Complications of Cholelithiasis
Content
COMPLICATIONS OF CHOLELITHIASIS Complications:-
Gallstones that do not cause symptoms rarely lead to problems. Death, even from gallstones with symptoms, is very rare. Serious complications are also rare. If they do occur, complications usually develop from stones in the bile duct, or after surgery. Gallstones, however, can cause obstruction at any point along the ducts that carry bile. In such cases, symptoms can develop. y
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In most cases of obstruction, the stones block the cystic duct, which leads from the gallbladder to the common bile duct. This can cause pain (biliary (biliary colic), colic), infection and inflammation (acute (acute cholecystitis), cholecystitis), or both. A bout 10% of patients with symptomatic gallstones also have stones that pass into and obstruct the common bile duct (choledocholithiasis). choledocholithiasis).
Infections
The most serious complication of acute cholecystitis is infection, which develops in about 20% of cases. It is extremely dangerous and life threatening if it spreads to other parts of the body (a condition called septicemia called septicemia), ), and surgery is often required. Symptoms include fever, rapid heartbeat, fast breathing, and confusion. Among the conditions that can lead to septicemia are the following: y
Gangrene
or Abscesses. If acute cholecystitis is untreated and becomes very severe, inflammation can cause abscesses.
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Inflammation can also cause necrosis (destruction of tissue in the gallbladder), which leads to gangrene. The highest risk is in men over 50 who have a history of heart disease and high levels of infection. erforated Gallbladder. An estimated 10% of acute P erforated cholecystitis cases result in a perforated gallbladder, which is a life-threatening condition. In general, this occurs in people who wait too long to seek help, or in people who do not respond to treatment. Perforation of the gallbladder is most common in people with diabetes. The risk for perforation increases with a condition called emphysematous cholecystitis, cholecystitis, in which gas forms in the gallbladder. Once the gallbladder has been perforated, pain may temporarily decrease. This is a dangerous and misleading event, however, because peritonitis (widespread abdominal infection) develops afterward. E mpyema. mpyema. Pus in the gallbladder (empyema) occurs in 2 - 3% of patients with acute cholecystitis. Patients usually experience severe abdominal pain for more than 7 days. The physical exam often fails to reveal the cause. The condition can be life-threatening, particularly if the infection spreads to other parts of the body. F istula. istula. In some cases, the inflamed gallbladder adheres to and perforates nearby organs, such as the small intestine. In such cases a fistula (channel) between the organs develops. Sometimes, in these cases, gallstones can actually pass into in to the small intestine, which can be very serious and requires immediate surgery. Ileus. A gallstone blocking the intestine is known Gallstone Ileus. as gallstone ileus. It primarily occurs in patients over age 65, and can sometimes be fatal. Depending on where the stone is located, surgery to remove the stone may be required.
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Infection in the Common Bile Duct (Cholangitis). Infection in the common bile duct from obstruction is common and serious. If antibiotics are administered immediately, the infection clears up in 75% of patients. If cholangitis does not improve, the infection may spread and become lifethreatening. Either surgery or a procedure known as endoscopic sphincterotomy is required to open and drain the ducts. Those at highest risk for a poor outlook also have one or more of the following conditions: K idney failure Liver abscess Cirrhosis Over 50 years old P ancreatitis. Common bile duct stones are responsible for most cases of pancreatitis (inflammation of the pancreas), a condition that can be life threatening. The pancreatic duct, which carries digestive enzymes, joins the common bile duct right before it enters the intestine. It is therefore not unusual for stones that pass through or lodge in the lower portion of the common bile duct to obstruct the pancreatic duct. o
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Other Complications Gallbladder
Cancer: Gallstones are present in about 80% of people with gallbladder cancer. There is a strong association between gallbladder cancer and cholelithiasis, chronic cholecystitis, and inflammation. Symptoms of gallbladder cancer usually do not appear until the disease has reached an advanced stage and may include weight loss, anemia, recurrent vomiting, and a lump in the abdomen. Research shows that survival rates for gallbladder cancer are on the rise, although the death rate remains high because many people
are diagnosed when the cancer is already at a late stage. When the cancer is caught at an early stage and has not spread beyond the mucosa (inner lining), removing the gallbladder (resection) can cure many people with the disease. If the cancer has spread beyond the gallbladder, other treatments may be required. This cancer is very rare, even among people with gallstones. Certain conditions in the gallbladder, however, contribute to a higher-than-average risk for this cancer. Gallbladder P olyps.
Polyps (growths) are sometimes detected during diagnostic tests for gallbladder disease. Small gallbladder polyps (up to 10 mm) pose little or no risk, but large ones (greater than 15 mm) pose some risk for cancer, so the gallbladder should be removed. Patients with polyps 10 - 15 mm have a lower risk, but they should still discuss gallbladder removal with their doctor. P rimary
Sclerosing Cholangitis. Primary sclerosing cholangitis is a rare disease that causes inflammation and scarring in the bile duct. It is associated with a lifetime risk of 7 - 12% for gallbladder cancer. The cause is unknown, although it tends to strike younger men with ulcerative colitis. Polyps are often detected in this condition and have a very high likelihood of being cancerous.
Anomalous Junction of the P ancreatic and Biliary Ducts. With this rare condition, which is present at birth (congenital), the junction of the common bile duct and main pancreatic duct is located outside the wall of the small intestine and forms a long channel between the two ducts. This problem poses a very high risk of cancer in the biliary tract. P orcelain Gallbladders.
Gallbladders are referred to as porcelain when their walls have become so calcified (covered in calcium deposits) that they look like porcelain on an x-ray. Porcelain
gallbladders have been associated with a very high risk of cancer, although recent evidence suggests that the risk is lower than was previously thought. This condition may develop from a chronic inflammatory reaction that may actually be responsible for the cancer risk. The cancer risk appears to depend on the presence of specific factors, such as partial calcification involving the inner lining of the gallbladder.
obstruction of the neck of the gall-bladder or the cystic duct cause destructive inflammation to develop due to stagnated bile, activation of infection and vascular disorders. When infection is spread in the abdominal cavity, peritonitis develops. Conservative therapy may cause unblocking of the gall-bladder.
