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Hepatic Encephalopathy
in End-Stage Liver Disease
Megan Dudley
End of Life Care for Adults and Families
The University of Iowa College of Nursing
Definition:
Hepatic Encephalopathy is a
reversible impairment of cognitive
function, or level of consciousness
in patients with liver disease.
Houlston and O’Neal (2009)
Why liver disease causes Hepatic
Encephalopathy
 When the liver is damaged over a long period of time (by such things as cirrhosis
or alcohol abuse), the liver forms scar tissue that replaces it’s normal soft tissue.
This causes two things to occur:

The scarred tissue makes it difficult for blood to travel through the liver causing an
increase of blood pressure within the veins in and around the liver, this is known as
portal hypertension.

The scarred tissue makes it difficult for the liver to filter toxins within the body.
When the liver is unable to filter toxins or when it is difficult for blood to
travel through the liver, toxins build up within the blood and may travel to
your brain.
American Liver Foundation (2015)
Pathophysiology of H.E.
There are three main theories of how hepatic encephalopathy is developed:
 Ammonia Theory:
 The damaged liver is unable to eliminate ammonia so it is carried in the blood stream to
the brain and the CNS.
 Ammonia has a toxic affect on cells in the CNS by causing structural and functional
damage.
 Neurotoxic effects can cause a change in brain function by inhibiting the metabolism of
amino acids and the use of energy in the brain.
Houlston and O’Neal (2009)
Pathophysiology of H.E.
cont.
 Gamma-amino butyric acid (GABA)/benzodiazepine theory:
 Gamma-amino butyric acid (GABA), is an inhibitory neurotransmitter that has a
calming effect.
 GABA, which is usually broken down in the liver can build up if the liver is
damaged.
 If an excess amount of GABA travels to the brain it can cause neuroinhibition.
 This may result in a decreased level of consciousness and impaired motor
function.
Houlston and O’Neal (2009)
Pathophysiology of H.E.
cont.
 False neurotransmitter theory:
 False neurotransmitters that are byproducts of the damaged liver are
produced
 These byproducts inhibit neurotransmission in the brain by replacing true
neurotransmitters
Dong and Ho, (2009)
Classification of H.E.:
The West Haven Criteria
Houlston and O’Neal (2009)
Grade 1




Trivial lack of awareness
Euphoria or anxiety
Shortened attention span
Impaired performance of addition
Grade 2
•
•
•
•
•
Lethargy or apathy
Minimal disorientation for time or place
Subtle personality change
Inappropriate behavior
Impaired performance of subtraction
Grade 3
•
•
•
Somnolence to semi-stupor, but responsive to verbal stimuli
Confusion
Gross disorientation
Grade 4
•
Coma (Unresponsive to verbal or noxious stimuli)
Precipitating Factors of H.E.:
 Sepsis or infection
 Constipation
 GI Bleeding
 Fluid and Electrolyte imbalances
 Use of sedatives
 Alcohol withdrawal
Houlston and O’Neal (2009)
Treatment of H.E.
 Treat the precipitating factor
 Reduction of the production and absorption of ammonia:
 Synthetic disaccharides such as lactulose
 Oral antibiotics to change the GI microflora
 Probiotics to improve flora in the gut
Bleibel and Al-Osaimi (2012)
Ongoing and Supportive Care:
 Ongoing neurological assessment
 Recognizing Symptoms
 Reorientation
 Fall Prevention
 Protein restriction no longer recommended
Houlston and O’Neal (2009)
Things to remember about H.E.
From the American Liver Foundation
 HE occurs in people with cirrhosis or
another type of severe liver disease
 HE seems to be caused by toxins that
build up in the blood and then reach
the brain
 Symptoms of HE can be both mental
and physical
 HE can start slowly, symptoms may not
be noticed at first.
 HE will not get better on its own.
Symptoms will get worse without
treatment
 Treatment for HE aim to control the
condition, improve well being and
quality of life and keep people out of
the hospital. Hospital admissions for HE
can be lengthy and costly.
 Lactulose and antibiotics are used to
treat HE and prevent toxins from
building up.
 With timely and proper treatment, the
progression of HE can be slowed and
sometimes even stopped.
American Liver Foundation(2012)
Information about HE from the
American Liver foundation:
http://he123.liverfoundation.org/
References:
American Liver Foundation. (2012). Living with hepatic encephalopathy [Brochure]
N.P.:n.p. available from: http://he123.liverfoundation.org/wpcontent/uploads/2013/05/Hepatic-Encephalopathy-Brochure-English-2012.pdf
Bleibel, W., Al-Osaimi, A.M.S., (2012). Hepatic encephalopathy. The saudi journal of
gastroenterology, 18(5), 301-305. doi: 10.4103/1319-3767.101123
H.E. 123. (2015). What is hepatic encephalopathy? (2015). Retrieved from:
http://he123.liverfoundation.org/what-is-he/the-connection-between-he-and-liverdisease/
Houlston, C., O’Neal, H., (2009). Hepatic encephalopathy. S. Sargeent (Ed.), Liver
diseases: An essential guide for nurses and health care professionals (pp. 79-89). doi:
0.1002/9781444322682