Gallbladder and Extrahepatic

Biliary System

Hamdy Sedky
Prof of GI Surgery
Embryology
Embryology
Embryology
Embryology
 Anatomy

 The gallbladder GB is related to the undersurface of the

liver between the 2 lobes

 GB is a pear-shaped sac, about 7–10 cm long. Average

capacity of 30–50 ml and can increase up to 300 ml.

 Unlike the rest of the GIT:

 GB wall consists of 3 layers as it lacks submucosa

 Mmuscularis mucosa and

 Muscolaris forms incomplete layer

 Anatomy
 The cystic artery is a branch of the right hepatic artery
(>90% ).

 The nerves of the gallbladder arise from the Vagus and

from sympathetic branches that pass through the celiac
plexus.

 Lymphatic drainage got to cystic LN, then to LNs along

the hepatic artery to Coeliac LNs
Anatomy
Calot’s triangle
 Anatomy
 The extrahepatic bile ducts include right and left hepatic
ducts, common hepatic duct, cystic duct and common bile
duct (CBD)
 The common hepatic duct is 1–4 cm in length and has a
diameter of approximately 4 mm.
 CBD is about 7–11 cm in length and 5–10 mm in diameter.
It consists of 3 parts.
Anatomy
Anatomy
Histology
 Anatomy
 CBD joins the MPD and enter the duodenal wall together in a
Y configuration to form a 2–10 mm long common channel that
often contains a dilation known as the ampulla of Vater.

 CBD runs obliquely downward within the wall of the

duodenum for 1–2 cm before opening on a papilla of mucous
membrane (major duodenal papilla), about 10 cm distal to the
pylorus (at the middle of D2).

 The sphincter of Oddi controls the flow of bile into the

duodenum.
Major papilla and sphincter of Oddi
 Anatomy
 The extrahepatic bile ducts are lined by a columnar mucosa
with numerous mucous glands in CBD. A fibroareolar tissue
containing scant smooth muscle cells surrounds the mucosa.

 The arterial supply to the bile ducts is derived from the

gastroduodenal and the right hepatic arteries, with major
trunks running along the medial and lateral walls of the
common duct.
Blood supply of the extra-
hepatic biliary system
 Anomalies
 The classic description of the extrahepatic biliary tree and its
arteries applies only in about 1/3 of patients.
 GB may have abnormal positions, be intrahepatic, be
rudimentary, have anomalous forms, or be duplicated.
 Anomalies of the hepatic artery and the cystic artery are quite
common, occurring in as many as 50% of patients.
 An accessory right hepatic duct occurs in 5% of patients.
 Small bile ducts (Duct of Luschka) may drain directly from
the liver into the body of the gallbladder.
Subvesical bile duct
 Physiology
Bile Formation and Composition
 The liver secrets 500–1000 ml of bile a day.

 With an intact sphincter of Oddi, bile flow is directed into the gallbladder.

 Bile is mainly composed of water, electrolytes, bile salts, proteins, lipids,

and bile pigments
Gallbladder Function
 The gallbladder, the bile ducts, and the sphincter of Oddi act together to
store and regulate the flow of bile.

 The main function of the gallbladder is to concentrate and store hepatic

bile and to deliver bile into the duodenum in response to a meal.

 Bile salts emulsify fat increasing its surface area.

Regulation of the GB function
 Diagnostic Studies
Laboratory investigations
 Liver FT (Bilirubin, AST, ALT,, ALP, GGT)

 CBC and CRP

 Tumour markers (CA 19-9)

Radiologic investigations
 Ultrasonography

 Computed Tomography (CT)

 Endoscopic ultrasonography (EUS)

 Intraoperative ultrasound (IUS)

 Diagnostic Studies

Radiologic investigations
 Biliary Radionuclide Scanning (HIDA Scan)

 Magnetic Resonance Imaging (MRI) & (MRCP)

 Percutaneous Transhepatic Cholangiography (PTC)

 Endoscopic Retrograde Cholangiopancreatography (ERCP)

 Intra-operative cholangipgraphy (IOC)

