Pathogenesis of chronic pancreatitis in the acute stage. Chronic pancreatitis. Etiology, pathogenesis, clinical picture, diagnosis, treatment. Difficulties of diagnosis and treatment

The diagnosis of “pancreatitis” is a collective concept that implies a group of pancreatic diseases accompanied by an inflammatory process. The definition of “chronic” implies that the disease lasts more than six months, from time to time accompanied by deterioration of the condition due to exposure to unfavorable factors. The pathogenesis of chronic pancreatitis describes a chain reaction of damage to interconnected organs and systems, indicating exactly how inflammation of the pancreas was caused and how it affected the body.

What is chronic pancreatitis

In a nutshell, the etiology and pathogenesis of chronic pancreatitis can be described as an inflammatory-destructive process in the pancreas (PG), caused by a violation of the outflow of pancreatic enzymes.

The pancreas exists to produce digestive enzymes, which pass through the ducts into the duodenum. On the way, the gallbladder duct joins them, and the exit into the intestine occurs through the large duodenal papilla and is regulated by the sphincter of Oddi.

Under the influence of factors such as poor diet, alcohol consumption, and diseases of neighboring organs, the outflow of digestive enzymes becomes more difficult, which leads to exocrine insufficiency of the pancreas. As a result, enzymes linger in the pancreas and begin to break it down. This is how organ tissues are destroyed. The disease can be aggravated by swelling, bleeding, purulent infection and other complications.

Moreover, the symptoms during exacerbation of chronic recurrent pancreatitis and the first-time acute condition are practically no different.

Origin

There are many reasons for the appearance of chronic pancreatitis:

1. Alcohol is first on the list, as it is responsible for the onset of the disease in 70% of cases. Any amount of ethyl alcohol irritates the surface of the gastrointestinal tract, increasing the production of certain hormones and enzymes. In addition, irritation of the surface of the duodenum causes the sphincter of Oddi to reflexively contract, making the release of bile and pancreatic juice impossible. The body perceives alcohol as a toxic substance, changing the composition of pancreatic secretions, which leads to the formation of stones.
2. Chronic diseases of the gallbladder and its ducts cause pancreatitis in 20% of cases. These diseases lead to a narrowing of the sphincter of Oddi, which makes it impossible for the outflow of pancreatic secretions. Bile itself does not have a negative effect on the pancreatic ducts. But disruption of the sphincter of Oddi leads to the reflux of the contents of the duodenum into the pancreatic ducts. Enzymes produced by the gland are activated and destroy its own tissue.

In the remaining 10% of cases, chronic pancreatitis is caused by:

• herbs;
• malnutrition with lack of protein foods;
• drug poisoning;
• viral infections;
• other diseases of the gastrointestinal tract;
• heredity.

Primary

Primary chronic pancreatitis includes those types of diseases in which external factors have a direct negative effect on the pancreas. This includes injuries, alcohol, poisoning, and poor nutrition.

Secondary

Secondary pancreatitis is called pancreatitis, which appears against the background of the active development of other diseases. In most cases, this is a blockage of the bile and pancreatic ducts with gallstones or as a result of inflammation and swelling of neighboring organs that compress the pancreatic ducts.

Kinds

The causes of the disease, differences in symptoms, the course of the disease, the degree of organ damage, complications that arise - all this provides the basis for the classification of chronic pancreatitis.

Some changes that have occurred in the pancreas can only be seen during surgery.

Indurative

When acute pancreatitis is complemented by infection and leads to the development of chronic pancreatitis, this type of disease is called indurative. The disease is characterized by:

• proliferation of connective tissue;
• violation of the patency of the gland ducts;
• increase in organ volume;
• decreased functionality.

Cystic

Chronic cystic pancreatitis is defined by the presence of cysts up to 1.5 cm in size. The cysts are filled with fluid. The organ is enlarged and has unclear boundaries. The gland ducts are dilated.

More than half of patients with this variant of the disease develop complications.

Pseudotumorous

“Pseudo” in Latin means “false,” and “tumor” translates as “tumor.” This type includes pancreatic diseases, in which the pancreas increases in size and puts pressure on neighboring organs. This occurs after a long course of chronic pancreatitis (more than 10 years) and is observed mainly among men.

Pseudotumorous pancreatitis causes subhepatic jaundice, disorders of many digestive functions and rapid weight loss of the patient. Surgical treatment is indicated.

Forms

Many factors influence the appearance, clinical picture and course of the disease. According to these criteria, forms of chronic pancreatitis are differentiated.

Calcifying

The formation of stones, or calcifications, in the pancreas and its ducts is a hallmark of this form of the disease. The causes of the disease are alcoholic, hereditary, idiopathic (unexplained) factors. But still, the formula that accurately characterizes the cause of the development of calcific pancreatitis is alcohol plus fatty foods.

The size of the stones ranges from half a millimeter to four centimeters. Such formations irritate the epithelium of the organ, which provokes worsening chronic inflammation and frequent relapses.

Obstructive

Obstruction of the main pancreatic duct means the impossibility of normal outflow of pancreatic secretions. The cause of obstruction may be trauma, abnormal organ structure, narrowing of the main pancreatic duct, or gallstone disease.

The last option is the most common. The gallstone blocks the exit of pancreatic secretion, after which the pathological mechanism is launched. The mucous membrane of the organ is irritated, which leads to insufficiency of the sphincter of Oddi, then the pressure inside the ducts increases. Digestive enzymes return to the gland, are activated, and damage the epithelium and pancreatic tissue.

Improving the outflow of pancreatic secretions immediately brings relief.

A separate type is alcoholic

In the classification of chronic pancreatitis, the alcoholic type is especially distinguished. This is not without reason, because 2/3 of pancreatic diseases occur precisely for this reason.

Alcohol hits the pancreas from two sides: outside and inside. Ethyl alcohol reaching the gland through the bloodstream destroys glandular cells.

Once alcohol enters the digestive system, it produces acetaldehyde, which is many times more toxic than ethanol. Acetaldehyde irritates the membrane of the gland ducts, disrupts the mechanism of calcium deposition, forming stones. The presence of stones impairs the patency of the ducts. It turns out to be a vicious circle.

With the regular presence of aceteldehyde, the cells responsible for the production of the liquid part of pancreatic juice are destroyed, leading to its thickening.

The disease is accompanied by classic clinical symptoms:

• girdle pain;
• vomiting that does not bring relief;
• constipation followed by diarrhea;
• pinpoint hemorrhages or bluish spots on the abdomen;
• renal failure.

Stages

There are several stages in the development of chronic pancreatitis.

Early

The early stage includes the first 10 years of the disease, although if medical instructions are violated, the transition from one stage to another can occur much faster. At this time, exacerbations alternate with remission, and acute periods may become more frequent.

The localization of pain depends on which part of the organ is affected. Inflammation of the head of the pancreas makes itself felt by pain in the middle of the upper abdomen. If the body of the organ is inflamed, the pain shifts to the left. When the tail of the pancreas is inflamed, the left side under the ribs hurts more.

At this stage, digestive disorders do not manifest themselves much.

Late

The late stage is complemented by pathological changes in the pancreas. Fibrosis and sclerosis develop, that is, as a result of the inflammatory process, connective tissue grows and replaces pancreatic tissue. As a result, exocrine insufficiency develops.

The patient’s well-being deteriorates significantly: pain increases, the digestion process is noticeably disrupted, accompanied by vomiting.

Ultimate

The last stage of chronic pancreatitis is accompanied by irreversible pathological changes in the organ, as a result of which other diseases develop.

At this time, the patient is tormented:

• belching;
• vomit;
• bloating;
• bowel dysfunction;
• weight loss;
• the formation of angiomas - red vascular formations on the abdomen.

Difficulties of diagnosis and treatment

Diagnosis begins with palpation of the abdomen. Due to the location of the organ, it cannot be felt directly, however, on the anterior abdominal wall there are pancreatic points that indicate the part of the organ in which the inflammatory process is taking place. By palpation it is also possible to detect a tumor or cyst.

Ultrasound examination can detect:

• liver enlargement;
• changes in the size, contours, density of the pancreas;
• stomach diseases;
• cysts, tumors, abscesses.

Regular ultrasound allows you to monitor the dynamics of the disease.

To establish an accurate diagnosis, an x-ray and computed tomography are done to detect calcifications.

In the diagnostic process, an important role is played by laboratory tests, through which the presence of enzymes in the blood is determined. Functional changes are visible in urine and stool tests. Before taking tests, it is not recommended to take medications containing enzymes and bile, so as not to “blur” the picture.

The patient is first prescribed fasting and active drug therapy. Only if the situation is severe and conservative treatment does not bring the expected results, surgeons intervene. A laparoscope is used for the operation. Due to the reduction in the area of ​​damaged tissue, compared to traditional surgery, faster recovery occurs.

For the first 3-4 days after an exacerbation, complete fasting is prescribed. You are only allowed to drink alkaline mineral water. After vomiting is relieved, nutrition is prescribed according to diet No. 5. The amount of proteins increases, the content of fats and carbohydrates in food decreases.

Treatment with pharmaceutical drugs is aimed at relieving spasms that cause pain (No-shpa, Baralgin). For severe pain, painkillers (Analgin) or narcotic substances (Promedol, Fortral) are prescribed. Morphine is contraindicated as it can lead to spasm of the sphincter of Oddi.

Pancreatic rest is ensured by antacids and antisecretory drugs (Phosphalugel, Maalox). To detoxify the body, a 5% glucose solution, Ringer-Locke solution, is administered intravenously. To improve digestion, enzymes (Creon, Mezim-Forte, Festal), as well as vitamin complexes, are prescribed.

What statistics say about morbidity and prognosis

As a result of daily consumption of even small amounts of alcohol, 90% develop pancreatitis.

According to statistics, since 1990, the number of patients with chronic pancreatitis has increased 2.5 times and is 63 people per 100,000 population. Early complications develop in 32% of patients, late ones - in 65%. Half of patients die within 20 years after the onset of the disease.

A patient with chronic pancreatitis has a 5-fold increased risk of developing pancreatic cancer.

The prognosis for the development of the disease sounds favorable only if you switch to a diet, stop drinking alcohol, and receive timely treatment. Otherwise, the disease leads to decreased ability to work, disability and death.

Chronic pancreatitis (CP)– chronic polyetiological inflammation of the pancreas, lasting more than 6 months, characterized by gradual replacement of parenchymal connective tissue and disruption of the exo- and endocrine functions of the organ.

