c 10 + 11 gallbladder and biliary tract

8/10/2019 C 10 + 11 GALLBLADDER AND BILIARY TRACT

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GALLBLADDER ANDBILIARY TRACT

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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, differentialdiagnosis, 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 liverby connective tissue and vessels, and it lies between the right, left, and quadrate hepatic lobes1-3or hepatic segments IV and V

The gallbladder occasionally has a complete peritoneal covering and true mesentery predisposingto torsion. Rarely, the organ is located so deeply within the liver parenchyma that it can bereached from the outside only by dividing an overlying layer of liver tissue (intrahepaticgallbladder).

The gallbladder is 7 to 10 cm long, with an average volume of about 30 mL. With markeddistention or acute obstruction, the viscus may contain up to 300 mL.


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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 theinfundibulum, or Hartmann pouch. The neck occupies the deepest part of the gallbladder fossaand lies in the free portion of the hepatoduodenal ligament).

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


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Vessels, Nerves, and Lymphatics The arteries of the gallbladder are derived from the cystic branch of the hepatic artery. Thecystic 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 thehepatocystic triangle, the area bound by the cystic duct, common hepatic duct and livermargin.

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 insertionof the cystic artery into the gallbladder wall.

The nerves of the gallbladder are branches of the vagus and sympathetic nerves, which passthrough the celiac plexus


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Normal and anomalous arterial supply to the gallbladder.


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Extrahepatic Biliary Ducts

Comm on Hepat ic Duct

The common hepatic duct is formed by the union of the right and left hepatic ducts close to their emergence fromthe liver.

The common hepatic duct is 1 to 2.5 cm long and normally has a diameter of about 4 mm. The duct passesdownward in the superior and lateral portion of the hepatoduodenal ligament and lies in front of the portal vein andto the right of the hepatic artery.

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

The cyst ic 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 ductpasses 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 mainhepatic duct and, after a spiral course, empty into its posterior or left side.

Variations in cystic

duct anatomy.


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Common Bi le Duct

The common bile duct (ductus choledochus) is formed by the union of the common hepatic andcystic ducts.

The common bile duct is usually about 7 to 9 cm long, but its length depends on the site of unionof the cystic and main hepatic ducts. Internal diameter averages about 5 mm; however, the ductmay be quite narrow or dilate to enormous dimensions when obstructed.

The anatomic divisions of the common duct


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The intramural portion of the common bile ductruns obliquely downward and laterallywithin the wall of the duodenum for 1 to 2 cm, opening on a papilla (VATER) of mucousmembrane about 10 cm from the pylorus.

The junction of the terminal common bile duct and pancreatic ductat the papilla takes one ofthree configurations that may be likened to a Y, V, or U. In about 70% of patients, there is acommon channel of the bile duct and pancreatic ducts, thus a Y configuration. In about 20%, thecommon channel is nonexistent (V configuration). In 10%, the two ducts enter the duodenum viaseparate openings (U configuration).

Cross section of the

sphincter of Oddi.


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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 connectivetissue, and serosa.

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

Motor Funct io n

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


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Motor Funct io n

In the postprandial state, about 70% of hepatic bile flows into the gallbladder before reaching theduodenum and entering the enterohepatic cycle.

Patterns of gallbladder storage and emptying depend on a pressure gradient between the bileducts 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 asmall fraction of the gallbladder bile enters the duodenum.

Following a meal, the gallbladder empties by a steady tonic contraction thought to be due torelease 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 toexplain cholesterol nucleationand 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 theinterdigestive phase would thus remove the less dense vesicles, and alterations in the normalmotor function would negate these favorable events and increase the risk of cholesterol stoneformation.


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MOTOR DYFUNCTION

Gallb ladder Dyskinesia

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

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

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

The most specific test for diagnosing gallbladder dyskinesia is CCK-enhanced cholescintigraphywith assessment of gallbladder ejection fraction. CCK is infused intravenously 15 to 30 minutesafter injecting an analogue of 99m Tc imminodiacetic acid, and the ejection fraction of the isotopeby the contracting gallbladder is calculated. An ejection fraction less than 35% is consideredabnormal and cholecystectomy may be indicated.

A number of factors may lead to decreased gallbladder contraction such as a primary abnormalityof 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 Dysfunct io n

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

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


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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 cholesteroland 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 thepathogenesis of gallstones and the mechanisms by which changes in the physical properties ofbile promote nucleation and stone formation.

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

For more than a century, cholecystectomy had been the gold standard for the management ofsymptomatic gallstone disease. In the 1980s, a number of new and innovative techniques were

developed for the nonoperative management of gallstones. The surgical management ofcholelithiasis 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 thedevelopment of laparoscopic cholecystectomy and related procedures.


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GALLSTONE CLASSIFICATION Gallstones may be s ing le or numerous, small or large, and they may differ in co lor, size,

shape, and conf igu rat ion.

the compositionof stones in individual patients is uniform.

