2.

01c
Diseases of the Gallbladder and Bile
Ducts
Dr. Carabeo
09/28/16

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
~3:1.
D. Gallbladder and Sphincteric Functions
II. DISEASES OF THE GALLBLADDER
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
PHYSIOLOGY OF BILE PRODUCTION AND FLOW colon.
BILE SECRETION AND COMPOSITION
ENTEROHEPATIC CIRCULATION
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.
GALLBLADDER AND SPHINCTERIC FUNCTIONS
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
1. CONGENITAL ANOMALIES
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
THE BILE ACIDS
herniation of the gallbladder.
Primary bile acids: Cholic acid and Chenodeoxycholic acid
(CDCA)
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)

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o Usually contain >50% cholesterol monohydrate plus an
admixture of calcium salts, bile pigments, and proteins.
Pigment stones (<20%)
o Composed primarily of calcium bilirubinate
o They contain <20% cholesterol and are classified into black
and brown types, the latter forming secondary to chronic
biliary infection.
2-3 times more common in females than in males
Prevalence higher in those >50 years old (25-30%)
ETHNIC PREDISPOSITON
Pima-Indians extremely high-risk population; 70% of
women have gallstones after age of 25
Scandinavians develop gallstone disease by age 50
Lowest risk: sub-Saharan Africa & Asia
First-degree relatives of index cases are 4.5 times
more likely to develop gallstones
MORPHOLOGY & COMPOSITION OF GALLSTONES
Categorized based on composition:
Cholesterol
Black pigment
Brown pigment
CHOLESTEROL STONES
Most common type
Purely cholesterol or have cholesterol as the major
chemical constituent
Mixed cholesterol stones slightly more common than
pure cholesterol stone
Risk factors
o Older age (40s-50s)
o Female gender (Estrogen)
o Obesity: BMI > 45 kg/m2 has 7-fold increased
risk
o Weight loss (Drastic)
o TPN
o Pregnancy
o Drugs: clofibrate, oral contraceptives, estrogen
treatment, progestogens, ceftriaxone, octreotide
o Genetic predisposition
o Diseases of the terminal ileum
o Lipid profile: decreased HDL, increased
triglycerides, apolipoprotein E-4(Previously, total
cholesterol was the focus but recently it was known that increased
triglycerides is one of the risk factor for Non-alcoholic fatty liver
disease (NAFLD) which can lead to cirrhosis)
Formation Cholesterol stones and biliary sludge
An excess of cholesterol in relation to phospholipids and bile acids
causes unstable, cholesterol-rich vesicles to remain
These vesicles aggregate into large multilamellar vesicles from which
cholesterol crystals precipitate
Mechanisms in the formation of lithogenic (stone-forming) bile:
The most important is increased biliary secretion of cholesterol.
o Occur in association with obesity, the metabolic syndrome, high-
caloric and cholesterol-rich diets, or drugs (e.g., clofibrate)
Genetic factors play an important role in gallstone disease.
o A single nucleotide polymorphism of the gene encoding the
hepatic cholesterol transporter ABCG5/G8 has been found in
21% of patients with gallstones
COMISO, DE DIOS, DE MANUEL, GONZAGA, GONZALES, KIM,
MACASIPOT, QUINAJON
2.01c
It is thought to cause a gain of function of the cholesterol
transporter and to contribute to cholesterol hypersecretion.
Impaired hepatic conversion of cholesterol to bile acids may also
occur, resulting in an increase of the lithogenic cholesterol/bile acid
ratio
Hyposecretion of bile acids or phospholipids may contribute.
After the mechanisms stated above, you now have supersaturation of
bile with cholesterol, however this is not sufficient by itself to produce
cholesterol precipitation. Most individuals with supersaturated bile do
not develop stones because the time required for cholesterol
crystals to nucleate and grow is longer than the time bile spends
in the gallbladder.
An important mechanism is nucleation of cholesterol monohydrate
crystals
o Either an excess of pronucleating factors or a deficiency of anti-
nucleating factors
Mucin and immunoglobulins, appear to be pronucleating
factors
Apolipoproteins A-I and A-II and other glycoproteins
appear to be ant nucleating factors.
o Continued growth of the crystals occurs by direct nucleation of
cholesterol molecules from supersaturated biliary vesicles.
Another important mechanism in cholesterol gallstone formation is
gallbladder hypomotility
Biliary sludge
Is a thick, mucous material that, upon microscopic examination,
reveals lecithin-cholesterol liquid crystals, cholesterol monohydrate
crystals, calcium bilirubinate, and mucin gels.
Forms a crescent-like layer in the most dependent portion of the
gallbladder and is recognized by characteristic echoes on
ultrasonography
The presence of biliary sludge implies two abnormalities:
o (1) the normal balance between gallbladder mucin secretion and
elimination has become deranged
o (2) Nucleation of biliary solutes has occurred.
