This document provides information about jaundice and obstruction of the biliary tract. It begins with an overview of the causes of yellow discoloration of the skin and mucous membranes, which is caused by bilirubin accumulation. It then describes the breakdown of red blood cells and how bilirubin is processed and excreted. The document outlines various causes of obstructive jaundice including gallstones, strictures, tumors, and external compression. Investigation methods and treatment approaches for different biliary obstructions are also summarized.
7. Water (98%)
Bile Salts
Bile pigments (Bilirubin)
Lecithin
Cholesterol
8. BROKEN DOWN RED CELLS ARE
REMOVED BY R.E.S.
HAEMOGLOBIN SPLITS INTO HAEM
&GLOBIN
GLOBIN & CELL WALL PROTEIN GO
DOWN
TO AMINOACIDS
THEY ENTER THE AMINO ACID POOL
9. HAEM SPLITS INTO IRON &
BILIRUBIN [pigments]
IRON STORED AS FERRITIN FOR
REUSE
10. BILIRUBIN IS NOT REUSED
[GOES TO THE LIVER]
COMBINE WITH GLUCOURINC ACID
TO FORM THE CONJUGATED [ DIRECT ]
BILIRUBIN [ WATER SOLUBLE ]
Van den Bergh reaction [DIRECT]
Alcohol added after van den Gergh [INDIRECT]
13. Typical Normal level of total bilirubin
0.1 -1mg /dl.
Typical Normal level of direct bilirubin
0-0.3 mg /dl.
Reference range of total bilirubin
0.2-1.2mg/dl.
Reference range for direct bilirubin
0.1-0.4mg/dl.
Elevated levels of total bilirubin > 2.5 -3 mg/dl.
Cause jaundice.
14. Normal value < 1mg/dl. (17u mol/L)
Ehrlich unit
A level of 2mg/dl. Represent a transition
from normal to abnormal level.
16. 1-STONES
2-STRICTURES; [BENIGN]
3-PERIAMPULLARY TUMOURS
4-CA. HEAD OF THE PANCREAS
5-CHOLANGIOCARCINOMA
6-PRESSURE FROM OUTSIDE;L.N.
7-CHOLEDOCHAL CYST
8-PARASITES; FILLING THE LUMEN
17. Luminal
Gallstone
Intra-mural
Benign stricture (e.g. As complication of
cholecystectomy )
Malignant stricture: cholangiocarcinoma
Extra-mural
Cancer Head of pancreas
Compression by malignant lymph nodes at
porta hepatis
20. L.N.
CANCER HEAD OF
THE PANCREAS
MIRIZZI SYND
ANY MASS
OUTSIDE
HARTMANN`S POUCH stone
Stone in
cystic duct
21. Secondary bile duct stones
STONES SLIPPING INTO THE BILIARY TREE
This is the commonest cause of obstructive
jaundice.
Retained bile duct stone after cholecystectomy.
Primary bile duct stone .
27. 1. Jaundice – onset
2. Pale stools, dark urine ?
YES = POST HEPATIC NO = PREHEPATIC & HEPATIC
PAIN?
YES NO PAIN
Colicky
Fatty food
intolerant
GALLSTONES
Wt loss
Back Pain
Non-specific
symptoms
MALIGNANCY
Hepatic:
IV Drug abuse
blood transfusion
flu-like illness
Excess alcohol intake
Liver cirrhosis
Obesity
Drug History
ASSOCIATED FEVER / RIGOR ?
Gram –ve Septicaemia
ADMIT
Pre-hepatic:
Family history of bleeding
disorders, tendency to bleed
28. PAIN
YELLOW DISCOLOURATION SKIN &M.M.
DARK URINE [TEA COLOUR]
CLAY COLOUR STOOL
ITCHING
FEVER and RIGORS IF CHOLANGITIS
SUPERVENE
LOSS OF APPETITE
LOSS OF WEIGHT IN MALIGNACY
29. LOSS OF Wt. IN MALIGNANCY
TOXIC IN CHOLANGITIS
[CHARCOT`S TRIAD,;PAIN, FEVER ,JAUNDICE]
YELLOW DISCOLOURATION OF SKIN,M.M.
TROISIER`S SIGN. VIRCHOW`S NODE
TENDER R.U.Q .[IN CHOLANGITIS ]
COURVOISIER` LAW[IN CA.HEAD OF PAN.]
ABDOMINAL MASS
ASCITES [IN MAIGNANCY]
34. Blood tests
Elevated WCC in ascending cholangitis)
Monitor renal function in case of hepato-renal syndrome
LFTs - ALP/GGT
Conjugated/unconjugated bilirubin
Clotting (INR maybe elevated)
USS
Look for gallstones, biliary tree dilatation, stone in CBD (though
often not seen due to bowel gas).
Look at pancreas to look for cancer (often poor views due to
overlying bowel gas)
Look at liver to exclude parenchymal disease.