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stone moves
into the cavity of the gall-bladder (rarely ± into choledoch), the contents of the gall-bladder spill through choledoch into the duodenum, and the attack subsides. Hydrops of the gall-bladder develops in the presence of obstruction with low virulent infection and high immune defense system. The attack subsides, a patient feels better. A painless and tensed gall-bladder is palpable at the right subcostal region. Acute
cholecystitis may be accompanied by jaundice, caused
by different factors. Prolonged history of the disease with multiple attacks leads to hepatic parenchyma being changed ± dystrophy,
hepatitis, biliary cirrhosis. A new attack of the disease causes exacerbation process in the liver presented as parenchymatous jaundice, which does not take a long course and can be easily treated conservatively. Progressive acute cholecystitis may lead to infiltrate formation with compression of extrahepatic biliary ducts with the resultant mechanical jaundice. Subsiding of the inflammatory process in the gall-bladder and the resolution of infiltrate will arrest jaundice. The most common cause of jaundice is calculous cholecystitis associated with choledocholithiasis. Stones of the bile-excreting ducts are usually of cystic origin. Obturative major duodenal papilla with an opening 3 mm in diameter leads to bile hypertension and mechanical jaundice. The consolidation of the head of the pancreas in cholecystopancreatitis causes constriction of the terminal choledoch in the site, where the duct crosses the parenchyma of the pancreas. The exacerbation of pancreatitis may lead to impaired bile outflow and the onset of jaundice. Intensive supporting care will abort the attack of cholecystopancreatitis, and jaundice passes.
Another
possible cause of jaundice is stenosis of major
duodenal papilla, which may be caused by: frequent spasms of papilla with blood supply disturbances and connective tissue development; migration of calculus through papilla with microtraumas of the mucous membrane. Isolated stenosis, however, can rarely cause jaundice. Stenotic rigid papilla becomes a place, where migrating calculi harbor; and a stone impacted at papilla will cause jaundice. It is necessary to note, that gallstones can be relatively rare formed in the bile-excretory passages. It occurs when there is an affected bile outflow due to stenosis of the distal choledoch. A bove
the area of stenosis, a ³biliary ointment´ is being formed.
This is an amorphous soft shapeless lump that grows into a soft crumble calculus. Mechanical jaundice may be caused only by a total obstruction of choledoch or major duodenal papilla. When there are floating calculi, jaundice is intermittent, what is associated with the episodes of total obstruction to the outflow of bile into the duodenum.
Stenosis of major duodenal papilla accompanies cholecystitis, its incidence is directly proportional to the duration of past history of calculous, or rarely acalculous cholecystitis. A
severe complication of cholecystitis is cholangitis ± acute
or chronic inflammation of the bilary ducts followed by severe intoxication, jaundice, cholangiovenous reflux with bacteriemia and sepsis, intrahepatic abscess formation, which can hardly respond to treatment. Pathological process, taking place in chronic cholecystitis behavior with the loss of the properties and the functions of the gall-bladder (reservoir-like, concentrated, and contractile), shrinking and sclerosing of the gallbladder wall, involves the biliary tree. Proximal spread of infection features the clinical picture of cholangitis. Chronic
cholecystitis is often associated with pancreatitis.
The common ostium of the bile-excreting and the pancreatic ducts causes the onset of biliopancreatic reflux. The pressure in the pancreatic duct is noramlly higher than in choledoch. This means there is no reflux. Bile hypertension levels the difference in pressure. Biliopancreatic reflux is not dangerous when there is a free outflow from Wirsungi¶s duct. With the rise of the pressure in
the duct of the pancreas with impaired passage through major duodenal papilla, reflux becomes pathological, what causes inactive forms of protolytic enzymes of the pancreas to turn into active forms with cytolytic effect. Recurrent reflux, may result in chronic, or acute pancreatitis in severe cases. Rare complications of cholecystitis include internal fistules between the gall-bladder and the intestine, followed by adhesions of these organs and the destruction of their walls. The contents of the gall-bladder spills through a fistule passage into the intestinal lumen. This abates the attack with a temporarily self-limitation. However, the presence of internal fistula defines reflux of the intestine contents into the gall-bladder what becomes the factor inducing chronic inflammation. Big calculi are able to migrate into the lumen of duodenum, small and large intestine only through a fistule. In some cases large stones may cause acute intestinal obstruction. Relatively small stones up to 5 mm in diameter may get into the duodenum through Vater¶s papilla. When patient with cholecystitis develops the signs of icteritious cuteneous and mucous membranes, it is necessary to make a differential diagnostic of jaundice.
Hemolytic (suprahepatic) jaundice is caused by intensive lysis of erythrocytes and excessive production of unconjugated bilirubin. A typical cause of jaundice is hemolytic anemia, associated with hyperfunction of the reticuloendotelial system (RES), mainly of the spleen in hypersplenism. Production of unconjugated bilirubin is so high, that the liver is in no condition to conjugate it in required amounts. Hemolytic jaundice may occur in intoxication with some poisons, resorption of decay products of large haematomas. In hemolytic jaundice the skin is of lemon-yellow color, there is no skin itch, a combination of pale and bile-tinged skin areas, liver is not enlarged, spleen is moderately enlarged, urine is brown, and stool is intensively colored. Blood serum shows elevated unconjugated bilirubin, anemia, reticulocytosis, increased ESR (erythrocyte sedimentation rate) and serum iron level. Parenchymatous (hepatic) jaundice more often occurs in viral hepatitis, cirrhosis of liver, intoxication with hepatotropic poisons (carbon tetrachloride, tetrachloretan, and compounds of arsenic, phosphorus). A lesion of hepatocytes results in a decrease in their ability to bind indirect blood bilirubin with glucuronic acid. Direct
bilirubin partly passes into biliary capillaries, and the significant part of directed bilirubin is diverted to blood. The disease has a marked prodromal period, which is manifested by the presence of malaise, loss of appetite, subfebrile fever. It is sometimes possible to reveal unfavorable epidemiologic past history. Patient complains of dull pains in the right subcostal region. Liver is enlarged and consolidated, spleen is sometimes palpable. The skin is of saffron-yellow color with tint of ruby, and in 3-4 weeks from the onset of the disease the skin turns yellowgreen, what is associated with accumulation of biliverdin in the skin. Skin itching is not expressed. Blood serum reveals elevated directed and indirected bilirubin, aminotransferases, and decreased concentration of prothrombin. Erythrocyte sedimentation rate (ESR) is moderately increased; urobilinogen and urobilin are revealed in urine; stool is colored, stercobilin reaction is positive. However in severe course of viral hepatitis with the advance of the disease, bile may not pass into intestine, what is followed by acholia of faeces, absence of urobilin in urine. Ultrasound scanning reveals a mixed structure of liver, a characteristic symptom of ³fading´ of an ultrasound wave.
