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Liver

Anatomy
• largest organ in the
body, weighing
approximately 1500 g
• Glisson’s capsule
• Falciform Ligament1
• left and right triangular
ligaments
• coronary ligament

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Anatomy
• Hepatoduodenal
ligament – porta
hepatis1
• Gastrohepatic ligament

Segmental Anatomy

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Segmental Anatomy
• Grossly separated into
the right and left lobes
by Cantlie’s line1 not by
the falciform ligament2

Segmental Anatomy
• Right lobe accounts for
60% to 70% of the liver
mass, with the left lobe
(and caudate lobe)
making up the
remainder

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Segmental Anatomy
• Caudate lobe lies to the
left and anterior of the
IVC and contains three
subsegments: the
Spiegel lobe, the
paracaval portion, and
the caudate process

Couinaud Segments

VII VIII II

IV

VI V III

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Blood Supply and Drainage


• Carry blood to the liver
– Hepatic Artery
– Portal Vein
• Carry blood from the
liver
– Hepatic Vein

Hepatic Artery
• Dual blood supply
– hepatic artery 25% blood
supply
– portal vein 75% blood
supply
• Classic anatomy
accounts for 76% cases,
while 24% having
variable anatomy

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Hepatic Artery Variations

Portal Vein
• Formed by SMV and
Splenic vein
• Main portal vein
traverses the porta
hepatis before dividing
into the left and right
portal vein branches

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Portal Vein
• Drains the splanchnic
blood from the
stomach, pancreas,
spleen, small intestine,
and majority of the
colon
• Vein pressure - is low at
3 to 5 mmHg

Hepatic Vein
• Right
– Drains segments 5 to 8
• Middle
– Drains segment 4 and
some from segment 5
and 8
• Left
– Drains segment 2 and 3
• Caudate lobe drains
directly to IVC

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Bile Ducts and Hepatic Ducts

Neural Innervation and Hepatic


Drainage
• Parasympathetic • Lymph is produced within
innervation of the liver the liver and drains via
comes from the left vagus the perisinusoidal space
• Sympathetic innervation of Disse and periportal
involves the greater clefts of Mall to larger
thoracic splanchnic lymphatics that drain to
nerves and the celiac the hilar cystic duct
ganglia lymph node as well as the
common bile duct,
hepatic artery, and
retropancreatic and celiac
lymph nodes

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PHYSIOLOGY

Liver Physiology
• Storage, metabolism, production, and secretion
• Plays important role in the metabolism of glucose,
lipids and proteins
• Responsible for the synthesis of most circulating
plasma proteins
– Albumin
– Factors of the coagulation and fibrinolytic systems,
– Compounds of the complement cascade
• Detoxification of many substances through drug
metabolism
• Immunologic responses - reticuloendothelial system

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Liver Physiology
• Bilirubin metabolism and formation of bile
– Bilirubin
• breakdown product of heme catabolism
• it is conjugated to glucuronic acid
• excreted in the urine or intestine as waste

Liver Physiology
• Bilirubin metabolism and formation of bile
– Bile
• main components of bile are water, electrolytes, and a
variety of organic molecules including bile pigments,
bile salts, phospholipids (e.g., lecithin), and cholesterol
• two fundamental roles of bile are to aid in the digestion
and absorption of lipids and lipid-soluble vitamins and
to eliminate waste products (bilirubin and cholesterol)
through secretion into bile and elimination in feces
• some reabsorbed through enterohepatic circulation

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LABORATORY EVALUATION OF THE


LIVER

Terms
• Liver Function
• Liver Damage
• Cholestasis

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Liver Function Test


Term frequently used to refer to measurement
of the levels of a group of serum markers for
evaluation of liver dysfunction:
- aspartate transaminase (AST)
- alanine transaminase (ALT)
- alkaline phosphatase(AP)
- γ-glutamyltranspeptidase (GGT)
- bilirubin

Liver Function Test


More accurate measurement of the liver’s
synthetic function:
- serum albumin levels
- prothrombin time (PT)

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Liver Function Test


The approach to evaluating abnormal laboratory
values also can be simplified by categorizing the
type of abnormality that predominates:
– Hepatocellular damage
• AST, ALT
– Abnormal synthetic function
• Serum albumin, Prothrombin time
– Cholestasis
• γ-glutamyltranspeptidase, alkaline phosphatase,
bilirubin

Liver Function Test


• Hepatocellular damage
– usually indicated by abnormalities in levels of the liver
aminotransferases AST and ALT
– Hepatocellular injury causes release of these enzymes into
the circulation
– Common causes of elevated aminotransferase levels
include:
• viral hepatitis
• Alcohol abuse
• medications
• genetic disorders (Wilson’s disease, hemochromatosis, α -
1

antitrypsin deficiency)
• autoimmune diseases.