35. CT
Used to assess pancreas in cases of suspected pancreatic cancer
Less sensitive that USS for picking up gallstones
MRCP
Used to assess biliary tree anatomy and determine cause of
obstruction (gallstone, stricture)
Diagnostic only but non-invasive
ERCP
Used to assess biliary tree anatomy and determine cause of
obstruction
Furthermore, obstruction can be relieved (diagnostic and
therepeutic, but invasive)
Stone extraction with balloon trawel
Sphincterotomy
Biliary stent (if stricture: benign or malignant)
Brushings for cytology (if stricture, to look for cholangiocarcinoma)
36. PTC (percutaneous transhepatic cholangiogram) –
performed by interventional radiologist
Diagnostic and therepeutic (biliary drain to relieve
obstruction) but invasive
More invasive and Higher complication rate than ERCP
(particularly haemorrhage) therefore used in situations where
ERCP is unavailable (out of hours in patient with cholangitis)
or unsuccesful
38. Detects intra/extra hepatic ductal dilatation
Less accuracy in defining etiology
Sensitivity – 94% if bilirubin > 10mg%
– 47% otherwise
39. Highly sensitive (esp.
with contrast) for
tumors.
Detects site & cause of
obstruction
Better anatomical
delineation
CT cholangiography
40. Bile – high signal
intensity on T2
weighted images
Visualises – biliary
dilatation (97-
100%), site of
obstruction (87%),
hepatic parenchyma
& vasculature
Only diagnostic
41. Extra hepatic bile
duct readily
visualized
Detects
choledocholithiasis
(>95%)
Sensitive in
diagnosis & staging
of malignancy
42. Helps in diagnosing
biliary leaks
Provides functional
assessment of
incomplete strictures and
surgical anastomosis
suggest complete biliary
obstruction if the small
intestine is not visualized
in 60 minutes
insensitive for helping
detect biliary dilatation or
the site and cause of bile
duct obstruction
43. Gold standard
Endoscopic/ percutaneous
Features:
◦ define the anatomy of the proximal biliary tree
◦ decompression of the biliary system
◦ allow for the simultaneous placement of
drainage catheters
◦ of assistance with regard to surgical
reconstruction
44.
45. PTC
The catheter is placed
into the intrahepatic
bile duct through
patient’s skin guided
by US and fixed on the
skin.
The radiographic image
is then taken.
Obstructive lesion can
be seen .
46.
47.
48. CORRECTION OF THE DERANGED
PARAMETRES AND DEHYDRATED PATIENT
ADMINISTRATION OF VITAMIN K
ANTIBIOTICS
MANNITOL PRE, INTRA and
POSTOPERATIVELY TO PREVENT
HEPATO-RENAL SHUTDOWN
49. Monitor for hepato-renal syndrome
Ensure fluid resuscitated and monitor urine output
Monitor INR
If deranged give vitamin K
Determine cause of obstructive jaundice
Danger is progression to ascending
cholangitis (Charcot’s triad) – can be life
threatening!
drain the Biliary tree to prevent development of
cholangitis
50. 1. STONE- ERCP -SPHINCTEROTOMY
2.STONE- LAP. OR OPEN EXPLORATION OF
C.B.D.
3.STRICTURE-STENT
4.STRICTURE-RESECTION ANASTOMOSIS FOR
SHORT STRICTURES
5. PERIAMPULLARY AND CA.HEAD OF
PANCREAS
=EARLY-WHIPPLE`S
OPERATION[PANCREATICO-DUODENECTOMY.
=LATE-BYPASS SURGERY[CHOLECYSTO-
JUJENOSTOMY
51. ERCP preferred method
Balloon trawl or dormia basket (for stones)
Sphincterotomy (to prevent future stones from
obstructing)
Stent (to allow free drainage of bile past a stricture)
PTC
Used where ERCP unavailable or unsuccesful ( more
invasive and higher complication rate)
Drain inserted percutaneously, trans-hepatically (through
the liver) and into the biliary tree to allow free drainage of
bile
52. Surgical
In the context of gallstones
At time of cholecystectomy an intra-operative
cholangiogram is performed to confirm stones in CBD
If present then consider:
Laparoscopic Trans-cystic (through cystic duct) removal using
fogarty catheter
Laparoscopic CBD exploration with choledochotomy
In context of malignancy (Ca head of
pancreas or external compression by
enlarged malignant lymph nodes)
Palliative bypass procedures such as hepaticojejunostomy
where ERCP/PTC + stenting has failed
55. Extrhepatic ductopenia or progressive
obliterative cholangiopathy.
A disease affecting all parts of biliary tract.
Untreated :cirrhosis,liver failure and death
56. 1 in 10,000 – Japan and China
1 in 17,000 – UK, USA, and Europe
F > M
57. The cause of BA is not known
Hypotheses
Developmental
Immunological overreaction
58. Type Incidence
(%)
Description
1 ∼5% Level of obstruction within the
common bile duct.
2 ∼2% Level of obstruction within the
common hepatic duct.
3 >90% Obstruction is within the porta hepatis
with no visible bile-containing
proximal lumen.
62. It is possible to make the correct diagnosis in
>80% of cases before laparotomy
Ultrasound
Liver biopsy
In Japan, use duodenal intubation and
measuement of intralumenal bile
ERCP,percutaneous cholangiography
64. Kasai-type portoenterostomy
Laparoscopic-assisted portoenterostomy has
been described although a true comparison
with the open procedure has to be
determined.