There are essentially three types of gallstonescholesterol, pigment, and mixedcholesteroland 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.

Primarycommon duct stones form exclusively in the intrahepatic or extrahepatic bile ducts andare generally soft, smooth, and yellowish. These stones usually conform to the shape of the bile

ductand rarely contain significant amounts of cholesterol.

Secondary (or retained) stones form in the gallbladder and subsequently pass into the commonbile duct, either through the cystic duct or a biliary fistula. These stones are chemically similar tocoexisting stones in the gallbladder.


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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 withdocumented 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 StonesAge (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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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 becritical in maintaining cholesterol in solution.

Bile acids are amphipathic compounds that contain both hydrophilic polar groups (amino acidsside chain) and hydrophobic nonpolar portions

Schematic representation of theorientation of bile acid molecules asamphipathic units with hydrophobicends pointed inward and hydrophilic

ends pointed outward.


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

Bile acidlecithincholesterol-mixedmicelle. Polar ends of bile acids andlecithin are oriented outward, andhydrophobic, nonpolar portions makeup the interior. Cholesterol is

solubilized within the hydrophobic,nonpolar center.


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Several independent investigators have demonstrated that although some cholesterol issolubilized in mixed bile acid lecithin micelles, much of the biliary cholesterol normally presentactually 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 istransported and solubilized in the vesicular form, with the remainder being transported in mixedmicelles. The relative amounts of cholesterol transported in vesicles or micelles is related to thedegree of bile concentration.

Unilamellar bile acidlecithincholesterolvesicle. The amphipathic molecules oflecithin and bile acids form a lipid bilayer.

Cholesterol is solubilized within thenonpolar portion of the bilayer.


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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 ofgallstones.

Theoretically, an increase in cholesterol concentration relative to bile acids can occur as a result ofaltered 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 bilesalts in both health and during cholesterol gallstone formation. Their data have been displayed usingtriangular 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 whichbile 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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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 ofcholesterol or decreased amounts of bile acids: in obese patients, in patients with ileal disorders orileal resection, during periods of starvation or fasting, normal people without gallstones secretecholelithogenic 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 tonucleation 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 comparedwith patients with cholesterol saturated bile but no stones.

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


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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 andnucleation-promoting6 factors and moreover, the manner in which this balance is disturbed duringcholesterol gallstone formation.

Schematic depicting the dynamic role ofvesicles as vehicles for cholesterol inbile and how they relate to nucleation.


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Biliary Calcium

Increased concentrations of calcium bilirubinate has long been recognized as an importantetiologic factor in the formation of pigment gallstones. Recent studies have suggested thatalterations 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 andwater 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 ofstone formation remain obscure.

Biliary Prostaglandins

Data suggest that arachidonic metabolism is significantly altered during the formation ofexperimentally 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 ofcholesterol feeding and have been linked with accumulation of gallbladder luminalfluid, a finding characteristic of patients with acute cholecystitis.


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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 unconjugatedbilirubin with precipitation of calcium bilirubinate and insoluble salts.

Classification

Pigment gallstones are characterized by their relatively high concentration of bilirubin (usually in excessof 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-pigmentstones are generally associated with hemolytic disorders or cirrhosis.These stones are typically tarry in appearance, are almost always located exclusively inthe 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 theintrahepatic or extrahepatic biliary tract, and are generally associated with infection.


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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 iswell known as the predominant component of most pigment gallstones).

Bacteria are found within the calcium bilirubinateprotein matrix of brown-pigmentstones but are absent from either black-pigment or cholesterol gallstones.

These findings are consistent with epidemiologic studies indicating that brown stonesare found in patients living in areas where biliary infections are endemic, whereasblack-pigment stones are typically found in patients with hemolytic disorders orcirrhosis.

Stasis of bile within the gallbladder has been implicated as an important etiologicfactor in the pathogenesis of pigment gallstones.

gallbladder stasis, tend to form calcium bilirubinate stones. gallbladder stasis, create conditions for infection.


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Biliary sludge

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

Sludge, as determined ultrasonographically, is partly composed of calcium bilirubinate crystalsand 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 bilirubinand contribute to biliary sludge remains unclear.

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


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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 upperquandrant pain (biliary colic).

Others will have symptoms consistent with acute cholecyst i t is, choledoc hol i th iasis, or gal lstonepancreatit is.

The difficulty lies in identifying those patients at risk for developing these specific complications ofgallstone 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 benignquestion: if early or prophylacticcholecystectomy 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 painbut instead havedyspepsia, vague epigastric discomfort, or even mildly increased flatulenceas the primarymanifestation of their disease.


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Up to 70% of such patients derive significant benefit from cholecystectomy, however, suggests thatthese nonspecific symptoms are frequently due to biliary calculi. Thus, designating these patients asasymptomatic 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

Abdom ina l Radiography

Although supine and upright abdominal radiographsare essential in the early evaluation of patientswith 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 patientswhose stones are grossly calcified, or the outlining of the gallbladder in patients with porcelaingallbladders or milk of calcium bile.

