Gall Bladder diseases

Dr Arun Aggarwal Gastroenterologist

 Ascertaining the true prevalence of GB disease
is difficult as most patient with GB disease are
asymptomatic.
 Various studies have shown prevalence rate
ranging from 0.13 – 2%.
Gall stones
 INTRODUCTION
 Gallstone disease is one of the most common
and costly of all digestive diseases.
 The third National Health and Nutrition
Examination Survey estimated that 6.3 million
men and 14.2 million women aged 20 to 74 in
the United States had gallbladder disease.
 Major risk factors for the development of
gallstones
 Age  Medications
 Female sex  Estrogen and oral contraceptives
 Genetic  Clofibrate
 Pima Indians and certain other
 Ceftriaxone
Native Americans  Octreotide
 Chileans  Terminal ileal resection
 Pregnancy  Gallbladder stasis
 Obesity  Diabetes mellitus
 Rapid weight loss  Total parenteral nutrition
 Very low calorie diet
 Postvagotomy
 Surgical therapy of morbid obesity
 Octreotide or somatostatinoma
 Spinal cord injury
 Cirrhosis
 Hemolytic anemias
 Reduced physical activity
 Hypertriglyceridemia
 Cystic fibrosis
 Age: exceedingly rare in children except in the
presence of hemolytic states; in addition, <5% of
all cholecystectomies are performed in children.
 Sex: F > M
 Pregnancy: frequency and no of pregnancies. Sex
hormones induce a variety of physiologic changes
in the biliary system, which ultimately cause bile
to become supersaturated with cholesterol,
thereby promoting gallstone formation. These
changes normalize 1-2 months following delivery.
obesity
 Diabetes mellitus: mechanism is not well
understood. Hepatic insulin resistance appears to
be important . Other contributing factors may be
hypertriglyceridemia and autonomic neuropathy
leading to biliary stasis due to gallbladder
hypomotility.
 Serum lipids: positively associated with
apolipoprotein E4 phenotype and elevated serum
triglycerides. Negative association exists between
gallstones and high density lipoprotein.
 There is no conclusive evidence linking elevated
serum cholesterol and gallstones.
 Cirrhosis: due to reduced hepatic synthesis and
transport of bile salts and nonconjugated bilirubin,
high estrogen levels, and impaired gallbladder
contraction in response to a meal.

