The gallbladder is located near the liver and stores and concentrates bile produced by the liver. It has three parts - the neck, body, and fundus. The cystic duct connects the gallbladder to the common hepatic duct. Gallstones can form in the gallbladder and cause problems like biliary colic, cholecystitis, cholangitis, or pancreatitis. Risk factors for gallstones include obesity, female gender, rapid weight loss, and certain medical conditions. Complications may include perforation or gangrene of the gallbladder.

1. Gallbladder
By: Krystle Rolle
Bobby Korah
& Oladapo
Samson

2. Anatomy of Gallbladder
 The gall bladder is located
in the junction of the right
ninth costal cartilage and
lateral border of the rectus
abdominis .
 It is a pear shaped sac
lying on the inferior surface
of the liver in a fossa
between the right and
quadrate lobes with a
capacity of about 30 to 50
mL.

3. Anatomy of Gallbladder
 The gallbladder is in direct
contact to the superior part
of the duodenum and
transverse colon.
 The gall bladder has three
parts the neck which
tapers into the narrow
cystic duct which connects
with the common duct.
 Body: contacts the visceral
surface of the liver the
transverse colon and
superior part of the
duodenum
 Fundus: The wide end of
the organ projects 1-2 cm
from the inferior border of

4. Anatomy of Gallbladder
 The cystic duct (3-4 cm long) connects the neck of the
gallbladder to the common hepatic duct .
 The spiral fold helps keep the cystic duct open ;thus
bile can easily be diverted into the gallbladder when
the distal end of the bile duct is closed by the
sphincter of the bile duct.
 The spiral fold also offers additional resistance to
sudden dumping of bile when the sphincters are
closed, and intra-abdominal pressure is suddenly
increased, as during a sneeze or cough.
 The cystic duct passes between the layers of the
lesser omentum, usually parallel to the common
hepatic duct, which it joins to form the bile duct.

5. Blood Supply of the Gall Bladder
 The cystic artery,
supplying the
gallbladder and cystic
duct commonly arises
from the right hepatic
artery.

6. CYSTOHEPATIC TRIANGLE OF
CALOT
In the angle between the
common hepatic duct and the
cystic duct cystohepatic triangle
(of Calot) which is formed by
the visceral surface of the liver
superiorly, the cystic duct
inferior-laterally and the
common hepatic duct medially.

7. Variations to the Cystic Artery
 Variations occur in the
origin and course of the
cystic artery .
 In approximately 12% of
cases, the right hepatic
artery arises from the
superior mesenteric artery.
 The cystic artery usually
arises from the right hepatic
artery, but other origins are
possible.
 The cystic artery may pass
posterior (75%) or anterior

8. Venous Drainage of the Gallbladder
 The cystic veins, draining the neck of the gallbladder
and cystic duct, enter the liver directly or drain through
the portal vein to the liver, after joining the veins
draining the hepatic ducts and upper bile duct.
 The veins from the fundus and body of the gallbladder
pass directly into the visceral surface of the liver and
drain into the hepatic sinusoids.
 Because this is drainage from one capillary
(sinusoidal) bed to another, it constitutes an addition
(parallel) portal system.

9. Lymphatic Drainage of Gallbladder
 The lymphatic drainage of
the gallbladder is to the
hepatic lymph nodes often
through cystic lymph
nodes located near the
neck of the gallbladder.
 Efferent lymphatic vessels
from these nodes pass to
the celiac lymph nodes.

10. Nerve Supply
 The nerves to the gallbladder and cystic duct pass
along the cystic artery from the celiac nerve plexus
(sympathetic and visceral afferent [pain] fibers), the
vagus nerve (parasympathetic), and the right phrenic
nerve (actually somatic afferent fibers).
 Parasympathetic stimulation causes contractions of
the gallbladder and relaxation of the sphincters at the
hepatopancreatic ampulla.
 However, these responses are generally stimulated
by the hormone cholecystokinin (CCK), produced by
the duodenal walls (in response to the arrival of a fatty
meal) and circulated through the blood stream

11. Functions
 Gall bladder
 It stores Bile
 It concentrates bile
 Ejects bile into lumen
 Bile
 Emulsify dietary lipids
 Formation of micelles with products of lipid digestion.