Oral Cholecystography

Traditionally, the oral cholecystogram has been the gold standard for the diagnostic evaluation ofpatients 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, poorpatient compliance, inability to absorb the tablets as a result of emesis, malabsorption, or diarrhea,

and jaundice or hepatic dysfunction


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Oral cholecystogram demonstratingmultiple radiolucent, free-floatingstones in the gallbladder.


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Abdom ina l Ul t rasonography

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 wallthickness, 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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Hepatobi l iary Scint igraphy

Radionuclides, such as 99mTcsubstituted iminodiacetic acid derivatives, can be used to providea direct image of the gallbladder and biliary tract.

These radionuclide agents, administered intravenously, are cleared from the blood by hepatocytesand excreted in an unconjugated form directly into the biliary ductular system.

The diagnostic role of hepatobiliary scintigraphy in patients with acute right upper quadrantsymptoms remains poorly defined.

The diagnosis of acute cholecystitis is established based on clinical criteria, although it may beconfirmed by biliary scintigraphy.

Bil iary Drainage and Cholecystokin in Cholecys tography

Common Clinical Features

Nonspeci fic Symptom s

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 themeal and pain.

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


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Classically, the pain of biliary colic is situated in the right upper quadrant or middle epigastrium.

The back discomfortthat is frequently observed in patients with biliary colic is usually located inthe 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 andemesis. These attacks are often precipitated by fatty meals,although most foods can also bring

about gallbladder contractions and painful episodes.Acu te Cholecyst i t is

The clinical manifestations of biliary colic and acute cholecystitis may overlap, and clinicaldistinction is often difficult.

It is helpful to think of them as distinct entities.

Diagram representing the chronologic painintensity of biliary colic. Characteristically, thepain is of sudden onset, builds in intensity,and then remains steady for several hours.


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

The onset and character of pain associated with acute cholecystitis is comparable to that observedin patients with biliary colic.

Unlike biliary colic, where the pain generally lasts for several minutes to hours, the pain of acutecholecystitispersists 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 comfortablelying still. The classic physical finding of acute cholecystitis is a positive Murphy sign,which refers toinspiratory arrest during deep palpation in the right upper quadrant. There is a wide variation in thespectrum of complaints and physical findingsin patients with acute cholecystitis, and often, onlypersistence of right upper quadrant pain and discomfort distinguishes this diagnosis from simplebiliary colic.

Acute cholecystitis occurs when astone becomes lodged in the cysticduct or Hartmann pouch.


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(Acute Cholecys t i t is)

Laboratory data are helpful but frequently nonspecific. Most patients with uncomplicated acutecholecystitis have mild leukocytosis, ranging from 12,000 to 15,000/mL. Mild jaundicemay bepresent 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 causesignificant 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 thickeningandobvious edema.

At the time of laparotomy, the gallbladder may be surrounded by omentum or adherent to theduodenum and contiguous structures. Depending on the evolution of the disease, there may begross evidence of ischemia, particularly in the least vascularized portion of the gallbladder, thefundus.

Histologically,acute cholecystitis is manifested by mucosal and subserosal edema, hypervascularity,and infiltration of the submucosa with polymorphonuclear leukocytes. In addition to the changestypical of acute cholecystitis, most acutely diseased gallbladders also have evidence of chronicinflammation, 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 bilecultures. Most of the bacteria cultured from these patients are of enteric origin, the most commonorganism 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 significantmorbidity and mortality.


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Preoperative evaluation

In addition to a careful history and physical examination, preoperative testing for 90 percent ofpatients with gallstone disease is minimal. An ultrasound of the right upper quadrant will usuallyconfirm the diagnosis, and the hepatic biochemical profile (alkaline phosphatase, SGOT, bilirubin,lactic acid dehydrogenase [LDH]) will usually determine the likelihood that common bile ductstones are present. Striking abnormalities in the hepatic profile, or an ultrasonographically dilatedcommon 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 ofintravenous morphine (which contracts the sphincter of Oddi) is a highly accurate predictor ofacute cholecystitis. When the ultrasound demonstrates nonuniform thickening of the gallbladderwall or pancreatic head, a CT scan should be performed to assess the likelihood of the presenceof gallbladder cancer. Intravenous cholangiography, rarely performed in the US, is popular inEurope for detecting common bile duct stones preoperatively in patients with abnormal liverfunction studies.


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(Acute Cholecys t i t is)

Prospective studies have demonstrated that the incidence of positive bile cultures increasessignificantly 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 onoperative 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 oncho lecystostomy andstone 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 beenpracticed 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 and1973 at 10 different institutions, from the United States and throughout the world, the overallmortality rate was l.6%.


