Pancreatic cysts and fistulas

Pancreatic fistulas are the pathological messages of the ducts of the gland with the external environment or internal organs.

There are external fistula when the mouth of the fistula opens on the skin, and internal, when the fistula communicates with the hollow organ (stomach, small or large intestine). They may be complete and incomplete.

When the proximal part of the duct is blocked (complete fistula), the entire pancreatic juice is excreted. In case of incomplete fistulas, the main part of pancreatic juice flows naturally into the duodenum, and only a part of it is separated by fistula.

external fistula of the pancreas most often occurs after an open injury of the abdomen or after surgery on the gland, combined with the opening of its ducts. Internal fistulas are usually the result of destructive changes in the gland, passing on to the wall of the adjacent organ (acute pancreatitis, penetration and perforation of the pancreatic cyst).

Clinic and diagnosis

for external fistula pancreas is characterized by the release of pancreatic juice through the external opening of the fistula. The amount of discharge depends on the type of fistula. With a full fistula (rarely occurs), up to 1 1.5 l of juice is secreted per day, with incomplete, often only a few drops. Depending on the severity of destructive and inflammatory changes in the gland and in the walls of the fistula, either pure pancreatic juice or pancreatic juice containing an admixture of blood and pus is secreted.

In case of incomplete fistulas due to the release of a large amount of pancreatic juice, maceration of the skin develops very quickly. A significant loss of pancreatic juice leads to a sharp deterioration in the patient's condition, pronounced violations of protein, fat and carbohydrate metabolism, significant losses of water, electrolytes and disorders of the acid-base state. Often, these losses lead to dehydration, exhaustion, adynamia, and in severe cases - to a comatose state.

In case of internal fistulas, secretion of the preatic juice occurs in the lumen of the stomach or intestines. In this regard, severe pathophysiological changes characteristic of external fistulas, does not happen.

Diagnosis of external fistula is not difficult. The final diagnosis is confirmed by examining the content of pancreatic enzymes in the fistula discharge. To clarify the diagnosis, fistulography should be used. If during fistulography contrast fills the pancreatic ducts, the diagnosis is beyond doubt.

Incomplete fistulae are usually closed under the influence of conservative treatment, which includes measures aimed at improving the general condition, combating exhaustion and dehydration.

To reduce the secretory activity of the gland, cytostatics, antispasmodics and a special diet limiting the secretion of pancreatic juice (rich in proteins and poor in carbohydrates) are prescribed.

Topical treatment consists of thorough care of the skin around the fistula, prevention of its maceration and introduction of a drainage into the fistula lumen, through which the contents are aspirated and the fistula is washed with a weak solution of lactic acid to inactivate proteolytic enzymes. Incomplete fistulas usually close under the influence of conservative treatment for several months.

For complete fistulas, surgical treatment is indicated. The most common types of operations are: excision of a fistula, insertion of a formed fistula into the stomach or small intestine, excision of a fistula with a single-stage resection of the distal pancreas affected by the pathological process

Gastroenterology - Cysts and pancreatic fistula

Cysts and pancreas fistula - Gastroenterology

Cysts and pancreas fistula is not uncommon. Cysts are capsules with liquid inside. Located on the gland itself, as well as on the surrounding tissues. This disease occurs at any age, and is not dependent on gender. Pancreatic cysts - a collective concept.

Cysts are divided into several types:

  1. Congenital These include cysts, which are formed as a result of the malformation of pancreatic tissue, as well as the ductal system.
  2. Acquired.
  • Acquired cysts, in turn, are divided into retention, degeneration, proliferation, parasitic.
  • Retention cysts result from the stricture of the excretory ducts of the gland, as well as when they are blocked with stones or tumors.
  • Degeneration cysts develop as a result of damage to the pancreatic tissue during pancreatic necrosis, after hemorrhage, injury, or during the tumor process.
  • Proliferation cysts are abdominal neoplasms. These are cystadenocarcinomas and cystadenomas.
  • Parasitic cysts occur during infection of the organism with Echinococcus and cysticercus.

Cyst depending on the structure of its walls.

There are false and true cysts of the pancreas, depending on the structure of its walls. True cysts are congenital dysontogenetic cysts, cystadenomas and cystadenocarcinomas, acquired retention cysts. True cysts make up about 20% of all gland cysts. Its main feature is the presence of epithelial lining, which is available on its inner surface. The size of the true cysts is much more false. Some of the cysts for surgeons become a real find.

The walls of a false cyst are compacted peritoneum and fibrous tissue. Unlike a real cyst, a false one does not have an epithelial lining inside. Inside, false cysts are surrounded by granulation tissue. In the cavity there is a fluid with necrotic tissues. This fluid has a different character. As a rule, it is purulent and serous exudate containing blood admixture and clots, and pancreatic juice may also be contained. False cyst is formed on the head, body and tail of the pancreas. The amount of fluid that is contained in a cyst sometimes reaches 1-2 liters or more. A large cyst often spreads in different directions. It can be positioned forward and upward in the direction of the omentum, while the liver pushes upwards, the stomach downwards. The cyst can also be directed towards the gastrocolic ligament, while pushing the stomach upward, and the transverse colon moves downward.

Large cysts.

Larger pancreatic cysts usually proceed without any symptoms. They arise in the event that the cyst has greatly increased and began to squeeze the adjacent organs. Frequent symptoms of cysts are pain in the upper abdomen, dyspeptic symptoms appear, the general condition is disturbed, weakness occurs, the person loses weight, the body temperature rises. During palpation, a tumor-like formation in the abdomen is felt.

The patient begins to appear dull, constant pain, in some cases, pain paroxysmal. They are shingles, bursting, while the patient has to take a bend position or knee-elbow position. The strongest pains appear when the cyst is pressurized on the solar plexus and celiac. But still, with huge cysts, the pain is insignificantly expressed, patients complain of pressure in the epigastric region. The most common dyspeptic symptoms are nausea, sometimes vomiting, and unstable stool.

During the study, the main feature is a tumor formation. If the cyst is large, it can be detected at the first examination. The borders are clear, the shape is oval or round, the surface of the cyst is smooth. Tumor formation depending on the location is determined in the umbilical region, in the epigastric, as well as in the left and right hypochondrium.

Cyst complication.

The most striking complications of the pancreatic gland cyst are hemorrhages in its cavity, purulent processes, various disorders that appear after squeezing of adjacent organs with cysts, external and internal fistulae, breaks with the subsequent development of peritonitis.

For the diagnosis, the clinical symptoms of the disease are taken into account, and special research methods are conducted. An increase in the number of pancreatic enzymes is observed in blood and urine. Computed tomography, including ultrasound scanning, helps to detect dense formation filled with fluid.

The treatment is performed surgically. A resection of the site of the pancreas affected by the cyst. When pseudocyst drainage operations are used.

