3. Anatomy and physiology
• The ampulla of Vater contains the distalmost portion of the common bile duct
and inserts into the wall of the duodenum. The pancreatic duct also joins the
ampulla and may fuse with the bile duct before passing through the wall of
the duodenum or within the wall of the duodenum, or it may have a separate
orifice within the ampulla.
• The most inferior portion of the common bile duct is encompassed by the head
of the pancreas. Superior to the intrapancreatic portion, the common bile duct
is divided into retroduodenal and supraduodenal segments. The insertion of
the cystic duct marks the differentiation of the common hepatic duct above
and the common bile duct below.
4. • The cystic duct drains the gallbladder, which is divided into the neck,
infundibulum with Hartmann pouch, body, and fundus. Roughly the size
and shape of a common light bulb, the gallbladder holds 30 to 60 mL of bile
as an extrahepatic reservoir. The gallbladder is attached to the inferior
surface of the liver and is enveloped by liver for a variable portion of its
circumference. Although some gallbladders are almost enveloped by liver
parenchyma, others hang on a mesentery, predisposing to volvulus. The
attachment of the gallbladder to the liver, known as the gallbladder fossa,
identifies the separation of the left and right lobes of the liver. Where the
gallbladder attaches to the liver, Glisson capsule does not form, and this
common surface provides most of the venous drainage of the gallbladder.
5. • The cystic duct drains at an acute angle into the common bile duct and can
range from 1 to 5 cm in length. There are a number of anatomic variations in
insertion of the cystic duct, including into the right hepatic duct. Within the
neck of the gallbladder and cystic ducts lie folds of mucosa oriented in a
spiral pattern, known as the spiral valves of Heister, which act to keep
gallstones from entering the common bile duct in spite of distention and
intraluminal pressure. The dependent portion of Hartmann pouch may
overlie the common hepatic or right hepatic ducts, thus placing these
structures at risk during the performance of a cholecystectomy.
• Above the cystic duct lies the common hepatic duct, draining the left and
right hepatic duct systems.
6. • The extrahepatic bile ducts consist of the right and left hepatic ducts, the
common hepatic duct, the cystic duct, and the common bile duct or
choledochus. The common bile duct enters the second portion of the
duodenum through a muscular structure, the sphincter of Oddi.
• The left hepatic duct is longer than the right and has a greater propensity for
dilatation as a consequence of distal obstruction. The two ducts join to form a
common hepatic duct, close to their emergence from the liver. The common
hepatic duct is 1 to 4 cm in length and has a diameter of approximately 4
mm. It lies in front of the portal vein and to the right of the hepatic artery.
The common hepatic duct is joined at an acute angle by the cystic duct to
form the common bile duct.
• The length of the cystic duct is quite variable. It may be short or absent and
have a high union with the hepatic duct, or long and run parallel, behind, or
spiral to the main hepatic duct before joining it, sometimes as far as at the
duodenum. Variations of the cystic duct and its point of union with the
common hepatic duct are surgically important
7. The common bile duct is about 7 to 11 cm in
length and 5 to 10 mm in diameter.
The common bile duct runs obliquely downward
within the wall of the duodenum for 1 to 2 cm
before opening on a papilla of mucous
membrane (ampulla of Vater), about 10 cm
distal to the pylorus. The union of the common
bile duct and the main pancreatic duct follows
one of three configurations. In about 70% of
people, these ducts unite outside the duodenal
wall and traverse the duodenal wall as a single
duct. In about 20%, they join within the duodenal
wall and have a short or no common duct, but
open through the same opening into the
duodenum. In about 10%, they exit via separate
openings into the duodenum. The sphincter of
Oddi, a thick coat of circular smooth muscle,
surrounds the common bile duct at the ampulla
of Vater . It controls the flow of bile, and in some
cases pancreatic juice, into the duodenum.
8. • 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 (sometimes referred to as 3 o’clock and 9
o’clock). These arteries anastomose freely within the duct walls. The density
of nerve fibers and ganglia increases near the sphincter of Oddi, but the
nerve supply to the common bile duct and the sphincter of Oddi is the same
as for the gallbladder
9.
10.
11.
12. Biliary Tract
Part of the digestive system.
Made up of:
• Intra hepatic ducts
• Exta hepatic ducts
• Gallbladder
• Common Bile Duct
13.
14. The Gallbladder
The GB- concentrates and stores bile.