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Liver Function Test


• Abnormal synthetic function
– The liver produces approximately 10 g of albumin
per day, however dependent on multiple factors1
– albumin is not a marker of acute hepatic
dysfunction due to long half-life of 15 to 20 days.
– Most clotting factors (except factor VIII) are
synthesized exclusively in the liver
– Prothrombin time (PT) and international
normalized ratio (INR) are some of the best tests
of hepatic synthetic function

Liver Function Test


• Cholestasis
– Cholestasis is a condition in which bile flow from
the liver to the duodenum is impaired
– often results in the release of certain enzymes and
thus can be detected by measuring the serum
levels of bilirubin, AP, and GGT

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Liver Function Test


• Cholestasis - cont
– patterns of elevation of the different fractions of
bilirubin provide important diagnostic clues as to
the cause of cholestasis
• elevated indirect bilirubin level suggests intrahepatic
cholestasis1
• elevated direct bilirubin level suggests extrahepatic
obstruction2

Liver Function Test


• Cholestasis - cont
– Alkaline phosphatase
• found in the liver and bones
• May take several days to normalize
– γ-glutamyltranspeptidase
• found in hepatocytes and released from the bile duct
epithelium
• Early marker and also a sensitive test for hepatobiliary
disease
• Increased levels of GGT can be induced by certain
medications, alcohol abuse, pancreatic disease, myocardial
infarction, renal failure, and obstructive pulmonary disease1

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Jaundice
Jaundice refers to the yellowish staining of the
skin, sclera, and mucous membranes with the
pigment bilirubin
• Prehepatic
• Intrahepatic
• Posthepatic

Jaundice
• Prehepatic
– conditions that interfere with proper conjugation
of bilirubin in the hepatocyte
– processes that result in excessive heme
metabolism

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Jaundice
• Intrahepatic
– involve the intracellular mechanisms for
conjugation
• Gildbert’s Syndrome, Crigler-Najjar syndrome
– excretion of bile from the hepatocyte
• Rotor’s syndrome, Dubin-Johnson syndrome
– multiple acquired conditions that result in
inflammation and intrahepatic cholestasis
– can also occur from the cytotoxic effects of many
medications

Jaundice
• Posthepatic
– usually the result of intrinsic or extrinsic
obstruction of the biliary duct system that
prevents the flow of bile into the duodenum

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RADIOLOGIC EVALUATION OF THE


LIVER

• Ultrasound
• Computed Tomography
• Magnetic Resonance Imaging
• Positron Emission Tomography

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• Ultrasound
– useful initial imaging test - inexpensive, widely
available, involves no radiation exposure, and is
well tolerated by patients
– excellent for diagnosing biliary pathology and focal
liver lesions.
– Limitations - include incomplete imaging of the
liver, because of the ribs; obesity and overlying
bowel gas also can interfere with image quality

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• Computed Tomography
– digitally processed cross-sectional image of the
body from a large series of x-ray images
– Tri-phasic CT scan
• Non-enhanced
• Arterial phase
• Portal Venous phase

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• Magnetic Resonance Imaging


– produces images based on magnetic fields and
radio waves
– Different tissues absorb and release radio wave
energy at different rates, and this information is
used to construct an image of the body
– T1 is a measure of how quickly a tissue can
become magnetized, and T2 measures how
quickly it loses its magnetization
– iodinated contrast media

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• Positron Emission Tomography


– produces images of metabolic activity in tissues by
detecting gamma rays emitted by a radioisotope
incorporated into a metabolically active molecule

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ACUTE LIVER FAILURE

Acute Liver Failure


• Acute liver failure (ALF) occurs when the rate
and extent of hepatocyte death exceeds the
liver’s regenerative capabilities.
• defined by the development of hepatic
encephalopathy occurring within 26 weeks of
severe liver injury in a patient without a
history of previous liver disease or portal
hypertension

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Etiology
• East and developing nations
– viral infections, primarily hepatitis B, A, and E
• West
– due to drugs and toxins, with acetaminophen
(paracetamol) being the most common etiologic
agent in the United States, Australia, United
Kingdom, and most of Europe

Clinical Presentation
• Female (73% )
• Median age 38
• Patients were ill for a median of 6 days before
the onset of encephalopathy
• median of 2 days between the onset of
jaundice and the development of
encephalopathy.

