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GALLBLADDER AND

BILIARY TRACT
4 hours

GALLBLADDER AND BILIARY TRACT

4 hours

C 10 - 2 hours
Normal anatomy, congenital abnormalities, phisiopathology of stone formation.
Gallbladder litiasis: acute cholecystitis, cronic cholecystitis (etiology, clinical findings,
evaluation, diagnosis, differential diagnosis, complications, treatment).
Choledocolitiasis: etiology, clinical findings, evaluation, diagnosis, differential
diagnosis, complications, treatment.
Bacterial cholangitis: etiology, classification, clinical findings, evaluation, diagnosis,
complications, treatment.

C 11 - 2 hours
Sclerosing cholangitis: etiology, classification, clinical findings, evaluation, diagnosis,
complications, treatment.
Malignant tumors of the bile ducts: pathology, classification, clinical findings,
evaluation, diagnosis, treatment.
Jaundice: etiology, classification, phisiopathology, clinical findings, evaluation,
diagnosis, differential diagnosis, complications, treatment;

GALLBLADDER AND BILIARY TRACT

The gallbladder is a pear-shaped organ bound to a fossa on the right inferior surface of the liver
by connective tissue and vessels, and it lies between the right, left, and quadrate hepatic lobes1-3
or hepatic segments IV and V
The gallbladder occasionally has a complete peritoneal covering and true mesentery predisposing
to torsion. Rarely, the organ is located so deeply within the liver parenchyma that it can be
reached from the outside only by dividing an overlying layer of liver tissue (intrahepatic
gallbladder).
The gallbladder is 7 to 10 cm long, with an average volume of about 30 mL. With marked
distention or acute obstruction, the viscus may contain up to 300 mL.

GALLBLADDER AND BILIARY TRACT

The gallbladder can be divided into four areasfundus, body, infundibulum, and neck

The neck usually has a gentle curve, the convexity of which may be enlarged to form the
infundibulum, or Hartmann pouch. The neck occupies the deepest part of the gallbladder fossa
and lies in the free portion of the hepatoduodenal ligament).

The cystic duct lumen contains a thin mucosal septum, called the spiral valve of Heister The
valve may make catheterization of the cystic duct difficult but does not have true valvular function.

GALLBLADDER AND BILIARY TRACT

Vessels, Nerves, and Lymphatics

The arteries of the gallbladder are derived from the cystic branch of the hepatic artery. The
cystic artery arises from the right hepatic artery in 95% of cases
The course of the cystic artery varies greatly but is nearly always found within the
hepatocystic triangle, the area bound by the cystic duct, common hepatic duct and liver
margin.
The cystic veins empty into the right branch of the portal vein and directly into the liver.
Gallbladder lymphatics drain into nodes at the neck of the gallbladder. Often, a visibly
enlarged lymph node MASCAGNI (cystic artery node or sentinel node) overlies the insertion
of the cystic artery into the gallbladder wall.
The nerves of the gallbladder are branches of the vagus and sympathetic nerves, which pass
through the celiac plexus

GALLBLADDER AND BILIARY TRACT

Normal and anomalous arterial supply to the gallbladder.

GALLBLADDER AND BILIARY TRACT


Extrahepatic Biliary Ducts
Common Hepatic Duct

The common hepatic duct is formed by the union of the right and left hepatic ducts close to their emergence from
the liver.
The common hepatic duct is 1 to 2.5 cm long and normally has a diameter of about 4 mm. The duct passes
downward in the superior and lateral portion of the hepatoduodenal ligament and lies in front of the portal vein and
to the right of the hepatic artery.

The common hepatic duct unites with the cystic duct to form the common bile ductCystic Duct

The cystic duct

is about 0.5 to 4 cm long, begins at the neck of the gallbladder, and is directed slightly to the left. The cystic duct
passes downward, backward, and to the left in the hepatoduodenal ligament and usually unites with the main
hepatic duct at an acute angle.
The cystic duct usually lies to the right of the hepatic artery and portal vein. Its course and mode of insertion into
the common duct is highly variable. The cystic duct may be extremely short or run behind or parallel to the main
hepatic duct and, after a spiral course, empty into its posterior or left side.

Variations in cystic
duct anatomy.

GALLBLADDER AND BILIARY TRACT

Common Bile Duct

The common bile duct (ductus choledochus) is formed by the union of the common hepatic and
cystic ducts.
The common bile duct is usually about 7 to 9 cm long, but its length depends on the site of union
of the cystic and main hepatic ducts. Internal diameter averages about 5 mm; however, the duct
may be quite narrow or dilate to enormous dimensions when obstructed.
The anatomic divisions of the common duct

GALLBLADDER AND BILIARY TRACT

The intramural portion of the common bile duct runs obliquely downward and laterally
within the wall of the duodenum for 1 to 2 cm, opening on a papilla (VATER) of mucous
membrane about 10 cm from the pylorus.
The junction of the terminal common bile duct and pancreatic duct at the papilla takes one of
three configurations that may be likened to a Y, V, or U. In about 70% of patients, there is a
common channel of the bile duct and pancreatic ducts, thus a Y configuration. In about 20%, the
common channel is nonexistent (V configuration). In 10%, the two ducts enter the duodenum via
separate openings (U configuration).

Cross section of the


sphincter of Oddi.

GALLBLADDER AND BILIARY TRACT


HISTOLOGY
Gallbladder

The gallbladder wall consists of five layers. The innermost layer is the epithelium, and the
succeeding layers are the lamina propria, smooth muscle, perimuscular subserosal connective
tissue, and serosa.

Most cells in the mucosa are columnar cells, and their main function is absorption.
Motor Function

As bile is secreted from the liver, it flows through the hepatic ducts into the common hepatic duct
and continues through the common bile duct into the duodenum. With an intact and contracted
sphincter of Oddi, bile flow is directed into the gallbladder, where it is concentrated and stored

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GALLBLADDER AND BILIARY TRACT

Motor Function
In the postprandial state, about 70% of hepatic bile flows into the gallbladder before reaching the
duodenum and entering the enterohepatic cycle.
Patterns of gallbladder storage and emptying depend on a pressure gradient between the bile
ducts and the gallbladder created by contraction of the sphincter.
Peptide hormones and neural factors influence this gradient.
During the interdigestive phase, 90% of bile from the liver enters the gallbladder, while only a
small fraction of the gallbladder bile enters the duodenum.
Following a meal, the gallbladder empties by a steady tonic contraction thought to be due to
release of endogenous cholecystokinin (CCK) from the mucosa of the small intestine.
The importance of these gallbladder motor events is speculative, but they have been invoked to
explain cholesterol nucleation and gallstone formation.
The bellows action of the gallbladder may reduce the vesicular phase (liquid crystals that lead to
stone formation) and increase the micellar phase of stored bile. Periodic emptying during the
interdigestive phase would thus remove the less dense vesicles, and alterations in the normal
motor function would negate these favorable events and increase the risk of cholesterol stone
formation.

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GALLBLADDER AND BILIARY TRACT


MOTOR DYFUNCTION
Gallbladder Dyskinesia

Motility abnormalities of the gallbladder and cystic duct present with symptoms suggesting
gallstones.

The most common presentation for patients with gallbladder motility disorders (chronic acalculous
cholecystitis or gallbladder dyskinesia) is recurrent biliary-type pain.

However, routine morphologic investigations of the biliary tree (by ultrasound or endoscopic
retrograde cholangiopancreatography [ERCP]) display no evidence of gallstones or other
anatomic abnormalities.

The most specific test for diagnosing gallbladder dyskinesia is CCK-enhanced cholescintigraphy
with assessment of gallbladder ejection fraction. CCK is infused intravenously 15 to 30 minutes
after injecting an analogue of 99m Tc imminodiacetic acid, and the ejection fraction of the isotope
by the contracting gallbladder is calculated. An ejection fraction less than 35% is considered
abnormal and cholecystectomy may be indicated.

A number of factors may lead to decreased gallbladder contraction such as a primary abnormality
of gallbladder muscle, motor dysfunction secondary to chronic inflammation or lithogenic bile,
suboptimal hormonal or neural stimulation or circulation of an inhibiting substance.
Sphincter of Oddi Dysfunction

Abnormalities of the sphincter of Oddi may cause symptoms that are referable to the biliary tree or
to the pancreas.

Sphincter of Oddi dysfunction may arise de novo or lead to symptoms after cholecystectomy.

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GALLBLADDER AND BILIARY TRACT

CALCULOUS BILIARY DISEASE

The first recognized case of cholelithiasis was reported more than 1500 years ago.

In 1882, Carl Langenbach, a German surgeon, performed the first successful cholecystectomy.

This event revolutionized the approach to cholelithiasis.

1950 The scientists recognized the importance of increased concentrations of biliary cholesterol
and alterations in hepatic biliary lipid metabolism as prerequisites for cholesterol stone formation.

In more recent years, attention has focused on the role of altered gallbladder function in the
pathogenesis of gallstones and the mechanisms by which changes in the physical properties of
bile promote nucleation and stone formation.

Calculous disease of the biliary tract continues to be a major national and international health
problem.

For more than a century, cholecystectomy had been the gold standard for the management of
symptomatic gallstone disease. In the 1980s, a number of new and innovative techniques were
developed for the nonoperative management of gallstones. The surgical management of
cholelithiasis was challenged by the introduction of oral agents suitable for medical dissolution,
reports of invasive techniques employing principles of contact dissolution, and biliary lithotripsy.

The management of gallstone disease has been revolutionized in recent years by the
development of laparoscopic cholecystectomy and related procedures.
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GALLBLADDER AND BILIARY TRACT

GALLSTONE CLASSIFICATION

Gallstones may be single or numerous, small or large, and they may differ in color, size,
shape, and configuration.
the composition of stones in individual patients is uniform.
There are essentially three types of gallstonescholesterol, pigment, and mixed cholesterol
and pigment stones. Pigment stones are further classified as brown or black.
These distinctions are important for understanding varyious causes but may have little influence
for surgical decision making.
Calculi may be found either in the gallbladder and extrahepatic biliary tract or in the intrahepatic
ductal system.
Stones situated in the extrahepatic biliary tract are classified as either primary or secondary,
depending on the site of origin.
Primary common duct stones form exclusively in the intrahepatic or extrahepatic bile ducts and
are generally soft, smooth, and yellowish. These stones usually conform to the shape of the bile
duct and rarely contain significant amounts of cholesterol.
Secondary (or retained) stones form in the gallbladder and subsequently pass into the common
bile duct, either through the cystic duct or a biliary fistula. These stones are chemically similar to
coexisting stones in the gallbladder.

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GALLBLADDER AND BILIARY TRACT

INCIDENCE

The incidence of biliary calculous disease varies widely throughout the world. In the United States,
about 10% of the population has cholelithiasis. In addition to the 25 million people with
documented gallstone disease, another 800,000 new cases are diagnosed each year.

EPIDEMIOLOGY
Age
Hereditary and Ethnic Factors
Gender and Hormones
Obesity
Diabetes
Cirrhosis
Vagotomy
Total Parenteral Nutrition

GALLBLADDER DISEASE PREVALENCE BY


AGE GROUP

Percentage With Stones


Age (y) Female Male
10-39
5.0
1.5
40-49
12.0
4.4
50-59
15.8
6.2
60-69
25.4
9.9
70-79
28.9
15.2
80-89
30.9
17.9
90+
35.4
24.4

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GALLBLADDER AND BILIARY TRACT

CHOLESTEROL GALLSTONES

The pathogenesis of cholesterol gallstones is multifactorial, and neither the liver nor the
gallbladder alone has an exclusive etiologic role in the formation of calculi.
Cholesterol calculi form as the result of a dynamic interaction between the liver and gallbladder,
wherein factors present in cholesterol-saturated bile induce a series of alterations in gallbladder
function that promote nucleation and stone growth.
Composition of Normal Bile
Bile is a solution secreted by the liver and is composed primarily of water, electrolytes, and
organic solutes.
This complex solution is isotonic with plasma and is essential for important physiologic functions,
including cholesterol solubilization and digestive function.
Bile salts, cholesterol, and phospholipids are the main solutes in bile and account for about 80%
of the dry weight of bile.
primary bile acids are synthesized from cholesterol in the liver.(In humans, chenodeoxycholic and
cholic acid)
They are conjugated with taurine or glycine in the liver to became hydrosoluble
Most of the cholesterol found in bile is synthesized de novo in the liver. Lecithin is the
predominant phospholipid found in human bile and accounts for more than 90% of the
phospholipid content.