Precursor form of gallstone disease
Can develop with disorders that cause gallbladder hypomotility; i.e.,
surgery, burns, total parenteral nutrition, pregnancy, and oral
contraceptivesall of which are associated with gallstone formation.
Cholelithogenic state during Pregnancy:
Caused by:
Marked increase in cholesterol saturation of bile during the 3rd
trimester
Sluggish gallbladder contraction in response to a standard meal,
resulting in impaired gallbladder emptying.
Although biliary sludge is a common finding during pregnancy, it is
usually asymptomatic and often resolves spontaneously after delivery.
1020% of persons with rapid weight reduction achieved through
very low calorie dieting develop gallstones.
.
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.
PIGMENT STONES
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.
o Rarely displaced to the CBD because it is heavy
Brown pigment stones
o Composed of calcium salts of unconjugated bilirubin with varying
amounts of cholesterol and protein
o Caused by the presence of increased amounts of unconjugated,
insoluble bilirubin in bile that precipitates to form stones.
o Especially prominent in Asians and is often associated with
infections in the gallbladder and biliary tree
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o Common where biliary infection are more
prevalent; can occur in the gallbladder or in the
biliary tree; also associated with duodenal
diverticula; more like to form de novo in bile ducts
DIAGNOSIS OF GALLSTONES
1. Ultrasonography of the gallbladder
ADVANTAGES:
Procedure of choice for the detection of stones
Rapid
Very accurate in the identification of cholelithiasis (>95%)
Stones as small as 1.5 mm in diameter may be confidently
identified
Simultaneous scanning of GB, liver, bile ducts, pancreas
Biliary sludge typically forms a layer in the most dependent
position of the gallbladder. This layer shifts with postural changes
but fails to produce acoustic shadowing; these two characteristics
distinguish sludges from gallstones.
Used to assess the emptying function of the gallbladder.
Principal imaging modality
Diagnosis: echogenic objects within the lumen of
gallbladder that produce an acoustic shadow
usually mobile and congregate in the dependent
portion of gallbladder
Able to detect as small as 2 mm stones
Overall sensitivity for detecting stone is > 95% for
stones larger than 2 mm
Specificity >95% when stones are seen with an
accompanying acoustic shadow
Gold standard for diagnosis of gallstones in
gallbladder
Sonographic Murphys sign: positive predictive
value of > 90% in detecting acute cholecystitis if
gallstone is present
Murphys sign: sudden cessation of inspiration
while you are pressing on RUQ
LIMITATIONS:
Bowel gas, Massive Obesity and Ascites
2. ENDOSCOPIC ULTRASOUND
Has the advantage of visualizing the CBD
Positive predictive value of 98% & a negative
predictive value of 88% for the diagnosis of CBD
stones using ERCP as the gold standard
3. Plain abdominal film/radiography
ADVANTAGES:
Low cost and readily available
May detect gallstones containing sufficient calcium to be
radiopaque (1015% of cholesterol and ~50% of pigment
stones).
Used in the diagnosis of emphysematous cholecystitis, porcelain
gallbladder, limey bile, and gallstone ileus
LIMITATIONS:
Relatively low yield
4. Oral cholecystography (OCG)
Useful procedure for the diagnosis of gallstones but has been
replaced by ultrasound and is regarded as obsolete.
May be used to assess the patency of the cystic duct and
gallbladder emptying function.
Can also delineate the size and number of gallstones and
determine whether they are calcified.
A secondary means of identifying GB stones
Can be used in Unusual cases in which the GB
cannot be identified sonographically (e.g.
contracted GB full of stones)
To determine if cystic duct is obstructed esp. in
patients with medical dissolution of stone or
lithotripsy is under consideration
Ingest oral agent which is taken up by the liver
and secreted into the bile & concentrated in the
GB
When GB has opacified, sensitivity & specificity for
detection of stone are approx. 90%
5. Radioisotope Scans (HIDA, DIDA, DISIDA, etc.)
COMISO, DE DIOS, DE MANUEL, GONZAGA, GONZALES, KIM,
MACASIPOT, QUINAJON
2.01c
Failure to image the gallbladder in the presence of biliary ductal
visualization may indicate cystic duct obstruction, acute or
chronic cholecystitis, or surgical absence of the organ.
Indicated in the diagnosis of acute cholecystitis.