Epidemiology: middle-aged and elderly men are more likely to suffer; frequency in adults 0.2-0.6%

Main etiological factors:

1) alcohol is the main etiological factor (especially when combined with smoking)

2) diseases of the gallbladder and biliary tract (chronic calculous and acalculous cholecystitis, biliary dyskinesia)

3) abuse of fatty, spicy, salty, pepper, smoked foods

4) drug intoxication (primarily estrogens and corticosteroids)

5) viruses and bacteria entering the pancreatic duct from the duodenum through the papilla of Vater

6) trauma to the pancreas (in this case, sclerosis of the ducts with increased intraductal pressure is possible)

7) genetic predisposition (often a combination of CP with blood group O(I)

8) late pregnancy (leads to compression of the pancreas and increased intraductal pressure)

Pathogenesis of chronic pancreatitis:

In the development of chronic pancreatitis, 2 mechanisms play a major role:

1) excessive activation of the pancreas’ own enzymes (trypsinogen, chymotrypsinogen, proelastase, lipase)

2) increased intraductal pressure and difficulty in the outflow of pancreatic juice with enzymes from the gland

As a result, autolysis (self-digestion) of pancreatic tissue occurs; areas of necrosis are gradually replaced by fibrous tissue.

Alcohol is both a good stimulator of the secretion of hydrochloric acid (and it already activates pancreatic enzymes), and leads to duodenostasis, increasing intraductal pressure.

Classification of chronic pancreatitis:

I. According to morphological characteristics: interstitial-edematous, parenchymal, fibrous-sclerotic (indurative), hyperplastic (pseudotumorous), cystic

II. According to clinical manifestations: pain variant, hyposecretory, asthenoneurotic (hypochondriacal), latent, combined, pseudotumorous

III. According to the nature of the clinical course: rarely recurrent (one exacerbation every 1-2 years), often recurrent (2-3 or more exacerbations per year), persistent

IV. By etiology: biliary-dependent, alcoholic, dysmetabolic, infectious, drug

Clinic of chronic pancreatitis:

1) pain- can be sudden, acute or constant, dull, pressing, occurs 40-60 minutes after a meal (especially large, spicy, fried, fatty), worsens when lying on your back and weakens when sitting with a slight bend forward, localized when if the head is affected - to the right of the midline, closer to the right hypochondrium; if the body is affected - along the midline 6-7 cm above the navel; if the tail is affected - in the left hypochondrium, closer to the midline; in 30% of cases the pain is of a girdling nature, in another 30% it has no specific localization; half of patients limit their food intake due to fear of pain

2) dyspeptic syndrome(belching, heartburn, nausea, vomiting); vomiting in some patients is accompanied by pain, repeated, does not bring any relief

3) exocrine pancreatic insufficiency syndrome:“pancreatogenic diarrhea” (associated with insufficient enzyme content in the secreted pancreatic juice, which is characterized by a large amount of feces containing a lot of neutral fat and undigested muscle fibers), malabsorption syndrome, manifested by a number of trophic disorders (weight loss, anemia, hypovitaminosis: dryness skin, brittle nails and hair loss, destruction of the skin epidermis)

4) endocrine deficiency syndrome(secondary diabetes mellitus).

Diagnosis of chronic pancreatitis:

1. Sonography of the pancreas: determination of its size, echogenicity of the structure

2. FGDS (normally, the duodenum, like a “crown,” goes around the pancreas; with inflammation, this “crown” begins to straighten out - an indirect sign of chronic pancreatitis)

3. X-ray of the gastrointestinal tract with a barium passage: the contours of the duodenum are changed, the “backstage” symptom (the duodenum straightens and moves apart, like the backstage on a stage, with a significant increase in pancreas)

4. CT – mainly used for differential diagnosis of CP and pancreatic cancer, because their symptoms are similar

5. Retrograde endoscopic cholangioduodenopancreatography - through an endoscope, a special cannula is used to enter the papilla of Vater and inject contrast, and then take a series of radiographs (allows you to diagnose the causes of intraductal hypertension)

6. Laboratory research:

a) OAC: during exacerbation - leukocytosis, acceleration of ESR

b) OAM: with exacerbation - increase in diastase

c) LHC: during exacerbation - increased levels of amylase, lipase, trypsin

c) coprogram: neutral fat, fatty acids, undigested muscle and collagen fibers

Treatment of chronic pancreatitis.

1. In case of exacerbation - table No. 0 for 1-3 days, then table No. 5p (pancreatic: limiting fatty, spicy, fried, spicy, peppered, salty, smoked foods); all food is boiled; meals 4-5 times/day in small portions; refusal to drink alcohol

2. Pain relief: antispasmodics (myolytics: papaverine 2% - 2 ml 3 times/day IM or 2% - 4 ml in saline IV, drotaverine / no-spa 40 mg 3 times/day, M-anticholinergics: platiphylline, atropine), analgesics (non-narcotic: analgin 50% - 2 ml IM, in severe cases - narcotic: tramadol orally 800 mg/day).

3. Antisecretory drugs: antacids, proton pump blockers (omeprazole 20 mg morning and evening), H2 receptor blockers (famotidine 20 mg 2 times a day, ranitidine) - reduce the secretion of gastric juice, which is a natural stimulator of pancreatic secretion

4. Protease inhibitors (especially with intense pain): gordox, contrical, trasylol, aminocaproic acid intravenously, slowly, in saline or 5% glucose solution, octreotide / sandostatin 100 mcg 3 times a day s.c.

5. Replacement therapy (for insufficiency of exocrine function): pancreatin 0.5 g 3 times a day during or after meals, Creon, pancitrate, mezim, mezim-forte.

6. Vitamin therapy - to prevent trophic disorders as a result of malabsorption syndrome

7. Physiotherapy: ultrasound, sinus-modeled currents of various frequencies, laser, magnetotherapy (in case of exacerbation), thermal procedures: ozokerite, paraffin, mud applications (in remission phase)

Dispensary observation: 2 times/year at the clinic level (examination, basic laboratory tests, ultrasound).

Operations: resection and surgical internal drainage, cholecystectomy, pancreaticectomy, choledochostomy, papillosphincteroplasty, virsungoplasty, formation of pancreatojejunal anastomosis

(OP) and chronic pancreatitis (CP) one of the leading mechanisms is the activation of pancreatic enzymes, primarily trypsin, and “self-digestion” of pancreatic tissue. Trypsin causes coagulative necrosis of acinar tissue with leukocyte infiltration. In turn, A- and B-phospholipases destroy the phospholipid layer of membranes and cells, elastase destroys the elastic “framework” of the vascular walls. In addition, activation of kallikrein and other vasoactive substances increases vascular permeability, which leads to hemorrhagic infiltration of pancreatic tissue.

Premature activation of trypsin from trypsinogen in the pancreatic ducts is carried out by a complex of components of duodenal contents coming from the duodenum during its dyskinesia and being a mixture of activated pancreatic enzymes, bile salts, lysolecithin, emulsified fat and bacterial flora (H. Schmidt, 1976). In the presence of an inflammatory process in the pancreas and an obstruction to the outflow of pancreatic juice, activation of trypsin, chymotrypsin and elastase can occur in the gland itself.

By origin, primary and secondary CP are distinguished

• In primary CP, the inflammatory-destructive process is initially localized in the pancreas. Primary CP develops against the background of AP, trauma, allergies, narrowing of the main pancreatic duct, chronic alcoholism, and circulatory disorders.
• Secondary CP is caused by pathology of neighboring organs that disrupts the functioning of the pancreas (cholelithiasis, peptic ulcer, duodenal diverticula, etc.).

CP, according to many researchers, is often a consequence of previous AP. In the majority of patients with CP (60% - according to P. Mallet-Guy), the acute phase of pancreatitis remains unrecognized, since instead of AP they are mistakenly diagnosed with foodborne toxic infection, cholelithiasis, cholecystitis, appendicitis, etc. Sometimes, for example, in conditions of chronic food poisoning, primarily protein deficiency, primary CP occurs without a history of attacks of AP.

V.M. Danilov and V.D. Fedorov (1995) believe that in most patients CP and AP are diseases with a single pathogenesis and that, as a rule, in these diseases we are talking about a single inflammatory-degenerative process in the pancreas. The concept that considers AP and CP as two independent diseases, which are characterized by different pathogenesis, was rejected by carefully conducted studies by Y. Kloppel, B. Maillet (1991), D.S. Sarkisov et al., 1985, which identified the stages of transition from AP to CP and a number of common morphological characteristics are described.

Y. Kloppel and B. Mailet (1986, 1992), based on retrospective anatomical, morphological and histological studies, suggested that CP is a consequence of repeated episodes of AP. According to their studies, macro- and microscopic changes in the pancreas in patients with AP and CP caused by alcohol are very similar. The authors consider necrosis of the peri- and intrapancreatic fat base to be one of the main changes in pancreatic tissue, which leads to the development of fibrous tissue, the formation of pseudocysts, and stenosis of the pancreatic ducts. Obstruction in the pancreatic ductal system causes thickening and precipitation of proteins in the pancreatic juice and subsequently the formation of stones. These data are confirmed by studies conducted in Zurich (R.W. Amman et al., 1994). Foci of steatonecrosis in the pancreas, even with the edematous form of pancreatitis, can lead to the development of scar tissue and obstructive phenomena in its ductal system. A distinctive feature of the proposed hypothesis is the fact that the primary factors in the development of CP are pathomorphological changes in the tissues of the pancreas, leading to narrowing and obstruction of the ductal system, and the secondary ones are the formation of precipitates and stones.

The pathomorphological basis of CP is a combination of destruction of the acinar apparatus with a progressive chronic inflammatory process, leading to atrophy and disorders in the pancreatic ductal system, mainly due to the development of strictures, micro- and macrolithiasis. There are also difficulties in lymphatic drainage (initially due to edema, and then due to sclerotic changes in acinar tissue), microcirculation disturbances due to the formation of fibrin threads in the capillaries and microthrombosis. At the same time, compaction of the pancreas occurs due to the proliferation of connective tissue and fibrosis of the gland.

As inflammatory-degenerative changes, sclerosis of the pancreatic parenchyma, and obliteration of the ductal system progress, its exocrine and then endocrine function is first disrupted. This process, as a rule, occurs in phases, with alternating periods of exacerbation, accompanied by destruction of pancreatic tissue, and periods of relative well-being, when the damaged parenchyma of the organ is replaced by connective tissue.

