THE LIVER

1.

U
nd
The LIVER er
st
 FORAMEN OF WINSLOW an
d
ex
tr
ah
ep
ati
c
o AKA: epiploic foramen an
d
int
ra
he
pa
Dr. Fidel Baldovino tic
liv
er
an
at
o
m
y
an
d
o Deep/dorsal to the porta hepatis

o connects directly to the lesser sac

KEY POINTS

o allows complete vascular inflow control to the liver when

the hepatoduodenal ligament is clamped using the Prin-

6.

physiology. D
es
cri
be
th
e
no
m
gle maneuver. en
cl
at
ur
2.
e
an
Understand hepatic molecular signaling pathways.
d
st
ep
s
in
pe
rf
or
mi
ng
an
an
at
3. Know the features of acute liver failure and cirrhosis, along with o
mi
c

treatment options.

rig
ht
or
le
4. ft
he
Formulate a plan for the work-up of an incidental liver lesion. pa
tic
re
se
cti
on
5. .

Understand the current treatment options for primary and meta-

static liver cancer.

ANATOMY OF THE LIVER

DUAL BLOOD SUPPLY

o surrounded by a fibrous sheath known as Glisson's cap-sule.

LIGAMENTS: holds the liver in place

o round ligament: remnant of the obliterated umbilical vein and enters

the left liver hilum at the front edge of the falci-form ligament.

o falciform ligament: separates the left lateral and left me-

LIVER

dial segments along the umbilical fissure

o largest organ in the body o 1500 g. anchors the liver to the anterior abdominal wall.

o right upper abdominal cavity beneath the diaphragm o ligamentum venosum: between the caudate lobe and the left lateral
protected by the rib cage. segment

o reddish brown obliterated ductus venosus

 Portal vein: Delivers 75%

covered by the plate of Arantius.

formed by the confluence of the splenic vein and the su-perior

mesenteric vein
o Left and Right ligaments: secure the two sides of the liver
to the diaphragm. on the liver are the

Coronary ligaments: Extending from the triangular liga-ments

anteriorly

Right coronary ligament: extends from the right un-dersurface of

the liver to the peritoneum overlying the right kidney

 anchors liver to the right retroperitoneum.

Hepatoduodenal ligament:

AKA porta hepatis

Hepatic Artery
contains the common bile duct, the hepatic artery, and the portal
vein.

DR. FIDEL BALDOVINO

Portal vein

Hepatic artery: delivers 25% of blood supply o arises from the

celiac axis/trunk
 Segment I: Caudate Lobe

Segments II and III: comprise left lateral segment

HEPATIC VENOUS SYSTEM

segment IV [aka: quadrate lobe]: left medial segment

divided the liver into eight

segments, numbering them IVA: cephalad, below diaphragm
in a clockwise direction
beginning with the:

IVB: caudad, adjacent to gallbladder fossa

Left and middle hepatic veins: form a common trunk approx-imately

95% of the time before entering the IVC

Right hepatic vein: inserts separately (in an oblique orienta-tion) into

the IVC.

large inferior accessory right hepatic vein

o 15 to 20% of cases

o runs in the hepatocaval ligament

can be a source of torrential bleeding if control is lost during right

hepatectomy.

COUINAUD'S SYSTEM

3 Hepatic veins: drain to suprahepatic IVC, right atrium o Right:

drains segments V to VIII

o Middle: drains segment IV as well as segments V and VIII

o Left: drains segments II and III

Caudate lobe: unique because its venous drainage feeds di-rectly into
the IVC.
 Bilirubin: breakdown product of normal heme catabolism o
Circulation: Bound to albumin, sent to the liver
LEFT LOBE:

left lateral segment (Couinaud's segments II and III)

o Liver: conjugated to glucuronic acid by glucuronyl trans-ferase,
which makes it soluble in water.
left medial segment (segment IV).

1 bilirubin molecule reacts with 2 uridine diphosphoglucuronic acid

Segment IV can be subdivided into segment IVB and molecules to form bilirubin diglucuronide

segment o Glucuronide is then excreted into the bile canaliculi.

