JAUNDICE
S1 UNIT
CONTENTS
? Surgical anatomy : Lakshmi Parvathy
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? Physiology and pathophysiology : Leon Francis? Etiopathogenesis : Maria Mathew
? Clinical Evaluation : Marlin T Abraham
? Investigations : Martin K Sebastian
? Management of calculous conditions : Megha Thomas
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? Management of benign conditions : Muhammed Afnas? Management of malignant conditions : Muhammed Galib
SURGICAL
ANATOMY OF
HEPATOBILIARY
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Lakshmi ParvathySYSTEM
Roll No: 84
SURGICAL ANATOMY OF LIVER
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Largest gland in our bodyLobes-right lobe,left
EMBRYOLOGY
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LIGAMENTS OF LIVERLOBES OF LIVER
ANATOMICAL RELATIONS
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CANTLIE'S LINE
? Imaginary vertical plane
? Divides liver into right and left lobes.
? Extends from IVC (posteriorly) to middle of
fossa for GB (anteriorly).
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SEGMENTAL ANATOMY
SEGMENTS OF LIVER
COUINAUD SEGMENTS
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FUNCTIONAL UNITBLOOD SUPPLY
LYMPHATIC DRAINAGE
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LIVER HISTOLOGY
EXTRAHEPATIC BILIARY SYSTEM
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COMMON BILE DUCT- PARTS
Sphincters-
superior & inferior choledochal sphincters,
ampullary sphincter, pancreatic sphincter
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GALL BLADDER
HARTMANN'S POUCH
Site for impaction of stone-
leads to mucocele GB.
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?Above-inferior surface of liver
?Below- cystic duct
?Left-Common hepatic duct
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PANCREAS
Retroperitonial (L1-L2 )
Behind stomach and lesser sac
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PANCREAS -RELATIONSPANCREAS - EMBRYOLOGY
PANCREAS - HISTOLOGY
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EHBS & PANCREAS -Arterial supply
PHYSIOLOGY
Leon Francis
Roll No:85
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BILE
? Complex fluid-
Inorganic & Organic
? Functions: digestion,
absorption, excretion
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? 600-1000ml/dayCOMPOSITION OF BILE
? Water(98%)
? Bile salts
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? Bile pigments? Cholesterol
? Inorganic salts
? Fatty acids
? Phosphatidyl choline
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? FatMECHANISM OF SECRETION
OF BILE
? Heptocyte secrete bile Biliary
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canaliculi? Additional secretion of Na & HCO3 ions
from epithelial cells lining biliary
duct(Secretin)
PHYSIOLOGICAL ROLE OF
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BILE?Digestion and absorption of fats
BILE ACID
?Major excretory route of lipid soluble
waste products
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BILIRUBINPATHOPHYSIOLOGY
JAUNDICE
? Normal serum bilirubin- 0.2 ? 0.8mg/dl.
? Manifested in sclera exceeds 2-
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2.5mg/dl.? Cutaneous icterus >5mg/dl
? Yellowish discoloration of skin , sclera
& mucous membrane
CLASSIFICATION OF
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JAUNDICE? PRE-HEPATIC (hemolytic) ? excessive
destruction of RBC
? HEPATIC (hepatocellular) ?liver
damage
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? POST-HEPATIC(obstructive)-obstruction to the bile flow
In obstructive jaundice (complete
obstruction)
? urine contains bilirubin and bile salts
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? urine urobilinogen is absent? stool devoid of stercobilinogen ? clay
coloured stools
? CARDIOVASCULAR
? Decreased cardiac contractility
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? Bradycardia due to direct effect of bile saltson SA node
? Decreased peripheral vascular resistance
? Reduced left ventricular pressure
? RENAL
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? Renal vasoconstriction? Shunting of blood from renal cortex
? Tubular and cortical necrosis
? Renal failure
? IMMUNITY
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? Bacterial translocation from the gut? WOUND HEALING
? Delayed wound healing
? High incidence of wound dehiscence
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? Defective synthesis of collagenAETIOPATHOGENESI
S OF
OBSTRUCTIVE
JAUNDICE
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Maria MathewROLL NO:86
OBSTRUCTIVE JAUNDICE
? Due to obstruction to the outflow of bile.