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GALLBLADDER AND BILIARY TRACT

Cholesterol Solubilization
Cholesterol is an organic molecule that is virtually insoluble in an aqueous medium such as bile.
For many years, the formation of mixed-bile acid-lecithin-cholesterol micelles was thought to be
critical in maintaining cholesterol in solution.
Bile acids are amphipathic compounds that contain both hydrophilic polar groups (amino acids
side chain) and hydrophobic nonpolar portions

Schematic representation of the


orientation of bile acid molecules as
amphipathic units with hydrophobic
ends pointed inward and hydrophilic
ends pointed outward.

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GALLBLADDER AND BILIARY TRACT

Incorporation of lecithin into the micelle induces swelling and facilitates incorporation of
cholesterol into this matrix

Bile acidlecithincholesterol-mixed
micelle. Polar ends of bile acids and
lecithin are oriented outward, and
hydrophobic, nonpolar portions make
up the interior. Cholesterol is
solubilized within the hydrophobic,
nonpolar center.

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GALLBLADDER AND BILIARY TRACT

Several independent investigators have demonstrated that although some cholesterol is


solubilized in mixed bile acid lecithin micelles, much of the biliary cholesterol normally present
actually exists in a vesicular form. These vesicles solubilize greater quantities of cholesterol than
micelles and are made up of lipid bilayers, similar to those normally found in cell membranes
Up to 70% of the total amount of cholesterol normally found in human gallbladder bile is
transported and solubilized in the vesicular form, with the remainder being transported in mixed
micelles. The relative amounts of cholesterol transported in vesicles or micelles is related to the
degree of bile concentration.

Unilamellar bile acidlecithincholesterol


vesicle. The amphipathic molecules of
lecithin and bile acids form a lipid bilayer.
Cholesterol is solubilized within the
nonpolar portion of the bilayer.

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GALLBLADDER AND BILIARY TRACT

Cholesterol Saturation

Regardless of the mode of cholesterol transport, failure to solubilize all cholesterol present, either as a
result of excessive quantity or alteration in the vehicle, is considered a critical step in the formation of
gallstones.
Theoretically, an increase in cholesterol concentration relative to bile acids can occur as a result of
altered secretion of any of the three biliary lipid moities present in bilecholesterol, bile acids, or lecithin.
In 1968, Admirand and Small first described the relation between cholesterol, phospholipids, and bile
salts in both health and during cholesterol gallstone formation. Their data have been displayed using
triangular coordinates and have since been modified by others
Tricoordinate phase diagram for determination of
cholesterol saturation index. A given single point
represents the relative molar ratios of bile salts,
lecithin, and cholesterol. The range of concentrations
found consistent with a clear, micellar solution (where
cholesterol is fully solubilized) is limited to a small
region in the lower left. The colored area directly above
this region corresponds to a metastable zone in which
bile initially appears clear but, with time, develops
cholesterol crystals. All other regions represent bile
solutions in which the cholesterol solubilization
capacity is exceeded and rapid formation of cholesterol
crystals occurs.

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GALLBLADDER AND BILIARY TRACT

Cholesterol Saturation

It is generally accepted that the cholesterol content of bile exceeds its solubilizing capacity in
patients with cholesterol gallstones.

Other factors than cholesterol saturation of bile may play an important etiologic role in the
pathogenesis of cholesterol gallstones (secretion of hepatic bile with either increased amounts of
cholesterol or decreased amounts of bile acids: in obese patients, in patients with ileal disorders or
ileal resection, during periods of starvation or fasting, normal people without gallstones secrete
cholelithogenic bile).

This finding suggests that factors other than cholesterol saturation of bile may play an important
etiologic role in the pathogenesis of cholesterol gallstones.
Nucleation and Mucus Secretion

Considerable evidence indicate that aggregation of cholesterolphospholipid vesicles is critical to


nucleation and formation of cholesterol crystals.

Nucleation refers to the process by which cholesterol monohydrate crystals form and agglomerate.

Nucleation occurs more rapidly in gallbladder bile of patients with cholesterol gallstones compared
with patients with cholesterol saturated bile but no stones.

Experimental and clinical studies have suggested that cholesterol gallstone formation is associated
with increased gallbladder mucus secretion.

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GALLBLADDER AND BILIARY TRACT

Nucleation and Mucus Secretion

These data suggest that mucin may be the elusive nucleating factor.

Efforts are underway to understand the physiologic balance between nucleation-inhibiting5 and
nucleation-promoting6 factors and moreover, the manner in which this balance is disturbed during
cholesterol gallstone formation.

Schematic depicting the dynamic role of


vesicles as vehicles for cholesterol in
bile and how they relate to nucleation.

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GALLBLADDER AND BILIARY TRACT

Gallbladder Stasis

Gallbladder stasis has long been considered an important etiologic factor in the pathogenesis of
cholesterol gallstones, but the manner in which it promotes stone formation continues to be investigated.
Stagnant pool of bile in the gallbladder would result in a decrease in the amount of bile salts available for
cholesterol solubilization and therefore predispose to saturation and crystal formation.
Stasis of bile in the gallbladder is thought to provide an ideal milieu for the precipitation of specific
factors present in gallbladder bile.
Recently, it has been proposed that alterations in gallbladder absorptive or secretory function may be a
sequela of biliary stasis.
The relation between gallbladder stasis and the concentration of nucleating or antinucleating factors
continues to be examined as a possible critical factor in the cascade of events leading to stone formation

Gallstone pathogenesis is a multifactorial


process that results from stasis of bile in
the gallbladder in combination with a
nucleation defect, all in the presence of
cholesterol-saturated bile.

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GALLBLADDER AND BILIARY TRACT

Biliary Calcium

Increased concentrations of calcium bilirubinate has long been recognized as an important


etiologic factor in the formation of pigment gallstones. Recent studies have suggested that
alterations in biliary calcium may be critical to the formation of cholesterol gallstones as well.

The mechanism by which biliary calcium is increased remains unclear.


Altered Gallbladder Absorption

Although the primary function of the gallbladder is to concentrate bile by absorbing sodium and
water during interdigestive periods, the manner in which this most fundamental activity is altered
during gallstone formation has not been well defined

The specific defects that occur in gallbladder epithelial ion transport during the early stages of
stone formation remain obscure.
Biliary Prostaglandins

Data suggest that arachidonic metabolism is significantly altered during the formation of
experimentally induced cholesterol gallstones

These changes in prostaglandin synthesis have been associated with mucus hypersecretion.

Alterations in endogenous synthesis and release of prostanoids occur as a result of


cholesterol feeding and have been linked with accumulation of gallbladder luminal
fluid, a finding characteristic of patients with acute cholecystitis.

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GALLBLADDER AND BILIARY TRACT

Proposed events that


occur during cholesterol
gallstone formation. A
relation can be seen
between hepatic
metabolism and altered
gallbladder physiology.

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GALLBLADDER AND BILIARY TRACT


PIGMENT GALLSTONES

Worldwide, pigment stones are the most common type of calculi found in the gallbladder.

Epidemiologic studies have indicated that although cholesterol calculi account for most gallstones in
the United States, pigment stones constitute about 30% of all gallbladder stones.

Despite the diverse settings in which pigment gallstones are known to occur, the final common pathway
in the pathogenesis of the various types of pigment calculi is altered solubilization of unconjugated
bilirubin with precipitation of calcium bilirubinate and insoluble salts.
Classification

Pigment gallstones are characterized by their relatively high concentration of bilirubin (usually in excess
of 40%) and their low cholesterol content.

Most pigment gallstones are mixed stones and contain calcium bilirubinate as the main component.

The pigment gallstones have been classified as black or brown stones.


Black-pigment stones are generally associated with hemolytic disorders or cirrhosis.
These stones are typically tarry in appearance, are almost always located exclusively in
the gallbladder, and are thought to occur as a result of alterations in biliary metabolism.
In contrast, brown stones are the most common type found in Asian patients, are similar
in composition to primary common bile duct stones, may be located throughout the
intrahepatic or extrahepatic biliary tract, and are generally associated with infection.

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GALLBLADDER AND BILIARY TRACT

Pathogenesis
Infection is thought to be a key factor in the pathogenesis of pigment gallstones.
Free unconjugated bilirubin produced by bacterial deconjugation is insoluble in water
and combines with calcium in bile to produce a calcium bilirubinate matrix (which is
well known as the predominant component of most pigment gallstones).
Bacteria are found within the calcium bilirubinateprotein matrix of brown-pigment
stones but are absent from either black-pigment or cholesterol gallstones.
These findings are consistent with epidemiologic studies indicating that brown stones
are found in patients living in areas where biliary infections are endemic, whereas
black-pigment stones are typically found in patients with hemolytic disorders or
cirrhosis.
Stasis of bile within the gallbladder has been implicated as an important etiologic
factor in the pathogenesis of pigment gallstones.
gallbladder stasis, tend to form calcium bilirubinate stones.
gallbladder stasis, create conditions for infection.

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GALLBLADDER AND BILIARY TRACT

Biliary sludge

The importance of biliary sludge as a precursor of cholesterol and pigment gallstones has
recently been recognized.

Sludge, as determined ultrasonographically, is partly composed of calcium bilirubinate crystals


and may be a consequence of biliary stasis.

Biochemical analysis of sludge demonstrates large amounts of phospholipids.

Nonetheless, the mechanism by which phospholipids alter the solubility of unconjugated bilirubin
and contribute to biliary sludge remains unclear.

Several possible explanations have been proposed, including direct binding of phospholipids to
unconjugated bilirubin and phospholipid-induced displacement of unconjugated bilirubin from
bile saltphospholipid micelles.

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GALLBLADDER AND BILIARY TRACT

Gallstone disease

The spectrum of clinical syndromes associated with cholelithiasis is varied


Studies suggest that about 50% of patients with gallstone disease are truly asymptomatic.
Most patients with symptoms secondary to cholelithiasis complain of recurring right upper
quandrant pain (biliary colic).

Others will have symptoms consistent with acute cholecystitis, choledocholithiasis, or gallstone
pancreatitis.

The difficulty lies in identifying those patients at risk for developing these specific complications of
gallstone disease.
Asymptomatic Stones

The optimal treatment for patients with asymptomatic gallstones has been debated for many years.

Less than 10% of patients with asymptomatic gallstones will develop significant symptoms over a 5year period.

The natural history of asymptomatic gallstones is benign question: if early or prophylactic


cholecystectomy is indicated( rarely )?.

An issue central to this controversy is the definition of what truly constitutes an asymptomatic
patient.

An issue central to this controversy is the definition of what truly constitutes an asymptomatic
patient.

A significant number of patients with cholelithiasis do not have postprandial pain but instead have
dyspepsia, vague epigastric discomfort, or even mildly increased flatulence as the primary
manifestation of their disease.
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GALLBLADDER AND BILIARY TRACT

Up to 70% of such patients derive significant benefit from cholecystectomy, however, suggests that
these nonspecific symptoms are frequently due to biliary calculi. Thus, designating these patients as
asymptomatic is inappropriate.

Early cholecystectomy should be considered in any patient with asymptomatic gallstones

Acute cholecystitis is a potentially life-threatening complication when it occurs in an


immunosuppressed patient.
Diagnosis
Abdominal Radiography

Although supine and upright abdominal radiographs are essential in the early evaluation of patients
with an acute abdomen, their usefulness is limited in patients with cholelithiasis.

Visualization of gallstones on plain abdominal radiographs is possible only in the 20% of patients
whose stones are grossly calcified, or the outlining of the gallbladder in patients with porcelain
gallbladders or milk of calcium bile.
Oral Cholecystography

Traditionally, the oral cholecystogram has been the gold standard for the diagnostic evaluation of
patients with calculous disease of the biliary tract

This test is based on the excretion of halogen compounds by the liver into bile with gallbladder
visualization after reabsorption of water and solutes, resulting in concentration of the dyes.

