PANCREATITIS

From Big Medical Encyclopedia

PANCREATITIS (pancreatitis; grech, pankreas, pankreatos a pancreas + - itis) — an inflammation of a pancreas.

In a wedge, practice two main forms of a disease — acute and chronic P.

Acute pancreatitis

Acute P. — the inflammatory and necrotic damage of a pancreas developing as a result of an enzymatic autolysis, or self-digestion meet.

Classification

St. 40 classifications of the acute Item V the All-Russian congress of surgeons in 1978 Are offered P. recommended to use the following classification acute: 1) edematous P.; 2) fatty pancreatonecrosis; 3) hemorrhagic pancreatonecrosis; 4) purulent Item. This classification based on morfol the principle, does not reflect other aspects of a disease which are important for to lay down. tactics. For more exact assessment the wedge, currents need to be allocated three phases of a disease: 1) phase of an enzymatic toxaemia; 2) a phase of times - ache remissions; 3) phase of sequestration and purulent complications.

At the complicated P.'s current it is necessary to estimate prevalence of peritonitis and character of an exudate in a peritoneal cavity. At distribution of process on retroperitoneal cellulose it is necessary to find out extent of defeat it. Besides, it is necessary to consider extent of defeat of tissue of pancreas, a cut can have limited, subtotal or total character. At a fatty pancreatonecrosis the centers of a necrosis on the surface of gland can have focal or drain character.

History

In 1841 N. Tulp reported about the abscess of a pancreas found during the opening of the patient who died at symptoms of an acute abdomen. E. Klebs in 1870 allocated acute P. as an individual disease. R. H. Fitz in 1889 made the message that he distinguished acute P. during lifetime of the patient. This diagnosis then was confirmed at a laparotomy and autopsy.

The first successful operation at acute P. was executed in 1890 by W. S. Halsted.

The first monographs about surgical diseases of a pancreas published A. V. Martynov in 1897, and then in 1898 to W. Korte, the abscess of a pancreas which for the first time successfully opened and recommending active surgical tactics at a pancreatonecrosis.

Statistics

Till 50th 20 century considered acute P. the rare disease found only during operation or at autopsy. According to V. M. Voskresensky (1951), domestic scientists from 1892 to 1941 described only 200 patients with acute P. S of the middle of the 50th along with improvement of diagnosis of a disease increase in incidence of the acute Item is noted. At the same time, according to V. S. Mayat and Yu. A. Nesterenko (1980), growth of number of patients with destructive forms of a disease is especially characteristic. Among acute surgical diseases of abdominal organs of P. takes on frequency the third place after an acute appendicitis and acute cholecystitis. According to G. N. Akzhigitov (1974), acute II. makes 0,47% of all somatopathies and 11,8% of all surgical diseases. Among sick women there were 80,4%, men — 19,6%. Patients with a pancreatonecrosis have a ratio of men and women makes 1: 1. Men aged up to 40 years suffer from P. twice more often than women.

The etiology

Acute P. is the polyetiological disease arising owing to damage of acinous cells of a pancreas, hypersecretion of pancreatic juice and difficulty of its outflow with development of acute hypertensia in pancreat ducts (pancreatic channels) that can lead to activation of enzymes in gland and to development of the acute Item.

Damage of acinous cells can happen at the closed and open injury of a stomach, operative measures on abdominal organs, sharply arising circulatory disturbances in a pancreas (bandaging, thrombosis, an embolism, a prelum of vessels, etc.), exogenous intoxications (alkalis, to-tami, etc.)? heavy allergic reactions, considerable alimentary disturbances, etc.

A role of diseases of bilious channels in genesis acute P. Obshchepriznana. Lansero (E. Lancereaux, 1899) stated a hypothesis of acute P.'s development owing to a pelting of bile in a pancreat duct.

Acute bilious and pancreatic pro-current hypertensia and a reflux of bile in pancreat ducts easily arise in the presence of the general ampoule for the general bilious channel and a pancreat duct in case of sudden blockade of the mouth of a big faterov of a nipple (a nipple of a duodenum), napr, a gallstone, etc. According to E. V. Smirnov with sotr. (1966), K. D. Toskina (1966), etc., in addition to biliary and pancreatic reflux (see), the duodenopankreatichesky reflux can appear an origin of acute P. also. If in the first case pancreatic enzymes are activated bile (see), in the second their activator is the enteropeptidaza. Flowing of duodenal contents in pancreat ducts is possible at a gaping of a big nipple of a duodenum and increase in duodenal pressure.

Pilot studies of N. K. Permyakov with sotr. (1973) showed that as the excess use of food, especially fats and carbohydrates, and its shortcoming, especially proteins, leads to damage of ultrastructures of acinous cells even in the conditions of undisturbed outflow of a pancreatic secret and promotes development primary atsi-noznoy forms P. (metabolic P.).

The role of an alimentary factor increases in acute P.'s development at reception of excess amount of sokogonny food in the conditions of disturbance of outflow of pancreatic juice.

In acute P.'s etiology in some cases can play a role and other factors: endocrine disturbances (giperparatireoidoz, pregnancy, prolonged treatment by corticosteroids, etc.), the inborn or acquired disturbance of a lipometabolism (sharply expressed hyperlipemia), nek-ry inf. diseases (viral parotitis and viral hepatitis).

Carry an allergy to the contributing factors. Still P. D. Solovoye in 1937 explained an origin of a pancreatonecrosis with a giperergichesky inflammation of vessels of a pancreas.

Afterwards it was proved that by a sensitization of animals foreign proteins or bacteritic toxins it is possible to reproduce acute P. in all phases.

M. N. Molodenkov (1964) vyzyvalg acute P., tying up pancreat ducts after a sensitization of rabbits quadruple hypodermic administration of normal horse serum.

V. V. Chaplinsky and A. I. Gnaty-shak (1972) reproduced acute P. at dogs by a sensitization of an organism a foreign protein and introductions on this background allowing exogenous (food) and endogenous (metabolitny) allergens. However numerous models of allergic P. are not identical to a similar disease at the person.

According to V. I. Eagle owl with sotr. (1973), G. N. Akzhigitova (1974), at the patients coming to surgical hospitals most often acute P.'s development of not traumatic origin is promoted by diseases of bilious channels and other digestive organs, diseases of cardiovascular system, alimentary disturbances, an alcohol abuse, etc.

the Pathogeny

the Greatest distribution was gained by the enzymatic theory of a pathogeny of the acute Item.

Activation own ферментов^ pancreas (trypsin, chymotrypsin, elastase, lipase., phospholipases, etc.) in the conditions of the increased function, also the subsequent enzymatic defeat of fabric of gland in the form of hypostasis and a necrosis is complicated go outflow of a pancreatic secret (fatty, hemorrhagic, mixed) are the most characteristic link in a pathogeny of the acute Item.

This process in a pancreas goes as chain reaction and begins usually with allocation from the damaged cells of a parenchyma of gland of a cytokinase. Under the influence of a cytokinase trypsinogen passes in trypsin (see). The pancreatic kallikrein activated by trypsin, working on kininogen, forms highly active peptide — collidine, to-ry quickly turns into bradykinin (see. Mediators, allergic reactions ). Bradykinin can be formed and directly of a kininogen. Under the influence of trypsin from various cells of a pancreas are released histamine (see) and serotonin (see). In lymphatic and circulatory ways pancreatic enzymes get to the general blood channel. In blood trypsin activates Hageman's factor (see. Coagulant system of blood ) and plasminogen and by that exerts impact on processes of hemocoagulation and a fibrinolysis.

Initial patol, changes in a pancreas and other bodies are shown by the expressed vascular changes: narrowing, and then vasodilatation, sharp increase in permeability of a vascular wall, delay of a blood-groove, an exit of a liquid part of blood and even uniform elements from a gleam of vessels in surrounding fabrics. There are serous, serous and hemorrhagic, hemorrhagic hypostasis and even massive hemorrhages in iron, retroperitoneal cellulose.

In the conditions of the broken local blood circulation, fabric exchange and direct action for cells of enzymes there are centers of a necrosis of a parenchyma of a pancreas and the fatty tissue surrounding it. It is promoted by a thrombogenesis, a cut is most characteristic of hemorrhagic forms P. From the destroyed cells are released lipases (see). The last, especially a phospholipase And, hydrolyze fats and phospholipids, causing a fatty necrosis of a pancreas, and extending a blood flow and a lymph, cause steatonecroses of the remote bodies.

The general changes in an organism are caused at the beginning of euzymatic (enzymatic), and then fabric (from the centers of a necrosis) by intoxication. Due to generalized impact on a vascular bed of vasoactive substances very quickly there are considerable circulatory disturbances at all levels: fabric, organ and system. Circulator frustration in internals (heart, lungs, a liver, etc.) lead to dystrophic, necrobiotic and even explicit necrotic changes in them then the secondary inflammation develops.

Considerable exudation in fabrics and a cavity, profound funktsionalnomorfologichesky changes of internals and other reasons cause the expressed disturbances water and electrolytic, carbohydrate, proteinaceous and a lipometabolism.

Pathological anatomy

Pathoanatomical primary destructive changes of an acinus caused by intraorganic (intracellular) activation of the digestive enzymes produced by a pancreas are the cornerstone of acute P. The developing fermental autolysis of acinous cells is followed by formation of the centers of a necrosis and aseptic (abacterial) inflammation. Therefore acute P.'s reference to group of inflammatory processes is very conditional; the term «pancreatonecrosis» captures the essence patol, process more precisely. Inf. the inflammation of gland, as a rule, is a complication of a pancreatonecrosis; it develops in late stages of a disease owing to microbic infection of the centers of a necrosis. Only occasionally purulent P. can be observed at a septicopyemia as the accompanying defeat owing to innidiation of a purulent infection.

The standard pathoanatomical classification of P. does not exist. Most of pathologists distinguish necrotic and hemorrhagic - intersticial acute P.'s forms, the acute serous, and also acute purulent Item.