12. BILE
 Bile is produced at a rate of 500–1500 mL/d by the
hepatocytes and the cells of the ducts
 The organic constituents of bile are bile salts (50%),
bile pigments such as phospholipids (40%),
cholesterol (4%), and bilirubin (2%) Bile also contains
electrolytes and water.
 Bile acids are conjugated with amino acids , glycine or
taurine to form bile salts.
 Bilirubin , a yellow- colored byproduct is the major
bile pigment.

13. Secretion and enterohepatic circulation
of bile salts

14. CHOLELITHIASIS
 Presence of one or more calculi
(gallstones) in the gallbladder.

15. Incidence and Epidemiology
 In the United States, about 20 million people (10-
20% of adults) have gallstones.
 Every year 1-3% of people develop gallstones and
about 1-3% of people become symptomatic.
 Prevalence of cholesterol cholelithiasis in other
Western cultures is similar to that of the United
States, but it appears to be somewhat lower in
Asia and Africa.
 Prevalence is highest in people of northern
European descent and in Hispanic populations
 Women are more likely to develop cholesterol
gallstones than men, especially during their
reproductive years, when the incidence is 2-3
times than that in men.

16. Risk factors
 Cholesterol stones:
 Obesity, age <50
 Estrogens: female, multiparity, OCPs
 Ethnicity: Caucasian > black
 Terminal ileal resection or disease (Crohn’s Disease)
 Impaired gallbladder emptying: starvation, DM type 1
 Rapid weight loss: rapid cholesterol mobilization and
biliary stasis
 Pigment stones :
 Chronic (contains calcium bilirubinate):
 Cirrhosis
 Chronic hemolysis
 Biliary stasis (strictures, dilation, biliary infection)

17. Pathophysiology
 Biliary sludge is often a precursor of gallstones. It
consists of Ca++ bilirubinate (a polymer of
bilirubin), cholesterol microcrystals, and mucin.
 Sludge develops during gallbladder stasis, as
occurs during pregnancy.
 Most sludge is asymptomatic or disappears when
the primary condition resolves.
 Alternatively, sludge can evolve into gallstones
and migrate into the biliary tract, obstructing the
ducts and leading to biliary colic, cholangitis, or
pancreatitis.

18. Pathophysiology
 Three types of stones, cholesterol,
pigment, mixed.
 Formation of each types is caused by
crystallization of bile.
 Cholesterol stones most common.
 Impaired motility can predispose to
stones.
 Pigment stones (15%) are from calcium
bilirubinate. Diseases that increase RBC
destruction will cause these. Also in
cirrhotic patients, parasitic infections.

19. Pathophysiology
 Cholesterol stones – vary in color from light yellow
to dark green or brown and are oval in shape, 2-3
cm in length, often having a tiny dark central spot.
 Pigmented stones – are small dark stones made
of bilirubin and calcium salts that are found in the
bile
 Mixed stones – calcium carbonate, palmitate
phosphate, bilirubin and other bile pigments.
Because of their calcium content, they are often
radiographically visible.

20. 4 Stages of Cholelithiasis
 Gallstone disease may be thought of as
having the following 4 stages:
 The lithogenic state, in which conditions
favor gallstone formation
 Asymptomatic gallstones
 Symptomatic gallstones, characterized by
episodes of biliary colic
 Complicated cholelithiasis

21. Symptoms and signs
 80% of gallstones are asymptomatic. The
remainder have symptoms ranging from biliary-
type pain (biliary colic) to cholecytitis to life-
threatening cholangitis. Biliary colic is the most
common symptom.
 RUQ (Right Upper Quadrant) pain which may
radiate to the back – described as colicky, but
more often is dull and constant.
 Nausea & Vomiting, fever and chills do not occur.
 Other symptoms include dyspepsia, flatulence,
food intolerance, particularly to fats, and some
alteration in bowel frequency.
 Restlessness

22. Biliary colic
 Biliary colic is pain associated with irritation of the
viscera secondary to cholecystitis and gallstones.
 Unlike renal colic, the phrase 'biliary colic' refers to the
actual cholelithiasis.
 Although it is frequently described as a colic, the pain
is steady, starts rapidly, becomes intense and lasts at
least 30 minutes and up to several hours.

