LIVER

ODESSA BACUD-TIANGCO, MD

ANATOMY

ANATOMY

HEPATIC VEIN

Small
short
hepatic
veins

HEPATIC ARTERY

Replaced
hepatic
artery
Accessory
hepatic
artery

PORTAL VEIN

PORTAL VEIN

75%
Posterior to the
bile duct & hepatic
artery

valveless

3-5 mm Hg

BILIARY SYSTEM

LYMPHATICS & INNERVATION

Spaces of Disse & clefts of Mall sub-Glissonian

&periportal cisterna chyli

Vagus nerve & celiac plexus

C3 & C4

LIVER LOBE

PHYSIOLOGY:
SYNTHETIC FUNCTIONS

Coagulation
factors
Plasma proteinseg. albumin

Glucose

Lipoproteins

Triglyceride

Cholesterol

Bile salt

BILIRUBIN METABOLISM

uncojugated

BILIRUBIN METABOLISM
uncojugated

BILIRUBIN METABOLISM

conjugated

BILE

Bile

85% water

10% bile salts

3% mucus & pigments

1% fats

0.7% inorganic salts

BILE ACIDS
Primary : cholic &
chenodeoxycholic
Secondary : deoxycholic
& lithocholic

BILE & ENTEROHEPATIC

CIRCULATION

500-1000ML/24H

LIVER FUNCTION TESTS

PARENCHYMAL- AST, ALT

BILIARY- Alkaline phosphatase

SYNTHETIC- INR, factors V & VII, bilirubin,

albumin

RADIOLOGIC EVALUATION OF THE

LIVER

ULTRASOUND

Economical

Screen for HCC

Biliary tract stones

Intrahepatic biliary
ductal dilation

ULTRASOUND

Microbubble
contrast

Doppler UTZ

laparoscopic

IOUS- gold standard

to detect number,
extent & blood vessel
association of tumors

COMPUTED TOMOGRAPHY SCANS

Highly sensitive
Dual- & triplephase IV contrast

3-D

COMPUTED TOMOGRAPHY SCANS

PRE-OPERATIVE
EVALUATIONinflow & outflow
of hepatic blood
vessel
-Liver volume

Primary vs.
metastatic

MAGNETIC RESONANCE IMAGING

Less sensitive at spatial discrimination

More sensitive for detecting early HCC &
distinguishing HCC for macroregenerative
nodules

Contrast- cystic vs. Hemangioma

MRC

PET Scan
F-flurodeoxyglycose

Angiography

Hepatic arterial chemoembolization

Percutaneous biopsy

Diagnostic laparoscopy

LIVER FAILURE

Hepatic insufficiency---> encephalopathy

ACUTE

Rapid massive loss of hepatocyte functional mass

without pre-existing liver disease

CHRONIC

Viral hepatitis, metabolic diseases, alochol abuse,

toxins
Ongoing & progressive hepatocyte necrosis
fibrosis & regeneration cirrhosis

ACUTE LIVER FAILURE

Development of encephalopathy within 26

weeks of onset of any hepatic symptom

Fulminant Hepatic Failure

Subfulminant Hepatic Failure

ACUTE LIVER FAILURE

Etiology

Acetaminophen overdose

Viral hepatitis

Other drug toxicities

20% will survive--> N liver function

HEPATIC ENCEPHALOPATHY

ACUTE LIVER FAILURE

Treatment

Supportive care/Medical Management

LIVER TRANSPLANT 60% survival rate

CRITERIA FOR SELECTION OF PATIENTS MOST LIKELY TO BENEFIT FROM

LIVER TRANSPLANTATION

ACETAMINOPHEN TOXICITY

PH< 7.3 regardless of grade of encephalopathy

PT > 100 sec (INR >6.5) & creatinine > 300
umol/L (in patients with grade 3-4
encephalopathy

VIRAL HEPATITIS/DRUG REACTION

PT > 100 sec (INR >6.5 regardless of grade of

encephalopathy)
or....

