Introduction of Disease
Hepatic encephalopathy is a decline in brain function when the blood chemistry is altered due to abnormal levels of electrolytes, amino acids, and excessive ammonia along with other chemicals that affect the central nervous system (Hubert & Meter., 2018). When the liver cannot properly remove toxins from the blood, this will cause a buildup in the bloodstream and ultimately lead to brain damage. According to the text Pathophysiology for the Health Professions “bleeding in the digestive tract due to ingestion of a high protein meal may cause elevated serum ammonia concentration and may precipitate severe encephalopathy” (Wolf., 2019). Hepatic encephalopathy has been characterized by persona changes, psychological impairment and a depressed degree of consciousness.
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There are three stages of hepatic encephalopathy and the first stage is characterized by inverted sleep wake pattern, the second stage is lethargy and personality changes, and the thirds stage is worsened confusion, the final stage is marked by progression to coma (Kahn., 2018). The epidemiology of Hepatic encephalopathy is that is occurs in 30-45 percent of patients with cirrhosis. According to National Center for Biotechnology Information (NCBI) Journal titled Hepatic encephalopathy, “There are approximately 7-11 million cases of HE prevalent in the United States, with approximately 150,000 patients newly diagnosed each year” (Mandiga., 2019).
Etiology and Risk Factors
There are several triggers of HE some of which include gastrointestinal bleeding, constipation, excessive dietary protein intake, dehydration, electrolyte imbalance, infection, consumption of alcohol, analgesics and diuretics consistent with chronic liver disease. Transjugular intrahepatic portosystemic (TIPS) shunt may follow HE in some cases (Mandiga., 2019). According to evidence-based research the root cause of HE is liver failure, however liver failure alone is rare, and is accompanied by other causes in association. The precipitating factors are excessive nitrogen, protein rich diet, GI-bleeding, bacterial peritonitis, renal failure and constipation. Those that are risk for getting HE are those with cirrhosis, HE is not gender specific, and it can occur in people of any age with acute/chronic live disease.
According to the Journal Pathogenesis of Hepatic Encephalopathy hyperammonemia is the main factor responsible for brain abnormalities in HE (Ciećko-Michalska, Słowik, Mach, & Szczepanek., 2012). The pathophysiological process has a lot to do with the substrate ammonia which is considered important for the enzymatic reaction in the brain. Bacteria is what produces ammonia in the gastrointestinal tract which in terms breaks down amino acids, purines and urea, from here the liver clears the excess. However, in advance liver disease there is a decrease in the number of functioning hepatocytes which results in decreased ammonia clearance which leads to hyperammonemia.
Clinical Manifestation and Complications
The clinical manifestations of HE is dependent on the current stages of disease. The signs and symptoms can range from mild to severe. HE is a complication a cirrhosis, and therefore there will be “swelling of the abdomen, spontaneous bacterial peritonitis, bleeding from varices, hepatorenal syndrome, hepatopulmonary syndrome, hypersplenism, and liver cancer” (Cunha., 2019). Many of the signs and symptoms will be very similar with cirrhosis and HE. One will experience fatigue, weakness, itching, jaundice, a loss of appetite and many others. However, HE directly affects the brain and one will experience a change in sleep patterns, memory loss, confusion, a depressed level of consciousness and in severe cases where HE is left untreated the outcome is either coma or even death.
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The Diagnostics test that are done for HE is electroencephalogram (EEG) changes can be observed with hepatic encephalopathy but it is not conclusive for the syndrome, however it is useful in ruling out seizure activity. The paper-and-pencil test, neuropsychometric test, and some computerized test, these tests are done in order to assess attention, processing speed and response inhibition, as well as to identify impairments in visuo-spatial functioning (Nabi & Bajaj, 2014).
- Ciećko-Michalska, I., Słowik, A., Mach, T., & Szczepanek, M. (2012, December 17). Pathogenesis of Hepatic Encephalopathy. Retrieved February 13, 2020, from https://www.hindawi.com/journals/grp/2012/642108/
- Cunha, J. P. (2019, July 3). What Is Cirrhosis of the Liver? Symptoms,Treatment, Causes & Stages. Retrieved February 13, 2020, from https://www.medicinenet.com/cirrhosis/article.htm
- Hubert, R. J., & Meter, K. V. (2018). Goulds pathophysiology for the health professions. St. Louis, MO: Elsevier.
- Kahn, A. (2018, June 14). Hepatic Encephalopathy. Retrieved February 13, 2020, from https://www.healthline.com/health/hepatic-encephalopathy-2
- Mandiga P, Foris LA, Kassim G, et al. Hepatic Encephalopathy. [Updated 2019 Jun 14]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430869/
- Nabi, E., & Bajaj, J. S. (2014, January). Useful tests for hepatic encephalopathy in clinical practice. Retrieved February 13, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918211/
- Wolf, D. C. (2019, November 10). Hepatic Encephalopathy: Definition, Pathogenesis, Clinical Features of Hepatic Encephalopathy. Retrieved January 23, 2020, from https://emedicine.medscape.com/article/186101-overview
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