 T-tube cholandiography
 Ultrasonography

1. Normal gallbladder 2. Gall stones

 Biliary Radionuclide Scanning (HIDA Scan)

A: liver parenchyma .Acute cholecystitis

B: gallbladder
C: small bowel
D: common bile duct
E: intra-hepatic bile duct
Diagnosis of:
Normal hepatobiliary scintigraphy  Acute cholecystitis
 Biliary leaks
Computed Tomography (CT)
Percutaneous Transhepatic Cholangiography
(PTC)
Magnetic Resonance Imaging (MRI)& (MRCP)
Endoscopic Retrograde Cholangiopancereaticography
(ERCP)
 Intra-oprative
cholangiography
(IOC)
 Gallstone Disease
 Incidence
 Autopsy reports have shown a prevalence of gallstones from 11–36 %.

 F:M ratio 3:1

 Obesity, pregnancy, dietary factors, Crohn disease, terminal ileal disease or resection, gastric

surgery, hereditary spherocytosis, and haemolytic anaemias.

 Natural History
 Mostly asymptomatic .. discovered accidently ..

 1-3% become symptomatic /year

 Symptomatic with biliary pain →→complications in 3-5%

 Over a 20-year period, about two-thirds of asymptomatic patients with gallstones remain

symptom free

 Formation
 Gallstone disease

 Types

1. Cholesterol Stones

 Due to supersaturation of bile with cholesterol.

 Colors range from whitish yellow and green to black.

 Most cholesterol stones are radiolucent

• Pure Cholesterol Stones (10%): single large stones with smooth

surfaces

• Mixed Cholesterol Stones (70%) at least 70% of their weight is

cholesterol. Multiple, of variable size, and may be hard and faceted or

irregular, mulberry-shaped and soft.

Pure cholesterol stone

Mixed cholesterol stone

 Gallstone disease

2. Pigment stones
 Black 15-20%
• Small, brittle, black, and sometimes spiculated.

• Secondary to hemolytic disorders and cirrhosis. Almost always

form in the gallbladder

 Brown
• Less than 1 cm in diameter, brownish-yellow, soft, and often

mushy.

• may form either in the gallbladder or in the bile ducts usually

secondary to bacterial infection caused by bile stasis

 Gallstone disease

 Complications
 In the gall bladder
 Mucocele of the gall bladder
 Acute calcular cholecystitis ,empyema, gangrene, perforation.
 Chronic calcular cholecystitis.
 Carcinoma of the gall bladder.

 Due to migration
 Obstructive jaundice.
 Cholangitis.
 Pancreatitis.
 Gallstone ileus.
 Chronic Calcular Cholecystitis

About two thirds of patients with gallstone disease present

with chronic cholecystitis
 Pathology

The pathologic changes, vary from an apparently normal

gallbladder with minor chronic inflammation in the mucosa, to
a shrunken, nonfunctioning gallbladder with gross transmural
fibrosis and adhesions to nearby structures
 Chronic Calcular Cholecystitis

 Clinical presentation
 Recurrent attacks of biliary pain.
• Caused by a stone obstructing the outflow of the GB.
• Severe, constant and increases in severity over the first half hour or so
and typically lasts 1–5 h.
• Comes on abruptly, typically during the night or after a fatty meal .
• It is located in the epigastrium or right upper quadrant and frequently
radiates to the right upper back or between the scapulae.
• It often is associated with nausea and sometimes vomiting.

 Mild right upper quadrant tenderness during an episode of pain.

 Chronic Calcular Cholecystitis

 Diagnosis
 Abdominal ultrasonography.
 Chronic Calcular Cholecystitis

 Management
 Until surgery , the
patient should be advised
to avoid dietary fats and
large meals.
 Elective laparoscopic or
open cholecystectomy.
Laparoscopic cholecystectomy
 Chronic Calcular Cholecystitis
 Management
 Since patients rarely develop complications without previous
biliary symptoms, prophylactic cholecystectomy in
asymptomatic persons with gallstones rarely is indicated.
 For post-transplant patients, patient dependent on life-long
TPN and in populations with increased risk of gallbladder
cancer, a prophylactic cholecystectomy may be advisable.
 Porcelain gallbladder, a rare premalignant condition in which
the wall of the gallbladder becomes calcified, is an absolute
indication for cholecystectomy..
 Acute Calculous Cholecystitis