 Gall bladder stasis: In the normal state, the

gallbladder avidly absorbs water from bile. Thus, if
bile remains within the gallbladder for a prolonged
period, it can become overly concentrated with
cholesterol, thereby promoting stone formation. Can
occur with spinal cord injuries, prolonged fasting
and the use of TPN, and excess somatostatin.
 Short bowel syndrome: Two factors are
thought to contribute: biliary stasis due to lack
of enteral stimulation; and, in patients with
ileal resection, interruption of the
enterohepatic circulation of bile acids results
in a reduction in hepatic bile acid secretion
and an altered composition of hepatic bile
which becomes supersaturated with respect to
cholesterol.
 Crohn’s disease: Gallstones in patients with
ileal Crohn's disease (or those who have
undergone ileal resection) are frequently
pigment based, reflecting an increased
concentration of bilirubin conjugates,
unconjugated bilirubin, and total calcium in
the gallbladder bile due to altered
enterohepatic cycling of bilirubin.
 Protective factors
 Statins
 Ascorbic acid
 Coffee (in moderation)
 Vegetable protein
 Poly and mono unsaturated fats
 CLINICAL FEATURES
When considering gallstone disease it is helpful to
categorize patients into the following clinical
groups:
 Gallstones on imaging studies but without symptoms
 Typical biliary symptoms and gallstones on imaging
studies
 Atypical symptoms and gallstones on imaging studies
 Typical biliary symptoms but without gallstones on
imaging studies
 Biliary type symptoms
 Biliary colic: recurrent pain attacks
 Complication of gall stones: acute
cholecystitis, acute biliary pancreatitis, acute
cholangitis, or choledocholithiasis with
extrahepatic cholestasis.
 Biliary colic
 Usually caused by the gallbladder contracting in response to
hormonal or neural stimulation usually due to a fatty meal, forcing a
stone (or possibly sludge or microlithiasis) against the gallbladder
outlet or cystic duct opening, and leading to increased
intragallbladder pressure and pain.
 The stones often fall back from the cystic duct as the gallbladder
relaxes. As a result, the discomfort progresses in less than an hour to
a steady plateau that ranges from moderate to excruciating and
remains constant for more than an hour, then slowly subsides over
several hours.
 Despite the term "colic", the pain is usually constant and not
colicky. The classic attack is described as an intense dull pressure-
like discomfort in the right upper or mid abdomen or in the chest
that may radiate to the back and the right shoulder blade . The pain
classically follows ingestion of a fatty meal (about one to two hours
after) and usually does not occur during fasting.
 The pain is often associated with diaphoresis,
nausea and vomiting. It is not exacerbated by
movement and not relieved by squatting,
bowel movements, or flatus.
 After the attack, the physical examination is
usually normal with the possible exception of
residual upper abdominal tenderness.
 Prolonged or recurrent cystic duct blockage
can progress to total obstruction causing acute
cholecystitis.
 Diagnosis
 Biliary colic is the most accurate predictor of
gallstone disease.
 Imaging studies can detect gallstones, there is
no clinical or laboratory test that can make the
diagnosis of biliary colic.
 The diagnosis is based upon a meticulous
history.
 Physical exam: usually not ill appearing, no
fever/ tachycardia, no peritoneal signs, ±
voluntary guarding.
 Labs
 LFT
 GGT
 Amylase, lipase
 CBC
 UA
 Imaging studies
 GGT
 GGT is sensitive for detecting hepatobiliary disease, but
its usefulness is limited by its lack of specificity.
 Elevated levels can occur in pancreatic disease,
myocardial infarction, renal failure, chronic obstructive
pulmonary disease, diabetes, and alcoholism.
 GGT be used to evaluate elevations of other serum
enzyme tests (eg, to confirm the liver origin of an
elevated alkaline phosphatase or to support a suspicion
of alcohol abuse in a patient with an elevated AST and
an AST:ALT ratio of greater than 2:1).
 An elevated GGT with otherwise normal liver tests
should not lead to an exhaustive work-up for liver
disease.
 USG
 Most useful test.
 It is non-invasive, readily available, relatively
inexpensive, and does not subject the patient
to ionizing radiation.
 Accuracy of USG is operator dependent.
 USG must be conducted with the patient
having fasted, because stones are best seen in a
distended gallbladder when they are
surrounded with bile.
 Ultrasound images of a gallbladder adenomatous
polyp (left ) compared to a gallstone (right). Note the
shadow cast by the stone (red arrow) compared to
the absence of a shadow behind the polyp.
AXR
 Plain abdominal x-rays are
generally not useful in
looking for gallstones in
symptomatic patients. Only
about 10 % of gallstones
have enough calcium in
their composition to make
them sufficiently radio-
opaque to be visible on a
plain radiograph. 
 Oral
cholecystography
 OCG is based upon an
orally administered contrast
agent that is absorbed
through the intestine, taken
up by the liver, and secreted
into bile. Gallstones appear
as filling defects within the
contrast .
 CT abdomen
 Endoscopic ultrasonographhy
 Management of biliary colic
 Pain control.
 Can usually be achieved with IV meperidine,
which is preferred to morphine since it has less
of an effect on sphincter of Oddi motility.
 NPO to prevent the release of cholecystokinin.
 IV fluids if vomiting +
 Anticholinergic agents, which are useful in the
management of renal colic due to their smooth
muscle relaxation effects, do not appear to
help biliary colic.
 Prophylactic treatment to prevent further attacks
and/or the development of complications