Pancreas fistula.

Pancreatic fistulas are pathological messages of the pancreatic ducts with internal organs or with the external environment. Fistulas are external when its mouth forms on the skin, and internal when the fistula communicates with hollow organs (small and large intestine, or stomach). Fistulas are complete and not complete. With a full fistula, pancreatic juice is expelled through the fistula to the outside. Incomplete fistula is characterized by the fact that pancreatic juice flows into the duodenum and part out through the fistula.

Most fistulas occur during abdominal trauma or after surgery on the pancreas, after opening its ducts. Internal fistulas appear as a result of changes in the pancreas, which pass on the wall of the adjacent organ (with pancreatitis, pancreatic cyst perforation and penetration).

For complete fistulas, surgical treatment is performed. The main types of operations are excision of the fistula, insertion of the resulting fistula either into the stomach or into the small intestine. The fistula is also removed along with the affected section of the pancreas.

Chronic pancreatitis

Chronic pancreatitis (CP) is a chronic relapsing inflammatory disease of the pancreas (PJ), leading to progressive atrophy of the glandular tissue of the organ, replacement of the cellular elements of the parenchyma with connective tissue, damage to the ducts, pain syndrome and loss of exo- and endocrine functions of the gland.

Over the past decades, the prevalence of chronic pancreatitis has increased, and it has acquired great medical and social importance.

Causes of pancreatitis and factors contributing to its occurrence. More than 140 factors are known that can cause pancreatitis or contribute to its occurrence. However, in the vast majority of surgical patients, pancreatitis is associated with three main factors, each of which can play an etiological role in both acute and chronic forms of the disease. These factors are (in order of importance):

  • 1) long and excessive drinking (alcoholism),
  • 2) diseases of organs adjacent to the pancreas, primarily of the biliary tract (cholelithiasis), less often of the duodenum, etc.,
  • 3) pancreas injury, including intraoperative.

It is believed that with alcoholism about 3/4 of cases of CP are associated, and the rapid increase in the prevalence of alcoholism, especially in our country, determines the sharp increase in the incidence of pancreatitis in recent decades, particularly among young and middle-aged men.

Cholelithiasis - the second most important cause of pancreatitis, which plays a predominant role in women of middle and old age. It is well known that for a long time in developed countries there was a marked increase in the number of patients with cholelithiasis, which also largely determines the increase in the frequency of associated pancreatitis.

Compared with the first two reasons injury - both “accidental”, including criminal, as well as operating room - is of less importance and primarily causes, as a rule, acute pancreatitis, which can later be transformed into chronic forms.

As an etiological factor, injury can have both direct and indirect effects on the gland. With direct exposure, direct damage to the gland tissue under the influence of mechanical force (closed or penetrating abdominal trauma, surgery on the gland itself or surrounding organs, especially on the duodenal papilla). The indirect effect of trauma is usually associated with microcirculatory ischemic disorders in the gland during traumatic shock, as well as with prolonged or imperfect extracorporeal circulation during cardiac surgery.

The number of traumatic pancreatitis is also prone to increase. This is due to the increase in the number of operations on the pancreas, endoscopic manipulations and surgical interventions on the major duodenal papilla (retrograde cholangiopancreatography (RCPG), endoscopic papillosphincterotomy (EPST)).

Thus, the impact of all three main causes of pancreatitis increased, which explains the huge increase in the prevalence of the disease during the twentieth century.

At the beginning of the XX century. pancreatitis was considered a rare disease, and the largest authority at the time in the field of diagnosis and surgical treatment of acute diseases of the abdomen French surgeon A. Mondor was proud that during many years of practice he was able to recognize acute pancreatitis twice in his lifetime. At the present time, even a novice surgeon working in an ambulance system can boast the same or even great achievement in one week, or even one duty.

Numerous other factors considered to be the cause or contributing to the development of pancreatitis are of less importance, rarely cause lesions of the pancreas, in particular requiring the attention of the surgeon. The more famous of these factors include:

  • • endocrine diseases (primary hyperparathyroidism, Cushing's disease),
  • • hyperlipidemia and hyperglyceridemia, in particular complicating pregnancy, as well as other genesis,
  • • drugs (oral contraceptives, corticosteroids, azathioprine and other immunosuppressants),
  • • allergic and autoimmune factors
  • • hereditary diseases (cystic fibrosis of the pancreas as a manifestation of cystic fibrosis, genetically determined diseases of metabolism and fermentopathy, in particular, congenital calcium deficiency, a stabilizing factor that increases the viscosity of pancreatic secretion and the formation of calcified calculus in the pancreatic duct, etc.)
  • • ischemia of the pancreas, in particular associated with compression stenosis of the celiac trunk and other causes,
  • • parasitic diseases (ascariasis, etc.).

Pathogenesis. It can be considered generally accepted that the basis of the pathogenesis of pancreatitis in the overwhelming majority of patients is damage to the gland tissue by the same digestive enzymes produced. Normally, these enzymes are released in an inactive state (except for amylase and some lipase fractions) and become active only after they enter the duodenum. Most modern authors distinguish three main pathogenetic factors that promote auto-aggression of enzymes in the body secreting them:

  • • the difficulty of outflow of secretion of the gland into the duodenum and intraductal hypertension,
  • • abnormally high volume and enzymatic activity of pancreatic juice,
  • • reflux into the ductal system of the pancreas contents of the duodenum and bile.

For a long time, the main enzyme guilty of pancreatic tissue damage in case of pancreatitis was trypsin (after activation of its precursor trypsinogen by cytokinase of damaged cells or duodenal enterokinase). Recently, much more importance is attached to the phospholipase BUT, activated from pro-enzyme bile acids and other factors, in particular trypsin. This enzyme is capable of destroying living acinar cells by cleaving their phospholipid membranes. Lipases are responsible for the occurrence of the main mass of pancreatic and parapancreatic necrosis (steato-necrosis). Trypsin and other activated proteolytic enzymes (elastase, collagenase, kallikrein) break down predominantly extracellular elements of the connective tissue, and the interstitium of the pancreas is an important object of their influence, with which hemorrhagic nature of pancreatic necrosis is associated in some patients.

The mechanisms of pathological intraorgan activation of enzymes and damage to the gland tissue differ depending on the cause of pancreatitis.

So, it is known that alcohol, especially in large doses, by reflex and humoral, dramatically increases the volume and activity of pancreatic juice. To this is added the stimulating effect of the alimentary factor. In addition, alcohol contributes to spasm of the sphincter hepatic-pancreatic ampoule (sphincter of Oddi), causes an increase in the viscosity of the pancreatic secretion, the formation of protein precipitates in it, further transforming into calculi characteristic of the chronic form of the disease. All this complicates the outflow of secretions and leads to intraductal hypertension, which at a level exceeding 350-400 mm of water column can cause damage to the epithelial cells of the ducts and acini and release of cytokinases that trigger the mechanism of enzyme activation. Spasm of the sphincter of Oddi leads to gall-pancreatic reflux and intraductal activation of enzymes due to bile acids. The direct damaging effect of high blood alcohol concentrations on glandular cells is also not excluded.