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? Surgical jaundice? Causes can be:
?Intrahepatic
?Extrahepatic
INTRAHEPATIC
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BILIARY OBSTRUCTIONCAUSES
? Primary biliary cirrhosis
? Primary sclerosing cholangitis
? Viral hepatitis
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? Cirrhosis? Alcohol
? Drug induced hepatitis
? Secondaries in liver
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EXTRAHEPATICBILIARY OBSTRUCTION
? INTRALUMINAL
? INTRAMURAL
? EXTRAMURAL
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IN THE LUMEN
? Choledocholithiasis
? Parasite
? Hemobilia
? Foreign body
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CHOLEDOCHOLITHIASIS
1.PRIMARY 4-12%
? Arise De novo
? Formed within CBD or intrahepatic duct.
CAUSES
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? Infections? Congenital
? Biliary dyskinesia
? Diabetes,malnutrition
PRIMARY CBD STONE
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FORMATIONBacteria
Hydrolyzes
Infection
secrete an
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bilirubinenzyme
glucuronides
Then
Form free
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precipitatesbilirubin
2.SECONDARY
? Stones originate in gallbladder and pass
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into bile ductPATHOPHYSIOLOGY OF
GALL STONE FORMATION
? Depends on the concentration and
type of phospholipids and bile acids in
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bile.? Micelles formed by phospholipid hold
cholestrol in stable state.
? CHOLESTEROL STONES - Precipitation of cholesterol give
rise to stones.
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? PIGMENT STONES1. BLACK- Bilirubin pigments mixed with calcium phosphate,
calcium bicarbonate
2. BROWN- Calcium bilirubinate, palmitate and stearate and
cholesterol
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? MIXED STONES - Contains cholesterolmonohydrate,calcium salts,bile pigments and
fatty acids.
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CHOLESTEROL
STONE
BLACK STONE
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BROWN STONEMIXED STONE
PARASITIC INFESTATION
BILIARY ASCARIASIS
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? Ascaris lumbricoides orRound worm
? Enter biliary tree through
the ampulla of Vater
? Complications :
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-strictures-supp. cholangitis
-liver abscess
-empyema of GB
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CHLONORCHIASIS? Oriental cholangiohepatitis
? Chlonorchis sinensis
? Inhabits bile ducts including
intra hepatic ducts.
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? Fibrous thickening of the ductwalls
BILIARY HYDATID
? Echinococcus granulosus
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? Large cyst obstruct thehepatic ducts
? rupture into the biliary tree
and its contents cause
obstructive jaundice.
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HEMOBILIA
? Bleeding into biliary tree from an abnormal
communication between a blood vessel and
bile duct
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? Rare condition? Causes: -Iatrogenic trauma
-Accidental trauma
-Gallstones
-Tumors
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-Inflammatory disorders-Vascular disorders
IN THE WALL
? Biliary atresia
? Primary sclerosing cholangitis
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? Tumors of bile duct? Cholangitis
? Choledochal cyst
? Caroli's disease
BILIARY ATRESIA
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? Extra hepatic ducts are progressivelydestroyed by inflammatory process which
starts at time of birth.
? Intrahepatic changes
? Biliary cirrhosis and portal hypertension
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PRIMARY SCLEROSING
CHOLANGITIS
? Fibrosing inflammatory condition of biliary
tree
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? Age 30-60(males)? Ass. with other autoimmune conditions
TUMORS OF BILE DUCT
Benign
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? Papilloma and adenoma- mc-arise from glandular epi lining bile
ducts
-more frequently in periampullary
region
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? Multiple biliary papillomatosis-rare
-multiple mucus secreting tumors of
biliary epithelium.
-malignant potential
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? Granular cell myoblastoma? Leiomyoma
? Endocrine tumours
CHOLANGIOCARCINOMA
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? Risk factors -? c/c inflammatory conditions
Primary sclerosing cholangitis
.
Oriental cholangiohepatitis
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Hepatitis C infection? parasitic infections
? congenital
? chemical agents & medications
? post surgical
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CHOLANGITIS
? Inflammation of biliary tree
? Obstruction of bile duct will lead to
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bacterial infection? Organisms causing
E.coli
,Klebsiella,Enterococci,Pseudomonas,
Proteus
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OUTSIDE THE WALL
? Carcinoma head of pancreas
? Periampullary carcinoma
? Enlarged lymph nodes in porta hepatis
? Mirizzi syndrome
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? Pseudocyst of pancreasPANCREATIC CARCINOMA
? 70% at head of pancreas
and periampullary region
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? Ductal adenocarcinoma.? Solid,scirrhous
tumours,characterised by
neoplastic tubular glands
within markedly
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desmoplastic fibrousstroma.
