Liver

Alain Neil Ancheta, MD

Hepatobiliary, Pancreatic and Upper GI Surgery
Liver Anatomy
• Wt 1500g
• RUQ under the diaphragm, protected by the rib cage
• Covered by Glisson’s capsule
• Capable of regeneration
• Minimum liver volume 20% of total - normal
• Minimum liver volume 40% of total - diseased
Liver Anatomy
• Liver ligaments
Liver Anatomy
• Liver Segments

VII VIII IVa II

VI V IVb III
Liver Anatomy
• Hepatic Artery
• Dual blood supply consisting of the hepatic artery and the portal vein
• Hepatic artery 25%
• Portal vein 75%.
Liver Anatomy
• Portal Vein
• Formed by union of superior mesenteric vein and splenic vein
• It divides into 2 main branches that drain into the right and left lobes
Liver Anatomy
• Portal Vein
• The right main branch divides further to drain into the right anterior
(segments 5,8) and right posterior (segments 6,7)
• The left main branch divides to drain into the left medial (segment 4a,4b) left
lateral segments (segment 2,3)
Liver Anatomy
• Portal Vein
• The portal vein drains the nutrient
rich blood from the stomach up to
the colon
• Portal vein pressure is low at 3 to 5
mmHg
• Valveless
• Pressure can be quite high (20 to
30 mmHg) if with obstruction
• Can lead to varicosities typically in
the left gastric (esophageal varices)
Liver Anatomy
• Hepatic Vein
• Right – 5,6,7,8
• Middle – 4b,5,8,4a Joins the left hepatic vein before draining into
• Left – 2,3 the IVC in 95%
• Caudate – drains directly to the IVC
Liver Anatomy
• Bile Ducts
• Anatomy is parallel to the portal vein and hepatic artery
Liver Physiology
Liver Physiology
• Functions
• Storage, metabolism, production and secretion
• Processing of absorbed nutrients including glucose, lipids and proteins
• Synthesis of plasma proteins (albumin), factors for coagulation and fibrinolysis
• Detoxification of toxic substances
• Immunologic response (reticuloendothelial system)
• Bilirubin metabolism from breakdown products of hemoglobin
• Excretion of metabolized products (medicines and toxins)
Liver Physiology
• Bilirubin Metabolism
• Bilirubin – byproduct of heme metabolism – transported to the liver - congjugated –
becomes water soluble – facilitating excretion
• Formation of Bile
• Composed of water, electrolytes, bile pigments, bile salts, phospholipids and
cholesterol
• Function:
• Aid in digestion and absorption (fat soluble vitamins)
• Elimination of waste products (bilirubin and cholesterol)
• Drug Metabolism
• Phase 1 – oxidation, reduction and hydrolysis
• Phase 2 – conjugation reactions
Liver Physiology
• Liver Function Test
• Used to refer to measurement of the levels of a group of serum markers for
evaluation of liver dysfunction.
• Aspartate aminotransferase, Alanine aminotransferase, Alkaline phosphatase,
y-glutamyltranspeptidase
• The approach to evaluating abnormal laboratory values also can be simplified
by categorizing the type of abnormality that predominates (hepatocellular
damage, abnormal synthetic function, or cholestasis).
Liver Physiology
• Hepatocellular Injury
• Indicated by elevation of enzymes released during hepatic destruction
• Aspartate Aminotransferase (AST, SGOT)
• Alanine Aminotransferase (ALT, SGPT)
• Found in the liver involved in the gluneogenisis– however they are released
into the bloodstream upon destruction of the hepatocyte
• When requested?
• Any injury that causes hepatocyte destruction (ex. acute drug injury,
infections, inflammation, alcohol toxicity, ischemic insults)
Liver Physiology
• Abnormal Synthetic Function
• Albumin and clotting factors are produced in the liver
• Measure the synthetic capacity of the liver – this gives a rough idea of the
remaining functional hepatocytes (ex. Liver cirrhosis)
• Serum Albumin, Prothrombin Time, INR

• When requested?
