1. October 23rd, 2013
Group: F2
Sub-group: C
Hepatic
Encephalopathy

2. Hepatic encephalopathy
• Is a reversible state in patients with
significant liver dysfunction.
• Is a wide range of neuropsychiatric
changes from subtle cerebral
dysfunction to deep coma.

3. Cause
• Accumulation of GIT derived toxins in the
systemic circulation due to impaired
hepatic extraction of these toxins.
• Most of its manifestations appear to be
attributable to a net increase in neuronal
inhibition.
• The pathogenesis is probably multifactorial.

4. Types
• Type A Acute liver failure-associated
hepatic encephalopathy (ALFA-HE)
• Type B Encephalopathy associated with
major porto-systemic bypass without
intrinsic liver disease.
• Type C Encephalopathy in patients with
chronic liver disease/cirrhosis

5. Symptoms of type C
• May present as
 Asymptomatic
 Acute spontaneous or precipitated
 Chronic persistent or fluctuating
 Hepato-cerebral degeneration
• Almost all clinically apparent hepatic
encephalopathy cases occur in patients
with cirrhosis.

6. Staging
• Stage 0 Lack of detectable changes in
personality or behavior. Asterixis absent.
• Stage 1 Trivial lack of awareness.
Shortened attention span. Impaired
addition or subtraction.
Hypersomnia, insomnia, or inversion of
sleep pattern. Euphoria or depression.
Asterixis can be detected.

7. Staging
• Stage 2 Lethargy or apathy. Disorientation.
Inappropriate behavior. Slurred speech.
Obvious asterixis.
• Stage 3 Gross disorientation. Bizarre
behavior. Semistupor to stupor. Asterixis
generally absent.
• Stage 4 Coma.

8. Treatment Goals
• Supportive Care
• Identification and Removal of
Precipitating Factors
• Reduction of Nitrogenous Load From
the Gut
• Assessment of the Need for Long Term
Therapy

9. Treatment options
• Nutritional Management

eg. Protein restriction
• Reduction in the Nitrogenous Load
Arising From the Gut

eg. Bowel cleansing
• Drugs That Affect Neurotransmission

eg. Flumazenil
• Manipulation of the Splanchnic
Circulation