With pancreatitis associated with diseases of the biliary tract, the main pathogenetic factor is a violation of the outflow of pancreatic juice into the duodenum, which is primarily due to the presence of the already mentioned “common channel” through which the bile stones develop and where the main pancreatic duct usually flows. With separate inflow of the gall and pancreatic ducts, as well as with a separate inflow into the duodenum of the accessory (Santorini) duct, which communicates with the main duct of the pancreas, biliary pancreatitis does not develop.

Passing through the Vater ampoule, the bile stones temporarily linger in it, causing spasm of the sphincter of Oddi and transient ductal hypertension, which causes enzymatic damage to the glandular tissue and, possibly, an attack of acute pancreatitis, in some cases, flowing with little or no symptoms of biliary colic. Repeated “pushing” of gallstones through the ampoule due to high pancreatic and biliary pressure can lead to injury of the duodenal papilla mucosa and stenotic papillitis, which increasingly obstructs the passage of bile and pancreatic juice, as well as re-discharge of stones. In this form of pancreatitis, bile reflux into the pancreatic duct can also play a role, and in the presence of cholangitis, microbial enzymes also contribute to the activation of pancreatic enzymes.

An independent role in the pathogenesis of pancreatitis can also play duodenal diseases, associated with duodenostasis and hypertension in the lumen and contributing to the reflux of duodenal contents into the pancreatic duct (including "afferent loop syndrome" after resection of the stomach according to Billroth II type). Parapapillary duodenal diverticulum can cause both spasm and (rarely) atony of the sphincter of Oddi.

With direct injury mechanical activation of the gland leads to intraorganic activation of the enzymes, with the release of activators (cytokinases) from the necrotic cells and subsequent development, in addition to the traumatic enzyme jacreonecrosis. During endoscopic interventions on the large duodenal papilla (RCP, EPST), the mucosa of the Vater ampulla and the terminal part of the main pancreatic duct are often injured. As a result of trauma, hemorrhage and reactive edema, the outflow of pancreatic secretion may be hampered and ductal hypertension develops, whose role in the pathogenesis of pancreatitis has already been considered. The duct walls can also be damaged by overpressure with the introduction of a contrast agent in the case of RCPG.

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

In chronic pancreatitis, not acting as a consequence of acute, enzymatic damage, necrobiosis, necrosis and autolysis of pancreatocytes also occur, occurring gradually, under the influence of a long-term factor, and acutely during the exacerbations of the chronic process.

Resorption of small disseminated foci of nacreonecrosis with their replacement with cicatricial tissue leads to sclerosis of the pancreas, compression of acini, deformity and cicatricial strictures of the excretory ducts, which plays an important role in the violation of secret outflow and the pathogenesis of chronic pancreatitis in general. The progression of the cicatricial process in the gland can lead to a significant reduction in both external and intrasecretory functions (digestive disorders, diabetes), as well as to compression of the common bile duct (obstructive jaundice) passing through the thickness of the pancreatic head (portal obstruction), portal vein (portal hypertension).

In the case of the encapsulation of small foci of necrosis, their secondary calcification, especially characteristic of alcoholic CP and pancreatitis associated with impaired calcium metabolism (hyperparathyroidism, deficiency of calcium-stabilizing factor). Calcification of the pancreatic parenchyma in chronic pancreatitis is indirect evidence of the small-focal pancreatic necrosis that was transferred in the past, since calcium salts are usually deposited in the devitalized, dead tissue.

Larger lesions pancreatonecrosis at its end in the encapsulation in some cases may proceed aseptically and be transformed into a false pancreatic, parapancreatic or combined cyst with fibrous walls formed initially necrotic tkanyo, and after its gradual degradation and dissolution - turbid gradually bleachable liquid, often comprising pancreatic secretion enzymes. The accession of the infection causes the occurrence of a sluggish pancreatic or parapancreatic abscess, usually containing pus and elements of pancreatic necrosis, which is in various stages of degradation. However, the addition of infectious inflammation in principle means a change in the fate of the necrotic tissue and the transition from unstable encapsulation to rejection.

Classification. Depending on the cause of the disease, chronic pancreatitis can be:

  • 1) alcohol,
  • 2) cholangiogenic (associated with diseases of the biliary tract),
  • 3) traumatic
  • 4) due to other factors.

By the nature of the morphological changes in the parenchyma of the gland should be allocated:

  • 1) diffuse sclerosing chronic pancreatitis,
  • 2) chronic pancreatitis with the presence of cavity formations (encapsulated foci of pancreatic necrosis, false cysts, sluggish abscesses).

Both of these types of diseases can occur:

  • a) without calcification
  • b) with calcification of the parenchyma of the gland.

According to the state of the duct system, one should single out:

  • 1) chronic pancreatitis without signs of ductal hypertension
  • 2) chronic pancreatitis with signs of ductal hypertension, including:
    • a) without intrastream concretions,
    • b) with intraductal calculus.

The prevalence distinguish chronic pancreatitis:

  • 1) regional with primary localization of changes (combinations are possible):
    • a) in the pancreatic head,
    • b) the body of the pancreas,
    • c) the tail of the pancreas,
  • 2) subtotal,
  • 3) total.

In addition, chronic pancreatitis is also distinguished:

  • a) without pronounced damage to parapancreatic fiber (parapancreatitis),
  • b) with a pronounced lesion of parapancreatic fiber.

In the clinical aspect can be distinguished:

  • 1) primary chronic pancreatitis,
  • 2) residual (residual) chronic pancreatitis, which is a continuation of acute pancreatitis.

The course of chronic pancreatitis can be:

  • 1) monotonous,
  • 2) periodically sharpening with phases:
    • a) aggravation
    • b) remission
  • 3) latent (including with long-term remission).

You can distinguish the form of chronic pancreatitis, depending on the presence of complications and their nature:

  • 1) chronic pancreatitis without complications,
  • 2) chronic pancreatitis, complicated:
    • a) acute massive pancreatic necrosis,
    • b) pancreatic fistula,
    • c) obstructive jaundice and (or) cholangitis,
    • d) violation of the duodenum,
    • e) portal hypertension,
    • e) bleeding,
    • g) alimentary exhaustion,
  • 3) diabetes,
  • and) other complications.

Clinical picture. The most frequent and relatively early manifestation of CP is pain syndrome. Pain is usually of considerable intensity. It is associated with impaired outflow of pancreatic juice and ductal hypertension, a chronic inflammatory process in the gland of aseptic or infectious nature, as well as involvement in the scar-inflammatory changes of the retroperitoneal nerve plexus and blood vessels that provide pancreatic circulation (ischemia).

