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7/30/2019 Long Case Periampullary Cancer
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Dr Ramdip Ray MS, MRCS ( Eng) Assistant Professor Medical College, Kolkata
obstructive jaundice
Periampullary carcinomaa long case discussion
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My dear boy !
you said that the Gall bladder is firm
This is a classic case of a hard gall bladder.
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Sir !
I . felt that it is firm .
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Are you sure ?
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I think so
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Okay go on
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obstructive jaundice
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Obstructive Jaundice
yellow sclera, skin, mucosa
dark urine
clay coloured stools
itching
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why itching ?
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the itch
accumulation of bile salts in blood/ tissues
sometimes precedes jaundice
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where to look for mild jaundice ?
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early jaundice
examine posterior hard palate
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why periampullary ?
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Periampullary CA
elderly male
not known patient of gallstones
progressive jaundice
anorexia
Courvoisiers law
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Courvoisier's law : 1890
If in the presence of jaundice the
gallbladder is palpable, then the
jaundice is unlikely to be due to a stone
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Courvoisier's law : 1890
With obstruction of the common bile duct by stone,
dilatation of gallbladder is rare. The organ is usually
shrunken. With obstruction of other kinds, on the
contrary, distention is the rule, shrinking occurs in only
one twelfth of these cases
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exceptions ?
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Exceptions to Courvoisier
pancreatic calculus at ampulla
double impaction
Oriental cholangiohepatitis
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Exceptions to Courvoisier
pancreatic calculus at ampulla
double impaction
Oriental cholangiohepatitis
( long standing stones in CBD + Clonorchis
sinensis from freshwater fish )
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Exceptions to Courvoisier
NOT mucocele GB
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define periampullary CA
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Periampullary CA
within 2 cm of ampulla
1 pancreatic head / CA2 intrapancreatic CBD
3 ampullary
4 duodenal
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differential diagnoses ?
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Differential diagnoses
pancreatic head CA
distal cholangioCA
CA Gall bladder
HCC
CBD stone
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Other differential diagnoses
chronic pancreatitis
enlarged pericholedochal lymph nodes
sclerosing cholangitis
oriental cholangiohepatitis
hydatid cyst
choledochal cyst
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Which type of periampullary ?
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Which type of periampullary ?
difficult to say
typical ampullary :
intermittent / waxing & waning jaundice
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confirm obstructive jaundice
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confirm obstructive jaundice
hyperbilirubinemia, mainly conjugated
elevated ALP & GGT normal or mildly elevated ALT/AST
low albumin
prolongation of P time
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normal LFT values ?
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normal values
Albumin : 3.55 mg / dL
ALP : 30300 IU / L ( adults )
ALT : 335 IU / L
AST : 335 IU / L
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Why does ALP rise ?
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Why ALP / GGT rise
ALP & GGT : bile duct epithelial damage
ALT & AST : hepatocyte damage
Albumin & P time : hepatic synthetic function
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other causes of high ALP ?
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ALP rise
Obstructive Jaundice
Hepatocellular Jaundice Malignant infiltration
Pagets disease
Pregnancy
Childhood
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elevated P time
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P time
Inj Vitamin K ( Vit K dependent II, VII, IX, X )
prefer I.V. to avoid risk of intramuscular
haematoma
FFP
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after LFT ?
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Ultrasonography
organ of origin GB
hepatomegaly, any liver SOL
distented GB / absence of gallstones dilated IHBR, CHD & CBD
dilated MPD
any periampullary SOL any enlarged LN, ascites
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spleen just palpable ?
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Splenomegaly
just palpable.. One & a half times
L sided portal hypertension
splenic vein thrombosis
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father had an abdominal cancer
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familial / hereditary ?
HNPCC
Familial Breast Cancer ( BRCA2 mutation )
Peutz Jeghers
Ataxia telangiectasia
FAMMM ( Familial Atypical Multiple Mole Melanoma )
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other risk factors ?
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Risk factors Pancreatic CA
age : strongest
smoking : Nnitroso compounds
hereditary / chronic pancreatitis
cystic fibrosis
carcinogens : DDT
diabetes mellitus ??
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diabetes mellitus
diabetes or abnormal GTT in 80 % of pancreatic CA
increased insulin, but reduced peripheral sensitivity
glucagon, somatostatin & amylin increased
amylin from peritumour tissue in response to a factor
produced by the tumour. Surgical resection may
improve !
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molecular genetics
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molecular genetics
The molecular genetics of pancreatic adenocarcinoma have been well
studied. Of these tumors, 80-95% have mutations in the KRAS2 gene, and
85-98% have mutations, deletions, or hypermethylation in the CDKN2 gene.