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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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Delayed Versus Early Cholecystectomy

The issue of delayed versus early cholecystectomy in patients with acute cholecystitis has long beenthe 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 theacute inflammatory process and to facilitate the operative procedure.

This traditional approach of intense medical management was challenged by a number of reports thatdemonstrated significant advantages to early cholecystectomy. These studies indicated that morbidityand mortality were no different in patients who underwent early or delayed cholecystectomyand thatearly 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 favorof early rather than delayed intervention as morbidity and mortality appear to be the same or even lesswhen 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 usesintraoperative cholangiography.

In most instances, this is accomplished by the placing a small catheter through the cystic duct andinstilling 10 to 20 mL of dye.


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Contact Dissolu t ion

Percutaneous transhepatic cholecystolitholysis (direct contact dissolution) has been recommendedas a potential therapy for patients with symptomatic cholesterol gallstone disease.

this technique is based on percutaneous transhepaticpigtail catheter placement in the gallbladderand 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 dissolvescholesterol.

potential candidates for MTBE dissolution include high-risk patients with symptomatic stones orthose who refuse operation.

Although this modality may have specific indications, its application to the general population is

limited.Bil iary Lithotr ips y (electrohydraul ic sho ck w ave l i thotr ipsy - ESWL)

In preliminary studies using lithotripsy combined with adjuvant and litholytic medications (usuallyUDCA), gallstone fragmentation has been achieved in virtually all selected patients. Fragmentclearance occurred within 2 months in 30% of patients, within 4 months in 48%, and in 21% ofpatients 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 causedthis concept to be reevaluated.


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Acalculous Cholecystitis(suite)

The estimated incidence of acute acalculous cholecystitis is about 3% of all surgical biliary tractcases

Acalculous cholecystitishas been reported as a postoperative complication and in critically illpatients following trauma or burns.

Most postoperative patients who develop acute acalculous cholecystitishave had an intraabdominalprocedure 2 to 14 days before the onset of symptoms.

Diagnosis of acalculous cholecystitisposes a considerable challenge to the clinician, especiallywhen it occurs in intensive care unit patients. These patients typically have multiple medical andsurgical problems, and as a result, the diagnosis may be delayed.

Several studies suggest that the associated morbidity and mortality ratesof 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 cho lecystostomy,either through a minilaparotomy or percutaneously, is theprocedure of choice. Percutaneous cho lecystostomycan be safely performed by interventional

radiologists in most centers. Although this procedure allows for the decompression and drainage ofinfected gallbladder bile, it obviously does not cure gangrenous cholecystitis.


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Cholecyst i t is in th e Elder ly

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 ofcholedocholithiasis, emphysematous cholecystitis, perforation of the gallbladder, and septiccomplications of cholecystitis in the elderly.

Although some have proposed that these findings are secondary to differences in the evolution ofthe 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 t imely diagnosis, ear ly stabi l izat ion,and semiurgent cholecys tectomy.

Choledocholithiasis has been reported in 20% to 54% of elderly patients undergoingcholecystectomy. This figure is in contrast to the 8% to 12% rate of common duct stones reported inthe general population. The increased incidence of common duct stones in the elderly probablyreflects 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 yearsand 7.6% to 29% in patients older than age 70 years.


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Cirrhosis and Cholecyst i t is 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 porta lhypertension, thromboc ytopenia secondary to hypersp lenism, and coagulopathy.

Indications for cholecystectomy in a cirrhotic patient should be more restrictivethan in the noncirrhoticpatient.

Operations should be undertaken only in patients who are truly symptomaticor who have developedone of thecomplicationsof gallstone disease, such as acute cholecystitis, perforation, fistula formation,or empyema of the gallbladder.

Total Parenteral Nutr i t io nInduc ed Gallbladder Disease

The reported incidence of asymptomatic and symptomatic gallstone disease in the subset of patientsreceiving 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 cholecystitiswas present in more than 50%.

Diabetes and Cho lecyst i t is

For many years, it has been assumed that diabetics have an increased incidence of cholesterolgallstones and are more likely to develop acute cholecystitis with a greater incidence of postoperativecomplications.


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Complications of gallbladder lithiasis

Hydrops

Obstruction of the cystic ductby an impacted stone can result in hydrops, in which the gallbladderbecomes filled with a clear or whitish mucoid material(white bile). Little is known about thepathophysiology of hydrops of the gallbladder except that the mucoid material probably results fromaltered gallbladder epithelial secretion.

The gallbladder frequently becomes enlarged, and patients may present with signs and symptomssuggestive of acute cholecystitis, although occasionally, their only complaint is of a mass in the rightupper quadrant. Cholecystectomy is the treatment of choice.

Emphy sematous Cholecyst i t is

Emphysematous cholecystitis is anpotentially lethal complicationof cholecystitis and is manifestedby the radiographic / ultrasonographic demonstration of gas within either the gallbladder lumen orwall.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 indiabetics.

