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05
Liver and Portal Hypertension

Dr. Karlos Noel Aleta June 30, 2015

OUTLINE
I. Liver Anatomy
A. Segmental Anatomy
B. Blood Supply
C. Hepatic Vein
D. Bile Duct
II. Liver Physiology
A. Liver Function Tests
B. Jaundice
III. Radiologic Evaluation of Liver
A. Ultrasound
B. Computed Tomography Scan (CT Scan)
C. Magnetic Resonance Imaging (MRI)
IV. Cirrhosis and Portal Hypertension
V. Liver Infection/Abscesses
A. Pyogenic Abscess
B. Amebic Abscess
C. Hydatid Disease
D. Ascariasis
E. Schistosomiasis Fig 2. In situ liver hilar anatomy with hepatoduodenal and gastrohepatic
VI. Liver Cysts ligaments. Foramen of Winslow is depicted.
A. Polycystic Liver Disease (PLCD)
B. Congenital Cysts SEGMENTAL ANATOMY
C. Biliary Cystadenoma  The liver has eight segments:
D. Caroli’s Disease o I - Caudate Lobe
VII. Benign Liver Lesions o II - Left lateral segment
A. Hemangioma
o III - Left lateral segment (parehas sila)
B. Adenoma
o IV - Left medial segment (quadrate lobe)
C. Focal Nodular Hyperplasia
D. Bile Duct Hamartoma o V-VIII- Right lobe
VIII. Malignant Liver Lesions  Caudate lobe has three subsegments:
A. Hepatocellular Carcinoma o Spiegel lobe
B. Cholangiocarcinoma o Paracaval portion
C. Metastatic Colorectal Cancer (MCRC) o Caudate process
D. Metastatic Neuroendocrine Cancer
IX. Treatment Options for Liver Cancer
A. Hepatic Resection
B. Liver Transplantation
C. Hepatic Resection Surgical Techniques
X. Laparoscopic Liver Resection

**This transcription was based mainly on the lecture. Some details were
lifted from the book.

LIVER ANATOMY
 Largest organ in the body, weighing approximately 1500 g
 Sits in the right upper abdominal cavity beneath the
diaphragm; protected by the rib cage
 Has two lobes, with larger right lobe
 The liver is held in place by several ligaments:
o Round ligament- remnant of umbilical ligament
o Falciform ligament- separates left lateral and left medial
segments, anchors liver to anterior abdominal word
o Ligamentum venosum- obliterated ductus venosus
o Triangular ligaments- secure liver to diaphragm
o Right coronary ligament- anchors the liver to the right
retroperitoneum
o Hepatoduodenal ligament- porta hepatis; contains the
common bile duct, the hepatic artery, and the portal vein

Fig 3. Couinaud’s liver segments (I through VIII) numbered in a

clockwise manner. The left lobe includes segments II to IV, the right lobe
includes segments V to VIII, and the caudate lobe is segment I. IVC =
inferior vena cava.
Fig 1. Hepatic ligaments suspending the liver to the diaphragm and
anterior abdominal wall

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 Liver and Portal Hypertension 1.05

BLOOD SUPPLY HEPATIC VEIN

 The liver has a dual blood supply consisting of the hepatic
artery (25%) and the portal vein (75%)
 There are three hepatic veins (right, middle, and left) that
drain to the suprahepatic IVC:
o Right hepatic vein drains segments V to VIII
o Middle hepatic vein drains segment IV as well as segments
V and VIII
o Left hepatic vein drains segments II and III
 Drainage of caudate lobe is direct to the IVC
 Left and middle hepatic veins form a common trunk 95% of
the time

Fig 4. Arterial anatomy of the upper abdomen and liver, including the
celiac trunk and hepatic artery branches. a. = artery; LHA = left hepatic
artery; RHA = right hepatic artery.

HEPATIC ARTERY
 The common hepatic artery then divides into the
gastroduodenal artery and the hepatic artery proper
 The hepatic artery proper divides into the right and left
hepatic arteries (75% of cases)

Fig 7. Confluence of the three hepatic veins (HVs) and the inferior vena
cava (IVC). Note that the middle and left HVs drain into a common trunk
before entering the IVC.

BILE DUCT
 The common bile duct lies anteriorly and to the right
 It gives off the cystic duct to the gallbladder and becomes the
common hepatic duct before dividing into the right and left
hepatic ducts
 The gallbladder sits adherent to hepatic segments IVB (left
lobe) and V (right lobe)

LIVER PHYSIOLOGY
 Bilirubin metabolism- heme breakdown
 Bile formation- absorption of lipids/lipid soluble vitamins
 Bile also functions to eliminate waste products (bilirubin and
cholesterol) via feces
Fig 5. Common hepatic artery anatomic variants. SMA = superior  The liver metabolizes drugs via the cytochrome 450 system
mesenteric artery. and conjugation reactions

PORTAL VEIN LIVER FUNCTION TESTS

 The portal vein is formed by the confluence of the splenic vein  Aspartate transaminase (AST)- used to assess hepatocellular
and the superior mesenteric vein injury
 The portal vein pressure in an individual with normal  Alanine transaminase (ALT)- used to assess hepatocellular
physiology is low at 3 to 5 mmHg injury; more specific for the liver
 The portal vein is valveless  Albumin levels, prothrombin time, INR- used to assess
abnormal synthetic function
 Cholestasis- impairment of bile flow from the liver to the
duodenum
 Diagnosis of cholestasis includes tests for:
o Alkaline phosphatase
o Gamma-Glutamyl Transpeptidase
o Bilirubin

JAUNDICE
 Jaundice refers to the yellowish staining of the skin, sclera,
and mucous membranes with the pigment bilirubin
 Types of jaundice
o Prehepatic- arises from conditions that interfere with proper
conjugation of bilirubin in the hepatocyte
o Intrahepatic- involve the intracellular mechanisms for
conjugation and excretion of bile from the hepatocyte
o Posthepatic- result of intrinsic or extrinsic obstruction of the
biliary duct system that prevents the flow of bile into the
duodenum
 Biliary diseases, including cholelithiasis,
Fig 6. Portal vein anatomy. The portal vein is formed by the confluence of
the splenic and superior mesenteric veins. The inferior mesenteric vein
choledocholithiasis, benign and malignant biliary
drains into the splenic vein. The coronary (left gastric) vein drains into strictures, cholangiocarcinoma, cholangitis, and papillary
the portal vein in the vicinity of the confluence. disorders