Mechanical (subhepatic, obturative) jaundice develops as a result of obstruction of the bile-excreting passages and impaired passage of bile into the intestine. The common causes of mechanical jaundice are as follows: choledocholithiasis, blastomatous processes in the gall-bladder, choledoch, major duodenal papilla, and the head of the pancreas. Rare causes of mechanical jaundice are as follows: ductal strictures, ascaridiasis of the bile-excreting ducts, the technical errors of operative intervention with ligation of the extrahepatic biliary ducts. In choledocholithiasis the pain attacks in the right subcostal region often accompany jaundice. Jaundice may occur in the presence of acute cholecystitis, or after subsiding of the attack due to migration of calculi through the cystic duct into choledoch. The skin is green-yellow, sometimes yellow-grey. There is a pronounced skin itch. The liver is often enlarged, the spleen is rarely enlarged. If cholangitis is added, fever may arise. The gall bladder is not often palpable, what is connected with its shrinking during the disease. In acute cholecystitis when the elastic features of the gall-bladder are intact, the gallbladder can be palpable, but palpation is painful (in contrast to Courvoisier's symptom in
carcinoma of the head of the pancreas, when there is jaundice and a painless gall-bladder). Mechanical jaundice of tumor genesis may occur with no pain attacks. Patients develop signs of cancer intoxication: cachexy, malaise, loss of appetite, a pale skin. X-ray films of stomach and duodenum as well as relaxative duodenography, duodenoscopy, which makes it possible to carry out a retrograde pancreaticocholangiography and stenting of the biliary ducts aids in verifying the cause of jaundice. Thus, at the present time in calculous cholecystitis verification of diagnosis does not cause any significant problems. The main general clinical methods of investigation as well as numerous laboratory tests and special diagnostic systems are available for the doctor. Let¶s
dwell on the technically difficult manipulations on the
bile-excreting passages. The indications for choledochotomy may be either absolute or relative. A bsolute
indications for choledochotomy:
- Mechanical jaundice at the time of the operation;
- Choledocholithiasis, verified by ultrasound scanning before the operation; - Palpable stones in choledoch; - The presence of filling defects in the bile-excreting ducts or the absence of evacuation of a contrast substance into the duodenum on cholangiogramm. Relative indications for choledochotomy: - The presence of mechanical jaundice in past history and at the time of admission to the clinic; - Contracted gall-bladder, a wide cystic duct (more than 3 mm), and small stones in the gall-bladder; - A wide extrahepatic ducts (more then 10 mm) with evidence of bile hypertension (more than 150 mm water); - Narrowing of the terminal choledoch with impaired evacuation of a contrast substance on cholangiogramm. A
generally accepted point for choledochotomy is the
supraduodenal part of choledoch. Duodenum must be mobilized (K ocher¶s method) to get a technical access and to perform an adequate exploration of the terminal choledoch. When choledoch
is incised, the instrumental exploration of the bile-excreting ducts is carried out, beginning with proximal and ending in distal parts. The patency of major duodenal papilla is checked by means of metal probes with an olive-like thickened end 3 -7 mm in diameter. If all probes pass through papilla, it can be considered free. At
the present time besides all the above-listed methods of
choledoch investigation, operative choledochoscopy and ultrasound investigation of choledoch by means of a special sterile sensor are used. Manipulations on choledoch along with exploration of the lumen always entail edema of the mucous membrane and papilla, with resultant bile hypertension. That is why placing external drainage is mandatory when terminating an operation on choledoch. A
primary suture of choledoch provides restoration of
anatomic tissues interrelations. However, this advantage of the primary suture is dangerous, because the following complication may develop:
- bile hypertension may cause suture dysfunction (suture incompetence, separation of suture); - at the place of tissue alignment, a stricture may arise, especially after operations, performed on a non-dilated choledoch. Holsted-Pikovsky¶s drainage of the stump of the cystic duct is able to decrease the level of bile hypertension while applying a primary suture on choledoch. K er¶s T-shape drainage helps to prevent stricture formation in the area of choledochotomy and instantly to provide an adequate bile outflow. The transverse part of drainage is inserted into the lumen of choledoch and serves as a frame (stricture prevention). The external outflow of bile takes place through a longitudinal part of drainage. The presence of cicatrical stenosis of major duodenal papilla or an impacted stone at papilla are the indications for papillosphincteroplasty. Papilla on the olive-like probe (olive is
10 mm in diameter), inserted into terminal choledoch through a choledochotomic opening, is protruded through the posterior wall of duodenum. At this level the anterior wall of the intestine is incised, papilla is incised above the olive of probe at the direction of 11-12 o¶clock, 7-12 mm deep. Step by step, as the opening grows, the mucous membranes of choledoch and duodenum are
sewed by means of interrupted stitches. A resultant triangle wound is being formed, at the base of which the ostium of the pancreatic duct must be located at the direction of 5 o¶clock. The mucous membranes must not be sutured in this place. If the operation is performed properly, the olive of probe will get a free access from choledoch to duodenum. The ostium of the pancreatic duct is checked for patency with a bulbous-end probe. The anterior wall of duodenum is sewed in transversely.
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T-shape drainage is
placed into choledoch. Together with papillosphincteroplasty it provides a double (internal and external) drainage of the bileexcreting ducts. The duration of choledoch drainage with T-shape drainage is determined individually, and normally lasts for 2-3 weeks. 2-3 days before the removal of the drainage, the tube is blocked 4-6 times a day for 1-2 hours, then for 24 hours, and after that it should be completely removed. Postcholecystectomy syndrome
Removal of the gall-bladder sometimes doesn¶t save a patient with cholelisiasis from various pathological symptoms.
