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Diseases of the Gallbladder and Bile
Dr. Carabeo

Lithocholic acid is much less efficiently absorbed from the colon than
OUTLINE deoxycholic acid.
I. PHYSIOLOGY OF BILE PRODUCTION AND FLOW Another secondary bile acid, found in low concentration, is
A. Bile Secretion and composition ursodeoxycholic acid (UDCA), a stereoisomer of CDCA.
B. The Bile Acids
In healthy subjects, the ratio of glycine to taurine conjugates in bile is
C. Enterohepatic Circulation
D. Gallbladder and Sphincteric Functions
A. Congenital Anomalies Bile acids are detergent-like molecules that form molecular aggregates
B. Gallstones called micelles.
C. Acute and Chronic Cholecystitis Solubility of cholesterol in bile depends on normal ratios of the total
D. The Hyperplastic Cholecystoses lipid concentration and the bile acids and lecithin thus facilitating the
III. DISEASES OF THE BILE DUCTS biliary excretion of cholesterol
A. Congenital Anomalies Abnormal ratios promote the precipitation of cholesterol crystals in
B. Choledocholithiasis bile
C. Trauma, Strictures and Hemobilia Bile acids also facilitate the normal intestinal absorption of dietary
D. Extrinsic Compression of the Bile Ducts
fats, mainly cholesterol and fat-soluble vitamins, via a micellar
E. Hepatobiliary Parasitism
transport mechanism
F. Sclerosing Cholangitis
Bile acids serve as a major physiologic driving force for hepatic bile
flow and aid in water and electrolyte transport in the small bowel and
Bile formed in the hepatic lobules Bile acids (unconjugated and conjugated) are absorbed by passive
diffusion along the entire gut
Important for bile salt recirculation, is the active transport
Secreted into network of canaliculi mechanism for conjugated bile acids in the distal ileum
Reabsorbed bile acids enter the portal bloodstream and are taken up
rapidly by hepatocytes, re-conjugated, and re-secreted into bile
Into Small bile ductules, and larger bile ducts in portal tracts situated (enterohepatic circulation)
between hepatic lobules The normal bile acid pool size is approximately 24 g.
During digestion of a meal, the bile acid pool undergoes at least one
or more enterohepatic cycles, depending on the size and composition
Interlobular bile ducts coalesce to form larger septal bile ducts of the meal.
Normally, the bile acid pool circulates ~510times daily
Intestinal absorption of the pool is about 95% efficient
Join to form the right and left hepatic ducts
Fecal loss of bile acids is in the range of 0.20.4 g/d.
In the steady state, this fecal loss is compensated by an equal daily
Unite to form the common hepatic duct. synthesis of bile acids by the liver
o Bile acids returning to the liver suppress de novo hepatic
synthesis of primary bile acids from cholesterol by inhibiting
Joined by the cystic duct of the gallbladder to form the common bile duct cholesterol 7-hydroxylase.
(CBD) Maximum rate of synthesis is ~5 g/d, which may be insufficient to
replete the bile acid pool size when there is pronounced impairment
of intestinal bile salt reabsorption.
Enters the duodenum (often after joining the main pancreatic duct) through
the ampulla of Vater.
Hepatic bile Sphincter of Oddi offers a high-pressure zone of resistance to bile
o Isotonic fluid with an electrolyte composition resembling plasma flow from the CBD into the duodenum during fasting
Gallbladder bile This tonic contraction serves to:
o Electrolyte composition differs from hepatic bile o Prevent reflux of duodenal contents into the pancreatic and bile
o Most of the inorganic anions, chloride and bicarbonate, have ducts
been removed by reabsorption across the gallbladder epithelium. o Promote filling of the gallbladder.
o As a result of water reabsorption, total solute concentration of The major factor controlling the evacuation of the gallbladder is the
bile increases from34 g/dL in hepatic bile to 1015 g/dL in hormone cholecystokinin (CCK)
gallbladder bile. o Released from the duodenal mucosa in response to the ingestion
Major solute components of bile: of fats and amino acids
o Bile acids (80%) o Produces (1) powerful contraction of the gallbladder, (2)
o Lecithin and traces of other phospholipids (16%) decreased resistance of the sphincter of Oddi, and (3) enhanced
o Unesterified cholesterol (4.0%) flow of biliary contents into the duodenum.
o In lithogenic state, the cholesterol can be as high as 810% o The normal capacity of the gallbladder is ~30 mL of bile.
Total daily basal secretion of hepatic bile: ~500600 mL
Three mechanisms important in regulating bile flow DISEASES OF THE GALLBLADDER
1. Active transport of bile acids from hepatocytes into the bile canaliculi
2. Active transport of other organic anions
3. Cholangiocellular secretion Phrygian cap is a clinically innocuous entity in which a partial or
complete septum (or fold) separates the fundus from the body.
Floating gallbladder predisposes to acute torsion, volvulus, or
herniation of the gallbladder.
Primary bile acids: Cholic acid and Chenodeoxycholic acid
Synthesized from cholesterol in the liver 2. GALLSTONES
Conjugated with glycine or taurine, and secreted into the bile. EPIDEMIOLOGY AND PATHOGENESIS
Secondary bile acids: Deoxycholate and lithocholate Gallstones are quite prevalent in most western countries.
Formed in the colon as bacterial metabolites of the primary bile acids. Divided into two major types:
Cholesterol stones account(>80% of total)