Useful in diagnosis of acalculouscholecystopathy
ADVANTAGES:
Accurate identification of cystic duct obstruction
Simultaneous assessment of bile ducts
6. Cholescintigraphy
Radionuclide-based imaging test of GB & biliary
tract
Most useful in patients suspected of acute
cholecystitis
By demonstrating the cystic duct, can rapidly (less
than or equal to 90 minutes) exclude acute
cholecystitis (Advantage: faster diagnosis)
Serial scans after injection show radioactivity in
GB, CBD, & small bowel within 30-60 minutes
Positive scan: non-visualization of GB with
preserved excretion into the CBD or small bowel
7. ERCP (Diagnostic and Therapeutic)
Gold standard for the diagnosis of
choledocholithiasis
Water-soluble dye is injected into the CBD &
pancreatic duct
CBD stones can be detected with sensitivity of
approximately 95%
Therapeutic potential: if stone is in an accessible
location, you can take the stone out through ERCP
8. CT & MRI
Main use lies in the detection of complications of
gallstones
Pericholecystic fluid in patients with acute
cholecystitis
Gas in GB wall with emphysematous cholecystitis
Perforation of GB
Abscess formation
Spiral CT & MR cholangiography have the
advantage over ERCP of being non-invasive, but
have no therapeutic potential
SYMPTOMS OF GALLSTONE DISEASE
Two mechanisms:
Obstruction of cystic duct or CBD
Erosion of gallbladder wall
Symptoms are caused either by inflammation or obstruction
following migration into the cystic duct or CBD
Asymptomatic stone 75%
Stone intermittently obstructing cystic duct causing
intermittent biliary colic 20%
Stone impacted in cystic duct causing acute
cholecystitis 10%
Stone in cystic duct compressing CBD (Mirizzis
syndrome) - <0.1%
Stone impacted in distal CBD 5%
Stone eroding thru the gallbladder into duodenum,
resulting in cholecysenteric fistula (gallstone ileus) -
< 0.1%
Long-standing cholelithiasis gallbladder carcinoma
Vast majority are asymptomatic & rarely warrants
intervention except
o Sickle cell anemia
o Amerindian ancestry high risk for CA
o Awaiting organ transplantation
o Porcelain gallbladder gallbladder CA
o Planning prolonged space travel or extremely
remote assignments.
The most specific and characteristic symptom is biliary colic
o Obstruction of the cystic duct or CBD by a stone produces
increased intraluminal pressure and distention of the viscus that
cannot be relieved by repetitive biliary contractions.
o The resultant visceral pain is characteristically a severe, steady
ache or fullness in the epigastrium or RUQ of the abdomen with
frequent radiation to the interscapular area, right scapula, or
shoulder.
o Biliary colic begins quite suddenly and may persist with severe
intensity for 15 min to 5 h, subsiding gradually or rapidly.
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o It is steady rather than intermittent as would be suggested by the
word colic (misnomer)
An episode of biliary pain persisting beyond 5 h should raise the
suspicion of acute cholecystitis
Nausea and vomiting frequently accompany episodes of biliary pain.
An elevated level of serum bilirubin and/or alkaline phosphatase
suggests a common duct stone.
Fever or chills (rigors) with biliary pain usually imply a complication,
i.e., cholecystitis, pancreatitis, or cholangitis.
Biliary colic may be precipitated by eating a fatty meal, by
consumption of a large meal following a period of prolonged fasting,
or by eating a normal meal; it is frequently nocturnal, occurring
within a few hours of retiring.
BILIARY COLIC
Most common clinical manifestation of gallstone
disease
Upper abdominal pain usually in the epigastrium or
RUQ
Precipitated by a meal, but more commonly there is
no inciting event
Steady rather than intermittent
Gradually increases over a period of 15 minutes to 1
hour; then remains at a plateau for about an hour
before going away
Pain lasting more than 6 hours suggest acute
cholecystitis
Location of pain: epigastrium>RUQ>LUQ>various
part of precordium or lower abdomen
PE usually normal (If (+) abnormal finding in PE
cholelithiasis)
NATURAL HISTORY OF GALLSTONES
Majority are asymptomatic and remain so
o Asymptomatic (Majority)
Initial presenting complaint in 90% is biliary
pain & not a biliary complication
Incidence of complication is low & prophylactic
removal of gallbladder is not necessary
o Symptomatic (Minority)
Risk of developing biliary complication is
estimated to be 1-2% per year & remains
constant over time
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
patient whose symptoms are not referable to cholelithiasis is a
common clinical problem.
Patients remaining asymptomatic for 15 years were found to be
unlikely to develop symptoms during further follow-up
Decision analysis has suggested that (1) the cumulative risk of death
due to gallstone disease while on expectant management is small, and
(2) prophylactic cholecystectomy is not warranted.
Complications requiring cholecystectomy are much more common in
gallstone patients who have developed symptoms of biliary pain.
Patients with diabetes mellitus and gallstones may be somewhat more
susceptible to septic complications, but the magnitude of risk of
septic biliary complications in diabetic patients is incompletely
defined.