Fig. 1. Microdrug of cellulose at acute pancreatitis: the center of a fatty necrosis is specified by shooters; coloring hematoxylin-eosine; x 80. Fig. 2. Macrodrug of a pancreas at diffusion and focal pancreatitis: small centers of a fatty necrosis. Fig. 3. Macrodrug of a pancreas at a total hemorrhagic pancreatonecrosis: increase in sizes and hemorrhagic treatment of fabric of gland. Fig. 4. Macrodrug of a normal pancreas (it is given for comparison). Fig. 5. The opened cavity of an adventitious cyst of the pancreas formed in the outcome of a hemorrhagic pancreatonecrosis. Fig. 6. Microdrug of a pancreas at acute pancreatitis: the arrow specified blood clot in a gleam of a vein; coloring across Mallori; x 80. Fig. 7. Microdrug of a pancreas at a hemorrhagic pancreatonecrosis: extensive hemorrhages (are specified by shooters) in fabric of gland; coloring across Mallori; x 80

Acute serous P. (acute hypostasis of a pancreas) most often is exposed to involution and only sometimes passes into a destructive form. However at fulminant development of a disease death can come from fermental shock in the first three days when destruction of gland did not come yet. These cases are difficult for pathoanatomical diagnosis since macroscopic changes of a pancreas (hypostasis) do not correspond to weight a wedge, currents. Only not numerous fatty can demonstrate defeat of gland necroses (see), found in surrounding cellulose (tsvetn. fig. 1). Microscopically at the same time in gland the changes corresponding diffusion focal P., as a rule, are found (tsvetn. fig. 2). The similar current of P. is observed, as a rule, at an alcoholism.

Pathoanatomical changes of gland at hemorrhagic-nekroti-cheskom P. (pancreatonecrosis) depend on scales of defeat and duration of a disease. Macroscopically in initial phases (1 — 3 days) gland is considerably increased in volume (tsvetn. fig. 3), it is condensed, the cut surface has a homogeneous gelatinous appearance, the lobular structure of its structure is erased, however the accurate centers of a necrosis are not visible yet. Only under the parietal peritoneum covering a pancreas (the so-called capsule) in small and big epiploons, the capsule of kidneys, a mesentery of intestines it is possible to find scattered the small centers of a fatty necrosis of yellow color in combination with a serous and serous and hemorrhagic exudate in a peritoneal cavity (tsvetn. fig. 4).

The macroscopic type of a pancreas in time 3 — 7 days from the beginning of a disease depends on prevalence of a pancreatonecrosis. In terms of the scope of defeats a pancreatonecrosis can be divided into three groups: diffusion and focal, macrofocal, subtotal (total).

At a diffusion and focal pancreatonecrosis in these terms the centers of a necrosis to dia. 0,2 — 1 cm yellow or reddish, are accurately delimited from the remained parenchyma of gland. The progressing sclerosis of necrotic sites, a gradual leucolysis and change of cellular composition of inflammatory infiltrate by limfoplazmokletochny and histiocytic elements is microscopically noted.

The centers of a fatty necrosis of surrounding cellulose either are absent, or are presented in a small amount. The capsule of a pancreas of destruction is not exposed.

In zones of defeat proliferation of small channels is found, the edge never comes to the end with regeneration of an acinus. An outcome of this form of a pancreatonecrosis is diffusion and focal fibrosis and lipomatoz a pancreas.

At a macrofocal form P. one or several centers of a necrosis by the sizes 2x3 — 3x4 cm having the wrong outlines unlike a heart attack are formed. The centers of a necrosis, as a rule, of yellow color also capture the capsule of gland. Their evolution, as well as outcomes of a disease, depend on depth of defeat and localization (a head, a body, a tail of gland). The necrosis of a tail of gland is most often replaced with fibrous fabric. At a necrosis of a body and a head of gland the outcome of a disease is caused by extent of secondary defeats of walls of vessels and large channels. The large centers of a necrosis of this localization quite often are exposed to diffusion fusion and sequestration with formation of abscess (intraorganic, an omental bursa) or an adventitious cyst (see. Pancreas ).

Cavity of a cyst (tsvetn. by fig. 5) it is, as a rule, connected with channels of gland, through to-rye there is a constant dumping of a secret.

At the progressing options of acute pancreatitis the initial stage of serous hypostasis of a pancreas very much early is replaced by a stage of a hemorrhagic necrosis with considerable hemorrhage (tsvetn. fig. 7) in fabric or without it. Then the stage of fusion and sequestration of the necrotic centers of a pancreas and retroperitoneal cellulose follows. In the last stage quite often there is suppuration, a cut has aseptic character in the beginning. Involution of the second stage and its transition to the third can be carried out through a stage of formation of massive inflammatory infiltrate in a zone of gland, at Krom not only gland, but also parapankreati-chesky retroperitoneal cellulose, and the next bodies (a stomach, a duodenum, a spleen and DR-) are involved in inflammatory process.

In most cases acute P.'s development stops at a stage of hypostasis or a necrosis, without passing into a stage of sequestration.

If hypostasis and a necrosis of a pancreas and retroperitoneal cellulose at acute P. develop usually in the next few hours of a disease, then fusion of the necrotic centers begins not earlier than 3 — the 5th day, and sequestration — in 2 — 3 weeks and is later from the beginning of a disease.

Sometimes the purulent inflammation of gland gains diffusion character. At the same time leukocytic infiltrates spread in a stroma of gland as phlegmon (phlegmonous P.) that usually demonstrates accession of an infection.

Walls of abscess of an omental bursa are formed at the expense of the bodies creating this cavity; their serous covers are exposed to fibrosis. Sclerous processes can be so intensive that all hollow bodies of an upper half of an abdominal cavity are accustomed to drinking in one conglomerate complicating a laparotomy. This conglomerate is taken sometimes for a tumor. Contents of abscess are usually presented by a fabric detritis, pus and a secret of a pancreas. Further evolution of abscess proceeds in the following main options: formation of an adventitious cyst, an erosion of walls of adjacent bodies (a stomach, duodenal, cross colonic guts) with formation of internal fistula, an arrosion of a large arterial trunk with bleeding in digestive tract, break in a free peritoneal cavity with development of purulent peritonitis (cm).

Weight of a current of macrofocal acute P. depends also on scales of fatty necroses. At crushing ekstraorganny defeats fusion of retroperitoneal cellulose with the subsequent formation of the parapancreatic phlegmon extending then on retroperitoneal space is observed.

The subtotal (total) form P. usually has character of a hemorrhagic necrosis and comes to an end with fusion and sequestration of gland with development of the complications described above.

Microscopically already in early phases of development of a pancreatonecrosis find, in addition to intersticial hypostasis, the multiple centers of a fatty necrosis and a necrosis of the acinus located preferential on the periphery of segments of a pancreas. In the centers of a necrosis thrombosis of capillaries, venules and a mural thrombosis of larger veins naturally comes to light (tsvetn. fig. 6). Disorders of haemo circulation in intraorganic veins are followed by extensive hemorrhages and hemorrhagic treatment of a parenchyma of gland. Extent of defeat of a venous bed, apparently, generally also defines both hemorrhagic character of a necrosis, and its scales.

Fig. 8. Microdrug of a pancreas at a pancreatonecrosis: the zone of a necrosis (1) is delimited by leukocytic infiltrate (2) and a granulyatsionny shaft (3); coloring hematoxylin-eosine; X 80. Fig. 9. Microdrug of a pancreas at chronic pancreatitis; the fresh center of a necrosis (1) against the background of fibrosis (2) glands; coloring hematoxylin-eosine; X 80. Fig. 10. Microdrug of a pancreas at chronic recurrent pancreatitis: in an expanded channel the concrement (1) is visible, fabric of gland is penetrated by tyazha of connecting fabric (2); coloring hematoxylin-eosine; X 80. Microdrugs of a pancreas at chronic sclerosing pancreatitis (Fig. 11 — 13). fig. 11. Against the background of a sclerosis (1) and a lipomatoz (2) a separate acinus (3) and lymphoid follicles (4), and also expanded channels are visible (5); coloring according to Van-Gizona, x 80. Fig. 12. Among fibrous fabric (1) the set of islets of Langerhans (2), an expanded channel (3) with papillomatous proliferation of an epithelium is visible; coloring hematoxylin-eosine, X 80. Fig. 13. In a circle of a separate acinus (1) the proliferating channels (2) creating the adenomatous centers are visible; coloring hematoxylin-eosine; h36

Disturbances of permeability of capillaries in the first 1 — 2 hour after destruction of an acinus are followed by emigration of leukocytes. In the same terms in an edematous stroma a large number of mast cells (labrocytes) appears, with to-rymi products of biologically active agents which are important in development of inflammatory reaction are connected (see. Inflammation ). In 1 — 2 days around the centers of a necrosis there is a demarcation shaft (tsvetn. fig. 8) consisting of leukocytes and a nuclear detritis. In the subsequent in it histiocytes and limfoplazmokletochny elements come to light. Feature of evolution of a pancreatonecrosis is the bystry activation of fibroblasts which is followed by intensive formation of collagen with formation of connective tissue capsules and fields of fibrosis (tsvetn. fig. 9 — 13).

At formation of a cyst or abscess microscopically their walls are presented by the hyalinized fibrous fabric with the diffusion and focal infiltrates consisting of lymphocytes, plasmocytes and histiocytes. The internal cover of abscess is usually covered with a necrotic plaque and fibrin with a leukocytic detritis and separate safe leukocytes.