The gas within the lumen of the gallbladder wall occurs as a result of gas-producing bacteria. Themost common organisms cultured are C perfringens, although mixtures of this anaerobe with E coliand species of Klebsiellaare also noted.

The clinical course of patients with emphysematous cholecystitis is frequently characterized by rapidonset with severe abdominal pain, constitutional symptoms of nausea and vomiting, and evidence ofsevere sepsis.


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Emphysematous Cholecystitis(suite)

Common sequelae are gangrene (74%) andperforation of the gallbladder(21%). The potential forserious 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 issimilar to acute uncomplicated cholecystitis, and the only significant difference is the presence ofpus in the gallbladder lumen. These patients are often toxic, and emergent cholecystectomy ismandated.

Gallbladder Perforat ion

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 fundusis the most common site of acute perforation.Anatomically, this areacorresponds to the least vascularized portionof the gallbladder.

In patients with subacute perforations or chronic perforationswith fistula formation, repeated boutsof cholecystitis probably lead to scarring and fibrosis, with adherence of adjacent structures.


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Gallston e ileus(suit e) 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 thesite of obstruction. Frequently, the stone is found in the terminal ileum.

The primary goals at laparotomy are correct ion of the obstru ct ion and removal of theof fending stone. Since many of these patients are elderly and ill, cholecystectomy and take-

down of the biliary enteric fistula may not be appropriate. Enterolithotomy alone, withoutcholecystectomy, has an associated mortality rate of 5% in

contrast to the 15% mortality rate for patients who undergo both procedures at the same time.


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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.


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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 sourceof bi le duct stonesas either primary or second ary : Primary common duct stones, which also may be :

Primary and Referredto 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 thecholedochus by the cystic duct or occasionally through a cholecystocholedochalfistula.

The distinction betweenprimaryand secondary common duct stones has long beenthought 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 recurrencerate 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 withoutlaparotomy.



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Incidence

The incidence of bile duct stones in patients undergoing cholecystectomy foreither 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 thatrequire further intervention.

Cri ter ia for pr imary common duct ston esinclude previous cholecystectomy; atleast 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 cysticduct 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 Morpholog y of Comm on Bi le Duct Stones

Pr imary bi le duc t stones

Primary bile duct stones are exclusively of the pigment variety. They areclassically 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 variableamount of sludge or pasty concretions. In addition, the shape of primary commonduct stones often conforms to that of the distal common bile duct. Biliary stasishas been implicated in the pathogenesis of primary common duct stones.

Ampullary stenosis and functional duct dilatation have been associated with anincreased risk of primary common duct stone formation. Manometric studiesindicate that aberrant patterns of sphincter of Oddi motility are present in patientswith common duct stones.



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The presence of paravaterian diverticulaof the duodenum has also been associated with anincreased risk of choledocholithiasis.

InfectionThere is an increased incidence of positive bile cultures in patients with primarycommon duct stone disease.

Bacterial deconjugation of bilirubin by-glucuronidase with the formation of insoluble bilirubinsaltsmay 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 gram-negative rods E coliand K pneumoniaeas well as anaerobes, including bacteroidesandClostridium sp.All these bacterial isolates possess-glucuronidase activity at physiologic pH.Natural History

Primary Stones may be present for years in the bile ductwithout 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 ofjaundice.Charcots triade:pain, fever, jaundince.

Although septic cholangitismay be the most dramaticmanifestation of choledocholithiasis, amore 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 ofpruritus, with or without jaundice, transient elevation of alkaline phosphatase, and episodic

abdominal or back discomfort.Small stones may enter the common bile duct from thegallbladder and actually pass into the duodenum without producing symptoms. Stones less than3 mm in diameter rarely have clinical manifestations unless they accumulate simultaneously inthe distal bile duct or become trapped in an abnormally narrowed bile duct or ampulla. Aspreviously stated, stones that exceed the diameter of the ampulla may remain for years, causingminimal difficulty, or they may be associated with severe cholangitis. The uncertainties aboutthe history of common duct stones suggest that the documentation of choledocholithiasis is anindication for stone removal. The best way to achieve this, however, is controversial.



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Clinical Evaluation and Diagnos is

The critical factor in both the diagnostic evaluation and pathophysiology of common ductstone disease is obstruction of the common bile duct.

Common bile duct(CBD) obstruction from stone disease is typically characterized byincomplete obstruction, low and fluctuating levels of hyperbilirubinemia, andfluctuating symptoms of pain and jaundice.

Pain is present in more than 90% of patients with primary common duct stone disease and isfrequently 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 benormal.

Laboratory evaluationprovides important clinical information about the cause of jaundice Serum alkaline phosphataseis the most sensitive indicator of ductal obstruction because

this enzyme is released from the biliary ductal epithelium. Levels rise rapidly in responseto duct obstruction.

Serum bilirubin (total) and especially the direct(conjugated) fraction assess theobstructive aetiology of the jaundice.

