Хирургические болезни. Практикум = Surgical diseases. Practice book. Учебное пособие

of the GB wall due to “leaking” of the infected bile from GB lumen through the Rokitansky-Aschoff passages into the abdominal cavity;

•GB empyema, which is a consequence of the previous AC accompanied by obturation of the cystic duct (with an interposed concrement), less often – by the development of obturation after frequent exacerbations of chronic recurrent cholecystitis (60–70% of cases). In the future, in view of the high virulence of the microflora, special conditions are created for suppuration of the GB contents;

•GB edema (or mucocele) which results from the obturation of the GB cervix (bladder duct) with a stone wedged into the cervix and accumulation of transparent mucous fluid in the cavity (due to the reverse absorption of the bile pigments by the GB mucosa) associated with unmarked virulence of microflora;

•perivesical infiltrate which is a complication of destructive ACC forms with the involvement of closely located structures and the greater omentum. Depending on the effectiveness of the treatment and specific features of the pathologic process, the infiltrate dissolves or develops into an abscess (called perivesical abscess).

Diagnosis. Diagnosis of ACC is based on the detection of signs of acute inflammation of GB on objective examination confirmed by instrumental and laboratory data. Among them ultrasound examination plays the main role (95% of information) as it includes the assessment of the acute process based on the size of GB, the configuration, as well as the nature of the contents and the thickness of the wall.

The main surgical intervention in acute calculous cholecystitis is cholecystectomy (CCE) performed both by means of traditional laparotomy (upper-middle access) and access to the right upper hypochondrium using Kocher-Fedorov’s method.

Recently, minimally invasive techniques of surgical interventions have been increasingly used in the treatment of ACC including videolaparoscopic cholecystectomy (since 1987), mini-access operations using special equipment (according to Prudkov’s method) and in the last decade – using high-resolution equipment (3D format); miniature ports for the introduction of mini-video cameras and instruments by means of installing a single port; besides, since 2008, NOTES technology has been used, which means performing CCE with the help of a flexible video camera allowing to perform interventions through natural holes.

9.2.2. Choledocholithiasis

Choledocholithiasis (CDL) is a complication of the gallstone disease associated with the presence of gallstones in the extrahepatic bile ducts.

If there is a “valvular” stone and there is no complete obturation of the common bile duct, the clinical manifestations of choledocholithiasis can

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be absent until the appearance of an attack of choledochal colic, which is caused by the migration of stones from the CBD to the duodenum and can proceed as follows:

•complete migration of stone to the duodenum;

•insertion of the stone into the MDP ampoule with the development of complete obstruction of CBD and subsequent manifestation of the phenomena of mechanical jaundice and acute cholangitis (AC). The course of the latter complication is especially severe and in a number of cases is treated as a case of abdominal surgical sepsis.

Treatment. The treatment of choledocholithiasis is based on the removal of concrements and the restoration of the passage of bile into the duodenum through interventions of two types:

•endoscopic, including removal of stones through MDP (after preliminary endoscopic papillosphincterotomy (EPST) using the Dormia basket or the inflated balloon Fogarty catheter. In some cases, the intervention is supplemented by contact shock wave or laser lithotripsy;

•choledocholithotomy, i.e. intervention by means of open laparotomy; mini-access laparotomy or videolaparoscopic interventions. After the elimination of choledocholithiasis and sanation of the bile ducts the final stage of the operation may be performed as follows:

“blind” suture on choledochus (in the absence of cholangitis);

external drainage of CBD using various methods;

creation of anastomoses between the CBD and duodenum (CDA) or the loop of the jejunum (types of internal biliodigestive anastomoses, most often performed using the method of Yurash-Vinogradov, Faulkner or Finsterer).

9.2.3. Obstructive (mechanical) jaundice

Obstructive (mechanical) jaundice (OJ) is a syndrome accompanied by icteritiousness of the skin, sclera and mucous membranes due to excessive bilirubinemia caused by mechanical obstruction of bile outflow.

Classification. According to the main causes, two forms of OJ are distinguished: due to benign (80% of all cases) and malignant processes (20%).

