gall bladder

1. GALL STONESGALL STONES

2. DEFINITIONDEFINITION
Cholelithiasis (calculi or gallstones) usually form inCholelithiasis (calculi or gallstones) usually form in
the gallbladder from the solid constituents of bilethe gallbladder from the solid constituents of bile
and vary greatly in size, shape and composition.and vary greatly in size, shape and composition.

3. ANATOMY OF GALL BLADDERANATOMY OF GALL BLADDER
 A pear-shaped, hollow, saclike organ, 7.5 to 10 cmA pear-shaped, hollow, saclike organ, 7.5 to 10 cm
(3-4 inch) long, lies in a shallow depression on the(3-4 inch) long, lies in a shallow depression on the
inferior surface of the liver, to which it is attached byinferior surface of the liver, to which it is attached by
loose connective tissue.loose connective tissue.
 The capacity of the gallbladder is 30 to 50 ml of bile.The capacity of the gallbladder is 30 to 50 ml of bile.
 Its wall is composed largely of smooth muscle.Its wall is composed largely of smooth muscle.
 The gallbladder is connected to the common bileThe gallbladder is connected to the common bile
duct by the cystic ductduct by the cystic duct

5. Fundus
Body
Neck
Infundibulum
Cystic duct

6. CYSTOHEPATIC TRIANGLE OF CALOTCYSTOHEPATIC TRIANGLE OF CALOT
Cystohepatic triangle (ofCystohepatic triangle (of
Calot) which is formed byCalot) which is formed by
the visceral surface of thethe visceral surface of the
liver superiorly, the cysticliver superiorly, the cystic
duct inferior-laterally andduct inferior-laterally and
the common hepatic ductthe common hepatic duct
medially. It contains cysticmedially. It contains cystic
artery and lymph nodes.artery and lymph nodes.

7. Blood supply of CBDBlood supply of CBD
 The blood supply of the supraduodenal duct isThe blood supply of the supraduodenal duct is
essentially axial.essentially axial.
 Most vessels to the common bile duct arise fromMost vessels to the common bile duct arise from
 1. the superior pancreaticoduodenal artery,1. the superior pancreaticoduodenal artery,
 2. the right branch of the hepatic artery,2. the right branch of the hepatic artery,
 3. the cystic artery,3. the cystic artery,
 4. the gastroduodenal artery, and4. the gastroduodenal artery, and
 5. the retroduodenal artery.5. the retroduodenal artery.
The most important of these vessels run along theThe most important of these vessels run along the
lateral borders of the duct and have been calledlateral borders of the duct and have been called
the 3 o’clock and 9 o’clock arteries.the 3 o’clock and 9 o’clock arteries.

9. ANATOMY :
The common duct courses downward anterior to the portal
vein, in the free edge of the lesser omentum;
CBD is closely applied to the hepatic artery, which runs
upward on its left, giving rise to the right branch of the
hepatic artery, which crosses the main bile duct usually
posteriorly, although in about 20% of cases, it crosses
anteriorly.
The cystic artery, arising from the right branch of the hepatic
artery, may cross the common hepatic duct posteriorly or
anteriorly

10. CBD, PORTAL VEIN & HEPATIC
ARTERY RELATION

11. PHYSIOLOGY OF GALLBLADDERPHYSIOLOGY OF GALLBLADDER
 It act as a storage depot for bileIt act as a storage depot for bile
 Between meals, when the sphincter of Oddi isBetween meals, when the sphincter of Oddi is
closed, bile produced by the hepatocytes entersclosed, bile produced by the hepatocytes enters
the gallbladderthe gallbladder
 During storage, a large portion of the water in bileDuring storage, a large portion of the water in bile
is absorbed through the walls of the gallbladder,is absorbed through the walls of the gallbladder,
so that gallbladder bile is 5-10 times moreso that gallbladder bile is 5-10 times more
concentrated than that originally secreted by theconcentrated than that originally secreted by the
liver.liver.