PERIAMPULLARY CARCINOMA
? Carcinoma arising at or near the ampulla of
vater
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It can arise from? Head of pancreas close to the ampulla
? Ampulla of vater itself
? Distal common bile duct-10%
? Duodenal mucosa adjacent to ampulla-10%
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PORTA HEPATIC
METASTASIS AND NODES
Secondaries from ca-stomach, pancreas
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and duodenumAll causes compression on the bile duct
and leads to obstructive jaundice.
MIRIZZI'S SYNDROME
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? Gallstone impacted in cysticduct or neck of gall bladder
? cause compression on
common bile duct or common
hepatic duct.
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? Resultant inflammation causecholecystocholedochal
fistula
PSEUDOCYST AT PANCREATIC
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HEAD? collection of amylase rich
fluid enclosed in a wall of
fibrous or granulation
tissue
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? arises following an attackof acute pancreatitis.
? Enlargement causes
pressure effects.
? ultimately leads to
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obstructive jaundice frombiliary compression ?
WADSWORTH SYNDROME
CLINICAL EVALUATION
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Marlin T AbrahamRoll No:87
HISTORY TAKING
Presenting complaints
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? Yellowishdiscolouration-
skin , sclera and
mucus membrane
? Generalised
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itching? Clay coloured
stools
? Dark coloured
urine
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? Epigastricdiscomfort
? Anorexia, weight loss in malignancy
? Melena / Dark silver stools
? Pain right upper quadrant
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? Intermittent feverPAST HISTORY
? h/o blood transfusion(Hepatitis B)
? h/o jaundice(Hepatitis B,C)
? h/o surgeries ? biliary surgery(post
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operative biliary strictures)? h/o pancreatitis
? h/o sudden onset diabetes
PERSONAL HISTORY
? Diet ? high consumption of meat
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? Cigarette smoking-carcinoma pancreas? Use of alcohol ? chronic pancreatitis
? h/o injections,drug abuse,tattoos-Hepatitis B
DRUG HISTORY
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? Cholestatic ?? anabolic steroids
? chlorpromazine
? carbamazepine
? antibiotics ? erythromycin,
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rifampicin? Hepatitis ?
?INH
?phenytoin
? halothane
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?methyl dopaEXAMINATION
General Examination
? Cachexic
? Pallor
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? Icterus? Clubbing
? Pitting pedal edema
? Pulse rate ? Bradycardia
? Blood Pressure ? hypotension
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? Scratch marks, silver nails? Stigmata of liver disease
? Migratory thrombophlebitis - Trousseau's
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Sign of malignancy? Indication of
Pancreatic carcinoma
Armand
Trousseau
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LOCAL EXAMINATION
Inspection
? Abdomen- distended/ scaphoid
? Gall bladder
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? Scars of previous surgeryPalpation
? Tender right upper quadrant
[cholangitis]
? Liver ? non tender, nodular, rounded
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edge - metastases? Gall bladder ? tense globular swelling
projecting downwards and forwards.
?Moves with respiration
?Better seen than felt
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?Dull on percussionCOURVOISIER'S
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LAWLudwig Georg
Courvoisier
EXCEPTIONS TO
COURVOISIER'S LAW
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? Double impaction of stone? Pancreatic calculus obstructing the
ampulla
? Oriental cholangiohepatitis
? Mucocele/empyema of gall bladder
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? Carcinoma gall bladder with multipleliver metastases
? Mirizzi's syndrome
? Nodes in porta hepatis.
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FEATURES OF METASTASIS
? Left supraclavicular lymph nodes
enlargement ? TROISIER'S SIGN [ Virchow's
node]
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Charles ?mileTroisier
? Per rectal examination ? BLUMER'S SHELF
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[secondaries in rectovesical/ rectouterinepouch]
? Ascitis- liver secondaries
CHOLEDOCHOLITHIASIS
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? Biliary colic? Nausea and vomiting
? Intermittent symptoms
? Physical examination ?