 Pathogenesis
 Secondary to gallstones in 90–95 % (Acute calculous cholecystitis)
 Obstruction of the cystic duct by a gallstone → gallbladder distention,
inflammation, and edema → Secondary bacterial contamination → empyema
 In 5–10 %, the inflammatory process progresses and leads to ischemia and
necrosis of the gallbladder wall.
 More frequently, the gallstone is dislodged and the inflammation resolves.

 Pathology
 The gallbladder wall becomes grossly thickened and reddish with subserosal
hemorrhages & pericholecystic fluid.
 The mucosa may show hyperemia and patchy necrosis.
 Acute Calculous Cholecystitis

 Clinical picture
 Attack of biliary pain, in which the pain does not subside and
may persist for several days.
 Fever, anorexia, nausea, and vomiting.

 Focal tenderness and guarding in the right upper quadrant.

 A mass (the gallbladder and adherent omentum) is occasionally

palpable; however, guarding may prevent this.
 (+) Murphy’s sign.
 Acute Calculous Cholecystitis

 Complication
 Perforation causing
generalized
peritonitis or
subphrenic abscess.
 Mirrizi syndrome.
 Gallstone ileus.
 Acute Calculous Cholecystitis

Gallstone ileus
Acute Calculous Cholecystitis
 Acute Calculous Cholecystitis
 Diagnosis
 +ve CRP and mild to moderate leukocytosis.

 Normal or mildly elevated liver function (Bilirubin less than 3.5 mg/dl) .

 Ultrasonography is the most useful radiologic test for diagnosing

acute cholecystitis.

 HIDA scan may be of help in the atypical case →→ non

visualization of the gallbladder.

 CT scan →→ thickening of the gallbladder wall, pericholecystic

fluid, and the presence of gallstones and air in the gallbladder wall.
 Acute Calculous Cholecystitis

 Treatment
1. Cholecystectomy (lap. or open) is the definitive treatment for acute cholecystitis.
• Emergency cholecystectomy: within 2-3 days ----(preferred).

• Delayed cholecystectomy: 6-10 weeks after initial medical treatment and recovery.

2. Medical treatment: When patients present late, after 3–4 days of illness, or are for some
reason unfit for surgery

• Intravenous fluids.

• Antibiotics (cover Gram negative aerobes and anaerobes).

• Analgesia.

 Approximately 30% of patients will either fail to respond to initial medical therapy, develop
relapse after initial improvement or develop complications and require an intervention. ………
percutaneous cholecystostomy or an open cholecystostomy
 Acute Acalculous Cholecystitis
 Etiology
 Acalculous cholecystitis typically develops in critically ill patients in ICU

 The cause is unknown, but gallbladder distention with bile stasis and ischemia have

been implicated as causative factors.

 Clinical picture
 In the alert patient is similar to acute calculous cholecystitis.

 In patient with disturbed conscious level ----- metabolic disturbance

 U/S is diagnostic.

 Treatment
 Ultrasound- or CT-guided cholecystostomy

 Open cholecystostomy or cholecystectomy is rarely possible

 Choledocholithiasis
(Common bile duct stones)

 Incidence
• Found in 15% of patients with gallbladder stones.

• The incidence increases with age reaching 20-25% above 60 y.

 Type
 Secondary: formed within the gallbladder and migrate down the cystic
duct to the common bile duct.
 Primary : that form in the bile ducts.
 Choledocholithiasis

GB STONE
100

CBD STONE
15

Asymptomatic Symptomatic
6 9

Biliary pain Pancreatitis Cholangitis Jaundice

2 1 3 3

The natural history of common bile duct stones

 Choledocholithiasis
 Clinical manifestations
 It may be silent ---- discovered incidentally.