A bout
10% of patients remain ill after cholecystectomy. These cases are defined as postcholecystectomy syndrome, thought the definition
itself does not seem to be felicitous. Never the less it is widely used and convenient for designating a group of pathological conditions in patients who have had cholecystectomy. Classification
of postcholecystectomy syndrome:
1. True postcholecystectomy syndrome. 2. Residual complaints after cholecystectomy due to one more disease of the abdominal organs. 3. Residual complaints due to the disease, associated with cholelithiasis. 4. Technical errors of a performed operation. 5. Inadequate correction of the pathological changes, which were present during the first operation. 6. True recurrence of the disease. 7. The onset of a new disease of the gastrointestinal tract. True postcholecystectomy syndrome. Removal of a functioning gall-bladder induces consequences for a patient. Instantly a functional state of the bile-excreting system arrives with no bile flow in portions, and no high concentrated bile. The function of the sphincter of Oddi may be disturbed involving both an icrease and a decrease of the tone .As a result, a patient may experience a dull pain in the right subcostal area, nausea, a bitter
taste in the mouth. These symptoms become more aggravating when taking a roasted and spicy food. Performed on a non-functioning gall-bladder, when the gallbladder functions became lost due to the disease (obturative cholecystitis with hydrops outcome; shrinking of the gall-bladder as a result of inflammation), cholecystectomy is better endured with less sequences arising for patients. However, an adaptation period after cholecystectomy in some patients with prolonged past history of the disease may be rather severe. In such cases, it is not the loss of the physiological functions of the gallbladder, which is of great importance, but the onset of various sequences, which does not let a patient recover his health quickly. Thus, true postcholecystectomy syndrome has a temporary character, different degrees of severity, and consists mainly of dyspeptic disorders. The duration of the syndrome is about 6-12 months. A patient has to follow some simple recommendations. One should take food piecemeal in small portions and at one and the same time during a day to gain a conditioned reflex and to decrease dyskinetic signs. Roasted, fatty, spicy and rich food should not be included in to a patient diet. The intake of carbonate
mineral water, tinctures of hips and herbs, contributing to choleresis are advisable. The spa cure treatment is recommended in 6 months after an operation One more disease of the abdominal organs. It is not always possible to diagnose timely the combination of diseases, mutually aggravating each other. Subsequent examination of a patient might be sometimes ceased when the diagnosis has been verified. Cholecystectomy
saves a patient from calculous cholecystitis, but
the other diseases still persist and are manifested by the pathological syndromes, which have nothing to do with the operation performed. Only a thorough work-up (examination) may help choose the proper approach of the treatment of patients with cholelithiasis, and probably, with other diseases of the abdominal cavity. When examining the patient it is necessary to keep in mind the traditionally associated diseases: - Saint¶s syndrome is hiatal hernia, colonic diverticulosis and calculous cholecystitis; - carcinoma of the colon and calculous cholecystitis; - duodenal and gastric ulcer and calculous cholecystitis.
The planned and combined operations are applicable when compensating diagnosed diseases and the vital bordily systems. The following are the diseases, directly associated with cholelithiasis, developed in a process of its clinical behavior, and determining the postcholecystectomy syndrome: cholangitis, cholangiohepatitis, biliary cirrhosis, chronic pancreatitis, refluxgastritis. The severity of residual complains in these pathological conditions often depends on the length of time the disease has been present and bile hypertension. Postoperative cholangitis may be quickly arrested provided that there is an adequate out flow of bile and after antibiotics treatment, which are excreted into the bile. An
acute suppurative form of cholangiohepatitis gives rise to
the foci of abscesses development in the liver. The disease takes a torpid course with recurrent acute cholangiohepatitis with the resultant hectic fever, remittent jaundice, enlarged and consolidated liver. The disease development results in biliary cirrhosis. The treatment must include desintoxification drugs, hepatoprotectors, corticosteroids.
Chronic
pancreatitis is a heavy-curable disease. Complaints,
that are still present after cholecystectomy in pancreatitis are especially persistent and sometimes do not respond to a medication (drug) correction. The main complaints of patients are pains in the epigastrium, and dyspeptic problems. Dietary habits and a regime have to be followed in the treatment of postoperative pancreatitis. Duodeneal motility disturbances may be functional in cholelithiasis due to dyskinesia of both Oddi¶s and Ocsner¶s sphincters (located in lower-vertical intestine). After the operation has been completed, disordered duodeneal patency may persist with an organic component being added to a functional one ± duodenum, united with the bed of the gall-bladder, acquires a new bend, which affect the passage of food. Grave intestinal motility disorders arise after choledochoduodenoanastomosis has been applied: a constant non-coordinated inflow of bile through anastomosis, with impaired duodeneal motility cause a pronounced duodeno-gastric reflux followed by reflux-gastritis development with the organic changes of the mucous membrane of the piloreantral part of the stomach. Patients with reflux-gastritis complain of pains in the epigastrium. They experience a feeling of heaviness, failing
appetite, nausea, bilious vomit, a bitter taste in the mouth. The treatment of reflux-gastritis is conservative, in severe cases it is advisable to remove previously applied anastomosis and to create another way for bile outflow. Technical errors of a previously performed cholecystectomy in the frame of the postcholecystectomy syndrome are as follows: a long stump of the cystic duct left (more than 12-15 mm), ligation of the main biliary ducts, sicatrical stricture of choledoch. Some surgeons consider, that there may be some stones left in a long stump of the cystic duct, or the stones might be formed and they may migrate into choledoch. During a technically difficult cholecystectomy there may be left not only the cystic duct, but also a part of the neck of the gall-bladder. Due to this process a small gall-bladder is being formed in patients. The signs of cholecystitis still persist. The treatment of such conditions is operative. Inadequate correction of the pathological changes which were present during the first operation include: a non-diagnosed before an operation and non-treated choledocholithiasis (false recurrence), stenosis of major duodenal papilla; formation of inadequate biliodigestive anastomosises; restenosis of major
duodenal papilla; formation of stenosis at the site of the suture on choledoch. The treatment of these complications is also operative. True recurrent cholelithiasis develops in cases, when a narrowing arising in the bile-excreting ducts affects the normal outflow of bile. The main differential sign of a true and false postoperative cholelithiasis is the length of time, when a patient has no complaints and the clinical signs of the disease can not be revealed. In false recurrent cholelithiasis this period of time may be either absent or may be too short, but in true recurrent cholelithiasis there may be a prolonged period. Clinically
true recurrent cholelithiasis may be manifested by
the presence of biliary colic, cholangitis attacks, jaundice, pancreatitis in association with stone formation as well as the presence of obstruction to the outflow of bile. Stones, overlooked in biliary passages after the first operation, are of cystic origin and mixed firm structure (cholesterol, bilirubin, calcium). In true recurrent cholelithiasis the stones look like an amorphous ointment. They sometimes may be firm, but easily crumbled. New diseases of the gastrointestinal tract may develop after an operation performend on biliary passages, and what can be associated with the new conditions of the bile-excretory system.
