2. Obstructive jaundice
Definition :
Conjugated hyperbilirubinemia
Is a condition characterized
by Yellow discoloration of
the skin , sclera & mucous
membrane as a result of an
elevated Sr. Bilirubin conc.
due to an obstructive cause.
4. Type II : Intermittent obstruction
Choledocholithiasis
Periampullary tumor
Duodenal diverticula
Choledochal Cyst
Papillomas of the bile duct
Intra biliary parasites
Hemobilia
5. TYPE III : Chronic incomplete
obstruction
Strictures of the CBD
Congenital
Traumatic
Sclerosing cholangitis
Post radiotherapy
Stenosed biliary enteric
anastamosis
Cystic fibrosis
Chronic pancreatitis
Stenosis of the Sphincter of
Oddi
ERCP showing distal common bile duct
stricture with proximal dilation
6. TYPE IV : Segmental Obstruction
Traumatic
Hepatodocholithiasis
Sclerosing cholangitis
Cholangio carcinoma
7. PATHOPHYSIOLOGY OF OBSTRUCTION
Alterations in
– Systemic and renal hemodynamics
– Hepatic function
– Hemostatic mechanism
– Gastrointestinal barrier
– Immune function
–Wound healing
• Protein synthesis,
• Reticulo-endothelial function
• Hepatic metabolism
8. Coagulation system
Prolonged bile duct obstruction leads to significant
defects in clotting factors
Before surgery these defects should be corrected by
Fresh frozen plasma andVitamin K
Even if there is no measurable coagulation
dysfunctionVitamin K should be given to all patients
with obstructive jaundice
17. Obstructive Jaundice
CBD stones (Choledocholithiasis) vs. tumor
Clinical features favoring CBD stones:
Age < 45
Biliary colic
Fever
Transient spike in AST or amylase
Clinical features favoring cancer:
Painless jaundice
Weight loss
Palpable gallbladder
Bilirubin > 10
18. Unconjugated vs. Conjugated
Unconjugated
production exceeds
ability of liver to
conjugate
Ex. Hemolytic anemia's,
hemoglobinopathies,
in-born errors of
metab., transfusion
rxn.
Conjugated
Can produce but not
excrete
Intra- or extra hepatic
obstruction Metabolic
defect
19. Choledocholithiasis
Defined as stones in the CBD
Patho physiology : intermittent obstruction of CBD
Often asymptomatic
Symptoms are indistinguishable from other causes of
Biliary pain
Predisposes to Cholangitis & Acute Pancreatitis
Elevated sr. bilirubin & Alk. Phos.
20. Evaluation
ERCP
Primary diagnostic and
therapeutic modality
Sphincterotomy and stone
extraction
Placement of stent if
stone extraction
unsuccessful
Mortality rate 1.5%
21. Open CBD Exploration
Indications
Presence of multiple stones (more than 5)
Stones > 1 cm
Multiple intra hepatic stones
Distal bile duct strictures
Failure of ERCP
Recurrence of CBD stones after sphincterotomy
22.
23. CBD Exploration – Surgical Options
Common bile duct exploration withT-tube
decompression
Choledochoduodenostomy
Transduodenal sphincterotomy and
sphincterplasty
Roux-en-Y Choledocho jejunostomy
24. CHOLEDOCHAL CYSTS
Congenital anomalies of the biliary tract that
manifest as cystic dilatation of the extra hepatic and
intra hepatic bile ducts
Females are most commonly affected
ETIOLOGY :
Congenital weakness of the bile duct wall
Congenital obstruction of the bile ducts
Reo virus association is seen in 78% of patients
40% of anomalies are seen at the junction of
pancreatic and common bile ducts
25. CLASSIFICATION OF CHOLEDOCHAL CYST
Proposed byTodani & colleagues
TYPE I : accounts for 80 – 90 % of cases
exhibit segmental or diffuse fusiform dilatation of the CBD.
TYPE II : consists of a true Choledochal diverticulum
TYPE III : consists of dilatation of the intra duodenal portion of the CBD.
