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By: Michelle Russell Case Study Presentation NUR 4216L 12-4-12 1.

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Presentation on theme: "By: Michelle Russell Case Study Presentation NUR 4216L 12-4-12 1."— Presentation transcript:

1 By: Michelle Russell Case Study Presentation NUR 4216L 12-4-12 1

2  Understand the pathophysiology of hepatic encephalopathy  Recogonize the signs/ symptoms  Understand relevance to clinical setting and patient scenarios 2

3  Hepatic Encephalopathy is a brain disorder that can occur when the liver is unable to remove toxins from the blood  Can be acute or chronic; and range from mild to severe; may progress slowly or rapid  Can be a medical emergency, patients usually hospitalized 3

4  Caused by disorders that affect the liver: Commonly hepatitis or cirrhosis Disorders that cause blood circulation to decrease to the liver 4

5 MILD SEVERE  Breath with a musty or sweet odor  Change in sleep patterns  Changes in thinking  Confusion that is mild  Forgetfulness  Mental fogginess  Personality or mood changes  Poor concentration  Poor judgment  Worsening of handwriting or loss of other small hand movements  Abnormal movements or shaking of hands or arms  Agitation, excitement, or seizures (occur rarely)  Disorientation  Drowsiness or confusion  Inappropriate behavior or severe personality changes  Slurred speech  Slowed or sluggish movement 5

6  Brain swelling  Permanent nervous system damage  Increased risk of heart failure, kidney failure, respiratory failure and sepsis (blood poisoning)  unconscious, unresponsive or coma  Death 6

7  Alcohol intoxication  Complicated alcohol withdrawal  Meningitis  Metabolic abnormalities such as low blood glucose  Sedative overdose  Subdural hematoma  Wernicke-Korsakoff syndrome 7

8  Asterixis “liver flap” Ask patient to hold their hands out in front of them, it will jerk  Neuro examination  CT scan or MRI of head  EEG  Liver function tests  Serum ammonia levels  PT/INR  Potassium/ sodium levels 8

9  Grade 0 - Minimal hepatic encephalopathy, asterixis not present; mild cognitive impairment  Grade 1 - Trivial lack of awareness. Asterixis can be detected.  Grade 2 - Lethargy or apathy. Disorientation. Obvious asterixis.  Grade 3 - Somnolent but can be aroused  Grade 4 - Coma with or without response to painful stimuli 9

10  Life support if in coma  Electrolyte/ fluid balance  Reduce protein level to lower ammonia level- possible long term diet change  Lactulose- prevent intestinal bacteria from creating ammonia 10

11  Can be treatable  Chronic typically gets worse, or comes back  If patient is put into a coma, 8 out of 10 patients die 11

12  Altered level of consciousness  Impaired nutrition  Fluid/ electrolyte imbalance 12

13  Interventions Temporarily decrease protein intake and increase carb intake Intestinal cleaning to remove nitrogen containing sources as a possible source of ammonia  Lactulose Antibacterials – influence ammonia flora, therefore decrease ammonia level Antipsychotics- theory (still inconclusive) that certain drugs preventing the binding of GABA decrease HE 13

14  Interventions Diagnosis of exclusion Correct underlying cause (if applicable) Lactulose (should be titrated to 3-4 loose stools daily, about 30-60g)  Supports bacterial growth… Antibiotics such as neomycin – lower ammonia levels in gut Establish healthcare proxy Education – recognize S/S, when to notify provider prevent falls, skin breakdown, aspiration 14

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16  A client is admitted with an elevated serum ammonia level and iron- deficiency anemia. The nurse knows this client has some degree of liver failure because: A. The liver is the storage center for iron B. The client is in acute renal failure and liver failure follows C. The liver converts ammonia to the harmless substance of urea D. Both A and C are correct 16

17  D. Both A and C are correct  The liver is the major storage center for iron. The liver is responsible for converting ammonia into urea for excretion by the kidneys. 17

18  A client is admitted with an alteration in neurological status and is in the process of being diagnosed with hepatic encephalopathy. Which of the following is known about this diagnosis? A. It is caused by a build up of urea B. It is caused by the build up of ammonia and protein metabolism malfunction C. reduced cardiac output is the leading cause of death in these clients D. It is caused by carbohydrate metabolism dysfunction 18

19  B. It is caused by the build up of ammonia and protein metabolism malfunction  This is the hallmark symptom of acute hepatic failure. Also termed hepatic coma, this is caused by a buildup of ammonia. Cerebral edema is the leading cause of death in this condition. 19

20  A client with acute hepatitis is prescribed lactulose. The nurse knows this medication will: A. Mobilize iron stores from the liver. B. Remove bilirubin from the blood. C. Prevent the absorption of ammonia from the bowel D. Prevent hypoglycemia. 20

21  C. Prevent the absorption of ammonia from the bowel  Lactulose helps prevent the absorption of ammonia from the bowel because it will cause frequent bowel movements, which facilitates the removal of ammonia from the intestines. 21

22  Exact cause of HE is unknown  It is still inconclusive about ‘correct’ interventions  Recognize S/S and risk factors in patients Change in LOC  Suspected in liver failure patients 22

23  American liver foundation. (2012, July 17). Retrieved from fo/hepaticencephalopathy/  Gerber, T., & Schomerus, H. (n.d.). Hepatic encephalopathy in liver cirrhosis. Disease Management, 1353-1367  Longstreth, G. (2011, October 16). Medline plus. Retrieved from cy/article/000302.htm  Wilson Childers, J., & Arnold, R. M. (2008). Hepatic encephalopathy in end-stage liver disease. Fast Facts and Concepts, 1341-1342  Wolf, D. (2011, March 9). Medscape. Retrieved from overview 23

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