CASE REPORT

54 year old gentleman presents to his GP with

increasing swelling of his abdomen and feet
over the last 2 months. He has been
increasing tired over this time and feels
nauseous and is off his food. His wife has
commented that his eyes have turned yellow
over the last few days. He works in a
warehouse and smokes 10 cigarettes a day.
He admits to drinking 4 cans of lager a night.
His wife says he drinks at least 8 cans a
night and a bottle of whisky a week.
On examination he is jaundiced but has no
hepatic flap and is orientated in time, place
and person. His abdomen is distended but
soft and non-tender. There is no palpable
organomegaly but there is shifting dullness.

DIFFERENTIAL DIAGNOSES
Decompensated Alcoholic liver
disease
Viral liver disease
Autoimmune liver disease, Wilsons,
HH etc
Hepatocellular Carcinoma
Pancreatic Cancer
Cryptogenic Liver Cirrhosis

Decompensated
Liver Cirrhosis

DEFINITION
Cirrhosis is defined
histologically as a diffuse
hepatic process characterized
by fibrosis and the conversion
of normal liver architecture into
structurally abnormal nodules

CAUSES OF LIVER
CIRRHOSIS
Viral Hepatitis B, C.
Alcoholic liver disease.
Non-alcoholic fatty liver
disease (NAFLD).
Autoimmune hepatitis.
Primary biliary cirrhosis.
Secondary biliary cirrhosis
(associated with chronic
extrahepatic bile duct
obstruction).
Primary sclerosing
cholangitis.
Hemochromatosis

 Wilson disease.
Alpha-1 antitrypsin deficiency.
Granulomatous disease (eg,
sarcoidosis).
Type IV glycogen storage
disease.
Drug-induced liver disease
(eg, methotrexate, alpha
methyldopa, amiodarone).
Venous outflow obstruction
(eg, Budd-Chiari syndrome,
veno-occlusive disease).
Cardiac cirrhosis: chronic
right-sided heart failure,
tricuspid regurgitation

SIGNS AND SYPTOMS

CAUSES OF HEPATIC
DECOMPENSATION
Alkalosis.
Hypokalemia.
GIT bleeding.
Hypotension.
Hepatotoxic drugs.
Infection.
Diuretic therapy.
General anesthesia.

PATH PHYSIOLOGY AND CLINICAL

PICTURE OF LIVER CELL FAILURE:
1) Liver:
Hyper-bilirubinemia (d.t secretory
function of the liver).
Hypo-albuminemia (d.t synthetic
function) tissue edema, ascites,
pleural effusion.
Elevated liver enzymes as a result of
hepatocellular damage.

STAGES OF LIVER DAMAGE

 2) GIT:
Portal hypert
Variceal Bleeding
Ascites:
SBP
3) Renal: Hepato-renal Syndrome

It is the occurrence of acute

renal dysfunction in patients
with preexisitng liver failure in
the absence of primary renal
disease.

4) PULMONARY
A) Hepato-pulmonary
Syndrome (HPS)
This is the presence of abnormal
intrapulmonary vascular
dilatation that can cause
profound hypoxemia

(B) Porto-pulmonary
hypertension (PPHTN)
PPHTN is defined as the
presence of a mean PAP
greater than 25 mmHg in
the presence of normal PCWP.
and can be very difficult to
treat.

5) CNS changes: Hepatic

encephalopathy
Hepatic encephalopathy is a
syndrome marked by
personality changes,
intellectual impairment, and a
depressed level of
consciousness occurring as a
result of diversion of portal
blood into the systemic
circulation (porto-systemic
shunting).

PATHOPHYSIOLOGY OF
HEPATIC ENCEPHALOPATHY

GRADES OF HEPATIC
ENCEPHALOPATHY
Grade 0 - Subclinical; normal mental status,
but minimal changes in memory,
concentration, intellectual function,
coordination.
Grade 1 - Mild confusion, euphoria or
depression, decreased attention, slowing of
ability to perform mental tasks, irritability,
disorders of sleep pattern (ie. inverted sleep
cycle).
Grade 2 - Drowsiness, lethargy, gross
deficits in ability to perform mental tasks,
obvious personality changes, inappropriate
behaviour, intermittent disorientation
(usually for time). Diminished short term
memory and concentration. Asterixis on
physical examination.
Grade 3 - Somnolent but arousable, unable
to perform mental tasks, disorientation to
time and place, marked confusion, amnesia,
occasional fits of rage, speech is present but
incomprehensible.
Grade 4 - Coma, with or without response
to painful stimuli.

6) BLOOD:
Anemia:
Thrombocytopenia
Coagulopathy
7) Metabolic changes:

Na and water retention

Hypokalemia:
Dilutional hyponatremia
Hyperkalemia
Hypomagnesemia

CHILD-TURCOTTE-PUGH
CLASSIFICATION:

Child-Turcotte-Pugh Scoring System for

Cirrhosis (Child Class A=5-6 points,
Child Class B =7-9 points, Child Class
C=10-15 points).

Acid base disorders:

Respiratory alkalosis: due to

hyperventilation 2ry to ascites
and hepatopulmonary $ (most
common).
Metabolic alkalosis: due to Klosing diuretics,
hyperaldosteronism, or
vomiting.
Metabolic acidosis: in renal
failure

8) CVS changes:
Hyperdynamic circulatory state due
to:
Peripheral vasodilation by
endogenous vasodilators that
bypass hepatic metabolism (NO
and glucagon).
Portal and systemic shunts.
s

OF GIT BLEEDING
(VARICEAL BLEEDING)

TREATMENT

Endoscopy
Gastric lavage
anti-shock measures
Vasopressin infusion
Balloon tamponade
Emergency sclerotherapy
IV nitro-glycerine and
propranolol
Octreotide
H2 Blockers:

TREATMENT OF
ENCEPHALOPATHY
Lactulose
colonic lavage
Neomycin
Rifaximin
Flumazenil

TREATMENT OF

HEPATORENAL $:

Expansion of intravascular volume with

albumin & FFP. Proper hydration.
Avoid nephrotoxic drugs as:
aminoglycosides, cyclosporine and
contrast dyes.
Mannitol to prevent renal failure.
Hemodialysis.
Liver transplantation: kidney
function usually recovers when
patients with cirrhosis and hepatorenal
syndrome undergo liver
transplantation.
If end stage renal failure develops
combined liver-kidney
transplantation is needed.

NUTRITION OF HEPATIC
PATIENT:
Caloric requirements:
25-30 Kcal/Kg/day of normovolemic BW.

Protein requirements:
Ptn restriction is controversial but still
routinely implemented).
Amount: 40-60 g/day or 0.8g/kg/day
(of normovolemic BW).
Type: rich in branched chain (nonaromatic) amino acids.
Some studies support that parentral
ptn carries less risk of encephalopathy
since not converted by colonic bacteria
into NH3.

Micronutrients: Thiamine, folic

acid, Mg, Zn.

AVOIDANCE OF
HEAPTOTOXIC MEDICATIONS:

Medications associated with

drug-induced liver disease
include:

NSAIDs
Isoniazide
valproic acid
Erythromycin
amoxicillin-clavulanate
Ketoconazole
chlorpromazine

Aminoglycosides are
considered obligate
nephrotoxins in patients with
cirrhosis and should be avoided.

ANALGESIA IN PATIENTS
WITH HEPATIC FAILURE
Acetaminophen
NSAID
Opiate