The pain is usually localized in the epigastric region, sometimes closer to the left or right hypochondrium, often radiating to the lower back or has a surrounding character. Localization of pain may depend on the location of the zone of most or primary damage to the gland (head, body, tail). Sometimes the pain is monotonous, but in most patients it is associated with food intake and begins or increases an hour or more after eating. In some cases, predominantly night pain. With recurrent pancreatitis, pain can only appear during exacerbations or increase during these periods.

Characteristic for pain in chronic pancreatitis is that they tend to increase in the position of the patient on his back and weaken with a change in body position. Acceptance of alcohol sometimes temporarily reduces pain, but in most patients it contributes to its strengthening. In chronic pancreatitis associated with cholelithiasis, pancreatogenic pain can be combined with pain in the right hypochondrium, characteristic of cholecystitis.

In patients with so-called painless CP or its latent course (usually with chronic alcoholic pancreatitis), the pain may be insignificant or it may be completely absent for a long time, which, most likely, may be due to the absence of marked ductal hypertension. Clinical manifestations in this group of patients are often associated mainly with a decrease in external and (or) internal secretion of G1G.

The group of frequently occurring symptoms of XII depends on the enzymatic deficiency of the gland and the corresponding digestive disorders. So, almost simultaneously with the pain, most patients have complaints about bloating and wasting belly and sometimes salivation after eating. These symptoms are aggravated by violations of the diet and after taking alcohol. Characteristic are also stool disorders.

In typical cases, constipation first occurs, which is then replaced by an unstable chair with alternating constipation and diarrhea. With often observable steatorrhea fecal masses acquire a grayish color, a characteristic oily sheen and may contain undigested food particles. In severe cases, persistent profuse diarrhea may occur with liquid watery stools containing fat drops. At the same time, the appetite is preserved, and even increased in some patients.

Digestive disorders, consisting in violations of the digestion and utilization of nutrients and vitamins, lead to weight loss and nutritional depletion of patients, accompanied by hypovitaminosis.

When a secondary infection process occurs in the gland zone (usually with pancreatitis associated with the formation of pathological cavities - festering false cysts) fever, sometimes accompanied by chilliness and sweats, and the general malaise associated with it, as well as increased pain in the area of ​​the pathological focus.

In the case of a secondary violation of the passage of bile due to compression of the terminal segment of the common bile duct with an enlarged and compacted gland head or cyst jaundiceand in cholangitis there is fever, heaviness and tenderness in the right hypochondrium.

With the compression of the duodenum, an accelerated feeling of saturation may be noted, nausea and vomiting after eating.

For large pancreatic and parapancreatic cysts, patients sometimes complain of abdominal asymmetry, painful bulging in its upper part.

Complications of pseudocysts or chronic abscess of the gland bleeding manifest well-known general symptoms of blood loss, and when there is communication between the cavity and the lumen of the gastrointestinal tract (most often pseudocystoduodenal fistula), a copious tarry stool appears. Pains sometimes amplify, and in the field of a cyst palpation begins or the volume education increases.

Complaints associated with endocrine insufficiency of the pancreas, usually occur late and do not always attract the attention of the patient. The reason for this may be a decrease in insulin requirements due to disruption of carbohydrate absorption, and the fact that in the insular apparatus along with insulin, the secretion of its antagonist, glucagon, decreases for the same reasons, and this contributes to the stabilization of glycemia and a more "soft" flow diabetes in a number of patients with CP.

Anamnesis of patients with chronic pancreatitis most often quite characteristic. For most of them, for several years before the onset of disorders associated with the pathology of the pancreas, there is an excessive consumption of alcohol as a result of severe alcohol dependence (alcoholism) or the so-called domestic drinking. Although in many cases, patients seek to hide from the doctor the true amount of alcohol consumed by them, it cannot yet be ruled out that sometimes alcoholic XII can be from taking moderate doses of hard liquor, and act as a result of individually increased sensitivity to them of the pancreas.

In a quantitatively smaller group of patients in which middle-aged and elderly women predominate, a history of cholelithiasis, including those complicated by episodes of obstructive jaundice and (or) cholangitis, the presence of the so-called postcholecystectomy syndrome, often associated with residual choledocholithiasis, is noted in history.Sometimes cholelithiasis, complicated by CP, can occur without classical symptoms, and cholecysto-or even choledocholithiasis is diagnosed in a patient with CP only with a special study.

Less commonly, a history of closed or open injury of the pancreas, surgery on the gland or adjacent organs, endoscopic interventions on the large duodenal papilla, etc.

In an even smaller number of patients in history, other endogenous or exogenous factors are established that may cause or contribute to the occurrence of CP (hyper-arythyroidism, cystic fibrosis, hereditary metabolic disorders, systematic intake of certain medications, etc.).

With objective clinical study It is relatively rare for a patient with uncomplicated XII to identify the signs specific to this disease. When viewed from a significant proportion of patients, there is a reduced nutrition, pale, sometimes the skin color of the face, sometimes with an icteric or earthy tint, and a tongue with a whitish bloom.

Percussion and auscultation of the chest rarely reveal effusion that is localized more often in the left pleural cavity and is associated either with a pancreato-pleural fistula or with suppuration of a pancreatic or para-pancreatic pseudocyst located under the left dome of the diaphragm. In the latter case, pleural effusion is called reactive.

An asymmetric increase in the volume of the abdomen in the upper section can be observed in the presence of large pancreatic or parapancreatic pseudocysts.

The presence of ascites, causing a general increase in the size of the abdomen and percussion dullness moving in shifting areas, is associated with secondary portal hypertension, which develops as a result of involvement in the scar-inflammatory process and (or) thrombosis of the portal vein and its main tributaries (upper mesenteric and splenic veins), passing in the immediate vicinity of the pancreas (subhepatic portal block). In this case, ascites is usually preceded and accompanied by splenomegaly, which is determined by palpation or percussion.

It is possible to palpate the pathologically altered pancreas itself mainly in exhausted patients in the form of a painful cushion located transversely in the epigastrium, and also in the presence of significant abdominal formations (pseudocysts, sluggish abscesses), including those which act as the substrate of the so-called tumor-like chronic pancreat. . Sometimes it is noteworthy that there is a mismatch between the intense pain syndrome and the slight pain caused by palpation.

In the case of obstructive jaundice, associated with an increase and compaction of the pancreas head surrounding the terminal part of the common bile duct, it is sometimes possible to palpate an enlarged and painless gallbladder (a variant of the Courvoisier symptom), and in case of duodenal obstruction, a distended stomach with a splashed noise phenomenon.

Sometimes systolic murmur is heard in the xiphoid process, indicating compression stenosis of the celiac trunk, which can cause ischemia of G1G (and other organs of the upper abdomen) and, as already mentioned, are related to the pathogenesis of chronic pancreatitis.

