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Running head: NURSING CARE FOR HEPATIC ENCEPHALOPATHY
Nursing Care For Hepatic Encephalopathy
Miranda Liang
April 24, 2016
University of New Hampshire
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NURSING CARE FOR HEPATIC ENCEPHALOPATHY
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In the United States, alcoholism is a major problem facing the population today.
An estimated 70% of adults in the United States drink alcohol, with 10% of them being
heavy drinkers and 5-10% alcohol-dependent (Robinson, 2015). It is the most widely
abused drug in the US. This substance is so addictive because it produces a general,
nonselective reversible depression of the central nervous system. Alcohol abuse is a
dangerous field because it is a drug that affects almost every part of the body. With
chronic alcohol use, some of the major consequences are gastritis, esophagitis, recurrent
pancreatitis, and most commonly, hepatitis and cirrhosis. Some other effects are
cardiomyopathy, sexual dysfunction, peripheral neuropathy, Korsakoff’s and Wernicke’s
syndrome, and leukopenia and thrombocytopenia. In the intoxication phase, some
symptoms are disinhibition, mood lability, impaired judgment, impaired social or
occupational functioning, slurred speech, incoordination, nystagmus, and unsteady gait.
Chronic alcoholism is characterized by a progressive and physical dependence on
alcohol, with withdrawal symptoms present in the absence of it (RN Mental health
nursing, 2013).
What makes alcoholism potentially life threatening is a complication of liver
disease that often occurs with liver failure called hepatic encephalopathy. Another name
for this is portosystemic encephalopathy. A patient with hepatic encephalopathy may
show no signs and symptoms but will have abnormalities in neurological assessments.
The pathophysiology behind this is that with chronic alcoholism, the liver, progressively
damaged by alcohol, is unable to detoxify the byproducts of metabolism, causing a build
up of ammonia in the blood. When ammonia enters the brain, it causes stimulation of
gamma-aminobutyric acid (GABA), a neurotransmitter that causes depression of the
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central nervous system causing sleep and behavioral changes, and in some severe cases,
coma (Hinkle & Cheever). Hepatic encephalopathy also causes portosystemic shunting,
which is the development of collateral vessels as a result of portal hypertension. The
collateral vessels allow the portal flood that is filled with toxins and unfiltered by the
liver to enter the systemic circulation, going to the brain and exaggerating the
neurological deficits (Carey, 2014).
Patients suffering with hepatic encephalopathy are a common and complicated
population often seen on medical surgical floors and in intensive care units.
Winningham’s book Critical Thinking Cases in Nursing covers a case study on hepatic
encephalopathy and the course of treatment for this acute illness. The case study will be
examined here, and the scenario is:
“John Doe, approximately 50 years old, is admitted to your unit for
observation from the emergency department (ED) with the diagnosis of rule out
hepatic encephalopathy with acute alcohol intoxication. This man was sent to the
ED by local police, who found him lying unresponsive along a rural road.
Examination and x-ray studies are negative for any injury, and you are awaiting
the results of the blood alcohol level and toxicology tests. He has no identification
and is not awake or coherent enough to give any history or to answer questions.
He is lethargic, has a cachectic appearance, does not follow commands
consistently, and is mildly combative when aroused. He smells strongly of alcohol
and has a notably distended abdomen and edematous lower extremities. He has a
Foley catheter and an IV of D5½NS with 20mEq KCl and 1 ampule of
multivitamins infusing at 75 mL/hr.
John Doe’s admission orders are:
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IV D5½NS with 20mEq KCl at 75 mL/hr; add 1 ampule multivitamins to 1L of
IV fluid per day
Insert Salem Sump NG tube and attach to low continuous suction
Insert Foley catheter to gravity drainage
Elevate HOB at 30-45 degrees at all times
Check all stools for occult blood
Lactulose (Cephulac) 45mL PO qid until diarrhea
Abdominal ultrasound in AM
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Vitamin K (AquaMEPHYTON) 10 mg/day IV or PO (when alert and able to
swallow) x3 doses
Vitamin B1/thiamine 100 mg/day IV; change to PO when alert and able to
swallow
Vitamin B9/folic acid 0.4 mg/day IM
Vitamin B6/pyridoxine 100 mg/day PO
Labs: CBC with differential, BMP, LFTs, PT/INR and PTT, serum ammonia now
and in AM
Once patient is alert and able to swallow, may have low-protein diet. Observe for
any difficult swallowing, and offer assistance with meals if needed
Call house officer for any sign of GI bleed; delirium tremens; systolic BP over
140 or less than 100 mmHg; diastolic BP less than 50 mmHg; or pulse over 120
beats/min,” (Harding, Snyder, Preusser, & Winningham, 2013).