RIGHT LOBE: V, VI, VII, and VIII,

Right Anterior Lobe: V and VIII

o Majority of conjugated bilirubin is excreted in the intestine as
waste

Right posterior lobe: VI and VII

some of the bilirubin and urobilinogens are reabsorbed in the portal

circulation; they are again excreted by the liver or enter the circulation
BILIRUBIN METABOLISM and are excreted in the urine

ENTERO
HEPATIC
CIRCUL
ATION

left lobe:
remainder
[with the
caudate
lobe]

caudate
lobe

o
three
subseg
ments

Spiegel
lobe
Cantlie’s line:

o Plane from the gallbladder fossa to the IVC

paracaval
o separates the liver into: portion

 caudate
right lobe: 60-70% of liver mass
process.
Falciform ligament: divides the left lateral segment from the left medial segment

COUINAUD'S SYSTEM

o Couinaud: French surgeon and anatomist in the early 1950s.

BALDOVINOFIDEL

DR..
 study of newly diagnosed cirrhotic patient

DIAGNOSTICS

evaluation of living transplant donor

LIVER FUNCTION TESTS

part of gallbladder workup

this term is a misnomer: most of these test measure not liver

function but rather cell damage
ULTRASOUND- “PULSE- ECHO PRINCIPLE”

more accurate measurement of the liver’s synthetic function is

provided by serum albumin levels and prothrombin time first modality to be requested o biliary stones

INTERPRETATION OF LIVER TESTS o ductal evaluation o liver texture

o Cirrhosis

Tests of synthetic liver function o Fatty infiltration

Tumor consistency (solid or Cystic)

INR

Intraoperative UTZ

Clotting factors

gold standard in detecting the number, extent, associa-tion of tumors

with intrahepatic blood vessels
Albumin

Test of parenchymal injury

laparoscopically or during laparotomy

requirement prior to hepatic resection for malignancy

AST (SGOT)
intraparenchymal vascular anatomy

o facilitates hepatic resection

ALT (SGPT)

used for image-guided biopsy

Test for biliary obstruction (Cholestasis)

ALP, GGT, Bilirubin (total, direct or indirect)

Ultrasound Elastography

LIVER IMAGING
Assess the degree of fibrosis or cirrhosis in the liver
Indications:

screening or assessment of malignancy

Low frequency vibrations--->elastic shear wave detected by pulse o T1: how quickly a tissue is magnetized
echo ultrasonography---> velocity of the wave correlates with the
liver stiffness (wave travels faster through fibrotic or cirrhotic tissues

87% sensitivity, 91% specificity

CT Scan

solid vs cystic lesion

based on the dual blood supply of the liver


o -arterial phase (20-30 secs) after contrast o -venous/potal
phase (60-70 secs) produces images based on magnetic fields and radio waves

can detect the ff:

presence of peritoneal disease

o T2: how quickly it loses its magnetization

portal lymphadenopathy

assess resectability of liver tumors

MRI
o with higher soft tissue contrast resolution w/o ionizing

radiation

excellent for evaluation of intrahepatic biliary tree (MRCP)

 o diagnostic workup of a patient with o potentially resectable hepatic
disease

sensitivity decreases by neoadjuvant chemotx—


reduced metabolic activity of the tumor
MR Venography
Disadvantages:

lack of exact localization of lesions due to poor reso-lution

 for this reason, integrated PET and CT are increasingly available to

potentially improve diagnostic accuracy over standard PET or CT alone
to study extrahepatic portal system

ANGIOGRAPHY

becoming less important because of CT and MRI

POSITRON EMISSION TOMOGRAPHY (HINDI NA DINISCUSS NI DOC)

canulate femoral a, insert catheter until reaching the celiac to the
hepatic artery

gamma rays emitted by radioisotope incorporated into a meta-

bolically active tissues
still used to confirm an atypical

whole body scan

hemangioma (vascular malformations)