The electronic microscopic examinations of a pancreas executed on various models of experimental P. open initial phases of damage of acinous cells. The progressing autolysis of an acinus is preceded, as a rule, by a partial necrosis of acinous cells with formation of a large number of auto-phagosomas, accumulation in cytoplasm of numerous lipidic vacuoles. These changes are followed by considerable reorganization of function of acinous cells that is shown by change of merokrinovy type of secretion, normal for gland, on apocrenic and mikrogolokrinovy, the Crimea sequestration of apical departments of cytoplasm together with granules of a secret is inherent. Also peculiar transfer of the granules of zymogen containing all set of synthesizable digestive enzymes in basal departments of cytoplasm of acinous cells is noted. At the same time any destruction of a basal membrane inevitably leads to paradoxical emission of secretory granules not in a gleam of a tubule, and in an interstitium from where they can rezorbirovatsya in blood and limf, a bed. The resorption of a secret is promoted by the accompanying damages of an endothelium of capillaries and intensive hypostasis of a stroma. The described changes are followed by bystry activation kallikrein - tryptic system and a phospholipase And that leads to the progressing autolysis with formation of the centers of an aseptic necrosis.

A clinical picture

the Expressed pain in an upper half of a stomach of the surrounding character — the leading and most constant symptom of the acute Item. In some cases irradiation of pains for a breast and to the area of heart is observed. Intensity of pain is connected with irritation of receptors, build-up of pressure in the general bilious channel and pancreat ducts, chemical influence of trypsin.

Because of sharp pains patients are uneasy and constantly change situation, without receiving simplification. Pains are especially expressed at a hemorrhagic pancreatonecrosis though severe pains can be observed also at an edematous phase P. With approach of a necrosis of nerve terminations intensity of pains decreases therefore on intensity of pain it is not always possible to judge extent of damage of a pancreas.

Nausea and vomiting — the second leading symptom acute P. Rvota quite often painful, unrestrained, not giving relief. Usually its first portions contain food masses, the last — bile and mucous contents of a stomach. At destructive P. sometimes owing to developing of acute stomach ulcers impurity of blood in the emetic masses (color of a coffee thick) appears.

Skin and mucous membranes at acute P. often pale, sometimes with a cyanochroic shade. At severe forms of a disease skin cold, is covered with a clammy sweat. Quite often acute P. is followed by mechanical jaundice (see), the caused obturation of the general bilious channel gallstones or a prelum its inflammatory infiltrate in a head of a pancreas.

Pathognomonic signs at destructive P. are described — sites of cyanosis of skin or hypodermic hemorrhages around a navel, on side areas of a stomach, a front abdominal wall, the person.

Body temperature, during the first hours diseases normal or lowered, with accession of the inflammatory phenomena increases. The high temperature which is not tending to decrease quite often is destructive P.'s sign, and late temperature increase of gektichesky character — a sign of purulent complications (retroperitoneal phlegmon, abscessing).

At the beginning of a disease bradycardia is quite often observed, later, at increase of intoxication, pulse rate usually gradually increases. At an edematous form of acute P. arterial hypertension is possible, and at destructive — hypotonia and even collapse (see).

Complications

It is possible to allocate two groups of complications acute P.: complications are local, connected with injury of a pancreas, and the complications caused by the general impact of a disease on an organism.

General complications: hepatonephric insufficiency, sepsis, mechanical jaundice, psychosis, diabetes mellitus.

Local complications: the peritonitis (delimited, extended); retroperitoneal phlegmon, abscesses of an abdominal cavity, omental bursa; necroses of a wall of a stomach, cross colon; pancreatic fistulas internal and outside; adventitious cyst of a pancreas; arrozivny bleedings.

At edematous P. complications are observed seldom. At destructive P. they arise almost at each patient.

Liver failure (see) and renal failure (see) are caused by intoxication of enzymatic and inflammatory genesis, hemodynamic disturbances, a hypoxia and the previous disturbances of a functional condition of a liver and kidneys.

Acute disorders of mentality are caused by intoxication and more often develop at the persons abusing alcohol. A diabetes mellitus (see. diabetes mellitus ) usually arises at destructive P. and destruction of all or almost all insular device of a pancreas, and at patients with the occult diabetes it can be shown also at edematous P.

the Diagnosis

Physical research. Language at acute P. usually dry, is laid over by a white or brown plaque. At a palpation during the first hours diseases a stomach sharply painful in epigastriß area, but rather soft in all departments. Gradually with development of paresis went. - kish. a path the stomach increases in sizes and does not participate in the act of breath. In the beginning inflation of an abdominal wall is noted locally in epigastriß area (a symptom Baud), then extends also to underlying areas. The peristaltics is sharply weakened or is not listened, gases do not depart.

The rigidity of a front abdominal wall in epigastriß area defined in a projection of a pancreas (a symptom to Kerta), is found almost in 60% of cases. Acute P. can be followed by tension of an abdominal wall, sometimes to doskoobrazny character. Shchetkin's symptom — Blyumberg is observed less than rigidity of a front abdominal wall. The symptom of Mayo-Robsona (morbidity in a costovertebral corner) is noted during the involvement in process of tail department of a pancreas and on the right at the left — at defeat of its head.

Also other symptoms at acute P. having a certain diagnostic value are described: Voskresensky's symptom (disappearance of a pulsation of an aorta in epigastriß area), Razdolsky (morbidity at percussion over a pancreas), Kacha (a hyperesthesia on the paravertebral line at the left, according to Thvn — ix segments), Makho-va (the hyperesthesia is higher than a navel), etc.

Laboratory methods of a research. Gematol, changes usually take place at destructive forms of a disease. At a part of patients hypochromia anemia comes to light though, according to V. V. Chaplinsky, V. M. Lashchevkera (1978), etc., at sharp dehydration in the first two days can be marked out a hyperglobulia. The leukocytosis is found approximately in 60% of patients. The lymphopenia, an aneosinophilia, acceleration of ROE are characteristic also neutrophylic shift due to increase in unripe forms, to the left. From enzymes of a pancreas (amylase, a lipase, trypsin) practical value has definition of amylase of urine (see. Volgemuta method ). The increase in its activity reaching 8192 — 32768 units (by Volgemut's method, at Krom normal indicators do not exceed 16 — 128 units), is noted more than at 70% of patients. However low activity of enzyme does not exclude the diagnosis of the acute Item. It can be caused by sclerous changes or a necrosis of acinous cells, a renal failure, early or, on the contrary, late arrival of the patient. At a heavy current of acute P. it is necessary to define amylase of blood serum since a number of patients can have normal amylase of urine, and in the blood which is sharply raised and to reach 400 — 500 units (by Smith's method — Rowe, at Krom normal indicators do not exceed 100 — 120 units). Usually activity of trypsin increases, and activity of its inhibitor decreases. Definition of activity of a lipase owing to considerable fluctuations it normal has smaller diagnostic value. By data A. A. Shelagurova (1970), increase in activity of enzymes of a pancreas in blood is found in 82,5 — 97,2% of patients. At the same time the dynamic research of activity of enzymes is important.

In acute P.'s diagnosis also the level of bilirubin of blood matters, to-ry at increase in a head of a pancreas can increase.

Definition allows to estimate weight of a condition of patients and extent of disturbance of the corresponding types of exchange at blood of ion concentration of potassium, sodium, calcium, and also sugar, crude protein and protein fractions.

Changes of coagulant system of blood also depend on a form of a disease. At an edematous form and a fatty pancreatonecrosis hypercoagulation is, as a rule, observed, at hemorrhagic P. — hypocoagulation. The fibrinosis and increase in S-reactive protein is almost always noted. According to V. S. Savelyev and soavt. (1973), G. A. Burom-skoy and soavt. (1979), changes in kallikrein-kinin system are characterized by decrease in level of a kininogen, an irekallikreina, inhibitor of kallikrein, a cut it is most expressed at the destructive Item.

Changes of indicators of a daily and hour urine to a certain extent depend on weight of damage of a pancreas. Falloff of a daily and hour urine, an anury are usually observed at a pancreatonecrosis. At patients with acute P. come to light also a proteinuria, mikr about a hamaturia, a cylindruria.

Radiodiagnosis. At a survey rentgenol, a research of a thorax and abdominal cavity find a high position of the left half of a diaphragm, restriction of its mobility, fluid accumulation in the left pleural cavity, a pneumatosis of a stomach and duodenum, paresis of separate loops of a jejunum.

At a contrast rentgenol, a research went. - kish. a path reveal the shift of a stomach of a kpereda, expansion of a duodenum, straightening of a medial contour of its vertical part, increase in so-called gastrolic distance in connection with increase in a pancreas and hypostasis of an omentulum and retroperitoneal cellulose.

A computer tomography (see. Tomography computer ) finds increase in a pancreas. At an edematous form of acute P. the shadow has it accurate contours. At hemorrhagic, necrotic and purulent P. outlines of gland disappear, and its shadow becomes intensive and heterogeneous; cavities of abscesses are sometimes distinguishable.

At tseliakografiya (see) the strengthened krovenapolneniye of vessels of a pancreas, increase in its volume, lengthening of a parenchymatous phase with heterogeneity of a shadow of gland is defined. At a pancreatonecrosis V. I. Prokubovsky (1975) noted easing or disappearance of a shadow of intraorganic vessels of a pancreas, a pushing off of a gastroduodenal artery, ugloobrazny deformation and a pushing off up of the general hepatic artery to the right.

Special methods of a research. Ultrasonic diagnosis (see) allows to distinguish borders and structure of a pancreas (focal and diffusion changes). At intersticial P. increase in the sizes of body comes to light, its accurate otgranichennost from surrounding fabrics remains, the transfer pulsation from an aorta appears. At destructive P. the pancreas loses uniformity, its contours merge with a surrounding background, unstructured sites are found. At development of a pseudocyst the homogeneous education with well outlined capsule which is pushing aside the next bodies is defined. In the presence of an exudate in an abdominal cavity echolocation allows to define it already in number of 200 ml.

At gastroscopies (see) and duodenoskopiya (see), made usually in hard diagnostic cases, it is possible to find the following signs acute P.: a) pushing off of a back body wall and pylorus; b) a hyperemia, hypostasis, slime and erosion in the field of a pushing off, and sometimes and symptoms of diffusion gastritis; c) turn of a loop of a duodenum, duodenitis, papillitis. A pushing off of a back wall of a stomach in combination with the expressed inflammatory changes sous of micron are symptoms of abscess stuffing.