23. CHOLECYCTITIS
A common condition that results from
inflammatory, infections, metabolic, neoplastic
and congenital disorders
 It is the inflammation of gallbladder that occurs
most commonly because of an obstruction of the
cystic duct from cholelithiasis.
 Acute acalculous cholecystitis – cholecystitis
without stones. It accounts for 5-10% of
cholecystectomies done for acute cholecystitis
 Acute calculous cholecystitis – cholecystitis with
stones. It accounts for 90-95%.

24. CHOLECYCTITIS
 Acute cholecystitis is inflammation of the
gallbladder that develops over hours, usually
because a gallstone obstucts the cystic duct.
 Symptoms include RUQ pain and tenderness,
sometimes accompanied by fever (usually low
grade), chills, nausea, and vomiting.
 Most patients have had prior attacks of biliary colic
or acute cholecystitis.
 Pain lasts longer (i.e. >6hr) than in biliary colic
and more severe.
 Acute cholecystitis begins to subside in 2 to 3
days and resolves within 1 week in 85% of
patients.

25. CHOLECYCTITIS
 Chronic cholecystitis is long-standing gallbladder
inflammation almost always due to gallstones.
 Chronic cholecystitis almost always results from
gallstones and prior episodes of acute
cholecystitis (even if mild). Damage ranges from a
modest infiltrate of chronic inflammatory cells to a
fibrotic, shrunken gallbladder. Extensive
calcification due to fibrosis is called porcelain
gallbladder.
 Gallstones intermittently obstruct the cystic duct
and so cause recurrent biliary colic. Such
episodes of pain are not necessarily accompanied
by overt gallbladder inflammation; the extent of
inflammation does not correlate with the intensity
or frequency of biliary colic. Upper abdominal

26. Physical findings:
 Fever, tachycardia, and hypotension;
alert you to more serious infections,
including cholangitis, cholecystitis.
 Murphy’s sign - it is performed by
asking the patient to breathe out and
then gently placing the hand below the
costal margin on the right side at the mid-
clavicular line (the approximate location
of the gallbladder). The patient is then
instructed to inspire (breathe in).
Normally, during inspiration, the
abdominal contents are pushed
downward as the diaphragm moves
down (and lungs expand). If the patient
stops breathing in (as the gallbladder is
tender and, in moving downward, comes

28. Physical findings:
 Lepenet’s symptom – tenderness is revealed by a
light tapping of the right hypochondrium with flexed
fingers on inspiration.
 Kehr’s symptom – tenderness in the zone of
gallbladder (Kehr’s point) especially evident on
inspiration)
 Mussi’s sign – detects pain by pressing a point of the
phrenic nerve between peduncles of the right
sternocleidomastoid muscle.
 Gausman’s symptom – light tapping of the right
hypochondrium with breath holding on deep
inspiration (inflated abdomen) – tenderness on
inspiration suggests chronic cholecystitis, and on
expiration – a likelihood of pyloro-duodenal pathology.

29. Differentials
 Abdominal Aorta Aneurysm
 Appendicitis
 Cholangitis, cholelithiasis
 Diverticulitis
 Gastroenteritis
 Hepatitis
 Inflammatory Bowel Disease
 Myocardial Infarction
 Pancreatitis, renal colic, pneumonia

30. CHOLECYCTITIS - complication
 Perforation
 Empyema – pus in the gallbladder
 Gangrene
 Mirizzi’s syndrome – rarely, a gallstone becomes
impacted in the cystic duct or Hartman’s pouch
and compresses and obstructs the common bile
duct, causing cholestasis.
 Gallstone pancreatitis: Gallstones pass from the
gallbladder into the biliary tract and block the
pancreatic duct.
 Cholecystoenteric fistula: Infrequently, a large
stone erodes the gallbladder wall, creating a
fistula into the small bowel (or elsewhere in the

31. CHOLEDOCHOLITHIASIS
 Is the presence of stones in bile ducts; the stones
can form in the gallbladder or in the ducts
themselves. These stones cause biliary colic,
biliary obstruction, gallstone pancreatitis, or
cholangitis (bile duct infection and inflammation).
 Stones may be described as:
 Primary stones (usually brown pigment stones), which
form in the bile ducts
 Secondary stones (usually cholesterol), which form in
the gallbladder but migrate to the bile ducts
 Residual stones, which are missed at the time of
cholecystectomy (evident < 3 years later)
 Recurrent stones, which develop in the ducts > 3 years
after surgery.