 To remove the offending stones to prevent

recurrent attacks of biliary colic and the
occurrence of more severe complications.
 Surgical removal of the gallbladder vs medical
dissolution of the stones while sparing the
gallbladder.
 Cholecystectomy is the most commonly recommended
modality. The gallbladder along with its contained
stones is removed under general anesthesia.
 Open vs laproscopic.
 Laparoscopic procedure has been associated with an
increased risk of common bile duct injury.
 Laparoscopic procedure may require conversion to an
open procedure due to a variety of technical or patient
issues.
 Interestingly, several other symptoms appeared to be
improved after cholecystectomy including abdominal
bloating, dyspepsia, heartburn, fat intolerance, nausea
and vomiting.
 However, these observations should not be
interpreted as suggesting that gallstones are a
possible cause of all these complaints.
 Relief of symptoms may have been due to the natural
history of some of these disorders, a placebo
response, or other nonspecific effect of the procedure.
 Gallstones but without symptoms
 These patients are unlikely to develop
symptoms and when they do occur they are
generally mild.
 Thus, patients should be educated about
symptoms potentially related to gallstones
(principally biliary colic) without
recommending specific therapy to address the
gallstones.
Typical biliary symptoms and gallstones

Such patients should generally undergo

treatment (generally cholecystectomy) since
they are likely to develop recurrent symptoms,
which can be severe.
Atypical symptoms and gallstones
 Such patients should undergo a search for non-
gallstone-related causes of symptoms.
 If investigation is unrevealing, treatment of
gallstones can be considered with the
understanding that the rate of persistent
symptoms is high.
 Typical biliary symptoms but without
gallstones 
 Clinical suspicion for gallstone disease should
be maintained in such patients.
 A repeat extracorporeal ultrasound should be
obtained.
 If results are unrevealing, Endoscopic US and
collection of duodenal bile for microscopy
should be considered.
 If results continue to be unrevealing, a search
for other causes of the pain is reasonable.
Nonsurgical treatment of gallstone disease
 Symptomatic gallstones are uncommonly treated with
medical therapy alone.
 Ursodiol: may have a role to enhance gallstone
dissolution and perhaps reduce symptoms in patients with
mild symptoms or those who are not candidates for
laparoscopic surgery (grade 2 B).
 ESWL and contact lithotripsy will likely be limited to
specialized centers with experience in these techniques
and in the majority of cases as an adjunct to endoscopic
or other invasive treatments.
 In patients with stones too large for dissolution therapy,
lithotripsy (plus bile salts) provided that patients have
fewer than three noncalcified stones (Grade 2B).
Acute cholecystitis
 Syndrome of right upper quadrant pain, fever, and leukocytosis
associated with gallbladder inflammation.
 Usually related to gallstone disease.
 Pain may radiate to the right shoulder or back. Characteristically,
acute cholecystitis pain is steady and severe. Associated
complaints may include nausea, vomiting, and anorexia.
 Should be suspected when a patient presenting with the clinical
manifestations outlined above is found to have gallstones on an
imaging study.
 Left untreated, symptoms of cholecystitis may abate within 7 to
10 days. However, complications can occur at high rates.
 Most common complication is the development of GB gangrene
(up to 20 % of cases) with subsequent perforation (2 % of
cases).
Radionuclide imaging/ Scintigraphy
 IV administered Technetium-99m hepatic iminodiacetic acid
(Tc-99m HIDA) is secreted from liver in to hepatic bile ducts,
but unable to enter GB if cystic duct is obstructed.
 If GB is not seen in 60 min: do delayed imaging at 4 hrs or
administration of morphine.
 Morphine increases pressure at sphincter of oddi and forces
bile in to GB if cystic duct is patent.
 Complications of acalculous cholecystitis (gangrene and