Bile:
• Secreted by the liver
• Cholesterol, bile pigments and
phospholipids
• Liver- hepatic ducts-GB -cystic duct
- common bile duct-Duodenum
• Digestion & absorption -fatty foods
and fat-soluble vitamins
15.
16. Gallstones – Pathophysiology
• Altered Ratio of cholesterol, phospholipids, and bile salts > cholesterol
crystals
• Gallstone formation :
• Cholesterol supersaturation
• Mucin hypersecretion
• Bile stasis
Four major factors explain most gallstone formation:
supersaturation of secreted bile, concentration of bile in
the gallbladder, crystal nucleation, and gallbladder
dysmotility.
17. Gallstones – Types
• Two main types:
• Cholesterol stones (85%):
Pure (90-100% cholesterol
• Solitary, whitish, and larger than 2.5 cm in diameter.
Mixed (50-90% cholesterol).
• Smaller, multiple in number, and occur in various shapes and colors.
• multiple, faceted
• Pigment stones (15%)
• Brown stones - calcium bilirubinate and calcium-soaps.
Bacteria - beta glucuronidase and phospholipase
Tend to be found in the bile ducts and are thought to be secondary to infection. The
difference in color comes from incorporation of cholesterol into the brown stones.
• Black stones - excess bilirubin - calcium bilirubinate
Eg. chronic hemolysis, cirrhosis
18. • Because black pigment stones occur in hemolytic states from concentration
of bilirubin, they are found almost exclusively in the gallbladder.
Alternatively, brown stones occur within the biliary tree and suggest a
disorder of biliary motility and associated bacterial infection
19. Epidemiology
• Common (20% population)
• Cholesterol stones in West
• Risk factors
• Sex (F:M=3:1)
• Age
• Genetics
• Obesity
• Estrogen
• Hypercholesterolaemia
• 5 F’s
• Disruption : Enterohepatic circulation- bile salt
• Biliary stasis
• Biliary infections
• DM
It is common in fat, fair,
fertile,, forty,
flatulent female.
20. Gallstones – Natural History
• 80% of patients, gallstones are clinically
silent
• 20% of patients develop symptoms over
15-20 years
• About 1% per year
• Almost all become symptomatic before
complications develop
21. Clinical manifestation
• Asymptomatic
• Biliary colic: pain that starts 10 -30 min after fatty food reach peak in 2 hrs
then decrease. If pain continue for more than 6hrs its not B.C
• the pain of biliary colic is usually constant and not colicky. The classic description is of an intense, dull discomfort
located in the right upper quadrant, epigastrium, or (less often) substernal area that may radiate to the back
(particularly the right shoulder blade)
• Ruq pain radiate to back [Boas sign]
• Dyspepsia
• Complications
• Cholecystitis
• Choledocholithiasis
• Pancreatitis
• Mirizzi syndrome:
• Cholangitis
• Gallstone ileus
• Carcinoma of gallbladder
22.
23. Complications of Gallstones
• In the gallbladder
• Biliary colic
• Acute and chronic cholecystitis
• Empyema
• Mucocoele
• Carcinoma
• perforation
• In the bile ducts
• Obstructive jaundice
• Pancreatitis
• Cholangitis
• In the Gut
• Gallstone ileus
Large gallstones can become impacted in the cystic duct
or in Hartmann's pouch. These stones can produce
common hepatic duct obstruction (the Mirizzi syndrome)
by two mechanisms: mechanical obstruction of the hepatic
duct because of the proximity of the cystic duct and the
common hepatic duct, and secondary inflammation with
frequent episodes of cholangitis.
•Type I – External compression of the common hepatic duct due to a stone
impacted at the neck of the gallbladder or at the cystic duct.
•Type II – The fistula involves less than one-third of the circumference of the
common bile duct.
•Type III – Involvement of between one-third and two-thirds of the
circumference of the common bile duct.
•Type IV – Destruction of the entire wall of the common bile duct.
24.
25. Investigations
• Ultrasound
• R/O Other causes of abd.pain
Eg. UGI Endoscopy
Treatment
• Cholecystectomy
• Symptomatic patients
• Fit for surgery
• Laparoscopic
Stone cast acoustic shadow
- DM [emphesematous GB]
- Pregnant
- Pts away from health care like pilots
26. Acute Cholecystitis
• Acute inflammation of the gallbladder
• Usually associated with calculi (stones)
• Obstruction at Hartmann's pouch or cystic
duct
• Less commonly with biliary sludge
• A-calculus (no-stone) cholecystitis rare
• Due to other systemic condition: sepsis,
burn, trauma
• Bacterial infection < 50%
• Recurrent attacks - fibrosed thickened
gallbladder (chronic cholecystitis)
• The production of lysolecithin from
lecithin is catalyzed by phospholipase A,
which is present in gallbladder mucosa.