In CP, exacerbations periodically occur, resembling the morphological and pathophysiological picture of acute pancreatitis, which are replaced by remissions. Each such exacerbation causes rapid progression of the disease. During exacerbations of chronic pancreatitis, the lobular tissue of the pancreas, which performs an exocrine function, is predominantly damaged. With fibrosis, both lobules and pancreatic islets are affected, which causes progressive disturbances of both exo- and endocrine function. All of the above changes gradually increase; in parallel, the functional reserves of the pancreas decrease, which then manifest clinically in the form of its exo- and endocrine insufficiency.

According to some data (Stephen Holt, 1993), exocrine insufficiency manifests itself clinically with the destruction of 90% of the gland parenchyma. The later stages of CP are characterized by a triad:

• gland calcification,
• diabetes,
• steatorrhea.

Steatorrhea occurs when lipase production by the pancreas falls below 16% of its normal level.

Thus, CP is currently considered more often not as an independent disease, but as a continuation and outcome of AP, which corresponds to the so-called fibro-necrotic theory of the development of CP. In 10% of patients, AP turns into CP immediately after the first attack of AP; in 20%, there is a long latent period (from 1 to 20 years) between the attack of AP and the development of CP; in 70% of patients, CP is detected after several attacks of AP. Its development is primarily promoted by chronic alcoholism, choledocholithiasis, chronic diseases of the stomach and intestines (peptic ulcer, papillitis, papillostenosis, duodenostasis), atherosclerotic damage to the vessels of the pancreas and some other factors to a lesser extent.

Early stages of chronic pancreatitis

A pathological examination in a relatively early stage of CP reveals a pronounced enlargement of the pancreas to varying degrees, a relatively slight uneven compaction of its tissue, edema, necrosis, hemorrhages, pseudocysts, indicating previous acute attacks. At the same time, both signs of acute inflammation, usually characteristic of AP, and chronic inflammation are detected, in particular, fibrosis of the lobules or interstitial tissue, pronounced cellular infiltration with the deposition of hemosiderin and microlites. These changes also extend to the pancreatic ducts, the epithelium of which is metaplastic, desquamated, and clogs their lumens. In the initial period of the disease, the pathological process can be limited (focal) in nature and not spread to the entire gland: left-sided, right-sided, paramedian CP (P. Mallet-Guy, 1960).

Late stages of chronic pancreatitis

In the late stages of CP, the pancreas, as a rule, is unevenly enlarged, dense, often with pseudocysts filled with colorless or yellowish-brownish liquid, fused with neighboring organs due to fibrous changes in the peripancreatic tissue, adjacent veins are often thrombosed. The stroma of the organ is represented by growths of wide layers of connective tissue of varying degrees of maturity; in some cases there are lime deposits both in the lumen of the ducts in the form of granular whitish-yellow stones, and among the growths of fibrous tissue in places of former necrosis of the parenchyma. The volume of exocrine parenchyma is sharply reduced.

Obliteration and deposition of lime inside the ducts cause the formation of retention cysts. When opening the main pancreatic duct, attention is drawn to the presence of uneven narrowings and expansions of its lumen. L. Leger (1961) distinguishes the following types of dilation of the gland ducts according to their predominant localization: dilatation throughout, ectasia in the head region, corpocaudal formation of pseudocysts.

The final stage of chronic pancreatitis

In the final stage of CP, the pancreas is atrophic, reduced in volume, woody in density. Diffuse intralobular and intraductal calcifications are often detected.

Thus, pathomorphological changes in CP are characterized by a combination of sclerotic, atrophic and regenerative processes, which are often accompanied by calcification of the organ parenchyma and the formation of true and false cysts. Therefore, several pathomorphological variants of CP are distinguished:

• inductive,
• cystic,
• pseudotumorous.

Indurated chronic pancreatitis

Indurative CP in most patients develops soon after AP and is manifested by diffuse proliferation of connective tissue with simultaneous atrophy of the gland parenchyma and expansion of its ducts. Hemorrhages and focal fat necrosis that occur during an acute inflammatory process are subsequently organized in most cases with the deposition of calcium salts and apatite hydroxide into foci of calcifications of various shapes and sizes.

Cystic chronic pancreatitis

Cystic CP is characterized by both cicatricial narrowing of the pancreatic ducts with impaired outflow of pancreatic juice and dilatation of the distal sections of the main pancreatic duct, and the development of pseudocysts in the area of ​​necrosis of the pancreas.

Pseudotumorous chronic pancreatitis

Pseudotumorous CP is caused by the predominance of a hyperplastic inflammatory process and is accompanied by an increase in the volume of the entire gland or part of it. The hyperplastic process often involves the head of the pancreas and is combined with the development of fibrous compactions, small foci of calcification and small cysts.

In the initial stage of CP, abdominal pain syndrome dominates, which develops primarily as a result of intraductal hypertension in the pancreas and pancreatitis-associated neuritis. Complications such as pseudocysts, jaundice, compression of the duodenum with its obstruction, pancreatic ascites, and pleural effusion are also typical.

Clinically pronounced jaundice can be detected in 8% of patients (A.A. Shalimov et al., 1997). The causes of jaundice in patients with CP can be: compression of the distal part of the common bile duct, cholelithiasis, stenosing papillitis, toxic hepatitis. In some patients, portal hypertension occurs due to compression and thrombosis of the splenic and portal veins. Against the background of long-term CP, the formation of pancreatic carcinoma is possible.

Thus, the main pathogenetic factors in CP are:

• a chronic inflammatory process, accompanied primarily by destruction of the exocrine apparatus of the gland and obligate destruction of its endocrine apparatus in the later stages of the disease;
• irreversible progressive atrophy and fibrosis of the acini and endocrine apparatus of the pancreas (P. Banks, 1988; J. Valenzuela, 1988; H. Sarles, 1989; J. Grendell, 1993; H. Spiro, 1994).

When considering the etiopathogenesis of CP, two main forms of the disease should be distinguished:

1. chronic calcific pancreatitis and
2. chronic obstructive pancreatitis.

These are the most common diseases of the pancreas in Western European countries (G. Cavallini, 1993). Chronic inflammatory fibrous pancreatitis is less common. At the same time, a number of experts (Prof. Henri Sarles from Marseille) believe that in terms of morphological changes, these two forms are not much different. The pathogenesis of primary and secondary CP, resulting from obstruction of the ductal system, can be very similar.

Pancreatic juice contains significant amounts of calcium combined with high levels of bicarbonates. The pathogenesis of CP in many cases is associated with impaired formation of soluble protein-calcium associates and the formation of calcifications. There are 3 types of pancreatic stones:

• calcium carbonate protein,
• calcium carbonate and
• protein (organic) - small insoluble protein plugs with no or weak degree of calcification.

According to the theory proposed by Sarles (1991), precipitation of proteins in the pancreatic ducts plays a major role in the pathogenesis of primary CP. In 1979, a glycoprotein - lithostatin (PSP - pancreatic stone protein) was discovered, which is directly related to the formation of stones in the pancreas. The protein intraductal aggregates include fibrillar insoluble peptides (LS-H 2), which are enzymes of the lithostatin protein (LS-S). Litostatin is produced by acinar cells. The main role of lithostatin is associated with the inhibition of nucleation, aggregation and the formation of crystals of calcium salts in pancreatic juice. Litostatin is considered the most important calcium stabilizer in soluble form. It is found in zymogenic granules of pancreatic acinar cells, and is present in pancreatic juice in healthy people, saliva (D. Hay, 1979) and urine (Y. Nakagawa, 1983). Precipitation of calcium and the formation of stones in the lumen of the pancreatic ducts are associated with a deficiency in the synthesis of the protein lithostatin (Horovitz, 1996). Already at the very early stages of CP formation, protein precipitates are found in the small pancreatic ducts, which are insoluble fibrillar protein with calcium deposits in the form of carbonates. According to this theory, certain congenital factors, as well as acquired ones (alcohol abuse, smoking) affect the secretion and stability of lithostatin. Protein precipitates and stones in the gland ducts cause damage to their covering epithelium and contribute to periductal inflammatory processes, leading to the development of fibrous tissue. The formation of protein precipitates and stones leads to obstruction of the ductal system, causing its stenosis, which subsequently leads to the emergence of new stones in the ductal system. Alcohol and nicotine affect the biochemical composition of pancreatic juice and thereby promote lithogenesis in the pancreatic ductal system. Studies have found that alcohol increases the secretion of proteins by acinar cells of the pancreas, while the secretion of the protein lactoferrin increases and the secretion of bicarbonates and citrates decreases, which leads to a change in the pH of pancreatic juice. This causes a decrease in the concentration of trypsin inhibitor, increasing the instability of trypsinogen (L.A. Scurro, 1990). In some cases, deficiency of lithostatin synthesis is caused by congenital genetic factors, which leads to the development of congenital, familial CP. This hypothesis practically excludes the formation of calcifying stones in the early stages of the disease.

Radioimmunoassay with monoclonal antibodies did not reveal significant differences in the lithostatin content in the pancreatic juice of patients with CP compared with controls (W. Schimigel, 1990). The concentration of lithostatin in pancreatic juice is not significant for the formation of precipitates; more significant is the reduction in the possibilities of synthesis, that is, the total pool of lithostatin (D. Giorgi, 1989). From these positions, the pathogenesis of precipitation of protein-calcium aggregates is considered as a result of decreased secretion of lithostatin under conditions of increased demand. Such conditions occur with increased protein hydrolysis in pancreatic juice, induction of polymerization of protein components, the appearance of a large number of poorly soluble proteins, and increased secretion of calcium salts (J. Bernard, 1994). A study of the composition of the organic matrix of pancreatic stones showed that it includes modified lithostatin, albumin, and globulins with high molecular weight.

Horovitz (1996) distinguishes 2 main pathogenetic types of CP - calcific and obstructive.

Calcific chronic pancreatitis

Calcifying CP is characterized by the presence of stones in the gland with a high degree of calcification and has a clear connection with alcohol consumption or insufficient (poor) nutrition. In the initial stages of CP, small insoluble protein plugs with no calcification may be detected. Such “microlites” are X-ray negative. The main issues of the pathogenesis of calcifying CP are currently being considered from the standpoint of the emergence of the mechanism of calcium and protein precipitation.