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 Liver and Portal Hypertension 1.05

RADIOLOGIC EVALUATION OF THE LIVER  Arterial and portal phase images allow for noninvasive
mapping of the hepatic arterial and venous anatomy
ULTRASOUND
o Crucial in the preoperative planning for patients undergoing
 Ultrasound technology is based on the pulse-echo principle
liver surgery
o Ultrasound transducer converts electrical energy to high-
frequency sound energy that is transmitted into tissue.
Table 1. Summary of Arterial and Portal Phase
o Although some of the ultrasound waves are transmitted
Arterial Portal Phase
through the tissue, some are reflected back, and the
Phase
ultrasound image is produced when the ultrasound receiver
Phase 20-30sec after 60-70sec after
detects those reflected waves.
contrast contrast
 Advantages:
delivery delivery
o Useful initial imaging test of the liver
o Inexpensive Function Enhance Enhance liver
o Widely available Hepatic artery parenchyma
o no radiation exposure supply
o Well tolerated by patients Hepatic Hypervascular Hypovascular
o Excellent for diagnosing biliary pathology and focal liver Tumor
lesions. Appearance Well delineated Hypoattenuated
o Liver injury can be evaluated in trauma patients using the of tumor in relation to
focused abdominal sonography for trauma examination. liver
 Limitations: parenchyma
o Incomplete imaging of the liver, most often at the dome or
beneath ribs on the surface CT CHOLANGIOGRAPHY
o Incomplete visualization of lesion boundaries.  Imaging modality for biliary disease
o Obesity and overlying bowel gas can interfere with image  Involves the use of contrast agents, which are excreted by
quality hepatocytes into the bile ducts
o Ultrasonographically detected masses usually require  Provides information on:
further evaluation by other imaging modalities o Hepatocyte function
o Lower sensitivity and specificity of ultrasound compared o Bile flow
with CT and MRI o High-resolution depiction of the biliary tree
 Doppler flow imaging  Advantages over Endoscopic Retrograde
o Augments realtime gray scale (B-mode) imaging Cholangiopancreatography (ERCP):
o Can detect the presence of blood vessels o Depicts small non-dilated peripheral biliary radicals
o Determines direction and velocity of blood flow o Useful in live liver donation or complex biliary surgery
 Contrast-enhanced ultrasound imaging of the liver aiding preoperative depiction of biliary anatomy
improves delineation of liver lesions through identification of  It also may be applicable in the postoperative setting for the
dynamic enhancement patterns and the vascular morphology detection of biliary leakage or obstruction
of the lesion  Its limitation is that the biliary tree may not be well visualized
 Intraoperative ultrasound is considered the gold standard for in patients with excessively dilated bile ducts or in those with
detecting liver lesions hyperbilirubinemia, as bilirubin excretion is impaired in these
 Elastography cases.
o Measures the stiffness of the liver by inducing an elastic
shear wave that propagates through the tissue MAGNETIC RESONANCE IMAGING (MRI)
o Promising non-invasive test in identifying patients with  Compared with CT scan, the major advantages of MRI is:
advanced fibrosis and cirrhosis o A higher soft tissue contrast resolution
o Excellent depiction of fluid-containing structures without
COMPUTED TOMOGRAPHY SCAN (CT SCAN) ionizing radiation.
 Produces a digitally processed cross-sectional image of the  Liver-specific MRI contrast agents relies on:
body from a large series of x-ray images. o Excretion by Kupffer cells - Ferumoxide
 In a single examination, modern-day CT scans provide o Secretion in bile by hepatocytes - Gadoxetate)
detailed morphologic information on the number, size,
distribution, and vascularity of liver lesions MAGNETIC RESONANCE ELASTOGRAPHY
 Diagnosis of hepatic fibrosis and cirrhosis
CONTRAST MEDIUM DELIVERY  Reduces need for biopsy
 Routinely used in CT evaluation of the liver because of the  High cost
similar densities of most pathologic liver masses and normal  Vibration device induces a shear wave in the liver
hepatic parenchyma. o Shear wave detected by MRI machine and generates color-
 A CT scan with a dual- or triple-phase bolus of intravenous coded image depicting wave velocity, and hence stiffness
contrast agent is performed to achieve the greatest throughout the organ.
enhancement of contrast between normal and pathologic
tissues. MAGNETIC RESONANCE
 Ideally, contrast media should be selectively delivered to CHOLANGIO-PANCREATOGRAPHY (MRCP)
either the tumor or the liver, but not both.  Indication: Biliary obstruction
 Rapid, non-invasive depiction of biliary tree & pancreatic duct
ARTERIAL AND PORTAL PHASE without radiation & IV contrast media
 Use dual blood supply of the liver to enhance contrast bet.  Provides visualization of dilated bile ducts
normal & pathologic tissues  The high spatial and contrast resolution enables accurate
 Portal vein – supplies 75%; Hepatic artery – supplies 25% assessment of the level of occlusion in the biliary tree
o Liver tumors – majority is supplied by Hepatic artery
 After injection of the contrast agent, the rapid scan time of CIRRHOSIS and PORTAL HYPERTENSION
helical CT allows for CT sections through the liver in both the
CIRRHOSIS
arterial dominant phase (20 to 30 seconds after the beginning
of contrast delivery) and venous or portal dominant phase (60  Final sequelae of chronic hepatic insult
to 70 seconds after contrast injection)  Characterized by fibrous septa throughout the liver
 Hepatic tumors that derive the majority of their blood supply subdividing it into hepatocellular nodules
from the hepatic artery as well as other hypervascular lesions  Consequence of “sustained wound healing in response to
are well delineated in the arterial phase. chronic liver injury.”
 Normal liver parenchyma is enhanced optimally in the portal
phase because the majority of its blood supply is derived from MORPHOLOGIC CLASSIFICATION OF CIRRHOSIS
the portal vein. MICRONODULAR
 Detection of hypovascular lesions becomes possible because  Characterized by thick regular septa
they will appear hypoattenuated in relation to the brighter  Small uniform regenerative nodules
normal liver parenchyma.  Involvement of virtually every hepatic lobule.

