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GALLBLADDER AND

BILIARY TRACT
4 hours

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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;

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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.

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GALLBLADDER AND BILIARY TRACT

• The gallbladder can be divided into four areas—fundus, 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.

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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

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GALLBLADDER AND BILIARY TRACT

• Normal and anomalous arterial supply to the gallbladder.

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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.

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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

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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.

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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 gallstones—cholesterol, 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 GALLBLADDER DISEASE PREVALENCE BY


AGE GROUP
• Age
• Hereditary and Ethnic Factors Percentage With Stones
• Gender and Hormones Age (y) Female Male
• Obesity 10-39 5.0 1.5
• Diabetes 40-49 12.0 4.4
50-59 15.8 6.2
• Cirrhosis 60-69 25.4 9.9
• Vagotomy 70-79 28.9 15.2
• Total Parenteral Nutrition 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 acid–lecithin–cholesterol-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 acid–lecithin–cholesterol


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 bile—cholesterol, 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 cholesterol–phospholipid 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 bilirubinate–protein 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 salt–phospholipid 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 5-
year 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 99mTc–substituted 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.
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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.

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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%.

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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: COMPLICATIONS OF LAPAROSCOPIC


OPEN CHOLECYSTECTOMY CHOLECYSTECTOMY IN 77,604 PATIENTS

Disease Status Complication Patients


Chronic Acute Complicated Bile duct injury 459 (0.6%)
Number 27,892 13,246 1336 Vascular injury 193 (0.25%)
Percentage Bowel injury 109 (0.14%)
of group 65.7% 31.2% 3.1% Mortality 33 (0.04%)
Morbidity rate 11.9% 19.4*% 25.2*%
Deaths 29 34 8 (Am J Surg 1993;165:9)
Mortality rate 0.10% 0.26*% 0.60*%
Length of
stay (d) 4.8 6.6* 8.6*
Cost ($) 5,881 9,043* 12,510*

* P <.0001 versus chronic cholecystitis.

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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 Langenbuch’s 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.

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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.

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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.

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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.

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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.

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