In acute P.'s diagnosis the laparoscopy is of great importance (see. Peritoneoskopiya ), edges allows to diagnose authentically the most severe form of a disease — a pancreatonecrosis.

Laparoskvpichesky signs of a pancreatonecrosis are the plaques of focal necroses of fatty tissue found on big and small epiploons, a gastrolic sheaf, sometimes on a peritoneum of a front abdominal wall, a round ligament of a liver, mesenteries of cross colonic and thin guts.

The second sign of a pancreatonecrosis is availability of exudate in a peritoneal cavity. At a fatty pancreatonecrosis it has serous character. The amount of exudate happens various — from 10 — 15 ml to several liters. The proof of the pankreatogenny nature of such peritonitis is sharp increase in activity of pancreatic enzymes in exudate. The research of activity of trypsin and a lipase in exudate has smaller value.

A frequent sign of a pancreatonecrosis is serous treatment of a fatty tissue (so-called vitreous hypostasis).

The hemorrhagic pancreatonecrosis differs in availability of exudate of red color — from brownish-brown to obviously hemorrhagic. The centers of hemorrhages in a gastrolic sheaf or a big epiploon are sometimes visible.

Unlike a pancreatonecrosis edematous P. usually has no characteristic laparoscopic data since patol, process, as a rule, does not go beyond an omental bursa. However in some cases in an abdominal cavity find a serous exudate with high activity of enzymes.

Differential diagnosis acute P. carry out with acute cholecystitis (see), holetsistopankreatity (see), perforated stomach ulcer and a duodenum (see. Peptic ulcer ), acute appendicitis (see), acute intestinal impassability (see. Impassability of intestines ), heart attack intestines (see), acute gastritis (see), food toxicoinfection (see. Toxicoinfections food ), myocardial infarction (see).

Differentiation of the edematous and destructive forms P. which are subject to various treatment remains difficult. Both an edematous, and destructive form P. quite often begin equally. However in several hours after carrying out an intensive care the wedge, manifestations at edematous P. abate, the condition of the patient improves. Destructive P.'s symptomatology, despite the carried-out therapy, it is long remains, the condition of the patient improves slightly. During the progressing of process it worsens: tachycardia amplifies, intoxication and the peritoneal phenomena accrue. At a total pancreatonecrosis from the first hours of a disease the wedge, a picture (the pointed features, frequent small pulse, an oliguria) develops heavy.

In cases, difficult for diagnosis, there are necessary a laparoscopy and other tool methods of a research.

Criteria are developed, to-rymi it is necessary to be guided at differential diagnosis of various forms II. (tab.).

Treatment

At serious condition of the patient to lay down. actions should be begun at a pre-hospital stage. They shall be directed to fight against sharply expressed pain syndrome and arterial hypotension, i.e. include elements of infusional therapy (Polyglucinum, Haemodesum, etc.), and also use of cardiac glycosides, the analeptics stimulating breath, analgetics except narcotic.

Hospitalization of patients with acute P. shall be made only in a surgical hospital. Character to lay down. the events held in a hospital the wedge, pictures of a disease, weight of a condition of the patient, these laboratory and tool methods of a research depends on expressiveness.

Treatment of the edematous form of acute P. which in most cases is not followed by heavy intoxication shall be complex. First of all it is directed to creation funkts, rest of a pancreas that is provided with hunger (3 — 5 days), purpose of ice to epigastriß area, reception of alkaline solutions, chreznazalny drainage of a stomach and duodenum, suppression of enzymatic activity of gland for what appoint cholinolytics (atropine, Scopolaminum, Platyphyllinum), derivatives of a pyrimidine (methyluracil, pentoxyl).

The prevention and elimination of the phenomena of bilious and pancreatic hypertensia are reached by means of spasmolysants (nitroglycerine, a papaverine, Nospanum, an Euphyllinum), intravenous administration of novocaine.

Elimination of pain and various neuroreflex frustration is reached purpose of analgetics, spasmolysants, ganglioblokator (Pentaminum, petrolhexonium, etc.), and also perinephric blockade (see. Novocainic blockade ) or blockade of a round ligament of liver.

For reduction of permeability of a vascular wall appoint antihistaminic drugs (Dimedrol, Pipolphenum, etc.). Treatment of the patients who are in a serious condition with the expressed toxaemia characteristic, as a rule, of destructive forms of acute P., shall be carried out in chamber of an intensive care or the intensive care unit together with the surgeon, the resuscitator, the therapist.

Lech. the events held at severe forms of a disease shall be directed to blockade of zymoplastic function of a pancreas, removal of pancreatic enzymes and intensive desintoxication of an organism, prevention of purulent complications.

Blockade of excretory function of a pancreas can be carried out by purpose of hunger, atropine and local cold. At a severe disease the local hypothermia of gland or introduction of tsitostatik are more effective.

Cooling of a pancreas is carried out by a local gastric hypothermia (see. Hypothermia artificial, local ) by means of a long gastric lavage a cold water (an open method) or the special cooling devices AGSh-1, etc. (the closed method). The hypothermia allows to suppress excretory function of cells of gland considerably. However duration of the procedure (4 — 6 hours), frequent emergence of complications from lungs, the expressed disturbances of acid-base equilibrium owing to losses of a gastric juice at an open method limit use of a hypothermia in a wedge, practice, especially at patients of advanced and senile age.

Since the beginning of the 70th more and more broad use for acute P.'s treatment various cytostatics (5-ftoruratsit find, Cyclophosphanum, Phthorafurum). Use of tsitostatik at regional introduction to a celiac trunk after its catheterization on Seldingera — to Edman is the most effective that allows to lower a dose of the administered drug, at the same time considerably having increased concentration it in tissues of a pancreas.

According to Johnson (R. M of Johnson, 1972), A. A. Karelina and soavt. (1980), the mechanism to lay down. actions of tsitostatik at acute P. consists in inhibition of excretory function of cells of a pancreas. Pilot studies of Yu. A. Nesterenko and sotr. (1979) it is established that Intra arterial introduction of a ftoruratsil in a dose of 5 mg on 1 kg of weight causes decrease in vneshnepankreatichesky secretion by 91% and is optimum to lay down. dose. At intravenous administration this dose can be increased by 2 — 3 times. Use of tsitostatik is shown at destructive to P. Netselesoobrazno their use for patients with a total pancreatonecrosis, purulent complications of P. and a renal liver failure.

Removal of pancreatic enzymes and desintoxication of an organism is carried out by means of methods intravenous or Intra arterial administrations of diuretics (for an artificial diuresis), peritoneal dialysis and drainage chest limf, a channel.

At an artificial diuresis pancreatic enzymes, components of kinin system, and also nek-ry products of cellular disintegration are removed by kidneys. The technique of an artificial diuresis includes water loading, administration of diuretics, correction of electrolytic and proteinaceous balance. 5 — 10% solution of glucose, Ringer's solution, reopoliglyukin, salt solution can be the main components of the entered liquid. At an intravenous method enter every day 5 — l of liquid for 3 — 10 days. Forcing of a diuresis carry out by introduction after infusion each 2 l of liquid of diuretic drugs (lasixum, Mannitolum) and try to obtain that the daily urine reached 3V2 — 4 of.

According to G. A. Buromskaya and sotr. (1980), Intra arterial administration of diuretics liquidates more effectively out of - and intracellular hydration, does not increase the central venous pressure, does not cause a hypervolemia. At the same time at this method toxic products are brought directly out of cells of a pancreas that causes more expressed disintoxication! effect. Volume entered vnutriarterial-but liquids depends on intoxication and degree of dehydration of the patient and averages 4 — 5 l a day. Duration of vnut-riarterialny administration of liquid usually makes 3 — 4 days. During the carrying out an artificial diuresis control of the central venous pressure, a hematocrit, average diameter of erythrocytes, indicators of volume of the circulating blood, acid-base equilibrium, level of electrolytes is necessary.

An important role in fight against an enzymatic toxaemia is played by antifer-mentny drugs (Trasylolum, Contrykal, Tzalolum, pantripin, Gordoxum, etc.). They need to be entered in high doses within 3 — 5 days.

Drainage chest limf, a channel (see. Grudnoy Canal ) carry out at destructive forms of pancreatitis for the purpose of removal from an organism of enzymes of a pancreas.

The quantity of the deleted lymph depends on degree of intoxication and opportunities of replacement therapy. The lymph cleared of toxic products and pancreatic enzymes by filtering through ion-exchange columns (see. Limfosorbtion ), reinfuzirut in a vein. According to V. M. Buyanov and sotr. (1979), a perspective method of desintoxication of an organism at acute P. is the intravenous liquid limfostimulyation.

Peritoneal dialysis (see) it is shown at detection in an abdominal cavity during a laparoscopy or a laparotomy of a large number of a serous or hemorrhagic exudate. Depending on function of drainages and a condition of the patient dialysis is continued by 2 — 4 days.

Prevention and treatment of tromboembolic episodes are made under control of indicators of a tromboelastogramma and koagulogramma. At destructive P. already during the first hours diseases with high fibrinolitic activity and a gipertripsinemiya for prevention of a widespread intravascular blood coagulation it is reasonable to enter, except antienzymes, also heparin, low-molecular solutions (5% solution of glucose, Haemodesum, reopoliglyukin, polyvinol, Neocompensanum, etc.).

Correction of electrolytic exchange is made introduction of isotonic or 10% of solution of sodium chloride, by 10% of solution of potassium chloride, 1% of solution of calcium chloride, Ringer's solution — Locke, etc. At disturbance of carbohydrate metabolism enter necessary doses of glucose and insulin. For the purpose of correction of protein metabolism transfuse blood, plasma, Aminonum, albumine.

For prevention of purulent complications, especially in a phase of fusion and sequestration of the necrotic centers in a pancreas, apply antibiotics of a broad spectrum of activity (Kanamycinum, gentamycin, Monomycinum, tseporin and dr-).