According to the course of the disease, the following forms are distinguished: complete, incomplete and intermittent, and the so-called “undulating course”.

In terms of the severity of hepatic failure, three types of disorders are distinguished: mild, moderate and severe.

Clinical picture. The main clinical manifestations in patients with OJ associated with bilirubinemia of more than 40 Mkmol / l are:

•icterus of skin and mucous membranes and icteric sclera;

•itchy skin (in some cases, its onset precedes the onset of jaundice itself);

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•discoloration of feces (or achiolia);

•GB enlarged and painless on palpation, which is called Courvoisier’s sign and determined in tumors of the terminal section of the choledochus, pancreas head or MDP;

•darkening of urine (dark, stagnant) due to the presence of a special pigment called urobilinogen.

Over time, jaundice ceases to be a syndrome and becomes the leading pathogenetic factor determining the outcome and the course of the process.

Diagnosis. Laboratory diagnosis of OJ is based on biochemical parameters including the syndromes of the enzyme-heptagram – cholestasis, cytolysis and inflammation.

The instrumental methods of diagnosis include:

•ultrasound examination of the abdominal cavity;

•endoscopic retrograde cholangiopancreatography (ERCP);

•percutaneous transhepatic cholangiography (PTHC);

•fistulography (through a previously imposed cholecystostomy);

•spiral computer tomography (SCT);

•magnetic resonance cholangiopancreatography.

Treatment. The treatment of OJ must be comprehensive and take into account the cause of the disease, the severity of the patient’s condition and the findings of laboratory and instrumental investigations.

In severe cases of OJ a two-stage approach is applied to the treatment plan:

1.Stage I. Minimally invasive interventions aimed at decompression of the bile ducts and restoration of bile outflow. In 20–40% of cases (more often in case of malignant neoplasms), such interventions are also the final method of treatment.

2.Stage II. Interventions mainly aimed at eliminating the cause of jaun-

dice and biliary hypertension. They include:

• percutaneous transhepatic cholecystostomy (cholangiostomy) for

decompression of the bile ducts by means of external bile withdrawal;

•endoscopic papillosphincterotomy (with lithotripsy or with extraction and nasobiliary drainage of the bile ducts as a variant of internal biliary excretion in case of complications of CL). This method can be combined with an endoscopic retrograde balloon dilatation of CBD in case of stricture in the terminal section or stent endoprosthesis (metal or mesh stents with a “Memory” form);

•formation of biliodigestive anastomoses. The method is used in presence of a mechanical obstacle to the outflow of bile in the terminal section of the choledochus, which cannot be eliminated with the help of the previously mentioned instrumental and retrograde interventions. These processes include: extensive cicatricial stenosis of MDP and terminal section of the choledochus; chronic inducible pancreatitis; location of the duodenal papil-

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lum in the portion of the large diverticulum; previous operations on the stomach and duodenum.

In addition to CDA, biliodigestive anastomoses include the creation of common bile duct anastomosis with the segment of the small intestine tied up due to the passage according to Roux’s method, as well as cholecystogastrotomy according to Bogoraz’s method (the creation of anastomosis of the gallbladder with the stomach).

In case of the neoplasms of the head of the pancreas, the major duodenal papilla (MDP), the terminal section of the common bile duct, and in the tumors of the confluence (the fusion of the right and left bile ducts or the Klatskin tumor), various bioliodigestive anastomoses are formed after their removal.

A pancreaticoduodenal resection (PDR), an operation first performed by A.Whipple in 1934, is referred to as a radical surgical aid in case of cancer of the pancreatic head, duodenum, major duodenal papilla and terminal section of the common bile duct.

The palliative operations in mechanical jaundice of tumor genesis include the creation of biliodigestive anastomoses including cholecystoenterostomy according to Mikulich.

9.2.4. Acute cholangitis

Acute cholangitis is an inflammatory process of bile ducts, which is bacterial in its nature and caused by other diseases. Currently, purulent cholangitis is considered in terms of cholangiogenic sepsis, the process characterized by local inflammatory changes in the bile ducts, general systemic inflammatory reaction and accompanied by the development of the syndrome of increasing multiple organ failure (MOF).