Doctors must be more watchful with diabetic patients because they
are considered immunocompromised
Must manage with or without symptoms
Incidental cholelithiasis is considered to be associated with increased
risk of serious complication even though asymptomatic
Natural history follows same pattern observed in non-diabetics
Mortality & complication rates comparable to those of other
published studies
Prophylactic cholecystectomy is generally not recommended for
diabetics
TREATMENT OF GALLSTONE DISEASE
SURGICAL THERAPY
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
enough to interfere with the patients general routine
COMISO, DE DIOS, DE MANUEL, GONZAGA, GONZALES, KIM,
MACASIPOT, QUINAJON
2.01c
o (2) The presence of a prior complication of gallstone disease, i.e.,
history of acute cholecystitis, pancreatitis, gallstone fistula, etc.
o (3) The presence of an underlying condition predisposing the
patient to increased risk of gallstone complications (e.g., calcified
or porcelain gallbladder and/or a previous attack of acute
cholecystitis regardless of current symptomatic status).
Patients with very large gallstones (>3 cm) and patients having
gallstones in a congenitally anomalous gallbladder might also be
considered for prophylactic cholecystectomy.
Laparoscopic cholecystectomy
o Its advantages include a markedly shortened hospital stay,
minimal disability, as well as decreased cost, and it is the
procedure of choice for most patients referred for elective
cholecystectomy.
o From several studies, the following key points emerge:
(1) complications develop in ~4% of patients
(2) conversion to laparotomy occurs in 5%
(3) The death rate is remarkably low (i.e., <0.1%)
(4) Bile duct injuries are unusual (i.e., 0.20.5%) but more
frequent than with open cholecystectomy.
o These data indicate why laparoscopic cholecystectomy has
become the gold standard for treating symptomatic
cholelithiasis.
MEDICAL THERAPYGALLSTONE DISSOLUTION
Ursodeoxycholicacid (UDCA)
o Decreases cholesterol saturation of bile
o Produce a lamellar liquid crystalline phase in bile that allows a
dispersion of cholesterol from stones by physical chemical means.
o May also retard cholesterol crystal nucleation.
o 50% of patients with a functioning gallbladder and with
radiolucent stones <10 mm in diameter, achieve complete
dissolution within6 months to 2 years.
o Should be limited to radiolucent stones smaller than 5 mm in
diameter.
o The dose of UDCA should be1015 mg/kg per day.
o Stones larger than 15 mm in size rarely dissolve.
o Pigment stones are not responsive to UDCA therapy.
o In addition to the vexing problem of recurrent stones (3050%
over 35 years of follow-up), there is also the factor of taking an
expensive drug for up to 2 years.
o The advantages and success of laparoscopic cholecystectomy
have largely reduced the role of gallstone dissolution
o Patients with cholesterol gallstone disease who develop recurrent
choledocholithiasis after cholecystectomy should be on long-term
treatment with ursodeoxycholic acid.
3. ACUTE AND CHRONIC CHOLECYSTITIS
ACUTE CHOLECYSTITIS
Pathophysiology
Most frequent complication of gallstone disease
Due to inflammation of GB wall
90% cause is gallstone obstructing the cystic duct
10% cases no stones; acalculouscholecystitis
Occurs when stone becomes impacted in the cystic
duct, causing chronic obstruction
If no stones found may be due to:
o Vasculitis
o Cholesterol emboli
Obstruction causes stasis of bile & damage to GB
mucosa
Bacteria not thought to contribute to actual onset of
acute cholecystitis
Antibiotics given in cases of suspected GB
perforation, gangrene, or in patients with toxic
presentation including fever > 102 F
Inflammatory response can be evoked by three factors:
o (1) mechanical inflammation produced by increased intraluminal
pressure and distention with resulting ischemia of the gallbladder
mucosa and wall
o (2) chemical inflammation caused by the release of lysolecithin
(due to the action of phospholipase on lecithin in bile) and other
local tissue factors
o (3) bacterial inflammation, which may play a role in 5085%of
patients with acute cholecystitis
Most frequently isolated by culture of gallbladder bile
include Escherichia coli , Klebsiella spp., Streptococcus spp.,
and Clostridium spp.
Signs and Symptoms
75% had prior attack of biliary colic
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Pain lasting for > 6 hours MEDICAL THERAPY

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

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The complication rate for acalculouscholecystitis exceeds that for
calculouscholecystitis.
Successful management of acute acalculouscholecystitis appears to
depend primarily on early diagnosis and surgical intervention, with
meticulous attention to postoperative care.
b. Acalculouscholecystopathy
Disordered motility of the gallbladder can produce recurrent biliary
pain in patients without gallstones.
The following criteria can be used to identify patients with
acalculouscholecystopathy:
recurrent episodes of typical RUQ pain characteristic of biliary tract
pain
Abnormal CCK cholescintigraphy demonstrating a gallbladder
ejection fraction of<40%
Infusion of CCK reproduces the patients pain.
Large gallbladder on ultrasound examination.