32. CHOLEDOCHOLITHIASIS
 Essentials for diagnosis:
 Biliary pain
 Jaundice
 Episodic cholangitis
 Gallstones in gallbladder or previous cholecystectomy
 Signs:
 Patient may be icteric and toxic, with high fever and
chills, or may appear to be perfectly healthy.
 A palpable gallbladder is unusual in patients with
obstructive jaundice.
 Dark-tea coloured urine.

33. Acute Biliary Pancreatitis
 Gallstones are the most
common cause of acute
pancreatitis (AP), a
potentially life-
threatening condition,
worldwide.
 accounting for at least
one half of the 4.8-24.2
cases of pancreatitis per
100,000 people that
occur in Western
countries. About 80,000
cases occur in the USA;

34. Etiology
 ? ?Unknown ?? - But Gender and Stone size may be
risk factors.
 Suggested possible initiating events in gallstone
pancreatitis include the reflux of bile into the
pancreatic duct due to transient obstruction of the
ampulla during passage of gallstones.
 The risk of developing acute pancreatitis in patients
with gallstones is greater in men; however, more
women develop this disorder since gallstones occur
with increased frequency in women.

35. Prevailing Theory of Pathogenesis
 Common Channel
Theory
 sterile bile does not
result in pancreatitis.
However, infected bile is
capable of activating
pancreatic enzymes
leading to auto digestion
of the gland.
 reflux of infected bile into
the pancreas activating a
cascade of proteolytic
enzymes, and
obstruction of pancreatic
duct causing acinar
disruption from raised
pressure.

36. History/PE
 Severe epigastric pain
 radiating to the back
 Grey Turner’s sign
 Flank discoloration
 Cullen’s sign
 Periumbilical discoloration
 Nausea, vomiting, weakness, fever, shock

37. Clues for Differentials
 Prior History of Biliary Colic
 Rule out other causes of acute Pancreatitis
 Heavy alcohol consumption
 Medications
 Genetic diseases
 Infectious agents
 Postoperative states
 Endoscopic procedure involving pancreatic and bile
ducts and other types of injury to pancreas.

39. Investigations
 In patients with suspected gallstone
complications, blood work should include:
 CBC with differentials
 LFT – Liver Function Test
 Amylase and lipase.
 Abdominal Ultra Sound – sensitivity and specificity
are 95%. It also accurately detects sludge.
 Endoscopic Ultra Sound accurately detects small
stones (<3mm) and may be needed if other tests
are ambiguous.
 CT, MRI – though accurate but are not cost
effective.

40. Labs
 Serological inflammatory markers
 Serum amylase
 elevated in at least 75% of cases of acute pancreatitis and
remains elevated for 5-10 days in most patients.
 However, amylase lacks specificity.
 Serum lipase
 Serum lipase has a longer half life than amylase and therefore
tends to remain elevated for longer.
 Using a cut-off of three times the upper limit of normal, the
sensitivity of serum lipase for pancreatitis approaches 90% in
patients presenting with abdominal pain.
 Calcium

41. Investigations
 Ultra Sound
 Should be considered for initial investigation
 Can show enlarged pancreas with
 Stranding
 Abscess
 Hemorrhage
 Necrosis
 Pseudocyst
 The sensitivity of this study in detecting pancreatitis is
62 to 95 percent. However, in 35 percent of cases, the
pancreas is obscured secondary to bowel gas.

42. Imaging studies: Ultra Sound
 → denotes
gallstones
→
→  denotes the
► acoustic
shadow due to
absence of
reflected sound
waves behind
the gallstone

43. Investigations cont.
 Computed Tomography (CT) scan
 provides the best imaging of the pancreas and surrounding
structures.
 useful when other diagnostic studies are:
 Inconclusive
 when the patient has severe symptoms
 when fever is present
 in the face of persistent leukocytosis that suggests secondary infection.
 findings in pancreatitis may show inflammation characterized by
diffuse or segmental enlargement of the pancreas, with irregular
contour and obliteration of peri-pancreatic fat, necrosis or a
pseudocyst.

44. CT scan
 Contrast-enhanced axial
computed tomographic
section of the upper
abdomen showing peri-
pancreatic and
retroperitoneal
edema (large
arrows) and stranding.
The pancreas
itself (small
rrow) appears relatively
normal.

45. CT
 Contrast-enhanced
axial computed
tomographic section
of the upper
abdomen showing
peripancreatic and
retroperitoneal
edema. Large non-
enhancing areas of
necrosis are visible
in the body and neck
of the
pancreas (arrows).