With this long list of orders, sometimes it is necessary for a registered nurse (RN) to
ease the workload and delegate certain tasks to nursing assistive personnel (NAP), as
long as these tasks are within their scope of practice. One of the above orders that can be
delegated to the NAP is positioning John Doe, by elevating the head of bed to 30 to 45
degrees. They can also alert the RN when stools are passed so they can be tested for
occult blood. NAP can also ensure a low-protein diet when receiving meals for John Doe,
as well as assisting with feeding if any difficulty swallowing is present. Lastly, they can
take vital signs on John Doe and notify the RN when any of the findings are out of the
expected parameters specified in the orders.
Some of the lab work drawn in the emergency department have come back. The
blood alcohol level is 320 mg/dL, and the blood ammonia level is 155 mcg/dL. His total
protein is 5.2 g/dL and albumin is 2.1 g/dL. This blood alcohol level is excessively high,
indicating John Doe has a significant amount of alcohol in his system. His blood
ammonia level is also excessively high, indicating his liver is not working correctly to
convert ammonia into its healthy byproducts and ammonia ends up in the blood. It
excites and stimulates GABA, the neurotransmitter that depresses the central nervous
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system, therefore causing John Doe to be drowsy. His protein level is low, showing that
alcohol has prevented the ability of his body to absorb proteins. Lastly, his low albumin
level indicates his body has the inability to main blood volume. Albumin plays an
important role in keeping the fluid from the blood from leaking out into the tissues.
The medication that would be most helpful with the elevated ammonia levels is
Lactulose (Cephulac), an ammonium detoxicant and osmotic laxative. The breakdown of
lactulose to organic acids by colonic bacteria acidifies colonic contents, thereby
subsequently inhibiting diffusion of ammonia back to the blood. It also enhances the
diffusion of ammonia from blood into the gut, where it is converted to ammonium
(Weber, 1996). Lactulose traps and expels the high levels of ammonia in the feces. Two
to three soft stools per day are expected, but excessive watery diarrhea is a sign of
overdose. Because it is a laxative, it is a perfect treatment for John Doe since constipation
can further exaggerate the effects of encephalopathy. While receiving Lactulose, the
patient will be closely monitored for hypokalemia and dehydration, which explains why
John Doe is receiving an intravenous infusion of dextrose 5% half normal saline with
potassium chloride as a supplement.
John Doe has a multitude of vitamins ordered. Due to his significant reduction in
food intake during his stay in the hospital, it is reasonable to conclude that these were
ordered to replenish necessary vitamins needed for regular functioning. Also, it is highly
likely that his diet prior to hospitalization was not providing adequate nutrition. In
cirrhosis, there is a decreased production of clotting factors due to deficient absorption of
vitamin K from the gastrointestinal tract because the liver cells are impaired and cannot
use vitamin K to make prothrombin. The absorption of other vitamins is also impaired
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from the decreased secretion of bile salts into the intestine (Hinkle & Cheever). John Doe
needs vitamin supplements to meet one hundred percent of his dietary allowance because
the stress of a lack of vitamins can further exaggerate his liver damage.
The case study progresses further:
“While you get John Doe settled, you continue your assessment.
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Neurological findings: PERRL (Pupils Equal, Round, Reactive to Light),
moves all extremities, but patient is sluggish, pulling away during assessment,
and follows commands sporadically.
Cerebrovascular findings: Pulse is regular but tachycardic without
adventitious sounds. All peripheral pulses are palpable, with 3+ bilateral and
3+ pitting edema in lower extremities.
Respiratory assessment: Breath sounds decreased to all lobes, no adventitious
sounds audible, patient not cooperating with cough and deep breathing, and
SaO2 at 90% on room air.