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 Liver and Portal Hypertension 1.05

MACRONODULAR between the portal system and the remnant of the umbilical
 Frequently has septa and regenerative nodules of varying vein)
sizes  Jaundice – does not appear until the bilirubin rises above 2 to
 Regenerative nodules consist of irregularly sized hepatocytes 3 mg/dL
with large nuclei and cell plates of varying thickness.  Asterixis in patients with hepatic encephalopathy
 Fetor hepaticus
 Malnutrition: weakness, weight loss, temporal muscle wasting
MIXED
 Present when regeneration is occurring in a micronodular liver
MANIFESTATION OF CIRRHOSIS
and over time converts to a macronodular pattern.
 Hx: fatigue, anorexia, weight loss, jaundice, abdominal pain,
 The morphologic categorization is limited, and cirrhosis is a peripheral edema, ascites, GI bleeding, hepatic
dynamic process in which nodule size varies over time encephalopathy
 The three patterns correlate poorly with etiology, and the  Reduced fat stores and muscle mass but with increased
same pattern can result from a variety of disease processes. energy expenditure
 A single disease process can demonstrate several  Muscle cramps
morphologic patterns. o Frequent in cirrhotic patients
 Irrespective of etiology and morphologic pattern, the cirrhotic o Correlated with ascites, low mean arterial pressure, and
liver frequently demonstrates: plasma renin activity
o Right hepatic lobe atrophy  Abdominal Hernias
o Caudate lobe and left lateral segment hypertrophy o Should be electively repaired only in patients with well-
o Recanalization of the umbilical vein compensated cirrhosis;
o Nodular surface contour o Hernia should be repaired at the time of or after hepatic
o Dilatation of the portal vein transplantation.
o Gastroesophageal varices  Hepatocellular Carcinoma (HCC)
o Splenomegaly on radiographic evaluation o Can occur in all forms of cirrhosis,
o Every cirrhotic patient should undergo screening for the
Table 2. Etiology of Cirrhosis development of HCC every 6 months via imaging and
measurement of a serum α-fetoprotein (AFP) level
 ↑ CO, HR; ↓ Systemic Vascular Resistance (SVR), BP
 Increased susceptibility to infections
o Decreased phagocytic activity of RES
o Bacterial infections
 Intrinsic drug metabolism is reduced

LABORATORY FINDINGS
 Mild normochromic, normocytic anemia
 Decreased WBC and platelet count
o Prolonged PT, does not respond to Vit. K therapy
 Bone marrow - Macroblastic
 Decreased serum albumin
 May have elevated transaminases, alkaline phosphatase, and
bilirubin
o Normal liver function test do not eliminate the possibility of
cirrhosis
 Urobilinogen is present and urinary sodium excretion is
diminished in the presence of ascites

END STAGE LIVER DISEASE (ESLD)
 Approximately 40% of cirrhotic patients are asymptomatic,
but progressive deterioration leading to the need for liver
transplantation or death is typical after the development of
end-stage liver disease (ESLD)
 5-year mortality of 50%, with 70% of deaths due to liver
failure
 Asymptomatic → progressive deterioration → ESLD → leading
to need for liver transplant or death
 Complications include:
o Progressive hyperbilirubinemia
o Malnutrition
o ↓ synthetic function of the liver
o Coagulopathy
o Portal hypertension (i.e., ascites & variceal bleeding)
o Hepatic encephalopathy
o Life-limiting fatigue
PHYSICAL EXAMINATION
 Finger clubbing – consequence of hypoalbuminemia
 Spider angioma & palmar erythema - caused by alterations in
sex hormone metabolism
 Males- features of feminization (gynecomastia, loss of
chest/axillary hair, testicular atrophy)
 Splenomegaly
 Cirrhotic liver – may be enlarged, normal or small
 Ascites & pleural effusion – fluid accumulation
 Portal hypertension
o Caput medusa
o Cruveilhier-Baumgarten murmur (venous hum that can be
auscultated in the epigastrium resulting from collaterals
LIVER BIOPSY
 Occasionally needed to confirm diagnosis of cirrhosis
 Can be performed via:
o Percutaneous
o Transjugular
o Laparoscopic approach
 Ultrasound elastography – noninvasive diagnosis of cirrhosis
(remember: this is not a biopsy)
HEPATIC RESERVE
 Patients undergoing surgery are in an increased risk for
surgical and anesthesia-related complications
o Actual risk depends on the type of anesthetic used, the
specific procedure performed, and the severity of liver
disease
o Emergency procedures, cardiac surgery, hepatic resections,
abdominal surgery, cholecystectomy, gastric resection, and
colectomy generate the highest operative risk among
cirrhotic patients
 (+) preop: Anemia, ascites, encephalopathy, malnutrition,
hypoalbuminemia, hypoxemia, infection, jaundice, portal
HPN, prolonged PT have been associated with inferior
outcomes after surgery
RISK ASSESMENT
CHILD-TURCOTTE-PUGH SCORE
 Originally developed to evaluate risk of portacaval shunt
procedures performed for portal hypertension
 Useful in predicting surgical risks of other intra-abdominal
operations on cirrhotic patients
 Surgical mortality rates per class:
o A - 10%
o B - 30%
o C - 75-80%

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 Liver and Portal Hypertension 1.05

 The problems with the CTP score are:

o Presence of subjective variables (encephalopathy and
ascites)
o Narrow range (5 to 15 points)
o Equal weighting given to each variable