65.
66. If fails, or the child develops significant
complications of chronic liver disease, then
liver transplantation will be required if
available
68. Prognosis post-KPE can be affected by
1. Age at surgery
2. Experience of surgeon/center
3. prognosis
69. Blockage of the biliary tree by biliary stones
Symptoms
◦ Pain, Jaundice, dark urine, pale stools
Signs
◦ Jaundice. Charcot triad
Investigations
◦ Bloods – LFT, Amylase, Hepatitis screen, Coagulation
profile, creatinin.
◦ Ultrasound of abdomen
Treatment
◦ ERCP
◦ LAPAROSCOPIC TREATMET
◦ OPEN SURGERY
70. ERCP
Open surgical treatment
Exploration of CBD followed by T tube insertion
exploration with Primary closure
choledochoduodenostomy
Laparoscopic treatment
Lap. transcystic exploration of CBD
Lap. Choledochotomy with choledochoscopy
Lap. Chledochoduodenostomy
71. Obstruction of biliary tree with bile duct infection
Symptoms
◦ Unwell, pain, jaundice, dark urine, pale stools
◦ Charcot triad (ie, fever, right upper quadrant pain, jaundice)
occurs in only 20-70% of cases
Signs
◦ Sepsis (Fever, tachycardia, low BP), Jaundice.
Investigations
◦ Blood – WBC, LFT, Amylase, CRP, Coagulation screen
◦ Ultrasound of abdomen
Treatment
◦ Intravenous antibiotics
◦ ERCP
72. Acute inflammation of pancreas and other
retroperitoneal tissues.
Symptoms
◦ Severe central abdominal pain radiating to back,
vomiting
Signs
◦ Variable – None to Sepsis (Fever, tachycardia, low BP),
Jaundice, acute abdomen
Investigations
◦ Blood WBC, LFT, Amylase,Lipase;CRP
◦ Ultrasound of abdomen
◦ MRCP
◦ CT Pancreas
Treatment
◦ Supportive
◦ ERCP ?
73.
74. Classification type : Csendes (1989)
Type I : External compression of the common duct because of a
stone impacted at the neck of the gall bladder or
at the cystic duct.
Type II : Cholecystobiliary fistula involving less than one-third of the
circumference of the common duct
Type III : Cholecystobiliary fistula that involves up to two-thirds of
its circumference
Type IV : Cholecystobiliary fistula with complete destruction of the
entire wall of the common duct
75. It has been reported in the literature that the
incidence of MS is approximately
0.3-3% of all patients undergoing
cholecystectomy
and in 0.1% of all patients with gallstone disease
76. The surgical technique depends on the type
of MS.
If the type of MS has not been classified
preoperatively, the best way to determine the
operative procedure is “fundus-first”
technique .
For type I cholecystectomy. For type II
cholecystectomy with T tube placement . For
type III and IV hepaticojejunostomy after
cholecystectomy.
77.
78. Biliary Stone Extraction
• Bile duct stones are a common clinical scenario .
• Their frequency may increase in the future given the
rise in gallstones linked to the obesity epidemic.
• Over the last decade, improved therapeutic tools have
been developed which have enhanced the overall
success and safety of endoscopic stone extraction.
• In some situations, mechanical lithotripsy may be
required. Rarely will surgery be required for stone
removal.
Wilcox, C.M , 2010 . Interventional and Therapeutic Gastrointestinal
Endoscopy. Basel, Karger, vol 27, pp 337–344
79.
80. Sphincterotomes
Balloons 10 and 15 mm
Basket
Mechanical lithotripter
Crank handle mechanical lithotripter
Accessories required for extraction of
common bile duct stones
83. Endoscopic Treatment of Benign Biliary Strictures
Some causes of benign biliary stricture
• surgery (Iatrogenic Biliary Stricture)
• chronic pancreatitis.
• Primary sclerosing cholangitis
• others.
The general endoscopic treatment of these strictures is
dilation followed by stent placement.
For postoperative strictures the data show that placement of
multiple, large bore (10-Fr) stents over the course of several
procedures is better than placement of fewer stents.
Care must be taken to exclude malignancy in cases where benignity
is not certain.
The use of temporary placement of covered, removable
SEMS for benign biliary strictures appears promising.
Baron,T.H , 2010 . Interventional and Therapeutic Gastrointestinal
Endoscopy. Basel, Karger, vol 27, pp 337–344
84. A Initial cholangiogram reveals stricture in the common hepatic duct near the previous
surgical clips.
b Balloon dilation of stricture.
c Placement of multiple stents over two procedures.
D Cholangiogram after stent removal showing stricture resolution.
Endoscopic treatment of post-cholecystectomy
biliary stricture using plastic biliary stents.
a
b c
d
86. Plastic
◦ Biliary
7 or 10 FG
Need to be removed/replaced within 3 months
◦ Pancreatic
5 FG
Need to be removed within 2-4 weeks
Metal
◦ 10mm
◦ Not removable (usually)
87. Plastic stents
Polyethylene , PTFE,polyurithane.