Laboratory diagnosis. In the study of patients with suspected chronic pancreatitis laboratory data have auxiliary diagnostic value. In general, a blood test can reveal some degree of anemia and phase changes characteristic of an exacerbation of the infectious-inflammatory process (leukocytosis, shifting the neutrophilic formula to the left, increasing erythrocyte sedimentation rate - ESR). Biochemical analysis reveals hypoproteinemia in exhausted patients, and hyperglycemia in secondary diabetes. With monotonically current CP, the increase in the level of enzymes in the blood, in particular hyperaemlasemia, may not be observed, and during exacerbations the level of enzymes, as a rule, increases, and sometimes significantly. The corresponding increase in the level of enzymes is observed in the urine.

In feces with steatorrhea, neutral fat and soaps are detected, and the content of bile acids is estimated to be normal (of course, with normal biliary tract patency). When creatorrhea is associated with insufficient enzymatic protein breakdown, feces contain little-altered muscle fibers.

A modern method for evaluating the exocrine function of the pancreas is the elastase test. Elastase - an enzyme that is produced by acinar cells of the gland is destroyed during the passage through the intestine of the ns; therefore, determining its concentration in the feces is an objective criterion for assessing the state of the exocrine function of the gland.

Some diagnostic value is the study of enzymes (mainly amylase) in the punctates of the contents of false cysts, as well as in the pleural exudate, sometimes complicating the course of CP.

Hardware and instrumental diagnostic methods. Survey radiography of the abdominal cavity (Fig. 20.1) is of more academic importance in the diagnosis of CP, however, characteristic changes can be identified only in patients with pronounced calcification of the gland parenchyma and (or) sufficiently large calcified calculi in the pancreatic duct.

Fig. 20.1.Survey radiograph of the abdominal organs in chronic calcific pancreatitis.

The picture shows large calcifications in the projection of the pancreas throughout (indicated by arrows)

Fibrogastroduodenoscopy (fibrogastroduodenoscopy) and retrograde cholangiopancreatography (rhPG) allow you to visually identify changes in the duodenum and major duodenal papilla (BDS), as well as to contrast pancreatic and bile ducts (Fig. 20.2).

Fig. 20.2.Retrograde pancreatography in chronic pancreatitis.

The picture shows a sharply expanded main pancreatic duct.

Contrast study of the biliary tract (cholangiography) is necessary first of all for patients with biliary CP or with suspicion of such. It is carried out either by an indirect method with oral or intravenous administration of a contrast agent, which, unfortunately, does not provide sufficient quality of images and is generally not applicable in patients with obstruction of the biliary tract, or by direct contrasting. The latter is achieved by RCCP (Fig. 20.3), as well as by percutaneous percutaneous puncture of the gallbladder or bile duct, including under the control of ultrasound, computed tomography or laparoscope.

Fig. 20.3.Retrograde cholangiopancreatography. Bile ducts, gallbladder and main pancreatic duct are contrasted. The picture shows prolonged narrowing (a symptom of a “mouse tail”) of the terminal part of the common bile duct (pancreatic part) and a sharp expansion of the main pancreatic duct with the vagueness of its contours.

When the gallbladder is blocked by stones or missing (after cholecystectomy), it is possible to inject a contrast agent by puncture of the intrahepatic bile ducts. In the presence of gall fistula, contrasting is achieved as a result of fistulography.

On the basis of cholangiography, it is possible to judge the presence of biliary stones, the expansion, deformation or stenosis of the biliary tract, the presence of obstacles to the flow of bile into the duodenum.

X-ray examination of the stomach and especially the duodenum is of significant diagnostic importance. When X-ray of the stomach, organic lesions that may be related to the pathogenesis of pancreatitis are excluded, and deformations associated with changes in the pancreas (Fig. 20.4), such as depression in the presence of a pseudocyst, CP tumor, etc., are sometimes detected.

Fig. 20.4.Deformation of the contour of the output section of the stomach and the turn of the duodenum with a cyst of the pancreatic head

Duodenography makes it possible to judge the free passage of barium through the duodenum or the presence of duodenostasis, as already mentioned, which is important in the pathogenesis of CP. An informative method is the X-ray examination of the duodenum under conditions of medical (artificial) hypotension, achieved by prior administration of antispasmodics, such as atropine. Characteristic features of chronic pancreatitis, which hypotonia contributes to, include dilated horseshoe duodenal ulcer due to an increase in the size of the pancreatic head and the presence of a wide filling defect on the medial wall of the descending part of the intestine, sometimes stenosing the lumen and making barium difficult to pass (Fig. 20.5).

Endoscopes with a side field of view are used to perform duodenoscopy. The study is usually carried out on an empty stomach, in a specially adapted X-ray room on an apparatus equipped with an electron-optical converter and a seriograph (if an RHIG is planned to be performed).

Fig. 20.5.Duodeiography with hypotension. The picture shows the expansion of the horseshoe duodenum and compression of the intestine at the level of the descending and lower horizontal branches of the enlarged head of the pancreas

With the help of an endoscope, the esophagus is preliminarily examined, where the dilated veins of the submucosal layer, which result from secondary portal hypertension, and then the stomach, are sometimes detected. In the stomach, there are often manifestations of gastritis, including erosive (during periods of exacerbations). Sometimes visible pushing back of the back of the stomach anteriorly (in the presence of pancreatic nsevdokist, tumor form XII).

In the duodenum, signs of duodenitis are often identified, the medial wall is pushed aside by an enlarged head of the gland, sometimes narrowing the lumen. Often erosions are visible on the mucous membrane, sometimes the changes acquire the character of the so-called pseudotumorous duodenitis, in which the intestinal wall becomes rigid, bleeding easily on contact, which requires a biopsy to exclude a cancerous lesion.

Examination of the MDP often reveals its changes that are associated with pancreatitis (papillitis, stenosis, papillomatous growths, sometimes also requiring biopsy to exclude papilla cancer, peripapillary duodenal diverticula, etc.).

If it is decided to carry out RCPG, a special Teflon catheter with an outer diameter of 1.8 mm is introduced into the Vater ampulla through the channel of the fibroscope, and through it a water-soluble radiopaque preparation (verographin, urographin, etc.), avoiding excessive pressure, and then taking a picture.

On the roentgenogram, signs characteristic of chronic pancreatitis can be found: an expansion of the main pancreatic duct (sometimes in the form of a contrasting “lake value”), the presence of strictures in the duct, calculus, and cavities associated with it (pseudocyst).

On the simultaneously performed cholangiogram, a stricture of the terminal part of the choledochus, expansion of the extrahepatic and intrahepatic bile ducts, choledocholithiasis, etc. can be detected. Considering the possible complications of rhPg (acute pancreatitis, acute cholangitis up to the development of bacterial toxic shock in the presence of infection in the ducts), this study is performed mainly according to absolute indications, before surgery or with simultaneous endoscopic ductal decompression and mandatory prophylaxis of OD (octreotide, antispasmodics) , infusion therapy).