o Usually contain >50% cholesterol monohydrate plus an It is thought to cause a gain of function of the cholesterol
admixture of calcium salts, bile pigments, and proteins. transporter and to contribute to cholesterol hypersecretion.
Pigment stones (<20%) Impaired hepatic conversion of cholesterol to bile acids may also
o Composed primarily of calcium bilirubinate occur, resulting in an increase of the lithogenic cholesterol/bile acid
o They contain <20% cholesterol and are classified into black ratio
and brown types, the latter forming secondary to chronic Hyposecretion of bile acids or phospholipids may contribute.
biliary infection.
2-3 times more common in females than in males After the mechanisms stated above, you now have supersaturation of
Prevalence higher in those >50 years old (25-30%) bile with cholesterol, however this is not sufficient by itself to produce
cholesterol precipitation. Most individuals with supersaturated bile do
ETHNIC PREDISPOSITON not develop stones because the time required for cholesterol
Pima-Indians extremely high-risk population; 70% of crystals to nucleate and grow is longer than the time bile spends
women have gallstones after age of 25 in the gallbladder.
Scandinavians develop gallstone disease by age 50 An important mechanism is nucleation of cholesterol monohydrate
Lowest risk: sub-Saharan Africa & Asia crystals
First-degree relatives of index cases are 4.5 times o Either an excess of pronucleating factors or a deficiency of anti-
more likely to develop gallstones nucleating factors
Mucin and immunoglobulins, appear to be pronucleating
Apolipoproteins A-I and A-II and other glycoproteins
Categorized based on composition:
appear to be ant nucleating factors.
Cholesterol o Continued growth of the crystals occurs by direct nucleation of
Black pigment cholesterol molecules from supersaturated biliary vesicles.
Brown pigment Another important mechanism in cholesterol gallstone formation is
gallbladder hypomotility
Most common type Biliary sludge
Purely cholesterol or have cholesterol as the major Is a thick, mucous material that, upon microscopic examination,
chemical constituent reveals lecithin-cholesterol liquid crystals, cholesterol monohydrate
Mixed cholesterol stones slightly more common than crystals, calcium bilirubinate, and mucin gels.
pure cholesterol stone Forms a crescent-like layer in the most dependent portion of the
Risk factors gallbladder and is recognized by characteristic echoes on
o Older age (40s-50s) ultrasonography
o Female gender (Estrogen) The presence of biliary sludge implies two abnormalities:
o Obesity: BMI > 45 kg/m2 has 7-fold increased o (1) the normal balance between gallbladder mucin secretion and
risk elimination has become deranged
o Weight loss (Drastic) o (2) Nucleation of biliary solutes has occurred.
o TPN Precursor form of gallstone disease
o Pregnancy Can develop with disorders that cause gallbladder hypomotility; i.e.,
o Drugs: clofibrate, oral contraceptives, estrogen surgery, burns, total parenteral nutrition, pregnancy, and oral
contraceptivesall of which are associated with gallstone formation.
treatment, progestogens, ceftriaxone, octreotide
o Genetic predisposition
Cholelithogenic state during Pregnancy:
o Diseases of the terminal ileum Caused by:
o Lipid profile: decreased HDL, increased Marked increase in cholesterol saturation of bile during the 3rd
triglycerides, apolipoprotein E-4(Previously, total trimester
cholesterol was the focus but recently it was known that increased
Sluggish gallbladder contraction in response to a standard meal,
triglycerides is one of the risk factor for Non-alcoholic fatty liver
resulting in impaired gallbladder emptying.
disease (NAFLD) which can lead to cirrhosis)
Although biliary sludge is a common finding during pregnancy, it is
usually asymptomatic and often resolves spontaneously after delivery.
Formation Cholesterol stones and biliary sludge
An excess of cholesterol in relation to phospholipids and bile acids 1020% of persons with rapid weight reduction achieved through
causes unstable, cholesterol-rich vesicles to remain very low calorie dieting develop gallstones.
These vesicles aggregate into large multilamellar vesicles from which .
cholesterol crystals precipitate Summary:
Cholesterol gallstone disease occurs because of several defects, which
include (1) bile supersaturation with cholesterol, (2) nucleation of
cholesterol monohydrate with subsequent crystal retention and stone
growth, and (3) abnormal gallbladder motor function with delayed
emptying and stasis.

Account for 10-25% in the US population; higher
percentage in Asians
Pigmented as a result of bilirubin precipitation
Black pigment stones
o Composed of either pure calcium bilirubinate or polymer-like
complexes with calcium and mucin glycoproteins.
o More common in patients who have chronic hemolytic states
(with increased conjugated bilirubinin bile), liver cirrhosis,
Gilberts syndrome, or cystic fibrosis.
o Gallbladder stones in patients with ileal diseases, ileal resection, or
ileal bypass generally are also black pigment stones.
Mechanisms in the formation of lithogenic (stone-forming) bile: o Rarely displaced to the CBD because it is heavy
The most important is increased biliary secretion of cholesterol. Brown pigment stones
o Occur in association with obesity, the metabolic syndrome, high- o Composed of calcium salts of unconjugated bilirubin with varying
caloric and cholesterol-rich diets, or drugs (e.g., clofibrate) amounts of cholesterol and protein
Genetic factors play an important role in gallstone disease. o Caused by the presence of increased amounts of unconjugated,
o A single nucleotide polymorphism of the gene encoding the insoluble bilirubin in bile that precipitates to form stones.
hepatic cholesterol transporter ABCG5/G8 has been found in o Especially prominent in Asians and is often associated with
21% of patients with gallstones infections in the gallbladder and biliary tree