46. CT
 Contrast-enhanced axial
computed tomographic
section of the upper
abdomen showing a well-
defined fluid collection in
the
retroperitoneum (arrow) just
below the level of the
pancreas.

47. Investigations cont.
 Early Endoscopic Retrograde
Cholangiopancreatography (ERCP)
 It is primarily indicated in patients with severe
disease who are suspected of having biliary
obstruction.
 The endoscope travels orally into the stomach,
through the pylorus into the duodenum where
the ampulla of Vater (the opening of the
common bile duct and pancreatic duct) exists.
 The sphincter of Oddi is a muscular valve that controls the
opening of the ampulla.
 Through the endoscope, the surgeon can see the inside of
the stomach and duodenum, and inject dyes into the ducts
in the biliary tree and pancreas so they can be further
visualized on X-rays.

48. ERCP
 Fluoroscopic image
of common bile duct
stone seen at the time of
ERCP.
 The stone is impacted in
the distal common bile
duct.
 A nasobiliary tube has
been inserted.

49. ERCP
 Fluoroscopic image
showing dilatation of the
pancreatic duct during
ERCP investigation.
 Endoscope is visible

50. HIDA SCAN
 A HIDA scan (hepatobiliary
iminodiacetic acid scan) is
radiodiagnostic procedure
that helps track the
production and flow of bile
from the liver to the small
intestine.
 It uses a radioactive
chemical, or tracer, that
helps highlight certain
organs on the scan. The
gallbladder should be
visualized between 1 – 4
hours.

51. HIDA SCAN
Normal Abnormal

52. Treatment
 Laparoscopic cholecystectomy with preoperative
endoscopic common bile duct clearance is
recommended as a treatment of choice for acute
biliary pancreatitis.
 Supportive care:
 IV fluids/electrolyte replacement
 Analgesia
 Bowel rest
 NG suction
 Nutritional support
 Oxygen

53. Treatment
 Symptomatic
 Laparoscopic cholecystectomy for symptomatic stones
 Open cholecystectomy, which involves a large
abdominal incision and direct exploration, is safe and
effective. Its overall mortality rate is about 0.1% when
done electively during a period free of complications.
 Asymptomatic
 For patients who decline surgery, or are at high risk of
surgical complications, but want to remove
asymptomatic stones; these gallstones can sometimes
be dissolved by ingesting bile acids orally for many
months.

54. Prognosis
 85-90% are mild and self-limiting
 10-15% are severe
 Which require ICU admission
 Mortality may approach 50% in severe cases
 Acute pancreatitis is a potentially fatal disease with an overall
mortality of 2 - 7% despite aggressive intervention.
 The outcome of acute pancreatitis is determined by two factors
which reflect the severity of the illness: organ failure and
pancreatic necrosis.
 About half of the deaths in patients with acute pancreatitis occur
within the first one/two weeks and are mainly attributable to multiple
organ dysfunction syndromes. When not treated, the risk of
recurrence in gallstone pancreatitis ranges from 32 to 61%.
 At least one study has shown that patients with severe biliary

55. Case 1 :
 46 year old female patient presents with RUQ
pain, jaundice, acholic stools, dark tea-colored
urine, no fevers
 Known history of cholelithiasis
 Exam: unremarkable
 WBC 8,000 per μl; Total Bilirubin is 8mg/dl,
increased AST/ALT , negative for Hepatitis B & C
 Ultrasound: Gallstones, Common Bile Duct stone,
dilated Common Bile Duct > 1cm
 CHOLEDOCHOLITHIASIS

56. Case 2
A 47-year-old man presents to the emergency room with sudden
onset of severe upper abdominal pain with vomiting. The pain is
focused in the epigastrium with radiation to the back. Serum
amylase levels are 2000 U/L.
 Which of the following are the most commonly encountered
predisposing factors for this patient‘s condition?
 A. Alcohol use and gallstones
 B. Helicobacter pylori infection and excess gastric acid secretion
 C. Hepatitis B infection and iron overload
 D. Obesity and high serum cholesterol
 E. Stress and cigarette use
 The correct answer is A. The clinical scenario is typical of acute
pancreatitis. The overwhelmingly most important contributing
factors for development of acute pancreatitis are gallstones
(particularly small ones) and alcohol abuse.