Although the accuracy for oral cholecystography has been reported to be as high as 95%

Several important conditions preclude satisfactory examination, including acute cholecystitis, poor
patient compliance, inability to absorb the tablets as a result of emesis, malabsorption, or diarrhea,
and jaundice or hepatic dysfunction
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GALLBLADDER AND BILIARY TRACT

Oral cholecystogram demonstrating


multiple radiolucent, free-floating
stones in the gallbladder.

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GALLBLADDER AND BILIARY TRACT

Abdominal Ultrasonography
Abdominal ultrasonography is the preferred test for evaluating patients with suspected cholelithiasis
Ultrasonography has advantages over conventional oral cholecystography:
- absence of radiation exposure,
- independence of patient compliance, and
- no requirement for intact digestive and hepatic function.
Most large series suggest that diagnostic accuracy and sensitivity for cholelithiasis exceeds 95%
Information derived from ultrasonography includes size and shape of the gallbladder, gallbladder wall
thickness, and the presence of pericholecystic fluid collections and in addition to identify stones in
the common bile duct.

Abdominal ultrasonogram
demonstrating echogenic foci within the
gallbladder causing acoustic shadowing
(arrow) typical of cholelithiasis.

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GALLBLADDER AND BILIARY TRACT

Hepatobiliary Scintigraphy
Radionuclides, such as 99mTcsubstituted iminodiacetic acid derivatives, can be used to provide
a direct image of the gallbladder and biliary tract.
These radionuclide agents, administered intravenously, are cleared from the blood by hepatocytes
and excreted in an unconjugated form directly into the biliary ductular system.
The diagnostic role of hepatobiliary scintigraphy in patients with acute right upper quadrant
symptoms remains poorly defined.
The diagnosis of acute cholecystitis is established based on clinical criteria, although it may be
confirmed by biliary scintigraphy.
Biliary Drainage and Cholecystokinin Cholecystography

Common Clinical Features


Nonspecific Symptoms

Patients with cholelithiasis may complain of vague, poorly localized abdominal discomfort

the pain typically occurs postprandially, patients may be unable to specify the interval between the
meal and pain.

The discomfort is generally localized in the right upper quadrant, although a significant number of
these patients complain of mid-epigastric pain. Other nonspecific complaints that may be present
in gallstone patients include increased flatulence, eructations, or heartburn.
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GALLBLADDER AND BILIARY TRACT


Common Clinical Features
Biliary Colic

Biliary colic usually results from an impacted stone in the cystic duct or Hartmann pouch or from
passage of a stone through this ductular structure.

Acute cholecystitis occurs when a stone becomes


lodged in the cystic duct or Hartmann pouch.

The term colic may be somewhat misleading in that the character of the pain is generally different
from pain that occurs with intestinal or ureteral obstruction.In the latter settings, the patient
typically describes an intermittent discomfort that is spasmodic and of relatively short duration.
In contrast, biliary colic is characterized by a rapid increase in pain intensity, with a plateau of
discomfort that lasts for several hours, followed by a gradual decrease in intensity

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GALLBLADDER AND BILIARY TRACT

Diagram representing the chronologic pain


intensity of biliary colic. Characteristically, the
pain is of sudden onset, builds in intensity,
and then remains steady for several hours.

Classically, the pain of biliary colic is situated in the right upper quadrant or middle epigastrium.
The back discomfort that is frequently observed in patients with biliary colic is usually located in
the inferomedial aspect of the right scapula,
Pain may also occur in the right shoulder.
Episodes of biliary colic typically occur postprandially and are often associated with nausea and
emesis. These attacks are often precipitated by fatty meals, although most foods can also bring
about gallbladder contractions and painful episodes.
Acute Cholecystitis
The clinical manifestations of biliary colic and acute cholecystitis may overlap, and clinical
distinction is often difficult.
It is helpful to think of them as distinct entities.
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GALLBLADDER AND BILIARY TRACT

The initiating factor in the pathogenesis of acute cholecystitis is impaction of a stone either in the
cystic duct or the pouch of Hartmann

Acute cholecystitis occurs when a


stone becomes lodged in the cystic
duct or Hartmann pouch.

The onset and character of pain associated with acute cholecystitis is comparable to that observed
in patients with biliary colic.
Unlike biliary colic, where the pain generally lasts for several minutes to hours, the pain of acute
cholecystitis persists and may be unremitting for several days.
With progression of the inflammatory process, the gallbladder may become more distended,
ultimately resulting in inflammation of the contiguous parietal peritoneum and surrounding organs.
At this juncture, the patient typically complains of more localized right upper quadrant pain. Many
patients have associated constitutional symptoms of anorexia, nausea, and vomiting.
As a result of associated peritoneal irritation, the patient is reluctant to move and is most comfortable
lying still. The classic physical finding of acute cholecystitis is a positive Murphy sign, which refers to
inspiratory arrest during deep palpation in the right upper quadrant. There is a wide variation in the
spectrum of complaints and physical findings in patients with acute cholecystitis, and often, only
persistence of right upper quadrant pain and discomfort distinguishes this diagnosis from simple
biliary colic.
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GALLBLADDER AND BILIARY TRACT

(Acute Cholecystitis)
Laboratory data are helpful but frequently nonspecific. Most patients with uncomplicated acute
cholecystitis have mild leukocytosis, ranging from 12,000 to 15,000/mL. Mild jaundice may be
present in up to 20% of patients and is typically due to contiguous inflammation.
Pathology
Obstruction of the cystic duct with a stone and the associated inflammatory response can cause
significant edema of the gallbladder wall as a result of venous and lymphatic outflow obstruction.
On gross examination, the gallbladder is typically distended with gallbladder wall thickening and
obvious edema.
At the time of laparotomy, the gallbladder may be surrounded by omentum or adherent to the
duodenum and contiguous structures. Depending on the evolution of the disease, there may be
gross evidence of ischemia, particularly in the least vascularized portion of the gallbladder, the
fundus.
Histologically, acute cholecystitis is manifested by mucosal and subserosal edema, hypervascularity,
and infiltration of the submucosa with polymorphonuclear leukocytes. In addition to the changes
typical of acute cholecystitis, most acutely diseased gallbladders also have evidence of chronic
inflammation, with lymphocytic infiltration of the submucosal layer and flattening of the mucosa.
Between 30% and 70% of patients with the clinical diagnosis of acute cholecystitis have positive bile
cultures. Most of the bacteria cultured from these patients are of enteric origin, the most common
organism being Escherichia coli. Other bacteria typically found include species of Enterobacter,
Klebsiella, and Enterococcus.
The presence of bacteria in the bile of patients with acute cholecystitis is a source of significant
morbidity and mortality.
37

GALLBLADDER AND BILIARY TRACT

Preoperative evaluation

In addition to a careful history and physical examination, preoperative testing for 90 percent of
patients with gallstone disease is minimal. An ultrasound of the right upper quadrant will usually
confirm the diagnosis, and the hepatic biochemical profile (alkaline phosphatase, SGOT, bilirubin,
lactic acid dehydrogenase [LDH]) will usually determine the likelihood that common bile duct
stones are present. Striking abnormalities in the hepatic profile, or an ultrasonographically dilated
common bile duct, may warrant a preoperative ERC or abdominal CT scan, or both, to search for
the cause (e.g., neoplasm or stricture) of bile duct obstruction.

The diagnosis of acute cholecystitis, when the diagnosis is in doubt, can be made with a nuclear
hepatobillary scan. Nonfilling of the gallbladder in one hour, especially after administration of
intravenous morphine (which contracts the sphincter of Oddi) is a highly accurate predictor of
acute cholecystitis. When the ultrasound demonstrates nonuniform thickening of the gallbladder
wall or pancreatic head, a CT scan should be performed to assess the likelihood of the presence
of gallbladder cancer. Intravenous cholangiography, rarely performed in the US, is popular in
Europe for detecting common bile duct stones preoperatively in patients with abnormal liver
function studies.

38

GALLBLADDER AND BILIARY TRACT


(Acute Cholecystitis)

Prospective studies have demonstrated that the incidence of positive bile cultures increases
significantly with age.

Septic complications continue to be a source of significant morbidity after cholecystectomy,


particularly when the indication for operation is acute cholecystitis.

Prospective studies have confirmed the benefit of prophylactic antibiotic therapy for these patients.

If a septic complication develops postoperatively, the choice of antibiotics should be based on


operative cultures as well as cultures from the wound or intraabdominal fluid collections.
Principles of treatment
Cholecystectomy

The earliest attempts at surgical treatment for gallstone disease focused on cholecystostomy and
stone removal; this approach was associated with a significant risk of gallstone recurrence,
approaching 50% to 80% within 5 years.

In 1882, Carl Langenbuch performed the first successful cholecystectomy and for the last 100 years,
open cholecystectomy has been the standard of care.
Open Cholecystectomy

Experience with open cholecystectomy is vast, spanning generations of surgeons and having been
practiced in virtually every country throughout the world.

Over time, this operation has proved to be safe and effective.

In a collected series of about 20,000 patients who underwent cholecystectomy between l946 and
1973 at 10 different institutions, from the United States and throughout the world, the overall
mortality rate was l.6%.
39

GALLBLADDER AND BILIARY TRACT

(Open Cholecystectomy)
More recently, a US population-based study examining the outcome of all open cholecystectomies
performed in a 12-month period in two states reported an overall mortality rate of 0.17%, morbidity
rate of 14.7%, and estimated incidence of bile duct injuries of 0.2%
In elective situations, open cholecystectomy is being performed in most hospitals throughout the
world on patients who are admitted the day of surgery with an overall stay of 2 to 4 days.
IMPACT OF DISEASE STATUS ON OUTCOME:
OPEN CHOLECYSTECTOMY

Chronic
27,892

Number
Percentage
of group
65.7%
Morbidity rate 11.9%
Deaths
29
Mortality rate 0.10%
Length of
stay (d)
4.8
Cost ($)
5,881

Disease Status
Acute
Complicated
13,246
1336
31.2%
19.4*%
34
0.26*%

3.1%
25.2*%
8
0.60*%

6.6*
9,043*

8.6*
12,510*

COMPLICATIONS OF LAPAROSCOPIC
CHOLECYSTECTOMY IN 77,604 PATIENTS
Complication
Bile duct injury
Vascular injury
Bowel injury
Mortality

Patients
459 (0.6%)
193 (0.25%)
109 (0.14%)
33 (0.04%)

(Am J Surg 1993;165:9)

* P <.0001 versus chronic cholecystitis.

40

GALLBLADDER AND BILIARY TRACT

Laparoscopic Cholecystectomy
In 1988, anecdotal reports suggested that the gallbladder could be removed laparoscopically
without the need for laparotomy.
In 1987, 105 years later, after Carl Langenbuchs first successful open cholecystectomy, Philipe
Mouret performed the first laparoscopic cholecystectomy in Lyon, France.
In recent years, laparascopic cholecystectomy has become the treatment of choice rather than
open cholecystectomy for managing calculous biliary disease.
As experience with this technology has increased, recommendations regarding contraindications
for it have evolved. Absolute contraindications include inability to perform laparascopic
cholecystectomy because of inadequate training or equipment, poor candidate for general
anesthesia, uncorrected coagulopathy, peritonitis, or suspected gallbladder carcinoma. Judgment
should be exercised when considering laparascopic cholecystectomy for patients with acute
cholecystitis, morbid obesity, previous upper abdominal surgery, cirrhosis and portal hypertension,
or pregnancy.

Widespread acceptance for this technique is growing because of the obvious


advantages of reduced hospital days, earlier return to normal activity, less pain, and
better cosmesis.

41

GALLBLADDER AND BILIARY TRACT

Laparoscopic
cholecystectomy :
(A)create a
pneumoperitoneum and
provide exposure. (B) Careful
identification of ductal and
vascular anatomy. (C)
Dissection of the gallbladder.
(D) Extraction.