Serum glutamic oxaloacetic transaminase(GOT) and serum glutamic pyruvic

transaminase(GPT) are released from injured hepatocytes, and although these levelsmay be elevated in patients with cholangitis, they are relatively normal in uncomplicatedcases 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 issueto resolve is whether there is intrahepatic or extrahepatic biliary dilatation orboth.



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The first issueto resolve is whether there is intrahepatic or extrahepatic biliary dilatation or both.

For that we can use several imagery tests:

Ultrasonographyhas been shown to be a simple, safe, and accurate way to identify biliarydilatation and stones and other pathological states.

CT scansprovide comparable information and also may identify mass lesions, such astumors in the distal bile duct, periampullary region, or in the head of the pancreas.

Percutaneous transhepatic cholangiography(PTC).

Endoscopic retrograde cholangiopancreatography (ERCP).ERCP offers certainadvantages over percutaneous transhepatic cholangiography. ERCP provides visualizationof the ampulla and periampullary region and allows for therapeutic intervention if

sphincterotomy is indicated and feasible. MRIis the best because is non invasive, whithout complications.

ERCP demonstrating multiple stones indistal common bile duct. Complete ductclearance was ultimately achieved in twosittings after endoscopic sphincterotomy.


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Clinical Syndromes

Management of Common Bile Duct Stones Found During Cholecys tectomy

About 7% of patients who undergo elective cholecystectomy are found to have unsuspected

common duct stones as documented by intraoperative cholangiography

Intraoperative cholangiogram performedduring OC demonstrating multiple, small,nonobstructing distal stones.



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Management of Common Bile Duct Stones Found During Cholecys tectomy(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 ductexploration. In addition to visualizing stones, the choledochoscope aids in their removal under directvision with the use of endoscopic grasping forceps.

Common bile duct stones found unexpectedly during a laparoscopic procedure present the surgeonwith 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 withpostoperative ERCP, sphincterotomy, and stone removal.

Secondary (Retained) Commo n B ile 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 thecommon bile duct by choledocholithotomy.

In addition to surgery, other modalities are now available for treating patients with retained commonduct stones, and their selection is generally based on the presence or absence of a T-tube.



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Secondary (Retained) Common Bile Duct Stones (suite)

Radiologic extraction (Burhenne technique) has become widely accepted for treatingpatients 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 isremoved and a Dormia basket catheter is passed down the matured T-tube tract.This basket is manipulated under fluoroscopic guidance, and multiple stones can beremoved. Using this technique success rates are ranging from 80% to 97%.

Illustration of Burhenne technique with placement ofbasket down matured tract and stone extraction.



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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 solventshave been applied topically to dissolve bile duct stones.MTBE hasbeen used successfully in the contact dissolution of gallbladder stones. To date, monooctanoic acidis the only agent that has been used with any success to dissolve cholesterolcommon duct stones.

When there is no T-tube in place the procedure of choice is endoscopic sphincterotomy

A B

B. ERCP demonstrating multiplestones in distal common bile duct.Complete duct clearance wasachieved after endoscopicsphincterotomy.

A.T-tube cholangiogram

demonstrating retainedgallstone in distal commonbile duct (white arrow).



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Secondary (Retained) Common B i le Duct Ston es (sui te) If, however, patients have multiple stones or subsequently develop evidence of retained

common bile duct stones after initial reexploration and require another reoperation, a biliarydrainage procedure is advised.Primary (Recurr ent) Common Bile Duct Stones

Experience has demonstrated the efficacy of ERCP with endoscopic sphincterotomy fortreating patients with primary common bile duct stones.

Success of this procedure depends on thesize of the stones, thenumberof stonesinvolved, the degree of stenosisor narrowingof the distal bile duct, and the expertise of theendoscopist.

Optimal treatment of patients with primary common bile duct stones should achieve twogoalsremoval of stones and prevention of recurrences. Many of these patients havemultiple 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, thegoal should be to select and perform a procedure that facilitates passage of any residual orrecurrent 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 butshould 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 bean 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 commonduct stones require a drainage procedure at the time of laparotomy, but rather whetherthey need an operation at all.

When surgery is indicated for patients with primary common duct stones, the surgeon hasthree optionstransduodenal sphincteroplasty, side-to-side choledochoduodenostomy, orRoux-en-Y choledochojejunostomy.



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choledochoduodenostomy.

A. The initial incision

is in the ampulla at11 oclock.

B. sphincteroplasty

A.

B.

GALLBLADDER AND BILIARY TRACT - BILIARY STRICTURES AND SCLEROSING

CHOLANGITIS


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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:

Postoperat ive Str ictures

Injury at primary biliary operations

Laparoscopic cholecystectomy Open cholecystectomy

Common bile ductexploration

Injury at other operative procedures

Gastrectomy

Hepatic resection

Portacaval shunt

Stricture of a biliaryenteric anastomosis

Blunt or penetrating trauma

Most biliary strictures occur after primary

operations on the gallbladder or biliary tree.With the introduction of laparoscopiccholecystectomy, bile duct injuries andassociated strictures have been seen withan increased frequency. Operative injury tothe bile ducts can also occur duringnonbiliary operations on the gallbladder or

biliary tree or as a result of externalpenetrating or blunt abdominal trauma.