12. PHYSIOLOGY OF GALLBLADDERPHYSIOLOGY OF GALLBLADDER
 When food enters the duodenum, the gallbladderWhen food enters the duodenum, the gallbladder
contracts and the sphincter of Oddi relaxes, allowingcontracts and the sphincter of Oddi relaxes, allowing
the bile to enter the intestine.the bile to enter the intestine.
 This response is mediated by secretion of theThis response is mediated by secretion of the
hormone cholecystokinin-pancreozymin (CCK-PZ)hormone cholecystokinin-pancreozymin (CCK-PZ)
from the intestinal wallfrom the intestinal wall

13. BILEBILE
 Bile is produced at a rate of 500–1500 mL/d by theBile is produced at a rate of 500–1500 mL/d by the
hepatocytes and the cells of the ductshepatocytes and the cells of the ducts
 The organic constituents of bile are water(98%),bileThe organic constituents of bile are water(98%),bile
salts, bile pigments, cholesterol, lecithin,fatty acidssalts, bile pigments, cholesterol, lecithin,fatty acids
and bilirubin. Bile also contains electrolytes. pH ofand bilirubin. Bile also contains electrolytes. pH of
bile is more than 7.bile is more than 7.
 Bile acids are conjugated with amino acids , glycineBile acids are conjugated with amino acids , glycine
or taurine to form bile salts.or taurine to form bile salts.

14. FunctionsFunctions
 Gall bladderGall bladder
 It stores BileIt stores Bile
 It concentrates bileIt concentrates bile
 Ejects bile into lumenEjects bile into lumen
 BileBile
 Emulsify dietary lipidsEmulsify dietary lipids
 Formation of micelles with products of lipidFormation of micelles with products of lipid
digestion.digestion.

15. Functions of bileFunctions of bile
1-1- The bile play a major role in the excretion of cholesterol
2- Solubilize cholesterol which prevent precipitation in the
GB. Alteration of bile composition lead to the formation of
GS.
3- Facilitate digestion of TG through emulsification .
4.Facilitate absorption of fat soluble vitamins(vit A,D,E,K).
5.Finally GB hypomotility & bile stasis promote GS formation .

16. CHOLELITHIASISCHOLELITHIASIS
 PresencePresence of one or more calculiof one or more calculi
(stones) in the gallbladder.(stones) in the gallbladder.
cholchol- (bile) +- (bile) +
lithlith- (stone) +- (stone) +
iasisiasis- (process).- (process).

17. Types of GallstonesTypes of Gallstones
 Mixed (80%)Mixed (80%)
 Pure cholesterol (10%)Pure cholesterol (10%)
 Pigmented (10%)Pigmented (10%)
 Black stones (containBlack stones (contain
Ca bilirubinate, a/wCa bilirubinate, a/w
cirrhosis andcirrhosis and
hemolysis)hemolysis)
 Brown stones (a/wBrown stones (a/w
biliary tract infection)biliary tract infection)

18. Pigment stones
Black pigment stones
Most common
Formed in gall bladder
Made of Calcium
bilirubinate,phosphate,bica
rbonate
Common in hemolytic
disorders,cirrhosis
Multiple , small & hard in
consistency
Brown pigment stones
•Rarely form in gall
bladder
•Formed in bile duct
•Related to bile stasis &
infected bile & foreign
body in bile duct like
stents.
•E.coli, Bacteroides

19. Factors Responsible for Formation
of Gallstones
1.Lithogenic bile
2. Nucleation
3. Stasis or gall bladder hypomotility

20. 1. Lithogenic bile
a. Increased Biliary Cholesterol: ₋
Obesity ₋ Cholesterol rich diet ₋ Clofibrate therapy
b. Decreased Bile Acids: ₋
i Primary biliary cirrhosis ₋
ii OCPs₋ Mutation of CYP7A1 gene (Mutation of CYP7A1 resulting in
deficiency of cholesterol 7-alpha hydroxylase, results in impaired
hepatic
conversion of cholesterol to bile acids)
iii. Impaired enterohepatic circulation of bile acids: Ileal disease or
resection, cholestyramine or colestipol (bile acid sequestrants)
c. Decreased Biliary Lecithin: ₋ MDR-3 gene mutation leads to
defective lecithin secretion in bile