Ultrasound examination (Fig. 20.6) - one of the most informative and, moreover, non-invasive methods of investigation of the pancreas - should be carried out in all cases when its pathology is suspected.

Fig. 20.6.Ultrasound for chronic pancreatitis:

DP - dilated pancreatic duct, L - liver, R - pancreas, VL - splenic vein, IVC - inferior vena cava, AO - aorta

The ultrasonic sensor is located in the epigastric region, and it is moved, respectively, by the projection of the gland on the left and right hypochondrium areas.

Normally, the pancreas has even, clear contours and a homogeneous structure, and the diameter of the main pancreatic duct does not exceed 1.5-2 mm. In pathology, a general increase in the size of the organ can be detected with a uniform decrease in echo density, indicating edema. Reducing the size of the gland, the heterogeneity of the structure, the presence of small areas of tissue consolidation, as well as the fuzziness of the contours may indicate fibrotic changes in the gland, and small sharply pronounced echo-positive nodules show focal calcification of the parenchyma.

High-density echostructures, located in the duct and giving the phenomenon of "ultrasonic track", are a sign of intraductal concretions.

Liquid formations (false cysts, sluggish abscesses) are represented on the echogram by rounded areas of significantly reduced echo density with more or less clear contours and dorsal amplification. Well-formed false cysts with liquid contents are round or oval in shape, homogeneous and surrounded by a well-defined capsule. The contents of unformed cysts and abscesses may be heterogeneous due to the presence of tissue sequesters and detritus in addition to fluid.

Computed tomography (CT) is a high resolution radiographic method, widely used in the study of the pancreas (Fig. 20.7). In principle, the method makes it possible to obtain data similar to echographic, but in some cases it makes it possible to clarify the latter, for example, when the patient is obese, the presence of meteorism, the preferential localization of pathological changes in the tail area of ​​the gland.

Fig. 20.7.Computed tomography for chronic calcific pancreatitis. The picture shows cysts of the head of the pancreas (U), advanced Wirsung duct and calcinate in its lumen (2)

At the same time, there are cases when focal changes detected by ultrasound are not detected at CT (isodens) or vice versa (iso-echogenic). Thus, both studies complement each other. Given the high cost of CT, its use should be considered necessary in cases where, on the basis of ultrasound, it is not possible to create a sufficiently clear picture of pathological changes in the pancreas (for example, when a partially isoechogenic focus is detected in the pancreas).

Normally, the pancreas is defined on computer tomograms in the form of a relatively homogeneous formation of a 5-shaped form. Signs of lesions of the gland are heterogeneity of the shadows with areas of compaction and dilution, expansion, contraction and deformation of the ducts, single or multiple cavitary fluid formations. For a false cyst, as with ultrasound, is characterized by the presence of a capsule and uniform or non-uniform (if there are sequesters in the cavity or putty-like detritus) contents. High resolution of CT in the presence of calcifications in the gland and duct stones. Malignant neoplasms appear at CT scan with foci whose density is lower than that of the gland.

Fine needle aspiration biopsy (TIAB) is used mainly for the differential diagnosis of a tumorous form of chronic pancreatitis and pancreatic cancer. It is carried out through the anterior abdominal wall under local anesthesia, and the direction of the needle is constantly monitored using an ultrasound scanner or a computer tomograph.The diagnostic effectiveness of the method depends on the experience of the physician who performs the puncture, the size of the punctured education and the number of punctures, as well as on the experience of the cytologist who studies the nunggates.

Despite the sufficient number and high information content of modern methods of preoperative diagnosis, not all patients can accurately recognize the nature of the lesion of the pancreas. In this regard, intraoperative diagnosis is of great importance. It includes the following elements:

  • • examination and palpation of the pancreas, biliary tract, stomach, duodenum, including the BDS area,
  • • direct puncture contrasting of the pancreatic and common bile duct with a picture on the operating table,
  • • puncture or incisional biopsy of pathological formations of the pancreas and altered regional lymph nodes.

Differential diagnosis. Chronic pancreatitis should be differentiated primarily with diseases manifested by chronic pain in the epigastric region, including those associated with food intake and occurring with periodic exacerbations. A radiographic and contrast study, especially EGD, makes it possible to exclude chronic gastric or duodenal ulcer, as well as painful forms of chronic gastritis. But it should be remembered that an ulcer penetrating into the pancreas may be a factor contributing to the occurrence of CP, and therefore, the detection of an ulcer cannot rule out the disease in question. This may impose a well-known imprint on the manifestation of peptic ulcer disease (irradiation of back pain, surrounding character), but usually does not bother the patient after the ulcer has healed in one way or another.

Gallstone disease is usually eliminated by ultrasound of the extrahepatic biliary tract (absence of calculus and other changes in the gallbladder). However, gallstone disease acts as a causative factor of pancreatitis, and the identification of stones in the bladder does not exclude this disease. Therefore, complaints of a patient with a verified gallstone disease of pain outside the projection of the gallbladder (in the middle part of the epigastrium), especially radiating to the lower back, make you think of chronic cholangiogenic (biliary) pancreatitis (or the so-called chronic cholecystopyscreatitis) and continue special studies in this direction.

Serious problems can arise from the differentiation of the pseudotumor form of chronic pancreatitis and pancreatic cancer. In chronic pancreatitis, it is possible to detect morphologically the proliferation of epithelial elements with signs of cellular atypism, which is considered to be a precancerous condition, and in cancer that surrounds the main pancreatic duct, manifestations of secondary pancreatitis are found. The combination of these two diseases as independent nosological forms occurs, apparently, infrequently.

At the same time, chronic pancreatitis, in particular, its pseudo-tumorous form, with predominant lesion of the glandular head, can cause compression of the terminal part of the common bile duct and give obstructive jaundice syndrome, characteristic of cancer of this localization, and manifest as pain in the case of pancreas lesion, which is also characteristic of neglected cancer of appropriate localization.

There are a number of clinical differences, in most cases allowing to differentiate the diseases in question. So, first of all, a relatively short history, not exceeding a few weeks or at most months, is characteristic of cancer, whereas in chronic pancreatitis, the history is more often longer. Operable cancer of the pancreas is almost never manifested by intense pain, and obstructive jaundice caused by it in the majority of cases occurs against the background of apparent health, as a result of which patients initially are usually hospitalized in the infectious diseases wards to exclude viral hepatitis. At the same time, in chronic pancreatitis obstructive jaundice occurs in patients most often with an alcohol history, who in the past had acute pancreatitis or had suffered from pain and periodic exacerbations of the infectious process associated with chronic pancreatitis for a long time. If obstructive jaundice occurs in patients with CP of cholangiogenic origin and is associated with difficult passage of bile calculus or impairment of it in a fatal ampoule, then, as a rule, there is a pronounced pain syndrome and other signs of exacerbation of calculous cholecystitis and cholangitis, which are not characteristic of jaundice associated with cancer of the head of the pancreas.