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Diagnosis and Clinical Management


• Medical History
– exposure to viral infections, medications, and
other possible toxins
– previous liver disease needs to be explored
– Asses patient’s mental status
– Identify findings of chronic liver disease

Diagnosis and Clinical Management


• initial laboratory
examination must
evaluate the severity of
the ALF as well as
attempt to identify the
cause

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Diagnosis and Clinical Management


• A liver biopsy - should be performed if
entertaining autoimmune hepatitis or
lymphoma

Diagnosis and Clinical Management


• Acetaminophen overdose
– Activated charcoal if within few hours
– N-acetylcysteine – antidote administered as early
as possible
• Other drugs
– Obtain details of all prescription and non
prescription drugs taken in previous year
• Most drug induced hepatotoxicity occur in the
first 6 months of intake

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Diagnosis and Clinical Management


• Admitted in the ICU
• Neuro examination should be performed
regularly
• CT-scan performed to rule-out mass or
hemorrhage
• Acute renal failure – maintain perfusion
• Severely affected patients have poor prognosis
with medical management – Liver
transplantation

CIRRHOSIS AND PORTAL


HYPERTENSION

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Cirrhosis and Portal Hypertension


• Cirrhosis
– the final sequela of chronic hepatic insult
– characterized by the presence of fibrous septa
throughout the liver subdividing the parenchyma
into hepatocellular nodules
– May progress to End Stage Liver Disease
• carries a 5-year mortality of 50%, with 70% of deaths
due to liver failure

Etiology of Cirrhosis

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Clinical Manifestations of Cirrhosis


• clinical history
– fatigue, anorexia, weight loss, jaundice, abdominal pain, peripheral edema,
ascites, GI bleeding, and hepatic encephalopathy
• physical examination
– Spider angiomata and palmar erythema
– Finger clubbing
– Males may develop features of feminization such as gynecomastia, loss of
chest and axillary hair, and testicular atrophy
– Splenomegaly
– Ascites and pleural effusion
– caput medusae
– Cruveilhier-Baumgarten murmur
– Jaundice
– Asterixis
– fetor hepaticus, as well as features suggestive of malnutrition such as
weakness, weight loss, and temporal muscle wasting

Laboratory Findings Associated with


Cirrhosis
Vary in the cirrhotic patient depending on the
degree of compensation
– Mild normocytic normochromic anemia
– white blood cell and platelet counts are reduced,
and the bone marrow is macronormoblastic
– PT is prolonged and does not respond to vitamin K
therapy
– serum albumin level is depressed
– Urobilinogen

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Hepatic Reserve and Assessment of


Surgical
Risk in the Cirrhotic Patient
• Patients with liver disease undergoing surgery
are at increased risk for surgical and
anesthesia-related complications.

• Child-Turcotte-Pugh Score

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Child-Turcotte-Pugh Score
• Numerous studies have
demonstrated overall
surgical mortality rates
of:
– 10% for patients with
class A cirrhosis
– 30% for those with class
B cirrhosis
– 75% to 80% for those
with class C cirrhosis

Portal Hypertension
• Portal Hypertension
– The normal portal
venous pressure is 5 to
10 mmHg
– As portal venous
pressure increases, a
large amount of blood
may be shunted around
the liver and into the
systemic circulation.

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Imaging of the Portal Venous System and


Measurement of Portal Venous Pressure
• The patency of the portal vein and the nature
of the collateral circulation should be
established
– Doppler ultrasound
– Abdominal CT and magnetic resonance
angiography
• The most accurate method of determining
portal hypertension is hepatic venography

Etiology and Clinical Features


of Portal Hypertension
• Causes
– Presinusoidal
– Sinusoidal
– postsinusoidal

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Management of Gastroesophageal
Varices
• Prevention of Variceal Bleeding
• Management of Acute Variceal Hemorrhage
• Luminal Tamponade
• Transjugular Intrahepatic Portosystemic Shunt
• Balloon-Occluded Retrograde Transvenous
Obliteration
• Surgical Shunting