o Common where biliary infection are more Failure to image the gallbladder in the presence of biliary ductal
prevalent; can occur in the gallbladder or in the visualization may indicate cystic duct obstruction, acute or
biliary tree; also associated with duodenal chronic cholecystitis, or surgical absence of the organ.
diverticula; more like to form de novo in bile ducts Indicated in the diagnosis of acute cholecystitis.
Useful in diagnosis of acalculouscholecystopathy
1. Ultrasonography of the gallbladder Accurate identification of cystic duct obstruction
ADVANTAGES: Simultaneous assessment of bile ducts
Procedure of choice for the detection of stones
Rapid 6. Cholescintigraphy
Very accurate in the identification of cholelithiasis (>95%) Radionuclide-based imaging test of GB & biliary
Stones as small as 1.5 mm in diameter may be confidently tract
identified Most useful in patients suspected of acute
Simultaneous scanning of GB, liver, bile ducts, pancreas cholecystitis
Biliary sludge typically forms a layer in the most dependent By demonstrating the cystic duct, can rapidly (less
position of the gallbladder. This layer shifts with postural changes than or equal to 90 minutes) exclude acute
but fails to produce acoustic shadowing; these two characteristics cholecystitis (Advantage: faster diagnosis)
distinguish sludges from gallstones. Serial scans after injection show radioactivity in
Used to assess the emptying function of the gallbladder. GB, CBD, & small bowel within 30-60 minutes
Principal imaging modality Positive scan: non-visualization of GB with
Diagnosis: echogenic objects within the lumen of preserved excretion into the CBD or small bowel
gallbladder that produce an acoustic shadow 7. ERCP (Diagnostic and Therapeutic)
usually mobile and congregate in the dependent Gold standard for the diagnosis of
portion of gallbladder choledocholithiasis
Able to detect as small as 2 mm stones Water-soluble dye is injected into the CBD &
Overall sensitivity for detecting stone is > 95% for pancreatic duct
stones larger than 2 mm CBD stones can be detected with sensitivity of
Specificity >95% when stones are seen with an approximately 95%
accompanying acoustic shadow Therapeutic potential: if stone is in an accessible
Gold standard for diagnosis of gallstones in location, you can take the stone out through ERCP
Sonographic Murphys sign: positive predictive 8. CT & MRI
value of > 90% in detecting acute cholecystitis if Main use lies in the detection of complications of
gallstone is present gallstones
Murphys sign: sudden cessation of inspiration Pericholecystic fluid in patients with acute
while you are pressing on RUQ cholecystitis
Gas in GB wall with emphysematous cholecystitis
LIMITATIONS: Perforation of GB
Bowel gas, Massive Obesity and Ascites Abscess formation
Spiral CT & MR cholangiography have the
2. ENDOSCOPIC ULTRASOUND advantage over ERCP of being non-invasive, but
Has the advantage of visualizing the CBD have no therapeutic potential
Positive predictive value of 98% & a negative
predictive value of 88% for the diagnosis of CBD SYMPTOMS OF GALLSTONE DISEASE
stones using ERCP as the gold standard Two mechanisms:
Obstruction of cystic duct or CBD
3. Plain abdominal film/radiography Erosion of gallbladder wall
Symptoms are caused either by inflammation or obstruction
Low cost and readily available following migration into the cystic duct or CBD
May detect gallstones containing sufficient calcium to be Asymptomatic stone 75%
radiopaque (1015% of cholesterol and ~50% of pigment
Stone intermittently obstructing cystic duct causing
intermittent biliary colic 20%
Used in the diagnosis of emphysematous cholecystitis, porcelain
Stone impacted in cystic duct causing acute
gallbladder, limey bile, and gallstone ileus
LIMITATIONS: cholecystitis 10%
Stone in cystic duct compressing CBD (Mirizzis
Relatively low yield
syndrome) - <0.1%
4. Oral cholecystography (OCG) Stone impacted in distal CBD 5%
Useful procedure for the diagnosis of gallstones but has been Stone eroding thru the gallbladder into duodenum,
replaced by ultrasound and is regarded as obsolete. resulting in cholecysenteric fistula (gallstone ileus) -
May be used to assess the patency of the cystic duct and < 0.1%
gallbladder emptying function. Long-standing cholelithiasis gallbladder carcinoma
Can also delineate the size and number of gallstones and Vast majority are asymptomatic & rarely warrants
determine whether they are calcified. intervention except
A secondary means of identifying GB stones o Sickle cell anemia
Can be used in Unusual cases in which the GB o Amerindian ancestry high risk for CA
cannot be identified sonographically (e.g. o Awaiting organ transplantation
contracted GB full of stones) o Porcelain gallbladder gallbladder CA
To determine if cystic duct is obstructed esp. in o Planning prolonged space travel or extremely
patients with medical dissolution of stone or remote assignments.
lithotripsy is under consideration The most specific and characteristic symptom is biliary colic
Ingest oral agent which is taken up by the liver o Obstruction of the cystic duct or CBD by a stone produces
increased intraluminal pressure and distention of the viscus that
and secreted into the bile & concentrated in the
cannot be relieved by repetitive biliary contractions.
o The resultant visceral pain is characteristically a severe, steady
When GB has opacified, sensitivity & specificity for ache or fullness in the epigastrium or RUQ of the abdomen with
detection of stone are approx. 90% frequent radiation to the interscapular area, right scapula, or
5. Radioisotope Scans (HIDA, DIDA, DISIDA, etc.) o Biliary colic begins quite suddenly and may persist with severe
intensity for 15 min to 5 h, subsiding gradually or rapidly.