42

GALLBLADDER AND BILIARY TRACT

Delayed Versus Early Cholecystectomy


The issue of delayed versus early cholecystectomy in patients with acute cholecystitis has long been
the focus of debate and controversy. Traditionally, the standard practice was to admit patients with
acute cholecystitis to the hospital for intravenous therapy and antibiotics.
As the inflammatory process resolved, these patients would be planned to perform an elective
cholecystectomy 6 to 10 weeks later. The rationale for this strategy was to allow resolution of the
acute inflammatory process and to facilitate the operative procedure.
This traditional approach of intense medical management was challenged by a number of reports that
demonstrated significant advantages to early cholecystectomy. These studies indicated that morbidity
and mortality were no different in patients who underwent early or delayed cholecystectomy and that
early cholecystectomy was associated with reduced hospitalization, cost, and episodes of recurrent
cholecystitis
In this era of laparascopic cholecystectomy as the treatment of choice, the debate has shifted in favor
of early rather than delayed intervention as morbidity and mortality appear to be the same or even less
when the gallbladder is removed expeditiously in patients with acute cholecystitis.
Performing laparascopic cholecystectomy in the presence of acute inflammation can be challenging,
and this procedure should only be undertaken by experienced laparoscopists.(surgeons)
Role of Intraoperative Cholangiography
Common bile duct stones are found in about 8% to 12% of all patients who undergo cholecystectomy
for symptomatic gallstone disease. An effective way to identify common duct calculi uses
intraoperative cholangiography.
In most instances, this is accomplished by the placing a small catheter through the cystic duct and
instilling 10 to 20 mL of dye.
43

GALLBLADDER AND BILIARY TRACT

Medical Dissolution
Medical dissolution of gallstones has been achieved only in cholesterol gallstones. Limited
information is available on the dissolution of noncholesterol, calcium bilirubinate stones. A series
of in vitro investigations, however, suggests that pigment gallstone material can be solubilized by
a solvent system that contains a mucolytic agent, a chelating agent, and a strong detergent.
Further research is clearly needed in the area of medical dissolution for both cholesterol and
noncholesterol gallstones.
chenodeoxycholic acid (CDCA).
The rate of complete stone disappearance was only 13.5% in the high-dose CDCA group, and
another 28% in this group had partial dissolution.
In addition to this disappointingly low success rate:

at least 9 months of intense therapy;


potential toxicity and side effects;
high cost;
a lifetime of maintenance therapy to prevent recurrence of stones;
the need to limit dietary cholesterol.

Ursodeoxycholic acid (UDCA) is now commercially available.


Initial data suggest that this agent may be a better, safer, and more effective drug for gallstone
dissolution than CDCA.
the rate of complete dissolution only approaches 40%.
The indications for the use of CDCA and UDCA are limited, particularly since the introduction of
laparascopic cholecystectomy.
44

GALLBLADDER AND BILIARY TRACT

Contact Dissolution
Percutaneous transhepatic cholecystolitholysis (direct contact dissolution) has been recommended
as a potential therapy for patients with symptomatic cholesterol gallstone disease.
this technique is based on percutaneous transhepatic pigtail catheter placement in the gallbladder
and infusion of an agent that has a high capacity for cholesterol dissolution.
Methyl tert-butyl ether (MTBE) is an aliphatic ether, liquid at body temperature, that rapidly dissolves
cholesterol.
potential candidates for MTBE dissolution include high-risk patients with symptomatic stones or
those who refuse operation.
Although this modality may have specific indications, its application to the general population is
limited.
Biliary Lithotripsy (electrohydraulic shock wave lithotripsy - ESWL)
In preliminary studies using lithotripsy combined with adjuvant and litholytic medications (usually
UDCA), gallstone fragmentation has been achieved in virtually all selected patients. Fragment
clearance occurred within 2 months in 30% of patients, within 4 months in 48%, and in 21% of
patients between 12 and 18 months.
Prior to 1989, ESWL appeared to be the most promising nonoperative modality for managing
symptomatic gallstones. The widespread application of laparascopic cholecystectomy has caused
this concept to be reevaluated.

45

GALLBLADDER AND BILIARY TRACT


Acalculous Cholecystitis

Acalculous cholecystitis is an unusual but potentially lethal complication of gallbladder disease.

The cause of this clinical entity has not yet been determined. Most clinical and experimental studies
suggest a multifactorial etiology that varies, depending on the clinical situation.
Pathogenesis

Stasis of bile in the gallbladder. Biliary stasis can occur as a result of :


ampullary spasm secondary to the administration of narcotics,
decreased gallbladder emptying during periods of prolonged fasting, or
cystic duct occlusion secondary to edema.

Altered viscosity of bile as a result of :


dehydration and
multiple transfusions with an associated increase in pigment load

The combination of biliary stasis and increased bile viscosity may lead to altered concentration of
specific biliary lipids and other luminal factors that may predispose to irritation and inflammation of
the gallbladder mucosa.

46

GALLBLADDER AND BILIARY TRACT

Acalculous Cholecystitis(suite)

The estimated incidence of acute acalculous cholecystitis is about 3% of all surgical biliary tract
cases
Acalculous cholecystitis has been reported as a postoperative complication and in critically ill
patients following trauma or burns.
Most postoperative patients who develop acute acalculous cholecystitis have had an intraabdominal
procedure 2 to 14 days before the onset of symptoms.
Diagnosis of acalculous cholecystitis poses a considerable challenge to the clinician, especially
when it occurs in intensive care unit patients. These patients typically have multiple medical and
surgical problems, and as a result, the diagnosis may be delayed.
Several studies suggest that the associated morbidity and mortality rates of acalculous cholecystitis,
when it occurs in intensive care patients, is between 40% and 60%.
The liberal use of ultrasound for early diagnosis and operative treatment may reduce the mortality
associated with this disease;
Cholecystectomy may be contraindicated because of the patients unstable overall condition. Under
these circumstances, a cholecystostomy, either through a minilaparotomy or percutaneously, is the
procedure of choice. Percutaneous cholecystostomy can be safely performed by interventional
radiologists in most centers. Although this procedure allows for the decompression and drainage of
infected gallbladder bile, it obviously does not cure gangrenous cholecystitis.

47

GALLBLADDER AND BILIARY TRACT

Cholecystitis in the Elderly


Considerable evidence indicates that gallstone disease is more virulent in the elderly than in the
younger population.
This contention is based on clinical observations demonstrating an increased incidence of
choledocholithiasis, emphysematous cholecystitis, perforation of the gallbladder, and septic
complications of cholecystitis in the elderly.
Although some have proposed that these findings are secondary to differences in the evolution of
the disease process and of delayed diagnosis.
Risk/benefit analyses suggest that elective cholecystectomy can be safely performed in elderly
patients with minimal morbidity and mortality.
Elderly patients with acute cholecystitis are best treated by timely diagnosis, early stabilization,
and semiurgent cholecystectomy.
Choledocholithiasis has been reported in 20% to 54% of elderly patients undergoing
cholecystectomy. This figure is in contrast to the 8% to 12% rate of common duct stones reported in
the general population. The increased incidence of common duct stones in the elderly probably
reflects long-standing, untreated disease. The clinical impact of this increased incidence of
choledocholithiasis in the elderly is underscored by the mortality rates for common duct exploration,
which increase with age.
The mortality rate associated with choledochotomy is 0.9% in patients younger than age 50 years
and 7.6% to 29% in patients older than age 70 years.

48

GALLBLADDER AND BILIARY TRACT

Cirrhosis and Cholecystitis

Regardless of the type of gallstones present, several studies have demonstrated that cholecystectomy
in cirrhotic patients is associated with significant rates of morbidity (50%) and mortality (10%).
Difficulties encountered in cirrhotic patients who undergo cholecystectomy are due to associated portal
hypertension, thrombocytopenia secondary to hypersplenism, and coagulopathy.
Indications for cholecystectomy in a cirrhotic patient should be more restrictive than in the noncirrhotic
patient.
Operations should be undertaken only in patients who are truly symptomatic or who have developed
one of the complications of gallstone disease, such as acute cholecystitis, perforation, fistula formation,
or empyema of the gallbladder.

Total Parenteral NutritionInduced Gallbladder Disease

The reported incidence of asymptomatic and symptomatic gallstone disease in the subset of patients
receiving long-term TPN (both children and adults) is between 40% and 45%.
40% of patients with TPN-induced gallbladder disease required emergency cholecystectomy, and
severe acute cholecystitis was present in more than 50%.

Diabetes and Cholecystitis

For many years, it has been assumed that diabetics have an increased incidence of cholesterol
gallstones and are more likely to develop acute cholecystitis with a greater incidence of postoperative
complications.
49

GALLBLADDER AND BILIARY TRACT

Complications of gallbladder lithiasis


Hydrops
Obstruction of the cystic duct by an impacted stone can result in hydrops, in which the gallbladder
becomes filled with a clear or whitish mucoid material(white bile). Little is known about the
pathophysiology of hydrops of the gallbladder except that the mucoid material probably results from
altered gallbladder epithelial secretion.
The gallbladder frequently becomes enlarged, and patients may present with signs and symptoms
suggestive of acute cholecystitis, although occasionally, their only complaint is of a mass in the right
upper quadrant. Cholecystectomy is the treatment of choice.
Emphysematous Cholecystitis
Emphysematous cholecystitis is an potentially lethal complication of cholecystitis and is manifested
by the radiographic / ultrasonographic demonstration of gas within either the gallbladder lumen or
wall. This entity accounts for about 1% of all cases of cholecystitis.
Stones are absent in about one third of patients with acute emphysematous cholecystitis.
Emphysematous cholecystitis is more common in elderly men, and about 40% of all cases occur in
diabetics.
The gas within the lumen of the gallbladder wall occurs as a result of gas-producing bacteria. The
most common organisms cultured are C perfringens, although mixtures of this anaerobe with E coli
and species of Klebsiella are also noted.
The clinical course of patients with emphysematous cholecystitis is frequently characterized by rapid
onset with severe abdominal pain, constitutional symptoms of nausea and vomiting, and evidence of
severe sepsis.
50

GALLBLADDER AND BILIARY TRACT

Emphysematous Cholecystitis (suite)


Common sequelae are gangrene (74%) and perforation of the gallbladder (21%). The potential for
serious morbidity and mortality in patients with acute emphysematous cholecystitis is so great that
emergent cholecystectomy is warranted when this diagnosis is suspected.
Empyema
Empyema of the gallbladder is a variant of acute cholecystitis. The pathogenesis of empyema is
similar to acute uncomplicated cholecystitis, and the only significant difference is the presence of
pus in the gallbladder lumen. These patients are often toxic, and emergent cholecystectomy is
mandated.
Gallbladder Perforation
Perforation of the gallbladder occurs in about 3% to 10% of all patients with acute cholecystitis.
This complication of biliary calculous disease has been traditionally classified into three types :

type 1, acute free perforation with bile stained peritoneal fluid;


type 2, subacute perforation with pericholecystic or right upper quadrant abscess formation;
type 3, chronic perforation with formation of either cholecystoenteric or cholecystocutaneous fistulas.

Acute and subacute perforation of the gallbladder have been associated with underlying vascular,
metabolic, or other disorders.
The gallbladder fundus is the most common site of acute perforation. Anatomically, this area
corresponds to the least vascularized portion of the gallbladder.
In patients with subacute perforations or chronic perforations with fistula formation, repeated bouts
of cholecystitis probably lead to scarring and fibrosis, with adherence of adjacent structures.