Table 3. Child-Turcotte-Pugh (CTP) Scoring

MELD
 Model for End Stage Liver Disease
 Linear regression model based on the following labs:
o Creatinine (SCr)
o Bilirubin (Tbil)
o INR
 Initially a tool to predict mortality after Transjugular
Intrahepatic Portosystemic Shunt (TIPS)
 Sole method of liver transplant allocation
 Formula - MELD SCORE = 9.57 ln(SCr) + 3.78 ln(Tbil) + 11.2
ln(INR) + 6.43
 MELD score recommendations:
o <10 - Can safely undergo elective surgery Figure 8. Intra-abdominal venous flow pathways leading to engorged
o 10-15 - May undergo surgery with caution veins (varices) from portal hypertension. 1, Coronary vein; 2, superior
o >15 - Should not undergo elective surgical procedures hemorrhoidal veins; 3, paraumbilical veins; 4, Retzius’ veins; 5, veins of
Sappey; A, portal vein; B, splenic vein; C, superior mesenteric vein; D,
inferior mesenteric vein; E, inferior vena cava; F, superior vena cava; G,
PORTAL HYPERTENSION hepatic veins; a, esophageal veins; a1, azygos system; b, vasa brevia; c,
 Portal venous system contributes approximately 75% of the middle and inferior hemorrhoidal veins; d, intestinal; e, epigastric veins.
blood and 72% of the oxygen supplied to the liver
 Normally, 1-1.5L/min of portal venous blood is supplied to the ETIOLOGY OF PORTAL HYPERTENSION
liver and this is significantly increased in the cirrhotic patient.  Presinusoidal, Sinusoidal or PostsinusoidaL
 Portal venous system is without valves and drains blood from:  Intrahepatic (Cirrhosis) - Most common cause of portal
o Spleen hypertension in the US
o Pancreas
o Gallbladder Table 4. Etiology of Portal Hypertension
o Abdominal portion of the alimentary tract into the liver PRE-SINUSOIDAL
 Tributaries of the portal vein communicate with veins draining
directly into the systemic circulation  Splenic vein thrombosis
Sinistral/
o Gastroesophageal junction  Splenomegaly
Extrahepatic
o Anal canal  Splenic arteriovenous fistula
o Falciform ligament
o Splenic venous bed
 Schistosomiasis
o Left renal vein and retroperitoneum
 Congenital hepatic fibrosis
 Normal Portal Vein pressure - 5-10mmHg
 Nodular regenerative hyperplasia
 Very little blood is shunted from the portal venous system
Intrahepatic  Idiopathic portal fibrosis
into the systemic circulation
 Myeloproliferative disorder
 As portal venous pressure increases, collateral
 Sarcoid
communications with systemic circulation dilate = a large
 Graft-versus-host disease
amount of blood may be shunted around the liver into the
systemic circulation
SINUSOIDAL
IMAGING
CIRRHOSIS
 Abdominal USG/ Doppler USG
 Viral infection
 Abdominal CT and MRI angiography - Visceral angiography  Alcohol abuse
and portal venography Intrahepatic  Primary biliary cirrhosis
 Most accurate method of determining portal HPN - Hepatic  Autoimmune hepatitis
venography  Primary sclerosing cholangitis
 HVPG = WHVP -FHVP  Metabolic abnormality
o HVPG - Pressure in the hepatic sinusoids and portal vein -
Measure of PV pressure
POST-SINUSOIDAL
 Clinically significant portal HPN is evident when HVPG exceeds
10mmHg Intrahepatic  Vascular occlusive disease

 Budd-Chiari syndrome
 Congestive heart failure
PostHepatic
 Inferior vena caval web
 Constrictive pericarditis

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 Liver and Portal Hypertension 1.05

CLINICAL FEATURES OF PORTAL HYPERTENSION MESO-CAVAL SHUNT (SMV-IVC)

 Development of GE varices  Most significant clinical finding
associated with PH
o GE varices - Mainly supplied by the Anterior branch of Left
gastric (coronary) vein
 Splenomegaly – Frequently associated with functional
hypersplenism which causes leukopenia, Thrombocytopenia,
Anemia
 Ascites - occurs in combination with hepatocyte dysfunction
o Umbilical vein may recannulate and dilate  Visible
collaterals on the abdominal wall
 Anorectal varices – must be distinguished with hemorrhoids
 VARICEAL BLEEDING  most significant manifestation and
leading cause of morbidity & mortality in PH
MANAGEMENT OF GASTROESOPHAGEAL VARICES
 Prevention of Variceal bleeding
o Nonselective β blockers (Propanolol, Nadolol)
o Prophylactic endoscopic surveillance with variceal band
ligation q 2weeks
 Acute Variceal Haemorrhage – ICU, Blood products,
antibiotics for SBP
o Vasoactive medications (Vasopressin, Octreotide)
o Endoscopy
 Luminal tamponade
o Using Sengstaken-Blakemore tube
o Limited duration  complications d/t overinflation or
pressure necrosis
o Should not exceed 36 hours
 Transjugular Intrahepatic Portosystemic Shunt (TIPS)
o Implantation of a metallic stent b/n an intrahepatic branch
of the portal vein and a hepatic vein radicle
o High rate of thrombosis – D/t intimal hyperplasia of the
metallic stent
 Balloon-Occluded Retrogade Transvenous Obliteration
(BRTO)
o Used for the Specific management of bleeding gastric
varices in patients with spontaneous Gastrorenal or
Splenorenal shunts
SURGICAL SHUNTING
 Reduced since TIPS & LT
 Recommendation: SS should only be considered in patients
with:
o MELD scores of <15
o Not candidates for hepatic transplantation
o limited access to TIPS & follow-up
 Aim of SS:
o To reduce PV pressure, maintain total Hepatic & Portal
blood flow, avoid high incidence of complicating hepatic
encephalopathy
 Patient survival is determined by Hepatic reserve
 Uses an 8- or 10-mm polytetrafluo-roethylene (PTFE) graft to
connect the SMV to the IVC (small lumen)
 Easier to perform
 Increased risk of Shunt thrombosis and rebleeding
DISTAL SPLENORENAL SHUNT (WARREN)
 Currently the most used
 Technically the most difficult to perform
 Selective shunt
 Advantage: Associated with a lower rate of hepatic
encephalopathy and decompensation and not interfering with
subsequent liver transplantation.
NONSHUNT SURGICAL MANAGEMENT
 Sugiura procedure – sugiurado ka na ba?
o Extrahepatic PV thrombosis with refractory bleeding
 Patient survival dependent on hepatic reserve during
procedure
 Extensive devascularization of stomach and distal esophagus,
transection of esophagus, splenectomy, truncal vagotomy,
pyloroplasty
HEPATIC/LIVER TRANSPLANT
 Cirrhosis + Portal hypertension + Variceal bleeding
o Usually die from hepatic failure and not from acute blood
loss
 Must be considered in End-stage Liver Disease
 Represents patient’s only chance for definitive survival
 Can be considered for patient with refractory variceal bleeding
BUDD-CHIARI SYNDROME
 Uncommon congestive hepatopathy characterized by
obstruction of hepatic venous outflow
 May be primary or secondary
o Primary when the obstructive process involves an
endoluminal venous thrombosis
o Secondary process when the veins are compressed or
invaded by a neighboring lesion originating outside the
vein.
 Primary Risk Factors:
o Primary myeloproliferative disorders
 Essential thrombocythemia
 Polycythemia rubra
o All known inherited thrombophilias
o Activated protein C resistance
 Related to factor V Leiden mutation
o Anticardiolipin antibodies
o Hyperhomocysteinemia
o Oral contraceptive use
 Clinically significant BCS
o Obstruction of 2 or more major hepatic veins resulting to:
 Hepatomegaly
 Liver congestion
 Right upper quadrant pain
o Liver perfusion via Portal vein may be decreased
o 70% of affected patients have noninflammatory
centrilobular necrosis on biopsy
o Caudate lobe hypertrophy due to direct venous drainage
into the IVC