perforation) can be identified by spill of radionuclide into
peritoneal cavity.
Ultrasound of the right
upper quadrant in a
patient with acute
cholecystitis reveals
marked thickening of
the gallbladder wall
(arrow) with fluid
surrounding the
distended gallbladder
(arrowhead).
 Treatment of acute cholecystitis
 Admit
 Analgesia (opioids)
 Antibiotics (unasyn/ zosyn/ rocephin + flagyl)
(grade 2C)
Treatment of acute cholecystitis
Acute cholangitis
 Clinical syndrome characterized by fever,
jaundice, and abdominal pain that develops as a
result of stasis and infection in the biliary tract.
 The classic triad of Charcot — fever, right upper
quadrant pain, and jaundice — occurs in only 50
to 75 % of patients .
 Confusion and hypotension can occur in patients
with suppurative cholangitis, producing
Reynold's pentad, which is associated with
significant morbidity and mortality.
 Differential diagnosis
 Biliary leaks
 Liver abscess
 Infected choledochal cysts
 Cholecystitis
 Mirizzi syndrome (chronic cholecystitis and large
gall stones resulting in compression of common
hepatic duct)
 Right lower lobe pneumonia/empyema
 Treatment
 Antibiotics (unasyn/ zosyn/ meropenem/
rocephin + flagyl)
 Establishment of biliary drainage (ERCP/ open
surgical decompression)
 IV fluids
 Correction of coagulopathy
 Monitoring
 80 % of patients with acute cholangitis will respond to
conservative management and antibiotic therapy.
 Biliary drainage can be performed on an elective basis.
 In 15- 20 % of cases, cholangitis fails to settle over the
first 24 hours with conservative therapy alone,
requiring urgent biliary decompression.
 Indications for urgent biliary decompression include:
 Persistent abdominal pain
 Hypotension despite adequate resuscitation
 Fever greater than 39ºC (102ºF)
 Mental confusion, which is a predictor of poor outcome
 Diagnosis and treatment of acute cholangitis with ERCP. Left: Multiple
small stones in the lower common bile duct (arrow). Ultrasonography had
shown borderline dilatation of the common bile duct but no stones.
Right : After sphincterotomy and stone extraction, the common bile duct
is free of stones.
Following cannulation of the distal common bile duct during
an ERCP examination (black arrow indicates cannula),
contrast material was injected, outlining a large stone
producing complete obstruction of the distal duct (white
arrow).
 Acalculous cholecystitis / Biliary
dyskinesia
 F>M
 Associated with systemic infection / surgery / trauma.
 Risk factors: prolonged fasting, PN, sepsis.
 Abdominal pain : RUQ, worse after eating.
 Examination and routine workup is generally normal.
 USG shows GB wall thickness > 3.5 mm.
 Hepatobiliary scintigraphy scan is usually diagnostic
(ejection fraction <35%).
 Cholecystectomy is usually helpful.
 Sphincter of oddi dysfunction
 There is effectively an obstruction at the level
of sphincter that may be caused by fibrosis /
inflammation / elevated sphincter tone.
 Symptoms usually similar to GB dyskinesia.
 ERCP with Manometry is usually diagnostic.
 Sphincterotomy is the treatment of choice.
 Cholecystectomy does not provide relief.
 Benign masses of gall bladder
 Usually polyps: primary or secondary
 Primary polyps include:
-Cholesterol polyps
-Inflammatory polyps
-hyperplastic adenomyoma
-Adenoma
-Heterotopic gastric and pancreatic tissue
• Can present with sign and symptoms of biliary colic
• USG usually diagnostic
 Malignant tumors of GB: usually follows
acute/chronic cholecystitis, rare in children.
 Congenital abnormalities of GB: rare, often found
incidently during imaging/surgery.
 Absent GB: can be associated with extra hepatic
biliary atresia, GB may appear absent in cystic
fibrosis(recurrent attacks of cholecystitis can lead
to fibrosis/atrophy of GB).
 Double GB: rare, usually asymptomatic.
Disease process USG Radio CT MRI / ERCP Misc
nuclide MRCP .
imaging
GB stone +++
Acute cholecystitis +++ ++
Acute acalculous +++ +
cholecystitis
Chronic acalculous + +++
cholecystitis
Sphincter of oddi spasm + ++ +++
Biliary leak post + +++ +
cholecystectomy
Bile duct obstruction +++ ++ ++ +++ +++ ±
chola
ngio
gram