• Want to know the synthetic capacity/hepatic reserve, severity of cirrhosis
Liver Physiology
• Cholestasis
• Condition in which bile flow from the liver to the duodenum is impaired
• Jaundice – clinical manifestation showing yellowish staining of skin, sclera and
mucus membranes with the pigment bilirubin – usually detectable when
blood levels rise above 2.5 to 3mg/dl
• Total Bilirubin, Indirect Bilirubin, Direct Bilirubin
• Alkaline phosphatase, Y-glutamyltranspeptidase
• Increased in conditions of biliary obstruction
Liver Physiology
• Workup of a patient with jaundice can be simplified by organizing
possible causes into groups based on location of bilirubin metabolism
• Prehepatic
• Often seen in processes that result in excessive heme metabolism
• Intrahepatic
• Inherited disorder in enzyme metabolism
• Defect in bilirubin excretion from hepatocytes
• Posthepatic
• Usually the result of intrinsic or extrinsic obstruction of the biliary duct system that
prevents the flow of bile into the duodenum
Liver Physiology
• Workup of a patient with jaundice can be simplified by organizing
possible causes into groups based on location of bilirubin metabolism
• Prehepatic (elevated Indirect Bilirubin/Unconjugated Bilirubin)
• Often seen in processes that result in excessive heme metabolism
• Intrahepatic (elevated Indirect Bilirubin or Direct Bilirubin)
• Inherited disorder in enzyme metabolism (elevated Indirect Bilirubin)
• Defect in bilirubin excretion from hepatocytes (elevated Direct Bilirubin)
• Posthepatic (elevated Direct Bilirubin/Conjugated Bilirubin)
• Usually the result of intrinsic or extrinsic obstruction of the biliary duct system that
prevents the flow of bile into the duodenum
Liver Physiology
• When requested?
• If you want to investigate the source of jaundice in a person
• Additionally request for alkaline phosphatase or GGT in patients with possible
obstruction as a cause – choledocholithiasis, tumors, strictures
Liver Imaging
Radiologic Evaluation of the Liver
• Ultrasound
Radiologic Evaluation of the Liver
• Computed Tomography
Radiologic Evaluation of the Liver
• Magnetic Resonance Imaging
Radiologic Evaluation of the Liver
• Positron Emission Tomography
Acute Liver Failure
Acute Liver Failure
• Occurs when the rate and extent of
hepatocyte death > liver’s
regenerative capabilities
• Also referred to as fulminant
hepatic failure.
• 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
• The manifestations of ALF may
include:
• cerebral edema
• hemodynamic instability
• increased susceptibility to
bacterial and fungal infections
• renal failure
• coagulopathy
• metabolic disturbances
Acute Liver Failure
• Even with current medical care, ALF can progress rapidly to hepatic
coma and death. The most common cause of death is intracranial
hypertension due to cerebral edema, followed by sepsis and
multisystem organ failure
Acute Liver Failure
• In the East and developing
portions of the world, the most
common causes of ALF are viral
infections, primarily hepatitis B,
A, and E.
• In contrast, 65% of cases of ALF
in the West are thought to be
due to drugs and toxins, with
acetaminophen (paracetamol)
Acute Liver Failure
• Diagnosis:
• The physical examination must assess and document the patient’s mental
status as well as attempt to identify findings of chronic liver disease.
• The initial laboratory examination must evaluate the severity of the ALF as
well as attempt to identify the cause
Acute Liver Failure
• Management:
• Patients with ALF should be admitted to the hospital (possibly ICU) and
monitored frequently
• N-acetylcysteine (NAC), the clinically effective antidote for acetaminophen
overdose, should be administered as early as possible to any patient with
suspected acetaminophen-associated ALF
• Despite advances in medical management, OLT remains the only definitive
therapy for patients unable to regenerate sufficient hepatocyte mass in a
timely manner.