DIAGNOSTIC PROCEDURE
 Ultrasonography
o Initial investigation of choice
o Can demonstrate the absence of:
 Hepatic vein flow
 Spider web hepatic vein
 Collateral hepatic veins
 CT Scan/MRI
o Capable of demonstrating hepatic vein thrombosis
o Evaluates the IVC but cannot show direction of blood flow
 Hepatic Venography
Fig 9. Surgical shunts for portal hypertension. A.Normal anatomy o Definitive radiographic study to evaluate BCS
B.Side-to-side C.End-to-side D.Mesocaval E.Warren o Determine presence and extent of hepatic vein thrombus
o Measure IVC pressures
PORTO-CAVAL SHUNT (ECK)
 Joins the portal vein to IVC TREATMENT
 Rarely performed d/t high incidence of hepatic encep  Systemic anticoagulation
o Side-to-side – Partial o Prevent extension of the hepatic vein thrombosis
 Maintains partial portal vein flow to the liver  Radiologic and surgical intervention
o End-to-side - Complete o Reserved for patients whose condition is nonresponsive to
 Completely disrupts portal vein flow to the liver medical therapy

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 Percutaneous angioplasty and TIPS, in combination with  Amebae multiply and block small intrahepatic portal radicles
thrombolytic therapy o Focal infarction of hepatocytes
o Preferred in restoring the outflow of blood from the liver o Amoeba has proteolytic enzyme that destroys parenchyma
 Thrombolytic therapy for acute thrombosis  Most common type of liver abscesses worldwide
 Surgical shunting  Abscesses are variable in size and can be single or multiple
o Side-to-side portacaval shunt  Most common location: superior-anterior aspect of the right
 Turns the portal vein into a hepatic outflow tract lobe near the diaphragm
 Most patients with portacaval shunt improvement in  Has necrotic central portion that contains a thick, reddish
hepatic function and fibrosis at 1 year without significant brown, pus-like material – like anchovy paste/chocolate sauce
hepatic encephalopathy
 High rate of operative mortality and shunt dysfunction DIAGNOSIS
 Hepatic transplantation for patients with progressive BCS and  Should be considered in patients who/with:
manifestations of ESLD o Travelled to an endemic area
o Present with right upper quadrant pain
LIVER INFECTION/ABSCESSES o Fever
PYOGENIC ABSCESS o Hepatomegaly
 Due to: o Hepatic abscess
o Impaired biliary drainage  Leukocytosis is common
o Subacute bacterial endocarditis  Elevated transaminase levels, jaundice, diarrhea are unusual
o Infected indwelling catheter  Mildly elevated AP level is the most common biochemical
o Dental work abnormality
o Direct extension of infection to the liver  Ultrasound and CT scan of the abdomen
 Diverticular disease o Very sensitive but nonspecific for amebic abscesses
 Crohn’s disease  CT scan
 The most common infecting agents are gram-negative o Well defined low-density round lesions that have
bacteria enhancement of the wall
o Escherichia coli (2/3 of cases), o Ragged appearance with a peripheral zone of edema
 Other common organisms include: o Central cavity may have septations as well as fluid levels
o Streptococcus faecalis o Useful in the detection of extrahepatic involvement
o Klebsiella
o Proteus vulgaris TREATMENT
o Bacteroides fragilis  DOC: Metronidazole 750mg 3x/day for 7 to 10 days
 Defervescence - 3 to 5 days
DIAGNOSTIC PROCEDURE  Time for the abscess to resolve  30 to 300 days
 Common presentation:  Both ultrasound and CT of the liver can be used as follow-up
o Right upper quadrant pain after the initiation of medical therapy
o Fever  Aspiration
o Jaundice (1/3 of cases) o For patients with large abscesses
 Common laboratory findings o Those who do not respond to medical therapy
o Leukocytosis o Superinfected
o Elevated sedimentation rate  Abscesses of the left lobe of the liver
o Elevated AP level o Risk for rupture into the pericardium
o Remaining liver function tests are unusual o Treated with aspiration and drainage
 Ultrasonography examination
o Round or oval hypoechoic lesions with well-defined borders HYDATID DISEASE
and a variable number of internal echoes  Caused by a tape, worm Echinococcus granulosus in its larval
 CT scan or cyst stage
o Highly sensitive in the localization of pyogenic liver o Treatment: Albendazole, intact cyst removal
abscesses  Gastric juice liberates ovum that burrows through the
o Hypodense with peripheral enhancement intestinal mucosa  carried by the portal vein to the liver
o May contain air-fluid levels indicating a gas-producing (site of development into adult cyst form)
infectious organism  Most cysts are caught in the hepatic sinusoids 70% of
 MRI of the abdomen hydatid cysts form in the liver
o High level of sensitivity but  Hydatid disease: most common in sheep-raising areas.
o Limited role - Inability to be used for image-guided  Commonly involve the RIGHT lobe of the liver, usually the
diagnosis and therapy anterior-inferior or posterior-inferior segments.

TREATMENT DIAGNOSIS
 Current cornerstones of treatment:  Affected patient resents with dull RUQ pain or abdominal
o Correction of the underlying cause distention
o IV antibiotic therapy  ELISA for echinococcal antigens
 Empiric antibiotic therapy should cover gram-negative  USG and CT: hydatid cysts visible as well-defined hypodense
and anaerobic organisms lesions with a distinct wall, ring-like calcifications; dead or
 Percutaneous needle aspiration and culture of the inactive dense calcification
aspirate may guide subsequent antibiotic therapy  MRI: evaluate pericyst, cyst matrix, and daughter cyst
 Should be continued for at least 8 weeks characteristics
 Placement of a percutaneous drainage catheter is beneficial
only for a minority of patients ASCARIASIS
o Most pyogenic abscesses are quite viscous and catheter  Ascariasis nidus for development of intrahepatic gallstones
drainage is often ineffective  Ova arrive in the liver by retrograde locomotion in the bile
 Surgical drainage (if initial therapies fail) ducts from the GI tract.
o Laparoscopic  Adult worm: 10 to 20 cm long; lodge in common bile duct
o Open approach partial bile duct obstruction and secondary cholangitic
 Anatomic surgical resection for patients with recalcitrant abscesses
abscesses
 Necrotic hepatic malignancy should not be mistaken for
DIAGNOSIS
hepatic abscesses
 Clinical manifestations:
o Biliary colic
AMEBIC ABSCESS
o Acute cholecystitis
 Entamoeba hystolytica o Acute pancreatitis
 Trophozoite in colon  ulcer  portal venous system  liver o Hepatic abscesses
 Flask-shaped ulcer in colonic mucosa