Unfortunately, special methods do not allow solving the considered differential diagnostic problem in all cases. Thus, a patient’s blood test for a carbohydrate antigen (CA 19–9) and a cancer embryonic antigen (CEA) gives a clearly positive response only at sufficiently large tumor sizes, often in inoperable cases. Examination of the pancreas using ultrasound or computed tomography gives an increase in the size of the gland, especially its head, and in chronic pancreatitis, and in cancer, and also reveals focal lesions of one size or another, moreover, a single hypoechoic mass is more characteristic of cancer pancreatitis, the pancreas is often diffusely altered, it is hyperechogenic (more dense), contains multiple calcifications, although it is not possible to precisely differentiate the nature of the lesions in all cases.

However, a significant expansion of the main pancreatic duct, and the more the presence of stones in it is not typical for cancer and, as a rule, indicates chronic pancreatitis. Identification of multiple foci in the liver in the presence of a pancreatic tumor indicates hematogenous dissemination of pancreatic cancer.

The already mentioned fine needle biopsy, performed through the anterior abdominal wall under the control of ultrasound or CT, also does not always solve the problems of differential diagnosis. Detection during cytological examination of a biopsy is undoubtedly cancer cells or their complexes, of course, indicates cancer. However, the absence of cancer elements in biopsy specimens in no way allows one to exclude oncological diagnosis, including after repeated punctures. If during diagnostic puncture it is possible to get pus, then the diagnosis of chronic pancreatitis becomes the most likely, although not absolutely reliable, since an obturating tumor can cause a secondary suppurative process in the ductal system of the gland.

In the case of the Nsevdotumoric form of CP, even a laparotomy, produced by an experienced surgeon in this field, does not always allow, by direct examination and palpation of the gland, to eliminate its cancerous lesion. Intraoperatively produced needle biopsy will make it possible to obtain material from the pathological focus with high confidence; however, even after an urgent cytological study, the situation does not become clear in all cases.

Direct incisional biopsy in cancer of the pancreas presents certain technical difficulties, especially with the deep location of the lesion in the head. However, even after obtaining a good biopsy, even experienced pathologists cannot always confidently distinguish cancer from epithelial proliferation characteristic of chronic pancreatitis, especially in the context of an urgent study. Therefore, even in specially equipped institutions that are specifically involved in the problem, diagnostic and, accordingly, tactical errors are sometimes made, some of which depend on underestimating purely clinical manifestations of the disease. As a result of this, the patients with pseudotumor pancreatitis of the head carry by no means the absolute pancreatoduodenal resection indicated by them, aimed at radical removal of the tumor. And patients with suspected inoperable cancer, which had palliative interventions such as biliodigestive anastomoses, live inexplicably long and sometimes are mistakenly considered to be miraculously spontaneously recovered from a hopeless cancer. Currently, most surgeons operating on the pancreas believe that if it is impossible to exclude cancer intraoperatively, one or another amount of its resection should be performed.

Surgery. The general indication for surgical treatment of CP is the ineffectiveness of conservative treatment conducted by gastroenterologist therapists. In rare cases, the indications can be considered as emergency, for example, in case of acute bleeding into the cavity, pseudocysts and (or) into the lumen of the gastrointestinal tract, as well as when a large cyst ruptures. Operations on urgent indications are performed much more often. They are shown in the exacerbation of an infectious process in the pancreas and its surrounding tissues, obstructive jaundice, as well as decompensated duodenal obstruction. In most cases, the treatment of CP is carried out in a planned manner after a thorough examination of the patient. The urgency of the indications for CP surgery increases when it is impossible to exclude a malignant tumor of the pancreas.

Surgical treatment of CP is associated with two fundamental difficulties.

The first of these is that the pathological changes in the gland affected by CP are severe, widespread and less reversible. At the same time, even in seriously ill patients, the gland continues to perform some of the exocon and endocrine functions vital for the patient. Therefore, in the full sense of the word, a radical operation in the form of pancreatectomy inevitably implies a complex and extremely expensive replacement therapy with digestive enzymes and hormones throughout life, and, moreover, is associated with great technical difficulties, possible complications and an immediate danger to the patient. It follows that most methods of surgical treatment of CP are, if not palliative, then to some extent compromise, i.e. suggest the preservation and functioning of the diseased gland tissue or, in any case, parts of it.

The second fundamental difficulty lies in the fact that the majority of patients with CP, as already mentioned, are chronic alcoholics, and the results of the application of most surgical methods greatly depend on how much the operated person wants and can cope with his or her vice. If patients after the operation continue to consume alcoholic beverages, the improvement of their condition is most often temporary, despite correctly executed labor-intensive, often multi-stage and costly interventions. Therefore, the treatment of patients with chronic alcoholic pancreatitis should be carried out successively by surgeons and narcologists.

In the surgical treatment of chronic pancreatitis, the following main tasks can and should be performed:

  • 1) the release of the pancreas and parapancreatic fiber from the affected areas of infected pancreatic necrosis and its derivatives (tissue sequesters, detritus, pus). This element of intervention, carried out with the most common in the surgical practice of abdominal forms of chronic pancreatitis, can be considered as a late necrotomy (sequestrectomy),
  • 2) elimination of ductal hypertension by ensuring the smooth flow of pancreatic secretions into the intestinal lumen,
  • 3) sanitation of the biliary tract and ensuring free flow of bile in chronic pancreatitis associated with cholelithiasis, as well as in secondary choledoch stenosis complicating other forms of chronic pancreatitis,
  • 4) resection of the most modified part of the pancreas with relatively localized forms of chronic pancreatitis (pancreatoduodenal resection (more often if it is impossible to exclude cancer of the pancreatic head), isolated resection of the pancreatic head, middle or left-side resection of the pancreas),
  • 5) the implementation of special measures aimed at the elimination of major pseudocysts and pancreatic fistulas that have independent significance (usually this problem is solved during the implementation of the first four tasks, see also paragraphs 20.2, 20.3).

Methods of pancreas denervation suggested in the past in so-called painful chronic pancreatitis (post-Yangiok-Vakabayashi postganglionic neurotomy, as well as sealing the ductal system of the gland with a liquid rapidly hardening plastic to turn off the excretory function) have hardly been used in recent years.

Surgical interventions for chronic pancreatitis are one- or two-step. Two-stage operations are planned in advance in accordance with the features of the pathology identified in the study, or are forced by unexpected circumstances discovered during the intervention. However, in many cases, patients have to undergo multiple surgeries for CP. This is due to the severity of the existing pathology, or to the insufficiency of the special qualifications of surgeons who take on the task that is too difficult for them, or to the patients in violation of the prescribed regimen (drinking and other violations of the diet).