Cirrhosis and Portal
Hypertension
 Cirrhosis
• Final sequela of chronic hepatic
injury
• Presence of fibrous septa
throughout the liver subdividing
the parenchyma into
hepatocellular nodules
• It is the consequence of
sustained wound healing in
response to chronic liver injury

Injury Cell death/Fibrosis Regeneration

Cirrhosis
• The complications of ESLD include
• progressive hyperbilirubinemia
• malnutrition
• decreased synthetic function of the liver
• coagulopathy,
• portal hypertension (i.e., ascites and variceal bleeding),
• hepatic encephalopathy
• life-limiting fatigue
Cirrhosis
• Cirrhosis can result from a wide
range of disease processes,
including viral, autoimmune,
drug-induced, alcohol-induced,
nonalcoholic fatty liver disease,
and metabolic diseases
• NAFLD is now the most common
chronic liver disease worldwide
• NASH is a progressive form of
NAFLD characterized by steatosis
with hepatocellular injury and
chronic inflammation.
• Aside from causing liver injury,
Fatty infiltration of the liver can
cause morbidity after liver
resection
Cirrhosis
• Clinical Manifestation • Physical Examination
• Spider angiomata
• fatigue • Palmar erythema
• anorexia • Finger clubbing
• abdominal pain • Feminization in males – gynecomastia, loss of
hair, testicular atrophy
• peripheral edema • Splenomegaly
• ascites • Ascitis and pleural effusion
• GI bleeding • Portal hypertension – caput medusa
• • Jaundice
hepatic encephalopathy
• Asterexis
• Fetor hepaticus
• Malnutrition
• Weight loss
Cirrhosis
• Laboratory Findings
• Mild normocytic, normochromic anemia
• Reduced wbc and platelet count
• Prolonged PT not responsive to Vit K
• Urobilinogen
• Serum levels of bilirubin, transaminases and alkaline phosphatase may be elevated
• Histopathologic examination
• Occasionally needed to confirm the diagnosis of cirrhosis and in determining
disease etiology, activity, and progression
• Ultrasound Elastography
• Non-invasive way to diagnose liver cirrhosis
Assessing Hepatic Reserve
 Hepatic Reserve and Assessment of Surgical
Risk in the Cirrhotic Patient
• Assessing the hepatic reserve of the cirrhotic patient is important because
cirrhosis and portal hypertension can have a negative impact on the
outcome of nontransplant surgical procedures.
• Patients with liver disease undergoing surgery are at increased risk for
surgical and anesthesia-related complications.
• Previous studies have demonstrated that emergency operations, cardiac
surgery, hepatic resections, and abdominal surgery, particularly
cholecystectomy, gastric resection, and colectomy, generate the highest
operative risk among cirrhotic patients.
• Nontransplant surgical procedures are contraindicated in patients with acute
fulminant hepatitis and those with severe decompensated chronic hepatitis.
Portal Hypertension
Portal Hypertension
• The portal venous system contributes
approximately 75% of the blood and
72% of the oxygen supplied to the liver
• The normal portal venous pressure is 5
to 10 mmHg, and at this pressure, very
little blood is shunted from the portal
venous system into the systemic
circulation
• Fibrosis restricts flow of blood and
some of these blood are channeled
through shunts into the systemic
circulation
 Imaging of the Portal Venous System and
Measurement of Portal Venous Pressure
• An understanding of portal vein patency and anatomy is crucial before
undertaking hepatic resection, hepatic transplantation or
portosystemic shunts
• Doppler ultrasound is capable of outlining the anatomy of the portal
vein, excluding the presence of thrombosis, and identifying the
direction of portal venous blood flow.
• The most accurate method of determining portal hypertension is
hepatic venography.
• The hepatic venous pressure gradient (HVPG) is then calculated by
subtracting the free from the wedged venous pressure (HVPG =
WHVP – FHVP).
• The HVPG represents the pressure in the hepatic sinusoids and portal
vein and is a measure of portal venous pressure. Clinically significant
portal hypertension is evident when HVPG exceeds 10 mmHg.
 Etiology and Clinical Features of Portal
Hypertension
• The causes of portal hypertension
can be divided into three major
groups: presinusoidal, sinusoidal,
and postsinusoidal.
• Although multiple disease
processes can result in portal
hypertension in the United States,
the most common cause of portal
hypertension is usually an
intrahepatic one, namely, cirrhosis.
