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 today because she noticed that her husband had increasing confusion and lethargy and was having difficulty walking. His wife states, “ He is probably acting a little fun because he is sleep deprived. He hasn’t slept very much in the past few days.”

Case Study:

Mr. Escobar is afebrile. His blood pressure is 136/68, pulse 88, and respiratory rate 18. His oxygen saturation is 98% on room air. He is awake, alert, and oriented to person only. His speech is slow and he appears tired. The nurse notices a foul odor to his breath. Upon physical examination, he is found to have a slightly distended abdomen. The health care provider (HCP) does not note any asterixis. The HCP requests an abdominal ultrasound, which reveals fatty infiltration of the liver, an enlarged spleen, a polyp in his gallbladder, and a moderate amount of ascites.

Laboratory Results:

CBC

WBC 4.8 cells/mm3

RBC 2.94 million/mm3

Hgb 9.8 g/dL

Hct 28.2%

platelet count 89,000 mm3

Comprehensive metabolic panel

sodium 145 mEq/L

potassium 3.6 mEq/L

chloride 112 mEq/L

carbon dioxide 25 mEq/L

glucose 185

BUN 42 mg/dL

creatinine is 1.6 mg/dL

total protein 5.7g/dL

albumin 3.1 g/dL

total bilirubin 1.8 mg/dL

AST 17 U/L

ALT 14 U/L

LDH 266 U/L

Ammonia 124 umol/L

Coagulation Studies: PT- 13.1 seconds

UA: WNL

Tests: Gastroscopy to rule out any GI bleeding.

IV fluids: D51/2NS is started at 100 ml/hr.

Medication prescribed: Lactulose & Neomycin sulfate.

Nursing Care: Daily weights, strict I&O, monitoring stool for occult blood, neurological assessment every four hours, and low protein, low sodium diet.

Instructions: Please provide detailed answers to the following questions. Please be sure to reference all of your answers. You may use only professional sources as references (if you copy and paste or fail to site your answer(s) you will not receive credit for them). With the exception of the references this does not need to be in APA format.

1. Mr. Escobar has cirrhosis. Discuss the pathophysiology of the disease.

Widespread, scarred connective tissue bands that occur over time and change the structural makeup of the liver (Ignatavicius, Workman, 2013). Toxins or diseases cause destruction and degeneration of liver cells (ignatavicius, 2013). The tissue becomes nodular and restricts blood flow as well as blocking the bile ducts. This causes impairments in blood and lymph flow from compression of the fibrous tissue excessiveness. Early stages of the disease are characterized by liver enlargement. The liver becomes hard and firm. As cirrhosis progresses, the liver will shrink and reduce in function. Liver enzymes such as AST and ALT will begin to elevate with advancement in cirrhosis. Some patients may be asymptomatic until serious damage and progression occurs. There are 3 different types of cirrhosis that can occur.

Postnecrotic cirrhosis occurs with viral hepatitis, drugs, or other toxins.

Laennec’s or alcoholic cirrhosis occurs after chronic alcoholism.

Biliary cirrhosis is caused by chronic biliary obstruction or automimmune disease. (Ignatavicius, 2013, pg 1294).

2. Explain how hepatic encephalopathy is related to cirrhosis.

Disorders such as cirrhosis greatly reduce the function of the liver. 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 hands would have coarse tremors that are rapid, nonrhythmic extensions or flexions in the wrists or fingers. These resemble a bird flap. This motor disturbance is seen in portal systemic encephalopathy. This is be recognized as positive signs of asterixis and is often called a “liver flap or “flapping tremor” (Ignatavicius, 2013, pg 1730).

4. Identify the characteristic clinical manifestations of hepatic encephalopathy consistent with Mr. Escobar’s presentation.

Patient has history of cirrhosis, increasing confusion, lethargy, and is having difficulty walking. Wife states, “He is acting funny because he is sleep deprived and hasn’t slept much in the past few days”. He is oriented only to person, his speech is slow, and he appears tired. He has a foul odor to his breath. (Ignatavicius, 2013, pg 1295).

5. Identify three priority nursing diagnosis for Mr. Escobar (be sure to put them in correct format and that they are priority diagnosis.

1. Risk for hemorrhage R/T esophageal varicies AEB decreased LOC, Decreased RBC’s, Hgb, Hct,Platelets, and enlarged spleen noted on Abdominal Ultrasound

2.Acute confusion R/T hyperammonia secondary to cirrhosis AEB pt is oriented to person only, speech is slow, tired appearance, difficulty walking, wife reports increasing confusion and lethargy.

3.Imbalanced nutrition less than body requirements R/T cirrhosis AEB decreased albumin and protein lab values (Ackley, Ladwig, 2014).

6. Identify which of the client’s admitting laboratory results are abnormal and provide a rationale for why each is above or below the normal range.

Decresed WBC of 4.8 cells/mm3 can be a result of the pre-existing liver disease and enlarged spleen. The decrease in RBC’s (2.94 million, mm3), Hgb( 9.8g/dL), Hct(28.2%), and Plt(89,000 mm3) counts can all be seen in cirrhosis as well as possible bleeds or hemorrhaging. There is a slight increase in Chloride at (112mEq/L) and can be a direct result of the increasing metabolic acidosis resulting from higher levels of ammonia. Glucose is elevated at (185) and could possibly be as a direct result of stress causing increased serum glucose levels. Elevated BUN (42mg/dL) can be a result of a GI bleed, an excessive catabolism of protein, overhydration or dehydration. There is a decrease in total protein (5.7g/dL) and albumin (3.1 g/dL). Albumin is synthesized by the liver and both are direct results of nutrition status. Total bilirubin is also increased (1.8 mg/dL). This elevated number is seen in hepatic damage as well as hemolysis. Bile is formed in the liver and has many components which also include bilirubin. The metabolism of bilirubin begins with the breakdown of RBC’s (Kathleen Pagana, 2013, pg 145).The ammonia levels are also elevated (124 umol/L). This is a direct result of the interruption in the urea cycle. The amounts of ammonia in the bloodstream continue to rise (Kathleen Pagana, 2013).