o It is steady rather than intermittent as would be suggested by the o (2) The presence of a prior complication of gallstone disease, i.e.,
word colic (misnomer) history of acute cholecystitis, pancreatitis, gallstone fistula, etc.
An episode of biliary pain persisting beyond 5 h should raise the o (3) The presence of an underlying condition predisposing the
suspicion of acute cholecystitis patient to increased risk of gallstone complications (e.g., calcified
Nausea and vomiting frequently accompany episodes of biliary pain. or porcelain gallbladder and/or a previous attack of acute
An elevated level of serum bilirubin and/or alkaline phosphatase cholecystitis regardless of current symptomatic status).
suggests a common duct stone. Patients with very large gallstones (>3 cm) and patients having
Fever or chills (rigors) with biliary pain usually imply a complication, gallstones in a congenitally anomalous gallbladder might also be
i.e., cholecystitis, pancreatitis, or cholangitis. considered for prophylactic cholecystectomy.
Biliary colic may be precipitated by eating a fatty meal, by Laparoscopic cholecystectomy
consumption of a large meal following a period of prolonged fasting, o Its advantages include a markedly shortened hospital stay,
or by eating a normal meal; it is frequently nocturnal, occurring minimal disability, as well as decreased cost, and it is the
within a few hours of retiring. procedure of choice for most patients referred for elective
o From several studies, the following key points emerge:
(1) complications develop in ~4% of patients
Most common clinical manifestation of gallstone
(2) conversion to laparotomy occurs in 5%
disease (3) The death rate is remarkably low (i.e., <0.1%)
Upper abdominal pain usually in the epigastrium or (4) Bile duct injuries are unusual (i.e., 0.20.5%) but more
RUQ frequent than with open cholecystectomy.
Precipitated by a meal, but more commonly there is o These data indicate why laparoscopic cholecystectomy has
no inciting event become the gold standard for treating symptomatic
Steady rather than intermittent cholelithiasis.
Gradually increases over a period of 15 minutes to 1
hour; then remains at a plateau for about an hour MEDICAL THERAPYGALLSTONE DISSOLUTION
before going away Ursodeoxycholicacid (UDCA)
Pain lasting more than 6 hours suggest acute o Decreases cholesterol saturation of bile
cholecystitis o Produce a lamellar liquid crystalline phase in bile that allows a
Location of pain: epigastrium>RUQ>LUQ>various dispersion of cholesterol from stones by physical chemical means.
part of precordium or lower abdomen o May also retard cholesterol crystal nucleation.
o 50% of patients with a functioning gallbladder and with
PE usually normal (If (+) abnormal finding in PE
radiolucent stones <10 mm in diameter, achieve complete
cholelithiasis) dissolution within6 months to 2 years.
o Should be limited to radiolucent stones smaller than 5 mm in
Majority are asymptomatic and remain so o The dose of UDCA should be1015 mg/kg per day.
o Asymptomatic (Majority) o Stones larger than 15 mm in size rarely dissolve.
Initial presenting complaint in 90% is biliary o Pigment stones are not responsive to UDCA therapy.
pain & not a biliary complication o In addition to the vexing problem of recurrent stones (3050%
Incidence of complication is low & prophylactic over 35 years of follow-up), there is also the factor of taking an
removal of gallbladder is not necessary expensive drug for up to 2 years.
o Symptomatic (Minority) o The advantages and success of laparoscopic cholecystectomy
Risk of developing biliary complication is have largely reduced the role of gallstone dissolution
o Patients with cholesterol gallstone disease who develop recurrent
estimated to be 1-2% per year & remains
choledocholithiasis after cholecystectomy should be on long-term
constant over time treatment with ursodeoxycholic acid.
Cholecystectomy offered to patients with
significant biliary symptoms
As many as 30% with one episode of pain will
not have a recurrent episode
Gallstone disease discovered in an asymptomatic patient or in a Most frequent complication of gallstone disease
patient whose symptoms are not referable to cholelithiasis is a Due to inflammation of GB wall
common clinical problem. 90% cause is gallstone obstructing the cystic duct
Patients remaining asymptomatic for 15 years were found to be 10% cases no stones; acalculouscholecystitis
unlikely to develop symptoms during further follow-up Occurs when stone becomes impacted in the cystic
Decision analysis has suggested that (1) the cumulative risk of death duct, causing chronic obstruction
due to gallstone disease while on expectant management is small, and If no stones found may be due to:
(2) prophylactic cholecystectomy is not warranted. o Vasculitis
Complications requiring cholecystectomy are much more common in o Cholesterol emboli
gallstone patients who have developed symptoms of biliary pain. Obstruction causes stasis of bile & damage to GB
Patients with diabetes mellitus and gallstones may be somewhat more mucosa
susceptible to septic complications, but the magnitude of risk of Bacteria not thought to contribute to actual onset of
septic biliary complications in diabetic patients is incompletely acute cholecystitis
defined. Antibiotics given in cases of suspected GB
Doctors must be more watchful with diabetic patients because they perforation, gangrene, or in patients with toxic
are considered immunocompromised presentation including fever > 102 F
Must manage with or without symptoms Inflammatory response can be evoked by three factors:
Incidental cholelithiasis is considered to be associated with increased o (1) mechanical inflammation produced by increased intraluminal
risk of serious complication even though asymptomatic pressure and distention with resulting ischemia of the gallbladder
Natural history follows same pattern observed in non-diabetics mucosa and wall
Mortality & complication rates comparable to those of other o (2) chemical inflammation caused by the release of lysolecithin
published studies (due to the action of phospholipase on lecithin in bile) and other
Prophylactic cholecystectomy is generally not recommended for local tissue factors
diabetics o (3) bacterial inflammation, which may play a role in 5085%of
patients with acute cholecystitis
TREATMENT OF GALLSTONE DISEASE Most frequently isolated by culture of gallbladder bile
SURGICAL THERAPY include Escherichia coli , Klebsiella spp., Streptococcus spp.,
and Clostridium spp.
A recommendation for cholecystectomy in a patient with gallstones
should probably be based on assessment of three factors:
o (1) The presence of symptoms that are frequent enough or severe Signs and Symptoms
enough to interfere with the patients general routine 75% had prior attack of biliary colic

Pain lasting for > 6 hours MEDICAL THERAPY

Pain localized in the RUQ For the period of in-hospital stabilization required before
Fever is common (low-moderate grade); usually < cholecystectomy
102 F unless gangrene or perforation has occurred Meperidine or NSAIDs for analgesia; may produce less spasm of the
20% mildly jaundiced sphincter of Oddi than drugs such as morphine.
Murphys sign Intravenous antibiotic therapy is usually indicated in patients with
Natural history of untreated cases severe acute cholecystitis
resolution of pain within 7-10 days Antibiotic therapy is guided by the most common organisms likely to
10% localized perforation be present, which are E. coli, Klebsiella spp., and Streptococcus spp.
1% free perforation & peritonitis Anaerobic coverage by a drug such as metronidazole should be added
Acute cholecystitis often begins as an attack of biliary pain that if gangrenous or emphysematous cholecystitis is suspected.
progressively worsens. Imipenem/meropenem represent potent parenteral antibiotics that
o Approximately 6070% of patients report having experienced cover the whole spectrum of bacteria causing ascending cholangitis.
prior attacks that resolved spontaneously.
o As the episode progresses, pain becomes more generalized in the SURGICAL THERAPY
RUQ The optimal timing of surgical intervention in patients with acute
o May radiate to the interscapular area, right scapula, or shoulder. cholecystitis depends on stabilization of the patient.
Peritoneal signs of inflammation such as increased pain with jarring The clear trend is toward earlier surgery
or on deep respiration may be apparent. Urgent (emergency) cholecystectomy or cholecystostomy is
Patient is anorectic and often nauseated. appropriate in most patients in whom a complication of acute
Vomiting is relatively common and may produce symptoms and signs cholecystitis such as empyema, emphysematous cholecystitis, or
of vascular and extracellular volume depletion. perforation is suspected or confirmed.
Jaundice is unusual early in the course disease but may occur when Patients with uncomplicated acute cholecystitis should undergo early
edematous inflammatory changes involve the bile ducts and elective laparoscopic cholecystectomy, ideally within 72 hours after
surrounding lymph nodes. diagnosis.
A low-grade fever is characteristically present, but shaking chills or Prognosis
rigors are not uncommon Approximately 75% of patients treated medically have remission of
The RUQ of the abdomen is almost invariably tender to palpation. acute symptoms within 27 days following hospitalization.
An enlarged, tense gallbladder is palpable in 2550% of patients. In 25%, a complication of acute cholecystitis will occur despite
Deep inspiration or cough during subcostal palpation of the RUQ conservative treatmentprompt surgical intervention is required.
usually produces increased pain and inspiratory arrest (Murphys Of the 75% of patients with acute cholecystitis who undergo
sign). remission of symptoms, ~25% will experience a recurrence of
Localized rebound tenderness in the RUQ is common, as are cholecystitis within 1 year, and 60% will have at least one recurrent
abdominal distention and hypoactive bowel sounds from paralytic bout within 6 years.
ileus Acute cholecystitis is best treated by early surgery whenever possible.
The diagnosis of acute cholecystitis is usually made on the basis of a
characteristic history and physical examination. Complications
The triad of sudden onset of RUQ tenderness, fever, and Mirizzis syndrome
leukocytosis is highly suggestive.
Stone becomes impacted in the neck of GB or cystic