CRITERIA FOR SELECTION OF PATIENTS MOST LIKELY TO BENEFIT FROM

LIVER TRANSPLANTATION

VIRAL HEPATITIS/DRUG REACTION

Any 3 of the following regardless of the grade of

encephalopathy)
1. age <11 & >40
2. duration of jaundice before the onset of
encephalopathy> 7 days
3. cause : non-HepA, non-HepB, halothane
hepatitis, idiosyncratic drug reaction

4. PT > 50 sec (INR > 3.5)

5. serum bilirubin > 300 umol/L (> 17.5 mg/dl)

CHRONIC LIVER FAILURE

CIRRHOSIS

CIRRHOSIS

Hepatic fibrosis

Nodular regeneration

Etiology

Pathogenesis

Clinical manifestations

CIRRHOSIS

Cirrhosis & portal hypertension negative

impact on the outcomes of nontransplant
surgical procedures

ULTRASOUND

ULTRASOUND

Coarsened
echotexture

Enlarged Left lobe

COMPUTED TOMOGRAPHY SCANS

CHILD-TURCOTTE-PUGH CLASSIFICATION

CHILD-TURCOTTE-PUGH
CLASSIFICATION

PORTAL HYPERTENSION

PORTAL HYPERTENSION

WHVP or direct portal venous pressure that is

>5 mmHg greater than the inferior vena cava
(IVC) pressure,
a splenic pressure of >15 mmHg,
or a portal venous pressure measured at
surgery of >20 mmHg

A portal pressure of >12 mmHg is necessary for

varices to form and subsequently bleed.

Etiology

Pathophysiology

Clinical manifestations

Clinical manifestations

Cruveilhier-Baumgarten murmur

Veins of Retzes- retroperitoneal

SURGICAL CONCERNS

Encephalopathy

Ascites

Variceal bleeding

VARICEAL BLEEDING
Prevention of bleeding

improvement of liver function (i.e., abstention from

alcohol),

avoidance of aspirin and NSAIDs,

propranolol or nadolol (nonselective beta blockers)

prophylactic endoscopic variceal ligation (EVL)

medium to large varices,

every 1 to 2 weeks until obliteration,

Esophagogastroduodenoscopy (EGD) 1 to 3 months

later
Surveillance EGD every 6 months

VARICEAL BLEEDING
Management of bleeding

ICU for resuscitation

Blood resuscitation to a hemoglobin level of ~ 8 g/dL. Overreplacment of
packed red blood cells and the overzealous administration of saline
rebleeding and increased mortality.

fresh-frozen plasma and platelets

short-term prophylactic antibiotics : ceftriaxone 1 g/day IV is often given.

Vasopressin, administered IV at a dose of 0.2 to 0.8 units/min,

Somatostatin and its analogue octreotide (initial bolus of 50 g IV followed by

continuous infusion of 50 g/h) also cause splanchnic vasoconstriction.
EGD & EVL

Even when aggressive pharmacologic and endoscopic therapies are

initiated and these treatment options are maximized, 10 to 20% of
patients with variceal bleeding will continue to bleed. Shunt therapy,
with either surgical shunts or TIPS, has been shown to control
refractory variceal bleeding in >90% of treated individuals. Shunt
surgery usually is considered only in patients with preserved hepatic
function (i.e., CTP class A); TIPS is used in patients with
decompensated liver disease (i.e., CTP class B or C). However, the use
of these treatment options is dependent on local expertise.

Balloon tamponade using a Sengstaken-Blakemore tube will control

refractory variceal bleeding in >80% of patients. However, its
application is limited due to the potential for complications, which
include aspiration and esophageal perforation. Therefore, use of a
Sengstaken-Blakemore tube should be limited to short-term therapy
(<24 hours) in those patients awaiting definitive care.