Classification. Cholangitis is classified by:

•etiological signs:

bacterial: the causative agents of which are often (80%) gramnegative (Escherichia coli, Proteus, Klebsiella) and Gram-positive bacteria, as well as nonclostridial germs and anaerobes;

helminthic;

toxic (toxic and allergic);

viral;

autoimmune;

•pathogenesis:

primary (primary-sclerosing or autoimmune);

secondary (bacterial), which may be caused by:

–choledocholithiasis;

–formation of cicatricial structures in BD;

–tumors;

–stenosis of MDP;

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Chapter 10

DISEASES OF THE PANCREAS

10.1. ACUTE PANCREATITIS

Acute pancreatitis (AP) (ICD 10: K 85) is an acute primary-aseptic inflammatory disease of the pancreas, which is based on autoenzymatic necrobiosis with intracellular activation of enzymes, autolysis of acinar cells, possible subsequent endogenous infection with involvement of the tissues of the retroperitoneal space, abdominal cavity and organ systems of extraabdominal localization.

The incidence of acute pancreatitis is about 10% of all emergency surgical in-patients and ranks 2nd–3rd place after acute appendicitis and complicated cholelithiasis.

In 15–20% of cases, the development of acute pancreatitis acquires a destructive character (pancreonecrosis) with the addition of purulent-septic complications in 40–70% of cases and results in a high mortality rate (20–65%).

Classification. Currently, the classification of acute pancreatitis depending on the phases of inflammation and destruction is used (Atlanta, USA, 1992):

•edematous (or interstitial pancreatitis);

•sterile pancreatic necrosis;

•infected pancreatic necrosis;

•pancreatogenic abscess;

•pseudocysts (including those infected). Etiology. The main etiological factors of AP are:

•diseases of extrahepatic biliary ducts accompanied by the development of cholestasis (chronic calculous cholecystitis, choledocholithiasis, diverticula of choledochus, etc.). This form of biliary pancreatitis occurs in 45– 75% of cases in women 50–60 years of age;

•diseases of the duodenum and major duodenal papilla (MDP): penetrating duodenal ulcer, duodenosis, duodenitis, duodenal diverticula;

•alimentary factors:

excessive food load (fatty, fried foods); medication stimulation of pancreatic secretion – prozerin, secretin, pancreosimin, etc.;

consumption of alcohol and / or its surrogates. They are triggering factors for the development of AP in 35–70% of cases in men aged 30–45 years.

•acute and chronic circulatory disorders that occur with microcirculatory lesions, spasm and ischemia of the pancreatic tissue (includes athero-

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sclerosis of the abdominal aorta and celiac trunk, vasculitis, arterial hypertension, hypotension due to shock, thrombosis and vascular embolism, etc.);

• allergic infectious factors that cause the Artyus-Shvartsman type of AP. Treatment. Therapeutic treatment of AP. The main principles of basic therapeutic AP treatment are creation of functional dormancy of the pan-

creas (“empty stomach”), which is provided by:

•nestiatria (up to 5 days);

•setting the nasogastrointestinal tube into the initial parts of the jejunum (behind gamentum suspensorium duodenum (a Treitz ligament) from 20 to 30 cm).

Suppression of the exocrine function of the pancreas is achieved by:

•artificial external or invasive hypothermia;

•the use of synthetic somatostatin analogues (octreotide or sandostatin in the dose of 300-600 mg / day 3 times), regulatory peptides (calcitonin) or 5-leukephalin derivatives (dalargin 75 mg / kg BW), suppressing both trypsin and amylase production and the general secretion of pancreatic juice (fluid);

•the use of cytostatics (5-fl uorouracil in the dose of 5 mg / kg BW for the first 2 days or fluoroufur in the dose of 20 mg / kg BW), pancreatic ribonuclease (intravenously or intra-arterially in the dose of 1–2 mg / kg BW). These drugs inhibit both the synthesis of DNA of protein molecules (primarily the proenzymes of the pancreas) and destroy RNA in pancreatic acids due to the direct action of ribonuclease;