F-fluorodexoyglucose (FDG) intravenous-MC radioisotope

as an adjunct in arterial chemo- embolization for unresec-table
malignant tumors

taken up by active tissues like malignant cells

NEEDLE BIOPSY OF THE LIVER

offers functional imaging of tisseus with high metabolic activity,

including most types of metastatic tumors
the only study that proved a pathologic diagnosis

almost 100% diagnostic accuracy rate

Uses:

very useful in diffuse diseases

o to rule out extrahepatic mets of o colorectal cancer

may miss focal lesions: neoplasm, abscesses, and granuloma

0.8% mortality rate

Complications (percutaneous approach)

o pain, pneumothorax, bleeding, peritonitis

DIAGNOSTIC LAPAROSCOPY

 minimally invasive

 can evaluate the entire abdomen

 laparoscopic ultrasound

 detects resectable or unresectable disease

o identifies contraindications to resection

 may be used as the final step in patient staging for hepatic

malignant disease

.
 nodular surface contour

useful in predicting surgical risks of other intraabdominal oper- dilatation of portal vein TR
ations performed on cirrhotic patients EA
T
o Class A Cirrhosis ---10% Surgical Mortality Rate o Class B M
Cirrhosis ---30% Surgical Mortality Rate o Class C Cirrhosis ---75- gastroesophageal varices
E
80% Surgical mortality rate N
T
splenomgaly

Pr
CIRRHOSIS AND PORTAL HYPERTENSION ev
en
t
fu
A 51 yr old man presents to the emergency room with hema-temesis rt
and a systolic BP of 80. After initial fluid resuscitation of isotonic he
crystalloid solutions, his BP- 120/80, and his pulse rate is 100. The r
next hospital day, EGD was done revealing large esophageal varices da
with overlying clot. Patient is a chronic alco-holic drinker.... m
ag
e
of
CIRRHOSIS th
e
liv
er
generalized hepatic fibrosis and nodular regeneration of the liver as
a response to hepatocyte necrosis

Tr
ea
8th leading cause of death in USA
t
co
m
pli
Ito cells – hepatic stellate cells
ca
o Principal mediators of hepatic fibrosis tio
n
of
cir
o Stimulated by hepatocyte necrosis, cytokine,growth fac-tors rh
os
is

CHARACTERISTICS

right hepatic love atrophy

caudate lobe and left lateral segment hypertrophy

recanalization of the umbilical vein

Prevent liver cancer or detect it early 

o HCC can occur in all forms of cirrhosis o does not rule out HCC

o Every cirrhotic patient should undergo screening for the Transplantation

development of HCC every 6 months

ASSESSMENT OF SURGICAL RISK IN THE CIRRHOTIC PATIENT

Measurement of serum alphafetoprotein (AFP) level

Child-Turcotte-Pugh Score (CTP)

o Only 60-75% of HCCs produce AFP; therefore, a normal se-rum
AFP level

Percutaneous approach o CT or UTZ Sp

le
no
m
Can determine the cause, activity, and eg
al
y

progress of the disease

o
En
Clinical features lar
ge
Laboratory values
d,
to
rt
Radiographic findings uo
us,
an
d
PORTAL HYPERTENSION ev
en
elevated pressure within the portal venous system an
eu
rys
m
normal: 5-10mmHg al
spl
en
ic
>10mmHg is clinically sig. portal HTN ve
ss
DIAGNOSIS Cirrhosis: MC cause of portal hypertension

Liver biopsy Gastroesophageal varices

Histopathologyc diagnosis o From the anterior branch of the left gastric or coronary vein
els frequently assocaited with
hypersplenism

Caput Medusa

o dilated umbilical vein

o visible collaterals on the abdominal

wall

Cruveilhier-Baumharten murmur

o Audible venous hum auscultated in the

epigastrium from collaterals b/n portal
system and remnant umbilical vein

Ascites

o Hepatic dysfunction

Anorectal varices

o In 45% of cirrhotic patients

o Must be distinguished from

hemorrhoids

Asterixis: hepatic encephalopathy

HEPATIC VENOGRAPHY

most accurate method of determining

portal hypertension

involves placing a balloon catheter directly

into the hepatic vein and measuring the
free hepatic venous pressure (FHVP) with
the balloon deflated, and the

wedged venous pressure (WHVP) with the

balloon inflated to occlude the hepatic vein
 endoscopic sclerotherapy (93% success rate) T
H
JLB E
LI
EGD VE
R

TIPS


M
 A
N
A
G
HVPG= WHVP-FHVP E
done by experienced interventional radiologist can control varical
 M
bleeding in >90% of cases <12 mmHg portal venous pressure E
Possible complications N
>10mHg: clinically significant portal HPN
T

bleeding intra-abdominally or in the biliary tree, infections, renal O
failure, decreased hepatic function--->hepatic en-cephalopathy(25- F
30% after the procedure) MECHANISM A
C
U
TE
 As portal venous collateral develop, diverting blood into the systemic V
ciculation, portal hypertension is maintained by increasing portal flow A