CHOLANGITIS


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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 drugsPathogenesis

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 laparoscopiccholecystectomy, including:

acute or chronic inflammation,

inadequate exposure,

patient obesity, and

failure to identify structures before clamping, ligating, or dividing them.

Inflammatory conditions and fibrosis due tochronic pancreatitis, gallstones within thegallbladder or the bile duct, stenosis of thesphincter of Oddi, or biliary tract infections canalso cause benign bile duct strictures. Finally,primary sclerosing cholangitis, a rare disease ofunknown cause, can result in multiple strictures

of the intrahepatic and extrahepatic bile ducts.


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SCLEROSING CHOLANGITIS


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Pathogenesis(suite)

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

Numerous surgical clips canbe seen in the area of thestricture.

right lobe segmental bile ductentering the cystic duct

Classic laparoscopic bile duct injury.




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Pathogenesis(suite)

Unfortunately, the recurrence of bile duct strictures after an initial attempt at repair is not uncommonand can also account for a number of anastomotic strictures.

Finally, long-term follow-up of a bile duct anastomosis is important because strictures can developyears 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 weeksof initialoperation usually present in one of two ways:

One presentation is theprogressive elevation of liver function tests, particularly total bilirubinand alkaline phosphatase levels. These changes can often be seen as early as the second orthird postoperative day.

The second mode of early presentation is with leakage of bile from the injured bile duct. Thispresentation appears to occur most often in patients presenting with bile duct injuries afterlaparoscopic cholecystectomy. Bilious drainage from operatively placed drains or through thewound after cholecystectomy is abnormal and represents some form of biliary injury.




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In patients without drains (including patients in whom the drains have been removed), thebile can leak freely into the peritoneal cavity, or it can loculate as a collection. Freeaccumulation 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 infectedsubhepatic or subdiaphragmatic abscess.

Patients with postoperative bile duct strictures who present months to yearsafter theinitial operation frequently have evidence of cholangitis. The episodes of cholangitisare often mild and respond to antibiotic therapy. Repetitive episodes usually occurbefore the definitive diagnosis. Less commonly, patientsmay 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 ofpatients developing symptoms isshown with respect to the time

interval from the procedure duringwhich the injury occurred until thepresentation of the symptoms.


CHOLANGITIS


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Laboratory invest igat ions

Liver function tests usually show evidence of cholestasis :

The serum bilirubincan 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 biliarycirrhosis has developed.

Serum alkaline phosphataseis usually elevated.

Serum transaminaselevels can be normal or minimally elevated except during episodes ofcholangitis. If advanced liver disease exists,

hepatic synthetic function can be impaired, with

lowered serum albumin and a prolongation of prothrombin time.

Serum electrolytesand

complete blood countare typically normal unless there is associated biliary sepsis.

Radiologic Examinat ions

The imaging techniquesof 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 mightrequire drainage


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GALLBLADDER AND BILIARY TRACT- BILIARY STRICTURES AND SCLEROSING

CHOLANGITIS


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In patients suspected of having early postoperative bile duct injury, a radionucleotide biliary scan canconfirm bile leakage.

In patients with postoperative external bile fistula, a sinography (injection of water-soluble contrastmedia through the drainage tract) can often define the site of leakage and the anatomy of the biliarytree. 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 apostoperative bile duct stricturedepends primarily onthe timing of the presentation.

Patients presenting in the early postoperative period can be septic with either cholangitis orintraabdominal bile collections.

Once sepsis is controlled, there is no hurry in proceeding with surgical reconstruction of the bile ductstricture.

The combination of proximal biliary decompression and external drainage allows most biliary fistulas tobe controlled or even to close.

In patients who present with a biliary stricture remote from the initial operation, symptoms of cholangitiscan necessitate urgent cholangiography and biliary decompression. Biliary drainage is bestaccomplished by the transhepatic method, although successful endoscopic stent placement can alsobe accomplished.


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GALLBLADDER AND BILIARY TRACT- BILIARY STRICTURES AND



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cl in ical pr esentat ion

intermittent jaundice, which beginsinsidiouslyin the fourth or fifth decadeof life.

Right upper quadrant pain,

pruritus,

fever, weight loss,and

fatigue can also occur.

cyclic remissions and exacerbations.