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

At necrotic forms P. it is necessary to stimulate reparative processes in a pancreas and other bodies also. For this purpose appoint pentoxyl, methyluracil, anabolic hormones.

It is reasonable to divide all operations at acute P. into three groups: 1) emergency and urgent, carried out during the first hours and days of a disease; 2) delayed, to-rye make in a phase of fusion and sequestration of the necrotic centers of a pancreas and retroperitoneal cellulose, in 10 — 14 days and is later from an onset of the illness; 3) planned, carried out during complete cessation of an acute inflammation in a pancreas, in 4 — 6 weeks from the beginning of an attack, after completion of inspection of the patient (these operations are intended for prevention of a recurrence of acute P.).

Indications to the immediate and urgent surgeries: diffuse enzymatic peritonitis; the acute P. caused by a choledocholithiasis (obturation of a big nipple of a duodenum).

At the immediate and urgent surgeries after a laparotomy through a verkhnesredinny section (see. Laparotomy ) make audit of an abdominal cavity, finding out a condition of a pancreas, retroperitoneal cellulose, a parietal peritoneum and biliary tract.

At edematous P. in an abdominal cavity sometimes find a serous or bilious exudate. The pancreas is increased in volume, is dense to the touch, on pale or its mat surface dot hemorrhages are visible. At a hemorrhagic pancreatonecrosis are found a bloody exudate, it is frequent with a putrefactive smell, is frequent with impurity of bile, at purulent P. — a muddy exudate with fibrin. The pancreas at an early stage of a hemorrhagic pancreatonecrosis is increased, its surface is covered with multiple hemorrhages. At a total pancreatonecrosis it brown or black color, on big and an omentulum, a parietal peritoneum, a mesentery of thin and thick guts and other bodies the centers of a steatonecrosis are often visible.

Exudate with impurity of bile, treatment of a hepatoduodenal sheaf by it, increase in the sizes of a gall bladder, expansion of the general bilious channel testify to P. complicated by bilious hypertensia.

At edematous P. after removal of an exudate the abdominal cavity is usually sewn up tightly after an obkalyvaniye of gland with solution of novocaine with antibiotics and anti-fermental drugs.

At the expressed hemorrhagic or bilious imbibition of retroperitoneal cellulose make broad opening of retroperitoneal space around gland and in side channels of a stomach (okoloobodochnoki-shechny furrows, T.). Operation is finished with drainage of an omental bursa, sometimes in combination with an omentopankreatopeksiya, or drainage of a peritoneal cavity with the subsequent peritoneal dialysis.

At an extensive hemorrhagic pancreatonecrosis A. A. Shalimov with sotr. (1978), V. I. Filin with sotr. (1979), Hollender (L. F. Hollender, 1976), etc. make a pancreatectomy, most often left-side.

At the acute P. proceeding with the jaundice caused by a choledocholithiasis make choledochotomy (see), delete stones, finishing operation with outside drainage of the general bilious channel (see. Drainage ). At the wedged stones of a big nipple of a duodenum make plastics of a big nipple of a duodenum — a transduodenal papillosfinkteroplasti-ka (see. Faterov of pacifiers ).

In a phase of fusion and sequestration of the necrotic centers of a pancreas make necretomies) and a sequestectomy.

The necretomy is possible not earlier than in 2 weeks from the beginning of a disease since the zone of a necrosis of gland accurately is defined not earlier than the 10th day from the moment of an attack of the acute Item. Ektomiya's sequester, i.e. removal of the torn-away nekrotizirovanny sites of gland and retroperitoneal cellulose, it is possible usually not earlier than 3 — 4th week from the beginning of a disease.

Operation in a phase of fusion and sequestration consists in broad opening of an omental bursa through a gastrolic sheaf, in audit of gland and retroperitoneal cellulose, removal of nekrotizirovanny fabrics, drainage and a tamponade of an omental bursa and retroperitoneal space. After operation through drainages carry out active aspiration of purulent separated.

Planned operations are directed generally to sanitation of a gall bladder and channels (a cholecystectomia, care a fur-coat of l an itotomiya, choledochoduodenostomy, etc.) and treatment of diseases of other digestive organs serving as the reason of a recurrence of acute P. (a peptic ulcer of a stomach, a duodenum, diverticulums of a duodenum, a duodenostaz, etc.).

In the postoperative period continue complex conservative treatment of the acute Item.

Tampons from an omental bursa change on 7 — the 8th day, trying to create the wide wound channel, to-ry periodically wash out antiseptic solutions (Furacilin, Rivanolum, Iodinolum).

In a phase of sequestration there can be arrozivny bleedings. Sometimes they can be caused by disturbances of coagulant system of blood. At profuse bleedings make an obshivaniye and bandaging of vessels in a wound or on an extent or their embolization, a tamponade or a pancreatectomy. At fibrinolitic bleedings direct hemotransfusions are shown (see. Hemotransfusion ) and administration of inhibitors of a fibrinolysis — e-aminokaironovoy to - you, antienzymes, etc.

Pancreatic fistulas arise owing to its continuing purulent destruction or after operation for a pancreatonecrosis. In most cases at conservative treatment, especially at use of a roentgenotherapy, fistulas heal within several weeks or months. If the quantity separated from fistula within 2 — 3 months does not decrease, operational treatment is shown.

The adventitious cyst of a pancreas is also formed owing to a local necrosis of body. At the same time through the destroyed output channels secretion of pancreatic juice in the center of destruction continues, to-ry it is delimited by again formed connecting fabric which is gradually forming a wall of a cyst. The pseudocyst of a pancreas can suppurate, perforate or, squeezing the next bodies, to cause impassability of intestines, the general bilious channel. Method of the choice at operational treatment of postnecrotic pseudocysts is pan-kreatotsistoentero-and pankreatotsi-stogastroanastomoz. At a distal arrangement of a cyst the pancreatectomy is shown; at an empyema of cyst make marsupialization (see).

Forecast and Prevention

Forecast at acute P. it is always serious. The over-all mortality makes from 3 to 7%, and a lethality at a pancreatonecrosis — from 20 to 50%. In the cases of a pancreatonecrosis which demanded operational treatment, the lethality fluctuates from 30 to 85%.

Long-term results of treatment acute II. at 50% of patients good, more than at 30% — satisfactory, at 15 — 20% develops hron. Item.

Prevention. Medical examination of the patients who transferred acute P is reasonable, Considering an important role of diseases of bilious ways in acute P.'s emergence, their sanitation is an effective measure of prevention of a recurrence of a disease. Also observance of a diet and an exception of an alcohol abuse is necessary. During remission recommend a dignity. - hens. treatment in sanatoria went. - kish. a profile (Borjomi, Zheleznovodsk, Truskavets, Krainka, Carat catch Varya).

Features of acute pancreatitis at advanced and senile age. Patients of advanced and senile age make more than 25% of patients acute P. Eto is explained first of all by increase in number of people of this age among the population. Important value also age changes in a pancreas, in particular such as deformation of channels with an obliteration and their expansion, for-pustevaniye circulatory a capillary network have, fibrosis of interlobular partitions, etc. Promote more frequent development of acute P. and funkts, the disturbances of digestive organs characteristic of this age, and also often found diseases of hepatic and bilious channels, a stomach, duodenal and thick guts, cardiovascular system.

Along with a usual patomorfol, a picture of a disease at patients of this age group the apoplexy of a pancreas or massive fatty necroses at a lipomatoza of a stroma of gland is quite often observed.

Wedge, acute P.'s manifestations in this group of patients are characterized by a number of features. Due to the frequent existence at them various associated diseases even easy forms of acute P. quite often proceed with the expressed disturbance of functions of vitals and systems. Therefore the course of a disease is followed by development of acute cardiovascular, respiratory, hepatonephric insufficiency, different types of encephalopathies and disturbance of incretory function of a pancreas more often. It is shown by jaundice, oligo-and an anury, hypo - or a hyperglycemia. At the same time insignificant morbidity at a palpation in epigastriß area is characteristic and the expressed paresis went. - kish. path. Complex conservative treatment of acute G1. at patients of advanced and senile age shall include surely measures for treatment of associated diseases, first of all cardiovascular and respiratory systems, prevention and treatment of hepatonephric insufficiency, disturbances of carbohydrate metabolism. In this regard treatment of such patients is carried out in chamber of an intensive care or the intensive care unit.

Features of acute pancreatitis

Acute P. at children occurs at children seldom. The etiology of a disease is very various (some infectious diseases, allergic states, etc.). In most cases etiol, factors remain not clear; in this regard at children it is accepted to call suddenly arising acute P. idiopathic.

The disease often begins with a febricula of the child, failure from food and outdoor games. Developing then the wedge, a picture to a certain extent depends on a form of the acute Item.

Acute hypostasis of a pancreas at children (especially younger age group) proceeds rather easily, symptoms are less expressed, than at adults, and are often regarded by pediatricians as «intoxication of not clear etiology». The carried-out symptomatic treatment leads to bystry improvement of the general state. Only special inspection allows to make the correct diagnosis. At children of advanced age the disease begins with the acute abdominal pains in the beginning poured, and then which are localized in epigastriß area or having the surrounding character. Gradual increase of pains is less often observed. At the same time there are repeated vomiting, plentiful salivation. The child adopts the forced provision, is more often on the left side. Body temperature normal or subfebrile, language is wet, laid moderately over white naletokhm. Pulse of satisfactory filling, is rhythmical, speeded up, normal or is slightly lowered by the ABP. At survey pallor of integuments is noted. The stomach of the correct form, is not blown up, participates in the act of breath. The palpation of a front abdominal wall is painless, a stomach soft. Such discrepancy between cruel abdominal pains and lack of the objective data speaking about existence of an acute disease of abdominal organs is characteristic of an edematous form acute II. In blood the moderate leukocytosis, without considerable change of a formula is noted. The most informative and precursory diagnostic character is increase in activity of amylase in blood. A bit later the content of amylase in urine increases. As a rule, the moderate hyperglycemia is observed.