 RI
and splanchnic vasodilation hyperdynamic portal venous
CE
  AL
circulation increased cardiac output generalized vasodilation
Sengstaken Blakemore Tube BL
EE
TIPS (Transjugular Intrahepatic, PS Shunt)
DI
N
 implantation of a metallic shent between an intrahepatic
G
branch of the portal vein and a hepatic vein radicle

<36 hrs to prevent tissue necrosis

aspiration, airway obstruction, perforation

control refractory bleeding

Balloon tamponade (Blakemore-Sengstaken tube)- luminal tam-

ponade

variceal band ligation

Admitted to an ICU for resuscitation and management. – PHARMACOLOGIC THERAPY

Started upon diagnosis SU

R
Blood resuscitation GE
RY
Vasopressin: the most potent vasoconstriction II

o haemoglobin level of approximately 8 g/dL.

Somatostatin and its analogue octreotide o also cause splanchnic

vasoconstriction
o avoid over replacement of packed red blood cells and the
overzealous administration of crystalloid solutions (per-missive
hypotension)
Octeotride

lead to both rebleeding and increased mortality.

o the preferred pharmacologic agent for initial management of

acute variceal bleeding
fresh-frozen plasma and platelets can be considered in patients
with severe coagulopathy

o can be administered for 5 days or longer

as
so
cia
te
d
wi
ESOPHAGEAL VARICES th
po
rta
l
submucosal plexus in the distal esophagus or upper stomach hy
pe
rte
nsi
rupture and bleeding of varices is the most serious complica-tion on

Factors: Ap
pr
o increased pressure in the varix oxi
m
o ulceration of the varix due to esophagitis
at
ely
30
%
VARICEAL BLEEDING
of
most significant manifestation of portal hypertension pa
tie
nt
s
leading cause of morbidity and mortality wi
th
co
mpensated cirrhosis and 60% of patients with decompensated for
cirrhosis have esophageal varices. pa
tie
nt
s
30% of patients with varices experience variceal bleeding wi
th
m
ed
One third of all patients with varices experience variceal bleed-ing.
iu
m
to
lar
20 to 30% risk of mortality.
ge
va
ric
Seventy percent of patients who survive the initial bleed will es
experience recurrent variceal hemorrhage within 1 year if left
untreated.

pe
rfo
ETIOLOGY OF VARICES rm
ed
ev
er
  y1
Obstruction of portal blood flow Elevated portal pressure (portal HPN)
to

reversal of portal blood flow enlargement of collaterals 2
we
ek
s
PREVENTION OF VARICEAL BLEEDING un
til
ob
lit
improvement of liver function
er
ati
on

avoidance of alcohol

avoidance of aspirin and NSAIDs, and

administration of propranolol or nadolol,

o reduces the index variceal bleed by approximately 45% o

reduces bleeding mortality by 50%.

prophylactic endoscopic variceal ligation (EVL)

for patients who cannot tolerate b-blockers

SURGERY FOR PORTAL HYPERTENSION

control manifestations/complications o ligation of varices

o transection procedures

o resection on varix-bearing areas o peritovenous shunts

reduction of portal pressure and flow

o splenectomy

Shunts
Surgiura
portocaval - portal vein to vena cava

splenorenal – splenic vein to renal vein SHUNT PROCEDURES

Surgical
Shunts for
mesocaval – mesenteric vein to IVC reduce portal venous pressure
Portal HPN:
non-selective

TRANSECTION/ DEVASCULARIZATION PROCEDURES

PORTOCAVAL
SHUNTS
o end to side PC shunt o side to side PC shunt o
central SR shunt
Sugiura

portal vein -->

IVC
Selective
o esophageal transection-anastomosis o esophagogastric
devascularization

end to side
o Distal splenorenal o H Graft shunt
o easiest
o Splenectomy
to perform
SHUNT OPERATIONS
o totally
diverts portal
most complete form of devascularization
blood flow
Hassab’s 
reduction of portal pressure decreased potential for
bleeding from varices
side to side
devascularization of the proximal stomach and distal esophagus
o 2-3%
*Encephalitis is common in Portocaval shunts rebleeding
o splenectomy
(sinceblood does not go to the liver anymore) rate
 o higher incidence of variceal rebleeding o lower THE LIVER
incidence of encephalopathy
o 14-40% post op encephalopathy rate o lower ammonia levels