• Portal Hypertension results in
• Splenomegaly with tortuous splenic vessels
• Splenomegaly will cause hypersplenisim causing leukopenia,
thrombocytopenia and anemia
• Ascitis
• Umbilical vein recanalization causing caput medusa
• Gastro-esophageal varices
 Management of Gastro-Esophageal Varices
• Prevention of bleeding
• Beta-blockers
• Endoscopic surveillance with prophylactic variceal band ligation
• Management of acute variceal bleeding
• Admitted to the ICU and resuscitated
• Avoid overzealous replacement of fluids/blood
• Correct bleeding parameters
• Antibiotics
• Vassopressin/Octreotide
• May refer to GI for rubber band ligation, or IR for embolization
 Management of Gastro-Esophageal Varices
• Luminal Tamponade
• Sengstaken – Blakemore tube
• Only used as a bridge
 Management of Gastro-Esophageal Varices
• Transjugular Intrahepatic
Portosystemic shunt
• The TIPS procedure involves
implantation of a metallic stent
between an intrahepatic branch of the
portal vein and a hepatic vein radicle.
• Possible complications include
bleeding either intra-abdominally or
via the biliary tree, infections, renal
failure, decreased hepatic function,
and hepatic encephalopathy, which
occur in 25% to 30% of patients after
the TIPS procedure.
Management of Gastro-Esophageal Varices
• Surgical Shunting
• Porto-caval shunt
• May worsen encephalopathy
• Difficulty in liver transplantation
• Mesocaval shunt
• May worsen ensephalopathy
• Does not interfere with transplantation
• Distal Spleno-Renal Shunt (Warren
Shunt
• Lower rate of encephalopathy
• Does not interfere with transplantation
 Management of Gastro-Esophageal Varices
• Non-shunt procedure
• Sugiura Procedure
• Hepatic Transplantation
• Therefore, hepatic transplantation
must be considered in the patient
with ESLD because it represents the
patient’s only chance for definitive
therapy and long-term survival.
• Hepatic transplantation also can be
considered for the patient with
variceal bleeding refractory to all
other forms of management.
Infections of the liver
Pyogenic Liver Abcess
• They may be single or multiple and are more frequently found in the
right lobe of the liver. The abscess cavities are variable in size and,
when multiple, may coalesce to give a honeycomb appearance.
• 40% Monomicrobial, 40% Polymicrobial, 20% Culture Negative
• Most common cause are gram negative bacteria (ex E coli.)
• In patients with endocarditis or infected indwelling catheters most
common organisms are gram positive
• Previously mainly caused by abdominal infections (ex appendicitis,
diverticulitis)
Pyogenic Liver Abcess
• Presentation
• RUQ pain with fever, occasional jaundice
• Leukocytosis
• Workup
• Ultrasound
• CT-scan/MRI
• Treatment
• IV antibiotic therapy directed at
underlying organism for 8 weeks
• Drainage (percutaneous or surgical) may
be necessary for persistent or large
abscesses
Amebic Liver Abcess
• Common in subtropical climates especially with poor sanitation
• Trophozoite invades colonic mucosa eventually gaining access to the
portal circulation and into the liver
• Commonly located in the right lobe
• Necrotic center contains reddish-brown pus-like material likened to
anchovy paste
Amoebic Liver Abscess
• Presentation
• RUQ pain with fever, hepatomegaly esp if from
endemic areas
• Leukocytosis
• Jaundice is unusual
• Diarrhea is unusual
• Workup
• Fluorescent antibody test for E hystolitica
• Ultrasound
• CT-scan/MRI
• Treatment
• Metronidazole 750mg 3x a day for 7 to 10 days
• Drainage (percutaneous or surgical) may be
necessary for persistent, large abscesses or
abscesses located in the left hepatic lobe
Infections of the liver
• Ascaris
• May enter the biliary tree and
cause obstruction or die and
become a nidus for stone
formation
• Schistosomiasis
• Causes presinusoidal portal
hypertension
• Viral Hepatitis
Liver Mass
Evaluation of Incidental Liver Mass
• History
• Abdominal pain, weight loss, previous liver disease, cirrhosis, alcohol abuse, blood transfusion, tattoos, oral
contraceptive use(women), Hx of cancer
• Physical Examination
• Jaundice, hepatomegaly, splenomegaly, palpable mass, signs of portal hypertension,
• Laboratory
• CBC with PC, Electrolytes, glucose, albumin, liver function test, serum ammonia, coagulation studies,
hepatitis profile, tumor markers AFP, Ca 19-9, Cea
• Imaging
• Ultrasound
• CT/MRI
• MRCP
• PET scan
• Liver biopsy
Hepatic Cyst
• Congenital Cyst
• Majority are asymptomatic
• are the result of excluded hyperplastic bile duct rests
• Simple cysts usually are identified in hepatic imaging
studies as thin-walled, homogeneous, fluid-filled
structures with few to no septations.