GI assessment: Tongue and gums are beefy red and swollen, abdomen is
enlarged and protuberant, girth is 141 cm, and abdominal skin is taught and
slightly tender to palpation. His Salem Sump NGT is patent, connected to
LCS with small to moderate greenish drainage; bowel sounds positive with
NGT clamped.
Genitourinary (GU) assessment: Foley to gravity drainage, with 75 mL dark
amber urine since admission (2 hours).
Skin: Pale on torso and lower extremities; heavily sunburned on upper
extremities and head. Skin appears thin and dry. Numerous spider angiomas
are found on the upper abdomen with several dilated veins across abdomen.
Vital signs: 120/60, 104, 32, 99.1 degrees F (37.3 C),” (Harding, Snyder,
Preusser, & Winningham, 2013).
The spider angiomas found are characteristic of alcoholic liver disease. Spider
angiomas are small lesions with tiny blood vessels radiating away from the center. They
are a result of neovascularization and the development of collateral vessels. The blood
pressure is so high in the portal vein that these tiny vessels are created and they transport
the toxic, unfiltered blood to systemic circulation. The dilated abdominal veins come
from resistance from the increased blood pressure from portal hypertension. Peripheral
edema is a result of John Doe’s low albumin levels, activating the renin-angiotensin-
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aldosterone-system (RAAS), causing the kidneys to retain salt and water. His distended
abdomen is another result of the portal hypertension and indicates ascites (Hinkle &
Cheever). The common cause of all these problems is portal hypertension, the abnormally
high blood pressure in the portal vein. This is the vein that brings blood from the intestine
to the liver.
John Doe’s distended abdomen is called ascites. It is caused by fluid that leaks
across the endothelium causing abdominal swelling. This is a result of both increased
pressure in the vein system and the development of collateral vessels, as well as his low
level of albumin, the protein responsible for maintaining blood volume and preventing
leakage. With portal hypertension, the blood being delivered to the liver meets resistance
and the pressure rises. Collateral blood vessels dilate, and blood is redirected away from
major organs and increased blood flow goes to the liver. The kidneys interpret this as a
low blood pressure and activate the RAAS further, and the retained water leaks out of the
vessels, causing ascites. The way to assess this is to inspect first, looking for signs of
injury, bruises, wounds, skin texture, and prominent veins. Next, the abdomen should be
auscultated before palpation and percussion because the external pressure can cause a
change in bowel sounds. Palpation detects pain and tenderness, while percussion detects
the accumulation of fluid. Percussion starts with the patient lying supine, and the free
fluid in the abdomen will collect around the flanks due to gravity. Next, the patient is
positioned on his/her side, and the fluid should move to the front of the abdomen and air
will be percussed at the top. This is called shifting dullness and presence of it indicates a
positive test for ascites. Nursing interventions include administering prescribed diuretics
and restricting sodium intake. Diuretics most commonly used are spironolactone and
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furosemide. Expected weight loss is about one to two pounds a day with careful
monitoring of electrolytes and renal functioning before administration. It is also essential
for nurses get daily weights of the patient at the same time of day wearing the same
amount of clothing for consistency, (Lee & Grap, 2008). Limiting sodium is a
controversial subject, because hyponatremia, a low sodium level in the blood, is a
common potential complication for this specific population of patients. As stated by
Fullwood and Purushothaman, “salt should be restricted to 70-90 mmol/day. This equates
to a non-added salt diet rather than the more traditional recommendation of a low salt diet
of 22-40 mmol/day. The traditional regimen has been found to compromise protein and
calorie intake in a patient group that is already experiencing malnutrition as a result of
chronic liver disease, and therefore is no longer recommended,” (Fullwood &
Purushothaman, 2014).
John Doe’s nutritional status is especially concerning because alcohol interferes
with the ability to absorb vitamins, and alcoholics typically have bad diets to begin with.
Objective findings indicating his poor nutrition are that he is sluggish and only follows
commands sporadically, and he has edema in lower extremities, a beefy red and swollen
tongue and gums, taut abdominal skin tender to palpation, dark amber urine, and pale,
thin, dry skin. It is evident he is malnourished and dehydrated by his poor skin quality
and concentrated urine. The most significant assessment factor is his abnormal
neurological status that is characteristic with a thiamine deficiency. Inadequate thiamine
can lead to beriberi, polyneuritis, and Wernicke-Korsakoff psychosis, a permanent form
of brain damage (Xiong, 2015).