 Symptomatic:

• They may cause obstruction, complete or incomplete, or they may manifest

with cholangitis or gallstone pancreatitis.
• Pain similar to that of biliary colic, Nausea and vomiting.
• Mild epigastric or right upper quadrant tenderness.
• Mild icterus.
• Elevation of serum bilirubin, alkaline phosphatase, and transaminases
 This picture may be intermittent (a ball valve stone).

 The stones may become completely impacted, causing severe progressive jaundice.
 Choledocholithiasis

 Diagnostic studies
 Commonly the first test, is Ultrasonography
 Magnetic resonance cholangiography (MRCP): non-invasive
 Endoscopic cholangiography (ERCP): it has the distinct advantage of
providing a therapeutic option at the time of diagnosis .
 Choledocholithiasis
 Treatment
1. Endoscopic sphincterotomy and ductal clearance of the stones
followed by a laparoscopic cholecystectomy is the optimal option
(one or two stages).
2. Laparoscopic cholecystectomy and Laparoscopic common bile
duct exploration (skills & instrumentation).
3. Open cholecystectomy and common bile duct exploration is an
option if the endoscopic method has already been tried and failed
or is for some reason not feasible. After CBD clearance, a T-tube
is usually left in the CBD.
 Choledocholithiasis
 Treatment
 If a common bile duct exploration was performed and a T-tube left in
place, a T-tube cholangiogram is obtained prior to its removal.
 Retained stones can be retrieved either endoscopically or via the T-tube
tract once it has matured (2–4 weeks).
 Stones impacted in the ampulla may be difficult for both endoscopic
ductal clearance and common bile duct exploration (open or
laparoscopic). In these cases the common bile duct usually is quite dilated
(about 2 cm in diameter). Choledochoduodenostomy or Roux-en-Y
choledochojejunostomy may be the best option for these circumstances.
 Retained or recurrent stones following cholecystectomy are best treated
 Ascending Cholangitis

 Is an ascending bacterial infection

in association with partial or
complete obstruction of the bile
ducts.
 Gallstones are the most common
cause of obstruction in cholangitis.
 The most common organisms
include Escherichia coli, Klebsiella
pneumoniae, Streptococcus
faecalis, and Bacteroides fragilis.
 Ascending Cholangitis
 Clinical presentation
 Cholangitis may present as anything from a mild, intermittent,
and self-limited disease to a fulminant, potentially life-
threatening septicemia.
 The most common presentation is fever, epigastric or right
upper quadrant pain, and jaundice. (Charcot triad)
 The illness may progress rapidly to Reynolds pentad (fever,
jaundice, right upper quadrant pain, septic shock, and mental
status changes).
 Ascending Cholangitis
 Diagnosis.
 +ve CRP, Leukocytosis, hyperbilirubinemia and elevation of alkaline
phosphatase and transaminases with above presentation in a patient
having gallstones.
 Both ERCP and PTC will show the level and the reason for the
obstruction, allow culture of the bile, possibly allow the removal of
stones if present, and drainage of the bile ducts with drainage
catheters or stents.
 CT scanning and MRI will show pancreatic and periampullary
masses, if present, in addition to the ductal dilatation .
 Ascending Cholangitis

 Management
 IV antibiotics and fluid resuscitation then, the obstructed
bile duct must be drained as soon as the patient has been
stabilized.
 Biliary decompression may be accomplished
endoscopically, via the percutaneous transhepatic route,
or surgically with a T-tube.
 Bile Duct Strictures
 Causes
 Iatrogenic injury,

 Fibrosis because of chronic pancreatitis, common bile duct

stones, acute cholangitis,

 Biliary obstruction because of cholecystolithiasis (Mirizzi

syndrome), and

 Strictures of a biliary-enteric anastomosis.

 Bile Duct Strictures

 Diagnosis and Treatment

 Progressive jaundice with repeated episodes of cholangitis.
 Laboratory: biliary obstruction and 2ry bacterial infection
 Ultrasound , CT scan, MRCP provide anatomic information
about the location and the degree of dilatation
 ERCP , PTC diagnostic and therapeutic by dilatation and
stenting for distal and proximal strictures respectively.
 Surgery with Roux-en-Y choledochojejunostomy or
hepaticojejunostomy is the standard of care
 Choledochal cysts
 incidence
 is 1:100,000 to 1:150,000, F:M=3-8:1
 The risk of cholangiocarcinoma is as high as 15 %

 Pathology
 Classified into five types.
 Lined with cuboidal epithelium and can vary in size from 2 cm in
diameter to giant cysts.