These diseases include malignant gastric, colonic, pancreatic tumors.
Gallstones that do not cause symptoms rarely lead to problems. Death, even from gallstones with symptoms, is very rare. Serious complications are also rare. If they do occur, complications usually develop from stones in the bile duct, or after surgery. Gallstones, however, can cause obstruction at any point along the ducts that carry bile. In such cases, symptoms can develop. y
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In most cases of obstruction, the stones block the cystic duct, which leads from the gallbladder to the common bile duct. This can cause pain (biliary (biliary colic), colic), infection and inflammation (acute (acute cholecystitis), cholecystitis), or both. A bout 10% of patients with symptomatic gallstones also have stones that pass into and obstruct the common bile duct (choledocholithiasis). choledocholithiasis).
Infections
The most serious complication of acute cholecystitis is infection, which develops in about 20% of cases. It is extremely dangerous and life threatening if it spreads to other parts of the body (a condition called septicemia called septicemia), ), and surgery is often required. Symptoms include fever, rapid heartbeat, fast breathing, and confusion. Among the conditions that can lead to septicemia are the following: y
Gangrene
or Abscesses. If acute cholecystitis is untreated and becomes very severe, inflammation can cause abscesses.
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Inflammation can also cause necrosis (destruction of tissue in the gallbladder), which leads to gangrene. The highest risk is in men over 50 who have a history of heart disease and high levels of infection. erforated Gallbladder. An estimated 10% of acute P erforated cholecystitis cases result in a perforated gallbladder, which is a life-threatening condition. In general, this occurs in people who wait too long to seek help, or in people who do not respond to treatment. Perforation of the gallbladder is most common in people with diabetes. The risk for perforation increases with a condition called emphysematous cholecystitis, cholecystitis, in which gas forms in the gallbladder. Once the gallbladder has been perforated, pain may temporarily decrease. This is a dangerous and misleading event, however, because peritonitis (widespread abdominal infection) develops afterward. E mpyema. mpyema. Pus in the gallbladder (empyema) occurs in 2 - 3% of patients with acute cholecystitis. Patients usually experience severe abdominal pain for more than 7 days. The physical exam often fails to reveal the cause. The condition can be life-threatening, particularly if the infection spreads to other parts of the body. F istula. istula. In some cases, the inflamed gallbladder adheres to and perforates nearby organs, such as the small intestine. In such cases a fistula (channel) between the organs develops. Sometimes, in these cases, gallstones can actually pass into in to the small intestine, which can be very serious and requires immediate surgery. Ileus. A gallstone blocking the intestine is known Gallstone Ileus. as gallstone ileus. It primarily occurs in patients over age 65, and can sometimes be fatal. Depending on where the stone is located, surgery to remove the stone may be required.
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Infection in the Common Bile Duct (Cholangitis). Infection in the common bile duct from obstruction is common and serious. If antibiotics are administered immediately, the infection clears up in 75% of patients. If cholangitis does not improve, the infection may spread and become lifethreatening. Either surgery or a procedure known as endoscopic sphincterotomy is required to open and drain the ducts. Those at highest risk for a poor outlook also have one or more of the following conditions: K idney failure Liver abscess Cirrhosis Over 50 years old P ancreatitis. Common bile duct stones are responsible for most cases of pancreatitis (inflammation of the pancreas), a condition that can be life threatening. The pancreatic duct, which carries digestive enzymes, joins the common bile duct right before it enters the intestine. It is therefore not unusual for stones that pass through or lodge in the lower portion of the common bile duct to obstruct the pancreatic duct. o
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Other Complications Gallbladder
Cancer: Gallstones are present in about 80% of people with gallbladder cancer. There is a strong association between gallbladder cancer and cholelithiasis, chronic cholecystitis, and inflammation. Symptoms of gallbladder cancer usually do not appear until the disease has reached an advanced stage and may include weight loss, anemia, recurrent vomiting, and a lump in the abdomen. Research shows that survival rates for gallbladder cancer are on the rise, although the death rate remains high because many people
are diagnosed when the cancer is already at a late stage. When the cancer is caught at an early stage and has not spread beyond the mucosa (inner lining), removing the gallbladder (resection) can cure many people with the disease. If the cancer has spread beyond the gallbladder, other treatments may be required. This cancer is very rare, even among people with gallstones. Certain conditions in the gallbladder, however, contribute to a higher-than-average risk for this cancer. Gallbladder P olyps.
Polyps (growths) are sometimes detected during diagnostic tests for gallbladder disease. Small gallbladder polyps (up to 10 mm) pose little or no risk, but large ones (greater than 15 mm) pose some risk for cancer, so the gallbladder should be removed. Patients with polyps 10 - 15 mm have a lower risk, but they should still discuss gallbladder removal with their doctor. P rimary
Sclerosing Cholangitis. Primary sclerosing cholangitis is a rare disease that causes inflammation and scarring in the bile duct. It is associated with a lifetime risk of 7 - 12% for gallbladder cancer. The cause is unknown, although it tends to strike younger men with ulcerative colitis. Polyps are often detected in this condition and have a very high likelihood of being cancerous.
Anomalous Junction of the P ancreatic and Biliary Ducts. With this rare condition, which is present at birth (congenital), the junction of the common bile duct and main pancreatic duct is located outside the wall of the small intestine and forms a long channel between the two ducts. This problem poses a very high risk of cancer in the biliary tract. P orcelain Gallbladders.
Gallbladders are referred to as porcelain when their walls have become so calcified (covered in calcium deposits) that they look like porcelain on an x-ray. Porcelain
gallbladders have been associated with a very high risk of cancer, although recent evidence suggests that the risk is lower than was previously thought. This condition may develop from a chronic inflammatory reaction that may actually be responsible for the cancer risk. The cancer risk appears to depend on the presence of specific factors, such as partial calcification involving the inner lining of the gallbladder.
obstruction of the neck of the gall-bladder or the cystic duct cause destructive inflammation to develop due to stagnated bile, activation of infection and vascular disorders. When infection is spread in the abdominal cavity, peritonitis develops. Conservative therapy may cause unblocking of the gall-bladder.