Sphincter of Oddi dysfunction can also give rise to recurrent RUQ
pain and CCK-scintigraphic abnormalities.
c. Emphysematous cholecystitis
Gas-forming organisms have secondarily infected the
GB wall
prone to rupture peritonitis
Pockets of gas evident in the area of GB fossa on
sonography, plain abdominal film, or abdominal CT
Scan
Treatment: anaerobic coverage & early
cholecystectomy
Risk of perforation is high
Common in diabetics or older men without gallstones
o Atherosclerosis of cystic artery with resulting
ischemia
Thought to begin with acute cholecystitis (calculous or acalculous)
followed by ischemia or gangrene of the gallbladder wall and
infection by gas-producing organisms.
Bacteria most frequently cultured include anaerobes, such as C.
welchii or C. perfringens, and aerobes, such as E. coli.
Occurs most frequently in elderly men and in patients with diabetes
mellitus.
Clinical manifestations are indistinguishable from those of
nongaseous cholecystitis.
The diagnosis is usually made on plain abdominal film by finding gas
within the gallbladder lumen, dissecting within the gallbladder wall to
form a gaseous ring, or in the pericholecystic tissues.
CHRONIC CHOLECYSTITIS
Almost always associated with the presence of gallstones
Thought to result from repeated bouts of subacute or acute
cholecystitis or from persistent mechanical irritation of the
gallbladder wall by gallstones.
Bacteria in the bile occurs in >25% of patients with chronic
cholecystitis.
May be asymptomatic for years, may progress to symptomatic
gallbladder disease or to acute cholecystitis, or may present with
complications
Intermittent obstruction of cystic duct by one or
more stones
DIAGNOSIS of CHRONIC CHOLECYSTITIS
Sonography: first imaging study preferred; highly
sensitive & specific means of establishing presence or
absence of stones in the GB
Oral cholecystography: essential to establish patency
of cystic duct
Meltzer-Lyon Test: examination of aspirated duodenal
bile for the presence of cholesterol or calcium
bilirubinate crystals
COMPLICATIONS OF CHOLECYSTITIS
1. Empyema
Empyema results from progression of acute cholecystitis with
persistent cystic duct obstruction to superinfection of the stagnant
bile with a pus forming bacterial organism.
Clinical picture resembles cholangitis with high fever; severe RUQ
pain; marked leukocytosis; and often, prostration.
Carries a high risk of gram-negative sepsis and/or perforation.
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Emergency surgical intervention with proper antibiotic coverage is
required as soon as the diagnosis is suspected.
2. Hydrops/Mucocele
Also result from prolonged obstruction of the cystic duct, usually by
a large solitary calculus.
The obstructed gallbladder lumen is progressively distended, over a
period of time, by mucus (mucocele) or by a clear transudate
(hydrops) produced by mucosal epithelial cells.
A visible, easily palpable, non-tender mass sometimes extending from
the RUQ into the right iliac fossa may be found on physical
examination.
Patient frequently remains asymptomatic, although chronic RUQ
pain may also occur.
Cholecystectomy is indicated, because empyema, perforation, or
gangrene may complicate the condition.
3. Gangrene and perforation
Gangrene results from ischemia of the wall and patchy or complete
tissue necrosis.
Underlying conditions often include marked distention of the
gallbladder, vasculitis, diabetes mellitus, empyema, or torsion
Gangrene usually predisposes to perforation of the gallbladder, but
perforation may also occur in chronic cholecystitis without
premonitory warning symptoms.
Localized perforations are usually contained by the omentum or by
adhesions produced by recurrent inflammation of the gallbladder.
Bacterial superinfection of the walled-off gallbladder contents results
in abscess formation.
Most patients are best treated with cholecystectomy
Some seriously ill patients may be managed with cholecystostomy and
drainage of the abscess.
Free perforation is less common but is associated with a mortality
rate of ~30%.
Patients may experience a sudden transient relief of RUQ pain as the
distended gallbladder decompresses; this is followed by signs of
generalized peritonitis.
4. Fistula formation and gallstone ileus
Fistulization into an adjacent organ adherent to the gallbladder wall
may result from inflammation and adhesion formation.
Fistulas into the duodenum are most common
Followed in frequency by: Hepatic flexure of the colon, stomach or
jejunum, abdominal wall, and renal pelvis.
Clinically silent biliary-enteric fistulas occur in 5 % of patients with
acute cholecystitis
Asymptomatic cholecystoenteric fistulas may sometimes be
diagnosed by finding gas in the biliary tree on plain abdominal films.
Treatment in the symptomatic patient usually consists of
cholecystectomy, CBD exploration, and closure of the fistulous tract.
Gallstone ileus refers to mechanical intestinal obstruction resulting
from the passage of a large gallstone into the bowel lumen.
Site of obstruction by the impacted gallstone is usually at the ileocecal
valve
The majority of patients do not give a history of either prior biliary
tract symptoms or complaints
Large stones,>2.5 cm in diameter, are thought to predispose to fistula
formation by gradual erosion through the gallbladder fundus.