 Clinical
 The classic clinical triad of abdominal pain, jaundice, and a mass.
 Adults commonly present with jaundice or cholangitis
 Choledochal cysts

 investigations
 U/S, CT, MRCP, PTC, ERCP.

• Treatment
– For types I, II, and IV, excision of the extrahepatic biliary
tree, including cholecystectomy, with a Roux-en-Y
hepaticojejunostomy .
– For type III, sphincterotomy is recommended.
 Carcinoma of the Gallbladder
 Incidence
 2-3 times more common in females than males.

 The peak incidence is in the seventh decade of life.

 Incidentally discovered in 1% of patients undergoing cholecystectomy for

gallstone disease.
 Etiology
 90% of patients with carcinoma of the gallbladder have gallstones.

 0.3-0.5% of patients with gallstones will develop carcinoma of the gallbladder.

 The risk of cancer, increases in gall bladder polyps larger than 10 mm.

 Porcelain gallbladder is associated with >20% incidence of gallbladder

carcinoma.
 Porcelain gallbladder
Carcinoma of the
Gallbladder
 Carcinoma of the Gallbladder
 Pathology

 Adenocarcinoma or rarely SCC.

 Spreads through the lymphatics, with venous drainage and with direct

invasion into the liver parenchyma.

 Clinical Manifestations and Diagnosis

 Abdominal discomfort, right upper quadrant pain, nausea and vomiting.

 Jaundice, weight loss, anorexia, ascites, and abdominal mass

 CEA and CA 19-9

 Ultrasound, CT, MRCP.

 Carcinoma of the Gallbladder

 Treatment
 Simple cholecystectomy is an adequate treatment for T1 tumors
identified incidentally, after cholecystectomy for gallstone disease.
 Extended cholecystectomy for T2 tumors (segments IVB and V, and
lymphadenectomy of the cystic duct, and pericholedochal, portal,
and posterior pancreatoduodenal lymph nodes)
 Palliative procedures for advanced cases.
 Prognosis
The 5-year survival rate of all patients with gallbladder cancer is
<5%.
Carcinoma of the Gallbladder
 Bile Duct Carcinoma
 Incidence: 0.3%
 Risk factors:

Primary sclerosing cholangitis, choledochal cysts, ulcerative colitis,

hepatolithiasis, biliary-enteric anastomosis and biliary tract infections with
Clonorchis.
 Pathology
 95 % of are adenocarcinomas.
 Morphologically It may be nodular (the most common type), scirrhous,
diffusely infiltrating, or papillary.
 Anatomically it may be distal, proximal, or perihilar (the commonest 2
thirds and referred to as Klatskin tumors).
Klatskin tumour
 Bile Duct Carcinoma
 Clinical Manifestations
 Painless jaundice is the most common presentation.

 Pruritus, mild right upper quadrant pain, anorexia, fatigue, and weight loss.

 Diagnosis
 CEA and CA 19-9

 The initial tests are usually ultrasound or CT scan.

 PTC defines the proximal extent of the tumor, which is the most important factor
in determining resectability.
 ERCP is used, particularly in the evaluation of distal bile duct tumors.

 MRI has the potential of evaluating the biliary anatomy, lymph nodes, and
vascular involvement and the tumor growth itself.
 Klatskin tumour,
Gross view

Klatskin tumour,
CT scan
 Klatskin tumour,
ERCP

Klatskin tumour,
MRCP
 Bile Duct Carcinoma

 Treatment
 Surgical excision is the only potentially curative treatment for resectable
tumour.
 The target of surgery is:
• Excision of the tumour with safety margin
• Dissection of the draining LNs
• Leaving sufficient residual liver volume draining its bile duct to Roux-
en-Y jejunal limb
 Palliative procedure is required for irresectable or metastatic disease.
Distal bile duct cancer