Hepatic Encephalopathy in End-Stage Liver Disease Megan Dudley
End of Life Care for Adults and Families The University of Iowa
College of Nursing 1
Slide 3
Definition: Hepatic Encephalopathy is a reversible impairment
of cognitive function, or level of consciousness in patients with
liver disease. Houlston and ONeal (2009)
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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 its
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)
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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 ONeal (2009)
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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 ONeal
(2009)
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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)
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Classification of H.E.: The West Haven Criteria Houlston and
ONeal (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)
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Precipitating Factors of H.E.: Sepsis or infection Constipation
GI Bleeding Fluid and Electrolyte imbalances Use of sedatives
Alcohol withdrawal Houlston and ONeal (2009)
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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)
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Ongoing and Supportive Care: Ongoing neurological assessment
Recognizing Symptoms Reorientation Fall Prevention Protein
restriction no longer recommended Houlston and ONeal (2009)
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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)
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Information about HE from the American Liver foundation:
http://he123.liverfoundation.org/
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References: American Liver Foundation. (2012). Living with
hepatic encephalopathy [Brochure] N.P.:n.p. available from:
http://he123.liverfoundation.org/wp-
content/uploads/2013/05/Hepatic-Encephalopathy-Brochure-English-2012.pdfhttp://he123.liverfoundation.org/wp-
content/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:
10.4103/1319-3767.10112310.4103/1319-3767.101123 H.E. 123. (2015).
What is hepatic encephalopathy? (2015). Retrieved from:
http://he123.liverfoundation.org/what-is-he/the-connection-between-he-and-liver-
disease/ Houlston, C., ONeal, 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