Diagnostic confirmation may occasionally be found on the plain
abdominal film (e.g., small-intestinal obstruction with gas in the
biliary tree and a calcified, ectopic gallstone)
Laparotomy with stone extraction (or propulsion into the colon)
remains the procedure of choice to relieve obstruction.
Cholecystenteric Fistula
Stone erodes the GB wall (usually the neck) & into a
hollow viscus
Most common entry point: duodenum, hepatic
flexure of colon, stomach, and jejunum
Symptoms similar to acute cholecystitis
Diagnosis: suspected on the basis of pneumobilia
on radiographs; confirmed with barium contrast
studies of upper and lower GIT
o pneumobilia: presence of air in biliary tree
If stone is > 25 mm, may cause small bowel
obstruction especially in elderly women at ileocecal
area causing obstruction
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5. Limey (milk of calcium) bile and porcelain gallbladder
Calcium salts in sufficient concentration may produce calcium
precipitation and diffuse, hazy opacification of bile or a layering effect
on plain abdominal x-ray. (limey bile, or milk of calcium bile)
Cholecystectomy is recommended when it occurs in a hydropic
gallbladder.
In porcelain gallbladder, calcium salt deposition within the wall of a
chronically inflamed gallbladder may be detected on the plain
abdominal film.
Cholecystectomy is advised in all patients with porcelain gallbladder
because in a high percentage of cases is associated with the
development of carcinoma of the gallbladder.
Porcelain Gallbladder
Intramural calcification of GB wall
Has a high incidence of developing carcinoma in 20%
of patients
Diagnosis: plain abdominal film or CT Scan
Treatment: prophylactic cholecystectomy
4. THE HYPERPLASTIC CHOLECYSTOSES
A group of disorders of the GB characterized by excessive
proliferation of normal tissue components.
Adenomyomatosis
o Benign proliferation of GB surface epith with gland like
formations, extramural sinuses, strictures, and/or fundal nodule
formation
Cholesterolosis
o Abnormal deposition of lipid, especially cholesteryl esters within
macrophages in the lamina propria of the GB wall.
o Diffuse form: (strawberry gallbladder), the GB mucosa is brick
red and speckled with bright yellow flecks of lipid.
o Localized form: solitary or multiple cholesterol polyps studding
the gallbladder wall.
Cholecystectomy is indicated in both adenomyomatosis and
cholesterolosis when symptomatic or when cholelithiasis is present.
DISEASES OF THE BILE DUCTS
1. CONGENITAL ANOMALIES
Biliary atresia and Hypoplasia
Most common biliary anomalies of clinical relevance in infancy
Clinical picture: Severe obstructive jaundice during the first month of
life, with pale stools.
Diagnosis is confirmed by surgical exploration and operative
cholangiography.
Approximately 10% of cases are treatable with roux-en-Y
choledochojejunostomy
Kasai procedure (hepatic portoenterostomy) is attempted in the
remainder in an effort to restore some bile flow.
Most patients, even those having successful biliary-enteric
anastomoses, eventually develop chronic cholangitis, extensive
hepatic fibrosis, and portal hypertension.
Choledochal cysts
Cystic dilatation involve the free portion of the CBD
Chronic reflux of pancreatic juice into the biliary tree can produce
inflammation and stenosis of the extrahepatic bile ducts leading to
cholangitis or biliary obstruction
The process is gradual so ~50% of patients present with onset of
symptoms after age 10.
The diagnosis maybe made by ultrasound, abdominal CT, MRC, or
cholangiography.
Only one-third of patients show the classic triad of abdominal pain,
jaundice, and an abdominal mass.
UTZ detection of a cyst separate from the gallbladder should suggest
the diagnosis of choledochal cyst, which can be confirmed by
demonstrating the entrance of extrahepatic bile ducts into the cyst.
Surgical treatment involves excision of the cyst and biliary-enteric
anastomosis.
Patients with choledochal cysts are at increased risk for the
subsequent development of cholangiocarcinoma.
Congenital biliary ectasia
Dilatation of intrahepatic bile ducts may involve either:
o Major intrahepatic radicles (Carolis disease)
Clinical manifestations: Recurrent cholangitis, abscess
formation in and around the affected ducts, and, often,
gallstone formation within portions of ectatic intrahepatic
biliary radicles.
o Inter- and intralobular ducts (congenital hepatic fibrosis)
COMISO, DE DIOS, DE MANUEL, GONZAGA, GONZALES, KIM,
MACASIPOT, QUINAJON
2.01c
o or both
Ultrasound, MRC, and CT are of great diagnostic value
Antibiotic therapy: Limits the frequency and severity of recurrent
bouts of cholangitis.
Progression to secondary biliary cirrhosis with portal hypertension,
extrahepatic biliary obstruction, cholangiocarcinoma, or recurrent
episodes of sepsis with hepatic abscess formation is common.