• Contains non-bilous clear fluid
• Treatment
• Managed conservatively
• Cyst-drainage with sclerotherapy
• Open or laparoscopic cyst fenestration
• Biliary Cystadenoma
• Slow growing
• Benign but may undergo malignant transformation
• Have thicker walls with sepations than congenital cyst
• Treatment is surgical resection
Hepatic Cyst
• Polycystic Liver Disease
• Autosomal Dominant
• Characterized by multiple hepatic cyst
• Clinical symptoms, including abdominal pain,
distension, shortness of breath, and early
satiety
• Cyst related complications include
hemorrhage, infection, rupture
• The principal aim of treatment for PCLD is to
ameliorate symptoms by decreasing liver
volume.
• Cyst aspiration
• Cyst fenestration
• Liver resection
• Liver transplantation
Hepatic Cyst
• Caroli’s Disease
• A syndrome of congenital ductal plate malformations of the intrahepatic bile ducts
and is characterized by segmental cystic dilatation of the intrahepatic biliary radicals.
• associated with an increased incidence of biliary lithiasis, cholangitis, and biliary
abscess formation
• The most common presenting symptoms include fever, chills, and abdominal pain.
• Approximately 33% of affected patients develop biliary lithiasis, and 7% develop
cholangiocarcinoma
• Diagnosis
• MRCP, ERCP
• Treatment
• Biliary Drainage, Liver resection if limited to one lobe
Benign Liver Tumors
Hemangioma
• Hemangiomas (also referred to as hemangiomata) are the most common solid
benign masses that occur in the liver.
• They consist of large endothelial-lined vascular spaces and represent congenital
vascular lesions that contain fibrous tissue and small blood vessels that eventually
grow.
• They are predominantly seen in women and occur in 2% to 20% of the population.
• They can range from small (≤1 cm) to giant cavernous hemangiomas (10 to 25 cm).
• Most hemangiomas are discovered incidentally with little clinical consequence.
However, large lesions can cause symptoms as a result of compression of adjacent
organs or intermittent thrombosis, which in turn results in further expansion of the
lesion.
Hemangioma
• Resection can be accomplished by enucleation or formal hepatic resection,
depending on the location and involvement of intrahepatic vascular
structures and hepatic ducts.
• On biphasic contrast CT scan, large hemangiomas show asymmetrical
nodular peripheral enhancement that is isodense with large vessels and
exhibit progressive centripetal enhancement fill-in over time (Fig. 31-18).
• On MRI, hemangiomas are hypointense on T1-weighted images and
hyperintense on T2-weighted images.
• Caution should be exercised in ordering a liver biopsy if the suspected
diagnosis is hemangioma because of the risk of bleeding from the biopsy
site, especially if the lesion is at the edge of the liver.
Focal Nodular Hyperplasia
• FNH is a solid, benign lesion of the liver believed to be a hyperplastic
response to an anomalous artery.
• Similar to adenomas, they are more common in women of
childbearing age, although the link to oral contraceptive use is not as
clear as with adenomas.
• A good-quality biphasic CT scan usually is diagnostic of FNH, on which
such lesions appear well circumscribed with a typical central scar
• They show intense homogeneous enhancement on arterial phase
contrast images and are often isodense or invisible compared with
background liver on the venous phase.
Focal Nodular Hyperplasia
• On MRI scans, FNH lesions are hypointense on T1-weighted images
and isointense to hyperintense on T2-weighted images. After
gadolinium administration, lesions are hyperintense but become
isointense on delayed images.
• The fibrous septa extending from the central scar are also more
readily seen with MRI. Unlike adenomas, FNH lesions usually do not
rupture spontaneously and have no significant risk of malignant
transformation.
