Hepatobiliary Surgery
Anil S. Paramesh, MD, FACS
Associate Professor of Surgery and Urology
Tulane Transplant Institute
Tulane University School of Medicine
New Orleans
Bile is 90% water
Bile Salts – 80%
1° Bile Acids – cholic and chenodeoxycholic
2° Bile Salts – lithocholic and chenodeoxycholic
Phospholipids – 15%
Cholesterol – 5%
Function of bile
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Bile facilitates fatty acid and monoglyceride
absorption via formation of micelles
Fat soluble vitamins A,D,E & K dependant on
this
Sole mechanism of cholesterol loss in the body
Gallbladder
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Actively absorbs salt and water to concentrate bile
Secretes H+ ions (keeps Ca+ soluble) and mucus
Contracts with parasympathetic and CCK
stimulation – normal contraction should be ~ 80%
Gallstones
Cholesterol
obesity, rapid wt loss, ileal resection, pregnancy, TPN
Pigment
Hemolytic anemias, brown vs. black
Calcium
PTH
Asymptomatic Cholelithiasis
Cholecystectomy only if:
1. diabetes mellitus
2. anticipated pregnancy
3. concurrent abdominal operation (bypass)
4. anticipated transplant
Also for polyps > 1cm
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HIDA scan
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Calculous and acalculous acute
cholecystitis the gallbladder is not
visualized as a result of cystic duct
obstruction
No visualization or delayed visualization
are common in chronic cholecystitis
<33%EF indication for surgery
Cholecystectomy
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Lap chole has higher risk of bile duct injury than
open
10% - 12% of pts with cholelithiasis will have
choledocholithiasis
Bile duct injury
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Sharp, < 2mm, consider primary repair, ± Ttube
Bovie injury, > 2mm, Roux en Y
hepaticojejunostomy
Use absorbable sutures!!
Compl of cholecystectomy
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Injury to R hepatic artery – may present with
biliary strictures/abscesses later on
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Hemobilia – pseudoaneurysm of traumatized
art. Presents with hematemesis, jaundice, RUQ
pain. Tx is embolization
Cholangitis
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Charcot’s Triad
Raynaud’s Pentad
Always treat with hydation and abx first –
chance of stone passage
CBD exploration vs. ERCP
Transduodenal sphincterotomy if above
unsuccessful
May do PTC first if pt is septic
Gallstone ileus
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Tumbling obstruction
X Ray- small bowel obstruction with pneumobilia
Most common site of obstruction is in the
terminal ileum
Initial therapy is appropriate resuscitation
followed by surgery
Proximal enterotomy with milking back of stone
Search for additional intestinal stones, which are
present in 10% of patients
Do not repair fistula if inflammation acute or hard
tissue
Choledochal cysts
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Type I most common
Risk of CCA, esp type I
& IV – comp excision
II/III – exc/endosc
opening
V (Caroli’s) diff from
PCLD – bile ducts are
involved. May need
resection/transplant
Sclerosing Cholangitis
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Primary vs. Secondary
Strong association with UC and
autoimmune diseases
Frequent biliary septic episodes
Tx is medical unless localized extrahepatic
Risk of development of cholangioca
Liver transplant for diffuse PSC
Cancer of the gallbladder
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Stage 1b (muscle) and higher requires
radical cholecystectomy
Wedge resection of Seg IVA and V, portal
lymphadenecetomy
Need to check cystic duct margin @
surgery
Good survival (>75%) if earlier stage and
completely excised
Surgical Anatomy of the Liver
GROSS ANATOMY
PROMETHEUS
WAS HE THE FIRST LIVER RESECTION?
Liver regenerates in 6 weeks
Hepatic Arteries
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Derived from the celiac axis, which becomes the
common hepatic artery after giving off the
gastroduodenal branch
15 to 20% of persons, the right hepatic artery can arise
from the superior mesenteric artery
the left hepatic artery originates from the left gastric
artery and is located in the gastrohepatic ligament in
15% of individuals
the arterial blood supply accounts for only 25% of
hepatic blood flow
Portal Vein
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Supplies 75% of blood to liver
Formed by SMV and SV
Portal vein pressure is 3 -5 mm Hg
No valves in the portal vein
Hepatic Veins
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3 hepatic veins!
Hepatic veins begin in the liver lobules and
coalesce to form the right, left, and middle
hepatic veins
Left and middle typically join just before reaching
IVC
Short hepatic veins
Each segment has it’s own triad
Elevated LFTs
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AST (SGOT), ALT (SGPT), and LDH are
indicators of the integrity of the
membranes and increase suggests
cellular damage
Bilirubin, alk phos, 5’-nucleotidase, leucine
aminopeptidase, and γGT reflect excretory
capacity and increase suggest biliary
stasis
Infections - Bacterial
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Most common cause of pyogenic liver abscess is
from biliary source
E.coli most common, may be anaerobes
May be from portal seeding – diverticulitis, etc.
Tx – drainage and antibiotics
Infection amebic
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Infection route via portal vein – may not have
diarrhea
History of third world country exposure
CT scan typically single collection with
peripheral rim of edema
“Anchovy paste” aspiration frequently neg –
need serologic testing for E. Histolytica
Tx – antibiotics (Flagyl) only
Infections - Echinococcal
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Dog are definitive host. Sheep and humans are
intermediate hosts
History of sheep exposure
Pain, cholangitis, anaphylaxis
CT scan - daughter cysts.
Dense calcification usually
signifies dead parasites and
may be left alone
Serolog testing – no aspirate!