mild epigastric/RUQ
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tendernessmild icterus
CHARCOT'S TRIAD
? Intermittent pain
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? Intermittent fever? Intermittent jaundice
REYNOLD'S PENTAD
? Intermittent pain , fever and jaundice
? Shock
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? Altered mental statusCA HEAD OF PANCREAS
? PAINLESS PROGRESSIVE
JAUNDICE ? 75% cases
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? Nausea,epigastricdiscomfort,pain
? Loss of weight and appetite
? Chills and rigor(cholangitis)
? New onset diabetes
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? Palpable liver? Palpable gall bladder
PERIAMPULLARY
CARCINOMA
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? Intermittent jaundice? Waxing and waning
of symptoms
? Dark silvery stools
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? Pain and weight loss- late features
CHOLANGIOCARCINOMA
? Abdominal pain, early satiety,
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anorexia and weight loss? Pruritus,jaundice
? Cachexia
? Gall bladder palpable
(obstruction-distal CBD)
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HEMOBILIA
? Triad of hemobilia(Sandbloom's
triad)
1. Biliary colic
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2. Obstructive jaundice3.Occult/gross intestinal bleeding
STRICTURES OF BILE DUCT
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? Slowly progressive painlessjaundice
? h/o cholecystectomy
? Pain abdomen
? Features of ascending
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cholangitis? Hepatomegaly due to back
pressure
CAROLI'S DISEASE
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? Presents with abdominalpain or sepsis
? Biliary stasis & stone
formation-biliary sepsis
? Complication-
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cholangiocarcinomaSCLEROSING CHOLANGITIS
? Right abdominal quadrant
discomfort, jaundice, fever,
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fatigue, pruritus and weightloss
? secondary biliary cirrhosis
and cholangiocarcinoma
can develop(long standing)
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PSEUDOCYST OF PANCREAS
? Epigastric pain
? Mild icterus and pallor
? Epigastric mass
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? Resonant on percussion? Mass - tender
? Does not move with
respiration
INVESTIGATIONS
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Martin K SebastianRoll No :88
oBiochemical investigations
oHematological investigations
oImaging and other investigations
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BIOCHEMICAL
INVESTIGATIONS
oBILIRUBIN
Normal
Total bilirubin: 0.2- 0.8mg/dL
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Direct: 0- 0.2 mg/dLIndirect :0.2-0.6 mg/dL
vConjugated hyperbilirubinemia
o Alkaline phosphatase
Normal: 60-300U/L
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>500U/L : suggestive of obstructivejaundice
o SGOT & SGPT
Modest Elevation
o 5' Nucleotide
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Elevatedo Gamma Glutamyl Transpeptidase
Elevated
? CA 19-9
Gross elevation (normal:0-37 unit/ml)
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suggest carcinomaHEMATOLOGICAL TEST
o Prothrombin time
Normal :12-16 sec
vProlonged but correctable with vitamin
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K in obstructive jaundice(10mg IM OD5days)
IMAGING AND
OTHER
INVESTIGATIONS
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PLAIN X-RAY
o Radio opaque gall stones in 10% of patients
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o Mercedes- Benz or sea gull signo Porcelain gall bladder: calcification
of gall bladder
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vAssociated with carcinoma up to25% cases
ULTRASONOGRAPHY
o Accurate , readily available,
inexpensive and quick
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o Intra hepatic and extra hepatic Biliarydilation
o level of obstruction
o Cause of obstruction
? gall bladder , CHD or CBD stones
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? Cholangiocarcinoma ,CA head of pancreas
Gall stones in USG
COMPUTED TOMOGRAPHY
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o More anatomical informationo Cause & site of biliary obstruction
o Staging CA liver,gallbladder,
o bile duct,pancreas
o Extend of primary tumour &
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relationship to other organs & vesselso Enlarged lymph nodes & metastasis
Carcinoma head of pancreas
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MAGNETIC RESONANCECHOLANGIOPANCREATOGRAPHY
Ductal obstruction,strictures,intraductal
abnormalities
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o ADVANTAGESvNon-invasive
vEqual or better imaging than ERCP
vLess complications
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ENDOSCOPIC RETROGRADECHOLANGIOPANCREATOGRAPHY
o Calculi or malignant strictures
o Bile aspirates
o Stone removal and stent placement
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o COMPLICATIONS
vCholangitis ( 1-2% patients)
vProphylactic antibiotics
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PERCUTANEOUS
TRANSHEPATIC
CHOLANGIOGRAPHY
o Strictures or obstruction
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o Bile for cytologyo Catheter for external biliary drainage
o PRECAUTIONS
Exclude bleeding tendency
PT should be normal
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Prophylactic antibioticso COMPLICATIONS
vInfections - cholangitis, septicemia
vBiliary leak
vHemorrhage
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ENDOSCOPIC
ULTRASONOGRAPHY
v Endoscopy aided ultrasound
v Distal common bile duct and ampulla
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v Staging & vascular invasionRADIOISOTOPE SCANNING
v Hydroxy Iminodiacetic acid scan
[HIDA]
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v Identification of bile flowv Obstruction of biliary tree and bile
leaks
PEROPERATIVE
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CHOLANGIOGRAPHYv During open or laparoscopic
cholecystectomy
v Exclude presence of stones
within bile duct
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OPERATIVE BILIARY
ENDOSCOPY
v Choledochoscopy
v Flexible fibreoptic endoscope passed
via cystic duct
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v Enable stone identification & removalunder direct vision
v T-tube
LAPAROSCOPIC
ULTRASONOGRAPHY
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v Biliary & pancreatic tumour stagingv Identify primary tumour and its
relationship to major vessels.