This enzyme may be released into the
gallbladder following trauma of the
gallbladder wall from an impacted
gallstone . Supporting this hypothesis is
the observation that lysolecithin (normally
absent in bile) is detectable in gallbladder
bile in patients with acute cholecystitis
27. Clinical manifestations.
• Symptoms
• Right upper quadrant pain – continuous, >4-6 hrs
• Patients with acute cholecystitis typically complain of
abdominal pain, most commonly in the right upper
quadrant or epigastrium. The 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. There is often a history of fatty food
ingestion about one hour or more before the initial
onset of pain.
• Signs
• Tachycardia, fever
• RUQ tenderness
• Murphy’s sign
28. Tenderness and the presence of Murphy sign help
distinguish acute cholecystitis from biliary colic, in
which there is no inflammatory process.
profound jaundice in the setting of a picture of
acute cholecystitis is rare and should raise the
suspicion of cholangitis, with obstruction of the
common bile duct, or Mirizzi syndrome, in which
inflammation or a stone in the gallbladder neck
leads to inflammation of the adjoining biliary
system, with obstruction of the common hepatic
duct.
29. • Investigations
• Leucocytosis…left shift
• CRP, LFT[moderately elevated]
• Ultrasound of abdomen
• Thickened gallbladder wall [> 4mm]
• peri-cholecystic fluid and stones
• Sonographic murphy’s sign
• Treatment
• Nil by mouth……IV fluid
• Analgesia
• Intravenous antibiotics: ceftriaxone and metrindazole
• Cholecystectomy
• once a patient develops symptoms or complications related to gallstones (such as biliary colic
or acute cholecystitis), treatment to eliminate the gallstones should be recommended, because
the likelihood of subsequent symptoms or complications is high.
Transabdominal ultrasonography is a sensitive,
inexpensive, and reliable tool for the diagnosis of acute
cholecystitis, with a sensitivity of 85% and specificity of
95%. In addition to identifying gallstones, ultrasound can
demonstrate pericholecystic fluid , gallbladder wall
thickening, and even a sonographic Murphy sign,
documenting tenderness specifically over the gallbladder.
31. • the primary pathophysiologic mechanism is unresolved cystic duct obstruction. Without resolution
of the obstruction, the gallbladder will progress to ischemia and necrosis. Eventually, acute
cholecystitis becomes acute gangrenous cholecystitis and, when complicated by infection with a gas-
forming organism, acute emphysematous cholecystitis
• When the gallbladder remains obstructed and secondary bacterial infection supervenes, an acute
gangrenous cholecystitis develops, and an abscess or empyema forms within the gallbladder. Rarely,
perforation of ischemic areas occurs.
• The perforation is usually contained in the subhepatic space by the omentum and adjacent organs.
However, free perforation with peritonitis, intrahepatic perforation with intrahepatic abscesses, and
perforation into adjacent organs (duodenum or colon) with cholecystoenteric fistula occur. When
gas-forming organisms are part of the secondary bacterial infection, gas may be seen in the
gallbladder lumen and in the wall of the gallbladder on abdominal radiographs and CT scans, an
entity called an emphysematous gallbladder.
34. Choledocholithiasis
• Presence of Stone –common Bile duct
• Most – secondary stones (GB)
Primary stones: Clinical manifestation
• Asymptomatic
• Biliary colic
• Obstructive jaundice
• Cholangitis
35. • Primary common duct stones arise de novo in the bile duct, and secondary
common duct stones pass from the gallbladder into the bile duct. Primary
choledocholithiasis is generally from brown pigment stones, which are a
combination of precipitated bile pigments and cholesterol.
• most choledocholithiasis remains clinically silent.When not clinically silent,
common duct stones may be manifested with symptoms ranging from biliary
colic to the clinical manifestations of obstructive jaundice, such as darkening
of the urine, scleral icterus, and lightening of the stools.
• Jaundice with choledocholithiasis is more likely to be painful because the
onset of obstruction is acute, causing rapid distention of the bile duct and
activation of pain fibers.
36. • The secondary stones are usually cholesterol stones, whereas the primary stones are usually of the
brown pigment type.