Infections - Echinococcal
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If has cholangitis – ERCP first to r/o biliary
connection
Tx – antihelminthics with drainage
PAIR
 Open surgery – pericystectomy vs. cyst unroofing
 20% NS
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Liver Mass - FNH
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Thought to be due to embyologic disturbance of
blood flow in liver. B9
Usually incidental
CT shows central scar
Confirmatory test – sulfur colloid scan.
Tx – resect only if symptomatic
FNH
Sulfur colloid scan – differentiate FNH vs HCC
FNH takes up dye because of normal liver parenchyma and increased Kuppfer
cells
Liver Mass - Adenoma
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History of OCP, steroids
CAN rupture, CAN turn malignant
Shows arterial enhancement on CT scan
May trial d/c steroids if small
Surgery if no improvement
Liver Mass - Hemangioma
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Looks solid on US
CT – slow filling of lesion from
periphery
Kassabach Merritt syndrome
Does not spontaneously rupture!
Enucleate only if symptomatic
Liver Mass - HCC
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Usually occurs in setting of chronic liver disease
CT scan shows classic arterial enhancement with
portal washout
AFP may be raised not diagnostic
Does NOT typically need biopsy!
Tx based on degree of liver disease
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Resection vs transplant vs ablation
Concerning Etiologies
Hepatitis B
Hepatitis C
Alcohol
NASH
HCC – arterial phase
HCC – venous phase
Child’s Pugh Score of Liver Cirrhosis
Parameter
Albumin (g/dL)
Bilirubin (mg/dL)
Ascites
Encephalopathy
PT (INR)
Score
Points
A
5-6
1
Points
2
3
> 3.5
2.8-3.5
< 2.8
<2
2-3
>3
Absent
Slight
Moderate
None
I - II
III - IV
< 1.7
1.8 – 2.3
> 2.3
B
7-9
C
10 - 15
Pugh, RNH, et al. British Journal of Surgery. 60(8): 646-649, 1973
Barcelona-Clinic-Liver-Cancer Screening
HCC
Child A-B
Child A
Very early stage,
Single <2 cm
T2 tumor
Single
Intermediate stage
multinodular
ECOG > 2, Child C
Advanced stage,
portal inv. N1, M1,
ECOG 1-2
Terminal stage
3 nodules, ≤ 3 cm
Portal pressure/bilirubin
Increased
Associated diseases
Normal
Resection
No
Transplant
Yes
PEI/RFA
Curative Treatments
Chemoembo New agents
Palliative Options
BSC
Adapted from Bruix, J. et al. Management of hepatocellular carcinoma. Hepatology. 2006 Feb; 43 (2): 373.
Radio Frequency Ablation of Cancer
RFA Probe
Liver Mass - CCA
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Typically occurs in setting of chronic biliary
inflammation (PSC)
Intra vs extrahepatic
CA 19-9
Tx - resection. Excise all involved duct – frozen
section! Transplant controversial
Klatskins – usually one duct involved more than
other
Cholangioca – biliary dilation
Cholangioca - ERCP
EUS Guided Biopsy
Spyglass cholangioscopy
Cholangico – resect the bile duct
Liver Mass - Hepatoblastoma
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Most common liver malignancy in children
Treatment is chemotherapy first – usually
shrinks tumor to make it more amenable for
resection or transplant
Liver Mass – Colorectal Mets
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Resect if feasible – will confer some survival
advantage! Surgery + chemo = > 50% 5 yr
survival
If initially unresectable – trial with chemo – may
shrink
Poor prognostic features
Extrahepatic disease
 DFI < 1 yr
 > 5 cm; > 4 tumors
 CEA > 60
 Positive resection margin
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Colorectal mets – do not enhance!
Neuroendocrine Mets
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Common:
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Less Common:
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Gastrinomas- gastrinZollinger-Ellison
Glucagonomas- alpha cell glucagon
Somatostatinomas-delta cellsomatostatin
nonfunctional neuroendocrine tumor
Insulinomas-beta cell insulin
Carcinoid-enterochromaffin cellserotonin
Most are slow growing and long term survival is
common without treatment
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Focus is directed at improving quality of life rather than
prolongation because most secrete active peptides
Rx Options:
Long-acting somatostatin analogues
 Hepatic arterial embolization
 Thermoablative approaches- RFA
 Surgery for persistent symptoms
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Resection – 50% -75% 5 yr survival with R0 resection
 Transplant
 Cytoreductive surgery - intention is to reduce symptoms
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Portal Hypertension
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Hepatic Portal Venous Gradient (HPVG)
normally less than 10. Above 12, variceal bleeds
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Causes
Presinusoidal – PVT, Schistosomiasis
 Sinusoidal – cirrhosis
 Post sinusoidal – Budd-Chiari syndrome
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Portal hypertension
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Umbilical hernia with
ascites – do not operate
if possible! Medical
therapy
Flood syndrome –
necrosis of skin with
leakage of ascites.
Surgical emergency as
represents risk of
infection. Fix primarily if
possible. High recurrence
rate
Portal hypertension - shunts
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Rare since development of TIPS
Patient may be transplant candidate – don’t
mess with the hilum!
Non-selective shunts – good for ascites, but
make encephalopathy worse
Selective shunts – less encephalopathy, worsens
ascites
Non selective shunts
Selective shunts
Liver trauma
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2nd most commonly injured organ in blunt
trauma (Spleen is first!)
Mainly nonoperative mgmt
Maneuvers – Pringle, TVI, embolization
Questions/Feedback
aparames@tulane.edu