v Micrometastasis of liver
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POSITRON EMISSIONTOMOGRAPHY SCAN
? Fluorodeoxyglucose
? Differenciate benign and malignant
? Diagnosis of metastatic diseases
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? To detect cancerous tissues thatmay not always be seen through
CT/MRI
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MANAGEMENT OFCALCULOUS
CONDITIONS
Megha Thomas
Roll No : 89
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?ERCP
?Cholecystectomy
a. Laparoscopic Cholecystectomy
b. Open Cholecystectomy
?Common bile duct exploration
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?Common bile duct drainageprocedures
?Trans duodenal Sphincterotomy
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ERCP?
Side viewing endoscope is used.
?
Ampulla of Vater is identified.
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?Sphincterotomy is done with a
sphincterotome
?
Extraction of stone with a balloon
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sweep?
Followed by cholecystectomy
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CAUSES OF FAILURE? large stones
? intrahepatic stones
? multiple stones
? altered gastric or
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duodenal anatomy? impacted stones
? duodenal diverticula
LAPAROSCOPIC
CHOLECYSTECTOMY
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INDICATION? Symptomatic gall stones
? Acute cholecystitis (early presentation)
? Acute biliary pancreatitis(after resolution of
signs and symptoms)
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POSITION: supine,head end up
(Reverse trendelenburg position) and
right side up
PORTS: 10 mm port - subumbilicus -
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to pass 10 mm telescope.10 mm port - midline
epigastrium- working
channel.
Two 5 mm ports -
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midclavicular & anterioraxil ary line in subcostal
region.
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OPEN CHOLECYSTECTOMY
? Right subcostal incision(Kocher's)
? Right paramedian
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? Horizontal incisionTECHNIQUE:
? Duct-first method:
?Calot's triangle is dissected.
Cystic artery and cystic duct
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ligated close to the gallbladder.?GB separated and removed.
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? Fundus-first method:? Done in the case of dense
adhesions.
? Fundus separated from the liver
bed. Dissection is carried
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proximally until cystic duct andcystic artery are identified, which
are then ligated.
COMPLICATIONS
?Bleeding from cystic artery,and from
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liver bed?Injury to CBD or hepatic duct
?Injuries to colon,duodenum,mesentry
?Infection and subphrenic abscess
?Bile leak and biliary fistula formation
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?Biliary stricture formationPOST CHOLECYSTECTOMY
SYNDROME
? Recurrent, new or persistent symptoms
after cholecystectomy In patients who
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have no demonstrable abnormality.? d/t loss of reserving function of GB,or
continuous bile flow into duodenum -
esophagitis / gastritis or diarrhea and
colicky pain.
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COMMON BILE DUCT
EXPLORATION:
1.LAPAROSCOPIC CBD
EXPLORATION
? Stone may be flushed with irrigation
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? A balloon catheter passed , inflated &withdrawn.
? A wire basket passed under
fluoroscopic guidance.
? if required a flexible choledochoscope
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can be usedTrans cystic approach
? Cystic duct is dilated and flexible
choledochoscope is passed down into CBD.
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? With identification of stone,wirebasketpassed to ensnare stone.
? C/I: Small ,friable cystic duct
Large stones( more than 1cm)
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Stones in common hepatic duct abovethe cystic duct insertion
Through CBD
INDICATION
? Jaundice,h/o jaundice or cholangitis
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? Palpable stones in CBD? Dilated CBD (>10 mm )
? Dilated cystic duct
? Abnormal LFT particularly elevated
ALP
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? Multi faceted stonesC/I: small caliber CBD
PROCEDURE
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? LongitudinalIncision in common
bile duct
? flexible
choledochoscope
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passed into duct? clearance of stones
? Choledochotomy is
sutured with T tube left
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inside with one endtaken out through the
abdominal wall
CARE OF T TUBE
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? After 14 days ,water soluble dye injected? X-ray taken
? If complete free flow - indicate no block
? T tube clamped for 24 hrs
? If no fever, jaundice or abdominal pain
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? T tube is removed? If blocked ? left for 6 weeks
? BURHENNE TECHNIQUE- After 6 weeks when T-
tube tract gets matured, Then either using
Dormia basket or Fogarty catheter or
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choledochoscope,stone is removed through T-tube tract under fluoroscopic guidance.