• Therefore, the management of FNH is usually reassurance and
prospective observation irrespective of size.
Adenoma
• They are 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, although they can occur
even in the absence of oral contraceptive use.
• On CT scan, adenomas usually have sharply defined borders and can
be confused with metastatic tumors. With venous phase contrast,
they can look hypodense or isodense in comparison with background
liver, whereas on arterial phase contrast, subtle hypervascular
enhancement often is seen
Adenoma
• On MRI scans, adenomas are hyperintense on T1-weighted images
and enhance early after gadolinium injection.
• Hepatic adenomas carry a significant risk of spontaneous rupture with
intraperitoneal bleeding.
• Hepatic adenomas also have a risk of malignant transformation to a
well-differentiated HCC. Therefore, it usually is recommended that
large hepatic adenomas (>4–5 cm) be surgically resected.
Malignant Liver Tumors
Malignant Liver Tumors
• Malignant tumors in the liver can be classified as primary (cancers
that originate in the liver) or metastatic (cancers that spread to the
liver from an extrahepatic primary site) (see Table 31-6). Primary
cancers in the liver that originate from hepatocytes are known as
hepatocellular carcinomas (HCCs or hepatomas), whereas cancers
arising in the bile ducts are known as cholangiocarcinomas.
Hepatocellular Carcinoma
• HCC is the fifth most common malignancy worldwide, with an
estimated 750,000 new cases diagnosed annually. Because of its high
fatality, it is the third most common cause of cancer death worldwide
• Major risk factors are viral hepatitis (B or C), alcoholic cirrhosis,
hemochromatosis, and NASH.
• HCCs are typically hypervascular with blood supplied predominantly
from the hepatic artery.
• Thus, the lesion often appears hypervascular during the arterial phase
of CT studies and relatively hypodense during the delayed phases due
to early washout of the contrast medium by the arterial blood.
• For patients without cirrhosis who develop HCC, resection is the
treatment of choice
• For patients with Child’s class A cirrhosis with preserved liver function
and no portal hypertension, resection also is considered
• If resection is not possible because of poor liver function and the HCC
meets transplant criteria, liver transplantation is the treatment of
choice
Cholangiocarcinoma
• Cholangiocarcinoma, or bile duct cancer, is
the second most common primary
malignancy of the liver.
• Subclassified into Peripheral and Central,
Central cholangiocarcinomas also called
Klatskins tumor, usually presents as
obstructive jaundice rather than a liver mass.
• In contrast, Peripheral or intrahepatic
cholangiocarcinoma presents as a tumor
mass in the liver.
• Surgical resection is the treatment of choice
of cholangiocarcinoma
• 3 year survival is 55%
Metastatic Colorectal Cancer
• Over 50% to 60% of patients diagnosed with colorectal cancer will
develop hepatic metastases during their lifetime.
• Proven that resection of metastasis improves survival of these
patients
• However limiting factor is the future liver remnant
Treatment Options for Malignant Liver
Cancer
• Hepatic Resection
• Liver Transplantation
• Radiofrequency Ablation
• Ethanol Ablation, Cryosurgery, Microwave ablation
• Chemoembolization and Hepatic Artery Pump Chemoperfusion
• Ytterium 90 Microspheres
• Stereotactic Radiosurgery and Intensity Modulated Radiation Therapy
• Systemic Chemotherapy
Hepatic Resection
Liver Transplantation
Radiofrequency Ablation
Chemoembolization and Hepatic Artery
Pump Chemoperfusion
Ytterium 90 Microspheres
Stereotactic Radiosurgery and Intensity
Modulated Radiation Therapy
Systemic Chemotherapy
Hepatic Resection Surgical Techniques
• Right Hepatectomy
• Left Hepatectomy
• Left Lateral Segmentectomy
• Anterolateral Segmentectomy
• Posterolateral Segmentectomy
Acute Viral Hepatitis
• AST, ALT
• TB
• DB
• IB
• Alk Phos
• Alb
• INR
Choledocholithiasis
• AST, ALT
• TB
• DB
• IB
• Alk Phos
• Alb
• INR
Hereditary Spherocytosis
• AST, ALT
• TB
• DB
• IB
• Alk Phos
• Alb
• INR