Calcifying CP is considered the most common form of CP found in Western Europe, accounting for 36 to 95% of all CP (T.T.White, 1978; J.Bernard, 1994). In highly developed countries, calcific CP is associated primarily with alcohol abuse and affects mainly men from wealthy segments of the population aged 30-40 years.

In Asian and African countries, calcific CP, as a rule, is not associated with alcohol consumption; it affects representatives of the least affluent segments of the population, and is equally often observed in men and women, starting from 10-20 years of age.

Obstructive chronic pancreatitis

The second most common form of CP is obstructive pancreatitis, characterized by the presence of stenosis of the pancreatic ducts at any level. Pancreatic biopsies usually reveal atrophy of acinar tissue with areas of fibrosis. Most often, obstruction is localized at the level of the ampullary region, and there is distal intraductal hypertension with the development of dilatation of the ductal system. In the case of anatomical fusion of the terminal sections of the bile ducts and the pancreatic ducts in obstructive CP, dilatation of the bile ducts may occur.

Alcoholic pancreatitis

Bordalo from Portugal (1984) proposed a new hypothesis for the development of CP. According to his data, based on anatomical and morphological studies, CP occurs with long-term alcohol intake, which leads to the accumulation of lipids inside pancreatic cells and to the development of periacinar fibrotic processes. The author came to the conclusion that, similar to the development of liver cirrhosis, pancreatic fibrosis occurs as a result of necrosis of acinar cells of the gland and chronic alcohol poisoning. This hypothesis was taken seriously by the Marseille school, whose experts believe that, as a result of alcohol poisoning, accumulation of oxidative products, peroxidases, and oxidative radicals occurs in the tissues of the pancreas (J.M. Braganza et al., 1983). It has been proven that long-term alcohol intake disrupts the functions of the liver and pancreas, which leads to the accumulation of oxidative radicals and a decrease in the level of antioxidants such as vitamins C, E, riboflavin, beta-carotene, and selenium. According to this theory, changes in the function of pancreatic cells lead to a decrease in the secretion of lithostatin and, as a result, to the formation of stones in its ducts. This hypothesis is important because for the first time the toxic effects of long-term alcohol intake on pancreatic dysfunction, degeneration of acinar cells, the development of intrapancreatic sclerosis, steatonecrosis and fibrosis were proven.

Currently, the most studied are the morphological and pathogenetic features of CP of alcoholic etiology (H. Sarles, 1981; Kloppel and Maillet, 1992; S.P. Lebedev, 1982), which is characterized by particularly severe morphological changes in the parenchyma and pancreatic ducts. The most likely case of alcohol abuse is the primary chronic course of the disease. Taking ethyl alcohol for a long time causes a cholinergic effect and leads to hypersecretion of protein by acinar cells.

A significant factor in the development of CP is necrosis of interstitial fatty tissue, which leads to the occurrence of perilobular fibrosis. When the connective tissue grows between the lobules of the pancreas, compression of the small ducts occurs and hypertension is formed in its ductal system, preventing the normal outflow of pancreatic juice. Under these conditions, protein secretion, unbalanced by the hyperproduction of water and bicarbonates, accumulates in small ducts in the form of protein precipitates, into which calcium salts are deposited and subsequently pancreatic calculi are formed. These changes contribute to the development of intra- and periductal sclerosis, local stenosis and obstruction of the pancreatic ducts with simultaneous dilatation of the ductal system.

Pathognomonic signs of alcoholic pancreatitis are:

1. dilation of the pancreatic ducts, metaplasia and desquamation of the ductal epithelium;
2. unevenness of pathological changes in different parts of the pancreas (W. Boecker et al., 1972; H. Sarles, 1974).

The previously discussed 3 theories of the development of CP show ways of damage to the acinar tissue of the pancreas, leading to disturbances in the ductal system. Boros and Singer (1984) suggest that long-term alcohol intake, combined with malnutrition, causes the development of destructive changes in the epithelium of the pancreatic ducts with the subsequent formation of precipitates and calculi in them. Using animal models of CP, the authors showed (1991, 1992) that with long-term alcohol intake in animals, obstructive processes in the pancreatic ducts may develop due to the formation of precipitates and calculi in them. Violation of the outflow of gland secretions causes the entire complex of the clinical picture of CP. The similarity of the morphological picture of periductal fibrosis in various types of CP leads to the idea of ​​a certain role of autoimmune processes in the development of chronic inflammation of the pancreas (J. Cavallini, 1997). Infiltration of pancreatic tissue by lymphocytes is a trigger process that causes a fibroplastic process in the periductal area. From this point of view, the pathogenesis of CP is as follows: poor outflow of pancreatic juice leads to precipitation of proteins, the formation of protein clots and subsequently stones, which causes obstructive processes in the ductal system, and to the development of the clinical picture of CP. Exogenous factors such as alcohol and nicotine affect the lithogenetic ability of pancreatic juice and cause damage to the epithelial cover of the pancreatic ductal system. All of these theories require clear confirmation. Thus, R.P. Jalleh et al. (1993), Cavallini (1997) indicate the presence of a genetic predisposition in the development of CP.

K.Hakamura (1982) distinguishes 2 stages in the morphogenesis of CP:

1. inflammatory - before the formation of stones; typical is the lobulated and multilobular nature of the spread of inflammatory foci; And
2. calcific - from the moment of appearance of calcified areas and stones in the gland; visible even on ordinary radiographs: this stage is characterized by obstruction of the pancreatic ducts.

Impaired digestion and absorption of nutrients in CP leads to loss of consumed proteins, fats and vitamins in feces. As a result, exhaustion, asthenia, and metabolic disorders of bone tissue and the blood coagulation system may develop.

A.A. Shalimov, V.V. Grubnik, Joel Horowitz, A.I. Zaychuk, A.I. Tkachenko / Chronic pancreatitis. Modern concepts of pathogenesis, diagnosis and treatment. 2000

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

Classification

Over 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 enzyme toxemia; 2) temporary remission phase; 3) phase of sequestration and purulent complications.

In case of complicated 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 extent of its damage 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 can be focal or confluent.

Story

In 1841, N. Tulp reported a pancreatic abscess discovered during an autopsy of a patient who died with symptoms of an acute abdomen. Klebs (E. Klebs) in 1870 identified acute pancreatitis as a separate disease. Fitz (R. N. Fitz) in 1889 reported that he recognized acute Pancreatitis during the patient’s lifetime. This diagnosis was subsequently 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 50s of the 20th century, acute pancreatitis was considered a rare disease, detected only during surgery or at autopsy. According to V. M. Voskresensky (1951), domestic scientists from 1892 to 1941 described only 200 patients with acute pancreatitis. Since the mid-50s, along with an improvement in the diagnosis of the disease, there has been an increase in the incidence of acute pancreatitis. At the same time, according to V. S. Mayat and Yu. A. Nesterenko (1980), the 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 the patients, 80.4% were women, 19.6% were men. In patients with pancreatic necrosis, the ratio of men to 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 the acinar cells of the pancreas, 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 trauma to the abdomen, surgical interventions on the abdominal organs, acute circulatory disorders in the pancreas (ligation, thrombosis, embolism, compression of blood vessels and others), exogenous intoxications (alkalies, acids and others) severe allergic reactions, significant nutritional disorders and others.

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

Acute bile-pancreatic ductal hypertension and reflux of bile into the pancreatic ducts easily occur in the presence of a common ampulla for the common bile duct and the pancreatic duct in the event of a sudden blockade of the orifice of the greater papilla of Vater (duodenal papilla), for example, with a gallstone, and others. According to E.V. Smirnov and his colleagues (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 full body of knowledge), then in the second their activator is enteropeptidase. Flow of duodenal contents into the pancreatic ducts is possible when the major duodenal papilla gapes and intraduodenal pressure increases.

Experimental studies by N.K. Permyakov and his colleagues (1973) showed that both excess consumption of food, especially fats and carbohydrates, and its deficiency, especially proteins, leads to damage to the ultrastructures of acinar cells even in conditions of undisturbed outflow of pancreatic secretions and promotes the development of primary -acinous form of Pancreatitis (metabolic Pancreatitis).

The role of nutritional factors in the development of acute pancreatitis increases when taking excess amounts of juice food in conditions of impaired outflow of pancreatic juice.

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

Predisposing factors include allergies. Pancreatitis D. Solovoe in 1937 explained the origin of pancreatic necrosis by hyperergic inflammation of the vessels of the pancreas.

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

M. N. Molodenkov (1964) caused acute Pancreatitis by ligating the pancreatic ducts after sensitizing rabbits with 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 resolving exogenous (food) and endogenous (metabolite) allergens against this background. However, numerous models of allergic pancreatitis are far from identical to a similar disease in humans.

According to V.I. Filin and his colleagues (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 is the enzymatic theory of the pathogenesis of acute pancreatitis.

Activation of the pancreas’s own enzymes (trypsin, chymotrypsin, elastase, lipase, phospholipase and others) under conditions of increased function, obstructed outflow of pancreatic secretions 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 occurs as a chain reaction and usually begins with the release of cytokinase from damaged cells of the pancreas parenchyma. Under the action of cytokinase, trypsinogen turns into 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 full body of knowledge: Mediators of allergic reactions). Bradykinin can also be formed directly from kininogen. Under the influence of trypsin, histamine (see full body of knowledge) and serotonin (see full body of knowledge) are released from various cells of the pancreas. Through the lymphatic and circulatory routes, pancreatic enzymes enter the general bloodstream. In the blood, trypsin activates the Hageman factor (see full body of knowledge: Blood coagulation system) and plasminogen and thereby affects the processes of hemocoagulation and fibrinolysis.

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

In conditions of impaired local blood circulation, tissue metabolism and the direct action of enzymes on cells, foci of necrosis of the pancreatic parenchyma and surrounding adipose tissue arise. This is facilitated by thrombus formation, which is most characteristic of hemorrhagic forms of 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, causing steatonecrosis of distant organs.

General changes in the body are caused initially 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 into tissues and cavities, profound functional and morphological changes in internal organs and other reasons cause severe disturbances in water-electrolyte, carbohydrate, protein and fat metabolism.

