

Surgical intervention may also be resorted to in case of doubts about the diagnosis and the likelihood of missing another surgical disease requiring surgical treatment. The postoperative period implies intensive measures for the prevention of purulent-septic complications and rehabilitation therapy.

Treatment of a mild form of pancreatitis, as a rule, is not difficult, and a positive trend has already been noted within a week. Severe pancreatitis takes much longer to heal.

Forecast and prevention

The prognosis for acute pancreatitis depends on its form, the adequacy of therapy and the presence of complications. The mild form of pancreatitis usually gives a favorable prognosis, and with necrotizing and hemorrhagic pancreatitis, the likelihood of death is high. Insufficient treatment and non-compliance with medical recommendations on diet and regimen can lead to relapses of the disease and the development of chronic pancreatitis.

Primary prevention is a rational healthy diet, the exclusion of alcohol, spicy, fatty plentiful food, smoking cessation. Acute pancreatitis can develop not only in people who regularly abuse alcohol, but also as a result of a single intake of alcohol-containing drinks for fatty, fried and spicy snacks in large quantities.