!!! Bile ducts

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The Biliary Tract

The Biliary TractSviatoslav Balaka (by Raymond W Pryor III M.D.)

History

HistoryCirca 200 AD Galen the gallbladder as a subsidiary organ for the liver & responsible for yellow bileRenaissance period Gallbladder seat of many emotions (gall)1652 - Thomas Bartholin gallbladder part of bile tract from liver to intestine1654 - Thomas Glisson formed more detailed anatomy of liver & biliary tract

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More relevant history1420 - Antonio Benevieni 1st account of gallstones1687 - Stal Pert Von Der Wiel 1st operation on gallstones1733 Jean-Louis Petit -1st successful removal of gallstones with fistula formation1859 J.L.W. Thudichum Two stage cholecystostomyJuly 15, 1867 Dr John Stough Bobbs Single stage cholecystostomy

1420 Antonis Benevieni had the first published case of gallstones after an autopsy of a female patient died after complaining of abdominal pain where he found a grossly inflamed and gangrenous gallbladder filled with stones.

In 1687 Stal Pert Von Der Wiel while operating on a patient with purulent peritonitis accidentally found gallstones, but did not know what to do with them.

In 1733 Jean Louis Petit suggested removal of gallstone and drainage of the gallbladder through a cutaneous fistula. His first successful surgery was in 1743, after several failed attempts.

His rigid criteria of surgical intervention was modified over the years. It involved adhering the gallblader to the abdominal wall and introduction of an indwelling trochar to remove stones and bile. This continued until 1859 when JLW Thudichum proposed a two stage elective cholecystostomy.In the 1st stage, the inflamed gallblader was sewed to the anterior abdominal wall. The second stage infolved making a direct incision over that site and removing stones.In 1867, a gynecologist fron Indiana, Dr John Stough Bobbs, while operating a patient with suspected ovarian cysts. Found a inflamed and adherant sac containing bullet like structures. He opened it and removed the stones, then closed it primairly and left it in the abdominal cavity. Thus the first recorded cholecystostomy. The patient recovered and actually outlived Dr Bobbs.4

Still More relevant History1630 & 1667 Zambecarri & Teckoff proved the gall bladder not essential to life1878 - Theodor Kocher refined cholecystostomy procedureJuly 15, 1882 Dr Langenbuch 1st open cholecystectomy1886 cholecystotomy 27% mortality vs 12% mortality for Langenbuchs cholecystectomy became gold standard1940s Mirizzi introduced cholangiography for CBD stones

Drs Zambecari & Teckoff, independent of one another, determined through experiments on pigs and dogs, that the gallbladder was not essential to life.1878, Dr Kocher refined the cholecystostomy procedure.

Dr Langenbuch, having observed the reports of Drs Kocher, Bobbs and Thudichum, observed that all these measures were only temporary andc rallied to find a definate solution to the disease.On july 15, 1882, at the age of only 27. Dr Langenbuch successfully removed the gallbladder of a 43 year old man who had been suffering from the disease for over 16 years.

His initial report was ignored by the medical community. He continued with his work and tallied up a mortality report. By 1886, it showed that his procedure had only a 12% mortality vs a 27% mortality with the traditional cholecystotomy. Thus, his procedure became the gold standard.

Fast forward to 1940 when Mirizzi introduced cholangiography.5

Anatomy

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Pear-shaped organ, hollow, thin-walled, Hartmanns pouch = infundibulumCystic duct contains prominent mucosal folds valves of Heister

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Anatomy

normal anatomyThe gallbladder lies between segment 4 & 5.The cystic artery is a branch off the right hepatic artery (90%), found in the triangle of Calot (cystic duct-lateral, CBD medial & liver-superiorLymphatics are on the R side of the CBD.Parasympatheic fibers from the left (anterior) trunk of the vagus nerve.Sympathetic fibers from the T7-T10 nerves coursing through the splanchnic and celiac ganglions. Thus the shoulder pain.Multiple variations of the R hepatic artery2nd most common is off the SMA in 17% populationABSITEIntrahepatic bile ductBile canaliculiSegmental bile ductLobal bile ductHepatic left and right hepatic ducts

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Variations in Bile Ducts

Great variability

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Gallbladder physiologyGallbladder wall has no muscularis mucosa or submucosaPredominantly columnar epithelial cellsRokitansky-Aschoff sinusesDucts of Luschka

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Biliary PhysiologyStorage and concentration of hepatic bileSecretion of water and electrolytesEmpting bile into the common bile ductcontroled by secretin, cholecystokinin (CCK) and gastrin.