•the use of protease inhibitors (contrikal, anpropotin, trasilol, gordoks, tsalol, ingitril, lexipafant, etc.) every 3–4 hours with the formation of inactive complexes with trypsin, kallikrein, plasmin and their subsequent excretion by forced diuresis. They are most effective only during the first 2 days of the disease – the initial stage of development of AP due to activation of the kallikrein-kinin system;

•the admistration of fat emulsions (intralipid, lipofundin, kabiven) with the addition of heparin to bind and immobilize the active lipase, as well as inhibit secretory activity of the pancrease and synthesize unsaturated fatty acids – substrates for excessive formation of prostaglandins, leukotrienes and other producers of lipid peroxidation.

Surgical interventions in AP are divided into 3 main groups, depending on the types of drainage of the pancreas and retroperitoneal tissue (fat):

•“closed” draining operations. They include techniques for active drainage of retroperitoneal tissue and abdominal cavity in conditions of restoring the anatomical integrity of the omental bursa and abdominal cavity by installing PVC or silicone drainage tubes for postoperative lavage with antiseptic solutions.

The technique of the “closed” operations is usually combined with repeated relaparotomies “on demand” (30–40% of their total volume), based on the results of clinical and instrumental methods of examination.

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In recent decades preference in the treatment of destructive AP has been given to minimally invasive drainage techniques through video-lapa- roscopic interventions or operations from mini-access using the video assistant “Liga-7” kit. Due to this, it has become possible to perform sanation of retroperitoneal tissue and retroperitoneal space through the lumbar mini-access or by percutaneous puncture drainage including cases of limited cystic-fluid formations drained under ultrasound or CT control. In the absence of the effect of “closed” operations “open” and “semi-open” drainage techniques are used.

In a number of cases, “closed” drainage techniques are complemented by VAG vacuum therapy with the creation of a constant rarefaction in the cavity within 100–120 mm Hg. for 2–3 days.

•“semi-open” draining operations (traditional) suggest removing the tubular drainage in combination with rubber-gauze (Penrose-Mikulicz drainage type) after necrosectomy, bursa pancreatolaparostomy or wide counterpunctures in the lumbar-lateral portions of the abdomen after lumbotomy with suturing the laparotomic wound in layers.

•“open” draining operations. They are performed in common forms of pancreatic necrosis involving retroperitoneal tissue and also after using other methods of “closed” or semi-open drainage (if their effectiveness is insufficient).

“Open” interventions are performed in combination with:

dynamic pancreato-omentobursostomy supplemented by lumbotomy;

pancreato-omentobursostomy in combination with laparostomy. Staged planned nec-, sequestrectomies are performed 48–72 hours

after previous interventions to achieve complete cleansing of the retroperitoneal space and omental bursa from purulent-necrotic tissues.

Complications. Within the period from 3 to 14 days 30–55% of AP patients develop focus of tissue necrosis, clinically manifested by parapancreatic infiltrate. The latter is a conglomerate of enlarged pancreas (with foci of necrosis) and involvement in periprocess of gastrointensinal ligament, a large omentum, mesentery of the transverse colon and jejunum, as well as posterior wall of the stomach.

There are two possible outcomes of parapancreatic infiltrate:

•aseptic (with the formation of postnecrotic cysts or fistulas of the pancreas, less often with complete restitution and restoration of structures and functions of the pancreas or with the formation of insufficiency of exometric functions and secondary diabetes mellitus (most often in case of involvement in the process of pancreatic tail);

•septic (with purulent complications) – begins at the end of the 2nd and beginning of the 3rd week of the disease.

In cases of formation of abscesses in the pancreas due to necrosis and changes in retroperitoneal tissue (purulent parapancreatitis or purulent-

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necrotic phlegmon) signs of systemic inflammatory response syndrome (SIRS) appear with the development of abdominal sepsis and septicopyemia.

10.2. CHRONIC PANCREATITIS

Chronic pancreatitis (ChP) (ICD 10: K 86.0-K 86.1) is a chronic multietiological nonspecific inflammatory degenerative dystrophic disease of the pancreas, accompanied by an obstruction of ducts, proliferative fibrosis, calcification, atrophy of the acini and impairment of its exoand endocrine function.