51

GALLBLADDER AND BILIARY TRACT

Gallbladder Perforation(suite)
Pressure necrosis and inflammation can develop around gallstones impacted in the wall of the
gallbladder, with subsequent erosion of the stone through the gallbladder wall into contiguous organs.
In most cases, this process occurs gradually so that protective adhesions between the gallbladder,
omentum, and colon are formed and prevent diffuse contamination. In this setting, either a localized
abscess or fistula results.
Computed tomography (CT) may be an inferior modality for detecting gallstones, it is better than
ultrasonography for detecting abscesses and free fluid that might be present in patients with either
type 1 or 2 perforations.
Barium upper gastrointestinal studies help define any fistulous communications among the stomach,
duodenum, and gallbladder. Acute free perforation of the gallbladder is less common than the other
types of perforation.
The clinical suspicion of acute perforation of the gallbladder warrants prompt and aggressive
treatment with fluid resuscitation, nasogastric decompression, intravenous administration of broadspectrum antibiotics, and expeditious laparotomy.
Gallstone ileus
Cholecystoenteric fistulas are the most common type of gallbladder perforation,
Depending on the size of the fistulous communication, a gallstone may pass through this tract. In
most cases, the stone passes through the intestinal tract without symptoms.
If a stone is large enough (greater than 2 cm in diameter), however, it may become lodged in a
portion of the gastrointestinal tract and cause a mechanical small bowel obstruction. This condition,
called gallstone ileus, is relatively rare and accounts for fewer than 5% of all cases of intestinal
obstruction.

52

GALLBLADDER AND BILIARY TRACT

Gallstone ileus(suite)

The diagnosis of gallstone ileus may be suggested by the presence of intrahepatic biliary air on
abdominal radiography.
Patients with gallstone ileus are best treated as if they had mechanical small bowel obstruction,
that is, with aggressive fluid resuscitation, broad-spectrum antibiotics, and early laparotomy.
In most cases, the diagnosis is made at the time of laparotomy when a gallstone is palpated at the
site of obstruction. Frequently, the stone is found in the terminal ileum.
The primary goals at laparotomy are correction of the obstruction and removal of the
offending stone. Since many of these patients are elderly and ill, cholecystectomy and takedown of the biliary enteric fistula may not be appropriate.
Enterolithotomy alone, without cholecystectomy, has an associated mortality rate of 5% in
contrast to the 15% mortality rate for patients who undergo both procedures at the same time.

53

GALLBLADDER AND BILIARY TRACT

gallstone ileus, showing air in the biliary tree


(arrows) and a gallstone (highlights) outside the
right upper quadrant. (S)

cholecystoduodenal fistula (arrow) with a large stone (S)


obstructing the duodenum.

54

GALLBLADDER AND BILIARY TRACT

Choledocolithiasis
Bile duct stones can be classified by :

Stone composition,
Location in the biliary tract,
Time relation to cholecystectomy, and
Source of stones.

The most clinically useful and relevant system of classification focuses on the source
of bile duct stones as either primary or secondary :
Primary common duct stones, which also may be :
Primary and
Referred to as recurrent, are calculi that form de novo outside the gallbladder in either
the intrahepatic or extrahepatic bile ducts.

Secondary, or retained stones, form in the gallbladder and pass into the
choledochus by the cystic duct or occasionally through a cholecystocholedochal
fistula.
The distinction between primary and secondary common duct stones has long been
thought to have great therapeutic implications.
Primary duct stones form as a result of biliary stasis and biliary infection;
therefore, removing the stone without correcting the underlying abnormality (a
biliary bypass or drainage procedure) may predispose to a high stone recurrence
rate for patients with primary common duct stones.
Secondary or retained stones can typically be removed without the need for a
biliary bypass or drainage procedure.
The widespread use of endoscopic sphincterotomy, many clinicians believe the issue
of stone type is no longer of paramount importance in therapeutic decision making,
since improved biliary drainage and stone removal can often be achieved without
laparotomy.
55

GALLBLADDER AND BILIARY TRACT

Incidence
The incidence of bile duct stones in patients undergoing cholecystectomy for
either acute or chronic cholecystitis is 8% to 15%. In addition, about 1% to 2% of
all patients who undergo cholecystectomy have stones left in the bile duct that
require further intervention.
Criteria for primary common duct stones include previous cholecystectomy; at
least a 2-year symptom-free period after cholecystectomy; the presence of soft,
easily crushable, light-brown stones or sludge; and no evidence of a long cystic
duct remnant or a biliary stricture resulting from prior surgery.
Using these criteria, recurrent or primary bile duct stones probably account for 4%
to 10% of all cases of choledocholithiasis.
Pathogenesis and Morphology of Common Bile Duct Stones
Primary bile duct stones
Primary bile duct stones are exclusively of the pigment variety. They are
classically described as earthy, soft, brown or yellowish tan, easily crushable,
noncholesterol in nature, and conforming to the shape of the duct.
Primary stones lack a crystalline nidus and typically are associated with a variable
amount of sludge or pasty concretions. In addition, the shape of primary common
duct stones often conforms to that of the distal common bile duct. Biliary stasis
has been implicated in the pathogenesis of primary common duct stones.
Ampullary stenosis and functional duct dilatation have been associated with an
increased risk of primary common duct stone formation. Manometric studies
indicate that aberrant patterns of sphincter of Oddi motility are present in patients
with common duct stones.
56

GALLBLADDER AND BILIARY TRACT

The presence of paravaterian diverticula of the duodenum has also been associated with an
increased risk of choledocholithiasis.
Infection There is an increased incidence of positive bile cultures in patients with primary
common duct stone disease.
Bacterial deconjugation of bilirubin by -glucuronidase with the formation of insoluble bilirubin
salts may play a critical role in primary common duct disease.
Bacterial microcolonies have been identified in the central matrix of common bile duct stones.
Bacterial isolates in patients with brown-pigment common duct stones include the aerobic gramnegative rods E coli and K pneumoniae as well as anaerobes, including bacteroides and
Clostridium sp. All these bacterial isolates possess -glucuronidase activity at physiologic pH.
Natural History
Primary Stones may be present for years in the bile duct without causing any problems and may
come to the attention of both patient and physician only when common duct obstruction occurs.
When obstruction is sudden and complete, the patient frequently experiences biliary colic,
bacteremia with chills, fever, leukocytosis, and the subsequent clinical development of jaundice.
Charcots triade:pain, fever, jaundince.
Although septic cholangitis may be the most dramatic manifestation of choledocholithiasis, a
more gradual, progressive obstruction may also occur, with minimal symptomatology.
When stones are in the bile duct but are not impacted, the symptom complex may be one of
pruritus, with or without jaundice, transient elevation of alkaline phosphatase, and episodic
abdominal or back discomfort. Small stones may enter the common bile duct from the
gallbladder and actually pass into the duodenum without producing symptoms. Stones less than
3 mm in diameter rarely have clinical manifestations unless they accumulate simultaneously in
the distal bile duct or become trapped in an abnormally narrowed bile duct or ampulla. As
previously stated, stones that exceed the diameter of the ampulla may remain for years, causing
minimal difficulty, or they may be associated with severe cholangitis. The uncertainties about
the history of common duct stones suggest that the documentation of choledocholithiasis is an
indication for stone removal. The best way to achieve this, however, is controversial.
57

GALLBLADDER AND BILIARY TRACT

Clinical Evaluation and Diagnosis


The critical factor in both the diagnostic evaluation and pathophysiology of common duct
stone disease is obstruction of the common bile duct.
Common bile duct(CBD) obstruction from stone disease is typically characterized by
incomplete obstruction, low and fluctuating levels of hyperbilirubinemia, and
fluctuating symptoms of pain and jaundice.
Pain is present in more than 90% of patients with primary common duct stone disease and is
frequently manifested by mid epigastric pain with radiation into the back. Charcot triad
(jaundice, pain, and fever) is present in less than 25% of patients with choledocholithiasis.
In the absence of significant obstruction (silent CBD litiasis), liver function tests may be
normal.
Laboratory evaluation provides important clinical information about the cause of jaundice
Serum alkaline phosphatase is the most sensitive indicator of ductal obstruction because
this enzyme is released from the biliary ductal epithelium. Levels rise rapidly in response
to duct obstruction.
Serum bilirubin (total) and especially the direct(conjugated) fraction assess the
obstructive aetiology of the jaundice.
Serum glutamic oxaloacetic transaminase(GOT) and serum glutamic pyruvic
transaminase(GPT) are released from injured hepatocytes, and although these levels
may be elevated in patients with cholangitis, they are relatively normal in uncomplicated
cases of choledocholithiasis.
While biochemical tests may provide evidence suggestive of extrahepatic biliary obstruction,
the definition of pathologic biliary anatomy is useful in developing a management strategy.
The first issue to resolve is whether there is intrahepatic or extrahepatic biliary dilatation or
both.
58

GALLBLADDER AND BILIARY TRACT

The first issue to resolve is whether there is intrahepatic or extrahepatic biliary dilatation or both.
For that we can use several imagery tests:
Ultrasonography has been shown to be a simple, safe, and accurate way to identify biliary
dilatation and stones and other pathological states.
CT scans provide comparable information and also may identify mass lesions, such as
tumors in the distal bile duct, periampullary region, or in the head of the pancreas.
Percutaneous transhepatic cholangiography(PTC).
Endoscopic retrograde cholangiopancreatography (ERCP). ERCP offers certain
advantages over percutaneous transhepatic cholangiography. ERCP provides visualization
of the ampulla and periampullary region and allows for therapeutic intervention if
sphincterotomy is indicated and feasible.
MRI is the best because is non invasive, whithout complications.

ERCP demonstrating multiple stones in


distal common bile duct. Complete duct
clearance was ultimately achieved in two
sittings after endoscopic sphincterotomy.

59

GALLBLADDER AND BILIARY TRACT

Clinical Syndromes
Management of Common Bile Duct Stones Found During Cholecystectomy
About 7% of patients who undergo elective cholecystectomy are found to have unsuspected
common duct stones as documented by intraoperative cholangiography

Intraoperative cholangiogram performed


during OC demonstrating multiple, small,
nonobstructing distal stones.

60

GALLBLADDER AND BILIARY TRACT

Management of Common Bile Duct Stones Found During Cholecystectomy (suite)


Complete stone removal is the goal for all common duct stones identified during
The first step is the successful exploration of the common bile duct by peroperative
cholangiography
Choledochotomy and stones extraction with forceps, irrigation, or baskets, or biliary balloons.
Choledochoscopy is a useful adjunct and improves the success rate of common bile duct
exploration. In addition to visualizing stones, the choledochoscope aids in their removal under direct
vision with the use of endoscopic grasping forceps.
Common bile duct stones found unexpectedly during a laparoscopic procedure present the surgeon
with a different set of choices from that for stones found during an open procedure where one would
invariably proceed to common duct exploration.
Although converting to an open procedure for the purposes of common duct exploration is
acceptable and should be considered based on the surgeons experience and expertise,
many surgeons may opt to complete the removal of the gallbladder and then proceed with
postoperative ERCP, sphincterotomy, and stone removal.
Secondary (Retained) Common Bile Duct Stones
Most large series suggest that retained calculi occur in about 1% to 5% of all patients who
undergo elective or emergency cholecystectomy.
Until recently, the only way of treating these patients was with reoperation and exploration of the
common bile duct by choledocholithotomy.
In addition to surgery, other modalities are now available for treating patients with retained common
duct stones, and their selection is generally based on the presence or absence of a T-tube.
61

GALLBLADDER AND BILIARY TRACT


Secondary (Retained) Common Bile Duct Stones (suite)

Radiologic extraction (Burhenne technique) has become widely accepted for treating
patients with retained stones who have a T-tube in place. This technique requires the
presence of a mature T-tube tract. Six to 8 weeks after operation, the T-tube is
removed and a Dormia basket catheter is passed down the matured T-tube tract.
This basket is manipulated under fluoroscopic guidance, and multiple stones can be
removed. Using this technique success rates are ranging from 80% to 97%.

Illustration of Burhenne technique with placement of


basket down matured tract and stone extraction.

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GALLBLADDER AND BILIARY TRACT

Secondary (Retained) Common Bile Duct Stones (suite)


biliary lithotripsy has been evaluated in a multicenter trial involving 56 patients with bile duct stones.
Stone fragmentation was successfully performed in 91% of patients, and clearance occurred in 79%.
A number of chemical solvents have been applied topically to dissolve bile duct stones. MTBE has
been used successfully in the contact dissolution of gallbladder stones. To date, monooctanoic acid
is the only agent that has been used with any success to dissolve cholesterol common duct stones.
When there is no T-tube in place the procedure of choice is endoscopic sphincterotomy

A. T-tube cholangiogram
demonstrating retained
gallstone in distal common
bile duct (white arrow).

B. ERCP demonstrating multiple


stones in distal common bile duct.
Complete duct clearance was
achieved after endoscopic
sphincterotomy.