TYPE IV : multiple intra hepatic & extra hepatic cysts
TYPEV or CAROLIS disease : consists of single or multiple dilatation of
the intra hepatic ductal system
26. Clinical features :
Disease often appears during first months of life
80% of pts. have cholestatic jaundice & acholic stools
Vomiting , irritability & failure to thrive may occur
Spontaneous perforation of a Choledochal cysts may occur
Progressive hepatic injury due to biliary obstruction
DIAGNOSIS :
BEST established by USG Abdomen
In Older children PTC or ERCP may help define the anatomy
of the cyst.
27. TREATMENT
Surgical excision of the cyst with Reconstruction
of the extra hepatic biliary tree
Biliary drainage is accomplished by Choledocho
– jejunostomy with a Roux – en –Y anastamosis
Long term follow up is necessary because of
complications like cholangitis , lithiasis ,
anastomotic stricture
28. Cholangiocarcinoma
90% are extra-hepatic
60’s and 70’s
Highest incidence in Japan, Israel, and Native
Americans
Increased 3 fold in the last 30yrs in the USA
M/F=3/2
31. Cholangiocarcinoma
Diagnosis and Initial Workup
Jaundice
Wt loss, anorexia, abdominal pain, fever
US then CT (CTA?) Followed by ERCP, PTC or
MRCP
CEA and CA 19-9 can be elevated
32. Cholangiocarcinoma
Intra-hepatic Disease
Suspicious mass on CT. Quadruple phase CT with 0.5 cm
cuts through the liver and portal hepatitis. Consider CTA
reconstruction.
Treatment
If adenoncarcinoma: look for primary with a chest CT and
upper/lower endoscopy.
Colon, pancreas, and stomach are common primary sites.
33. Cholangiocarcinoma
Intra-hepatic Disease-Surgery/Ablation
Extent of surgical therapy is determined by the location,
hepatic function, and underlying cirrhosis.
Anatomic resections have lowest recurrence rates.
However non anatomic resection increases potential
surgical candidates and improves survival
Hepatic devascularization prior to resection is preferred
Ablative therapy gives good local control.
39. Pathology
Adeno carcinoma accounts for 95%
Arises from 4 different tissues of origin
Head of pancreas
Distal Bile duct
Ampullary ofVater
Periampullary duodenum
40. Pathology
Prognosis for each of these are different.
Five year survival for pancreas: 18%
Five year for ampulla: 36%
Five year for distal bile duct: 34%
Five year for duodenum: 33%
Determination of tissue origin is important for
prognosis, extent of resection.
41. Pathology
Determination of tissue origin from FNA,
endoscopic biopsy.
Also from thin section CT scan, ERCP
Determination of k-Ras also helps (95% of
pancreatic cancer).
42. Spread
Loco regional spread results from lymphatic
invasion and direct tumor spread to adjacent
soft tissue.
Ampullary lesions spread to LN 33%, typically
to a single LN in the posterior
pancreatcoduodenal group.
Duodenal has intermediate spread.
Pancreas metastasizes 88% to multiple sites.
43.
44. Treatment
StandardWhipple pancreaticoduodenectomy
thought to provide adequate tumor clearance in
the case of non-pancreatic ampullary tumor,
because tumor spread is localized.
Biopsy proven paraduodenal LN is thought by
most to preclude curative resection
45. Surgery and Chemotherapy
Low risk patients had 5 year local control and
survival of 100% and 80% respectively.
High risk patients had 5 year local control and
survival of 50% and 38%, respectively.
Based on these findings, some have proposed a
course of preoperative chemoradiation to
improve local disease control in these high risk
patients.
46. Whipple Procedure
Five basic techniques are used to resect pancreatic
cancers
Standard pancreaticoduodenectomy
Pylorus preserving pancreaticoduodenectomy
Total pancreatectomy
Regional pancreatectomy
Extended resection (MD Anderson)
52. Adjuvant Therapy
Autopsy series show that 85% of patients will
experience recurrence in operative field.
70% have metastases to liver.
So need to address local control (radiation) and
distant disease (chemotherapy).
Most commonly used is 5 FU and this only has a
15-28% response on its own, but it’s a radio
sensitizer, so it improves response to chemo.