21. 2. Nucleation :
• Cholesterol monohydrate crystal agglomerate to become
macroscopic crystal by nucleation
Pro-nucleating Factors: Mucin, Non-mucin glycoprotein
Infection
Anti-nucleating Factors:
• Apolipoprotein A-I and A-II
• Excess of pro-nucleating factors or deficiency of anti-nucleating
factors results in formation of gallstones

22. 3. Stasis or gall bladder hypomotility :
• Prolonged TPN
• Prolonged fasting
• Pregnancy
• Octreotide
• OCPs
• Massive burns

23. Pathogenesis of Cholesterol Gallstones
• Cholesterol is insoluble in water (water is major constituent
of bile, 85-95%).
• Bile acid and phospholipids in bile keep cholesterol in
solution by the formation of micelles.
• An excess of cholesterol relative to bile acids and
phospholipids allows cholesterol to form crystals and such bile
is called lithogenic or supersaturated bile
Bacterial infection and an increase in bilirubin load play a role
in the development of black and brown gallstones

24. PATHOPHYSIOLOGYPATHOPHYSIOLOGY
Decreased bile acid synthesisDecreased bile acid synthesis
oror
Increased cholesterol synthesis in the liverIncreased cholesterol synthesis in the liver
Super saturation of bile with cholesterolSuper saturation of bile with cholesterol
Formation of precipitatesFormation of precipitates
Gall stones (Cholelithiasis)Gall stones (Cholelithiasis)
Inflammatory changes (Cholecystitis)Inflammatory changes (Cholecystitis)

26. PredisposingPredisposing factorsfactors forfor gallstonegallstone formationformation
 1.For cholesterol and mixed stones.1.For cholesterol and mixed stones.
 Demographic and genetic factorsDemographic and genetic factors – familial disposition;– familial disposition;
hereditary aspects; greater prevalence in Northern Europehereditary aspects; greater prevalence in Northern Europe
and North America, lower – in Asiaand North America, lower – in Asia
 ObesityObesity – increased biliary secretion of cholesterol– increased biliary secretion of cholesterol
 DietDiet - high fat and caloric diet- high fat and caloric diet
 Weight lossWeight loss – mobilization of tissue cholesterol leads to– mobilization of tissue cholesterol leads to
increased biliary cholesterol secretion while enterohepaticincreased biliary cholesterol secretion while enterohepatic
circulation of bile acids is decreasedcirculation of bile acids is decreased

27.  Female sex hormonesFemale sex hormones
• Estrogens stimulate hepatic lipoproteins receptors,Estrogens stimulate hepatic lipoproteins receptors,
increase uptake of dietary cholesterol, and increaseincrease uptake of dietary cholesterol, and increase
biliary cholesterol secretionbiliary cholesterol secretion
• Natural and synthetic estrogens lead to decrease bileNatural and synthetic estrogens lead to decrease bile
salt secretion and decreased conversion of cholesterolsalt secretion and decreased conversion of cholesterol
to cholesterol estersto cholesterol esters
 Ileal disease or resectionIleal disease or resection – malabsorption of bile acids– malabsorption of bile acids
leads to decreased bile acids pool and decreased biliaryleads to decreased bile acids pool and decreased biliary
secretion of bile saltssecretion of bile salts
 Increasing ageIncreasing age – increased biliary secretion of cholesterol,– increased biliary secretion of cholesterol,
decreased size of bile acid pool, biliary secretion of biledecreased size of bile acid pool, biliary secretion of bile
salts, and gallbladder motilitysalts, and gallbladder motility

28. PredisposingPredisposing factorsfactors forfor gallstonegallstone formationformation
 Gallbladder hypomotilityGallbladder hypomotility leading to stasis andleading to stasis and
formation of sludgeformation of sludge
• FastingFasting
• PregnancyPregnancy
• Drugs: octreotideDrugs: octreotide
• Prolonged parenteral nutritionProlonged parenteral nutrition
 Clofibrate therapyClofibrate therapy - increased biliary secretion of- increased biliary secretion of
cholesterol.cholesterol.
 Cholestyramine –Cholestyramine – decreases the bile saltdecreases the bile salt
concentration.concentration.
 Decreased bile acid secretionDecreased bile acid secretion
• Primary biliary cirrhosisPrimary biliary cirrhosis
• Chronic intrahepatic cholestasisChronic intrahepatic cholestasis