duct & extrinsically compresses the CBD with

Laboratory Findings resulting jaundice & bile duct obstruction
Leukocytosis in the range of 10,00015,000 cells per microliter with a Treatment: open cholecystectomy; endoscopic
left shift on differential count is found. stenting & laparoscopic cholecystectomy
Mildly elevation of serum bilirubin [<85.5 mmol/L (5 mg/dL)] in Pre-op diagnosis is important to avoid CBD injury
fewer than half of patients, while about one-fourth have modest A rare complication in which a gallstone becomes impacted in the
elevations in serum aminotransferases (usually less than a fivefold cystic duct or neck of the gallbladder causing compression of the
elevation). CBD, resulting in CBD obstruction and jaundice.
UTZ will demonstrate calculi in 9095% of cases and is useful for Ultrasound shows gallstone(s) lying outside the hepatic duct.
detection of signs of gallbladder inflammation including: Endoscopic retrograde cholangiopancreatography (ERCP) or
o Thickening of the wall percutaneous transhepatic cholangiography (PTC) or magnetic
o Pericholecystic fluid resonance cholangiopancreatography (MRCP) will usually
o Dilation of the bile duct demonstrate the characteristic extrinsic compression of the CBD.
The radionuclide (e.g., HIDA) biliary scan may be confirmatory if bile Surgery consists of removing the cystic duct, diseased gallbladder, and
duct imaging is seen without visualization of the gallbladder. the impacted stone.
DIAGNOSIS OF ACUTE CHOLECYSTITIS The preoperative diagnosis of Mirizzis syndrome is important to
Sonographic Murphys sign avoid CBD injury.
GB wall thickening to > 4 mm
Ability to exclude acute cholecystitis a. Acalculouscholecystitis
Cholescin- 510% of patients with acute cholecystitis, have no calculi found
allow to focus on non-biliary causes
tigraphy obstructing the cystic duct at surgery.
of acute abdominal pain
An increased risk for the development of acalculouscholecystitis is
Used to confirm presence of
especially associated with:
Abdominal complication such as o Serious trauma or burns
CT scan emphysematous cholecystitis or o The postpartum period following prolonged labor
perforation of GB o Orthopedic and other non-biliary major surgical operations in the
postoperative period.
TREATMENT OF ACUTE CHOLECYSTITIS Other precipitating factors include:
IV fluids & electrolyte correction o Vasculitis, obstructing adenocarcinoma of the gallbladder,
NPO: to rest the GB diabetes mellitus, torsion of the gallbladder, unusual bacterial
NGT should be inserted if with abdominal distention infections of the gallbladder
or persistent vomiting o Acalculouscholecystitis may also be seen with a variety of other
Antibiotics: reserved for complicated cases systemic disease processes
o Toxic-appearing The setting of acute gallbladder inflammation complicating
o Perforation of GB severe underlying illness is characteristic of acalculous disease.
o Emphysematous cholecystitis UTZ, CT, or radionuclide examinations demonstrating a large,
Definitive treatment: cholecystectomy tense, static gallbladder without stones and with evidence of poor
emptying over a prolonged period may be diagnostically useful in
some cases.



The complication rate for acalculouscholecystitis exceeds that for Emergency surgical intervention with proper antibiotic coverage is
calculouscholecystitis. required as soon as the diagnosis is suspected.
Successful management of acute acalculouscholecystitis appears to
depend primarily on early diagnosis and surgical intervention, with 2. Hydrops/Mucocele
meticulous attention to postoperative care. Also result from prolonged obstruction of the cystic duct, usually by
a large solitary calculus.
b. Acalculouscholecystopathy The obstructed gallbladder lumen is progressively distended, over a
Disordered motility of the gallbladder can produce recurrent biliary period of time, by mucus (mucocele) or by a clear transudate
pain in patients without gallstones. (hydrops) produced by mucosal epithelial cells.
The following criteria can be used to identify patients with A visible, easily palpable, non-tender mass sometimes extending from
acalculouscholecystopathy: the RUQ into the right iliac fossa may be found on physical
recurrent episodes of typical RUQ pain characteristic of biliary tract examination.
pain Patient frequently remains asymptomatic, although chronic RUQ
Abnormal CCK cholescintigraphy demonstrating a gallbladder pain may also occur.
ejection fraction of<40% Cholecystectomy is indicated, because empyema, perforation, or
Infusion of CCK reproduces the patients pain. gangrene may complicate the condition.
Large gallbladder on ultrasound examination.
3. Gangrene and perforation
Sphincter of Oddi dysfunction can also give rise to recurrent RUQ
Gangrene results from ischemia of the wall and patchy or complete
pain and CCK-scintigraphic abnormalities.
tissue necrosis.
Underlying conditions often include marked distention of the
c. Emphysematous cholecystitis
gallbladder, vasculitis, diabetes mellitus, empyema, or torsion
Gas-forming organisms have secondarily infected the
Gangrene usually predisposes to perforation of the gallbladder, but
GB wall perforation may also occur in chronic cholecystitis without
prone to rupture peritonitis premonitory warning symptoms.
Pockets of gas evident in the area of GB fossa on Localized perforations are usually contained by the omentum or by
sonography, plain abdominal film, or abdominal CT adhesions produced by recurrent inflammation of the gallbladder.
Scan Bacterial superinfection of the walled-off gallbladder contents results
Treatment: anaerobic coverage & early in abscess formation.
cholecystectomy Most patients are best treated with cholecystectomy
Risk of perforation is high Some seriously ill patients may be managed with cholecystostomy and
Common in diabetics or older men without gallstones drainage of the abscess.
o Atherosclerosis of cystic artery with resulting Free perforation is less common but is associated with a mortality
ischemia rate of ~30%.
Thought to begin with acute cholecystitis (calculous or acalculous) Patients may experience a sudden transient relief of RUQ pain as the
followed by ischemia or gangrene of the gallbladder wall and distended gallbladder decompresses; this is followed by signs of
infection by gas-producing organisms. generalized peritonitis.
Bacteria most frequently cultured include anaerobes, such as C.
welchii or C. perfringens, and aerobes, such as E. coli. 4. Fistula formation and gallstone ileus
Occurs most frequently in elderly men and in patients with diabetes Fistulization into an adjacent organ adherent to the gallbladder wall
mellitus. may result from inflammation and adhesion formation.
Clinical manifestations are indistinguishable from those of Fistulas into the duodenum are most common
nongaseous cholecystitis. Followed in frequency by: Hepatic flexure of the colon, stomach or
The diagnosis is usually made on plain abdominal film by finding gas jejunum, abdominal wall, and renal pelvis.
within the gallbladder lumen, dissecting within the gallbladder wall to Clinically silent biliary-enteric fistulas occur in 5 % of patients with
form a gaseous ring, or in the pericholecystic tissues. acute cholecystitis
Asymptomatic cholecystoenteric fistulas may sometimes be
CHRONIC CHOLECYSTITIS diagnosed by finding gas in the biliary tree on plain abdominal films.
Almost always associated with the presence of gallstones Treatment in the symptomatic patient usually consists of
Thought to result from repeated bouts of subacute or acute cholecystectomy, CBD exploration, and closure of the fistulous tract.
cholecystitis or from persistent mechanical irritation of the Gallstone ileus refers to mechanical intestinal obstruction resulting
gallbladder wall by gallstones. from the passage of a large gallstone into the bowel lumen.
Bacteria in the bile occurs in >25% of patients with chronic Site of obstruction by the impacted gallstone is usually at the ileocecal
cholecystitis. valve
May be asymptomatic for years, may progress to symptomatic The majority of patients do not give a history of either prior biliary
gallbladder disease or to acute cholecystitis, or may present with tract symptoms or complaints
complications Large stones,>2.5 cm in diameter, are thought to predispose to fistula
Intermittent obstruction of cystic duct by one or formation by gradual erosion through the gallbladder fundus.
more stones Diagnostic confirmation may occasionally be found on the plain
abdominal film (e.g., small-intestinal obstruction with gas in the
DIAGNOSIS of CHRONIC CHOLECYSTITIS biliary tree and a calcified, ectopic gallstone)
Sonography: first imaging study preferred; highly Laparotomy with stone extraction (or propulsion into the colon)
sensitive & specific means of establishing presence or remains the procedure of choice to relieve obstruction.
absence of stones in the GB
Oral cholecystography: essential to establish patency Cholecystenteric Fistula
of cystic duct Stone erodes the GB wall (usually the neck) & into a
Meltzer-Lyon Test: examination of aspirated duodenal hollow viscus
bile for the presence of cholesterol or calcium Most common entry point: duodenum, hepatic
bilirubinate crystals flexure of colon, stomach, and jejunum
Symptoms similar to acute cholecystitis
COMPLICATIONS OF CHOLECYSTITIS Diagnosis: suspected on the basis of pneumobilia
1. Empyema on radiographs; confirmed with barium contrast
Empyema results from progression of acute cholecystitis with studies of upper and lower GIT
persistent cystic duct obstruction to superinfection of the stagnant o pneumobilia: presence of air in biliary tree
bile with a pus forming bacterial organism. If stone is > 25 mm, may cause small bowel
Clinical picture resembles cholangitis with high fever; severe RUQ obstruction especially in elderly women at ileocecal
pain; marked leukocytosis; and often, prostration. area causing obstruction
Carries a high risk of gram-negative sepsis and/or perforation.