DISTAL SPLENORENAL SHUNT

o low protein

o no GI bleeding
AKA: Warren Shunt

distal splenic vein --> left renal vein

provides selective decompression of

esophageal varices while maintaining

hepatic blood flow

difficult to construct

low incidence of encephalopathy

SPLENORENAL SHUNT

Central splenorenal shunt

o proximal splenic vein --> left renal vein o used in patients

where portal vein is

o Obstructed or cannot be used for shunting o difficult to

construct

o “small side to side shunt”

 LIVER MASSESS AND TRANSPLANTATION

INTERPOSITION MESOCAVAL SHUNT

H-shunt, jump shunt,

synthetic material or autologous vein graft is anastomosed

between the IVC and superior mesenteric vein

easy to perform

used in emergencies

variceal bleeding is low

encephalitis is low

long term patency of the graft is questionable

CLASSIFICATION OF LIVER MASSES

Mesocaval H-Shunt
THE LIVER

tionable; hyperplastic response to

BENIGN SOLID NEOPLASMS OF THE LIVER

IISURGERY
an anomalous artery

high risk of hemorrhage

A 25 year old woman on oral contraceptives develops right unlikely but uncertain
upper
and malignant transfor-

mation is recognized
quadrant abdominal pain. A ct scan demonstrates a hypodense,
6cm

consists of hepatocytes w/o

contains Kupffer cells along with a

bile ducts or Kupffer cells

mass in the right lobe of the liver. Helical CT scan reveals a
defect in central stellate scar surrounded by

fibrous tissues

the area of the mass. Angiographic study reveals a Helical CT: absence of
hypervascular
presence of Kuppfer cells enables

Kuppfer cells, it does not

uptake of radioisotopes, well cir-

tumor with a peripheral blood supply.....
take up radioisotope, hy-

cumscribed with a typical central

podensity with a central

Scarring

defect
HEPATIC ADENOMA VS FOCAL NODULAR
HYPERPLASIA

liver specific MRI con-

HEPATIC ADENOMA improved the ability to differentiate

FOCAL NODULAR HYPERPLASIA rast(gadoxetate)-increase

child bearing age HA from FNH

child bearing age enhancement during

OCPs and anabolic steroids

association with steroids is ques-

hepatobliary phase of imag-
ing BENIGN VASCULAR HEPATIC TUMOR

Management: An asymptomatic 45 yr old woman is found to have a 7 cm liver mass. A ct

scan demonsrates an initial hypodense lesion with peripheral to central
enhancement by contrast material.MRI shows a dense T2 weighted
phase....
percutaneous biopsy is not

Reassurance and prospective ob-

recommended HEMANGIOMA

servation irrespective of size

regression does not reliably

surgical resection can be recom- ● Most common solid benign tumor of the liver

occur with cessation of

mended: symptomatic, HA or HCC

OCPs
● Congenital vascular lesions that contains fibrous tissue and
cannot be definitely excluded

4 cm lesions, trial of cessa-

tion of OCPs maybe at-

blood vessels that eventually grow

tempted

surgical resection is the

organs or intermittent thrombosis causes further expansion of

treatment of choice

●
Embolization is useful for
Incidental findings on utrasound with little clinical consequence

treating spontaneous intra-

● Giant cavernous hemangiomas- causes compression of adjacent

peritoneal bleeding (10-

25%)
the lesion

Diagnostics:

o CT Scan: asymmetrical nodular peripheral enhancement

that is isodense with large vessels and exhibit progressive

centripetal enhancement fill-in overtime

 temic circulation--> lung/ brain abscess o Hx of travel to endemic area

Therapeutics:

o observation- asymptomatic lesions DIAGNOSTICS

o Enucleation or formal hepatic resection o Transarterial 1.) Ultz- round or oval hypoechoic lesions with well defined borders and
Embolization (TAE) variable number of internal echoes

