Decompensated

Liver Cirrhosis
M. Dzikrul haq, MD
Emergency Medicine Kediri General Hospital

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:

1) Viral Hepatitis B, C.
2) Alcoholic liver disease.
3) Non-alcoholic fatty
liver disease (NAFLD).
4) Autoimmune hepatitis.
5) Primary biliary
cirrhosis.
6) Secondary biliary
cirrhosis (associated
with chronic
extrahepatic bile duct
obstruction).
7) Primary sclerosing
cholangitis.
8) Hemochromatosis

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

Causes of hepatic decompensation:

Alkalosis.
Hypokalemia.
GIT bleeding.
Hypotension.
Hepatotoxic drugs.
Infection.
Diuretic therapy.
General anesthesia.
Surgery and general anesthesia place the
cirrhotic liver at risk for decompensation.
Why? Anesthesia reduces cardiac output,
induces splanchnic vasodilation and causes
a 30-50% in hepatic blood flow.

Pathophysiology 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.

2) GIT:
Portal hypertension: defined as a
pressure gradient of > 10 mmHg between
the portal vein and IVC. It is a major
contributory factor for ascites and
esophageal varices.
Variceal Bleeding
Ascites: as a result of portal HTN. It is a
transudate in nature with protein
concentration less than 2.5 mg/dL.
SBP: appears to be caused by the
translocation of GI tract bacteria across the
gut wall and also by the hematogenous
spread of bacteria. The most common
causative organisms are Escherichia coli,
Streptococcus pneumoniae, Klebsiella, and
other gram-negative enteric organisms.
C/P: abdominal pain, fever, leukocytosis,

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.
May be caused by an imbalance between renal
vasoconstrictors (eg. Angiontensin, ADH, NE)
and vasodilators (eg. PGE2, PGI2, ANF). Plasma
levels of vasoconstrictors are elevated resulting in
decreased renal perfusion. NSAIDS inhibit PG
synthesis and hence potentiate renal
vasoconstriction with a resulting drop in
glomerular filtration. Thus the use of NSAIDS is
contra indicated in patients with decompensated
cirrhosis.
It is diagnosed by:
Creatinine clearance < 40 ml/min
Serum creatinine > 1.5 mg/dL
Oliguria urine volume < 500 ml/day
Urine Na < 10 mlEq/L

4) Pulmonary:
(A) Hepato-pulmonary Syndrome
(HPS)

This is the presence of abnormal

intrapulmonary vascular dilatation that can
cause profound hypoxemia and can be very
difficult to treat. It may be explained by
decreased hepatic clearance of endogenous
vasodilators (eg. NO).
HPS is marked by the symptom of platypnea
(shortness of breath occurring more in the
upright position) and othrodeoxia (O2
desaturation occurring more in the upright
position).
It can be diagnosed by echocardiography. Pts
are diagnosed when their PaO2 is less than 70
mmHg. Some cases may be corrected by liver
transplantation and pts may receive a speedy

(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.
It results from excessive pulmonary
vasoconstriction and vascular remodelling
that eventually leads to right-heart failure.
It is also diagnosed by Doppler
echocardiography.
Many liver transplantation programs rule out
the presence of PPHTN in pts on the transplant
waiting list. Pts who develop PPHTN require
aggressive medical therapy in effort to stabilize
PAP and decrease perioperative mortality

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).
It is believed to be caused by the passage of neurotoxins
which bypass hepatic detoxification and reach the brain
via porto-systemic shunting. Neurotoxins include shortchain fatty acids, mercaptans, false neurotransmitters
(eg, tyramine, octopamine), ammonia (NH3), and
gamma-aminobutyric acid (GABA). Patients may have
altered brain energy metabolism and increased
permeability of the blood-brain barrier.
Today it is believed that neurosteroids may play a key
role in hepatic encephalopathy. They are elevated in
patients with encephalopathy and are capable of binding
to their receptor within the neuronal GABA receptor
complex and can increase inhibitory neurotransmission.
Acute encephalopathy occurs in fulminating hepatic
failure. There is cerebral edema and increased ICP.

Symptoms are graded on the following scale:

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.

 Diagnosis of hepatic encephalopathy :

a) Elevated free serum ammonia level.
b) EEG: shows non-specific high amplitude low frequency
waves and triphasic waves.
c) CT scan and MRI of the brain may be necessary in
ruling out intracranial lesions. In acute encephalopathy
brain edema may be seen.

Common precipitating factors:

Renal failure, GIT bleeding, infection, constipation,

increased dietary protein intake. Opiates,
benzodiazepines, anti-depressants and anti-psychotics
may also worsen encephalopathy. Hypokalemia and
alkalosis (due to vomiting or excessive use of K-losing
diuretics) increase solubility of NH3 thus increase its
passage across the blood brain barrier.

Differential diagnosis of encephalopathy (other

causes of coma):

Intracranial lesions (intracranial hge, tumour, abcess),

infections (meningitis, encephalitis), metabolic

encephalopathy (hypoglycaemia, uremia, electrolyte
imbalance), alcoholic encephalopathy, post-seizure
encephalopathy.