5. Limey (milk of calcium) bile and porcelain gallbladder o or both

Calcium salts in sufficient concentration may produce calcium Ultrasound, MRC, and CT are of great diagnostic value
precipitation and diffuse, hazy opacification of bile or a layering effect Antibiotic therapy: Limits the frequency and severity of recurrent
on plain abdominal x-ray. (limey bile, or milk of calcium bile) bouts of cholangitis.
Cholecystectomy is recommended when it occurs in a hydropic Progression to secondary biliary cirrhosis with portal hypertension,
gallbladder. extrahepatic biliary obstruction, cholangiocarcinoma, or recurrent
In porcelain gallbladder, calcium salt deposition within the wall of a episodes of sepsis with hepatic abscess formation is common.
chronically inflamed gallbladder may be detected on the plain
abdominal film. 2. CHOLEDOCHOLITHIASIS
Cholecystectomy is advised in all patients with porcelain gallbladder Pathophysiology and clinical manifestations
because in a high percentage of cases is associated with the Occurrence of stones in the CBD
development of carcinoma of the gallbladder. May remain asymptomatic for years
May cause life-threatening complications
Porcelain Gallbladder o Cholangitis
Intramural calcification of GB wall o Pancreatitis
Has a high incidence of developing carcinoma in 20% Occurs in ~1015% of patients with cholelithiasis.
of patients
Incidence of common duct stones increases with increasing age
Diagnosis: plain abdominal film or CT Scan
Majority are cholesterol stones formed in the GB, which then migrate
Treatment: prophylactic cholecystectomy into the extrahepatic biliary tree through the cystic duct.
Primary calculi arising de novo in the ducts are usually pigment
4. THE HYPERPLASTIC CHOLECYSTOSES stones developing in patients with
A group of disorders of the GB characterized by excessive o Hepatobiliary parasitism
proliferation of normal tissue components. o Chronic, recurrent cholangitis
Adenomyomatosis o Congenital anomalies of the bile ducts (especially Carolis disease)
o Benign proliferation of GB surface epith with gland like o Dilated, sclerosed, or strictured ducts
formations, extramural sinuses, strictures, and/or fundal nodule o An MDR3 (ABCB4) gene defect leading to impaired biliary
formation phospholipids secretion (low phospholipidassociated
Cholesterolosis cholelithiasis)
o Abnormal deposition of lipid, especially cholesteryl esters within May remain asymptomatic for years, may pass spontaneously into the
macrophages in the lamina propria of the GB wall. duodenum, or (most often) may present with biliary colic or a
o Diffuse form: (strawberry gallbladder), the GB mucosa is brick complication.
red and speckled with bright yellow flecks of lipid. Clinical manifestations depend on the rate of onset &
o Localized form: solitary or multiple cholesterol polyps studding degree of obstruction & the amount of bacterial
the gallbladder wall.
contamination of the bile
Cholecystectomy is indicated in both adenomyomatosis and o Acute obstruction: causes biliary colic and
cholesterolosis when symptomatic or when cholelithiasis is present.
o Chronic obstruction: develops gradually over
several months may present initially with pruritus
1. CONGENITAL ANOMALIES or jaundice alone
Biliary atresia and Hypoplasia If bacteria proliferates, cholangitis may result
Most common biliary anomalies of clinical relevance in infancy PE is usually completely normal if obstruction is
Clinical picture: Severe obstructive jaundice during the first month of intermittent
life, with pale stools. Rise of bilirubin concentration is proportional to the
Diagnosis is confirmed by surgical exploration and operative degree of obstruction
cholangiography. Increase in ALP has no relationship to either degree
Approximately 10% of cases are treatable with roux-en-Y of obstruction or its cause
choledochojejunostomy o It means there is an obstruction but does not tell
Kasai procedure (hepatic portoenterostomy) is attempted in the the severity
remainder in an effort to restore some bile flow. Transient spikes of transaminases or amylase
Most patients, even those having successful biliary-enteric suggest passage of a CBD stone into the duodenum
anastomoses, eventually develop chronic cholangitis, extensive
hepatic fibrosis, and portal hypertension.
Choledochal cysts May pass from GB to CBD or primarily in the duct
Cystic dilatation involve the free portion of the CBD All gallstones from one patient are of the same type,
Chronic reflux of pancreatic juice into the biliary tree can produce either pigment or cholesterol
inflammation and stenosis of the extrahepatic bile ducts leading to Cholesterol stones only form in the GB; any
cholangitis or biliary obstruction cholesterol stones found in CBD must have migrated
The process is gradual so ~50% of patients present with onset of from the GB
symptoms after age 10. Black pigment stones also form in the GB but rarely
The diagnosis maybe made by ultrasound, abdominal CT, MRC, or migrate into the CBD (heavy weight of black
cholangiography. pigmented stone)
Only one-third of patients show the classic triad of abdominal pain, Brown pigment stones form de novo in the CBD as
jaundice, and an abdominal mass. a result of bacterial action on phospholipid & bilirubin
UTZ detection of a cyst separate from the gallbladder should suggest in bile; frequently associated with cholangitis
the diagnosis of choledochal cyst, which can be confirmed by o 95% of patients with CBD stone also have GB
demonstrating the entrance of extrahepatic bile ducts into the cyst. stone
Surgical treatment involves excision of the cyst and biliary-enteric o Normal pressure in the CBD = 10-15 cmH20
anastomosis. o CBD obstruction = 25-40 cmH20
Patients with choledochal cysts are at increased risk for the o Bile flow decreases at 15 cmH20
subsequent development of cholangiocarcinoma. o Bile flow ceases at 30 cmH20