OPEN CBD
EXPLORATION
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? When endoscopic and laparoscopicmethods fails
? Palpate distal bile duct , find the stone
which may milked backward.
? Choledochotomy performed in the
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supraduodenal part.COMMON BILE DUCT
DRAINAGE PROCEDURES
? When stones cannot be cleared
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? Duct is very dilatedCHOLEDOCHODUODENOSTOMY
mobilizing the second
part of the duodenum
and anastomosing it
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side to side with thecommon bile duct.
ADVANTAGE: Continues to allow
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endoscopic access to entire biliarysystem.
DISADVANTAGE: Bile duct distal to
anastomosis , doesnot drain well which
collect debris - obstruction of
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anastomosis/pancreatic duct(SUMPSYNDROME)
CHOLEDOCHOJEJUNOSTOMY
bringing up a 45-cm Roux-en-Y limb
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of jejunum and anastomosing it endto side to the common bile duct.
? ADVANTAGE: No risk of sump
syndrome and excellent drainage
? DISADVANTAGE: Does not allow future
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endoscopic evaluation.TRANSDUODENAL
SPHINCTEROTOMY
? Unsuccessful
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endoscopic attemptswith nondilated
biliarytree.
? Longitudinal
duodenotomy to identify
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ampulla? The sphincter is then
incised at the 11 o'clock
position to avoid injury
to the pancreatic duct
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? The impacted stonesare removed
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MANAGEMENT OFBENIGN
CONDITIONS
Muhammed Afnas
Roll no: 90
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PRIMARY SCLEROSING
CHOLANGITIS
? No specific medical therapy
? Choleretic agent ursodeoxycholic acid
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? Immunosuppresives? Antibiotics ,Vitamin K,
Steroids
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Mx:1.Endoscopic balloon dilatation of dominant
strictures improve pruritis,cholangitis and
prolong survival
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2.Biliary reconstruction -
pts with dominant
stricture at biliary
bifurcation
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Resection of affectedpart & long term
silastic stenting
3.Orthotopic liver
transplantation - only
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life saving option--- Content provided by FirstRanker.com ---
MIRIZZI SYNDROME? Cholecystectomy, which may
require repair of the CBD
? In case of cholecysto-
choledochal fistula,
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choledochojejunostomyBILIARY STRICTURES
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1.ERCP withsphincterotomy,
balloon dilatation,
stent placement
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2. Anastomosising a loop of jejunum
( Roux-en-Y jejunal limb) to dilated
portion above the stricture
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CHOLEDOCHOJEJUNOSTOMY
HEPATICOJEJUNOSTOMY
CHOLEDOCHAL CYST
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TYPE 1? Complete surgical excision followed
by Roux- en- Y hepaticojejunostomy
TYPE II
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? Excision of diverticulumwith suturing of CBD
? Anomalous pancreaticobiliary jn [
APBJ ] ?
biliary enteric diversion by
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Roux-en-Y hepaticojejunostomyTYPE III - CHOLEDOCHOCELE
? ERCP with sphincterotomy
- ( cyst < 3cm)
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? Transduodenal excision orsphincteroplasty - ( cyst >3cm )
TYPE IV
? Only extrahepatic biliary dilatation
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excision and hepaticojejunostomy [ liketype I ]
? Intrahep extension ( 1 lobe ) partial
hepatectomy + reconstruction
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TYPE V ?CAROLI'S DISEASE? UNILOBAR Hepatic
lobectomy
? BILOBAR
liver
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transplantationLILLY `S TECHNIQUE
? If the cyst adheres to portal vein
secondary to inflammatory
reactions
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posterior serosal wall of cyst is left
behind & mucosa of cyst is
obliterated
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POLYPS OF GBRx:
?Laparoscopic cholecystectomy
?Risks factor for CA
- Radical cholecystectomy
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?Asymptomatic/no risk factors / no USGfeatures of CA ? observation with seirial
USG
BENIGN BILIARY MASS
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? ADENOMASComplete resection along with small
rim of normal epithelium by
transduodenal approach
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? Papillomatosisliver resection /
liver transplantation
BILIARY ATRESIA
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EXTRA HEPATIC BILIARY ATRESIATYPE I
TYPE 2 & 3
Roux en Y
Kasai
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hepaticojejunostomyportoenterostomy
BILIARY ATRESIA
