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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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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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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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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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Terms
• Liver Function
• Liver Damage
• Cholestasis
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antitrypsin deficiency)
• autoimmune diseases.
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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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• 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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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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Etiology of Cirrhosis
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• 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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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
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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.
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• 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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• 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.
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