More recently newer stens have been designed
• 2 layer sent
• Stent with antireflux valve
Shape : Sraight,angled ,curved,pig-tailed
Diameters : vary 5-12 F
88. Metallic Stents
a) Wall stent covered and uncovered (Boston Scientific).
• B) WallFlex Stent – platinum-cored nitinol construction (Boston Scientific).
• C) Zilver stent (Wilson Cook).
• D) Viabil® stent.
a
b
c
d
89. Distal Malignant Obstruction
• Pancreatic cancer, responsible for more than 90% of the cases
• Ampullary tumors.
• Cholangiocarcinoma
• Gallbladder cancer
• Malignant lymphadenopathy
The site of malignant obstruction
Drainage with plastic sten insertion
90. Hilar Malignant Obstruction
The most common malignant etiology
• cholangiocarcinoma,
• gallbladder carcinoma
• nodal metastases
• hepatocellular carcinoma
• hepatic metastases
Bismuth classification for hilar tumors
I II III A III B IV
96. Primary tumor (T)
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ
T1 Tumor limited to the pancreas, ≤ 2 cm in greatest dimension
T2 Tumor limited to the pancreas, > 2 cm in greatest dimension
T3
Tumor extends beyond the pancreas but without involvement of
the celiac axis or the superior mesenteric artery
T4
Tumor involves the celiac axis or the superior mesenteric artery
(unresectable primary tumor)
Regional lymph nodes (N)
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Regional lymph node metastasis
Distant metastasis (M)
M0 No distant metastasis
M1 Distant metastasis
Pancreatic cancer TNM staging
97. Intraoperative Assessment of Resectability
• Inaccurate
• Incomplete gross
resection provides no
survival benefit
compared to
chemoradiation
without surgery
99. R DesignationGross ResectionMicroscopic Margin
R0completenegative
R1completepositive
R2incompletepositive
Exocrine Pancreas. In Greene FL, Page DL, Fleming ID, et al., eds.
AJCC Cancer Staging Manual. Chicago, IL: Springer, 2002. pp. 157-164.
100. Resectable:
no extension to celiac, CHA, SMA
patent SMV-PV confluence
stage I, II (T1-3, Nx, M0)
Locally Advanced:
celiac, SMA encasement (> 1800)
stage III (T4, Nx, M0)
Borderline:
arterial abutment (< 1800)
stage III (minimal T4)
Varadhachary GR, et al. Ann Surg Oncol. 2006;13(8):1035-46
Katz MHG, et al. J Am Coll Surg. 2008;206(5):833-46
101. Resectable:
no extension to celiac, CHA, SMA, SMV-PV
confluence
stage I, II (T1-3, Nx, M0)
Borderline:
a) venous abutment or encasement (with
option for reconstruction)
b) arterial abutment (< 1800)
Locally Advanced:
celiac, SMA encasement (> 1800)
stage III (T4, Nx, M0)
110. Tumor size and location
Tumor and veins relationship – SMV, portal
vein and splenic vein
Tumor and arteries relationship – SMA, celiac
axis, common hepatic artery
Presence or absence of distant metastases –
liver, lung, peritoneum
MDACC Multidisciplinary Pancreatic Cancer Study Group
111. Treatment of Borderline Resectable Pancreatic Cancer
Underlying hypothesis / assumption
1. Neoadjuvant treatment sequencing used to:
• select those with favorable biology
• treat radiographically occult M1 disease
• enhance the chance of a complete (R0,
R1) resection
2. Outcome for R1 different than R2 (ie, better)
115. Summary of treatment of pancreatic cancer
• Local tumor resectability is best determined by
high quality CT (exploratory surgery is out-dated)
• Resectable tumors may be treated with upfront
surgery or a neoadjuvant approach
• Borderline resectable tumors are best treated with
upfront systemic therapy/chemoradiation
• Locally advanced tumors, as defined by arterial
encasement, are not resectable and surgery is not a
realistic treatment option
117. Mortality rates from intrahepatic
cholangiocarcinoma have steeply risen over
the course of the last 30y and continue to
rise
Men = Women
Previously no clear national consensus for
optimal diagnosis and treatment
118. Age (65% are >65y)
PSC (lifetime risk = 5-15%)
Chronic intraductal gall stones
Bile duct adenoma + biliary papillomatosis
Caroli’s disease (cystic dilatation of ducts)
◦ Lifetime risk = 7%
Choledochal cysts (5% will transform with time)
Smoking
Chemical Exposure ( Thorotrast, aircraft,
rubber)
Tropiocal (liver flukes, chronic typhoid carriers)
120. Type 1
◦ Below the confluence
Type 2
◦ Involving the confluence but not the L or R
duct
Type 3
◦ Occluding the CHD and involving either the R
(IIIa) or the L (IIIb) hepatic duct
Type 4
◦ Multicentric or
◦ Involve the CHD + both the L and the R
hepatic ducts
121.