• The causes of biliary stasis that lead to the development of primary stones include biliary stricture,
papillary stenosis, tumors, or other (secondary) stones, cystic fibrosis
• The pain is often more prolonged than is seen with typical biliary colic and resolves with
either spontaneous passage or removal of the CBD stone. Some patients have intermittent
pain due to transient blockage of the CBD. Transient blockage occurs when there is
retention and floating of stones or debris within the bile duct, a phenomenon referred to
as a "ball-valve" effect. right upper quadrant or epigastric pain, nausea, and vomiting.
• Clinical manifestation
Pancreatitis and cholangitis could be
complications
37. • Investigations
• LFT- ALP, Bilirubin (T&D), GGT[gamma-glutamyl transpeptidase]
• Ultrasound of abdomen: stones in the gallbladder (if still present), as well as
determining the size of the common bile duct. [(>8 mm in diameter)], stone in CBD
• Endoscopic cholangiography is the gold standard for diagnosing common bile duct
stones. It has the distinct advantage of providing a therapeutic option at the time
of diagnosis.
• Complications like pancrititis, bleeding, perforations
• MRCP, ERCP
• Treatment
• Endoscopic Retrograde CholangioPancreatogram
• Open Choledocholithotomy
• Cholecystectomy
• If a choledochotomy is performed, a T tube is left in place. T- tube for
drainage and therapeutic for inserting contrast
38.
39. Ascending Cholangitis
• Infection of the obstructed biliary system
• The organisms typically ascend from the duodenum; hematogenous spread from the portal vein
is a rare source of infection
• Mechanical hindrance to bile flow facilitates bacterial contamination.
• The most common organisms cultured from bile in patients with cholangitis include
Escherichia coli, Klebsiella pneumoniae, enterococcus , Streptococcus faecalis, Enterobacter,
and Bacteroides fragilis.
• Chronic biliary obstruction raises the intrabiliary pressure, a central pathogenetic event in the
development of acute cholangitis. High pressure promotes the migration of bacteria from the
portal circulation into the biliary tract and subsequent colonization.
• When the barrier mechanism is disrupted, as occurs after endoscopic sphincterotomy,
choledochal surgery, or biliary stent insertion, pathogenic bacteria enter the biliary system at
high concentrations. Thus, cholangitis frequently develops after endoscopic or percutaneous
manipulation with incomplete biliary drainage or as a late complication of stent blockage.
40. • Symptoms
• Charcot’s triad : fever, RUQ pain, jaundice (50%)
• Vomiting and Abnormal mentation
• Reynolds’ pentad (e.g., fever, jaundice, right upper quadrant pain, septic shock, and
mental status changes).
• Signs
• Sepsis (Fever, tachycardia, low BP), Jaundice & RUQ tenderness
• Done during the same admission
41. • Investigations
• Leucocytosis
• LFT- Abnormal[elevations in the serum alkaline phosphatase,
gammaglutamyl transpeptidase (GGT), and bilirubin
(predominantly conjugated) concentration]
• Ultrasound of abdomen: dilation of common and intrahepatic
duct, stone
• ERC: endoscopic retrograde cholangiography.
• Blood culture
• Bile cultures: Obtain to facilitate proper antibiotic treatment;
offending organisms are usually enteric gram negatives and
enterococc.
• Treatment
• IV fluid resuscitation
• Intravenous antibiotic- Gm Negatives , Anaerobes
• Persistent sepsis- Emergency biliary decompression by ERCP or
T tube: if not responding to anti biotic in 24 hrs
• choledochotomy , Cholesystectomy & CBD exploration / ERCP
with bile duct clearance
• Surgery deferred until cholangitis is treated
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
42. • Primary sclerosing cholangitis (PSC) is a chronic progressive disorder of
unknown etiology that is characterized by inflammation, fibrosis, and
stricturing of medium size and large ducts in the intrahepatic and
extrahepatic biliary tree . The great majority of cases have underlying
ulcerative colitis.
• Fatigue and pruritus are common features at presentation. Fevers, chills,
night sweats, and right upper quadrant pain can also be present. These
features may represent episodic bacterial cholangitis from biliary obstruction
rather than advanced disease. Liver biochemical tests may worsen during
these episodes, but persistent jaundice usually reflects advanced disease.
• Continued destruction of bile ducts in PSC leads to end-stage liver disease
and portal hypertension. Patients with PSC also may develop a number of
other complications, including:
• Cholestasis-associated problems, Biliary stricture, Cholangitis and
cholelithiasis, Cholangiocarcinoma, Colon cancer (in patients with
concomitant ulcerative colitis)
46. Choledochal cysts
Choledochal cysts are
congenital dilations of the intra- and/or
extrahepatic biliary system.