Let us return to the fulfillment of the five main objectives of the surgical treatment of CP, as applied to specific clinical situations.

If the patient comes over chronic pancreatitis, which occurs with periodic exacerbations or during exacerbations (which happens very often), and it has clinical signs of an infectious process (temperature reaction, increased epigastric pain, acute white blood reaction, etc. .), and with ultrasound or CT scan of the pancreas, large-focal, presumably cavitary, formations are detected, one should think of the cavity form of chronic pancreatitis with sluggish or exacerbated suppuration in the zone of old lesions pancreatic necrosis. In such patients, intervention should be possible as early as possible, which has the main purpose of dissection, emptying and drainage of pancreatic and parapancreatic foci of chronic infection, i.e. perform some form of the already mentioned late necrotomy. At the same time, if necessary, the operation is usually carried out on the biliary tract.

After the upper midline laparotomy, the operator first assesses the state of the extrahepatic biliary tract and, in the event of a pathology, performs their surgical rehabilitation. In the presence of calculous cholecystitis, cholecystectomy is performed, in choledocholithiasis, cholechotomy and stone removal, revision of the terminal part of the common bile duct, and intervention on the biliary tract often ends with drainage of the choledoch by T-shaped drainage.

If, in the absence of cholelithiasis, there are signs of secondary biliary hypertension (enlargement of the gallbladder, expansion of the choledochus), in order to decompress, impose cholecystostomy.

The main part of the operation begins with a wide dissection of the gastrocolic ligament and a thorough revision of the pancreas, and for the access to the back surface of the head it is necessary to mobilize the duodenum according to Kocher (Fig. 20.8 and 20.9).

Fig. 20.8.Dissection of the parietal peritoneum along the edge of the duodenum

Fig. 20.9.The duodenum together with the head of the pancreas bluntly exfoliates from the retroperitoneal tissue and palpation of the mobilized organs is performed.

The inflammatory infiltrates found in the gland and surrounding tissue (often with signs of central softening and even fluctuations) are punctured, and when they receive a turbid liquid, pus and tiny detritus, the needle is opened, removing semi-melted tissue sequesters and liquid pus from the cavities. Comparing the operating finding with the data of ultrasound and CT, you should make sure that all foci of pancreatic necrosis are found and emptied. The open cavities are drained by individual tubes, which are fixed to the surrounding tissues and are displayed on the anterior abdominal wall.

In many cases, during this intervention, an expanded pancreatic duct is opened and reorganized with external drainage of the proximal and distal parts of it (fig. 20.10).

Fig. 20.10.External drainage of the main pancreatic duct after a transverse incision of the pancreas in the body area (to the posterior wall of the main pancreatic duct)

In some cases, form a longitudinal pancreatojejunostomy (Fig. 20.11 and 20.12).

Fig. 20.11.The stage of the operation of the formation of a longitudinal nanocreatojejunostomy (operation Pewstau-N). Pancreatic duct cut longitudinally(1),jejunum is lined up to the pancreas (2) (the back lip of the anastomosis is formed)

Fig. 20.12.The final form of the operation of the formation of a longitudinal nanocreatojejunostomy (operation Piustau-I)

The imposition of nancreatojejunostomy (PEA) at this stage of surgical treatment is contraindicated in cases of infectious inflammatory process in the gland or parapancreatic fiber, exacerbation of chronic pancreatitis. In these cases, there is always the risk of divergence of the anastomotic sutures, so you should limit yourself to external drainage of the main pancreatic duct.

In the postoperative period, in the event of a message of open foci with the ductal system of the gland, as well as after external drainage of the duct, a pancreatic fistula (fistula) is usually formed, which, with free flow of pancreatic juice, heals naturally, and if there is an obstacle in the proximal duct, it continues to function until the next stages of surgical treatment - imposition of NAP.

Operations aimed at ensuring the free flow of secretion of the gland into the intestine are carried out in patients with signs of ductal hypertension (dilation of the duct due to stricture of its terminal section, duct stones, persistent pancreatic fistula). Endoscopic interventions on the DB C (EPST) (Fig. 20.13) and transduodenal operations such as papillosphinctero-and virsungoplasty are ineffective due to the usually prolonged stenosis of the terminal part of the pancreatic duct, as well as the risk of severe exacerbation of CP. Therefore, preference is given to the longitudinal PEA with the Ru initial loops of the jejunum turned off according to the type of operation of Pewstau-P.

Fig. 20.13.Schematic representation of endoscopic intervention on the major duodenal papilla

In patients with chronic pancreatitis with more or less localized gross pathological changes in the gland (a large isevdocist or a group of pseudocysts, a dense volumetric formation if it is impossible to exclude a tumor, etc.), removal of the affected areas is indicated. After resection of the caudal region, the main pancreatic duct is sought to drain retrogradely (to eliminate ductal pancreatic hypertension) by imposing a terminolateral (term terminal) anastomosis of the transverse section of the gland with the loop of the jejunum turned off along Roux (Pewstau-1 operation) (Fig. 20.14).

Fig. 20.14.Operation Pewstau-I. Overlay pancreatoenteroanastomosis with a loop of jejunum, turned off by Roux, after distal resection of the pancreas

Some authors, who consider such an anastomosis to be insufficient, additionally dissect the duct longitudinally and connect it to the intestine, as if combining the methods of Pyustau-I and Pyustau-N.

During the resection of the middle section (body) of the gland, the loop of the intestine turned off along the anastomosis with the ends of the remaining proximal and distal parts of the gland (Fig. 20.15).

Fig. 20.15.Type of reconstruction after midline resection of the pancreas

Pancreatoduodenal resection (PDR), if it is impossible to exclude cancer of the pancreatic head, is performed, as a rule, according to the well-developed Whipple technique (for more details see paragraph 21.2).

A special feature of PDR in chronic pancreatitis is the difficulty associated with extensive cicatricial peripancreatitis, especially in isolating the posterior surface of the head and the hooked process, between which is located the portal vein with the tributaries and the superior mesenteric vein.

Interventions on the extrahepatic biliary tract but for cholelithiasis are of independent significance mainly in patients with milder forms of chronic biliary pancreatitis, in which severe morphological changes in the gland are usually absent, and exacerbations of cholecystitis or discharge of concretions through the Vater ampoule are accompanied by transient swelling of the gland and the corresponding combination symptomatology.

Surgeries aimed at the treatment of duodenal pathology, which, as already mentioned, are important in the pathogenesis of the disease (duodenostasis, duodenal, especially peripapillary, diverticula, etc.) have a certain value in the treatment of CP.

Watch the video: Pancreatic Cysts: Diagnosis & Management (April 2020).