Pathological anatomy

Pathologically, acute pancreatitis is based on primary destructive changes in the acini, caused by intraorgan (intracellular) activation of digestive enzymes produced by the pancreas. The developing enzymatic autolysis of acinar cells is accompanied by the formation of foci of necrosis and aseptic (abacterial) inflammation. Therefore, the classification of acute pancreatitis into 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 is usually a complication of pancreatic necrosis; it develops in the late stages of the disease due to microbial infection of foci of necrosis. 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 pathological classification of Pancreatitis. Most pathologists distinguish between necrotic and hemorrhagic-interstitial forms of acute pancreatitis, acute serous, and acute purulent pancreatitis

Acute serous pancreatitis (acute swelling of the pancreas) most often undergoes reverse development and only sometimes becomes destructive. However, with lightning-fast development of the disease, death can occur from enzyme shock in the first three days, when destruction of the gland has not yet occurred. These cases are difficult for pathological diagnosis, since macroscopic changes in the pancreas (edema) do not correspond to the severity of the clinical course. Damage to the gland can be indicated only by a few fat necrosis (see full body of knowledge) found in the surrounding tissue (color figure 1). Microscopically, changes corresponding to diffuse focal pancreatitis are usually found in the gland itself (color figure 2). A similar course of Pancreatitis is observed, as a rule, in chronic alcoholism.

Pathoanatomical changes in the gland in hemorrhagic-necrotizing 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 increased 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 omentum, kidney capsule, and intestinal mesentery, scattered small yellow foci of fat necrosis can be found in combination with serous and serous-hemorrhagic effusion in the peritoneal cavity (color Figure 4 ).

The macroscopic appearance 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 during these periods, foci of necrosis with a diameter of 0.2-1 centimeters are yellow or reddish in color, clearly demarcated from the remaining parenchyma of the gland. Microscopically, progressive sclerosis of necrotic areas, gradual disintegration of leukocytes and a change in the cellular composition of the inflammatory infiltrate by lymphoplasma cell and histiocytic elements are noted.

Foci of fat necrosis of the surrounding tissue are either absent or present in small quantities. The pancreatic capsule is not subject to destruction.

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

In the large-focal form of pancreatitis, one or several foci of necrosis are formed measuring 2 × 3 - 3 × 4 centimeters, which, unlike a heart attack, have irregular outlines. Foci of necrosis are usually yellow in color and involve the capsule of the gland. Their evolution, as well as the outcome of the disease, depend on the depth of the lesion and location (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 damage to the walls of blood vessels and large ducts. Large foci of necrosis of this localization often undergo diffuse melting and sequestration with the formation of an abscess (intraorgan, omental bursa) or false cyst (see full body of knowledge: Pancreas).

The cyst cavity (color figure 5), as a rule, is associated with the ducts of the gland, through which secretions are constantly discharged.

With progressive variants of acute pancreatitis, the initial stage of serous edema of the pancreas very early gives way to 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 tissue. 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 stage of formation of a massive inflammatory infiltrate in the gland area, in which not only the gland is involved in the inflammatory process, but also 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 moving into the stage of sequestration.

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

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

The walls of the omental bursa abscess are formed by 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 fused into one conglomerate, making laparotomy difficult. This conglomerate is sometimes mistaken for a tumor. The contents of an abscess are usually represented by tissue detritus, pus and pancreatic secretions. Further evolution of the abscess occurs in the following main variants: 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, breakthrough into the free peritoneal cavity with the development purulent peritonitis (cm).

The severity of large-focal acute pancreatitis also depends on the extent of fat necrosis. In severe extraorgan lesions, melting of the retroperitoneal tissue is observed, followed by the formation of parapancreatic phlegmon, which then spreads throughout the retroperitoneal space.

Subtotal (total) form of 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 fat necrosis and acini necrosis, located mainly along the periphery of the pancreatic lobules, are detected. In foci of necrosis, thrombosis of capillaries, venules and parietal thrombosis of larger veins is naturally detected (color figure 6). Disorders of hemocirculation in the intraorgan veins are accompanied by extensive hemorrhages and hemorrhagic penetration of the gland parenchyma. The degree of damage to the venous bed, apparently, mainly determines both the hemorrhagic nature of necrosis and its scale.

Violations of capillary permeability already in the first 1-2 hours after the destruction of 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 the inflammatory reaction (see 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 lymphoplasma 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 fields of fibrosis (color figure 9-13).

When a cyst or abscess forms, microscopically, their walls are represented by hyalinized fibrous tissue with diffuse focal infiltrates consisting of lymphocytes, plasma cells and histiocytes. The inner lining of the abscess is usually covered with necrotic plaque and fibrin with leukocyte detritus and individual preserved 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 the 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 from the normal merocrine type of secretion 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, into the basal sections of the cytoplasm of acinar cells. Moreover, any destruction of the basement membrane inevitably leads to the 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. Secretion resorption is facilitated by concomitant damage to the capillary endothelium and intense stromal edema. 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 half of the abdomen of a girdle nature is the leading and most constant symptom of acute pancreatitis. In some cases, irradiation of pain behind the sternum and into the heart area is observed. The intensity of pain is associated with irritation of receptors, increased pressure in the common bile duct and pancreatic ducts, and the chemical effect of trypsin.

Due to the sharp pain, patients are restless and constantly change positions without getting relief. Pain is especially pronounced during temorrhagic 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, so the intensity of pain cannot always be used to judge the extent of damage to the pancreas.

Nausea and vomiting are the second leading symptom of acute pancreatitis. Vomiting is often painful, indomitable, and does not bring 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 and covered with sticky sweat. Quite often, acute pancreatitis is accompanied by obstructive jaundice (see full body of knowledge), caused by obstruction of the common bile duct with gallstones or compression of it by the inflammatory infiltrate in the head of the pancreas.

Pathognomonic signs of destructive Pancreatitis are described - areas of cyanosis of the skin or subcutaneous hemorrhages around the navel, on the lateral areas of the abdomen, the anterior abdominal wall, and face.

Body temperature, in the first hours of the disease, is normal or low, but increases with the addition of inflammatory phenomena. A high temperature that does not tend to decrease is often a sign of destructive pancreatitis, and a later increase in temperature of a hectic nature is a sign of purulent complications (retroperitoneal phlegmon, abscess formation).

At the beginning of the disease, bradycardia is often observed; later, as intoxication increases, the pulse rate usually gradually increases. With the edematous form of acute pancreatitis, arterial hypertension is possible, and with 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 bursa; necrosis of the stomach wall, transverse colon; pancreatic fistulas internal and external; false pancreatic cyst; arrosive bleeding.

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

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

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

Diagnosis

Physical examination. The tongue in acute pancreatitis is usually dry, covered 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 parts. 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 areas. Peristalsis is sharply weakened or cannot be heard, gases do not pass away.

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

Other symptoms of acute pancreatitis that have a certain diagnostic value are described: Voskresensky’s symptom (disappearance of aortic pulsation in the epigastric region), Razdolsky’s (pain on percussion over the pancreas), Kach’s (hyperesthesia along the paravertebral line on the left, corresponding to segments Th VII-IX), Machova (hyperesthesia above the navel) and others

Laboratory research methods. Hematological changes usually occur in destructive forms of the disease. Some patients exhibit hypochromic anemia, although, according to V.V. Chaplinsky, V.M. Lashchevker (1978) and others, with severe dehydration in the first two days, erythrocytosis may be observed. 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 ROE 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: Wolgemut method). An increase in its activity, reaching 8192-32768 units (according to the Wolgemut method, in which normal values ​​do not exceed 16-128 units), is observed in more than 70% of patients. However, low enzyme activity 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 may be normal, but in the blood it may be sharply increased and reach 400-500 units (according to the Smith-Rowe method, in which normal values ​​do not exceed 100-120 units ). Typically, trypsin activity increases and trypsin inhibitor activity decreases. Determination of lipase activity due to significant fluctuations in normal conditions 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. In this case, it is important to dynamically study enzyme activity.

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

Determining the concentration of potassium, sodium, calcium ions in the blood, as well as sugar, total protein and protein fractions allows us to assess the severity of the patient’s condition and the degree of disruption of the corresponding types of metabolism.

Changes in the blood coagulation system also depend on the form of the disease. In the edematous form and fatty pancreatitis, hypercoagulation is usually observed; in hemorrhagic pancreatitis, hypocoagulation is observed. Hyperfibrinogenemia and increased C-reactive protein are almost always observed. According to V. S. Savelyev and co-authors (1973), G. A. Buromskaya and co-authors (1979), changes in the kallikrein-kinin system are characterized by a decrease in the level of kininogen, prekallikrein, kallikrein inhibitor, which is most pronounced in destructive pancreatitis

Changes in daily and hourly diuresis to a certain extent depend on the severity of damage to the pancreas. A sharp decrease in daily and hourly diuresis, anuria is 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 abdominal cavity 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.

With a contrast X-ray examination, the gastrointestinal tract is revealed due to an enlargement of the pancreas and swelling of the lesser omentum and retroperitoneal tissue, 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 full body of knowledge: Computed tomography) reveals an enlargement of the pancreas. In 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 abscess cavities are visible.

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 are determined. With pancreatic necrosis, V.I. Prokubovsky (1975) noted a weakening or disappearance of the shadow of the intraorgan vessels of the pancreas, displacement of the gastroduodenal artery to the right, angular deformation and upward displacement of the common hepatic artery.

Special research methods. Ultrasound diagnostics (see full body of knowledge) allows you to distinguish 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 demarcation from the surrounding tissues remains, and transmission pulsation from the aorta appears. With destructive pancreatitis, the pancreas loses its homogeneity, its contours merge with the surrounding background, and structureless areas are found. With the development of a pseudocyst, a homogeneous formation with a well-defined capsule is determined, pushing aside neighboring organs. If there is effusion in the abdominal cavity, echolocation allows you to determine it in the amount of 200 milliliters.

With gastroscopy (see full body of knowledge) and duodenoscopy (see full body of knowledge), usually performed in difficult diagnostic cases, the following signs of acute pancreatitis can be detected: a) pushing back of the posterior wall of the body and the pylorus of the stomach; 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. Retraction of the posterior wall of the stomach in combination with pronounced inflammatory changes are signs of an abscess of the omental bursa.

Laparoscopy is of great importance in the diagnosis of acute pancreatitis (see 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 omentum, gastrocolic ligament, sometimes on the peritoneum of the anterior abdominal wall, round ligament of the liver, mesenteries 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 is serous in nature. The amount of exudate varies - from 10-15 milliliters to several liters. Evidence of the pancreatogenic nature of such peritonitis is a sharp increase in the activity of pancreatic enzymes in the exudate. The study of trypsin and lipase activity in the exudate is of less importance.