The hemorrhagic and fatty necrosis is followed by the expressed symptomatology and a heavy current. At children of younger age the disease is shown by quickly increasing concern. The child shouts and rushes about from pains, adopts the forced provision. Gradually motive concern is replaced by an adynamia. Children of advanced age usually point to localization of pains in upper parts of a stomach, their surrounding character, irradiation to the supraclavicular area, a shovel. There is repeated vomiting exhausting the child. The general state progressively worsens. Integuments are pale, with a cyanochroic shade. Develop eksikoz, heavy intoxication. Language dry, is laid over. Pulse is frequent, sometimes weak filling, the ABP gradually decreases. Body temperature is usually subfebrile, in rare instances increases to 38 — 39 °.

At purulent P. at the beginning of a disease discrepancy between subjective signs of an acute abdomen and absence or small expressiveness of objective data is even more expressed. / the Icon case at the child actively participates in the act of breath. Percussion and a palpation are slightly painful. The muscle tension of a front abdominal wall is expressed poorly. Then paresis of intestines develops, morbidity at a palpation amplifies, symptoms of irritation of a peritoneum appear» Body temperature increases, the considerable leukocytosis is characteristic. There comes disturbance of water and electrolytic balance, the amount of sugar in blood increases. Sharply concentration of amylase in blood and urine increases. Decrease in its level is a bad predictive sign.

Sometimes at children of younger age the heavy hemorrhagic or fatty necrosis is shown a wedge, a picture of the acute progressing ascites.

Rentgenol, a research at children, as a rule, a little informatively.

At children of advanced age at reasonable suspicion on a pancreatonecrosis it is possible to apply a laparoscopy.

The differential diagnosis of acute P. at children is carried out with an acute appendicitis, intestinal impassability and perforation of hollow bodies.

Acute P.'s treatment at children preferential conservative. To all children after establishment of the diagnosis appoint a complex to lay down. the actions directed to fight against a pain syndrome, intoxication and consecutive infection. An important task is creation funkts, rest of a pancreas, blockade of its zymoplastic function, fight against disturbances of water and electrolytic balance.

Complex conservative treatment at children at the acute P. diagnosed in early terms (1 — the 2nd days), usually leads to recovery.

At accurate a wedge, purulent P.'s signs or peritonitis an operative measure is shown. At children of preschool age complexity of differential diagnosis often results in need to distinguish acute P. in vrvkhmya the laparotomy made concerning an estimated acute appendicitis or other disease. Operational treatment is carried out by the same principles, as at adults.

All children who had acute P. need in long (up to 2 years) dispensary observation at the surgeon and the endocrinologist.

Chronic pancreatitis

Hron. The item meets often — according to section data, from 0,18 to 6% of cases. However in a wedge, practice this disease, apparently, meets still more often, but is not always diagnosed. Usually hron. The item comes to light on average and advanced age, is slightly more often at women, than at men. Hron. The item occurs at children seldom.

Distinguish primary hron. The item, at Krom inflammatory process is from the very beginning localized in a pancreas, and so-called secondary, or accompanying, P. which is gradually developing against the background of other diseases went. - kish. path, napr, peptic ulcer, gastritis, cholecystitis, etc.

Aetiology and pathogeny

Aetiology primary hron. The item it is various. In hron, can pass a form heavy or prolonged acute P. No is more often hron. The item arises gradually under the influence of such factors as unsystematic irregular food, the frequent use of spicy and greasy food, hron, alcoholism, especially in combination with deficit in food of proteins and vitamins. According to Benson (J. A. Benson), in the USA hron, recurrent P. in 75% of cases arises at the patients suffering hron. alcoholism. The penetration of stomach ulcer or a duodenum in a pancreas can also lead to development hron, inflammatory process in it. Among other etiol, factors it is necessary to call hron, disturbances of blood circulation and atherosclerotic defeat of vessels of a pancreas, inf. diseases, exogenous intoxications. Sometimes P. arises after operations on the bilious ways or a stomach. Damage of a pancreas is more rare reason at a nodular periarteritis, a Werlhof's disease, hemochromatosis, a hyperlipemia. In some cases, according to nek-ry researchers, in 10 — 15% the reason hron. The item remains not clear. The contributing factors in emergence hron. Items are also the obstacles for release of pancreatic juice in a duodenum caused by a spasm or a stenosis of an ampoule of a sphincter of Oddi, and also its insufficiency, edges are facilitated by hit of duodenal contents in a pancreat duct.

One of the leading mechanisms of development hron. inflammatory process in a pancreas the delay of allocation and intraorganic activation of pancreatic enzymes, first of all the trypsin and a lipase (a phospholipase And) which are carrying out an autolysis of a parenchyma of gland is. Activation of elastase and nek-ry other enzymes leads to defeat of vessels of a pancreas. Action of kinin on the smallest vessels leads to edematization. The hydrophilic effect of decomposition products in the centers of a necrosis of tissue of pancreas also promotes hypostasis, and in the subsequent — to formation of adventitious cysts. In development, especially progressing hron. inflammatory process, processes of an autoaggression are of great importance.

At hron, gastritis (see) and duodenitis (see) development by enterokhromaffinny cells about a lysis - that cover of a stomach and a duodenum of polypeptide hormones is broken, to-rye participate in regulation of secretion of a pancreas.

At hron. Item inf. origins the activator can get into a pancreas from a duodenum (e.g., at dysbacteriosis, enterita) or from bilious ways (at cholecystitis, a cholangitis) through pancreat ducts in the ascending way to what promote dyskinesia went. - kish. a path, followed by a duodenopankreatichesky and hole-dokhopankreatichesky reflux.

Pathological anatomy

Pathoanatomical hron. Items subdivide on hron, recurrent P. and hron, sclerosing P.

Hron, recurrent P. in essence is the prolonged option of an acute melkoochagovy pancreatonecrosis as any palindromia is followed by formation of the fresh centers of a necrosis of a parenchyma of a pancreas and surrounding fatty tissue.

Macroscopically in the period of an aggravation of iron it is represented a little increased in volume and diffuzno condensed. Microscopically in it the fresh and organized centers of a necrosis of a parenchyma and a fatty tissue alternating with the cicatricial fields, the centers of calcification, small pseudocysts deprived of an epithelial vystilka are found. Also considerable deformation and expansion of a gleam of the output channels containing the condensed secret and quite often microlites is noted. In some cases diffusion and focal calcification of an interstitium is observed, and then speak about hron, the kaltsifitsiruyushchy Item.

Inflammatory infiltration from leukocytes is observed only in the centers of a fresh necrosis of a parenchyma. It gradually abates in process of the organization of the centers of destruction, being replaced by diffusion and focal infiltrates from lymphoid, plasmocytes and histiocytes. Many researchers consider these infiltrates manifestation of the autoimmune reaction of the slowed-down type arising in response to continuous antigenic influence from the centers of destruction of an acinus.

Hron, sclerosing P. differs in diffusion consolidation and reduction of a pancreas in sizes. Fabric of gland gets stony density and macroscopically reminds a tumor. Microscopically find a diffusion focal and segmented sclerosis with the progressing growth of connecting fabric around channels, segments and in an acinus. The constant decrease of a parenchyma proceeding as a necrosis or an atrophy of a separate acinus and groups of an acinus is the reason of a sclerosis. In far come cases against the background of diffusion fibrosis small islands of an atrofichny parenchyma hardly are found. Along with it the expressed proliferation of an epithelium of channels with formation of adenomatous structures is noted, to-rye it is sometimes difficult to differentiate with an adenocarcinoma. In gleams of the expanded removing channels the condensed secret, crystal deposits of lime, microlites constantly meet. In a circle of channels a large number of giperplazi-rovanny pancreatic islands (Langergans) is found. The new growth of an acinus does not occur, the necrosis of a parenchyma of gland is replaced with a hem.

As well as at a recurrent form P., among fields of fibrous fabric it is possible to find the limfoplazmotsitarny infiltrates which are reflection of autoimmune processes. At the same time morphologically in a pancreas not necrotic, but dist-roficheski-atrophic changes of an acinus with their slow substitution by connecting fabric prevail.

At all options hron. Items are observed identical complications. Most often the cicatricial stricture of a pancreat duct, and also obstruction by its stone or an adenomatous polyp meets. At the same time obturation of the general bilious channel with development of mechanical jaundice is possible. Thrombosis of a splenic vein is sometimes observed. Quite often against the background of hron. The item develops a diabetes mellitus though unlike an acinus islets of Langerhans well regenerate, and among cicatricial fabric they can always be found.

Clinical picture

Clinical picture hron. The item it is very variable, but in most cases includes the following symptoms: pain in epigastriß area and left hypochondrium; dispeptic phenomena; so-called pankreatogenny ponosa; weight loss, hypoproteinemia, symptoms of a polyhypovitaminosis; signs of a diabetes mellitus.

Pain is localized in epigastriß area on the right (at preferential localization of process in the field of a head of a pancreas); during the involvement in inflammatory process of her body pain is observed in epigastriß area; at damage of her tail — in left hypochondrium. Quite often pain irradiates in a back (at the X—XII level of chest vertebrae) or has the surrounding character, amplifies in position of the patient lying on spin and can weaken in a sitting position, especially at a small inclination forward. Pain can irradiate also to the area of heart, imitating stenocardia, in a left shoulder-blade, the left shoulder, and sometimes to the left ileal area. Intensity and the nature of pains are various; they can be the constants (pressing, aching), to appear through a nek-swarm time after food (as at a peptic ulcer), especially after reception of greasy or spicy food, or to be pristupoobrazny as pancreatic colic.