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GALLBLADDER AND BILIARY TRACT

Secondary (Retained) Common Bile Duct Stones (suite)


If, however, patients have multiple stones or subsequently develop evidence of retained
common bile duct stones after initial reexploration and require another reoperation, a biliary
drainage procedure is advised.
Primary (Recurrent) Common Bile Duct Stones
Experience has demonstrated the efficacy of ERCP with endoscopic sphincterotomy for
treating patients with primary common bile duct stones.
Success of this procedure depends on the size of the stones, the number of stones
involved, the degree of stenosis or narrowing of the distal bile duct, and the expertise of the
endoscopist.
Optimal treatment of patients with primary common bile duct stones should achieve two
goalsremoval of stones and prevention of recurrences. Many of these patients have
multiple stones in both the choledochus and intrahepatic ducts, and complete removal may
not be feasible. Furthermore, it may be difficult to prevent stone recurrence. Therefore, the
goal should be to select and perform a procedure that facilitates passage of any residual or
recurrent stones into the small bowel and thereby reduces the likelihood of cholangitis,
jaundice, or pancreatitis.
The procedure selected should be simple and safe with minimal morbidity and mortality but
should effectively minimize the need for a second operation or endoscopic procedure.
The presence of primary common duct stones has been considered by most authors to be
an absolute indication for formal drainage of the biliary tree with either
choledochoduodenostomy, choledochojejunostomy, or transduodenal sphincteroplasty.
The introduction of endoscopic techniques has added a new dimension to an already
existing dilemma. The central question is no longer whether patients with primary common
duct stones require a drainage procedure at the time of laparotomy, but rather whether
they need an operation at all.
When surgery is indicated for patients with primary common duct stones, the surgeon has
three optionstransduodenal sphincteroplasty, side-to-side choledochoduodenostomy, or
Roux-en-Y choledochojejunostomy.

64

GALLBLADDER AND BILIARY TRACT

A. The initial incision


is in the ampulla at
11 oclock.

B. sphincteroplasty

A.

B.
choledochoduodenostomy.
65

GALLBLADDER AND BILIARY TRACT - BILIARY STRICTURES AND SCLEROSING


CHOLANGITIS

Biliary strictures and sclerosing cholangitis

Benign strictures of the biliary tree are one of the most difficult challenges that a surgeon faces.
Although numerous technologic developments have facilitated diagnosis and management, bile duct
strictures remain a significant clinical problem.

If unrecognized or managed improperly, life-threatening complications, such as biliary cirrhosis,


portal hypertension, and cholangitis, can develop.
Benign bile duct strictures can have numerous causes:
Postoperative Strictures

Injury at primary biliary operations


Most biliary strictures occur after primary

Laparoscopic cholecystectomy
operations on the gallbladder or biliary tree.

Open cholecystectomy
With the introduction of laparoscopic

Common bile duct exploration


cholecystectomy, bile duct injuries and
associated strictures have been seen with

Injury at other operative procedures


an increased frequency. Operative injury to

Gastrectomy
the bile ducts can also occur during

Hepatic resection
nonbiliary operations on the gallbladder or

Portacaval shunt
biliary tree or as a result of external

Stricture of a biliaryenteric anastomosis


penetrating or blunt abdominal trauma.

Blunt or penetrating trauma

66

GALLBLADDER AND BILIARY TRACT - BILIARY STRICTURES AND SCLEROSING


CHOLANGITIS

Strictures Due to Inflammatory Conditions

Chronic pancreatitis
Cholelithiasis and choledocholithiasis
Primary sclerosing cholangitis
Stenosis of the sphincter of Oddi
Duodenal ulcer
Crohns disease
Viral infections
Toxic drugs

Inflammatory conditions and fibrosis due to


chronic pancreatitis, gallstones within the
gallbladder or the bile duct, stenosis of the
sphincter of Oddi, or biliary tract infections can
also cause benign bile duct strictures. Finally,
primary sclerosing cholangitis, a rare disease of
unknown cause, can result in multiple strictures
of the intrahepatic and extrahepatic bile ducts.

Pathogenesis
Over 80% of strictures occur after injury to the bile ducts during cholecystectomy.
The incidence of bile duct injury during laparoscopic cholecystectomy is clearly higher.
A number of factors are associated with bile duct injury during either open or laparoscopic
cholecystectomy, including:
acute or chronic inflammation,
inadequate exposure,
patient obesity, and
failure to identify structures before clamping, ligating, or dividing them.

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GALLBLADDER AND BILIARY TRACT - BILIARY STRICTURES AND


SCLEROSING CHOLANGITIS

Pathogenesis(suite)
More specific causes of bile duct injury also exist:
Bleeding from the cystic or hepatic arteries
The generous application of Liga clips at either open or laparoscopic cholecystectomy to hilar
areas not well visualized
Failure to recognize congenital anatomic anomalies of the bile ducts,
Technical factors are associated with laparoscopic cholecystectomy that can also increase
the risk of bile duct injury when compared with the open procedure.
End-viewing laparoscope, which alters the surgeons perspective of the operative field.
Excessive cephalad retraction of the gallbladder fundus can cause the cystic duct and common
bile duct to become aligned in the same plane.
The role of intraoperative cholangiography in preventing bile duct injury during laparoscopic
cholecystectomy is controversial.
the experience of the surgeon in performing laparoscopic cholecystectomy can be correlated with
the risk of bile duct injury.

The importance of ischemia of the bile duct in the formation of postoperative strictures has been
emphasized.
Unnecessary dissection around the bile duct during cholecystectomy or bile duct anastomosis can
divide or injure the major arteries of the bile duct
the intense connective tissue response with fibrosis and scarring that can occur after bile duct
injury.
After cholecystectomy and common bile duct exploration, the two most common operations
associated with bile duct injury are gastrectomy and hepatic resection.
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GALLBLADDER AND BILIARY TRACT - BILIARY STRICTURES AND


SCLEROSING CHOLANGITIS

Pathogenesis(suite)
In addition to iatrogenic bile duct injury occurring during cholecystectomy or other operations, bile
duct strictures can also occur at biliary anastomoses.

Numerous surgical clips can


be seen in the area of the
stricture.

Classic laparoscopic bile duct injury.


right lobe segmental bile duct
entering the cystic duct

69

GALLBLADDER AND BILIARY TRACT - BILIARY STRICTURES AND


SCLEROSING CHOLANGITIS

Pathogenesis(suite)
Unfortunately, the recurrence of bile duct strictures after an initial attempt at repair is not uncommon
and can also account for a number of anastomotic strictures.
Finally, long-term follow-up of a bile duct anastomosis is important because strictures can develop
years after the original anastomosis.
Clinical presentation
Most patients with benign postoperative bile duct strictures present early after their initial operation.
After open cholecystectomy, only about
10% of postoperative strictures are actually suspected within the first week,
70% are diagnosed within the first 6 months,
20% are diagnosed within 1 year after surgery.
Patients suspected of having a postoperative bile duct stricture within days to weeks of initial
operation usually present in one of two ways:
One presentation is the progressive elevation of liver function tests, particularly total bilirubin
and alkaline phosphatase levels. These changes can often be seen as early as the second or
third postoperative day.
The second mode of early presentation is with leakage of bile from the injured bile duct. This
presentation appears to occur most often in patients presenting with bile duct injuries after
laparoscopic cholecystectomy. Bilious drainage from operatively placed drains or through the
wound after cholecystectomy is abnormal and represents some form of biliary injury.

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GALLBLADDER AND BILIARY TRACT - BILIARY STRICTURES AND


SCLEROSING CHOLANGITIS

In patients without drains (including patients in whom the drains have been removed), the
bile can leak freely into the peritoneal cavity, or it can loculate as a collection. Free
accumulation of bile into the peritoneal cavity results in either biliary ascites or bile peritonitis.
Similarly, a loculated bile collection can result in sterile biloma (Fig. 43-6) or in an infected
subhepatic or subdiaphragmatic abscess.

Patients with postoperative bile duct strictures who present months to years after the
initial operation frequently have evidence of cholangitis. The episodes of cholangitis
are often mild and respond to antibiotic therapy. Repetitive episodes usually occur
before the definitive diagnosis. Less commonly, patients may present with painless
jaundice and no evidence of sepsis. Finally, patients with markedly delayed
diagnoses may present with advanced biliary cirrhosis and its complications.

The cumulative percentage of


patients developing symptoms is
shown with respect to the time
interval from the procedure during
which the injury occurred until the
presentation of the symptoms.

71

GALLBLADDER AND BILIARY TRACT - BILIARY STRICTURES AND SCLEROSING


CHOLANGITIS

Laboratory investigations
Liver function tests usually show evidence of cholestasis :
The serum bilirubin can fluctuate; occasionally, it is normal. In patients with bile leakage, the
bilirubin can be normal or minimally elevated owing to absorption from the peritoneal cavity.
When elevated, serum bilirubin usually ranges from 2 to 6 mg/dL unless secondary biliary
cirrhosis has developed.
Serum alkaline phosphatase is usually elevated.
Serum transaminase levels can be normal or minimally elevated except during episodes of
cholangitis. If advanced liver disease exists,
hepatic synthetic function can be impaired, with
lowered serum albumin and a
prolongation of prothrombin time.
Serum electrolytes and
complete blood count are typically normal unless there is associated biliary sepsis.
Radiologic Examinations
The imaging techniques of abdominal ultrasound and computed tomography (CT) play an
important initial role in the evaluation of patients with benign postoperative biliary strictures.
In patients who present in the early postoperative period with evidence of a bile leak or biliary
sepsis, these studies are useful to rule out the presence of intraabdominal collections that might
require drainage

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GALLBLADDER AND BILIARY TRACT- BILIARY STRICTURES AND SCLEROSING


CHOLANGITIS

Large bile duct collection (biloma;


arrow) occurring after bile duct injury.

CT and ultrasound are also important in the


initial evaluation of the patient presenting
with a bile duct stricture months to years
after initial operation.
Both studies can confirm biliary obstruction
by demonstrating a dilated biliary tree. CT
is especially useful in identifying the level of
obstruction of the extrahepatic bile duct.

Percutaneous
transhepatic
cholangiogram
demonstrating bile
duct stricture (arrow)
at hepatic duct
bifurcation with
proximal duct
dilation.

ERCP: The common bile


duct (CBD), however, does
not fill beyond the large clip
that appears to be placed
across the duct.

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GALLBLADDER AND BILIARY TRACT- BILIARY STRICTURES AND SCLEROSING


CHOLANGITIS

In patients suspected of having early postoperative bile duct injury, a radionucleotide biliary scan can
confirm bile leakage.
In patients with postoperative external bile fistula, a sinography (injection of water-soluble contrast
media through the drainage tract) can often define the site of leakage and the anatomy of the biliary
tree. Sinography can also identify intraabdominal collections and facilitate nonoperative drainage.
The gold standard for evaluation of patients with bile duct strictures is cholangiography.
Percutaneous transhepatic cholangiography (PTC)
more valuable than endoscopic retrograde cholangiography (ERC)
it defines the anatomy of the proximal biliary tree that is to be used in the surgical reconstruction
PTC can be followed by placement of percutaneous transhepatic catheters, which can be useful in
decompressing the biliary system to either treat or prevent cholangitis.
Endoscopic retrograde cholangiography (ERC).
Preoperative Management
The preoperative management of a patient with a postoperative bile duct stricture depends primarily on
the timing of the presentation.
Patients presenting in the early postoperative period can be septic with either cholangitis or
intraabdominal bile collections.
Once sepsis is controlled, there is no hurry in proceeding with surgical reconstruction of the bile duct
stricture.
The combination of proximal biliary decompression and external drainage allows most biliary fistulas to
be controlled or even to close.
In patients who present with a biliary stricture remote from the initial operation, symptoms of cholangitis
can necessitate urgent cholangiography and biliary decompression. Biliary drainage is best
accomplished by the transhepatic method, although successful endoscopic stent placement can also
be accomplished.

