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.

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 colic), infection and inflammation (acute cholecystitis), or both.

About 10% of patients with symptomatic gallstones also have stones that pass into and obstruct the common bile duct (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), 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:

Gangrene or Abscesses. If acute cholecystitis is untreated and becomes very severe, inflammation can cause abscesses.

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.

Perforated Gallbladder. An estimated 10% of acute 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, 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.

Empyema. 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.

Fistula. 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 the small intestine, which can be very serious and requires immediate surgery.

Gallstone Ileus. A gallstone blocking the intestine is known 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.

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 life-threatening. 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:

o Kidney failureo Liver abscesso Cirrhosiso Over 50 years old

Pancreatitis. 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.

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 Polyps. 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.

Primary 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 Pancreatic 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.

Porcelain 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.

Above the area of stenosis, a “biliary 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 yellow-

green, 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 “fading” 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.

Absolute 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

(Kocher’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. Ker’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 bile-

excreting 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. About

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, reflux-

gastritis. 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.