29. PredisposingPredisposing factorsfactors forfor gallstonegallstone formationformation
2.2.Pigment stonesPigment stones
Demographic/genetic factors: Asia, ruralDemographic/genetic factors: Asia, rural
settingssettings
Chronic hemolysisChronic hemolysis
Alcoholic cirrhosisAlcoholic cirrhosis
Chronic biliary tract infections, parasiteChronic biliary tract infections, parasite
infestationinfestation
Increasing ageIncreasing age

30. 4 Stages of Cholelithiasis4 Stages of Cholelithiasis
 Gallstone disease may be thought of asGallstone disease may be thought of as
having the following 4 stages:having the following 4 stages:
 The lithogenic state, in which conditionsThe lithogenic state, in which conditions
favor gallstone formationfavor gallstone formation
 Asymptomatic gallstonesAsymptomatic gallstones
 Symptomatic gallstones, characterized bySymptomatic gallstones, characterized by
episodes of biliary colicepisodes of biliary colic
 Complicated cholelithiasisComplicated cholelithiasis

31. Clinical featuresClinical features
 More common in femalesMore common in females
 Fat,fertile,forty,flatulentFat,fertile,forty,flatulent
 Asymptomatic in 10 to 20% casesAsymptomatic in 10 to 20% cases
 Symptoms-Symptoms-
 Biliary colic- Right hypochondrium & epigastrium,Biliary colic- Right hypochondrium & epigastrium,
radiating to chest,back & shoulder, severe , on &radiating to chest,back & shoulder, severe , on &
off, spasmodic, occurs within hours afteroff, spasmodic, occurs within hours after
meal,usually self limiting and recurring,precipitatedmeal,usually self limiting and recurring,precipitated
by fatty meal.by fatty meal.
 VomitingVomiting
 FeverFever

32.  MURPHY’s SIGN
Patient winces in pain
with catch of
breath when
inflamed gall
bladder strikes
palpating fingers on
inspiration
A positive Murphy's
sign may suggests
acute inflammation
and may be
associated with a
leucocytosis and
moderately
elevated liver

33. Courvoiser’s LawCourvoiser’s Law
 In a patient with jaundice a palpable non tender gall
bladder it is not due to gall stones but-
 Results from a distal common bile duct obstruction
secondary to a peripancreatic malignancy
 Rarely a non tender palpable gall bladder results
from complete obstruction of the cystic duct by the
stone with reabsorption of the intraluminal bile and
secretion of uninfected mucus secreted by the
epithelium, leading to a mucocele of the gall bladder.

34. Complications of Gall stonesComplications of Gall stones
In Gall Bladder-
Acute cholecystitis
Chronic cholecystitis
Empyema of gall bladder
Mucocele gall bladder
Perforation – leading to
biliary peritonitis
Gangrene of gall bladder
Carcinoma
In Bile duct-
•Obstructive jaundice
•Cholangitis(charcot’s
triad)
•Acute pancreatitis
•Secondary CBD
stones(choledocholithia
sis)
In Intestine-
•Acute intestinal
obstruction(gall stone
ileus)

35. ComplicationsComplications
 Acute cholecystitis:
 Due to obstruction of the neck of gallbladder or
cystic duct by a stone resulting in a chemical
inflammatory reaction. Bacteria are cultured from
the bile in approximately 1/2 of patients with
gallstones and unrelieved obstruction in the
presence of this infected bile may produce an
empyema
 Boas' sign :hyperaesthesia below the right scapula in
cholecystitis.