122. WHO Classification of Intrahepatic
Carcinomas
Hepatocellular Ca
Combined Hepatocellular
Cholangiocarcinoma
Cholangiocarcinoma, intrahepatic
Bile duct cystadenocarcinoma
Undifferentiated carcinoma
123.
124. WHO Classification of Extrahepatic bile duct
carcinomas
Carcinoma in situ
Adenocarcinoma (95%, graded 1-4 on glandular tissue)
Papillary adenocarcinoma
Adenocarcinoma, intestinal type
Mucinous adenocarcinoma
Clear Cell adenocarcinoma
Signet ring adenocarcinoma (grade 3)
Adeno-squamous carcinoma
Squamous carcinoma (graded on degree of undifferentiation)
Small cell carcinoma (“oat cell”) (grade 4)
Undifferentiated carcinoma
125. Inactivation of tumour suppressor genes
◦ P53, APC, p16
Mutations in Oncogenes
◦ K-ras, C-myc, C-erbB-2, C-neu
Chromasomal aneuploidy
◦ 25% of perihilar tumours
These mutations can lead to phenotypic
changes
Diagnostic and prognostic usefulness is
unclear
127. Obstructive LFTs
Transaminases ( Normal, high with acute
obstruction)
Deficiency in Vit D,E,A,K (in chronic obstruction)
Chronic Systemic Markers (Hb, Alb, LDH)
CA 19-9 (85%)
◦ Can be elevated by obstruction alone
◦ > 100 U/ml = sensitivity of 75% and specificity of 80%
CA 125 (40-50%)
◦ May signify the presence of peritoneal involvement)
CEA (30%)
129. U/S
◦ 1st line for obstruction
◦ Small lesions missed
◦ Colour doppler can reveal compression/ thrombosis
of the portal V or hepatic A
CT
◦ Localises lymphadenopathy
◦ Enhanced spiral/ helical CT should be used if
involvement of hilum or vascular system suspected
MRI
◦ Optimal for anatomy + extent
◦ MRCP for ductal involvement
◦ MRA for hilar/vascular involvement
130. Cholangiography
◦ Essential for early diagnosis and assessing
resectability
◦ MRCP is non-invasive
◦ ERCP (preferred) or PTC allows cytology and
stenting
◦ Cytology (+ in 30%)
◦ Angiography will predict resectability
NB = Biopsies should be avoided if resectability is
possible
132. 5y Survival for intrahepatic Ca = 9-18%
5y Survival for proximal Ca = 9-18%
5y Survival for distal Ca = 20-30%
Survival depends on
◦ stage with tumour free margins
◦ absence of LN involvement
133. Contra-indicated due to rapid recurrence and
death within 3y
Survival may improve in some with
chemoradiation
135. Pre-op biliary drainage / stenting is not
advised if resection being considered
May be necessary in severely malnourished or
in acute suppurative cholangitis
Preop placement of biliary catheters may be a
helpful technical aid when dissecting a
proximal Ca
136. Complex CholangioCa
◦ MRCP will help planning management
◦ ? Bilateral > unilateral
Plastic Vs Metal
◦ Metal stents in those due to survive >6/12
◦ Metal = shorter hospital stay
◦ Stenosis of metal stents can be treated with
Cotton-Leung plastic stent through lumen
Mesh metal stent
covered stents (?reduce Ca ingrowth)
137. Response correlates to performance status at
onset
No strong evidence for a survival benefit, but
phase II trials suggest
◦ Single agent 5FU partial response = 10-20%
◦ Single agent gemcitabine partial response =
20-30%
◦ Combination partial response = 20-40%
◦ Gemcitabine + cisplatin partial response =
30-50%
Downstaging can convert to operability
138. External Beam XRT (+ChemoTx)
◦ Palliation of painful mets
◦ No evidence for adjuvant post op XRT
◦ No improvement of QOL or Survival in advanced
tumour
Local radiation
◦ intra-operative or intra-luminal brachytherapy
◦ No good data to support their use
◦ could be promising
143. Direct invasion of the liver
by gallbladder cancer in a
66-year-old woman
Should differentiate
gallbladder cancer from
acute cholecystitis
T?N?M?
case
144. Treatment
Radical surgery including segment liver resection,
bile duct resection and extensive
lymphadenectomy
Poor prognosis in patients with unresectable
tumor
External radiation therapy may provide palliative
benefit.
5-Fu and Gemcitabine can be used as
chemotherapy.
150. Obstructive jaundice
Cholangitis – Charcot’s triad
jaundice; fever, usually with rigors; and right upper quadrant
abdominal pain.
– Reynold’s pentad
+ hypotension and an altered mental state
Past history of cholecystectomy/ other GI
surgery (eventful)
History s/o pancreatitis, trauma, radiation,
alcohol abuse
151. Icterus
s/o hepatocellular failure
Courvoisier's sign
biliary fistula, peritonitis, biloma
Nutritional deficiencies
pale stools
dark urine
Itching marks (pruritus)
152. Under a microscope, the individual hepatocytes will have a
brownish-green stippled appearance within the cytoplasm,
representing bile that cannot get out of the cell.
Canalicular bile plugs between individual hepatocytes or
within bile ducts may also be seen, representing bile that
has been excreted from the hepatocytes but cannot go any
further due to the obstruction.