INFECTIONS OF THE LIVER 2.) CT Scan- hypodense with peripheral enhancement and may contain
air-fluid levels indicating gas producing infectious or-ganisms

A 50 yr old man is found to have 10x5x4 cm oval hypoechoic lesions

3.) ELISA (Amebic abscess)- high sensitivity, amebiasis is unlikely if test is
with well defined borders and variable number of inter-nal echoes of
negative
the right hepatic lobe. Patient had a 1 week histo-ry of right upper
quadrant pain with associated fever, chills and sweating. He was
diagnosed to have uncomplicated diverticuli-tis 1 mo prior to the
present condition...
THERAPEUTICS

INFECTIONS OF THE LIVER Pyogenic Liver Abscess

Pyogenic Liver Abscess a.) Antibiotic Tx- IV tx for 2 weeks the P.O for 1 mo based on etiology

Etiology:

b.) Surgical Drainage

ascending biliary infection (biliary tract manipulation, ercp)

open/ lap
hematogenous: portal system

percutaneous(ct or ultz guided)

trauma/ direct extension
Amebic Liver Abscess
E. coli (gram neg), Streptococcus, Bacteroides (Anaerobes)

a.) Metronidazole 750mg/tab TID for 7-10 days b.) Surgical Drainage
Amebic Liver Abscess (same as pyogenic type)

Entamoeba histolytica by fecal oral route INDICATIONS OF SURGERY

a.) percutaneous (utz or ct scan guided)

Cyst (stomach and small intestine)---> trophozoite form (colon)---->

portal venous system--->(liquefaction necrosis in the liver producing
anchovy sauce appearance)--> sys- failure of medical management
  Multivesicular (multiple cysts)
o UTZ: low sensitivity
 Complications
>5cm hepatic abscess 1. Compression
2. Cyst infection
3. Rupture into the biliary tree- MC
 Communication between cyst and bile duct
 obstruction in bile flow  obstructive
unstable patients
jaundice  cholangitis (Charcot’s triad:
fever, RUQ pain, jaundice)
b.) open or laparoscopic surgery  Treat problem in biliary tree and the cyst
 Cholangiogram: map of biliary tree
o Use of stent: removes
obstruction
o Surgical decompression: put tube
ruptured abscess in liver to allow bile flow to
external organs to prevent
cholangitis
4. Rupture into peritoneum – rare; pericyst has thick cyst
wall
loculated
 Treatment
1. Albendazole – drug diffusion through the cyst membrane, initial
treatment for small, asymptomatic cysts
2. Open/ Lap Cystectomy or Hepatectomy (Liver Resection)
left sided abscess near the pericardium
o ***Peritoneal rupture may lead to anaphylactic reaction and
inevitable recurrence
“I would rather have a patient who will have a rupture into the
biliary tree than a rupture in the peritoneum” -FB

HEPATIC CYSTS
A 50 year-old woman is found to have a 8 cm solitary, homogenous fluid filled right
hepatic lobe lesion with no internal echoes on ultrasound imaging. Patient
complains of recurrent RUQ pain with no associated jaundice and weight loss but
with early satiety. She had undergone laparoscopic cholecystectomy 1 year PTA.

SIMPLE CYST ADPLD

MC benign lesion of the Autosomal dominant disease with
liver association to PKD1 and PKD2
mutations
Single or multiple with Hormone mediated hepatic lesion
female predominance 2nd to estrogen effect
results from excluded hyperplastic Associated with renal, hematologic
bile duct rest and cranial manifestations;
pathology based on genetic make-
up of individual
No malignant transformation No to low malignant
transformation
Biliary Cystadenoma-have
malignant transformation,
(+) septations – any kind of cysts
along the biliary tree in the presence
HYDATID DISEASE of septations  malignancy
 Etiology: Echinococcus granulosus- tapeworm in canids which are Ultrasound: absence of Complex cysts and presence of
infected by eating the viscera of sheep that contain hydatid cyst internal echoes, homogenous, internal echoes with septations
fluid filled
CT Scan:

*
*
*

*hydatid cysts at the periphery

 Diagnostics
Treatment:
o Diagnostic test of choice: ELISA - (+) for echinococcal
1. Aspiration (percutaneous/surgical)
antigen  clinch diagnosis
- shrinkage of cyst but once point of puncture heals or fibrose, fluid-filled cyst
o Clinical manifestations are attributed to gross and
may recur
imaging modalities:
-higher recurrence rate!
o Diagnostic imaging modality: CT Scan: presence of ring
More aggressive treatment:
like calcifications of the pericysts (demonstrate
2. Sclerotherapy
characteristic daughter cysts or hydatid sand within
-to prevent recurrence
the cyst: honeycomb or rosette appearance)
- apply alcohol or sclerosant
 2 types of pericysts:
-high recurrence
 Univesicular ( 1 cyst only)
. Marsupialization 1. Associated with cirrhosis- limits range of therapeutic options and increases
-only unroofs the cyst  maintains floor  no more accumulation of fluid  morbidity and mortality of any therapy
lower recurrence 2. Asymptomatic at early stages- great propensity for intravascular or
intrabiliary extension--> resulting to advanced stage with few effective
treatment options
MALIGNANT LIVER MASSES 3. Resistant to most cytotoxic chemotherapy- limits the array of non-operative
CASE: A 37 year old physician sought consult with a complaint of RUQ pain form of treatment
and easy fatigability. He was a medical technology graduate, occasional
alcoholic beverage drinker, non smoker. Denied any history of other METASTATIC COLORECTAL CANCER
illnesses. Abdominal ultz revealed 5x4cm solid hepatic mass in the right lobe.  Cancers that spread to the liver from an extrahepatic primary site
Helical CT scan revealed 6x5 cm liver mass with arterial enhancement and  Most common malignant liver tumor is metastatic colorectal
portal washout. AFP=>400ng/ml. Hepa profile-(+)HBsAg adenocarcinoma (venous drainage of colon  portal vein  liver)
 Liver- 2nd to LN as sites of metastasis
HEPATOCELULAR CARCINOMA  25-50% of patients dying with cancer have liver metastasis
 5th MC malignancy globally
 Major risk factor: ROUTES OF LIVER METASTASIS
o viral hepatitis B or C  Portal venous system – MC
o alcoholic cirrhosis  Lymphatics
o hemochromatosis  Hepatic arterial system
o NASH (Non-alcoholic steatohepatosis)  Direct extension (Gastric cancer can directly invade the liver 2nd to
 Most common primary tumor of the liver proximity)
 Annual conversion rate of cirrhosis to HCC: 2-6%
 HCC can also occur before the onset of cirrhosis Growth pattern of metastasisis more rapid than primary tumor
o HCC not equivalent to cirrhosis and vice versa Signs and symptoms
o 90-95% cirrhotic liver, after 6 months, may evolve into HCC o Hepatic pain, ascites, jaundice, anorexia, weight loss
 Signs and symptoms: o Hepatic nodularity
o Weight loss and weakness o Portal hypertension
o Abdominal pain Diagnosis
o Hepatomegaly, splenomegaly: abdominal mass is the 1st sign in o Elevated AFP, SGOT
children o Negative AFP
o Ascites and jaundice o Elevated CEA (colon cancer)
o Signs and symptoms of portal hypertension o MRI, UTZ
 Diagnostic Studies: Treatment
o Elevated alkaline phosphatase o Metastasectomy
o Serum bilirubin is usually normal  Primary tumor is controlled
o Alpha-Feto Protein (AFP): present in the fetusbut disappears after  No systemic or intraabdominal metastasis (the metastasis
birth should only be in the liver for you to perform this procedure)
 Cirrhotic liver may not necessarily have increased AFP,
 Good patient condition
may have normal AFP, still depend on liver biopsy for
 Total metastasectomy is feasible
diagnosis
o Also positive in embryonal testicular ovarian tumors o Intra-arterial chemotherapy using 5-FU
o Liver biopsy o Radiotherapy and chemotherapy
 Of all cancers in the body, biopsy is needed for o Debulking procedures
diagnosis BUT HCC is the only tumor that is the  Improve quality of life but will not affect survival rates
exception for a biopsy-confirmed diagnosis. “Liver cancer sucks because prognosis-wise – it’s too low, treatment wise – limited
 The sensitivity and specificity of classical findings of range of options for the patient. Medicine sucks.” - FB
HCC in CT Scan PLUS increased AFP is sufficient to
clinch the diagnosis of HCC.
o Imaging TREATMENT OF LIVER CANCER
 CT with contrast  Hepatic Resection
 Lesions are hypervascular during the arterial phase of  Liver Transplantation
CT studies  Ablation Techniques:
 Arterial phase 1st 20-30 seconds of injecting dye = o RFA
arterial enhancement 30-40 seconds = portal washout o Cryoablation
 Relatively hypodense during the delayed menses
o Ethanol ablation
 MRI
o Microwave ablation
TREATMENT
 Regional Liver Therapies
o TAE/TACE
o Hepatic Artery Pump Chemoperfusion
o Internal Radiation Therapy (yttrium 90)
o External Beam Radiation
HEPATECTOMY....