Management of Gastroesophageal
Varices
• Prevention of Variceal Bleeding
– Beta blockers
– Prophylactic endoscopic surveillance with variceal
band ligation1

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Management of Gastroesophageal
Varices
• Management of Acute Variceal Hemorrhage
– acute variceal hemorrhage should be admitted to an
ICU for resuscitation and management
– Blood resuscitation should be performed carefully to
reach a hemoglobin level of approximately 8 g/dL1
– fresh frozen plasma and platelets can be considered in
patients with severe coagulopathy
– Vasoactive medications
• Vassopressin
• Somatostatin

Management of Gastroesophageal
Varices
• Luminal Tamponade
– balloon tamponade using a Sengstaken-Blakemore
tube
– Should not exceed 36 hours to avoid tissue
necrosis
– considered a temporary bridge

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Management of Gastroesophageal
Varices
• Transjugular Intrahepatic Portosystemic Shunt
– involves implantation of a metallic stent between
an intrahepatic branch of the portal vein and a
hepatic vein radicle
– high rate of thrombosis

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Management of Gastroesophageal
Varices
• Balloon-Occluded Retrograde Transvenous
Obliteration
– a balloon-occlusion catheter is directed through
the left renal vein into the spontaneous shunt,
which is then obliterated with the use of a
sclerosing agent

Management of Gastroesophageal
Varices
• Surgical Shunting
– Eck shunt (porto-caval)
• Portal vein to the IVC
– Mesocaval shunt
• PTFE graft from SMV to
IVC
– Warren shunt (spleno-
renal)
• Splenic vein to renal vein
• Non-shunt
– Sugiura procedure2

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Management of Gastroesophageal
Varices
• Hepatic Transplantation
– Patients with cirrhosis, portal hypertension, and
variceal bleeding usually die as a result of hepatic
failure and not acute blood loss
– patient’s only chance for definitive therapy and
long-term survival

INFECTIONS OF THE LIVER

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Infections of the Liver


• Pyogenic liver abscess
– The abscess cavities are variable in size and, when
multiple, may coalesce to give a honeycomb
appearance
– In the past usually associated with intestinal
infections like appendicitis and diverticulitis
– Presents as RUQ pain and fever, only 1/3 presents
with jaundice

Infections of the Liver


• Pyogenic liver abscess
– Ultrasound - round or oval
hypoechoic lesions with
well-defined borders and a
variable number of internal
echoes
– CT - hypodense with
peripheral enhancement
and may contain air-fluid
levels indicating a gas-
producing infectious
organism
– MRI

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Infections of the Liver


• Pyogenic liver abscess
– cornerstones of treatment include correction of
the underlying cause and IV antibiotic therapy
– IV antibiotic therapy should be continued for at
least 8 weeks
– Surgical drainage either via the laparoscopic or
open approach may become necessary if initial
therapies fail

Infections of the Liver


• Amebic Abscesses1
– Amebae multiply and block
small intrahepatic portal
radicles with consequent
focal infarction of
hepatocytes
– Commonly located in the
superior-anterior aspect of
the right lobe of the liver
– Anchovy sauce - necrotic
central portion that
contains a thick, reddish
brown, pus-like material
– Ultrasound and CT-scan

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Infections of the Liver


• Amebic Abscesses
– Metronidazole 750 mg three times a day for 7 to
10 days is the treatment of choice and is
successful in 95% of cases
– Aspiration of the abscess rarely is needed and
should be reserved for patients with large
abscesses, those who do not respond to medical
therapy

• Hydatid Liver Cyst


Echinococcosis (hydatid disease) is a zoonosis
caused by Echinococcus granulosus .
• Humans are accidental intermediate hosts,
whereas animals can be both intermediate hosts
and definitive hosts.
• humans, 50–75% of the cysts occur in the liver,
25% are located in the lungs, and 5–10%
distribute along the arterial system.

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The typical hydatid cyst has a three-layer wall surrounding a fluid
cavity. The outer layer is the pericyst, a thin, indistinct fibrous tissue
layer representing an adventitial reaction to the parasitic infection.
The pericyst acts as a mechanical support for the hydatid cyst . As
the cyst grows, bile ducts and blood vessels stretch and become
incorporated within this structure, which explains the biliary and
hemorrhagic complications of cyst growth . Over time, the pericyst
calcifies.
The intermediate layer of the cyst itself is the ectocyst or laminated
membrane and is bluish-white, gelatinous.
The inner layer or endocyst is the germinal membrane, responsible
for the production of clear hydatid fluid, the ectocyst, scoleces, and
daughter cysts.