A
stone moves
into the cavity of the gall-bladder (rarely ± into choledoch), the contents of the gall-bladder spill through choledoch into the duodenum, and the attack subsides. Hydrops of the gall-bladder develops in the presence of obstruction with low virulent infection and high immune defense system. The attack subsides, a patient feels better. A painless and tensed gall-bladder is palpable at the right subcostal region. Acute
cholecystitis may be accompanied by jaundice, caused
by different factors. Prolonged history of the disease with multiple attacks leads to hepatic parenchyma being changed ± dystrophy,
hepatitis, biliary cirrhosis. A new attack of the disease causes exacerbation process in the liver presented as parenchymatous jaundice, which does not take a long course and can be easily treated conservatively. Progressive acute cholecystitis may lead to infiltrate formation with compression of extrahepatic biliary ducts with the resultant mechanical jaundice. Subsiding of the inflammatory process in the gall-bladder and the resolution of infiltrate will arrest jaundice. The most common cause of jaundice is calculous cholecystitis associated with choledocholithiasis. Stones of the bile-excreting ducts are usually of cystic origin. Obturative major duodenal papilla with an opening 3 mm in diameter leads to bile hypertension and mechanical jaundice. The consolidation of the head of the pancreas in cholecystopancreatitis causes constriction of the terminal choledoch in the site, where the duct crosses the parenchyma of the pancreas. The exacerbation of pancreatitis may lead to impaired bile outflow and the onset of jaundice. Intensive supporting care will abort the attack of cholecystopancreatitis, and jaundice passes.
Another
possible cause of jaundice is stenosis of major
duodenal papilla, which may be caused by: frequent spasms of papilla with blood supply disturbances and connective tissue development; migration of calculus through papilla with microtraumas of the mucous membrane. Isolated stenosis, however, can rarely cause jaundice. Stenotic rigid papilla becomes a place, where migrating calculi harbor; and a stone impacted at papilla will cause jaundice. It is necessary to note, that gallstones can be relatively rare formed in the bile-excretory passages. It occurs when there is an affected bile outflow due to stenosis of the distal choledoch. A bove
the area of stenosis, a ³biliary ointment´ is being formed.
This is an amorphous soft shapeless lump that grows into a soft crumble calculus. Mechanical jaundice may be caused only by a total obstruction of choledoch or major duodenal papilla. When there are floating calculi, jaundice is intermittent, what is associated with the episodes of total obstruction to the outflow of bile into the duodenum.
Stenosis of major duodenal papilla accompanies cholecystitis, its incidence is directly proportional to the duration of past history of calculous, or rarely acalculous cholecystitis. A
severe complication of cholecystitis is cholangitis ± acute
or chronic inflammation of the bilary ducts followed by severe intoxication, jaundice, cholangiovenous reflux with bacteriemia and sepsis, intrahepatic abscess formation, which can hardly respond to treatment. Pathological process, taking place in chronic cholecystitis behavior with the loss of the properties and the functions of the gall-bladder (reservoir-like, concentrated, and contractile), shrinking and sclerosing of the gallbladder wall, involves the biliary tree. Proximal spread of infection features the clinical picture of cholangitis. Chronic
cholecystitis is often associated with pancreatitis.
The common ostium of the bile-excreting and the pancreatic ducts causes the onset of biliopancreatic reflux. The pressure in the pancreatic duct is noramlly higher than in choledoch. This means there is no reflux. Bile hypertension levels the difference in pressure. Biliopancreatic reflux is not dangerous when there is a free outflow from Wirsungi¶s duct. With the rise of the pressure in
the duct of the pancreas with impaired passage through major duodenal papilla, reflux becomes pathological, what causes inactive forms of protolytic enzymes of the pancreas to turn into active forms with cytolytic effect. Recurrent reflux, may result in chronic, or acute pancreatitis in severe cases. Rare complications of cholecystitis include internal fistules between the gall-bladder and the intestine, followed by adhesions of these organs and the destruction of their walls. The contents of the gall-bladder spills through a fistule passage into the intestinal lumen. This abates the attack with a temporarily self-limitation. However, the presence of internal fistula defines reflux of the intestine contents into the gall-bladder what becomes the factor inducing chronic inflammation. Big calculi are able to migrate into the lumen of duodenum, small and large intestine only through a fistule. In some cases large stones may cause acute intestinal obstruction. Relatively small stones up to 5 mm in diameter may get into the duodenum through Vater¶s papilla. When patient with cholecystitis develops the signs of icteritious cuteneous and mucous membranes, it is necessary to make a differential diagnostic of jaundice.
Hemolytic (suprahepatic) jaundice is caused by intensive lysis of erythrocytes and excessive production of unconjugated bilirubin. A typical cause of jaundice is hemolytic anemia, associated with hyperfunction of the reticuloendotelial system (RES), mainly of the spleen in hypersplenism. Production of unconjugated bilirubin is so high, that the liver is in no condition to conjugate it in required amounts. Hemolytic jaundice may occur in intoxication with some poisons, resorption of decay products of large haematomas. In hemolytic jaundice the skin is of lemon-yellow color, there is no skin itch, a combination of pale and bile-tinged skin areas, liver is not enlarged, spleen is moderately enlarged, urine is brown, and stool is intensively colored. Blood serum shows elevated unconjugated bilirubin, anemia, reticulocytosis, increased ESR (erythrocyte sedimentation rate) and serum iron level. Parenchymatous (hepatic) jaundice more often occurs in viral hepatitis, cirrhosis of liver, intoxication with hepatotropic poisons (carbon tetrachloride, tetrachloretan, and compounds of arsenic, phosphorus). A lesion of hepatocytes results in a decrease in their ability to bind indirect blood bilirubin with glucuronic acid. Direct
bilirubin partly passes into biliary capillaries, and the significant part of directed bilirubin is diverted to blood. The disease has a marked prodromal period, which is manifested by the presence of malaise, loss of appetite, subfebrile fever. It is sometimes possible to reveal unfavorable epidemiologic past history. Patient complains of dull pains in the right subcostal region. Liver is enlarged and consolidated, spleen is sometimes palpable. The skin is of saffron-yellow color with tint of ruby, and in 3-4 weeks from the onset of the disease the skin turns yellowgreen, what is associated with accumulation of biliverdin in the skin. Skin itching is not expressed. Blood serum reveals elevated directed and indirected bilirubin, aminotransferases, and decreased concentration of prothrombin. Erythrocyte sedimentation rate (ESR) is moderately increased; urobilinogen and urobilin are revealed in urine; stool is colored, stercobilin reaction is positive. However in severe course of viral hepatitis with the advance of the disease, bile may not pass into intestine, what is followed by acholia of faeces, absence of urobilin in urine. Ultrasound scanning reveals a mixed structure of liver, a characteristic symptom of ³fading´ of an ultrasound wave.