When these plugs occur within the bile duct, sufficient
pressure (caused by bile accumulation) can cause them to
rupture, spilling bile into the surrounding liver tissue,
causing hepatic necrosis. These areas are known as bile
lakes, and are typically seen with extra-hepatic
obstruction.
HISTOPATHOLOGY
153.
154.
155. Type A: Cystic duct leak or
leaks from small ducts in the
liver bed
Type B: Occlusion of a part of
the biliary tree, almost
invariably the aberrant right
hepatic duct
Type C: Transection without
ligation of the aberrant right
hepatic duct
Type D: Lateral injuries to
major bile duct
Type E: Subdivided as per
Bismuth classification into E1
to E5
156. E: injury to main duct
(Bismuth)
E1: stricture >2cm from
confluence
E2: stricture <2cm from
confluence
E3: stricture reaching the
confluence
E4:stricture with Separation
of the Right and Left ducts
E5: Type C plus injury in
hilum
157. Only 25-33% of injures are recognized intraoperatively
If experienced, convert to Open Procedure and perform
Cholangiography (determine extent of injury)
If not experienced, perform the cholangiogram laparoscopically with
intent of referring patient (placement of drains)
Consult an experienced hepatobiliary surgeon
Urgent intraoperative and Early postoperative
Management of Bile Duct Injury
Quicker the repair, the better the outcome!!!
Biliary catheter for decompression of biliary tract and control of
bile leaks
Drainage of intraperitoneal bile collection
158. Controlling sepsis, establish biliary drainage, postulate
diagnosis, type and extent of the bile duct injury.
Broad-spectrum antibiotics
No need for an biliary reconstruction in the presence of
peritonitis with worse outcome .
No need for urgent reconstruction of the biliary tree
The inflammation, scar formation and development of
fibrosis take several weeks to subside.
Reconstruction of the biliary tract is best performed
electively after an interval of at least 6 .
159. Patient presents with…
Vague abdominal pain, nausea, fever, jaundice, vomiting
Investigation
◦ Ultrasonagraphy and CT (ductal dilatation and
intra-abdominal collection)
◦ Cholangiogram
MRCP—noninvasive (can miss minor leaks)
ERCP—biliary anatomy and assess the injury
PTC—define biliary anatomy proximal to injury
◦ MR angiography—vascular injuries
160. Endoscopic stenting and dilation for
strictures
T-tube placement for minor lacerations
Primary duct-to-duct repair only if tension
free anastomosis is available
Biliary anastomosis with jejunal loop for
major transection or ligation injuries (Roux
en Y hepaticojejunostomy )
161. Attention to operative details
Stasberg’s critical view of safety
Appropriate Handling of Gallbladder
Careful use of diathermy
Recognition of Biliary and Vasculature
Anomalies
162. Options:
Endoscopic or percutaneous balloon dilatation and
insertion of stent
Surgery
Pre-procedure antibiotic prophylaxis
164. Operative management : biliary enteric
anastomosis
◦ to surgically re-establish bile flow within the
biliary tree and into the proximal
gastrointestinal tract in a manner that prevents
cholestasis, cholangitis, sludge and stone
formation, restricture, or biliary cirrhosis
Non–operative management: ERCP or
perctaneous dilation and stenting
◦ to correct the increased resistance to biliary
flow caused by a reduction in the diameter of
the lumen
167. Cystic dilatation of the extrahepatic bile
ducts
Female to male is about 4:1
The majority are now diagnosed in
childhood
Classified into five types
Associated with various biliary tumors
Choledochal cysts
168. • Type I approximately 80 %
• Type II
• Type III
• Type IV
• Type V
174. • Majority of choledochal cysts have
anomalous junction of common bile duct
with pancreatic duct (90%).
• This allows reflux of pancreatic
secretions and enzymes into common bile
duct.
• Results in inflammation and weakening of
bile duct wall.
• Formation of choledochal cyst.
175. • Rare in US and western countries.
• Reported 1 case per 2 million live births.
• Prevalent in Asia 33% cases Japan = 1:1000.
• Females 3-4:1
176. • Infants and children – pancreatitis,
cholangitis and histological evidence of
hepatocellular inflammation and damage.
• cholangiocarcinoma 9-28%.
187. •Associated with
U.Colitis in 70% of
cases
•May lead to
malignancy
•Unknown aetiology
•Symptoms of
cholangitis
•Treatment;Antibiotics
• Or liver transplant
Rosary beads
188. o Primary sclerosing cholangitis (PSC) is a chronic liver
disease caused by progressive inflammation and scarring
of the bile ducts of the liver.
o The inflammation impedes the flow of bile to the gut, which
can ultimately lead to liver cirrhosis and liver failure.
o The underlying cause of the inflammation is believed to be
autoimmunity.
o The definitive treatment is liver transplantation.
189.
190. The cause(s) for PSC are unknown.
It is often considered to be an autoimmune disorder.
PSC is associated with inflammatory bowel disease and
particularly ulcerative colitis, which coexists in
approximately 70% of patients.