2. CHOLEDOCHOLITHIASIS
Pathophysiology and clinical manifestations
Occurrence of stones in the CBD
May remain asymptomatic for years
May cause life-threatening complications
o Cholangitis
o Pancreatitis
Occurs in ~1015% of patients with cholelithiasis.
Incidence of common duct stones increases with increasing age
Majority are cholesterol stones formed in the GB, which then migrate
into the extrahepatic biliary tree through the cystic duct.
Primary calculi arising de novo in the ducts are usually pigment
stones developing in patients with
o Hepatobiliary parasitism
o Chronic, recurrent cholangitis
o Congenital anomalies of the bile ducts (especially Carolis disease)
o Dilated, sclerosed, or strictured ducts
o An MDR3 (ABCB4) gene defect leading to impaired biliary
phospholipids secretion (low phospholipidassociated
cholelithiasis)
May remain asymptomatic for years, may pass spontaneously into the
duodenum, or (most often) may present with biliary colic or a
complication.
Clinical manifestations depend on the rate of onset &
degree of obstruction & the amount of bacterial
contamination of the bile
o Acute obstruction: causes biliary colic and
jaundice
o Chronic obstruction: develops gradually over
several months may present initially with pruritus
or jaundice alone
If bacteria proliferates, cholangitis may result
PE is usually completely normal if obstruction is
intermittent
Rise of bilirubin concentration is proportional to the
degree of obstruction
Increase in ALP has no relationship to either degree
of obstruction or its cause
o It means there is an obstruction but does not tell
the severity
Transient spikes of transaminases or amylase
suggest passage of a CBD stone into the duodenum
ETIOLOGY
May pass from GB to CBD or primarily in the duct
All gallstones from one patient are of the same type,
either pigment or cholesterol
Cholesterol stones only form in the GB; any
cholesterol stones found in CBD must have migrated
from the GB
Black pigment stones also form in the GB but rarely
migrate into the CBD (heavy weight of black
pigmented stone)
Brown pigment stones form de novo in the CBD as
a result of bacterial action on phospholipid & bilirubin
in bile; frequently associated with cholangitis
o 95% of patients with CBD stone also have GB
stone
o Normal pressure in the CBD = 10-15 cmH20
o CBD obstruction = 25-40 cmH20
o Bile flow decreases at 15 cmH20
o Bile flow ceases at 30 cmH20
Complications
Cholangitis
May be acute or chronic, and symptoms result from inflammation
The characteristic presentation of acute cholangitis involves biliary
pain, jaundice, and spiking fevers with chills (Charcots triad).
Blood cultures are frequently positive, and leukocytosis is typical.
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Non-suppurative acute cholangitis is most common; respond to
supportive therapy
Suppurative acute cholangitis (presence of pus under pressure in a
completely obstructed ductal system) leads to symptoms of severe
toxicitymental confusion, bacteremia, and septic shock.
o Response to antibiotics alone in this setting is relatively poor
o Multiple hepatic abscesses are often present
o Mortality rate approaches 100% unless prompt endoscopic or
surgical relief of the obstruction and drainage of infected bile are
carried out.
o ERCP with endoscopic sphincterotomy is safe and the preferred
initial procedure for both establishing a definitive diagnosis and
providing effective therapy.
Obstructive jaundice
Gradual obstruction of the CBD (weeks to months): Initial
manifestations of jaundice or pruritus without associated symptoms
of biliary colic or cholangitis.
Painless jaundice may occur
o But is much more characteristic of biliary obstruction secondary
to malignancy
Associated chronic calculous cholecystitis is very common
Absence of a palpable gallbladder in most patients with biliary
obstruction from duct stones is the basis for Courvoisiers law
o Courvoisiers Law: The presence of a palpably enlarged
gallbladder suggests that the biliary obstruction is secondary to an
underlying malignancy rather than to calculous disease.
Obstruction causes progressive dilatation of the intrahepatic bile
ducts as intrabiliary pressures rise.
Bile flow is suppressed, and reabsorption and regurgitation of
conjugated bilirubin into the bloodstream lead to jaundice
accompanied by dark urine (bilirubinuria) and light-colored (acholic)
stools.
CBD stones should be suspected in any patient with cholecystitis
whose serum bilirubin level is >85.5 mmol/L (5 mg/dL).
The maximum bilirubin level is seldom >256.5 mmol/L (15.0
mg/dL) in patients with choledocholithiasis unless concomitant
hepatic disease or another factor exists.
Serum bilirubin levels >342.0 mmol/L (20 mg/dL) should suggest
the possibility of neoplastic obstruction.
Alkaline phosphatase level is almost always elevated in biliary
obstruction.
o Precedes clinical jaundice and may be the only abnormality in
routine liver function tests.
There may be a two- to tenfold elevation of serum aminotransferases
Following relief of the obstruction, serum aminotransferase
elevations usually return rapidly to normal
Bilirubin level may take12 weeks to return to normal.