• Uncommon abnormality
• 50% present with combination of
jaundice, abdominal pain, and an
abdominal mass.
• ? Due to anomalous union of the
pancreatic and biliary ductal system.
47. • Patients may present at any age with
jaundice, fever, abdominal pain and a
right upper quadrant mass on
examination,
• however, 60 per cent of cases are
diagnosed before the age of ten years.
Pancreatitis is not an infrequent
presentation in adults.
• Patients with choledochal cysts have an
increased risk of developing
cholangiocarcinoma with the risk
varying directly with the age at
diagnosis
48.
49. • More in female
• Weakness of the bile duct wall and increased
pressure secondary to partial biliary obstruction
are required for biliary cyst formation.
• More than 90% of patients have an anomalous
pancreaticobiliary duct junction, with the
pancreatic duct joining the common bile duct >1
cm proximal to the ampulla. This results in a
long common channel that may allow free reflux
of pancreatic secretions into the biliary tract,
leading to inflammatory changes, increased
biliary pressure, and cyst formation.
• Ultrasonography or CT scanning will confirm
the diagnosis, but endoscopic cholangiography,
transhepatic cholangiography, or MRC is
required to assess the biliary anatomy and to
plan the appropriate surgical treatment.
50. • Todani classification- 5 types
• Complications
-Ascending cholangitis (Recurrent)
-Cholangiocarcinoma
-Biliary cirrhosis
• Treatment - surgical (excision of the cyst with
construction)
54. Endoscopic retrograde cholangiopancreatography
(ERCP) is an endoscopic technique in which a
specialized side-viewing upper endoscope is guided
into the duodenum, allowing for instruments to be
passed into the bile and pancreatic ducts. These are
opacified by injection of a contrast medium, thereby
permitting their visualization and allowing for a variety
of therapeutic interventions. It is a relatively complex
endoscopic procedure since it requires specialized
equipment and has a long learning curve to develop
proficiency. Its benefits in the minimally invasive
management of biliary and pancreatic disorders are
challenged by a higher potential for serious
complications than any other standard endoscopic
technique
Complications: pancreatitis [most common], bleeding ,
infection, perforation
61. Carcinoma of the gall bladder
• This is a rare disease, but extremely variable by geographical region and
racial–ethnic groups. The highest incidence is among Chileans, American
Indians and residents in parts of northern India, where it accounts for as
much as 9 per cent of all biliary tract disease. Women appear to have a
higher incidence across all geographic areas.
• The aetiology is unclear, but there appears to be an association with pre-
existing gallstone disease suggesting that chronic inflammation may play a
role in a manner similar to tumours of the common bile duct. Calcification
of the gall bladder wall, presumably due to chronic inflammation
(porcelain gall bladder), is also associated with an increased risk of cancer,
Chronic infection may also promote development of gall bladder cancer and
the risk in typhoid carriers is significantly increased over the general
population.
62. • The majority (90 per cent) of cases are adenocarcinoma.
• The tumour spreads by direct extension into the liver, seeding of the
peritoneal cavity and involvement of the perihilar lymphatics and neural
plexuses. At the time of presentation, the majority of tumours are advanced.
• Clinical features
• Patients may be asymptomatic at the time of diagnosis. Symptoms, if present, are usually
indistinguishable from those of benign gall bladder disease, such as biliary colic or
cholecystitis, particularly in older patients. Jaundice and anorexia are late features. A
palpable mass is a late sign.
• Laboratory findings are generally non-specific, but may be consistent with
biliary obstruction. Non-specific findings, such as anaemia, leukocytosis,
mild elevation in transaminases and increased inflammatory markers, such
as ESR or C-reactive protein, may be present. Serum CA19-9 is elevated in
approximately 80 per cent of patients. The preoperative diagnosis is often
made on ultrasonography, and confirmed by a MDR-CT scan or MRI/MRCP
63.
64. • Courvoisiers Law
• In a patient with jaundice if there is a palpable gallbladder it is not due to stones.
• In pathology of gallbladder like calculus cholecystitis there will be fibrosis of the
gallbladder and hence it can not enlarge if there is a distal obstruction
• But if the pathology is there outside gallbladder due to CBD carcinoma, pancreatic
carcinoma you can palpate the gallbladder.
• Exceptions to this Law
• Double impaction of stone—one in CBD and other in cystic duct
• Oriental cholangiohepatitis
• Pancreatic calculus obstructing ampulla of vater
• Mucocele due to stone in cystic duct.