TRANSJUGULAR INTRAHEPATIC
PORTOSYSTEMIC SHUNT

Control variceal bleeding in

>90% refractory to medical
treatment
Complications : bleeding,
infection, renal failure,
decreased hepatic function,
hepatic encephalopathy

PORTOCAVAL SHUNT
Eck fistula

high incidence of
hepatic
encephalopathy
decreased liver
function
makes subsequent
hepatic transplantation
much more technically
difficult

MESOCAVAL SHUNT

technically easier
does not adversely
affect subsequent
hepatic
transplantation.

higher incidence of
shunt thrombosis and
rebleeding

DISTAL SPLENORENAL (WARREN)

Used most often

lower rate of hepatic
encephalopathy and
decompensation,
not interfering with
subsequent hepatic
transplantation

DISTAL SPLENORENAL (WARREN)

Used most often

lower rate of hepatic
encephalopathy and
decompensation,
not interfering with
subsequent hepatic
transplantation

SUGIURA PROCEDURE

In patients with
extrahepatic portal
vein thrombosis
and refractory
variceal bleeding

BENIGN SOLID LIVER TUMORS

CYSTIC DISEASES OF THE LIVER

Congenital cysts

Biliary cystadenoma

Polycystic liver disease

Caroli's disease

LIVER INFECTIONS

Pyogenic liver abscess

Amoebic liver abscess

Hydatid Disease

Ascariasis

Schistosomiasis

Viral hepatitis

The most common source of liver abscess is the biliary tree in

patients with cholecystitis, choledocholithiasis, or cholangitis
Less common sources include other intra-abdominal processes,
such as appendicitis or diverticulitis, and hematogenous spread from
sources such as an infected heart valve or the oral cavity a the
vascular route is associated with multiple abscesses
The right hepatic lobe is affected more than twice as frequently as
the left, due to vascular anatomy
Aspiration of abscess fluid and subsequent culture guide antibiotic
choice
Failure to culture pathogenic organism(s) may be due to prior
antibiotic treatment or inadequate anaerobic culture
Treatment includes antibiotics and often either percutaneous or
surgical drainage/debridement, depending on the size, number, and
complexity of the abscess(es)

Less common sources include other intra-abdominal processes, such as

appendicitis or diverticulitis, and hematogenous spread from sources such as an
infected heart valve or the oral cavity
Amebic liver abscess should be considered in endemic areas or patients who
have been to the tropics
Fungal microabscesses are seen primarily in patients with compromised
immune systems
Rarely, liver abscess may be due to trauma, secondary infection from an
amebic abscess or a necrotic malignant hepatic tumor, or direct extension from
local structures

Common pathogens include Streptococcus spp., Escherichia coli, Klebsiella,

and Bacteroides spp. Polymicrobial infections occur in 15% to 20% of patients;
approximately the same percentage have multiple abscesses

Amebic liver abscess follows vascular spread of Entamoeba histolytica

from the colon in patients with the intestinal infection amebiasis. Amebic
abscesses may be very large; they contain aspirate with 'anchovy-sauce'
color and consistency
Liver abscess in a child suggests immunocompromise

A single abscess is the most common presentation; spread to the liver via
the vascular route is associated with multiple abscesses
The right hepatic lobe is affected more than twice as frequently as the
left, due to vascular anatomy
Aspiration of abscess fluid and subsequent culture guide antibiotic
choice
Failure to culture pathogenic organism(s) may be due to prior antibiotic
treatment or inadequate anaerobic culture
Treatment includes antibiotics and often either percutaneous or surgical
drainage/debridement, depending on the size, number, and complexity of
the abscess(es)

MALIGNANT LIVER TUMORS

3rd most common cancer mortality

Risk factors : Hep B, Hep C, Cirrhosis, aflatoxins, flukes

Inc serum AFP in 55-95%

Resection if :

Single lesion < 5 cm, up to 3 lesions each < 3 cm

Childs A & B

No portal hypertension

Tumor recurrence : 70% at 5 years