TREATMENT OF HCCA Segmentation not for HCC

Therapeutic Challenges of HCCA: Do not perform left hepatectomy
What is important in liver resection is the amount of liver tissue retained =
future liver remnant  dictates how a particular patient will survive (20% or
more liver to maintain life)

GENERAL PRE-OP ASSESSMENT

 Important considerations pre-operatively:
1. Tumor staging A-2nd week post-embolization. B-3rd week post-embolization
2. Baseline LFTs
3. Size of the future liver remnant LIVER TRANSPLANT
4. Co-morbidity  Milan Criteria for Transplant
a. 1 tumor < 5cm in size
TUMOR STAGING b. 3 or fewer lesions <3 cm in size
In which of the ff situations would resection of an isolated hepatic segment  Hard to comply with the Milan Criteria, thus many patients are excluded
for malignancy be contraindicated? for liver transplantation
a. Primary Hepatocellular cancer  60-80% survival after 5 years post-transplant for those who meets the
b. Malignant tumor in a non cirrhotic liver requirement of the Milan Criteria
c. Malignant tumor with extrahepatic metastasis  Resection – 2 to 3 years survival, for smaller tumors, if larger, refer to
d. Metastatic colorectal cancer Milan criteria

BASELINE LFTS (no need to memorize the values! Just the variables ) Transarterial Chemoembolization (TACE)
Chemoembolization
 Injecting chemotherapeutic drugs combined with embolization
particles into the hepatic artery that supplies the liver tumors
 Procedure: palpate femoral artery. Insert wire until arterial hepatic
system viewed with fluoroscopic guidance. Once in the hepatic lobe,
block arterial system while chemo drugs are given. There will be no exit
of embolization particles.
 In case of bleeding hepatic HCCs, surgical intervention may be difficult.
TACE may be used. Bleeding stops because feeding vessel of the tumor
is blocked.
 However, tumor is not removed. It will remain in the liver. Only the
vessels supplying the tumor are blocked.
 Percutaneous, transfemoral
 MC used
Hepatitis Profile
 Cisplatin in lipiodol (so that it will not readily diffuse)
● AFP/CEA/Ca 19-9
RADIOFEQUENCY ABLATION
● → >2 cm hepatic mass can be diagnose as HCC with classical CT
scan finding + AFP> 400 ng/ml without the need of a biopsy  Destroys liver tumors by thermal destruction
(90-95% specificity and sensitivity)  Heat is generated by radiofrequency energy delivered through a needle
electrode inserted into the tumor  radiofrequency energy will change
FUTURE LIVER REMNANT direction of ions on alternating charges  high frictional energy, heat
 Measured by CT volumetry conduction and thermal destruction  tissue temperature above 45°C
causes apoptosis, above 90°C creates irreversible zone of coagulation
a. Healthy, non cirrhotic liver- FLR of 20% is adequate
b. Cirrhotic liver- FLR of 40% is adequate for acceptable risk necrosis
 Preferred to be done laparoscopically
 Portal Vein Embolization (PVE)- induce hypertrophy to contralateral SYSTEMIC CHEMOTHERAPY
liver to potentiate growth of FLR
SHARP trial (Sorafenib HCC Assessment randomized protocol)
 602 patients with Child’s class A cirrhosis and inoperable HCC
 Survival benefit was found in the treatment group
 Sorafenib led to a 44% improvement in overall survival compared with
placebo
 Sorafenib received accelerated FDA approval for the treatment of
advanced unresectable HCC – low effectivity

Block right lobe for preferential flow of blood to contralateral liver.