• The clinical features of hydatid liver disease


depend on the site, size, stage of development,
whether the cyst is alive or dead, and whether
the cyst is infected or not. Pain in the RUQ or
epigastrium is the most common symptom,
whereas hepatomegaly and a palpable mass are
the most common signs. Nonspecific fever,
fatigue, nausea, and dyspepsia may also be
present . Approximately one-third of patients will
have eosinophilia, and only 20% will present with
jaundice and hyperbilirubinemia

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• Serological test e.g’ The Casoni test are no longer


used due to their low sensitivities. Determination
of specific antigens and immune complexes of
the cyst with enzyme-linked immunosorbent
assay (ELISA) give a positive result in more than
90% of patients. The arc 5 antibody test involves
precipitation during immunoelectrophoresis of
the blood of patients with the antigen. Positivity
for this test is 90%.

• Radiology
Chest radiographs may show an elevated
diaphragm and concentric calcifications in the
cyst wall, but are of limited value. Ultrasound
and CT are considered the first choice for
imaging . Classic findings of hydatid cysts are
calcified thick walls, often with daughter cysts.
Ultrasound defines the internal structure,
number, and location of the cysts and the
presence of complications

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• Computed tomography gives similar information to


ultrasound, but more specific information about the
location and depth of the cyst within the liver.
Daughter cysts , and the volume of the cyst can be
estimated. CT is imperative for operative management,
especially when a laparoscopic approach is utilized.MRI
provides structural details of the hydatid cyst, but adds
little more than ultrasound or CT, and is more
expensive. Endoscopic retrograde
cholangiopancreatography (ERCP) may show
communication between the cysts and bile ducts and
can be used to drain the biliary tree before surgery

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• Treatment
Most hydatid cysts are asymptomatic on presentation. Medical,
surgical, and percutaneous approaches may be part of the
treatment . Small cysts (<4 cm) located deep in the parenchyma of
the liver, if uncomplicated, can be managed conservatively.
Antihelminthics
Medical therapy for echinococcosis is limited to the benzimidazoles
(mebendazole and albendazole) and used alone is only 30%
successful. Mebendazole is poorly absorbed and is inactivated by
the liver. Albendazole is thus the drug of choice for medical therapy.
Given for at least 3 months preoperatively, albendazole reduces the
recurrence rate when cyst spillage, partial cyst removal, or biliary
rupture has occurred. Duration of therapy in these instances is at
least 1 month.

• The PAIR technique (percutaneous aspiration,


injection and re-aspiration) has also been
combined with albendazole therapy with 70%
success rates and a low rate of recurrence

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• The surgical options range from liver resection or local


excision of the cysts to de-roofing with evacuation of
the contents Contamination of the peritoneal cavity at
the time of surgery with
active hydatid daughters should be avoided by
continuing drug
therapy with albendazole and adding peroperative
praziquantel.
This should be combined with packing of the
peritoneal cavity
with hypertonic (2 mol l–1) saline-soaked packs and
injection
2 mol l–1 saline into the cyst before it is opened.

BENIGN LIVER LESIONS

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Benign Liver Lesions


• Cyst
– most frequently encountered liver lesion overall
– majority of hepatic cysts are asymptomatic
– Asymptomatic simple cysts are best managed
conservatively
– preferred treatment for symptomatic cysts is
ultrasound- or CT-guided percutaneous cyst
aspiration followed by sclerotherapy
– laparoscopic or open surgical cyst fenestration

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Benign Liver Lesions


• Hemangioma
– Most common solid benign masses in the liver
– Most hemangiomas are discovered incidentally
– can cause symptoms as a result of compression of
adjacent organs or intermittent thrombosis
– surgical resection can be considered if the patient
is symptomatic

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Benign Liver Lesions


• Adenoma
– most commonly seen in premenopausal women older
than 30 years of age and are typically solitary
– Prior or current use of estrogens (oral contraceptives)
is a clear risk factor for development of liver
adenomas
– carry a significant risk of spontaneous rupture with
intraperitoneal bleeding
– also have a risk of malignant transformation to a well-
differentiated HCC1