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 Liver and Portal Hypertension 1.05

 Abdominal radiographs, USG, and ERCP demonstrate Ascaris LIVER CYSTS

as linear filling defects within the bile ducts  Polycystic Liver Disease (PCLD)
 Congenital
TREATMENT  Biliary Cystadenoma
 Medical (Albendazole, Mebendazole)  Caroli’s Disease
 Endoscopic retrieval
 Surgery if ERCP does not remove Ascaris **Only PCLD was discussed in the lecture. Other liver cysts
diseases were lifted from the book
SCHISTOSOMIASIS
 Leads to portal fibrosis POLYCYSTIC LIVER DISEASE (PCLD)
 Hepatic schistosomiasis occurs when emboli of the ova in the  May be small, single; Large, multiple
intestines reach the liver via mesenteric venous system.  Small number and size of cysts (<2 cm): asymptomatic
o Widespread hematogenous dissemination  Large number and size of cysts: develop abdominal pain,
o Those entering the intrahepatic portal system grow distension, shortness of breath, early satiety
rapidly granulomatous reaction  Disease progression  renal failure
 Degree of consequent portal fibrosis is related to adult worm  Liver parenchymal volume and synthetic function are
load. preserved despite extensive cystic disease
 3 Stages of clinical symptomatology:  Principal aim of treatment: ameliorate symptoms by
o 1st: itching of the skin (entry of cercariae) decreasing liver volume
o 2nd: fever, urticarial, eosinophilia o Cyst aspiration
o 3rd: hepatic fibrosis followed by presinusoidal portal HPN o Cyst fenestration
liver shrinks, spleen enlarges, develops complications of o Hepatic Resection
portal HPN  Orthotopic Liver Trasplantation (OLT): only definite treatment
for symptoms or complications
DIAGNOSIS
 Stool exam: detect active infection CONGENITAL CYSTS
 Serologic tests: indicate past exposure, but no information  Usually asymptomatic; identified incidentally and occur
regarding the timing of infection anytime throughout life
 Decreased serum albumin: result of frequent GI bleeds and  Simple cysts  result of excluded hyperplastic bile duct rests
malnutrition  Imaging: thin-walled, homogenous, fluid-filled structures with
few to no septations
TREATMENT  Cyst epithelium: cuboidal; secretes a clear non-bilous serous
 Education on hygiene and avoidance of infected water fluid
 DOC: Praziquantel (40-75 mg/kg single dose)  Large cysts  may cause abdominal pain, epigastric fullness,
 GI bleeding: controlled by endoscopic variceal ligation and early satiety
 Treatment of choice: Ultrasound or CT- guided percutaneous
**Viral Hepatitis: included in Schwartz under Infections of the Liver (10 th cyst aspiration followed by sclerotherapy
Ed, pp. 1286-1287), but not discussed in the lecture  Alternative: laparoscopic or open surgical cyst fenestration

BILIARY CYSTADENOMA
 Slow-growing, unusual, benign lesions that most commonly
resent as large lesion on RIGHT lobe of the liver
 Commonly present with abdominal pain
 PE: abdominal mass
 Thicker wall than congenital cysts with soft tissue nodules and
septations
 Preferred mode of treatment: Surgical resection

CAROLI’S DISEASE
 Syndrome of congenital ductal plate malformations of the
intrahepatic bile ducts
 Characterized by segmental cystic dilatation of the
intrahepatic biliary radicals
 Associated with increased incidence of biliary lithiasis,
cholangitis, and biliary abscess formation
 Occurs in the absence of cirrhosis, but associated with cystic
renal disease
 Most common presenting symptoms: fever, chills, abdominal
pain
 Diagnosis: MR-Cholangiopancreatography, ERCP, and
percutaneous transhepatic cholangiography
 Treatment: biliary drainage, hepatic resection

BENIGN LIVER LESIONS

 The liver is commonly involved either primarily or secondarily
with vascular, metabolic, infectious, and malignant processes.
 Classification schemes used to narrow the differential
diagnosis of liver lesions:
o Solid or cystic
Figure 10. Algorithm for diagnostic work-up of an incidental liver lesion
o Single or multiple
Table 5. Classification of Liver Lesions o Cell of origin (hepatocellular, cholangiocellular, or
LIVER LESION CLASSIFICATION mesenchymal)
BENIGN MALIGNANT o Benign or malignant
 Benign liver lesions occur in up to 20% of the general
 Cyst  Hepatocellular CA
population and are much more common than malignant
 Hemangioma  Cholangiocarcinoma (bile
tumors.
 Focal nodular hyperplasia duct cancer)
 The most common benign lesions:
 Adenoma  Gallbladder cancer
o Cysts
 Biliary hamartoma  Metastatic colorectal cancer
o Hemangiomas
 Abscess (MCRC)
o Focal nodular hyperplasia (FNH)
 Metastatic neuroendocrine
o Hepatocellular adenomas
cancer (carcinoid)
 Other metastatic cancers

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 Liver and Portal Hypertension 1.05
Table 6. Benign lesions and their features
BENIGN LESIONS FEATURES
Hemangioma  Most common benign solid masses of
(Hemangiomata) the liver
 Consist of large endothelial-lined
vascular spaces
 Represent congenital vascular lesions
that contain fibrous tissue and small
BV’s that eventually grow
Adenoma  Benign solid neoplasms usually in
post-menopausal women
 Typically solitary but can be multiple
 Risk factor: Prior use of estrogen
(OC’s)
 Appear soft and encapsulated, tan to
light brown
 Lack bile ducts glands and Kupffer
cells, no true lobules, congested
heptocytes
Focal Nodular  Hyperplastic response to an
Hypeplasia anomalous artery
 Do not rupture spontaneously and
have no significant risk of malignant
transformation
Bile Duct  2-4mm, excision is needed to
Hamartoma establish diagnosis
 Firm, smooth, whitish yellow
**more details in the book (pp. 1289-1291 10th ed Schwartz)

Fig 12. Computed tomographic (CT) images of hepatocellular carcinoma

(HCC) and peripheral cholangiocarcinoma. CT scans reveal a large (upper
panel) and small (middle panel) hypervascular HCC. A hypovascular left
lobe peripheral cholangiocarcinoma (CholangioCA) is also shown (lower
panel).