36.  The thickened gallbladder becomes intenselyThe thickened gallbladder becomes intensely
inflamed, edematous and occasionally gangrenousinflamed, edematous and occasionally gangrenous
 The fundus of the distended, inflamed gallbladderThe fundus of the distended, inflamed gallbladder
may perforate giving rise to localised abscessmay perforate giving rise to localised abscess
formation and occasionally to biliary peritonitisformation and occasionally to biliary peritonitis
 The commo organism implicated in inflammation ofThe commo organism implicated in inflammation of
the gallbladder are E coli, Klebsiella sp. and Strepthe gallbladder are E coli, Klebsiella sp. and Strep
faecalisfaecalis
 Staphylococci, clostridia and salmonella areStaphylococci, clostridia and salmonella are
occasionally can infectoccasionally can infect

37. Chronic cholecystitisChronic cholecystitis
 Repeated bouts of biliary colic or acute cholecystitisRepeated bouts of biliary colic or acute cholecystitis
culminate in fibrosis, contraction of the gallbladderculminate in fibrosis, contraction of the gallbladder
and chronic inflammatory change my be present inand chronic inflammatory change my be present in
the absence of gallstones, as is the case in thethe absence of gallstones, as is the case in the
gallbladders of typhoid carriersgallbladders of typhoid carriers
 The incidence of carcinoma of the gallbladder isThe incidence of carcinoma of the gallbladder is
increased in patients with long standing gallstonesincreased in patients with long standing gallstones

38. MucoceleMucocele
 A mucocele develops when the outlet of theA mucocele develops when the outlet of the
gallbladder becomes obstructed in the absence ofgallbladder becomes obstructed in the absence of
infectioninfection
 The imprisoned bile is absorbed, but clear mucusThe imprisoned bile is absorbed, but clear mucus
continues to be secreted into the distendedcontinues to be secreted into the distended
gallbladder.gallbladder.

39. CholedocholithiasisCholedocholithiasis
 When gallstones enter the common bile duct, theyWhen gallstones enter the common bile duct, they
may pass spontaneously or give rise to obstructivemay pass spontaneously or give rise to obstructive
jaundice, cholangitis or acute pancreatitisjaundice, cholangitis or acute pancreatitis
 Gallstone pancreatitis most commonly occurs whenGallstone pancreatitis most commonly occurs when
a small stone becomes temporarily arrested at thea small stone becomes temporarily arrested at the
ampulla of vater.ampulla of vater.

40. CLINICAL FEATURESCLINICAL FEATURES
 The natural history of CBD stones isThe natural history of CBD stones is
unpredictable, with many small stonesunpredictable, with many small stones
passing spontaneously.passing spontaneously.
 In patients who have cholecystectomy forIn patients who have cholecystectomy for
gallbladder stones, approximatelygallbladder stones, approximately 10% to10% to
18%18% also have common bile duct (CBD)also have common bile duct (CBD)
stonesstones much lower percentage of patientsmuch lower percentage of patients
developed clinical sequelae of CBD stones indeveloped clinical sequelae of CBD stones in
series that utilized a more selective approachseries that utilized a more selective approach
to cholangiographyto cholangiography

41. COMPLICATIONSCOMPLICATIONS
CholangitisCholangitis
Obstructive JaundiceObstructive Jaundice
PancreatitisPancreatitis
Secondary Biliary CirrhosisSecondary Biliary Cirrhosis
4141

42. CHOLANGITISCHOLANGITIS
 NonsuppurativeNonsuppurative acute cholangitisacute cholangitis
 most common and respond rapidly to antibioticsmost common and respond rapidly to antibiotics
 Suppurative acute cholangitisSuppurative acute cholangitis
 Pus in completely obstructed ductal systemPus in completely obstructed ductal system  symptomssymptoms
of severe toxicity such as mental confusion and septicof severe toxicity such as mental confusion and septic
shockshock
 Poor response to antibiotics and mortality is 100% unlessPoor response to antibiotics and mortality is 100% unless
prompt endoscopic or surgical relief of the obstructionprompt endoscopic or surgical relief of the obstruction
and drainage of infected bile are carried out.and drainage of infected bile are carried out.
Mx : ERCP with endoscopic sphincterotomyMx : ERCP with endoscopic sphincterotomy
4242