Congenital biliary ectasia Complications

Dilatation of intrahepatic bile ducts may involve either: Cholangitis
o Major intrahepatic radicles (Carolis disease) May be acute or chronic, and symptoms result from inflammation
Clinical manifestations: Recurrent cholangitis, abscess The characteristic presentation of acute cholangitis involves biliary
formation in and around the affected ducts, and, often, pain, jaundice, and spiking fevers with chills (Charcots triad).
gallstone formation within portions of ectatic intrahepatic
biliary radicles. Blood cultures are frequently positive, and leukocytosis is typical.
o Inter- and intralobular ducts (congenital hepatic fibrosis)

Non-suppurative acute cholangitis is most common; respond to presence of CBD stones

supportive therapy but not definitely
Suppurative acute cholangitis (presence of pus under pressure in a exclude
completely obstructed ductal system) leads to symptoms of severe choledocholithiasis
toxicitymental confusion, bacteremia, and septic shock. Better visualization of
o Response to antibiotics alone in this setting is relatively poor CBD
o Multiple hepatic abscesses are often present Endoscopic Ultrasound
Sensitivity & specificity
o Mortality rate approaches 100% unless prompt endoscopic or
approx. 95%
surgical relief of the obstruction and drainage of infected bile are
carried out. Gold standard for
o ERCP with endoscopic sphincterotomy is safe and the preferred choledocholithiasis
initial procedure for both establishing a definitive diagnosis and Sensitivity & specificity
providing effective therapy. approx. 95%
Can confirm
Obstructive jaundice Percutaneous
Gradual obstruction of the CBD (weeks to months): Initial TranshepaticCholangio-
Accomplished in the
manifestations of jaundice or pruritus without associated symptoms graphy
setting of dilated IHDs
of biliary colic or cholangitis.
Used in the surgical
Painless jaundice may occur Laparoscopic
o But is much more characteristic of biliary obstruction secondary suite prior to
to malignancy mobilization of GB
Associated chronic calculous cholecystitis is very common Diagnosis of choledocholithiasis is usually made by cholangiography
Absence of a palpable gallbladder in most patients with biliary either preoperatively by endoscopic retrogradecholangiogram (ERC)
obstruction from duct stones is the basis for Courvoisiers law or MRCP or intraoperatively at the time of cholecystectomy.
o Courvoisiers Law: The presence of a palpably enlarged Endoscopic removal of CBD stone
gallbladder suggests that the biliary obstruction is secondary to an o Can be performed without the need for
underlying malignancy rather than to calculous disease. cholecystectomy
Obstruction causes progressive dilatation of the intrahepatic bile o Subsequent cholecystectomy for symptoms is
ducts as intrabiliary pressures rise. required in only 10% of patients
Bile flow is suppressed, and reabsorption and regurgitation of When CBD stones are suspected prior to laparoscopic
conjugated bilirubin into the bloodstream lead to jaundice cholecystectomy, preoperative ERCP with endoscopic papillotomy
accompanied by dark urine (bilirubinuria) and light-colored (acholic) and stone extraction is the preferred approach.
stools. CBD stones should be suspected in gallstone patients who have any
CBD stones should be suspected in any patient with cholecystitis of the following risk factors:
whose serum bilirubin level is >85.5 mmol/L (5 mg/dL). o History of jaundice or pancreatitis
The maximum bilirubin level is seldom >256.5 mmol/L (15.0 o Abnormal tests of liver function
mg/dL) in patients with choledocholithiasis unless concomitant o Ultrasonographic or MRCP evidence of a dilated CBD or stones
hepatic disease or another factor exists. in the duct.
Serum bilirubin levels >342.0 mmol/L (20 mg/dL) should suggest Endoscopic Biliary Sphincterotomy followed by spontaneous passage
the possibility of neoplastic obstruction. or stone extraction is the treatment of choice in the management of
Alkaline phosphatase level is almost always elevated in biliary patients with common duct stones, especially in elderly or poor-risk
obstruction. patients.
o Precedes clinical jaundice and may be the only abnormality in 3. TRAUMA, STRICTURES AND HEMOBILIA
routine liver function tests. Most benign strictures result from surgical trauma
There may be a two- to tenfold elevation of serum aminotransferases Strictures may present with bile leak or abscess formation in the
Following relief of the obstruction, serum aminotransferase immediate postoperative period or with biliary obstruction or
elevations usually return rapidly to normal cholangitis as long as 2 years or more following the inciting trauma.
Bilirubin level may take12 weeks to return to normal. When positive exfoliative cytology is obtained, the diagnosis of a
Alkaline phosphatase level usually falls slowly, lagging behind the neoplastic stricture is established.
decrease in serum bilirubin. o Especially important in patients with primary sclerosing
cholangitis (PSC) who are predisposed to cholangiocarcinomas.
Pancreatitis Hemobilia may follow traumatic or operative injury to the liver or
bile ducts, intraductal rupture of a hepatic abscess or aneurysm of the
The most common associated entity discovered in patients with
hepatic artery, biliary or hepatic tumor hemorrhage, or mechanical
nonalcoholic acute pancreatitis is biliary tract disease.
complications of choledocholithiasis or hepatobiliary parasitism.
The common factor appears to be the passage of gallstones through
Patients often present with a classic triad of biliary pain, obstructive
the common duct.
jaundice, and melena or occult blood in the stools.
Coexisting pancreatitis should be suspected in patients with
Although minor episodes of hemobilia may resolve without operative
symptoms of cholecystitis who develop:
intervention, surgical ligation of the bleeding vessel is frequently
o (1) back pain or pain to the left of the abdominal midline
o (2) prolonged vomiting with paralytic ileus
o (3) A pleural effusion, especially on the left side.
Surgical treatment of gallstone disease is usually associated with 4. EXTRINSIC COMPRESSION OF THE BILE DUCTS
resolution of the pancreatitis. The most common cause is carcinoma of the head of the pancreas.
May also occur as a complication of either acute or chronic
Secondary biliary cirrhosis pancreatitis or involvement of lymph nodes in the portahepatis by
lymphoma or metastatic carcinoma.
More common in cases of prolonged obstruction from stricture or
neoplasm. The latter should be distinguished from cholestasis resulting from
May be progressive even after correction of the obstructing process massive replacement of the liver by tumor.
Increasingly severe hepatic cirrhosis may lead to portal hypertension
or to hepatic failure and death. 5. HEPATOBILIARY PARASITISM
Prolonged biliary obstruction may also be associated with deficiencies Infestation of the biliary tract by adult helminths or their ova may
of the fat-soluble vitamins A, D, E, and K. produce a chronic, recurrent pyogenic cholangitis with or without
multiple hepatic abscesses, ductal stones, or biliary obstruction.
Organisms most commonly involved are trematodes or flukes,
Diagnosis and treatment
including Clonorchis sinensis, Opisthorchis viverrini or O. felineus ,
and Fasciola hepatica
Dilatation of CBD > 6
The biliary tract also may be involved by intraductal migration of
mm in diameter seen in adult Ascaris lumbricoides or by intrabiliary rupture of hydatid cysts
Sonography approx. 75% of the liver produced by Echinococcus spp.
Can be used to confirm Diagnosis: cholangiography and ova on stool examination.
or at least suggest the