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Benign Liver Lesions


• Focal Nodular Hyperplasia
– solid, benign lesion of the liver believed to be a
hyperplastic response to an anomalous artery
– Child bearing age, link to oral contraceptive use is
not as clear
– Unlike adenomas, FNH lesions usually do not
rupture spontaneously and have no significant risk
of malignant transformation
– management is usually reassurance and
observation`

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MALIGNANT LIVER TUMORS

Malignant Liver Tumors


• Hepatocellular Carcinoma
– Major risk factors are viral hepatitis (B or C),
alcoholic cirrhosis, hemochromatosis, and NASH
– typically hypervascular with blood supplied
predominantly from the hepatic artery
• appears hypervascular during the arterial phase of CT
studies
• relatively hypodense during the delayed phases due to
early washout of the contrast

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Malignant Liver Tumors


• Hepatocellular Carcinoma
– The treatment of HCC is complex and is best
managed by a multidisciplinary liver transplant
team
– Child’s class A cirrhosis with preserved liver
function and no portal hypertension - resection
– poor liver function and the HCC meets transplant
criteria – transplantation is the treatment of
choice

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Malignant Liver Tumors


• Cholangiocarcinoma
– is an adenocarcinoma of the bile ducts
– Central (extrahepatic)
• Located proximal known as hilar cholangiocarcinoma or
Klatskin tumor
• Usualy present as obstructive jaundice
– Peripheral (intrahepatic)
• Presents as a tumor mass within the hepatic lobe or
periphery of the liver

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Malignant Liver Tumors


• Cholangiocarcinoma
– Surgical resection offers the only chance for cure
of cholangiocarcinoma
– The location and extent of tumor dictate the
operative approach

Malignant Liver Tumors


• Metastatic Colorectal Cancer
– Over 50% to 60% of patients diagnosed with
colorectal cancer will develop hepatic metastases
during their lifetime.
– Resection for hepatic metastases has been a
routine part of treatment for colorectal cancer

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TREATMENT OPTIONS FOR LIVER


CANCER

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Treatment Options for Liver Cancer


• Hepatic Resection
• Liver Transplantation
• Radiofrequency Ablation
• Ethanol Ablation, Cryosurgery, and Microwave Ablation
• Chemoembolization and Hepatic Artery Pump
Chemoperfusion
• Yttrium-90 Microspheres
• Stereotactic Radiosurgery and Intensity-Modulated
Radiation Therapy
• Systemic Chemotherapy

Treatment Options for Liver Cancer


• Hepatic Resection
– Treatment of choice for primary liver cancers or
hepatic metastases
– For HCC with cirrhosis liver transplantation offers
the potential for long-term survival1
– Many large series of patients undergoing major
hepatectomy now report mortality rates of <5%.

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Treatment Options for Liver Cancer


• Liver Transplantation
– rationale supporting OLT for HCC includes the fact that
most HCCs (>80%) arise in the setting of cirrhosis
– The cirrhotic liver often does not have enough reserve
to tolerate a formal resection
– recurrence rates are high at 5 years after resection
(>50%)
– OLT is an appealing treatment, because it removes
both the cancer and the cirrhotic liver that leads to
cancer

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Treatment Options for Liver Cancer


• Liver Transplantation
– Although indications for liver transplantation have
increased, the supply of donor livers has failed to
keep pace with the numbers of potential
recipients
– partial solution - use of living donor grafts

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Treatment Options for Liver Cancer


• Radiofrequency Ablation
– Radiofrequency waves cause local tissue destruction
with uniform necrosis
• Ethanol Ablation, Cryosurgery, and Microwave
Ablation
– Percutaneous ethanol injection has been shown to be
a safe and effective for small HCCs
– Microwave ablation - thermal ablative technique used
in unresectable liver tumors to produce a coagulation
necrosis

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Treatment Options for Liver Cancer


• Chemoembolization and Hepatic Artery Pump
Chemoperfusion
– injecting chemotherapeutic drugs combined with
embolization particles into the hepatic artery that
supplies the liver tumor
• Yttrium-90 Microspheres
– microspheres delivered in hepatic artery supplying
the tumor delivering doses of high-energy, low-
penetration radiation selectively to the tumor

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Treatment Options for Liver Cancer


• Systemic Chemotherapy
– Chemotherapy has not demonstrated great
efficacy in patients with HCC, especially in patients
with significant cirrhosis

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