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? INTRAHEPATIC- Liver transplantation
DUODENAL DIVERTICULUM
? A/C diverticulitis
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IV antibiotics and bed rest? Surgical removal is done as an interval
procedure when the
a/c attack subsides
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HEMOBILIATo stop bleeding and to
relieve biliary obstruction
? Antibiotics
? Blood transfusions
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? Transarterial embolisation (TAE)? Surgical intervention - ligation of
bleeding vessel or hepatic artery or
excision of aneurysm
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PSEUDOCYST OFPANCREATIC HEAD
? Endoscopic drainage under EUS guidance
with tube drain
? Cystoduodenostomy via
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laparotomyMANAGEMENT OF
MALIGNANT
CONDITIONS
Muhammed Galib
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Roll no:91? CARCINOMA HEAD OF THE PANCREAS
? PERIAMPULLARY CARCINOMA
? CHOLANGIOCARCINOMA
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CARCINOMA HEAD OF THE
PANCREAS
MANAGEMENT
? SURGICAL RESECTION
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? ADJUVANT THERAPY? NEOADJUVANT THERAPY
? PALLIATIVE THERAPY
SURGICAL RESECTION
SIGNS OF INOPERABILITY
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a)Distant metastasis including non regional LNb)Head/uncinate process:
-solid tumor contact of >180deg with SMA or
CA
-solid tumor contact with 1st jejunal SMA
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branch-unreconstructible SMV/PV d/t
tumor/occlusion
-contact with most proximal draining jejunal
branch into SMV
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c)Body and tail:
-solid tumor contact of >180deg with SMA or
CA
-solid tumor contact with CA & aortic
involvement
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-unreconstructible SMV/PV d/ttumor/occlusion
PREOPERATIVE PREPARATIONS
i. Hydration
ii. Nutrition(glucose orally or iv)
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iii. Vitamin K 10mg IM started 3 days prior tosurgery
iv. Correction of anemia
v. ERCP stenting (severe cholangitis)
vi. Antibiotics 1 day prior to surgery
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vii.Total parenteral nutrition if neededWHIPPLE'S RESECTION
(PANCREATICODUODENECTOMY
) STEPS
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Incision: midline from xiphoid toumbilicus or bilateral sub costal
Liver, peritoneal surfaces assessed for
metastasis
Hepatic flexure of colon is reflected
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medially (Cattell Braasch maneuver)Kocher's maneuver done and duodenum
along with head of pancrease is mobilised
to midline
SMV identified and
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assessedGastroepiploic vein and
artery ligated
Porta hepatis examined
Assess operability
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? CHOLECYSTECTOMY ANDRESECTION OF
COMMON HEPATIC DU CT
RESECTION OF ANTRUM OF
STOMACH
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Stomach resected atthe level of the third
or fourth transverse
vein on the lesser
curvature
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WHOLE DUODENUM ALONG
WITH 20 ? 30 CM OF JEJUNUM
REMOVED
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DIVISION OFF NECK ANDREMOVAL OF HEAD OF
PANCREAS
Tributaries from the portal
vein and superior mesenteric
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vein ligated and divided? PANCREATICOJE JUNOSTOMY
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HEPATICOJEJUNOSTOMY
GASTROJEJUNOSTOMY
TRAVERSO-LONGMIRE PYLORUS
PRESERVING
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PANCREATICO-DUODENECTOMY(PPPD)POST OP MANAGEMENT
? High dependency observation for1-2 days
? Drain may be put
? Early feeding can be commenced
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? Fluid and electrolyte balance? Observation for feeding and DIC
? Respiratory support(ventilation may be
necessary)
? Vitamin K continued for 5 days
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? Monitor urine output? Octreotide for 5 days to prevent leak
COMPLICATIONS
a. Infections
b. Haemorrhage
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c. Leak from anastomosis between bowel andpancreas(octreotide)
d. Pancreatic fistula
e. Recurrence
f. Hepatorenal syndrome
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g. Delayed gastric emptyingh. Bile leak
i. Mortality 3%(sepsis,hemorrhage,
cardiovascular events)
ADJUVANT THERAPY
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? High recurrence rate followingresection
? CHEMOTHERAPY AND RADIATION
? 5FU
? Gemcitabine (less toxic)
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? I125 external radiotherapy? Immunotherapy (allogenic tumor cell
vaccine)
NEOADJUVANT THERAPY
? Administration of chemotherapy with or
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without radiotherapy before surgery? For borderline resectable
? ADVANTAGES
? Increased R0 resection status
? Reduces node positivity rate
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? Reduce tumour burden? Decrease recurrence
? Decrease chance of fistula
PALLIATIVE THERAPY