43.  CholecystoentericCholecystoenteric fistulafistula: Infrequently, a large stone: Infrequently, a large stone
erodes the gallbladder wall, creating a fistula into theerodes the gallbladder wall, creating a fistula into the
small bowel (or elsewhere in the abdominal cavity);small bowel (or elsewhere in the abdominal cavity);
the stone may pass freely or obstruct the smallthe stone may pass freely or obstruct the small
bowel (bowel (gallstone ileusgallstone ileus).).
 Mirizzi’s syndromeMirizzi’s syndrome – Rarely, a gallstone gets– Rarely, a gallstone gets
impacted in the GB wall, mostly in the Hartman’simpacted in the GB wall, mostly in the Hartman’s
pouch or fundus of GB and compresses it causingpouch or fundus of GB and compresses it causing
pressure necrosis and its adherence to the commonpressure necrosis and its adherence to the common
bile duct, and occasionally it can leads to cholecysto-bile duct, and occasionally it can leads to cholecysto-
choledochal fistula.choledochal fistula.

44. Biliary colicBiliary colic
 Severe gripping pain after meals an in the eveningSevere gripping pain after meals an in the evening
which is maximal in the epigastrium and rightwhich is maximal in the epigastrium and right
hypochondrium with radiation to the back.hypochondrium with radiation to the back.
 Transient obstruction of GB from an impacted stone.Transient obstruction of GB from an impacted stone.
 Despite being continuous the pain may wax andDespite being continuous the pain may wax and
wane in intensity over several hours, vomiting andwane in intensity over several hours, vomiting and
retching are common. Resolution occurs when theretching are common. Resolution occurs when the
stone falls back into the gallbladder lumen or passesstone falls back into the gallbladder lumen or passes
onwards into the CBD.onwards into the CBD.
 If the obstruction does not resolve then the patientIf the obstruction does not resolve then the patient
develops acute cholecystitis.develops acute cholecystitis.

45. Differential diagnosis of cholecystitisDifferential diagnosis of cholecystitis
 CommonCommon
 AppendicitisAppendicitis
 Perforated pepticPerforated peptic
ulcerulcer
 Acute pancreatitisAcute pancreatitis
 uncommonuncommon
 Acute pyelonephritisAcute pyelonephritis
 Myocardial infarctionMyocardial infarction
 Pneumonia- rightPneumonia- right
lower lobe
 Ultrasound scan aidsUltrasound scan aids
diagnosisdiagnosis
 Uncertain diagnosis- doUncertain diagnosis- do
CT scanCT scan

46. Laboratory findingsLaboratory findings
 For patients with uncomplicated cholelithiasis, bloodFor patients with uncomplicated cholelithiasis, blood
work results usually are normal.work results usually are normal.
 However, labs can detect complications of gallstoneHowever, labs can detect complications of gallstone
disease; complications might alter the course ofdisease; complications might alter the course of
treatment.treatment.
 CBCCBC
 Chemistry panel, including electrolytes, liver enzymes,Chemistry panel, including electrolytes, liver enzymes,
and bilirubin.and bilirubin.
 Choledocholithiasis can manifest with onlyCholedocholithiasis can manifest with only
elevation of serum alkaline phosphatase orelevation of serum alkaline phosphatase or
bilirubin.bilirubin.
 Nearly 50% of patients with symptomatic gallstoneNearly 50% of patients with symptomatic gallstone
disease will have abnormal transaminasesdisease will have abnormal transaminases
 Serum lipase and amylase levels are helpful in cases ofSerum lipase and amylase levels are helpful in cases of
diagnostic uncertainty or suspected concurrentdiagnostic uncertainty or suspected concurrent
pancreatitispancreatitis