Dispeptic symptoms (pancreatic dyspepsia) meet often, especially at an exacerbation of a disease or heavy disease. Many patients note also loss of appetite, disgust for greasy food. At the same time at development of a diabetes mellitus patients can feel strong hunger and thirst. The increased salivation, an eructation, nausea, vomiting, a meteorism are often observed. The chair in mild cases normal, in heavier is observed tendency to a diarrhea or alternation of locks and ponos. However in the typical far come cases hron. Items (in the presence of strong indications, vneshnesekretorny insufficiency of a pancreas) more characteristic are pancreatogenous diarrheas with allocation plentiful kashitseobrazny fetid with a greasy luster a calla.

Owing to development of vneshnesekretorny insufficiency of a pancreas and disturbance of processes of digestion and absorption in intestines weight loss accrues. It is promoted by the loss of appetite which was usually observed at patients, and also accession of a diabetes mellitus.

At severe forms of a disease the depression, morbid depression and other mental disturbances are possible. At alcoholic P. disturbances of mentality can be caused by long effect of alcohol on c. N of page.

The course of a disease usually has long character. Allocate 5 forms of a disease: 1) the recurrent form which is characterized by the clear periods of remission and aggravations of process; 2) the painful form proceeding with the constant pains dominating in a clinical picture; 3) pseudo-tumoral form; 4) latent (bezbolevy) form; 5) a sclerosing form, for a cut the arising and progressing signs of insufficiency of functions of a pancreas are characteristic early. At the last form mechanical jaundice owing to a prelum of the general bilious channel is sometimes observed by the sclerosed head of a pancreas. T. G. Reneva with sotr. (1978) allocates 3 forms of a current hron. P.: easy, medium-weight and heavy. The last proceeds with persistent ponosa, dystrophic frustration, the accruing exhaustion.

Complications: cysts, calcificats of a pancreas, diabetes mellitus, thrombosis of a splenic vein, stenosis of a pancreat duct. Against the background of a long hron. P1. development of cancer of pancreas is possible.

Diagnosis

Physical research. At a palpation of a stomach at patients hron. The item morbidity in epigastriß area and left hypochondrium is usually characteristic. A number of researchers described painful points and zones, morbidity in to-rykh is especially characteristic. So, at defeat of a head of a pancreas pain can be noted with a pressure in the so-called pancreatic point of Dezharden which is located in the field of a projection to a front abdominal wall of distal department of a pancreat duct (approximately at distance of 5 — 7 cm from a navel on the line connecting a navel to the right axillary hollow), or in wider holedokhopankreatichesky zone of Shoffar which is located between the line stated above, a front midline of a body and the perpendicular lowered to the last line from Dezharden's point. Morbidity of a point in a costovertebral corner (a symptom of Mayo-Robsona) is quite often noted. The zone of a skin hyperesthesia according to a zone of an innervation 8 — the 10th chest segment at the left (a symptom Kacha) and nek-paradise the atrophy of hypodermic cellulose in the field of a projection of a pancreas to a front abdominal wall described by A. A. Shela-gurov (1970) is sometimes noted. To Propalpirovat the increased and condensed pancreas at hron. The item works well very seldom.

Nek-roye auscultation of epigastriß area at a full exhalation can have diagnostic value: systolic noise is sometimes heard, to-ry arises owing to a prelum of a belly part of an aorta the increased and condensed pancreas.

Laboratory methods of a research quite often reveal at patients hron. The item moderate hypochromia anemia, acceleration ROE, a neutrophylic leukocytosis, a disproteinemia at the expense of the increased content of globulins, increase in activity of transaminases and zymohexase in blood serum. At defeat of the insular device of a pancreas comes to light hyperglycemia (see) and glycosuria (see), however identification of easy extents of disturbance of carbohydrate metabolism requires a research of a sugar curve with double loading glucose (see. Carbohydrates, methods of definition ). At disturbances of vneshnesekretorny function of a pancreas more or less expressed hypoproteinemia usually comes to light; in more hard cases — disturbance of electrolytic exchange, in particular hyponatremia (see). Definition in duodenal contents, and also in blood and urine of content of enzymes of a pancreas allows to give an assessment funkts, conditions of body. In the duodenal contents received by means of the two-channel probe (see. Duodenal sounding ), before stimulation of a pancreas determine by secretin and pancreozymin total quantity of juice, its bicarbonate alkalinity, content of trypsin, a lipase and amylase; in blood — the content of amylase, a lipase, antitrypsin; in urine — amylases. Simultaneous carrying out a research of content of pancreatic enzymes allows to reflect in duodenal juice, blood, and also an amilasuria much more precisely a condition of vneshnesekretorny function of a pancreas at patients hron. The item, than separate carrying out these researches in different days.

The hyperamilasuria reaching at hron. The item sometimes of figures 2048 — 4096 units (on Volgemuta), comes to light more often than a hyperamilasemia, however increase in amylase of urine (to 256 — 512 units) it is sometimes observed also at other diseases of abdominal organs.

Content of enzymes in blood and urine increases in the period of P.'s aggravation, and also at obstacles to outflow of pancreatic juice (inflammatory hypostasis of a head of gland and a prelum of channels, a cicatricial stenosis of a big nipple of a duodenum, etc.). In duodenal contents concentration of enzymes and total amount of juice in an initial stage of a disease can be a little increased, however at the expressed atro-ficheski-sclerous process in iron these indicators decrease.

The Koprologichesky research (see. Kal ) reveals the increased maintenance in Calais of undigested food (a steatorrhea, a creatorrhea, an amylorrhea, kitarinoreya). In opinion OST yes (W. J. Austad, 1979), a resistant steatorrhea at hron. The item appears when external secretion of a pancreas decreases not less than by 90%.

Fig. 1. Roentgenogram of a stomach and duodenum of the patient with chronic pancreatitis: the stomach is displaced up, the duodenum is developed by the increased pancreas.
Fig. 2. Roentgenogram of area of a pancreas: multiple limy a fireplace on the course of a pancreat duct.

Radiodiagnosis. At rentgenol, a research went. - kish. a path find in case of increase in a pancreas the shift of a stomach up and kpered, expansion of a duodenal loop and flattening of a medial contour of the descending part of a duodenum (fig. 1). By means of a relaxation duodenografiya (see. Duodenografiya relaxation ) on this contour it is possible to reveal short rigid sites, a number of the pointed deepenings in the form of needles (spicules), impressions at the edges of a big nipple of a duodenum. In survey pictures of a pancreas define also stones or deposits of salts of calcium (fig. 2), and on computer tomograms find the expanded and deformed pancreat duct. At holegrafiya (see) sometimes find narrowing of distal department of the general bilious channel.

Great value in diagnosis hron. The endoscopic retrograde holangiopankreato-grafiya has the item (see. Pankreatokholangiografiya retrograde ). At the beginning of a disease pancreat ducts are not changed or deformation of small output pancreat ducts is noted. Further these channels are narrowed, a part them is obliterated, and in others — small cystiform expansions can be defined. The gleam of a pancreat duct becomes uneven, on its walls there are roughnesses and impressions. In case of formation of abscesses and pseudocysts a contrast agent from the destroyed channels gets into a parenchyma of gland and depicts in it cavities, allowing to specify their situation and size. Unlike pseudocysts in abscesses necrotic masses can come to light at the same time.

Fig. 3. Tseliakogramma patient with chronic pancreatitis: increase in a shadow of a pancreas (it is specified by shooters), the strengthened its krovenapolneniye.
Fig. 4. Fistulogramma of the patient with chronic posttraumatic pancreatitis with outside fistula: the contrasted distal part of the pancreatic canal (1), is reported by the fistular course with a cavity in subphrenic space (2) and wide fistula with a cross colon (3) (a shadow of a drainage at the left).

At a tseliakografiya it is possible to allocate two forms hron. P. Increase in a pancreas, its gipervas-kulyarization and not homogeneous contrasting in a parenchymatous phase (fig. 3) are typical for the first form. The second form is more characteristic of P. with the expressed fibrous changes in a pancreas. It differs in the shift and vasoconstriction and depletion of the vascular drawing. The parenchymatous phase is absent or is weakened. At all forms of Tileni Arneshyyo (and. Tu1yop, V. of Arnesjo, 1973) stenoses of large arteries out of a pancreas — own hepatic, gastroduodenal, splenic observed. Contours of the narrowed sites remained equal while at a pancreatic cancer they had «corroded» character. Pseudocysts look as the roundish avaskulyarny educations displacing adjacent arterial branches. During operation and in the postoperative period (if in pancreat ducts or a cavity of a cyst the catheter for a drainage is left) for specification of a condition of channels it is possible to carry out pankreatografiya (see). If after operation for a cyst the outside or internal pancreatic fistula was formed, carrying out is reasonable fistulografiya (see), edges allows to characterize the fistular course and a residual cavity of a cyst (fig. 4).

Radio isotope scanning of a pancreas with marked selenium-75 methionine also has a certain diagnostic value.

Ekhografiya allows to reveal existence, character and extent morfol, changes in a pancreas.

Differential diagnosis it is often very difficult. Hron. The item needs to be differentiated first of all with a tumor pancreas (see); at the same time methods of tool diagnosis are of great importance: tseliakografiya, endoscopic retrograde holangiopankreatogra-fiya, computer tomography, ekhografiya and radio isotope scanning of a pancreas.

The differential diagnosis is carried out also with cholelithiasis (see), a peptic ulcer of a stomach and duodenum, hron, by enteritis, etc.

Treatment

Conservative treatment is carried out in initial stages of a disease and in the absence of complications. In the period of the expressed aggravation hospitalization is shown, as well as at the acute Item.

Conservative treatment hron. To the item it is directed to creation of optimum conditions for functioning of a pancreas and elimination of the factors supporting inflammatory process on fight against a pain syndrome, compensation of disturbances externally - and intra secretory insufficiency of a pancreas.