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GALLBLADDER AND BILIARY TRACT- BILIARY STRICTURES AND


SCLEROSING CHOLANGITIS

Surgical Management
The goal of operative management of bile duct stricture is:
the establishment of bile flow into the proximal gastrointestinal tract in a manner that prevents :
cholangitis,
sludge or
stone formation,
restricture, and
biliary cirrhosis.
This goal is best accomplished with a number of surgical alternatives for primary repair of bile duct
strictures, including:
end-to-end repair,
Roux-en-Y
hepaticojejunostomy or
choledochojejunostomy,
choledochoduodenostomy.
The choice of repair depends on a number of factors, including the extent and location of the
strictures, the experience of the surgeon, and the timing of the repair.

75

GALLBLADDER AND BILIARY TRACT- BILIARY STRICTURES AND


SCLEROSING CHOLANGITIS

Nonoperative Management
Operative management of bile duct strictures is technically difficult and continues to be associated
with significant postoperative morbidity and mortality.
Recurrent strictures develop in a proportion of patients.
Technical advances in the fields of therapeutic radiology and endoscopy, have led to the development
of nonoperative techniques for management of bile duct strictures:
Percutaneous Balloon Dilation
Endoscopic Balloon Dilation

Primary Sclerosing Colangitis


Primary sclerosing cholangitis is an idiopathic disease characterized by intrahepatic and
extrahepatic inflammatory strictures of the bile ducts that cannot be attributed to other
specific causes.
The cause of primary sclerosing cholangitis is unknown. Many experts consider primary
sclerosing cholangitis to be an autoimmune reaction
It is likely that a number of causes, including viral or bacterial infections, toxic drug
reactions, and congenital anomalies, can all result in the same end-stage injury that is
recognized as primary sclerosing cholangitis.

76

GALLBLADDER AND BILIARY TRACT- BILIARY STRICTURES AND


SCLEROSING CHOLANGITIS
DISEASES ASSOCIATED WITH PRIMARY SCLEROSING CHOLANGITIS
Disease
Ulcerative colitis
Pancreatitis
Diabetes mellitus
Retroperitoneal fibrosis
Riedel thyroiditis
Crohns disease
Histiocytosis X
Sicca complex
Rheumatoid arthritis
Hypertrophic osteoarthropathy
Sarcoidosis
Angioimmunoblastic lymphadenopaty
Acquired immunodeficiency syndrome

Frequency (%)
40-60
12-25
5-10
Rare
Rare
Rare
Rare
Rare
Rare
Rare
Rare
Rare
Rare

clinical presentation

intermittent jaundice, which begins


insidiously in the fourth or fifth decade
of life.

Right upper quadrant pain,

pruritus,

fever,

weight loss, and

fatigue can also occur.

cyclic remissions and exacerbations.

Cholangiogram of a patient with primary sclerosing


cholangitis. Multiple irregular strictures and dilation
(beading) of intrahepatic bile ducts can be seen.

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GALLBLADDER AND BILIARY TRACT- BILIARY STRICTURES AND


SCLEROSING CHOLANGITIS

Diagnosis
The diagnosis is suggested by:
Clinical presentation associated with
Cholestatic liver function test abnormalities:
The levels of bilirubin often fluctuate with respect to the remissions and exacerbations
of the disease and the extent of hepatic injury.
Alkaline phosphatase is usually elevated out of proportion to the serum bilirubin and is a
more persistent finding.
The diagnosis, however, usually is confirmed by cholangiography, which reveals multiple dilations
and strictures (beading) of the intrahepatic and extrahepatic bile ducts (Fig. 43-14).
ERC is the preferred procedure because of difficulties in cannulation of the intrahepatic ducts by
the percutaneous transhepatic route because the ducts are usually nondilated and fibrotic.
The disease should be followed closely by cholangiography and liver biopsy to provide
appropriate management before the development of biliary cirrhosis.
Treatment
No known specific medical therapy is effective for primary sclerosing cholangitis.
The most encouraging results, are with ursodeoxycholic acid which significantly improves serum
liver function tests and liver histologic appearance.
Nonoperative dilation therapy (discussed earlier), by either the transhepatic or endoscopic route.
The results of endoscopic dilation and stenting may be more favorable.
Because of the lack of effective medical therapy, an aggressive surgical approach is advocated
for most symptomatic patients with primary sclerosing cholangitis.
In patients with biliary cirrhosis, hepatic transplantation is recommended.
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GALLBLADDER AND BILIARY TRACT- BILIARY STRICTURES AND


SCLEROSING CHOLANGITIS
Bile Duct Strictures Secondary to Chronic Pancreatitis
Chronic pancreatitis is a cause of benign bile duct strictures, resulting in less than 10% of cases.
In chronic pancreatitis, the clinical problem is distal bile duct obstruction due to inflammation and
parenchymal fibrosis of the gland and are associated with dilation of the entire proximal biliary
tree.
In most cases, the cause of the chronic pancreatitis is alcoholism.
clinical presentation = variable

no symptoms, with the diagnosis of bile duct strictures


suggested only by abnormal liver function tests:

The serum alkaline phosphatase appears to be the most sensitive


laboratory finding and is elevated in over 80% of patients.

Abdominal pain with or without jaundice is another common


presentation.
pancreatic calcification, diabetes, and malabsorption with jaundice
Finally, the development of jaundice in patients with chronic
pancreatitis must be differentiated from periampullary malignancy.
The definitive evaluation of patients with a bile duct stricture due to
chronic pancreatitis is cholangiography. Either endoscopic
retrograde cholangiopancreatography (ERCP) or PTC can be
useful.

Cholangiogram of a patient with a long


distal common bile duct stricture
(arrow) due to chronic pancreatitis.

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GALLBLADDER AND BILIARY TRACT- BILIARY STRICTURES AND


SCLEROSING CHOLANGITIS

Treatment
The indications for surgical management of common bile duct strictures due to chronic pancreatitis
are clear in patients with significant pain, jaundice, or cholangitis.
In general, biliary bypass is indicated :
Choledochoduodenostomy and
Roux-en-Y choledochojejunostomy are acceptable methods of biliary bypass.
The results of surgical management of distal bile duct structures due to chronic pancreatitis are
usually excellent, with a low rate of perioperative complications and excellent long-term results.

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GALLBLADDER AND BILIARY TRACT- BILIARY NEOPLASMS

Benign Tumors Of Gallbladder And Bile Ducts

Benign gallbladder and bile duct tumors are extremely rare.


gallbladder tumors and pseudotumors occur more frequently than benign tumors of the bile ducts.
BENIGN TUMORS OF THE GALLBLADDER
polyps or polyploid lesions
pseudotumors or hyperplastic conditions
adenomas, which are most likely premalignant lesions
Other benign tumors, such as
adenomyosis,
heterotopia, or
tumors of the supporting tissues of the gallbladder, are rarely seen.
Pseudotumors
Cholesterolosis, or strawberry gallbladder, is manifested by yellow spots visible on the surface of
the mucosa. This proliferation of foamy macrophages filled with cholesterol in the lamina propria
can also result in the formation of polyps, called cholesterol polyps. These polyps are thought to
result from a disturbance in cholesterol metabolism.
Inflammatory polyps, which are composed of a vascular connective tissue stalk with a single layer
of columnar epithelial cells and have a chronic inflammatory cell infiltrate. These lesions are not
considered to be premalignant lesions and are thought to result from chronic inflammation.

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GALLBLADDER AND BILIARY TRACT- BILIARY NEOPLASMS

Adenomas
Adenomas with hyperplasia of the epithelial layer of the gallbladder, can be sessile or papillary.
Carcinoma in situ has been reported in these lesions, and they are thought to be premalignant
lesions.
The cause of adenomas of the gallbladder is unknown. The role of gallstones in the formation of
adenomas is also unknown; most are not associated with the presence of gallstones.
Adenomyosis
An adenomyoma of the gallbladder is a rare intramural mass or nodule. This lesion is characterized
by proliferation of the mucosal epithelium and hypertrophy of the muscular layers of the gallbladder.
Because most of these rare tumors have been reported to occur in the fundus, it has been
postulated that a functional cystic duct obstruction or biliary dyskinesia is responsible for the
muscular hypertrophy and the development of adenomyosis of the gallbladder.
The cause of this condition is unknown.
Other Benign Gallbladder Tumors
Heterotopic lesions Heterotopia consists of nodules of ectopic tissue not normally seen in the
gallbladder, such as intestinal, pancreatic, or gastric epithelium.
Tumors of the supporting tissues of the gallbladder, have been reported and are extremely rare.
Tumors of the supporting tissues, such as hemangiomas, lipomas, leiomyomas, or granular cell
tumors, can also occur in the gallbladder.

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GALLBLADDER AND BILIARY TRACT- BILIARY NEOPLASMS

BENIGN BILE DUCT TUMORS


Benign tumors of the extrahepatic bile ducts are extremely rare. Only 2 cases in 5200 biliary tract
surgeries were reported.
Papillomas can occur in the extrahepatic bile ducts, as can multiple polyps or papillomatosis of the
bile ducts.
Adenomatous lesions (Isolated reports) in association with adenocarcinoma suggest these may
be premalignant lesions.
Tumors of the supporting tissues, such as fibromas, leiomyomas, angioleiomyomas, or carcinoids,
are rarely found in the bile ducts.
Clinical Findings
Benign gallbladder tumors cause symptoms similar to cholelithiasis: right upper quadrant pain and
discomfort,
fatty food intolerance,
nausea, vomiting,
increase in flatulence, are common complaints
Often, it is difficult to separate symptoms caused by these tumors from those caused by
concomitant gallstones because many of these benign tumors are diagnosed as incidental
findings at the time of cholecystectomy.
Benign tumors of the bile ducts present with symptoms relating to bile duct obstruction. Most
often, these tumors are diagnosed during evaluation of jaundice or after treatment for biliary
infection. The jaundice is often intermittent. Other patients have nonspecific symptoms, such as
dyspepsia or elevated serum alkaline phosphatase levels.
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GALLBLADDER AND BILIARY TRACT- BILIARY NEOPLASMS


Diagnosis and Treatment

Gallbladder tumors, when diagnosed preoperatively, by ultrasound must be operated cholecystectomy. Because ultrasound can not distinguish benign from malignant lesions, all
gallbladders that contain polypoid lesions should be removed.

Benign tumor of the bile duct Ultrasound can also be used for initial evaluation of jaundice in a
patient with a benign tumor of the bile duct, but unequivocal demonstration of these tumors requires
either PTC or ERCP.

Whenever tumors in the bile ducts are demonstrated, surgical excision is indicated to relieve
intermittent jaundice and cholangitis.

Excision of a benign tumor with reanastomosis of the bile duct is often possible.

If so much duct is removed that a tension-free anastomosis cannot be done, reconstruction of the
biliary tree with a biliaryenteric anastomosis is preferred, usually by choledochojejunostomy.

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GALLBLADDER AND BILIARY TRACT- BILIARY NEOPLASMS

Gallbladder Cancer

Incidence
Gallbladder cancer is a rare disease which accounts for 3% to 4% of all gastrointestinal tract tumors,
and about 2% of all biliary tract procedures are done for gallbladder cancers.
Gallbladder cancer is much more frequent in women, with a female/male ratio of 3:1. The disease is
most commonly seen in elderly women, with the mean age of 65 years at diagnosis .
The association of gallstones with gallbladder cancer is well known. Seventy to 90% of all patients with
gallbladder cancer have gallstones, and about 0.4% of all patients with gallstones have gallbladder
cancer. The association of gallstones with cancer can be related to gallstone size; larger stones have a
greater cancer risk.
Calcification of the wall of the gallbladder, the so-called porcelain gallbladder, is associated with a 25%
to 60% incidence of gallbladder cancer. The presence of a porcelain gallbladder, should alert the
physician to the high probability of a malignancy.
Pathology
Classification
Well-differentiated adenocarcinomas. 80 to 90% of gallbladder cancers are Adenocarcinomas which
can be subdivided into:
papillary,
serous,
colloid, or
glandular carcinomas.
Squamous cell epiteliomas A small percentage of gallbladder cancers are squamous cell cancers, but
this type accounts for only about 5% of all gallbladder cancers.
Anaplastic neoplasms. The remainder of gallbladder cancers, about 10%, are anaplastic neoplasms.
85

GALLBLADDER AND BILIARY TRACT- BILIARY NEOPLASMS

The mode of spread can be predicted by the lymphatic and venous drainage of the gallbladder.
Direct extension into the liver, particularly, liver segments IV and V.
The lymphatic drainage of the gallbladder is to the cystic duct lymph node, to periportal lymph
nodes, and then to celiac and superior mesenteric lymph nodes.
These tumors also can spread into and around the cystic duct and can extend into the common
bile duct, causing biliary obstruction. Thus, the first clinical symptom encountered is often jaundice
distant metastasis is possible but is less commonly seen.