Fig 11. Computed tomographic scans showing classic

appearance of benign liver lesions. Focal nodular hyperplasia
(FNH) is hypervascular on arterial phase, isodense to liver on
venous phase, and has a central scar (upper panels). Adenoma
is hypovascular (lower left panel). Hemangioma shows
asymmetrical peripheral enhancement (lower right panel).
MALIGNANT LIVER TUMORS
MALIGNANT FEATURES
LESIONS
Hepatocellular CA  Major risk factors: viral hepatitis
(B or C), alcoholic cirrhosis,
hemochromatosis, NASH
 Hypervascular with blood
suppliead predominantly from
hepatic artery
Cholangiocarcinoma  Peripheral (intrahepatic)
 Central (extrahepatic)  hilar
cholangiocarcinoma or Klatskin’s
tumor
 r/o primary sclerosing cholangitis
for resection
 Bile duct cancer or adenoCA of
bile ducts
 Forms in the biliary epithelial cells
Metastatic colorectal  Resection for hepatic metastases
cancer (MCRC) has been a routine part of
treatment
Metastatic  Hepatic metastases from NE
neuroendocrine cancer tumors are associated with
endocrinopathies
 Treatment: aggressive surgical
approach of debulking surgery
**more details in the book (pp.1291-1294 10th ed Schwartz)
Fig 13. Algorithm for the management of hepatocellular Carcinoma
(HCC). The treatment algorithm for HCC begins with determining
whether the patient is a resection candidate or liver transplant candidate.
Bili = bilirubin level (in milligrams per deciliter);
Child’s = Child-Turcotte-Pugh class; lap = laparoscopic; LDLT = living-
donor liver transplantation;
MELD = Model for End-Stage Liver
Disease; OLTreatment = orthotopic liver transplantation;
Perc = percutaneous; RFA = radiofrequency ablation; TACE =
transarterial chemoembolization;
Treatment = transplantation; UNOS = United Network for Organ Sharing;
vasc. = vascular.
TREATMENT OPTIONS FOR LIVER CANCER
 Treatments listed are not mutually exclusive; the important
point is to select the most appropriate initial treatment after a
complete evaluation
 Surveillance imaging (CT or MRI) is performed every 3 to 4
months during the first year after diagnosis to observe for
response, progression, or recurrence
 The treatment plan is individualized and modified according to
the response of the patient
HEPATIC RESECTION
 For primary liver cancers or hepatic metastases, hepatic
resection is the gold standard and treatment of choice
 For HCC with cirrhosis, liver transplantation also offers the
potential for long-term survival, albeit with the consequences
of immunosuppression
 Hepatic resection also has been advocated for HCC in select
patients with cirrhosis before secondary liver transplantation
 Previously, a 1-cm tumor margin; recent studies have
reported comparable survival rates with smaller margins

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 Liver and Portal Hypertension 1.05

Table 8. Treatment options for liver cancer.

Fig 14. Hepatic anatomy. Hepatic segments removed in the formal major
hepatic resections are indicated. IVC = inferior vena cava; LHV = left
hepatic vein; MHV = middle hepatic vein; RHV = right hepatic vein.

LIVER TRANSPLANTATION
 Rationale supporting OLT for HCC includes the fact that most
HCCs (>80%) arise in the setting of cirrhosis
o Cirrhotic liver often does not have enough reserve to
tolerate a formal resection
o HCC tumors are commonly multifocal and are
underestimated by CT or MRI imaging
o OLT is an appealing treatment, because it removes both the
cancer and the cirrhotic liver that leads to cancer
 Survival rates were markedly improved when OLT was limited
to patients with early-stage HCC (stage I or stage II) with one
tumor .5 cm, or up to three tumors no larger than 3 cm,
along with the absence of gross vascular invasion or
extrahepatic spread
 In an attempt to prioritize patients with preserved liver
function and progressive HCC, patients with stage I or stage
II HCC are allocated exception points (currently 22 MELD
points, increasing every 3 months as long as they continue to
meet transplant criteria)

HEPATIC RESECTION SURGICAL TECHNIQUES

BRISBANE 2000 LIVER TERMINOLOGY (NOMENCLATURE) Fig 15. Completed right hepatic lobectomy (right hepatectomy) with the
OLDER HEPATIC BRISBANE 2000 HEPATIC right portal vein, right hepatic artery, and right bile duct ligated and
RESECTION RESECTION TERMINOLOGY divided. The right hepatic vein is ligated and divided. Middle hepatic vein
branches inside the liver are divided.
TERMINOLOGY
 Right hepatic  Right hepatectomy/ right
lobectomy hemipatectomy (V,VI, VII, VIII)
 Left hepatic  Left hepatectomy/ Left
lobectomy hemipatectomy (II, III, IV)
 Right hepatic  Right trisectionectomy/ Extended
trisegmentectomy righ hepatectomy (or
 Left hepatic hemipatectomy, IV, V, VI, VII, VIII)
trisegmentectomy  Left trisectionectomy/ Extended left
 Left lateral hepatectomy (or hemipatectomy,
segmentectomy II, III, IV, V, VIII)
 Right posterior  Left lateral sectionectomy/
lobectomy Bisegmentectomy (II, III)
 Caudate lobectomy  Right posterior sectionectomy (VI,
VII)
 Caudate lobectomy/
Segmentectomy (I)
ALTERNATIVE “SECTOR” TERMINOLOGY
 Right anterior sectorectomy
 Right posterior sectorectomy or right lateral
sectorectomy
 Left medial sectorectomy or left paramedian
sectorectomy (bisegmentectomy, III, IV)
 Left lateral sectorectomy (segmentectomy, II)
**The book discussed surgical techniques extensively (as in
step by step), we didn’t included it since it was not discussed. Fig 16. Completed left hepatic lobectomy (left hepatectomy) resecting
segments II, III, and IV.