7. Define ascites. Explain what cause ascites and how the nurse will assess for this condition.

Ascites is the connection of free fluid within the peritoneal cavity caused by increased hydrostatic pressure from portal hypertension. The collection of plasma protein in the peritoneal fluid reduces the amount of circulating plasma protein in the blood. When this decrease is combined with the inability of the liver to produce albumin because of impaired liver cell functioning, the serum colloid osmotic pressure is decreased in the circulatory system (Ignatavicius, 2013 pg. 1294). The result is a fluid shift from the vascular system into the abdomen (Ignatavicius, 2013). The nurse would assess liver function tests and electrolytes (Ignatavicius, 2013). The nurse would also assess for nausea, vomiting, abdominal pain, fatigue, and a significant change in weight (Ignatavicius, 2013, pg 1296). The nurse would inspect for gross asymmetries across the abdomen. The nurse would then assess the flanks for bulging or shifting dullness. The nurse would also assess for a positive fluid wave (http://depts.washington.edu/physdx/liver/tech.html)

8. Mr. Escobar has been prescribed 30 ml of lactulose every six hours and neomycin sulfate, 500 mg four times a day. Explain why each of these medication has been included in the client’s medical management plan. What should the nurse teach Mr. Escobar regarding the potential adverse effects of each medication?

The lactulose prevents absorption of ammonia in the colon by acidifying the stool. The lactulose will help with excreting the ammonia in the stool since it is unable to be converted to urea by the liver. The patient should report diarrhea because it could indicate overdose (Skidmore-Roth, 2015, pg. 677). In hepatic encephalopathy, lactulose can reduce ammonia levels by 25-50% (Skidmore-Roth, 2015). Neomycin was the antibiotic chosen due to the ability to kill intestinal bacteria. This medication inhibits the bacteria from breaking down protein in the intestine so it would not be converted to more ammonia and waste products. This would cause the levels of ammonia to rise even higher (Lehne, 2013). Some adverse reactions can include severe renal damage, bowel obstruction, and ototoxicity (Skidmore-Roth, 2015).

9. When should the nurse anticipate the onset of the effects of the lactulose, and describe the therapeutic effects of lactulose on Mr. Escobar’s bowel pattern. While evaluating the effectiveness of the lactulose what finding would indicate a potential lactulose overdose? If the dose is given rectally for liver damage, the effects on mental status can be seen within 2 hours. If the medication is given orally, therapeutic effect may take 24 to 48 hours. The goal is to have at least 2-3 soft stools per day with this medication. Dosage is based on the medical condition and the response to therapy. Symptoms of overdose may include severe stomach cramps and diarrhea ( WebMD 2005-2015).

10. Provide a rationale for the low protein, low sodium diet the HCP prescribed.

The decreased protein in the diet is needed to reduce the amount of ammonia production. Ammonia is produced with the breakdown of protein. Therefore, lowering the protein of the diet keeps from adding or introducing more ammonia. The low sodium in the diet will keep the fluid retention to a minimum. The goal is to attempt to excrete the high levels of ammonia from the bloodstream. Sodium attracts water and therefore would retain higher levels of ammonia in the bloodstream. So, lowering the sodium intake would in turn keep from retaining as much fluid. Both are beneficial in helping to manage issues with ascites and edema from portal hypertension (Ignatavicius, 2013).

11. A gastroscopy reveals esophageal varices, which are treated with banding. Discuss what esophageal varices are and the banding procedure used to treat them.

Esphogeal varices are caused by portal hypertension. They occur when the thin walled, delicate esophageal vein becomes distended because of increased pressure (Ignatavicius, 2013). If the varices are bleeding, this is considered a life threating emergency. The patient can lose massive amounts of blood. Melena and hematemesis can occur and patient may lose consciousness before any bleeding is observed (Ignatavicius, 2013). The banding procedure called EVL or endoscopic variceal ligation involves application of small “O” bands around the base of varices to decrease the blood supply to the varices (Ignatavicius, 2013, pg, 1302).

References

Betty Ackley, G. L. (2014). Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care, 10th Edition.

Donna Ignatavicius, M. L. (2013). Medical- Surgical Nursing: Patient Centered Collaborative Care, 7th edition. St. Louis, Missouri: Elsevier.

Kathleen Pagana, T. P. (2013). Mosby's Diagnostic and Laboratory Test Reference, 11th edition. St. Louis, Missouri: Elsevier.

Lehne, R. A. (2013). Pharmacology for Nursing Care, 8th edition. St. Louis, Missouri: Elsevier.

Medicine, U. o. (n.d.). Advanced Physical Diagnosis Learning and Teaching at the Bedside Volume 1. Retrieved from University of Washington Department of Medicine.

Skidmore-Roth, L. (2015). Mosby's 2015 Nursing Drug Reference, 28th edition. St. Louis, Missouri: Elsevier.

WebMD. (2005-2015). Retrieved from WebMD Drugs and Medications: http://www.webmd.com/drugs/2/drug-3367-7202/lactulose-oral/lactulose-oral,rectal/details#overdose