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BILIARY OBSTRUCTION? Surgical biliary
bypass(choledochojejunostomy &
gastroenterostomy)
? ERCP stenting
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? PTC stenting? PTBD
1.internal drainage
2.external drainage
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DUODENAL OBSTRUCTION? Gastrojejunostomy
? Duodenal stent
PAIN
? Antiinflammatory drugs
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? Opioids? Celiac nerve block(inj.3ml 0.25% bupivacaine and
10 ml absolute alcohol)
ROUX EN Y CHOLEDOCHOJEJUNOSTOMY
AND GASTROJEJUNOSTOMY
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It is a palliative procedure done along with gastrojejunostomy aftercholecystectomy
ADVANTAGES
Ease of flow of food
Decreased risk of cholangitis
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Easier management of biliaryanastomotic leaks
PALLIATIVE CHEMOTHERAPY AND
RADIATION
? Locally advanced unresectable
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disease and stage 4 diseases? Folfirinox(5FU+Oxaliplatin+Irinotecan+leuco
vorin)
? Gemcitabine+nabpaclitaxel(albumin
bounded paclitaxel particle)
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? Gemcitabine,erlotinib? 5FU and capecitabine with radiotherapy
PROGNOSIS
? After surgical resection and adjuvant
therapy for CA pancreas,the median
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survival is approximately 22 months.? 5 year survival of 15-20%
PERIAMPULLARY
CARCINOMAS
? Periampullary cancer includes tumors
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arising from the distal bile duct, duodenalmucosa, or pancreas just adjacent to the
ampulla
? Management : Pancreaticoduodenectomy
(PD) with or without pylorus preservation
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CHOLANGIOCARCINOMA
? Cholangiocacinoma(bile duct carcinoma)
is a rare malignancy
Distal bile duct tumours
Proximal bile duct tumours
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? Resection and hepaticojejunostomy? Endoscopic stent placement
? Signs of unresectability : hepatic
metastasis,peritoneal metastasis
DISTAL CHOLANGIOCARCINOMA
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? PANCREATICODUODENECTOMYPROXIMAL
CHOLANGIOCARCINOMA
? En block resection of common bile
duct with hepatic parenchyma as
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necessary to achieve negative margins? Resection of regional lymph node
? Taj Mahal resection: central liver
resection> 1,4,5 segments& relevant
bile ducts removed
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? No proven role for adjuvant therapy
? Adjuvant chemoradiation ?patient with nodal
disease,R1 resection,undergoing clinical
trial.
OUTCOMES
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? Depend on stage at presentation? Negative margins
COLORECTAL LIVER
METASTASIS
RESECTION
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? To be resectable CRLM must be removablewith neg margins with min preservation 2
contiguous supported liver segments
? Vol of FLR depends on parenchymal function
-n/l liver:20%
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-damaged by chemo:30 or 40%SMALL FUTURE LIVER
REMNANT
CONVERSION
? Chemotherapy conversion-downsizing
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unresectable liver d/s burden toresectability
Eg: FOLFOX4 regimen
TWO STAGE LIVER RESECTION
Prior to hepatectomy>portal vein
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occlusion> hypertrophy of small FLR-operative ligation (PVL)
-percutaneous trans hepatic
embolization(PVE)
ASSOCIATING LIVER PARTITION &
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PORTAL VEIN LIGATION(ALPPS)? Stage 1: portal vein ligated & parenchyma
transected to separate FLR from
hepatectomy specimen
-rapid FLR hypertrophy(7-10 days)
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? Stage 2: completion hepatectomyp-ALPPS: partial transection of FLR in
stage 1
Salvage-ALPPS: FLR refractory to
hypertrophic stimulus of portal vein
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occlusionCOMBINED INTRAOPERATIVE
ABLATION & RESECTION
? Resection of larger& superficial lesions +
ablation of sub 4cm, deeper lesions
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? Minimizing parenchymal loss- FLR preservedABLATION
? Not sufficiently fit to undergo liver
resection are considered
? Ablation +systemic chemo
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? Radiofrequency ablation? Microwave ablation
IRREVERSIBLE ELECTROPORATION
? Non thermal technique
? Induce cell death with electric pulse
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? Preservation of vessels and bile duct? To manage anatomically challenging
lesions
Overview
? Jaundice due to obstruction of flow of
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bile to intestine.? Causes are Intrahepatic and
Extrahepatic.
? Clinical features are jaundice, clay
coloured stools, itching, epigastric
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discomfort, anorexia etc.? Investigations include USG, plain X-ray ,
MRCP, ERCP, CT scan, radioisotope
scanning, PTC and endoscopic
ultrasound.
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? Management is mainly surgical anddepends on the cause.