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

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

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

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

Differentiation of edematous and destructive forms of Pancreatitis, which are 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 of edematous pancreatitis subside, and the patient’s condition improves. The symptoms of destructive pancreatitis, despite the therapy, persist for a long time, the patient’s condition improves slightly. As the process progresses, it worsens: tachycardia intensifies, 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 cases that are difficult to diagnose, laparoscopy and other instrumental research methods become necessary.

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

Treatment

If the patient’s condition is serious, treatment measures should begin at the pre-hospital stage. They should be aimed at combating severe pain and arterial hypotension, that is, include elements of infusion therapy (polyglucin, hemodez and others), as well as the use of cardiac glycosides, analeptics, stimulating respiration, analgesics, except narcotics.

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

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

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

Elimination of pain and various neuroreflex disorders is achieved by prescribing analgesics, antispasmodics, ganglion blockers (pentamine, benzohexonium, etc.), as well as perinephric blockade (see full body of knowledge: Novocaine blockade) or blockade of the round ligament of the liver.

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

Therapeutic measures carried out 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 prescribing hunger, atropine and local cold. In severe cases of the disease, local hypothermia of the gland or the administration of cytostatics are more effective.

Cooling of the pancreas is carried out by local gastric hypothermia (see 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, and severe disturbances in acid-base balance due to loss of gastric juice during the open method limit the use of hypothermia in clinical practice, especially in elderly and senile patients.

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

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 the inhibition of the excretory function of pancreatic cells. Experimental studies by Yu. A. Nesterenko and co-workers (1979) established 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. When administered intravenously, this dose can be increased by 2-3 times. The use of cytostatics is indicated for destructive pancreatitis. Their use is inappropriate in patients with total pancreatic necrosis, purulent complications of pancreatitis and renal and hepatic failure.

The removal of pancreatic enzymes and detoxification of the body is carried out using 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 products of cellular breakdown are excreted by the kidneys. The method of forced diuresis includes water load, administration of diuretics, correction of electrolyte and protein balance. The main components of the administered fluid can be 5-10% glucose solution, Ringer's solution, rheopolyglucin, saline solution. With the intravenous method, 5-6 liters of liquid are administered daily for 3-10 days. Diuresis is forced by introducing diuretics (Lasix, mannitol) after infusion of every 2 liters of liquid and ensuring that the daily diuresis reaches 3½-4 liters.

According to G. A. Buromskaya and co-workers (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, with this method, toxic products are removed directly from the pancreatic cells, which causes a more pronounced detoxification effect. The volume of intra-arterial fluid administered depends on the intoxication and 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, monitoring of central venous pressure, hematocrit, average diameter of erythrocytes, indicators of circulating blood volume, acid-base balance, and electrolyte levels is necessary.

Anti-enzyme drugs (trasylol, contrical, tzalol, pantrypin, gordox and others) play an important role in the fight against enzymatic toxemia. They must be administered in large doses over 3-5 days.

Drainage of the thoracic lymphatic duct (see full body of knowledge: Thoracic duct) is carried out in 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, cleared of toxic products and pancreatic enzymes by filtration through ion exchange columns (see full body of knowledge: Lymphosorption), is reinfused into a vein. According to V.M. Buyanova and coworkers (1979), a promising method of detoxifying the body in acute pancreatitis is intravenous liquid lymphostimulation.

Peritoneal dialysis (see full body of knowledge) is indicated when a large amount of serous or hemorrhagic effusion is detected in the abdominal cavity during laparoscopy or laparotomy. Depending on the function of the drains and the patient’s condition, dialysis is continued for 2-4 days.

Prevention and treatment of thromboembolic complications is carried out under the control of thrombosis lastogram and coagulogram indicators. In case of destructive pancreatitis, already in the first hours of the disease in the presence of high fibrinolytic activity and hypertrypsinemia, to prevent widespread intravascular coagulation, it is advisable, in addition to antienzymes, to also administer heparin, low molecular weight solutions (5% glucose solution, hemodez, rheopolyglucin, 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, aminon, 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, zeporin and others) are used.

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

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

It is advisable to divide all operations for acute pancreatitis into three groups: 1) emergency and urgent, performed in the first hours and days of the disease; 2) delayed, which occur in the phase of melting and sequestration of necrotic foci of the pancreas and retroperitoneal tissue, 10-14 days or 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 from the onset of the attack, after completion of the examination of the patient (these operations are intended to prevent relapse of acute pancreatitis).

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

During emergency and urgent operations after laparotomy through the upper midline incision (see full body of knowledge: Laparotomy), an audit of the abdominal cavity is performed, determining the condition of the pancreas, retroperitoneal tissue, parietal peritoneum and biliary tract.

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

Effusion mixed with bile, penetration of the hepatoduodenal ligament with it, an increase in the size of the gallbladder, and dilation 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 injecting the gland with a solution of novocaine with antibiotics and antienzyme drugs.

In case of 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 (pericocolic grooves) is performed. The operation is completed by drainage of the omental bursa, sometimes in combination with omentopancreatopexy, or drainage of the peritoneal cavity followed by peritoneal dialysis.

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

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

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 area of ​​gland necrosis is clearly defined no earlier than the 10th day after an attack of acute pancreatitis. Sequestrectomy, that is, removal of rejected necrotic areas of the gland and retroperitoneal tissue, is usually possible no earlier than 3-4 th weeks from the onset of the disease.

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

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

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

Tampons from the omental bursa are changed on the 7-8th day, trying to form a wide wound channel, which is periodically washed with antiseptic solutions (furacilin, rivanol, iodinol).

In the sequestration phase, arrosive bleeding may occur. Sometimes they can be caused by disorders of the blood coagulation system. In case of profuse bleeding, vessels are sutured and ligated in the wound or throughout, or they are embolized, tamponade or pancreatic resection. For fibrinolytic bleeding, direct blood transfusions are indicated (see full body of knowledge: Blood transfusion) and the introduction of fibrinolysis inhibitors - γ-aminocaproic acid, antienzymes and others

Pancreatic fistulas occur as a result of ongoing purulent destruction or after surgery for pancreatic necrosis. In most cases, with conservative treatment, especially when using 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, through the destroyed excretory ducts, the secretion of pancreatic juice continues into the site of destruction, which is delimited by newly formed connective tissue, which gradually forms the wall of the cyst. A pancreatic pseudocyst can suppurate, perforate, or, by squeezing neighboring organs, cause obstruction of the intestine or common bile duct. The method of choice for surgical treatment of postnecrotic pseudocysts is pancreatocystoentero and pancreatocystogastroanastomosis. If the cyst is located distally, pancreatic resection is indicated; When suppuration occurs, the cysts produce marsupialization (see full body of knowledge).

Prevention

Clinical examination of patients who have suffered acute pancreatitis is advisable. Considering the important role of diseases of the biliary tract in the occurrence of acute pancreatitis, their sanitation is an effective measure to prevent relapse 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 gastrointestinal sanatoriums (Borjomi, Zheleznovodsk, Truskavets, Krainka, Karlovy Vary).

Features of acute pancreatitis in elderly and senile age

Elderly and senile patients make up more than 25% of patients with acute pancreatitis. This is explained primarily by the increase in the number of people of this age in the population. Age-related changes in the pancreas are also of no small importance, in particular such as deformation of the ducts with obliteration and expansion, desolation of the blood 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 liver and bile ducts, stomach, duodenum and colon, and cardiovascular system.

Along with the usual pathomorphological picture of the disease, patients in this age group often experience pancreatic apoplexy or massive fat necrosis due to lipomatosis of the glandular stroma.

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 severe dysfunction of vital organs and systems. Therefore, the course of the disease is often accompanied by the development of acute cardiovascular, respiratory, hepatic-renal failure, 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. Complex conservative treatment of acute pancreatitis in elderly and senile patients must necessarily include measures for the treatment of concomitant diseases, primarily the cardiovascular and respiratory systems, prevention and treatment of hepatic-renal failure, and carbohydrate metabolism disorders. In this regard, treatment of such patients is carried out in the intensive care ward or resuscitation department.

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, the etiological factors remain unclear; In this regard, suddenly occurring acute pancreatitis in children is usually called idiopathic.

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

Acute edema of the pancreas in children (especially 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.” Symptomatic treatment leads to a rapid improvement in general condition. Only a special examination allows you to make a correct diagnosis. In older children, the disease begins with acute pain in the abdomen, initially diffuse and then localized in the epigastric region or of a girdling nature. Less commonly, a gradual increase in pain is observed. At the same time, repeated vomiting and 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 satisfactory, rhythmic, rapid, blood pressure is normal or slightly reduced. On examination, pallor of the skin is noted. The abdomen is of the correct shape, not swollen, and participates in the act of breathing. Palpation of the anterior abdominal wall is painless, the abdomen is soft. Such a discrepancy between severe abdominal pain and the lack of objective data indicating the presence of an acute disease of the abdominal organs is typical specifically for 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 amylase activity in the blood. Somewhat later, the amylase content in the urine increases. As a rule, moderate hyperglycemia is observed.

Hemorrhagic and fat necrosis is accompanied by severe symptoms and a severe course. In young children, the disease manifests itself as rapidly increasing anxiety. The child screams and rushes about in pain, takes a forced position. Gradually, motor restlessness gives way to adynamia. Older children usually indicate the localization of pain in the upper abdomen, its encircling nature, irradiation to the supraclavicular region, the scapula. Repeated vomiting appears, exhausting the child. The general condition is progressively worsening. The skin is pale, with a cyanotic tint. Exicosis and severe intoxication develop. The tongue is dry and coated. The pulse is frequent, sometimes weak, and 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 stomach actively participates in the act of breathing. Percussion and palpation are slightly painful. Tension of the muscles of the anterior abdominal wall is weakly expressed. Then intestinal paresis develops, pain on palpation intensifies, and symptoms of peritoneal irritation appear. Body temperature rises, significant leukocytosis is characteristic. A disturbance in the water-electrolyte balance occurs, and the amount of sugar in the blood increases. The concentration of amylase in the blood and urine increases sharply. A decrease in its level is a poor prognostic sign.

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

X-ray examinations in children, as a rule, are not very 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 diagnosis, all children are prescribed a set of therapeutic measures aimed at combating pain, intoxication and secondary infection. An important task is to create functional rest of the pancreas, block its enzyme-forming function, and combat water-electrolyte imbalances.