Food of the patient shall be fractional, 5 — 6-times, small portions. Exclude alcohol, marinades, fried, greasy and spicy food, strong broths at possessing a promoting effect on a pancreas. The diet shall contain to 150 g of proteins, from them 60 — 70 g of animal origin (low-fat grades of meat, fish, low-fat cottage cheese, not strong cheese). Content of fats in a diet is limited to 80 — 70 g a day, generally at the expense of rough fats of animal origin (pork, mutton). At a considerable steatorrhea the content of fats in a diet is reduced to 50 g. Amount of carbohydrates also limit, oso-bennno mono - and disaccharides; at development of a diabetes mellitus they are completely excluded. All food is given in a warm look since cold dishes can strengthen dyskinesia) intestines to cause a spasm of a sphincter of Oddi.

From medicines appoint derivatives a feast them dyne (pentoxyl, methyluracil) for 3 — 4 weeks. At severe pains perinephric, juxtaspinal, celiac novocainic blockade, non-narcotic analgesics, reflexotherapy are shown; in especially hard cases — narcotic analgetics in combination with cholinolytic and antispasmodics.

At vneshnesekretorny insufficiency of a pancreas for the purpose of replacement therapy appoint fermental drugs: Pancreatinum, abomin, Cholenzymum, panzinorm, festal, Vitohepatum, etc., and also vitamin drugs: Riboflavinum (B2), a pyridoxine (B6), cyanocobalamine (B12), pangamat calcium (B15), Retinolum (A), nicotinic and ascorbic to - you. Appoint also anabolic hormones (methandrostenolone, retabolil), glutaminic to - that, cocarboxylase. In fight against the accruing disproteinemia use of proteinaceous blood preparations is reasonable (Amincrovinum, a hydrolyzate of casein, etc.). Intra secretory insufficiency of a pancreas demands the corresponding diet and to lay down. actions.

After removal of the acute phenomena and for the purpose of prevention of an aggravation in a stage of remission the resort therapy in sanatoria gast-roenterol is recommended. profile (Borjomi, Yessentuki, Zheleznovodsk, Pyatigorsk, Karlovy Vary).

Operational treatment. Indications: cysts it is also long not healing outside pancreatic fistulas; concrements of channels of gland; a stenosis of a pancreat duct with disturbance of outflow of pancreatic juice; indurative (pseudo-tumoral) P., especially in the presence of jaundice; the persistent pain syndrome which is not giving in to conservative actions.

A type of an operative measure on a pancreas at hron. The item depends on the nature of defeat of its parenchyma and channels, in particular on level and the extent of their impassability and the reasons which brought to it. The most important problem of operation is creation of the conditions excluding development of intra pro-current pancreatic hypertensia.

At occlusive (gallstone) and the stenosing defeats of a big nipple of a duodenum operation of the choice is the transduodenal papil-losfinkterotomiya (plastics). In the presence of a simultaneous stenosis of the mouth of a pancreat duct or obstruction by its stone make also a virzungotomiya (plastics).

At a widespread stricture of a pancreat duct in the field of a head and expansion of a channel as «a chain of lakes» at the level of a body and a tail of gland it is shown punk reatoyeyunostomiya. At the same time as much as possible open all cavities and pockets of a pancreat duct and its branches, exempt them from stones and zamazkoobrazny weight. The small bowel is anastomosed with all is longitudinal dissect fabric of gland.

At a combination hron. The item with a parapancreatic cyst, in a cavity a cut opens fistula of a pancreatic channel, make a pankreatotsi-hundred-jejunostomy.

At macrofocal polycystic or calculous P., combined with impassability of a pancreat duct in a zone of the greatest defeat of gland, its resection is shown. At localization of such changes in a tail and an adjacent part of a body of gland make a left-side resection of gland, and at localization in a head — a pankreatoduodenalny resection (see. Pancreatoduodenectomy ).

Recurrent P. can be complicated by a focal polycystosis of gland and pancreatic fistula. At an arrangement of these changes in a tail or a body of gland carry out a left-side pancreatectomy.

At recuring hron. The item with considerable defeat of fabric of gland in a tail and a body in some cases can be made a left-side subtotal resection of gland. Various operations for century of N of page (a silankhnikotomiya, neurotomy) were not repaid.

Since the end of the 70th in a wedge, practice began to apply intraoperative occlusion of pancreat ducts alloplastichesky material that leads to oppression of its external secretion.

Pancreas operations at hron. Items can be complicated by a pancreatonecrosis, peritonitis, bleeding, etc. In the postoperative period the complex of the held conservative events shall include surely preventive administration of anti-fermental drugs, tsitostatik.

The forecast at hron. The item depends on the frequency of an exacerbation of a disease and character of the arisen complications. At an uncomplicated current in a stage of remission working capacity in most cases remains. At an aggravation of process, and also emergence of complications it, as a rule, is considerably broken, especially at severe forms of a diabetes mellitus.

Prevention consists in timely treatment of the diseases promoting emergence hron. Item, elimination of an opportunity hron, intoxications, first of all alcohol abuse, providing a balanced diet. In this regard medical examination of patients hron is reasonable. The item

Features of chronic pancreatitis at advanced and senile age

Various forms hron. Items occur at persons of advanced and senile age more often than in earlier age groups. At the same time it is usually combined with various diseases of other bodies went. - kish. path (hron, gastritis, cholecystitis, colitis etc.). According to A. A. Shelagurov (1970), etc., with age in a pathogeny of G1. gain bigger value the progressing atherosclerotic defeat of vessels of a pancreas, and also reduction of its compensatory opportunities owing to fiziol. aging, atrophic and sclerous processes in a pancreas, decrease in its excretory and incretory functions.

Wedge, picture hron. The item at people of advanced age of a polimorfn; sometimes associated diseases shade clinic of a disease. However comparative study of a current of a painful form hron. The item reveals that often the disease from the very beginning accepts hron, a current. Strong-willed attacks at elderly people are usually less intensive. They arise at errors in a diet, especially after an exercise stress. At the long course of a disease considerable weight loss is noted more often than at young people, dispeptic frustration meet. Vneshnesekretorny function of a pancreas at advanced age decreases that complicates use of data of its research for diagnosis of a disease.

Treatment hron. The item at advanced age has the features. At purpose of a diet it is necessary to consider the associated diseases which are quite often available for such patients (atherosclerosis, coronary heart disease, a hypertension, etc.). Owing to the age decrease in vneshnesekretorny function of a pancreas aggravated hron. The item, to such patients showed more prolonged treatment by enzymatic drugs of a pancreas (Pancreatinum, panzinormy, festal, etc.). Surgical treatment hron. Items in this group of patients apply only at not allowed jaundice caused by a prelum of the general bilious channel the increased head of gland is long not healing outside fistulas of gland, and also an empyema of cyst.

Experimental pancreatitis

For the first time acute P. was got by K. Bernard in 1856 by retrograde introduction to a pancreat duct of luccu oil, and chronic — I. P. Pavlov in 1877 by bandaging of a pancreat duct of a dog. These experiments laid the foundation for search of various models experimental 11.

The most suitable animals for. P.'s reproduction dogs owing to similarity of an anatomic structure of their output channels to channels of the person are. At the same time white rats — a convenient object for studying of efficiency of therapy of experimental pancreatitis. There are not less than 100 models P., to-rye it is conditionally possible to systematize as follows.

1. The Obturatsionno-gipertenzionny P. caused by temporary or continuous build-up of pressure in system of pancreat ducts by their bandaging or retrograde administration of various substances (bile, natural or synthetic bilious to - t, trypsin, a lipase, elastase, enterokinase or mix of the last with bile or blood and t. and.). In addition to increase in intra pro-current pressure at the time of introduction, these substances activate pancreatic enzymes or stimulate own secretion of a parenchyma of gland. By I. P. Pavlov's works it is proved that bandaging of a pancreat duct does not cause P., and is followed by a gradual atrophy of an exocrine parenchyma. If on this background to stimulate secretion, then P., as a rule, develops. It is necessary to carry the models P. caused by the dosed or long duodenal hypertensia promoting a pelting of contents of a gut in pancreat ducts to the same group.

2. Intoksikatsionno-metabolichesky P. is caused by means of a row pharmakol, and chemical agents or deficit of amino acids in food. Models acute and hron use the greatest distribution. The items caused by introduction these they on in a parenchyma of a pancreas or intraperitoneally and also by means of enteral administration of alcohol against the background of proteinaceous and scarce food.

3. Allergic models P. create by a sensitization of animals horse serum or meningococcal endotoxin. The allowing dose of the agent is entered into one of pankreatoduodenalny arteries or into fabric of gland. Carry the so-called parallergic models P. created by a sensitization of rabbits or dogs by horse serum according to the practical standard to the same group however as the allowing factor use bandaging of a channel or medicamentous stimulation of secretion of gland. Acute and hron. Items cause also by means of pankreatotoksichesky serum.

4. Ischemic (hypoxemic) models P. cause by bandaging of a splenic vein or intraorganic vessels. The same effect is reached by embolization of an arterial bed a fatty emulsion. However without additional stimulation of secretion or influence of other damaging agents of convincing model P., as a rule, it is not possible to receive.

5. Neurogenic models P. receive by disturbance of an innervation of a pancreas or electrostimulation of sympathetic and parasympathetic nervous trunks with simultaneous introduction to channels of gland of the damaging agents.

The most effective models of experimental P. are the combined techniques combining hypertensia of channels of gland and activation of its enzymes against the background of hypersecretion or ischemia of body.

At all models of experimental P. enzymatic is the cornerstone of a disease autolysis (see), the developing owing to disturbance of synthesis and release of enzymes, focal focal or widespread pancreatonecrosis with the secondary inflammatory reaction which is followed by a vein thrombosis and also a microcirculator bed and hemorrhages in a parenchyma of gland.

Table. Differential diagnostic characters of the main forms of acute pancreatitis

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Of H. Akzhigitov, A. L. Grebenev, Yu. A. Nesterenko, V. I. Filin; G. A. Bairov (it is put. hir.), L. D. Lindenbraten (rents.), N. K. Permyakov (stalemate. An.), G. P. Titova (experimental pancreatitis).

Яндекс.Метрика