Tumor spread in gallbladder cancer. Gallbladder cancer


commonly spreads by direct extension into surrounding tissues.
86

GALLBLADDER AND BILIARY TRACT- BILIARY NEOPLASMS

A staging system has been developed that takes into consideration the lymphatic and venous
drainage of the gallbladder. This system is used to describe the extent of gallbladder carcinoma and
has been shown to be of prognostic value. Unfortunately, most patients with gallbladder carcinoma
present with stage V disease.
Stage

Extent of Tumor

Mucosa only

II

Muscularis and mucosa

III

Subserosa, muscularis, and


mucosa

IV

Cystic lymph node


involvement and all layers
of the gallbladder wall

Distant spread

STAGING SYSTEM FOR


GALLBLADDER CANCER

As outlined by the American Joint Committee on Cancer, a TNM classification is also being used to
describe the extent of disease with gallbladder cancer.
The primary tumor (T) is designated as:

T1 when it is confined to the mucosa (T1a) or to the muscle layer of the gallbladder (T1b).
T2 tumors invade the perimuscular connective tissue
T3 tumors perforate the serosa or invade into one adjacent organ (2-cm extension into the liver or less).
T4 tumors have local extension into several adjacent organs, or they extend into the liver for more than 2 cm.

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GALLBLADDER AND BILIARY TRACT- BILIARY NEOPLASMS


The regional lymph node metastases are:

(N1) to cystic duct, pericholedochal, or hilar lymph nodes or to


(N2). peripancreatic, periduodenal, periportal, celiac, or superior mesenteric lymph nodes

Staging depends on the primary tumor, the regional lymph nodes, and metastatic disease
Distant metastasis

(M0) No distant metastasis


M(1) With distant metastasis

TNM CLASSIFICATION FOR STAGING OF CANCER


OF THE GALLBLADDER
Stage
I
II
III
IVA
IVB

Stage Grouping
T1, N0, M0
T2, N0, M0
T1, T2 or T3, N0 or N1, M0
T4, N0 or N1, M0
Any T, N2, M0 or any T, any N, M1

Diagnosis
The signs and symptoms of gallbladder cancer are similar to those of gallstones. For smaller
tumors, it may be difficult to distinguish the symptoms of concomitant gallstones from those of
gallbladder carcinoma.

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GALLBLADDER AND BILIARY TRACT- BILIARY NEOPLASMS

Right upper quadrant pain,


discomfort, and dyspepsia.
nonspecific signs of malaise,
weight loss and anorexia, or
obstructive jaundice Jaundice occurs when the tumor extends into the common bile duct.
a mass in the right upper quadrant.
Tumor invasion of the cystic duct causing cystic duct obstruction can result in the development of acute
cholecystitis.

The diagnosis often is not made preoperatively but is made at the time of laparotomy for jaundice or
acute cholecystitis.
Tumors with the best prognosis are those found incidentally at the time of cholecystectomy for
symptomatic gallstone disease.
This emphasizes the importance of opening all gallbladders at the time of cholecystectomy so that
any suspicious lesions can immediately be examined histologically.
Treatment
When gallbladder cancer is limited to the mucosa, cholecystectomy is adequate treatment and has a
good prognosis, with up to 100% 5-year survival rate.
When the cancer involves the mucosa and submucosa 5-year survival rate was 64% whereas
cancer involving all layers of the gallbladder wall none of the patients survived longer than 2.5 years.
Even though these tumors were relatively localized at the time of cholecystectomy, cholecystectomy
alone was not adequate therapy for long-term survival.
Considering the lymphatic and venous drainage of the gallbladder, it has been recommended that
gallbladder cancer to be treated by cholecystectomy with a wide resection of the liver around the
gallbladder bed (liver segments IV and V) and regional lymphadenectomy. This procedure has been
termed radical cholecystectomy or extended cholecystectomy and at times can also involve
resection of the adjacent bile duct.
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For stage V disease, the goal of treatment is palliation. Because these patients
frequently present with obstructive jaundice, a major goal of treatment is relief of
jaundice and its attendant symptoms, such as pruritus and cholangitis.
Percutaneous, endoscopic, or operative drainage of the biliary tree can be performed.
When both the diagnosis and unresectability of the tumor are determined before
operation, drainage of the biliary tree for palliation can be performed by stent
placement, either endoscopically or by the transhepatic route.
Although radiation and chemotherapeutic regimens have been tried, none has been associated with
a good response.
Laparoscopic removal of a gallbladder cancer is not recommended.
If gallbladder cancer is suspected, an open cholecystectomy and exploration is warranted.
Prognosis
The prognosis of gallbladder cancer remains poor, with an average survival in the range of 6 months.
Less than 5% of patients survive 5 years, because 90% of gallbladder cancer patients present
with stage V disease.

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Treatment for invasive gallbladder


cancer is cholecystectomy and a
wedge resection of the liver along
with a regional lymphadenectomy.
The lymph node regions that drain
the gallbladder and that should be
removed during operation for
gallbladder cancer.

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Carcinoma Of The Bile Ducts

Incidence
Cancer of the bile ducts is even less common than gallbladder carcinoma and is seen in 0.01% to
0.46% of all autopsies.
males have a higher incidence of bile duct cancer.
The average age range of diagnosis is between 50 and 70 years.
Pathogeny
There is an association between bile duct cancer and gallstones, only 25% to 57% of patients with
bile duct cancer have gallstones.
Biliary tract infection is associated with these tumors; patients with Clonorchis sinensis infection and
chronic typhoid carriers have a higher incidence of bile duct cancer
Congenital hepatic fibrosis and choledochal cysts are also associated with bile duct cancer.
Patients with ulcerative colitis have a markedly increased incidence.
This predisposition is independent of whether the patient has had adequate treatment, either medical
or surgical, of their colonic disease. In addition, bile duct tumors in colitis patients tend to follow a
more aggressive course.
Staging
Bile duct cancer is classified according to its location within the ductal system. The tumors are
generally divided into three major locations:

upper third,
middle third, and
lower third.

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The most common location is the upper third, where the confluence of the hepatic ducts is involved.
Tumors in the upper third have been called Klatzkin tumors, after Gerald Klatzkin, who reported on
13 such patients with tumors at the bifurcation of the hepatic ducts.
Middle-third tumors are located between the cystic duct and the upper border of the duodenum.
Lower-third lesions are located between the upper border of the duodenum and up to but not
including the Vater ampulla.

Distribution of bile duct cancers

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Staging for bile duct cancer with the TNM classification


T refers to the primary tumor, with

Tis as carcinoma in situ, and with


T1 denoting tumor invasion into the mucosa (T1a) or into the muscle layer of the bile duct (T1b).
T2 is used to designate tumors invading the perimuscular connective tissue.
T3 lesion when the tumor invades adjacent structures, such as the liver, pancreas, or duodenum.

N,refers to the limph nodes involvment lymph node metastases can be either

N1, with metastasis in the cystic duct, pericholedochal, or hilar lymph nodes, or
N2, with metastases in the peripancreatic, periduodenal, celiac, or mesenteric lymph nodes.

M Distant metastasis
(M0) No distant metastasis
M(1) With distant metastasis

Stage I denotes T1 tumors, without lymph node or metastatic disease.


Stage II is for T2 tumors without metastases.
Stage III includes lymph node metastases with T1 or T2 primary tumors.
Stage IV is for locally invasive disease, T3 tumors but no distant metastasis, and
Stage V indicates distant metastatic disease. The use of this classification in addition to sitespecific information is recommended to promote more uniform description of extent of disease for
these rare tumors.

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Clinical Findings
Similar to gallbladder cancer, bile duct cancers spread by direct extension.
With the close proximity of the bile ducts to the branches of the portal veins and hepatic
arteries, these tumors are often unresectable because of vascular invasion,.
Jaundice is the most frequent presenting symptom, occurring in about 90% of patients.
Abdominal pain (30% to 50%) and
Cholangitis (10% to 30%) are other common initial findings.
Weight loss, anorexia,
pruritus, or
anemia. Patients uniformly have elevated alkaline phosphatase levels, which may be the
only clinical finding.
Diagnosis
Diagnosis is most often made during evaluation of jaundice.
ultrasound scan to detect ductal dilation. Ultrasound examination demonstrates
intrahepatic ductal dilation and, depending on the site of the tumor, variable degrees of
common bile duct dilation. Ultrasound or CT demonstrates intrahepatic biliary obstruction
but rarely the tumor itself.
The visualization of the biliary tree, either through PTC or ERCP.
Percutaneous transhepatic cholangiography is preferred for more proximal lesions because
ERCP can fail to visualize the proximal portion of the biliary tree adequately. For lower bile
duct lesions, ERCP may be the preferred route of cholangiography.
It has the advantages of providing opportunity to obtain brushings for cytologic diagnosis
and having a lessened chance for bile leak because a liver puncture is avoided.
Selective celiac angiography helps to determine whether there is involvement of major
adjacent vascular structures, such as the portal veins, to aid in determination of surgical
resectability.
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Surgical Therapy
Middle- and Lower-Third Bile Duct Tumors
For lesions of the middle and lower thirds of the bile duct, resection of the bile duct tumor
with reanastomosis is the procedure of choice when possible. For small middle-third bile duct
carcinomas, resection with reanastomosis of the common bile duct may be possible, but for
larger lesions, reconstruction with a biliaryenteric anastomosis, usually a
choledochojejunostomy (anastomosis of the common bile duct to the jejunum) is required.
For lower-third lesions, the Whipple procedure (pancreaticoduodenectomy) is necessary.
Overall, both middle and lower-third lesions have a better prognosis than tumors in the hilum.
Hilar Tumors
The prognosis for patients with hilar bile duct cancer is extremely poor, with mortality rates of
80% to 90% at 5 years.
Poor survival reflects the fact that most of these tumors are unresectable at the time of
diagnosis.
Determination of Resectability
Hilar bile duct tumors are considered unresectable under the following conditions:
There is metastatic disease, growth into surrounding structures, or peritoneal metastasis.
There is extensive vascular invasion, that is, tumor invading the main portal vein or
tumor involving both right and left portal veins or right and left hepatic arteries.
There is tumor within the second-order biliary radicles of both hepatic lobes.
CT scans help to delineate the extent of local invasion.
Cholangiography not only is the gold standard for diagnosis but also is helpful in determining
resectability because if both the right and left biliary ducts have extension of tumor beyond
the secondary biliary radicles, these tumors are unresectable.
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GALLBLADDER AND BILIARY TRACT- BILIARY NEOPLASMS

Surgical Treatment of Unresectable Tumors


Hepatico-jejunoanastomosis:
Longmire procedure, the lateral portion of the left lobe is transected, and
the dilated left hepatic duct is identified and anastomosed to a loop of
jejunum.
the round ligament approach.
Nonsurgical Palliative Stenting
Improved palliation of patients with extensive unresectable disease is
possible with nonsurgical percutaneous or endoscopic stenting.
Stents can be placed across an obstructing, unresectable bile duct cancer
either at the time of ERCP or by the percutaneous transhepatic approach
Patients with surgical bypass for palliation have less cholangitis and may
have improved quality of life and survival.20
Adjuvant Therapy
Adjuvant radiotherapy has been proposed in an effort to improve the
survival with bile duct carcinoma.
Various chemotherapeutic regimens have been tried, but no effective
treatment for bile duct cancers has been developed.
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