PRINGLE AND ISCHEMIC PRECONDITIONING

 Pringle maneuver was initially described for controlling
bleeding due to traumatic liver injury; it is commonly used
during elective hepatic resections
 To minimize blood loss and hypotension

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 Liver and Portal Hypertension
 Liver has been shown to tolerate up to 1 hour of warm
ischemia
 Variation: intermittent vascular occlusion with cycles of
approximately 15 minutes on and 5 minutes off
o Studies have demonstrated the efficacy of intermittent
vascular occlusion in decreasing ischemia/reperfusion injury
compared with continuous vascular occlusion
 Variation: selective hemihepatic vascular occlusion, which can
reduce the severity of visceral congestion and total liver
ischemia
o Both total and partial clamping were found to be equally
effective for patients with normal livers, but greater liver
damage was observed with total inflow occlusion in cirrhotic
livers
 To decrease the ischemic damage associated with inflow
occlusion, some have advocated ischemic preconditioning
 Ischemic preconditioning – brief interruption of blood flow,
followed by a short reperfusion period, and then a more
prolonged period of ischemia
o 10-minute clamp, a 10-minute reperfusion, and then a 30-
minute clamp
o Patients with steatosis were especially protected by
ischemic preconditioning, related in part to preservation of
the adenosine triphosphate content of liver tissue
PREOPERATIVE PORTAL VEIN EMBOLIZATION (PVE)
 Tumor thrombosis of a major portal vein branch induced
ipsilateral lobar atrophy and contralateral lobe hypertrophy
led to the concept of intentional preoperative PVE
 To induce compensatory hypertrophy of the remnant liver
 Accomplished via a percutaneous, transhepatic route
 Usually performed in the setting of:
o Planned right trisectionectomy or extended left
hepatectomy (also referred to as a left trisectionectomy;
resection of Couinaud’s segments II, III, IV, V, and VIII of
the liver)
o Extended hepatic lobectomy when the remnant liver will be
too small to support liver function
 If the future liver remnant is thought to be too small, then
PVE should be considered to increase the size of the future
liver remnant
 In general, surgery is planned approximately 4 weeks after
PVE to allow adequate time for hypertrophy
 No universal agreement on what constitutes a future liver
remnant adequate to avoid postoperative liver failure
 It is thought that 25% to 30% of the total liver volume is
adequate in patients with a normal liver
 One study demonstrated that PVE had no beneficial effect on
the postoperative course in patients with normal livers but
significantly reduced postoperative complications in patients
with chronic liver diseases
 A larger remnant may be necessary in:
o Patients with normal livers when a complex hepatectomy is
planned or when the background liver is steatotic
o Fatty liver disease
o Received preoperative chemotherapy
o Suggested that 40% of the total hepatic volume should
remain to minimize postoperative complications
 PVE-related complications occur at a low rate:
o Bleeding
o Hemobilia
o Liver abscess
o Incomplete embolization
o Small bowel obstruction
 To augment the ability to increase liver function reserve in
patients who have undergone PVE, some add ipsilateral
hepatic artery embolization and ipsilateral hepatic vein
embolization
STAGED HEPATECTOMY AND REPEAT HEPATIC
RESECTION FOR RECURRENT LIVER CANCER
 A two-stage hepatectomy is a sequential resection strategy to
remove all metastatic liver tumors when it is impossible to
resect all in a single procedure
 First-stage hepatectomy: clearance of the left hemiliver by
nonanatomic resection, followed by right portal vein ligation
or embolization to induce left lobe hypertrophy
 Second-stage: major right hepatectomy or extended right
hepatectomy to resect the right liver metastases
 Most commonly used in cases of initially unresectable
colorectal hepatic metastases and has yielded very good
results
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1.05
 Majority of patients undergoing hepatic resection for
colorectal cancer metastases experience a recurrence
o For disease recurrence confined to the liver, repeat
hepatectomy is a reasonable option
LAPAROSCOPIC LIVER RESECTION (LLR)
 Minimally invasive surgery
 Because of the increased technical demands in LLR, stringent
criteria based on surgeon experience and lesion size and
location must be used
 Surgeons should have an advanced understanding of liver
anatomy, extensive experience in open liver surgery, and the
technical skills to control major vascular and biliary structures
laparoscopically before embarking on LLR
 Familiarity with laparoscopic ultrasonography is needed
 Smaller, more peripheral lesions, particularly those located in
the anterolateral segments (segments II to VI) are most
amenable to LLR
 Laparoscopic liver resection can now be performed safely by
experienced surgeons in selected patients
 Benefits of the laparoscopic approach include less operative
blood loss, reduced postoperative pain and narcotic
requirements, a shorter length of hospital stay, and
comparable postoperative morbidity and mortality rates to
open liver resection
---end---
Sample Quiz:
1. What are the signs of portal hypertension?
2. This is used to evaluate risk of portacaval shunt?
3. Infectious agent in pyogenic liver abscess?
4. Manifestations of liver cirrhosis?
5. Segments of the caudate lobe?
6. Gold standard for detecting liver lesions intraoperatively?
7. What is the normal portal vein pressure?
8. Most common cause of portal hypertension in the US?
9. Most common type of liver abscess worldwide?
10. Most common location of amebic abscess?
Answers:
1. Gastroesophageal varices, splenomegaly, ascites, anorectal varices
2. Child-Turcotte-Pugh Score
3. Escherichia coli (2/3 of cases) –most common
Other common organisms include: Streptococcus faecalis, Klebsiella,
Proteus vulgaris, and Bacteroides fragilis
4. Madami. Haha. Basta liver failure signs and symptoms.
E.g. Fatigue, anorexia, weight loss, jaundice, abdominal pain, peripheral
edema, ascites, GI bleeding, hepatic encephalopathy, Reduced fat stores
and muscle mass but with increased energy expenditure, Muscle cramps,
Abdominal Hernias, Hepatocellular Carcinoma, ↑ CO, HR; ↓ Systemic
Vascular Resistance (SVR), BP.
5. Spiegel lobe, Paracaval portion, and Caudate process
6. Ultrasound
7. 5-10mmHg
8. Intrahepatic (Cirrhosis)
9. Amebic abscess
10. Superior-anterior aspect of the right lobe near the diaphragm
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 Liver and Portal Hypertension 1.05

**This table is not in the book but was in the lecture

SOURCE: http://www.thecco.net/article/view/2528/3943

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