Of these cancers, 50% have mutations in TP53 and about 55% havehomozygous deletions or mutations of Smad4. Some of these mutations
can also be found in high-risk precursors of pancreatic cancer. For
example, in chronic pancreatitis, 30% of patients have detectable
mutations in TP16 and 10% have K-ras mutations. Although studies are
underway, the genetic mutations associated with pancreaticadenocarcinoma are not yet clinically useful in screening for or
diagnosing the disease.
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molecular genetics
The molecular genetics of pancreatic adenocarcinoma have been well
studied. Of these tumors, 80-95% have mutations in the KRAS 2 gene,and 85-98% have mutations, deletions, or hypermethylation in the CDKN2
gene. Of these cancers, 50% have mutations in TP53 and about 55%have homozygous deletions or mutations of Smad4. Some of these
mutations can also be found in high-risk precursors of pancreatic cancer.
For example, in chronic pancreatitis, 30% of patients have detectable
mutations in TP16 and 10% have K-ras mutations. Although studies areunderway, the genetic mutations associated with pancreatic
adenocarcinoma are not yet clinically useful in screening foror diagnosing the disease.
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after USG ?
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CECT
confirm USG findings
liver mets, LN, distant mets
hypodense mass on venous phase
abutment, encasement or occlusion of portal
vein / SMV / SMA or coeliac axis vascular anomalies
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best imaging ?
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Current standard
helical CECT with 3D reconstruction
further imaging in equivocal cases
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other imaging options
MRCP
MR Angiography
EUS
PET
Laparoscopy
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role of EUS
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EUS
more sensitive for lesions < 2cm
better for L N mets
guided FNAC : esp for Neoadjuvant
Issues : availibility, expertise, cost, invasive
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role of ERCP
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ERCP
to visualise / biopsy ampullary / duodenal
brush cytology & delineation of cholangioCA
for stenting : plastic or metallic
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pre operative stenting
unresolved debate
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pre operative stenting
biliary tract sepsis
elderly / comorbidities very high bilirubin levels
( as per institutional policy )
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pre op biopsy
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pre operative biopsy
non issue
not required in good risk patient with double
duct sign negative bx will not change plan
positive bx may help in counselling
if neo adjuvant planned
10 % benign after Whipples
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diagnostic laparoscopy
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diagnostic laparoscopy
very large tumours
no need of palliative surgery ( stent in place )
body / tail tumours
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Pathological dilemma
abundant desmoplastic stroma
widely scattered neoplastic glands
few cancer cells in FNAC / Bx specimens !
more host tissue than cancer cells
atypia often in chronic pancreatitis
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differential behaviour
similar perioperative M & M
post operative diabetes rare .. In all
long-term survival different
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differential behaviour
pancreatic most clinically aggressive
K ras mutations for codon 12 specific for
pancreatic
Jaundice more common in cholangio &
ampullary
Waxing & waning in ampullary
But none present at earlier stage
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differential behaviour
Location Mediansurvival
5 yr survival L N mets Perineuralinvasion
Pancreatic 1118 mo 626 % 5679 % Most
Cholangio 2233 mo 1343 % 5669 % 86 %
Ampullary 3849 mo 3348 % 3050 % 517 %
Duodenal 86 mo 3267 % 3647 % -
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ampullary & duodenal
no ampulla in two-thirds
pathological distinction difficult
similar presentation / outcome
proposal : classified as one !
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Assessment of fitness
Hb, TLC, DLC
Sugar, Urea, Creatinine
CXRPA, ECG
Echo, Stress Echo, TMT in some centres
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Informed consent
discuss diagnosis with patient
natural course & treatment options
the surgical procedure chances of inoperability / surgical bypass
Risk of death ( < 4 % )
Risk of morbidities ( 3050 % )
Residual disease / Recurrent disease
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pre operative preparation
adequate hydration : urine output
mannitol / diuretics : unproven role
Inj Vit K 10 mg I.m. / I.v. 35 days
FFP if required
prophylactic I.v. antibiotics at induction
stenting if indicated
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Complications of obstructive jaundice ?
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Obstructive jaundice
Cholangitis : pain, fever & jaundice
Toxic cholangitis : also shock, confusion
Infective complication
Coagulopathy
Hepatorenal syndrome
Impaired immune function
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plan
Whipples operation in good risk
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signs of inoperability
liver / distant metastases
peritoneal metastases
SMVportal vein / SMA fixity
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palliative bypass
hepaticojejunostomy
NOT cholecystojejunostomy unlesslaparoscopic palliation
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margins
pancreatic parenchymal
C B D
G I mucosal
retroperitoneal / uncinate / mesenteric
vascular margin : most important
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controversies
pre op biopsy : resolved
pre op stenting
pre-op mannitol / diuretics
prophylactic octreotide
PP-PDR vs Classic PDR
Classic vs extended PDR
Adjuvant therapy
Prophylactic G J : resolved
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thank you