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

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:

References: American Liver Foundation. (2012). Living with hepatic encephalopathy [Brochure] N.P.:n.p. available from: 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), doi: / / H.E (2015). What is hepatic encephalopathy? (2015). Retrieved from: disease/ Houlston, C., O’Neal, H., (2009). Hepatic encephalopathy. S. Sargeent (Ed.), Liver diseases: An essential guide for nurses and health care professionals (pp ). doi: /