Conversely, the prevalence of PSC in ulcerative colitis
patients is ~4%.
There is a 2:1 male-to-female predilection of PSC.
There is an increased prevalence of HLA alleles A1, B8, and
DR3 in PSC.
191. The disease normally starts from age 30 to 60,
though may begin in childhood.
PSC progresses slowly, so the disease can be
active for a long time before it is noticed or
diagnosed.
192. Signs and symptoms
Fatigue
Severe jaundice with intense itching
Malabsorption (especially of fat) and steatorrhea,
leading to decreased levels of the fat-soluble vitamins,
A, D, E and K.
Signs of cirrhosis
Ascending cholangitis, or infection of the bile duct.
Pale stool due to biliary obstruction
Dark urine due to excess conjugated bilirubin, which is
water soluble, being excreted by the kidneys
193. Investigations
MRCP
ERCP
Approximately 80% of patients have perinuclear
antineutrophil cytoplasmic antibodies, also called p-
ANCA, however this finding is not specific for PSC.
Antinuclear antibodies and anti-smooth muscle
antibodies are found in 20%-50% of PSC patients and,
likewise, are not specific for the disease.
Full blood count, liver enzymes, bilirubin levels (usually
grossly elevated).
Faecal fat determination is occasionally ordered when the
symptoms of malabsorption are prominent.
The differential diagnosis include: primary biliary
cirrhosis, drug induced cholestasis, cholangiocarcinoma,
and HIV-associated cholangiopathy.
194. Primary sclerosing cholangitis. Single-shot fast spin-echo MRCP image
shows multifocal strictures and dilatations of the intrahepatic bile ducts
198. Treatment
Ursodiol, a bile acid naturally produced by the liver, which has been
shown to lower elevated liver enzyme in PSC, but has not yet been
proven effective at prolonging the life of the liver.
Medications to relieve itching (antipruritics) and bile acid
sequestrants (cholestyramine), antibiotics to treat infections, and
vitamin supplements, as people with PSC are often deficient in
vitamin A, D, E and K.
In some cases, ERCP, whth stenting of the bile duct, may be
necessary (dominant strictures).
Liver transplantation is the only proven long-term treatment of PSC.
Indications for transplantation include recurrent bacterial cholangitis,
jaundice refractory to medical and endoscopic treatment,
decompensated cirrhosis and complications of portal hypertension.
199.
200. Primary biliary cirrhosis is an autoimmune disease of
the liver marked by:
The slow progressive destruction of the small bile
ducts (bile canaliculi) within the liver.
When these ducts are damaged, bile builds up in the
liver (cholestasis) and over time damages the tissue.
This can lead to scarring, fibrosis and cirrhosis.
It was previously thought to be a rare disease, but more
recent studies have shown that it may affect up to 1 in
3-4,000 people; the sex ratio is about 9:1 (women to
men)
PRIMARY BILIARY CIRRHOSIS
201.
202. In some areas of the US and UK the prevalence is
estimated to be as high as 1 in 4000. This is much
more common than in South America or Africa ( may
be due to better recognition in the US and UK ).
First-degree relatives may have as much as a 500
times increase in prevalence,
After liver transplant, the recurrence rate may be as
high as 18% at 5 years, and up to 30% at 10 years.
There is no consensus on risk factors for
recurrence of the disease
203. The cause of the disease is unknown
An immunological basis for the disease, making it an
autoimmune disorder.
Most patients (>90%) have anti-mitochondrial
antibodies (AMAs) against pyruvate dehydrogenase
complex (PDC-E2), an enzyme complex that is found
in mitochondria.
An increase in GGT could indicate presence of
Primary Biliary Cirrhosis.
57% of patients with acute liver failure have anti-
transglutaminase antibodies suggesting a role of
gluten sensitivity in primary biliary cirrhosis, and
primary biliary cirrhosis is considerably more common
in gluten sensitive enteropathy than the normal
population..
204. The following signs may be present in PBC:
• Fatigue
• Pruritus (itchy skin)
• Jaundice (yellowing of the eyes and skin)
• Xanthelasmata (focal collections of cholesterol in the
skin, especially around the eyes)
• Complications of cirrhosis and portal hypertension:
• Fluid retention in the abdomen (ascites)
• Hypersplenism
• Esophageal varices
• Hepatic encephalopathy, up to coma
in extreme cases.
• Association with extra-hepatic autoimmune disorder[s]
such as Rheumatoid arthritis or Sjögren's syndrome (up
to 80% incidence).
205. To diagnose PBC
distinctions should be established from
other conditions with similar symptoms,
such as autoimmune hepatitis or primary
sclerosing cholangitis (PSC).
206. Investigations include:
Abnormal liver function tests (high alkaline phosphatase, elevated
AST, ALT)
Presence of certain antibodies: antimitochondrial antibody,
antinuclear antibody (the M2-IgG antimitochondrial antibody is the
most specific test)
Abdominal ultrasound ,MRCP and CT are usually performed to rule
out blockage to the bile ducts , and - if uncertainty remained - ERCP
may be done.
