Hepatic Encephalopathy

2199 Words Jan 21st, 2016 9 Pages
Hepatic Encephalopathy

Name________

Directions:

Gender: Male

Age: 47

Setting: Hospital

Ethnicity: African American

Preexisting Conditions: Cirrhosis secondary to alcohol hepatitis, hypertension, esophageal varices

Coexisting Conditions:

Disability: Unemployed (on disability) for past four years

Socioeconomic: Married, father of two boys (ages 19 and 17 years old), history of drinking one quart of hard liquor each day for three years prior to diagnosis of cirrhosis

Pharmacologic: Lactulose (Cephulac), neomycin sulfate (mycifradin sulfate)

Client Profile: Mr. Escobar is a 47-year old male with a history of cirrhosis. He lives with his wife and teenage sons. His wife brought him to the emergency department
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Ammonium is absorbed in the intestines. It is used to create bicarb using carbon dioxide and oxygen. The bi-product that is left is ammonia. It is excreted as urea. When there is cirrhosis in the liver, the urea cycle cannot occur normally. This may be due to hepatocyte death or issues with circulation caused by portal hypertension. When the circulation is compromised, the liver is unable to remove toxins from the bloodstream and convert the ammonia to urea. Thus, causing a buildup of ammonia and toxins in the the bloodstream. This buildup of toxins interferes and worsens brain function. This would be observed more with decompensated liver function where liver function is impaired and manifestations of liver failure are present. In compensated cirrhosis, there is still some liver function still occurring. Therefore, there are four stages that occur with hepatic encephalopathy. All are directly related to the decreased function of the liver (Ignatavicius, 2013, pg 1295).

3. Upon initial examination, the HCP did not note any asterixis. What asterixis, and how did the HCP assess Mr. Escobar for this condition?

Asterixis is a tremor seen in patients with hepatic encephalopathy due to the buildup of ammonia in the brain. The HCP would ask the patient to extend their arms and dorsiflex both wrists. In a patient with no liver damage or asterixis, the hands would remain still. In a patient with hepatic encephalopathy that shows signs of asterixis, the