Alkaline phosphatase level usually falls slowly, lagging behind the
decrease in serum bilirubin.
Pancreatitis
The most common associated entity discovered in patients with
nonalcoholic acute pancreatitis is biliary tract disease.
The common factor appears to be the passage of gallstones through
the common duct.
Coexisting pancreatitis should be suspected in patients with
symptoms of cholecystitis who develop:
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
resolution of the pancreatitis.
Secondary biliary cirrhosis
More common in cases of prolonged obstruction from stricture or
neoplasm.
May be progressive even after correction of the obstructing process
Increasingly severe hepatic cirrhosis may lead to portal hypertension
or to hepatic failure and death.
Prolonged biliary obstruction may also be associated with deficiencies
of the fat-soluble vitamins A, D, E, and K.
Diagnosis and treatment
Dilatation of CBD > 6
mm in diameter seen in
Sonography approx. 75%
Can be used to confirm
or at least suggest the
COMISO, DE DIOS, DE MANUEL, GONZAGA, GONZALES, KIM,
MACASIPOT, QUINAJON
2.01c
presence of CBD stones
but not definitely
exclude
choledocholithiasis
Better visualization of
CBD
Endoscopic Ultrasound
Sensitivity & specificity
approx. 95%
Gold standard for
choledocholithiasis
ERCP
Sensitivity & specificity
approx. 95%
Can confirm
Percutaneous
choledocholithiasis
TranshepaticCholangio-
Accomplished in the
graphy
setting of dilated IHDs
Used in the surgical
Laparoscopic
suite prior to
Ultrasound
mobilization of GB
Diagnosis of choledocholithiasis is usually made by cholangiography
either preoperatively by endoscopic retrogradecholangiogram (ERC)
or MRCP or intraoperatively at the time of cholecystectomy.
Endoscopic removal of CBD stone
o Can be performed without the need for
cholecystectomy
o Subsequent cholecystectomy for symptoms is
required in only 10% of patients
When CBD stones are suspected prior to laparoscopic
cholecystectomy, preoperative ERCP with endoscopic papillotomy
and stone extraction is the preferred approach.
CBD stones should be suspected in gallstone patients who have any
of the following risk factors:
o History of jaundice or pancreatitis
o Abnormal tests of liver function
o Ultrasonographic or MRCP evidence of a dilated CBD or stones
in the duct.
Endoscopic Biliary Sphincterotomy followed by spontaneous passage
or stone extraction is the treatment of choice in the management of
patients with common duct stones, especially in elderly or poor-risk
patients.
3. TRAUMA, STRICTURES AND HEMOBILIA
Most benign strictures result from surgical trauma
Strictures may present with bile leak or abscess formation in the
immediate postoperative period or with biliary obstruction or
cholangitis as long as 2 years or more following the inciting trauma.
When positive exfoliative cytology is obtained, the diagnosis of a
neoplastic stricture is established.
o Especially important in patients with primary sclerosing
cholangitis (PSC) who are predisposed to cholangiocarcinomas.
Hemobilia may follow traumatic or operative injury to the liver or
bile ducts, intraductal rupture of a hepatic abscess or aneurysm of the
hepatic artery, biliary or hepatic tumor hemorrhage, or mechanical
complications of choledocholithiasis or hepatobiliary parasitism.
Patients often present with a classic triad of biliary pain, obstructive
jaundice, and melena or occult blood in the stools.
Although minor episodes of hemobilia may resolve without operative
intervention, surgical ligation of the bleeding vessel is frequently
required.
4. EXTRINSIC COMPRESSION OF THE BILE DUCTS
The most common cause is carcinoma of the head of the pancreas.
May also occur as a complication of either acute or chronic
pancreatitis or involvement of lymph nodes in the portahepatis by
lymphoma or metastatic carcinoma.
The latter should be distinguished from cholestasis resulting from
massive replacement of the liver by tumor.
5. HEPATOBILIARY PARASITISM
Infestation of the biliary tract by adult helminths or their ova may
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,
including Clonorchis sinensis, Opisthorchis viverrini or O. felineus ,
and Fasciola hepatica
The biliary tract also may be involved by intraductal migration of
adult Ascaris lumbricoides or by intrabiliary rupture of hydatid cysts
of the liver produced by Echinococcus spp.
Diagnosis: cholangiography and ova on stool examination.
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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.
stones
Occurs up to 75% in association with IBS, especially ulcerative colitis.
May also be associated with autoimmune pancreatitis
TREATMENT
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
TREATMENT
Therapy with cholestyramine may help control symptoms of pruritus
==============END==============
Antibiotics are useful when cholangitis complicates the clinical
picture
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.

7. CHOLANGITIS (BACTERIAL)
ETIOLOGY & PATHOPHYSIOLOGY
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
perfringens

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

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