The incidence of ChP is 5–7 new cases per 100,000 adults or 0.1–0.4% of the total adult population, reaching 9–10% of all diseases of the abdominal cavity. Over the past 20 years, there has been an increase in the incidence rate of 1.7 to 1.9 times among the population of the developed countries. The peak incidence is observed at the age of 40–45; men suffer 3 times as often as women.

Classification. Classification of ChP:

•according to the Marseilles-Rome classification (1989) the following ChP forms are distinguished:

chronic calcifying pancreatitis (80% of cases);

chronic obstructive pancreatitis;

chronic fibrotic indurative pancreatitis;

chronic cysts and pseudocysts of the pancreas;

•according to the predominant character of morphological changes:

parenchymal;

ductal (retentional);

pseudotumorous (with primary damage to the head of the pancreas);

•according to the complications:

mechanical jaundice;

duodenal obstruction;

pseudocysts of the pancreas;

internal and external fistulas;

regional sub-hepatic portal hypertension;

secondary diabetes mellitus;

false aneurysms of the branches of the arterial trunk.

Etiology. Etiological factors of chronic pancreatitis include:

•chronic alcoholism (occurs in 70–80% of cases);

•congenital and acquired diseases of bile ducts, which contribute to the development of complications of cholelithiasis (30–35% of cases);

•isolated autoimmune ChP or the development of this process against the background of other autoimmune diseases that occur with the prevalence of fibro-sclerotic processes;

•congenital defects predominantly transmitted through the autosomal dominant pathway and accompanied by disorders in the secretion of tryp-

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sinogen (due to defects in chromosomes: 7g35 (alleles 29 and 122); and gene mutations-GCFTR (alleles 22 and 23);

•long-term exposure to exogenous factors including:

protein deficiency and prevalence of predominantly protein food in the diet;

long-term use of glucocorticoids, cytostatics, sulfonamides or estrogens;

lack of food antioxidant substances (zinc, copper, selenium);

chronic processes: cystic fibrosis; hyperparathyroidism (hypercalcemia); chronic renal insufficiency (CRI);

•diseases of the gastroduodenal area, which contribute to increased intraluminal pressure in the duodenum: duodenal ulcer, duodenitis, papillitis, diverticulitis, pyloroduodenal stenosis, chronic duodenal obstruction.

The combination of the presented etiological factors leads to a change in the viscosity of protein molecules (protein precipitation) with occlusion of the final sections of acinar cells of the pancreas, which is accompanied by stasis of secretion, precipitation of protein precipitates, disturbances in the outflow of acinar contents into the intersegmentary ducts of the pancreas and which triggers local autolytic processes of activation of trypsinogen and other enzymes. Subsequently, local sites of autodigestion in the pancreatic tissue result in the formation of small-focal necrosis, atrophy and fibrous degeneration. Fibrous changes, in turn, aggravate secondary inflammatory fibrous disorders in closely located organs, contribute to stenosis of the MDP, regional hypertension and duodenal stasis, and also predict the onset of secondary exocrine pancreatic insufficiency.

Prolonged inflammatory process in the pancreas is accompanied by the formation of ossificates in both the main pancreatic duct and in the tissues of the pancreas and causes progressive intraductal hypertrophy of the pancreas, leukocyte infiltration of perineural sympathetic nerve fibers and sensitive receptors that trigger the development of persistent pain syndrome.

Treatment. Indications for surgical treatment of ChP are:

•complicated course (3–4–5–6 variants of clinical course) in the presence of:

large-sized pseudocysts (> 5–8 cm in the diameter);

abscess formations of the pancreas or suppuration of pseudocysts;

regional portal hypertension with episodes of repeated acute gastroduodenal bleeding, thrombosis of portal or splenic veins (with secondary involvement due to parapancreatic infiltration);

pancreatic stenosis of the common bile duct or duodenal obstruction;

mechanical jaundice;

internal or external fistulas of the pancreas;

•persistent dilatation of the main pancreatic duct in the presence of confirmed virsungolithiasis and distal ductal hypertension;

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