When obstruction is present, the treatment of choice is laparotomy DIAGNOSIS

under antibiotic coverage, with common duct exploration and a Ultrasound: choledocholithiasis seen in approx.
biliary drainage procedure.
50% of cases; can be inferred by the finding of a
dilated CBD in 75% of cases
6. SCLEROSING CHOLANGITIS CT Scan: useful in excluding existence of stones in
Primary or idiopathic sclerosing cholangitis is characterized by a CBD
progressive, inflammatory, sclerosing, and obliterative process
ERCP: Gold standard in the diagnosis of CBD
affecting the extrahepatic and/or the intrahepatic bile ducts.
Occurs up to 75% in association with IBS, especially ulcerative colitis.
May also be associated with autoimmune pancreatitis
Patients often present with signs and symptoms of chronic or
intermittent biliary obstruction: RUQ abdominal pain, pruritus, Antibiotics
jaundice, or acute cholangitis. o Mild cases: single drug is sufficient
Late in the course, complete biliary obstruction, secondary biliary o Severe cases: more intensive therapy
cirrhosis, hepatic failure, or portal hypertension with bleeding varices Improvement should be expected within 6-12 hours
may occur. o How to tell if there is an improvement?
Diagnosis: Multifocal, diffusely distributed strictures with intervening o Lysis of fever
segments of normal or dilated ducts, producing a beaded appearance o improvement of sensorium
on cholangiography o decreased pain
The cholangiographic techniques of choice in suspected cases are o stabilization of BP
MRCP and ERCP. In most cases infection will come under control
When a diagnosis has been established, a search for associated within 2-3 days with defervescence, relief of
diseases should be carried out. discomfort, & decreased WBC count
Small duct PSC is defined by the presence of chronic cholestasis and If after 6-12 hours clinical status is declining with
hepatic histology consistent with PSC but with normal findings on worsening fever, pain, mental confusion or
cholangiography. hypotension, CBD must be decompressed on
o May represent an earlier stage of PSC associated with a emergency basis
significantly better long-term prognosis. ERCP with stone extraction or at least decompression
o May progress to classic PSC and/or end-stage liver disease with of bile duct is the treatment of choice
consequent necessity of liver transplantation.
Must contain and subside the infection with-in 24
hours before operation can be done
Therapy with cholestyramine may help control symptoms of pruritus
Antibiotics are useful when cholangitis complicates the clinical
Vitamin D and calcium supplementation may help prevent the loss of
bone mass frequently seen in patients with chronic cholestasis.
In cases where high-grade biliary obstruction (dominant strictures)
has occurred, balloon dilatation or stenting may be appropriate.
Only rarely is surgical intervention indicated.
The prognosis is unfavorable, with a median survival of 9 to 12 years
following the diagnosis, regardless of therapy.
Four variables (age, serum bilirubin level, histologic stage, and
splenomegaly) predict survival in patients with PSC and serve as the
basis for a risk score.
PSC is one of the most common indications for liver transplantation.

85% - impacted stone in CBD
Others: neoplasm, biliary stricture, parasitic
infection, congenital abnormalities of bile ducts
Bile duct obstruction is necessary but not sufficient
to cause cholangitis
Most likely to result when a bile duct that already
contains bacteria becomes obstructed; common with
choledocholithiasis & stricture
Malignant obstruction more complete than due to
stricture or CBD stones; less commonly permits
reflux of bacteria from duodenal contents
Most common bacteria: Escherichia coli, Klebsiella,
Pseudomonas, enterococcus, Proteus, anaerobic
bacteria such as Bacillus fragilis or Clostridium

Charcots triad: pain, jaundice & fever
o hallmark & present only in 70% of cases
Accompanied by chills & rigors
o Fever in 95%
o RUQ tenderness in 90%
o Jaundice in 80%
o Hypotension & mental confusion in severe cases