Functions:Storage and concentration of hepatic bileSecretion of water and electrolitesOmpting bile into the common bile ductAmount of bile up to 1000 ml/dayVagal stimulation contraction, sympathetic reverse (relaxation?)10

Storage and concentrationNormal capacity of 40-50 mLLiver secretes >600 mL of bile dailyGreatest absorptive capacityConcentrates bile 5-10 foldNaCl transport by epithelium is driving force and water passively absorbed

Gallbladder mucosa has per unit area of any structure in body

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Composition of BileCharacteristic (mEa/L)HepaticGallbladderNa160270K510Cl62-1121-10HCO34510Ca425Water95-98%85-90%Bilirubin1.515Protein (mg/dL)250700Bile Acids3-50290-340Phospholipids840Cholesterol (mg/dL)60-70350-930Total Solids--125pH7.0 - 7.86.0 - 7.2

Biliary MotilityContraction of ampullary sphincter (Sphincter of Oddi)After meal, sphincter of Oddi relaxes & CCK released contraction of gallbladderWhen stimulated, 50-70% of contents ejected over 30-40 minutesRefills over next 60-90 minutes

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Gallstones

Cholelithiasis10-20% of Europeans and Americans carry gallbladder stonesMajority are asymptomaticSymptoms and severe complications - 25%1-2% of asymptomatic individuals develop symptoms per yearEach year, an estimated 700,000 cholecystectomies (US)$6.5 billion (US)

10e20% of Europeans andAmericans carry gallbladder stones,1,2 and the prevalence of gallstone disease seemsto be rising as a result of longer life expectancyApprox 65% of asymptomatic patients remain symptom free after 20 years

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Classification of gallstones

Cholesterol gallbladder stonesGallstones are classified as cholesterol stones or pigment stones (Table 2). More than80% of gallstones consist mainly of cholesterol crystals and are formed within the gallbladder.8 Three key mechanisms contribute to the formation of cholesterol gallbladderstones: cholesterol supersaturation of bile, gallbladder hypomotility, and destabilizationof bile by kinetic protein factors. Cholesterol is virtually insoluble in water, and its solubilityin bile depends on the detergent properties of bile salts and phospholipids.9Cholesterol-supersaturated bile contains more cholesterol than can be solubilizedby mixed micelles at equilibrium (cholesterol saturation index (CSI) > 1) (Figure 1).The CSI is defined as the ratio of the actual biliary cholesterol concentration andthe maximal concentration that would be soluble at phase equilibrium in model bilewith equal lipid composition.10 Cholesterol-supersaturated bile contains multilamellarvesicles (liquid crystals), fusion and aggregation of which precede the formation ofsolid cholesterol crystals (Figure 1). As illustrated in the ternary phase diagram,9,10solid crystals occur in bile at high relative bile salt and low phospholipid concentrations,and at cholesterol:phospholipid ratios >1.An excess of biliary cholesterol in relation to bile salts and phospholipids can resultfrom hypersecretion of cholesterol, or from hyposecretion of bile salts or phospholipids(Table 3). Cholesterol hypersecretion, which is the most common cause of supersaturation,8 might be caused by increased hepatic uptake or synthesis of cholesterol,decreased hepatic synthesis of bile salts, or decreased hepatic synthesis ofcholesteryl esters for incorporation in very-low-density lipoproteins (VLDL). In nonobeseindividuals who form cholesterol-rich gallbladder stones, gallstones were associatedwith a small bile salt pool cycling at a normal frequency within the enterohepaticcirculation.11 Furthermore, it has been suggested that slow intestinal transit increasesbacterial degradation of primary to secondary bile salts in the colon.12 Bile then containsa greater proportion of deoxycholate conjugates which, in turn, increases biliary cholesterolsecretion and saturation, thereby enhancing gallstone formation.13In humans, most cholesterol present in gallstones is of dietary origin, consistentwith the observation that hepatic biosynthesis contributes 1) (Figure 1).The CSI is defined as the ratio of the actual biliary cholesterol concentration andthe maximal concentration that would be soluble at phase equilibrium in model bilewith equal lipid composition.10 Cholesterol-supersaturated bile contains multilamellarvesicles (liquid crystals), fusion and aggregation of which precede the formation ofsolid cholesterol crystals (Figure 1). As illustrated in the ternary phase diagram,9,10solid crystals occur in bile at high relative bile salt and low phospholipid concentrations,and at cholesterol:phospholipid ratios >1.An excess of biliary cholesterol in relation to bile salts and phospholipids can resultfrom hypersecretion of cholesterol, or from hyposecretion of bile salts or phospholipids(Table 3). Cholesterol hypersecretion, which is the most common cause of supersaturation,8 m