DISEASES ASSOCIATED WITH PRIMARY SCLEROSING CHOLANGITIS

Disease Frequency (%)

Ulcerative colitis 40-60Pancreatitis 12-25

Diabetes mellitus 5-10Retroperitoneal fibrosis RareRiedel thyroiditis RareCrohns disease RareHistiocytosis X RareSicca complex RareRheumatoid arthritis RareHypertrophic osteoarthropathy RareSarcoidosis RareAngioimmunoblastic lymphadenopaty RareAcquired immunodeficiency syndrome Rare

Cholangiogram of a patient with primary sclerosingcholangitis. Multiple irregular strictures and dilation(beading) of intrahepatic bile ducts can be seen.




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Diagnosis

The diagnosis is suggestedby:

Clinical presentation associated with

Cholestatic liver function test abnormalities: The levels of bilirubin often fluctuatewith respect to the remissions and exacerbations

of the disease and the extent of hepatic injury.

Alkaline phosphataseis usually elevated out of proportion to the serum bilirubin and is amore persistent finding.

The diagnosis, however, usually is confirmed by cholangiography, which reveals multiple dilationsand 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 bythe percutaneous transhepatic route because the ducts are usually nondilated and fibrotic.

The disease should be fol low ed closelyby cholangiography and liver biopsy to provideappropriate 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 ursodeoxycho l ic ac idwhich 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 advocatedfor most symptomatic patients with primary sclerosing cholangitis.

In patients with biliary cirrhosis, hepatic transplantation is recommended.




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Bile Duct Strictures Secondary to Chronic Pancreatitis

Chronic pancreatitisis 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 andparenchymal fibrosis of the gland and are associated with dilation of the entire proximal biliarytree.

In most cases, the cause of the chronic pancreatitis is alcoholism.

Cholangiogram of a patient with a longdistal common bile duct stricture(arrow) due to chronic pancreatitis.

cl in ical presentat ion = variable

no symptom s, with the diagnosis of bile duct stricturessuggested only by abnormal liver function tests:

The serum alkaline phosphatase appears to be the most sensitivelaboratory finding and is elevated in over 80% of patients.

Abdominal painwith or withoutjaundiceis another commonpresentation.

pancreatic calcification, diabetes, and malabsorption with jaundice

Finally, the development of jaundice in patients with chronicpancreatitis must be differentiated from periampullary malignancy.

The definitive evaluationof patients with a bile duct stricture due tochronic pancreatitis is cholangiography. Either endoscopicretrograde cholangiopancreatography (ERCP) or PTCcan beuseful.


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GALLBLADDER AND BILIARY TRACT- BILIARY NEOPLASMS


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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 GALL BLA DDER

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 propriacan also result in the formation of polyps, called cholesterol polyps.These polyps are thought toresult from a disturbance in cholesterol metabolism.

Inflammatory polyps, which are composed of a vascular connective tissue stalk with a single layerof columnar epithelial cells and have a chronic inflammatory cell infiltrate. These lesions are notconsidered to be premalignant lesions and are thought to result from chronic inflammation.



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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

Anadenomyomaof the gallbladder is a rare intramural mass or nodule. This lesion is characterizedby 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 responsiblefor themuscular hypertrophy and the development of adenomyosis of the gallbladder.

The cause of this condition is unknown.

Other Benign Gallb ladder Tumors

Heterotopic lesions Heterotopiaconsists of nodules of ectopic tissuenot normally seen in thegallbladder, such as intestinal, pancreatic, or gastric epithelium.

Tumors of the supporting tissuesof the gallbladder, have been reported and are extremely rare.Tumors of the supporting tissues, such as hemangiomas, lipomas, leiomyomas, or granular celltumors, can also occur in the gallbladder.



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BENIGN BILE DUCT TUMORS

Benign tumors of the extrahepatic bile ducts are extremely rare. Only 2 cases in 5200 biliary tractsurgeries were reported.

Papillomascan occur in the extrahepatic bile ducts, as can multiple polyps or papillomatosis of thebile ducts.

Adenomatouslesions (Isolated reports) in association with adenocarcinomasuggest these maybepremalignant lesions.

Tumors of the supporting tissues, such as fibromas, leiomyomas, angioleiomyomas, or carcinoids,are rarely found in the bile ducts.

Clin ical Finding s

Benign gallbladder tumorscause symptoms similar to cholelithiasis: right upper quadrant pain anddiscomfort,

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 byconcomitant gallstones because many of these benign tumors are diagnosed as incidental

findings at the time of cholecystectomy.

Benign tumors of the bile ductspresent with symptoms relating to bile duct obstruction. Mostoften, these tumors are diagnosed during evaluation of jaundice or after treatment for biliaryinfection. The jaundice is often intermittent. Other patients have nonspecific symptoms, such asdyspepsia or elevated serum alkaline phosphatase levels.



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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 ductUltrasound can also be used for initial evaluation of jaundice in apatient with a benign tumor of the bile duct, but unequivocal demonstration of these tumors requireseither PTCor ERCP.

Whenever tumors in the bile ducts are demonstrated, surgical excision is indicated to relieveintermittent 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 thebiliary tree with a biliaryenteric anastomosis is preferred,usually by choledochojejunostomy.


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