Now most patients are diagnosed without invasive investigation since
the combination of anti-mitochondrial antibodies and typical
(cholestatic) liver function tests are considered diagnostic. However, a
liver biopsy is necessary to determine the stage of disease.
Anti-nuclear antibodies appear to be prognostic in PBC. Anti-
glycoprotein-210 antibodies, and to a lessor degree anti-p62
antibodies correlate with progression toward end stage liver failure.
Anti-centromere antibodies correlate with developing portal
hypertension..
207. Contrast-enhanced helical CT image obtained through liver during hepatic
arterial phase shows several small, homogeneously enhancing lesions
(arrows). Multiple lesions were seen throughout remainder of liver as well.
208. STAGES OF DISEASE
• Stage 1 - Portal Stage: Normal sized triads; portal
inflammation, subtle bile duct damage.
Granulomas are often detected in this stage.
• Stage 2 - Periportal Stage: Enlarged triads; periportal
fibrosis and/or inflammation. Typically characterized by the
finding of a proliferation of small bile ducts.
• Stage 3 - Septal Stage: Active and/or passive fibrous
septa.
• Stage 4 - Biliary Cirrhosis: Nodules present; garland or
jigsaw pattern.
209. Treatment :
No known cure, but medication may slow the progression
Ursodeoxycholic acid (Ursodiol) is the most frequently
used treatment. This helps reduce the cholestasis and
improves blood test results (liver function tests).
To relieve itching caused by bile acids in circulation,
which would normally be removed by the liver,
cholestyramine (a bile acid sequestrant) may be prescribed
to absorb bile acids in the gut and be eliminated, rather
than re-enter the blood stream.
Alcoholic beverages are contraindicated.
Multivitamins (esp. Vitamin D) and calcium are also
recommended as patients with PBC have poor lipid-
dependent absorption of Vitamins A, D, E, K.
In advanced cases, a liver transplant, if successful, results
in a favourable prognosis.
210.
211. Treatment of malignant obstruction
Adjunct to surgery - Treatment of stricture
or recurrent stones after hepaticojejunostomy
Failed ERCP
Treatment of CBD calculi
Treatment of benign strictures
214. Malignant or benign disease
Gastroenterologists
Surgeons
Radiologists
Other Healthcare Workers
215. PTC and Internal/External biliary drainage
PTC and metallic Stent
216. ERCP treatment of choice
PTC and internal/external drain or plastic
stent. May enable successful ERCP later
217. INR < 1.4. Consider vitamin K, FFP and also
Beriplex/Octaplex.
Platelets > 100,000. If less, consider platelet
transfusion
218. WHO performance status
Check coagulation
Explain procedure at least 1 day before
Risks. Bleeding, bile leak, infection,
pneumothorax and failure
220. At start of procedure
Discuss with Microbiology
221. Use what works best for you
Chiba needle 22 gauge
Trochar needle 18 gauge
Stiff Terumo wire
Amplatz wire
Catheters.
Self expanding stent
Internal/External drains 8.5/10.5F.
222. Ascites present? Drain first
Ultrasound?
Right lobe. Mid axillary line. Aim for
xyphisternum.
Left lobe. Locate with U/S and usually aim for
segment III.
Very gently inject 1/3 strength contrast as
needle is withdrawn
Duct entered when contrast flows away from
needle and persists
Duct not entered. Change angle and try not to
exit liver capsule
Duct normally anterior to portal vein
224. Pre-surgery for cholangiocarcinoma. Discuss
lobe to drain. Usually the lobe being
preserved.
Pre-surgery for pancreatic cancer. Right lobe
puncture.
Palliative. Drain right, left or both?
1. Chiba needle to opacify ducts then choose
duct for trochar puncture and wire etc.
2. Single puncture (NEF set ), then wire,
dilator and access sheath
Consider bile for cytology if no diagnosis
225. Cross lesion with wire.
Torque
Stent/Drain
1 or 2 stage procedure?
Temporary drain followed by stent?
Plug track? Coils, gelfoam etc.
Technical success >95%
226. Unable to cross stricture, establish external
drainage (8.5F internal/external drain).
Further attempt after decompression usually
successful.
Care with drainage bag essential.
227. In hospital mortality 19.8%.
Death or major complication 21.2% overall, 18.3%
benign, 21.7% malignant.
Major complications in 7.9%, haemorrhage 3.5%,
renal failure 1.8% and sepsis 1.6%.
Minor complications in 26.0%, pain 14.3%, sepsis
7.7% and haemorrhage 4.5%.
Association with ascites, elevated INR and low
platelets.
1 year survival <20% for malignant disease.
Drainage more effective if stents placed across
ampulla
228.
229.
230.
231. Recurrent obstructive jaundice
It will depend on
• stones
• Benign or malignant stricture
• Recurrent obstructive jaundice after ERCP
• Recurrent obstructive jaundice after lap. Or open CBD
exploration
• Recurrent obstructive jaundice after
choledochojejunostomy or hepaticojejunostomy
232. Follow up of patients after treatment of
obstructive jaundice
• Very important to achieve good results
• Early detection of recurrent jaundice and
treatment of complications .
• Short and long term follow up .