Hepatic Encephalopathy

As the largest internal organ in the body, the liver is responsible for many functions including iron metabolism, plasma-protein production, and the detoxification of drugs and other materials (Sanders, 2007).  Once the liver fails, it is unable to neutralize toxins, which then start to build up.  These toxins “escape through the intestines and enter the systemic circulation, causing neurochemical changes in the brain.”  These neurochemical changes in the brain, as a result of liver failure, are known as hepatic encephalopathy or portal-systemic encephalopathy.  It is believed that “the accumulation of unmetabolized toxins (primarily ammonia) in the brain, false neurotransmitters, and neuroinhibitory substances are believed to be the main mechanisms of [hepatic encephalopathy]” (de Melo, Charneski, & Hilas, 2008).

Most often hepatic encephalopathy is seen in patients who suffer from cirrhosis of the liver.  In fact, it is estimated that 50-70% of patients who present with hepatic encephalopathy are a result of cirrhosis of the liver.  Besides the patient’s medical history, patients who are suffering from hepatic encephalopathy will also present with signs and symptoms that resemble impairment of the brain (de Melo, Charneski, & Hilas, 2008).  Altered mental status, hepatic coma or coma hepaticum, cerebral edema, and death are commonly associated with hepatic encephalopathy.  Early in the disease process some patients may have a “day-night reversal,” in which the patient sleeps during the day but stays awake at night (Wikipedia).  Some patients may also experience dementia, spastic paraparesis, cerebellar degeneration, or extrapyramidal movement disorders, which the clinician may attribute to another cause besides hepatic encephalopathy (de Melo, Charneski, & Hilas, 2008).  According to Wikipedia, “the hallmark of hepatic encephalopathy on the physical examination is the presence of asterixis;” which is a tremor in the patient’s wrists while patient’s arms are outstretched and the wrist is extended.  Some have said this resembles “a bird flapping its wings” and it is believed this is due to the inability of the liver to metabolize ammonia to urea.  However, asterixis may also be seen in “states such as renal failure and carbon dioxide retention” (Wikipedia).

In the prehospital environment, not much can be done for the treatment of hepatic encephalopathy.  Prehospital treatment is primarily supportive care because treatment is long term through the use of medications and diet, which “focus on the resolution of ammonia accumulation and identification/removal of precipitating factors.”  Currently Lactulose is used in the treatment of hepatic encephalopathy, however other drugs, such as Rifaximin, are being studied for the use in hepatic encephalopathy.  For patients who are being treated using diet, “protein should be restricted and uresase-producing colonic bacteria should be inhibited” (de Melo, Charneski, & Hilas, 2008) (de Melo, Charneski, & Hilas, 2008).

Works Cited

de Melo, R., Charneski, L., & Hilas, O. (2008). Rifaximin for the Treatment of Hepatic Encephalopathy. American Journal of Health-System Pharmacy , 65 (9), 818-822.

Sanders, M. (2007). Mosby's Paramedic Textbook (3rd Edition ed.). St. Louis, Missouri: Elsevier Mosby.

Wikipedia. (n.d.). Asterixis. Retrieved August 4, 2008, from Wikipedia: http://en.wikipedia.org/wiki/Asterixis.

Wikipedia. (n.d.). Hepatic encephalopathy. Retrieved August 3, 2008, from Wikipedia: http://en.wikipedia.org/wiki/Hepatic_encephalopathy.