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, surgical intervention 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 require long-term (up to 2 years) follow-up with a surgeon and endocrinologist.

Chronic pancreatitis

Chronic Pancreatitis occurs frequently - according to sectional data, from 0.18 to 6% of cases. However, in clinical practice, this disease seems to occur even more often, but is not always diagnosed. Typically, 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 in the pancreas from the very beginning, 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 prolonged acute Pancreatitis can become chronic. But more often, chronic Pancreatitis occurs gradually under the influence of factors such as unsystematic irregular nutrition, frequent consumption of spicy and fatty foods, chronic alcoholism, especially in combination with a deficiency of proteins and vitamins in food. According to J. A. Benson, in the USA, chronic recurrent Pancreatitis occurs in 75% of cases 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 damage to the vessels of the pancreas, infectious diseases, and exogenous intoxications. Sometimes Pancreatitis occurs after surgery on the biliary tract or stomach. A more rare cause is damage to the pancreas with periarteritis nodosa, thrombocytopenic purpura, hemochromatosis, and 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 secretion of pancreatic juice into the duodenum, caused by spasm or stenosis of the ampulla 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 carry out autolysis of the pancreatic parenchyma. Activation of elastase and some other enzymes leads to damage to the blood vessels of the pancreas. The action of kinins on the smallest vessels leads to the development of edema. The hydrophilic effect of decomposition products in foci of necrosis of pancreatic tissue also contributes to edema, and subsequently to the formation of false cysts. In the development, especially the progression of the chronic inflammatory process, the processes of autoaggression are of great importance.

In chronic gastritis (see full body of knowledge) and duodenitis (see 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 case of chronic pancreatitis of infectious origin, the pathogen can enter 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 divided into chronic recurrent Pancreatitis and chronic sclerosing Pancreatitis

Chronic recurrent Pancreatitis is essentially a prolonged version of acute small-focal pancreatic necrosis, since any 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 to be slightly increased in volume and diffusely denser. Microscopically, fresh and organizing foci of necrosis of parenchyma and fatty tissue are found in it, alternating with scar fields, foci of calcification, and small pseudocysts devoid of epithelial lining. There is also significant deformation and expansion of the lumen of the excretory ducts, containing compacted secretions and often microliths. In some cases, diffuse focal calcification of the interstitium is observed, and then they speak of chronic calcific pancreatitis

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

Chronic sclerosing pancreatitis is characterized by diffuse thickening and a decrease in the size of the pancreas. The gland tissue acquires a stony density and macroscopically resembles a tumor. Microscopically, diffuse focal and segmental sclerosis is detected with progressive proliferation of connective tissue around the ducts, lobules and inside the acini. The cause of sclerosis is a constant loss of parenchyma, occurring 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 difficult to detect. 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 lumens of the dilated excretory ducts, thickened secretions, crystalline deposits of lime, and microliths are constantly found. A large number of hyperplastic pancreatic islets (Langerhans) are found in the circumference of the ducts. New formation of acini does not occur; necrosis of the gland parenchyma is replaced by a scar.

As with the recurrent form of Pancreatitis, lymphoplasmacytic infiltrates can be found among the fields of fibrous tissue, which are a reflection of autoimmune processes. In this case, morphologically in the pancreas, it is not necrotic, but dystrophic-atrophic changes in the acini with their slow replacement by connective tissue that predominate.

With all variants of chronic pancreatitis, the same complications are observed. Most often, cicatricial stricture of the pancreatic duct occurs, as well as blockage by a stone or adenomatous polyp. In this case, obstruction of the common bile duct with the development of obstructive jaundice is possible. Thrombosis of the splenic vein is sometimes observed. Diabetes mellitus often develops against the background of chronic pancreatitis, although, unlike acini, the islets of Langerhans regenerate well, and they can always be found among 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 symptoms; 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 process predominantly localized in the head of the pancreas); when her body is involved in the inflammatory process, pain is observed in the epigastric region; if her tail is affected - in the left hypochondrium. Often the pain radiates to the back (at the level of the X-XII thoracic vertebrae) or has a girdling character, intensifies when the patient lies on his back and can weaken in a sitting position, especially with a slight bend forward. The pain can also radiate to the heart area, simulating angina pectoris, to the left shoulder blade, left shoulder, and sometimes to the left iliac region. The intensity and nature of the pain varies; they can be constant (pressing, aching), appear some time after eating (as with a peptic ulcer), especially after eating fatty or spicy foods, or be paroxysmal like pancreatic colic.

Dyspeptic symptoms (pancreatic dyspepsia) are common, especially with exacerbation of the disease or severe course of the disease. Many patients also note loss of appetite and aversion to fatty foods. At the same time, with the development of diabetes, patients may feel severe hunger and thirst. Increased salivation, belching, nausea, vomiting, and flatulence are often observed. In mild cases, stool is normal; in more severe cases, there is a tendency to diarrhea or alternating constipation and diarrhea. However, in typical advanced cases of chronic pancreatitis (in the presence of obvious signs of exocrine pancreatic insufficiency), pancreatic diarrhea with the release of copious mushy, foul-smelling, greasy feces is more typical.

Due to the development of exocrine pancreatic insufficiency and disruption of the processes of digestion and absorption in the intestines, 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 caused by the long-term effect of alcohol on the central nervous system

The course of the disease is usually protracted. There are 5 forms of the disease: 1) a recurrent form, characterized by distinct periods of remission and exacerbations of the process; 2) painful form, occurring with constant pain dominating the clinical picture; 3) pseudotumor form; 4) latent (painless) form; 5) sclerosing form, which is characterized by early 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 and her colleagues (1978) distinguish 3 forms of chronic pancreatitis: mild, moderate and severe. The latter occurs with persistent diarrhea, dystrophic disorders, and increasing exhaustion.

Diagnosis

Physical examination. When palpating the abdomen in patients with chronic pancreatitis, pain in the epigastric region and left hypochondrium is usually characteristic. A number of researchers have described pain points and areas in which pain is especially characteristic. Thus, if the head of the pancreas is affected, pain can be observed with pressure at the so-called pancreatic point of Desjardins, located in the area of ​​projection onto the anterior abdominal wall of the distal pancreatic duct (approximately 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 midline of the body and the perpendicular lowered to the last line from Desjardins’ point. Often there is a painful point in the costovertebral angle (Mayo-Robson symptom). Sometimes there is a zone of cutaneous 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 area of ​​​​the projection of the pancreas onto the anterior abdominal wall, described by A. A. Shelagurov (1970). It is very rare to palpate an enlarged and thickened pancreas in chronic pancreatitis.

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

Laboratory research methods often reveal in patients with chronic pancreatitis moderate hypochromic anemia, accelerated ROE, neutrophilic leukocytosis, dysproteinemia due to increased globulin content, increased activity of transaminases and aldolase in the blood serum. When the islet apparatus of the pancreas is damaged, hyperglycemia (see full body of knowledge) and glycosuria (see full body of knowledge) are detected, however, to identify mild degrees of carbohydrate metabolism disorders, it is necessary to study the sugar curve with a double load of glucose (see full body of knowledge: Carbohydrates, methods of determination) . In cases of violations of the exocrine function of the pancreas, more or less pronounced hypoproteinemia is usually detected; in more severe cases - disturbance of electrolyte metabolism, in particular hyponatremia (see full body of knowledge). 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 full body of knowledge: Duodenal intubation), 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 testing of the content of pancreatic enzymes in duodenal juice, blood, as well as amylasuria makes it possible to reflect the state of the exocrine function of the pancreas in patients with chronic pancreatitis much more accurately than conducting these studies separately on different days.

Hyperamylasuria, which sometimes reaches 2048-4096 units in chronic pancreatitis (according to Wolgemut), 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 the period of exacerbation of pancreatitis, as well as when there are 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 examination (see full body of knowledge: Feces) reveals an increased content of undigested food in the feces (steatorrhea, creatorrhoea, amilorrhea, kitarhinorrhea). According to Austad (W. J. Austad, 1979), persistent steatorrhea in chronic II. appears when the external secretion of the pancreas decreases by at least 90%.

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

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

With celiacography, two forms of chronic pancreatitis can be distinguished. For the first form, enlargement of the pancreas, its hypervascularization and inhomogeneous contrast in the parenchymal phase are typical (Figure 3). The second form is more typical for Pancreatitis with pronounced fibrous 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 Tylen Arnesjo (H. Tylen, B. Arnesjo, 1973), stenoses of large arteries outside the pancreas were observed - the proper hepatic, gastroduodenal, and splenic. The contours of the narrowed areas remained smooth, while in pancreatic cancer they had a “corroded” character. Pseudocysts appear as rounded avascular formations that displace adjacent arterial branches. During surgery and in the postoperative period (if a catheter is left in the pancreatic ducts or cyst cavity for drainage), pancreatography can be performed to clarify the condition of the ducts (see full body of knowledge). If, after surgery for a cyst, an external or internal pancreatic fistula has formed, 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.

Echography allows us 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 pancreatic tumor (see full body of knowledge); In this case, instrumental diagnostic methods 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), gastric and duodenal ulcers, chronic enteritis and others.

Rice. 1. Microscopic specimen of fiber for acute pancreatitis: the focus of fat necrosis is indicated by arrows; hematoxylin-eosin staining; × 80. Rice. 2. Macroscopic specimen of the pancreas for diffuse focal pancreatitis: small foci of fat necrosis. Rice. 3. Macropreparation of the pancreas for total hemorrhagic pancreatic necrosis: increase in size and hemorrhagic penetration of the gland tissue. Rice. 4. Macroscopic specimen 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. Microscopic specimen of the pancreas in acute pancreatitis: the arrow indicates a thrombus in the lumen of the vein; Mallory staining; × 80. Rice. 7. Microscopic specimen of the pancreas for hemorrhagic pancreatic necrosis: extensive hemorrhages (indicated by arrows) into the gland tissue; Mallory staining; × 80.