Mechanical (subhepatic, obturative) jaundice develops as a result of obstruction of the bile-excreting passages and impaired passage of bile into the intestine. The common causes of mechanical jaundice are as follows: choledocholithiasis, blastomatous processes in the gall-bladder, choledoch, major duodenal papilla, and the head of the pancreas. Rare causes of mechanical jaundice are as follows: ductal strictures, ascaridiasis of the bile-excreting ducts, the technical errors of operative intervention with ligation of the extrahepatic biliary ducts. In choledocholithiasis the pain attacks in the right subcostal region often accompany jaundice. Jaundice may occur in the presence of acute cholecystitis, or after subsiding of the attack due to migration of calculi through the cystic duct into choledoch. The skin is green-yellow, sometimes yellow-grey. There is a pronounced skin itch. The liver is often enlarged, the spleen is rarely enlarged. If cholangitis is added, fever may arise. The gall bladder is not often palpable, what is connected with its shrinking during the disease. In acute cholecystitis when the elastic features of the gall-bladder are intact, the gallbladder can be palpable, but palpation is painful (in contrast to Courvoisier's symptom in
carcinoma of the head of the pancreas, when there is jaundice and a painless gall-bladder). Mechanical jaundice of tumor genesis may occur with no pain attacks. Patients develop signs of cancer intoxication: cachexy, malaise, loss of appetite, a pale skin. X-ray films of stomach and duodenum as well as relaxative duodenography, duodenoscopy, which makes it possible to carry out a retrograde pancreaticocholangiography and stenting of the biliary ducts aids in verifying the cause of jaundice. Thus, at the present time in calculous cholecystitis verification of diagnosis does not cause any significant problems. The main general clinical methods of investigation as well as numerous laboratory tests and special diagnostic systems are available for the doctor. Let¶s
dwell on the technically difficult manipulations on the
bile-excreting passages. The indications for choledochotomy may be either absolute or relative. A bsolute
indications for choledochotomy:
- Mechanical jaundice at the time of the operation;
- Choledocholithiasis, verified by ultrasound scanning before the operation; - Palpable stones in choledoch; - The presence of filling defects in the bile-excreting ducts or the absence of evacuation of a contrast substance into the duodenum on cholangiogramm. Relative indications for choledochotomy: - The presence of mechanical jaundice in past history and at the time of admission to the clinic; - Contracted gall-bladder, a wide cystic duct (more than 3 mm), and small stones in the gall-bladder; - A wide extrahepatic ducts (more then 10 mm) with evidence of bile hypertension (more than 150 mm water); - Narrowing of the terminal choledoch with impaired evacuation of a contrast substance on cholangiogramm. A
generally accepted point for choledochotomy is the
supraduodenal part of choledoch. Duodenum must be mobilized (K ocher¶s method) to get a technical access and to perform an adequate exploration of the terminal choledoch. When choledoch
is incised, the instrumental exploration of the bile-excreting ducts is carried out, beginning with proximal and ending in distal parts. The patency of major duodenal papilla is checked by means of metal probes with an olive-like thickened end 3 -7 mm in diameter. If all probes pass through papilla, it can be considered free. At
the present time besides all the above-listed methods of
choledoch investigation, operative choledochoscopy and ultrasound investigation of choledoch by means of a special sterile sensor are used. Manipulations on choledoch along with exploration of the lumen always entail edema of the mucous membrane and papilla, with resultant bile hypertension. That is why placing external drainage is mandatory when terminating an operation on choledoch. A
primary suture of choledoch provides restoration of
anatomic tissues interrelations. However, this advantage of the primary suture is dangerous, because the following complication may develop:
- bile hypertension may cause suture dysfunction (suture incompetence, separation of suture); - at the place of tissue alignment, a stricture may arise, especially after operations, performed on a non-dilated choledoch. Holsted-Pikovsky¶s drainage of the stump of the cystic duct is able to decrease the level of bile hypertension while applying a primary suture on choledoch. K er¶s T-shape drainage helps to prevent stricture formation in the area of choledochotomy and instantly to provide an adequate bile outflow. The transverse part of drainage is inserted into the lumen of choledoch and serves as a frame (stricture prevention). The external outflow of bile takes place through a longitudinal part of drainage. The presence of cicatrical stenosis of major duodenal papilla or an impacted stone at papilla are the indications for papillosphincteroplasty. Papilla on the olive-like probe (olive is
10 mm in diameter), inserted into terminal choledoch through a choledochotomic opening, is protruded through the posterior wall of duodenum. At this level the anterior wall of the intestine is incised, papilla is incised above the olive of probe at the direction of 11-12 o¶clock, 7-12 mm deep. Step by step, as the opening grows, the mucous membranes of choledoch and duodenum are
sewed by means of interrupted stitches. A resultant triangle wound is being formed, at the base of which the ostium of the pancreatic duct must be located at the direction of 5 o¶clock. The mucous membranes must not be sutured in this place. If the operation is performed properly, the olive of probe will get a free access from choledoch to duodenum. The ostium of the pancreatic duct is checked for patency with a bulbous-end probe. The anterior wall of duodenum is sewed in transversely.
A
T-shape drainage is
placed into choledoch. Together with papillosphincteroplasty it provides a double (internal and external) drainage of the bileexcreting ducts. The duration of choledoch drainage with T-shape drainage is determined individually, and normally lasts for 2-3 weeks. 2-3 days before the removal of the drainage, the tube is blocked 4-6 times a day for 1-2 hours, then for 24 hours, and after that it should be completely removed. Postcholecystectomy syndrome
Removal of the gall-bladder sometimes doesn¶t save a patient with cholelisiasis from various pathological symptoms.
