Hepatic Encephalopathy - PowerPoint Presentation

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Hepatic Encephalopathy

By: Michelle RussellCase Study PresentationNUR 4216L12-4-12

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Objectives

Understand the pathophysiology of hepatic encephalopathyRecogonize the signs/ symptoms

Understand relevance to clinical setting and patient scenarios

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What is it?

Hepatic Encephalopathy is a brain disorder that can occur when the liver is unable to remove toxins from the bloodCan be acute or chronic; and range from mild to severe; may progress slowly or rapid

Can be a medical emergency, patients usually hospitalized

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Causes

Caused by disorders that affect the liver:Commonly hepatitis or cirrhosis

Disorders that cause blood circulation to decrease to the liver

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Symptoms

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 confusionInappropriate behavior or severe personality changesSlurred speechSlowed or sluggish movement

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Complications

Brain swellingPermanent nervous system damageIncreased risk of heart failure, kidney failure, respiratory failure and sepsis (blood poisoning) unconscious, unresponsive or coma

Death

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Diseases that masks symptoms

Alcohol intoxicationComplicated alcohol withdrawalMeningitisMetabolic abnormalities such as low blood glucose

Sedative overdose

Subdural hematoma

Wernicke-Korsakoff

syndrome

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Objective findings/ diagnostics

Asterixis “liver flap”Ask patient to hold their hands out in front of them, it will jerk

http://www.youtube.com/watch?v=1yFRzxbJnqQ

Neuro examination

CT scan or MRI of head

EEG

Liver function tests

Serum ammonia levels

PT/INR

Potassium/ sodium levels

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Stages

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

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Treatment

Life support if in comaElectrolyte/ fluid balanceReduce protein level to lower ammonia level- possible long term diet change

Lactulose- prevent intestinal bacteria from creating ammonia

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Prognosis

Can be treatableChronic typically gets worse, or comes backIf patient is put into a coma, 8 out of 10 patients die

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Nursing Diagnosis

Altered level of consciousnessImpaired nutritionFluid/ electrolyte imbalance

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ARTICLE 1: Hepatic encephalopathy in liver cirrhosis

InterventionsTemporarily 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

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ARTICLE 2: Hepatic Encephalopathy in End-Stage Liver Disease

InterventionsDiagnosis 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

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NCLEX style review questions

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Question #1

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

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D is correct

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.

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Question #2

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

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B is correct

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.

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Question #3

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.

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C is correct

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.

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Conclusion

Exact cause of HE is unknownIt is still inconclusive about ‘correct’ interventionsRecognize S/S and risk factors in patients

Change in LOC

Suspected in liver failure patients

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References

American liver foundation. (2012, July 17). Retrieved from http://www.liverfoundation.org/abouttheliver/in 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 http://www.nlm.nih.gov/medlineplus/en cy/article/000302.htmWilson Childers, J., & Arnold, R. M. (2008). Hepatic encephalopathy in end-stage liver disease.

Fast Facts and Concepts, 1341-1342Wolf, D. (2011, March 9). Medscape. Retrieved from http://emedicine.medscape.com/article/186101- overview23Slide24

Thank you!

Questions???

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