Rice. 8. Microscopic specimen of the pancreas for pancreatic necrosis: the necrosis zone (1) is delimited by a leukocyte infiltrate (2) and a granulation shaft (3); hematoxylin-eosin staining; × 80. Rice. 9. Microscopic specimen of the pancreas for chronic pancreatitis; fresh focus of necrosis (1) against the background of fibrosis (2) of the gland; hematoxylin-eosin staining; × 80. Rice. 10. Microscopic specimen of the pancreas in chronic recurrent pancreatitis: a calculus is visible in the dilated duct (1), the gland tissue is penetrated by strands of connective tissue (2); hematoxylin-eosin staining; × 80. Microscopic specimens of the pancreas for 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; Van Gieson staining, × 80. Rice. 12. Among the fibrous tissue (1) many islets of Langerhans (2), an enlarged duct (3) with papillomatous proliferation of the epithelium are visible; hematoxylin-eosin staining, × 80. Rice. 13. In the circle of individual acini (1) proliferating ducts (2) are visible, forming adenomatous foci; hematoxylin-eosin staining; × 36.

Treatment

Conservative treatment is carried out in the initial stages of the disease and in the absence of complications. During periods of severe exacerbation, hospital 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, combating pain, and compensating for disorders of external and intrasecretory pancreatic insufficiency.

The patient's meals should be divided, 5-6 times a day, in small portions. Avoid 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 proteins, of which 60-70 g are of animal origin (lean meats, fish, low-fat cottage cheese, mild cheese). The fat content 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 mellitus they are completely excluded. All food is given warm, since cold dishes can increase intestinal dyskinesia and cause spasm of the sphincter of Oddi.

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

In case of exocrine pancreatic insufficiency, enzyme preparations are prescribed for replacement therapy: pancreatin, abomin, cholenzym, 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, and cocarboxylase are also prescribed. In the fight against increasing dysproteinemia, it is advisable to use protein blood products (aminoblood, casein hydrolysate, etc.). Intrasecretory pancreatic insufficiency requires an appropriate diet and therapeutic measures.

After the removal of acute phenomena and in order to prevent exacerbation in the remission stage, resort treatment in gastroenterological sanatoriums (Borjomi, Essentuki, Zheleznovodsk, Pyatigorsk, Karlovy Vary) is recommended.

Surgical treatment. Indications: cysts and long-term non-healing external pancreatic fistulas; gland duct calculi; stenosis of the pancreatic duct with impaired outflow of pancreatic juice; indurative (pseudotumor) Pancreatitis, especially in the presence of jaundice; persistent pain syndrome that does not respond to conservative measures.

The type of surgical intervention on the pancreas for chronic pancreatitis depends on the nature of the damage to 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 prevent the development of intraductal pancreatic hypertension.

For obstructive (gallstone) and stenotic 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 blockage with a stone, a virzungotomy (plasty) is also performed.

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

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

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

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

In case of recurrent chronic pancreatitis with significant damage to the gland tissue in the area of ​​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 70s, intraoperative occlusion of the pancreatic ducts with alloplastic material has been used in clinical practice, which leads to inhibition of its external secretion.

Surgeries on the pancreas for chronic pancreatitis can be complicated by pancreatic necrosis, peritonitis, bleeding and others. In the postoperative period, the complex of conservative measures taken must necessarily include the prophylactic administration of antienzyme drugs and cytostatics.

Prevention

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

Features of chronic pancreatitis in old and senile age

Various forms of chronic pancreatitis in elderly and senile people are more common than in earlier age groups. Moreover, 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. Shelagurova (1970) and others, with age, in the pathogenesis of Pancreatitis, progressive atherosclerotic damage to 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 elderly people is polymorphic; Sometimes concomitant diseases obscure the clinical picture of the disease. However, a comparative study of the course of the painful 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 when there are errors in the diet, especially after physical activity. With a long course of the disease, significant weight loss is observed, and dyspeptic disorders occur more often than in young people. The exocrine function of the pancreas decreases in old age, which makes it difficult to use its study data to diagnose the disease.

Treatment of chronic pancreatitis in old age has its own characteristics. When prescribing a diet, one should take into account the concomitant diseases that such patients often have (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 indicated for longer treatment with pancreatic enzymatic preparations (pancreatin, panzinorm, festal, etc.). Surgical treatment of chronic pancreatitis in this group of patients is used only for unresolved jaundice caused by compression of the common bile 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 ligating 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: reproduction of Pancreatitis 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 therapy for experimental pancreatitis. There are at least 100 models of Pancreatitis, which can be roughly systematized as follows.

Obstructive-hypertensive Pancreatitis„ caused by a temporary or permanent increase in pressure in the pancreatic duct system by ligating them 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 own secretion of the gland parenchyma. The works of I. Pancreatitis Pavlov have proven that ligation of the pancreatic duct does not cause Pancreatitis, but is accompanied by gradual atrophy of the exocrine parenchyma. If secretion is stimulated against this background, then Pancreatitis, as a rule, develops. This group should also include models of pancreatitis caused by dosed or prolonged duodenal hypertension, which promotes the reflux of intestinal contents into the pancreatic ducts.

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

Allergic models of Pancreatitis are created by sensitizing animals with horse serum or meningococcal endotoxin. A resolving dose of the agent is injected into one of the pancreaticoduodenal arteries or into the gland tissue. This group also includes the so-called paraallergic models of Pancreatitis, created by sensitizing rabbits or dogs with horse serum according to the generally accepted method, but 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 the sympathetic and parasympathetic nerve trunks with the simultaneous introduction of damaging agents into the gland ducts.

The most effective models of experimental pancreatitis are combined techniques 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 basis of the disease is enzymatic autolysis (see full body of knowledge), developing as a result of impaired synthesis and release of enzymes, focal focal or widespread pancreatic necrosis with a secondary inflammatory reaction, accompanied by thrombosis of the veins, as well as the microvasculature and hemorrhages in the parenchyma of the gland.

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Delayed secretion and intraorgan activation of pancreatic enzymes - trypsin and lipase, which carry out autolysis of the pancreatic parenchyma, reactive growth and cicatricial wrinkling of connective tissue, which then leads to sclerosis of the organ, chronic circulatory disorders in the pancreas. In the professionalization of the inflammatory process, the processes of autoaggression are of great importance. In chronic pancreatitis of infectious origin, the pathogen can enter the pancreas from the lumen of the duodenum (for example, with dysbacteriosis) or from the bile ducts through the pancreatic ducts in an ascending manner, which is facilitated by dyskinesia of the digestive tract, accompanied by duodeno- and choledochopancreatic reflux. Predispose to the occurrence of chronic pancreatitis are spasms, inflammatory stenosis or tumor of the papilla of Vater, 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 the intestinal juice, which activates trypsin. The inflammatory process can be diffuse or limited only to the head or tail of the pancreas. There are chronic edematous (interstitial), parenchymal, sclerosing and calculous pancreatitis.

In the case of severe exacerbation of CP due to the presence of gallstones, indications for cholecystectomy arise.

Basic mechanisms:

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

> Obstruction of 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.

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

Diseases of the duodenum (DPC) and major duodenal papilla (MDP)

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

> Presence of insufficiency of the BDS (hypotension) - papillitis, diverticulitis, stone passage, impaired motor skills;

> Development of duodenal stasis (chronic duodenal obstruction);

> Combinations of these two states.

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

Penetration of an ulcer into the pancreas (secondary pancreatitis).

Nutritional factor

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

Genetically determined pancreatitis

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

Drug-induced pancreatitis

They are rare. Pancreatic-damaging 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, and mumps virus is assumed.

Impaired blood supply

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

Dysmetabolic pancreatitis

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 (Friderichsen I and V). In pathogenesis, obstruction of gland vessels by fatty particles, fatty infiltration of acinar cells, and the appearance of free fatty acids formed as a result of activation of TAG hydrolysis are important.

With hyperparathyroidism, secondary pancreatitis occurs in 10-19% of cases. The calcium content in acinar cells increases (stimulation of enzyme secretion) and 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 blood pressure in the duodenum and pancreatic ducts, relieves spasm of the sphincter of Oddi.

Under the influence of secretin deficiency:

> Pressure in the duodenum increases;

> Spasm of the sphincter of Oddi;

> Pressure in the pancreatic ducts increases;

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

> Reduced bicarbonate secretion;

> Thickening of pancreatic juice and increasing 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 a spasm of the sphincter of Oddi.

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

With a significant periodic increase in the secretory activity of the pancreas (alcohol, spicy food), dilation of the gland ducts initially occurs; in the future, while maintaining secretory activity, the pancreatic secretion is released into the surrounding interstitial tissue,

causing swelling of the pancreas.

In conditions of edema as a result of mechanical compression and disruption 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, the basal membrane of the acinar cells ruptures with the release of enzymes into the surrounding tissue (activation of proteases and limited self-digestion of the gland (tryptic recurrent form).

Activation of KKS is important in the pathogenesis of chronic pancreatitis,

coagulation and fibrinolytic systems (development of thrombosis, hemorrhages,

necrosis, microcirculation disturbance).

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 a violation of the formation of soluble protein-calcium associates. At the earliest stages of CCP formation, protein precipitates are detected in the pancreatic ducts. They are insoluble fibrillar protein combined with calcium carbonate deposits. This protein was 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 CCP, the possibility of synthesizing the total pool of lipostatin decreases under conditions of increased need 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 etiology

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 characteristics

1) Edema form

2) Sclerotic-atrophic form

3) Fibrous (diffuse, diffuse nodular form)

4) Pseudotumorous form

5) Calcifying form

III. According to the specifics 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) Mild pancreatitis (I stage of the disease - initial)

2) Moderate pancreatitis (grade II)

3) Severe pancreatitis (III degree - Terminal, cachetic).

At stage I signs of disturbance of intra- and exocrine function are not expressed.

At II and III stages. there are signs of impairment of external and/or intrasecretory function (secondary diabetes mellitus).

At stage III persistent “pancreatogenic” diarrhea is observed,

polyhypovitaminosis, exhaustion.

Marseille-Roman classification (1988)

I. Chronic calcific pancreatitis. 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 ducts of the pancreas, thickening of the secretion occurs with the formation of plugs rich in protein and calcium. In this process, a decrease in the concentration of lithostatin (a protein that prevents stone formation) plays an important role.

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 is preserved. Occurs infrequently.

III. Chronic fibrous-indurative (parenchymal, inflammatory) pancreatitis. It is characterized by fibrosis, mononuclear cell infiltration and atrophy of exocrine tissue. 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) Parenchymatous

3) Fibrous-sclerotic

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 (hypochondriacal)

4) Latent

5) Combined

Intravenous According to the nature of the clinical course

1) Rarely recurrent

2) Often recurrent

3) With constant symptoms of chronic pancreatitis

Clinical picture, course options, complications, outcomes

The clinical picture is characterized by 3 main syndromes:

> Pain syndrome;