6) Blood:

Anemia: may result from folic acid

deficiency, hemolysis, hypersplenism, or

GIT bleeding.
Thrombocytopenia: usually is
secondary to hypersplenism and
decreased levels of thrombopoietin.
Coagulopathy: results from decreased
hepatic production of coagulation
factors. Decreased vitamin K absorption
results in reduction of Vit-K-dependent
factors: II, VII, IX, and X. Patients with
cirrhosis also may experience
fibrinolysis and DIC.

7) Metabolic changes:
Fasting hypoglycemia: due to reduced glycogen
stores.

Electrolytes:
Na and water retention: occurs 2ry to relative

hypovolemia and 2ry hyperaldosteronism.

Dilutional hyponatremia: occurs due to increased
ADH, 2ry hyperaldosteronism, impaired renal handling
of free water and decreased dietary Na.
Hypokalemia: due to diuresis and 2ry
hyperaldosteronism.
Hyperkalemia: may occure due to the use of Ksparing diuretics, renal failure and metabolic acidosis.
Hypomagnesemia: due to poor dietary intake,
intestinal malabsorption hyperaldosteronism and
diuretic therapy.

 Acid base disorders:

Respiratory alkalosis: due to
hyperventilation 2ry to ascites and
hepatopulmonary $ (most common).
Metabolic alkalosis: due to K-losing
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.

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).

Moemen Modified Classification of Liver Disease:

Scoring Points

Variables
1)
Encephalopath
y
2) Ascites

2 (Class B)

3 (Class C)

I, II

III, IV

Mild

Moderate,
severe

4.0-5.0

> 5.0

3.5-2.8

< 2.8

1-4

>4

130-120

< 120

1.5-2.5

> 2.5

1 (Class A)

3) Serum
bilirubin
< 4.0
(mg/dL)
4) Serum
> 3.5
albumin (g/L)
5) Prothrombin
Time prolonged
0
(seconds)
6) Serum
Sodium
> 130
(mmol/L)
7) Serum
creatinine
< 1.5
(mg/dL)
The
surgical risk is classified
8) Leucocytic
mild
moderate
count(9-10 points), <
10
3

according to the scoring points

(11-14
severe (15-2
10-12 points) and
> 12

Treatment

(1) ttt of GIT bleeding (variceal bleeding):

Upper GIT endoscopy to exclude other causes of

hematemesis as peptic ulcer and gastritis.

Gastric lavage through a NG tube using cold saline.
Replacement of blood loss by IV fluids and blood products
(anti-shock measures).
Vasopressin infusion (or its analogue Terlispressin):
IV infusion: 0.3-0.8 units/min
Localised infusion into Superior mesenteric artery
(identified by selective arteriography): 0.15-0.2
untis/min
Balloon tamponade by Sengstaken-Blakemoore,
Minnesota tubes.
Emergency sclerotherapy.
IV nitroglycerin and propranolol can decrease portal
pressure.
Octreotide:somatostatin analogue that acts as intestinal
vasocontrictor.
H2 Blockers: eg. Ranitidine

(2) ttt of Encephalopathy:

Treatment of the precipitanting factors of hepatic

encephalopathy (eg. metabolic disturbances, GI
bleeding, infection, constipation).
Lactulose is a nonabsorbable disaccharide that
stimulates the passage of ammonia from tissues into
the gut lumen and inhibits intestinal ammonia
production.
Other cathartics, including colonic lavage also may
be effective in patients with severe encephalopathy.
Neomycin and other antibiotics (eg. metronidazole,
oral vancomycin) serve as second-line agents. They
work by decreasing the colonic concentration of
ammoniagenic bacteria. Neomycin dosing is 2501000 mg orally 2-4 times daily.
Rifaximin is a nonabsorbable antibiotic that can
decrease colonic levels of ammoniagenic bacteria,
with resulting improvement in symptoms of hepatic
encephalopathy.
Flumazenil: a benzodiazepine receptor antagonist
that has been tried successfully in hepatic
encephalopathy.

(3) ttt 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.

(4) Nutrition of hepatic patient:

Caloric requirements:
25-30 Kcal/Kg/day of normovolemic BW.

Protein requirements:
Ptn restriction is controversial but still routinely
implemented (esp. in pts with TIPSS).
Amount: 40-60 g/day or 0.8g/kg/day ( of
normovolemic BW).

Type: rich in branched chain (non-aromatic)

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.

(5) Avoidance of heaptotoxic

medications:
Medications associated with druginduced 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.

(6) Analgesia in patients with hepatic

failure:
Although high-dose acetaminophen is a wellknown hepatotoxin, most hepatologists permit
the use of acetaminophen in patients with
cirrhosis at doses up to 2 g/d.
NSAID use may predispose patients with
cirrhosis to develop GI bleeding. Patients with
decompensated cirrhosis are at risk for NSAIDinduced renal insufficiency, because of
prostaglandin inhibition and worsening of renal
blood flow.
Opiate analgesics are not contraindicated
but must be used with caution in patients with
preexisting hepatic encephalopathy.