A bout
10% of patients remain ill after cholecystectomy. These cases are defined as postcholecystectomy syndrome, thought the definition
itself does not seem to be felicitous. Never the less it is widely used and convenient for designating a group of pathological conditions in patients who have had cholecystectomy. Classification
of postcholecystectomy syndrome:
1. True postcholecystectomy syndrome. 2. Residual complaints after cholecystectomy due to one more disease of the abdominal organs. 3. Residual complaints due to the disease, associated with cholelithiasis. 4. Technical errors of a performed operation. 5. Inadequate correction of the pathological changes, which were present during the first operation. 6. True recurrence of the disease. 7. The onset of a new disease of the gastrointestinal tract. True postcholecystectomy syndrome. Removal of a functioning gall-bladder induces consequences for a patient. Instantly a functional state of the bile-excreting system arrives with no bile flow in portions, and no high concentrated bile. The function of the sphincter of Oddi may be disturbed involving both an icrease and a decrease of the tone .As a result, a patient may experience a dull pain in the right subcostal area, nausea, a bitter
taste in the mouth. These symptoms become more aggravating when taking a roasted and spicy food. Performed on a non-functioning gall-bladder, when the gallbladder functions became lost due to the disease (obturative cholecystitis with hydrops outcome; shrinking of the gall-bladder as a result of inflammation), cholecystectomy is better endured with less sequences arising for patients. However, an adaptation period after cholecystectomy in some patients with prolonged past history of the disease may be rather severe. In such cases, it is not the loss of the physiological functions of the gallbladder, which is of great importance, but the onset of various sequences, which does not let a patient recover his health quickly. Thus, true postcholecystectomy syndrome has a temporary character, different degrees of severity, and consists mainly of dyspeptic disorders. The duration of the syndrome is about 6-12 months. A patient has to follow some simple recommendations. One should take food piecemeal in small portions and at one and the same time during a day to gain a conditioned reflex and to decrease dyskinetic signs. Roasted, fatty, spicy and rich food should not be included in to a patient diet. The intake of carbonate
mineral water, tinctures of hips and herbs, contributing to choleresis are advisable. The spa cure treatment is recommended in 6 months after an operation One more disease of the abdominal organs. It is not always possible to diagnose timely the combination of diseases, mutually aggravating each other. Subsequent examination of a patient might be sometimes ceased when the diagnosis has been verified. Cholecystectomy
saves a patient from calculous cholecystitis, but
the other diseases still persist and are manifested by the pathological syndromes, which have nothing to do with the operation performed. Only a thorough work-up (examination) may help choose the proper approach of the treatment of patients with cholelithiasis, and probably, with other diseases of the abdominal cavity. When examining the patient it is necessary to keep in mind the traditionally associated diseases: - Saint¶s syndrome is hiatal hernia, colonic diverticulosis and calculous cholecystitis; - carcinoma of the colon and calculous cholecystitis; - duodenal and gastric ulcer and calculous cholecystitis.
The planned and combined operations are applicable when compensating diagnosed diseases and the vital bordily systems. The following are the diseases, directly associated with cholelithiasis, developed in a process of its clinical behavior, and determining the postcholecystectomy syndrome: cholangitis, cholangiohepatitis, biliary cirrhosis, chronic pancreatitis, refluxgastritis. The severity of residual complains in these pathological conditions often depends on the length of time the disease has been present and bile hypertension. Postoperative cholangitis may be quickly arrested provided that there is an adequate out flow of bile and after antibiotics treatment, which are excreted into the bile. An
acute suppurative form of cholangiohepatitis gives rise to
the foci of abscesses development in the liver. The disease takes a torpid course with recurrent acute cholangiohepatitis with the resultant hectic fever, remittent jaundice, enlarged and consolidated liver. The disease development results in biliary cirrhosis. The treatment must include desintoxification drugs, hepatoprotectors, corticosteroids.
Chronic
pancreatitis is a heavy-curable disease. Complaints,
that are still present after cholecystectomy in pancreatitis are especially persistent and sometimes do not respond to a medication (drug) correction. The main complaints of patients are pains in the epigastrium, and dyspeptic problems. Dietary habits and a regime have to be followed in the treatment of postoperative pancreatitis. Duodeneal motility disturbances may be functional in cholelithiasis due to dyskinesia of both Oddi¶s and Ocsner¶s sphincters (located in lower-vertical intestine). After the operation has been completed, disordered duodeneal patency may persist with an organic component being added to a functional one ± duodenum, united with the bed of the gall-bladder, acquires a new bend, which affect the passage of food. Grave intestinal motility disorders arise after choledochoduodenoanastomosis has been applied: a constant non-coordinated inflow of bile through anastomosis, with impaired duodeneal motility cause a pronounced duodeno-gastric reflux followed by reflux-gastritis development with the organic changes of the mucous membrane of the piloreantral part of the stomach. Patients with reflux-gastritis complain of pains in the epigastrium. They experience a feeling of heaviness, failing
appetite, nausea, bilious vomit, a bitter taste in the mouth. The treatment of reflux-gastritis is conservative, in severe cases it is advisable to remove previously applied anastomosis and to create another way for bile outflow. Technical errors of a previously performed cholecystectomy in the frame of the postcholecystectomy syndrome are as follows: a long stump of the cystic duct left (more than 12-15 mm), ligation of the main biliary ducts, sicatrical stricture of choledoch. Some surgeons consider, that there may be some stones left in a long stump of the cystic duct, or the stones might be formed and they may migrate into choledoch. During a technically difficult cholecystectomy there may be left not only the cystic duct, but also a part of the neck of the gall-bladder. Due to this process a small gall-bladder is being formed in patients. The signs of cholecystitis still persist. The treatment of such conditions is operative. Inadequate correction of the pathological changes which were present during the first operation include: a non-diagnosed before an operation and non-treated choledocholithiasis (false recurrence), stenosis of major duodenal papilla; formation of inadequate biliodigestive anastomosises; restenosis of major
duodenal papilla; formation of stenosis at the site of the suture on choledoch. The treatment of these complications is also operative. True recurrent cholelithiasis develops in cases, when a narrowing arising in the bile-excreting ducts affects the normal outflow of bile. The main differential sign of a true and false postoperative cholelithiasis is the length of time, when a patient has no complaints and the clinical signs of the disease can not be revealed. In false recurrent cholelithiasis this period of time may be either absent or may be too short, but in true recurrent cholelithiasis there may be a prolonged period. Clinically
true recurrent cholelithiasis may be manifested by
the presence of biliary colic, cholangitis attacks, jaundice, pancreatitis in association with stone formation as well as the presence of obstruction to the outflow of bile. Stones, overlooked in biliary passages after the first operation, are of cystic origin and mixed firm structure (cholesterol, bilirubin, calcium). In true recurrent cholelithiasis the stones look like an amorphous ointment. They sometimes may be firm, but easily crumbled. New diseases of the gastrointestinal tract may develop after an operation performend on biliary passages, and what can be associated with the new conditions of the bile-excretory system.
These diseases include malignant gastric, colonic, pancreatic tumors.