47. Imaging StudiesImaging Studies
 X-rays
 Approximately 15% of gallstones are radiopaque and can beApproximately 15% of gallstones are radiopaque and can be
visualized on plain x-ray.visualized on plain x-ray.
 A porcelain gallbladder (heavily calcified) should be removedA porcelain gallbladder (heavily calcified) should be removed
surgically because of increased risk of gallbladder cancer.surgically because of increased risk of gallbladder cancer.
 Other causes of abdominal pain diagnosed with the assistanceOther causes of abdominal pain diagnosed with the assistance
of x-rays include perforated viscus, bowel obstruction, calcificof x-rays include perforated viscus, bowel obstruction, calcific
pancreatitis, and renal stones.pancreatitis, and renal stones.
 UltrasoundUltrasound is the most sensitive and specific test for theis the most sensitive and specific test for the
detection of gallstones. Posterior acoustic shadowing is seen.detection of gallstones. Posterior acoustic shadowing is seen.
 US provides information about the size of the common bile ductUS provides information about the size of the common bile duct
and hepatic duct and the status of liver parenchyma and theand hepatic duct and the status of liver parenchyma and the
pancreas.pancreas.
 Thickening of the gallbladder wall and the presence ofThickening of the gallbladder wall and the presence of
pericholecystic fluid are radiographic signs of acute cholecystitispericholecystic fluid are radiographic signs of acute cholecystitis

48. Imaging studies: Ultra SoundImaging studies: Ultra Sound
 →→ denotesdenotes
gallstonesgallstones
 ►► denotes thedenotes the
acousticacoustic
shadow due toshadow due to
absence ofabsence of
reflected soundreflected sound
waves behindwaves behind
the gallstonethe gallstone
→
→
►

49. CTCT scanningscanning often is used in workup of abdominal pain
without specific localizing signs or symptoms.
CT scanning is not a first-line study for detection of
gallstones because of greater cost.
When present, gallstones usually are observed on CT
scan.

50. CholangiographyCholangiography
 IV cholangiography has been replaced by MRCPIV cholangiography has been replaced by MRCP
which is increasingly used to assess the biliary treewhich is increasingly used to assess the biliary tree
non invasively whereas ERCP is reserved fornon invasively whereas ERCP is reserved for
removing common bile duct stones by endoscopicremoving common bile duct stones by endoscopic
sphincterotomysphincterotomy
 Complications occur in up to 7% of patients and mayComplications occur in up to 7% of patients and may
include cholangitis, bleeding and acute pancreatitisinclude cholangitis, bleeding and acute pancreatitis

51. Treatment-IndicationsTreatment-Indications
 Symptomatic gallstonesSymptomatic gallstones
 Complicated gallstonesComplicated gallstones
 Silent gallstonesSilent gallstones
 DiabeticsDiabetics
 Patients undergoing bariatric surgeryPatients undergoing bariatric surgery
 There is generally no reason for prophylacticThere is generally no reason for prophylactic
cholecystectomy in an asymptomatic person unlesscholecystectomy in an asymptomatic person unless
 the gallbladder is calcifiedthe gallbladder is calcified
 gallstones are > 3cm in diametergallstones are > 3cm in diameter

52. TreatmentTreatment
 SymptomaticSymptomatic
 Laparoscopic cholecystectomy forLaparoscopic cholecystectomy for symptomaticsymptomatic stonesstones
 Open cholecystectomy, which involves a largeOpen cholecystectomy, which involves a large
abdominal incision and direct exploration, is safe andabdominal incision and direct exploration, is safe and
effective. Its overall mortality rate is about 0.1% wheneffective. Its overall mortality rate is about 0.1% when
done electively during a period free of complications.done electively during a period free of complications.

53.  AsymptomaticAsymptomatic
 For patients who decline surgery, or are at high risk of surgicalFor patients who decline surgery, or are at high risk of surgical
complications, but want to remove asymptomatic stones; thesecomplications, but want to remove asymptomatic stones; these
gallstones can sometimes be dissolved by ingesting bile acidsgallstones can sometimes be dissolved by ingesting bile acids
((ursodeoxycholic and chenodeoxycholic acid)ursodeoxycholic and chenodeoxycholic acid) orally for manyorally for many
months. They dissolve gallstones made of pure cholesterol, butmonths. They dissolve gallstones made of pure cholesterol, but
not the calcified stones and it may take months or years.not the calcified stones and it may take months or years.
 ESWL shatters the stone into small fragments that can either beESWL shatters the stone into small fragments that can either be
dissolved more quickly using dissolution treatment withdissolved more quickly using dissolution treatment with
ursodeoxycholic or may pass spontaneously into the intestine.ursodeoxycholic or may pass spontaneously into the intestine.

54. Thank YouThank You