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Although John Doe’s protein levels are low, he still has an order for a low protein
diet. This is because John Doe’s alcoholism has impaired the ability to absorb and digest
proteins. The breakdown of protein actually increases the production of ammonia, and
would therefore exaggerate his hepatic encephalopathy. The high ammonia levels are
responsible for his neurological changes of being sleepy and unresponsive. Although the
science behind it supports a low protein diet, research has been done regarding the
effectiveness of it. Protein restriction could perhaps worsen the nutritional status of a
patient with cirrhosis and may have no resulting improvements in hepatic
encephalopathy. A study was done to see if a low-protein diet for fourteen days resulted
in improvements in neurological status compared to a normal-protein diet in cirrhotic
patients with episodic hepatic encephalopathy. It was found that there was no significant
difference between the two groups, showing that diets with normal protein content could
be safely administered to cirrhotic patients to improve their metabolic status and will not
have any negative effects on hepatic encephalopathy, (Córdoba et.al, 2004). This
randomized study had a population size of only 30, so more research should be done on
this topic to investigate the best protein diet for patients with cirrhosis to ensure proper
nutrition without decreasing neurological function.
When an alcoholic is admitted to the hospital, it is common for nurses to
stereotype and judge them, with remarks like “Why are we wasting time with this
‘wino’? He isn’t worth the time or money. Why don’t they let him die?” In a situation
like this, it is important to remember that as nurses, our responsibility is to treat our
patients rather than passing judgments. In addition, he has not provided a specific history
so we do not know if there is a reason why he is a heavy drinker. Our nursing ethics of
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beneficence, nonmaleficence, and justice require us to do good, avoid harm, and give fair
treatment of all patients, regardless of their condition and social habits.
A nursing problem relative to John Doe’s care is the possibility of injury.
Ensuring safety is a priority when caring for a person who might be withdrawing from
alcohol. Because of his excessive alcohol abuse, his body has built up a tolerance over
time to GABA. When the body is so used to it and the alcohol is stopped abruptly, the
opposite effect of GABA happens, called delirium tremens (DT). DT is alcohol
withdrawal symptoms with an altered mental status and sympathetic overdrive,
characterized by anxiety, tremors, diaphoresis, arrhythmias, irritability, agitation,
tremors, and seizures (RN Mental health nursing, 2013). A calm environment should be
maintained to reduce stimulation. Seizure precautions must be implemented for John Doe
ensuring he has IV access, seizure pads and his bed in the lowest position, and potentially
having a tele-sitter to continuously monitor him. Some medications that can prevent
seizures are benzodiazepines and barbiturates, but they can only be given if there is an
order. Often times, giving benzodiazepines is concerning because of the highly addictive
nature of these drugs, which is especially dangerous in a population already addicted to
alcohol. When used in combination, there is a high risk for toxicity and respiratory
depression (Doyle, Keogh, & Lynch, 2010). Another reason he is at a fall risk is because
he is not alert and oriented and might try to ambulate, even though he is unaware of his
situation. Lastly, his poor nutrition and fluid balance puts him at an even higher risk for
falls. It is important to reorient him as appropriate and prevent dehydration and
malnutrition.
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In monitoring John Doe for signs and symptoms of alcohol withdrawal and DT,
he is restless, has tremors, and a low-grade fever. Some more severe symptoms of DT are
hallucinations, extreme diaphoresis, tachycardia, and vomiting, (Doyle, Keogh, & Lynch,
2010). It is important to educate John Doe of early signs of withdrawal and to report them
to prevent him from developing the more serious symptoms.
Falls are especially important in John Doe because his cirrhosis indicates he has
low clotting factors. If he were to fall, it could cause bleeding that could not stop and puts
him at risk for hemorrhage. In addition, a fall could cause trauma to his face, dislocating
the NG tube hooked up to suction. Lastly, his poor nutrition would cause poor wound
healing, so if he were to sustain a fall, he would have a complicated and lengthy recovery
process with a high risk for infection.
During John Doe’s hospitalization, a staff psychiatrist evaluates him for mental
decline associated with alcohol abuse and dependence, including alcoholic dementia, or
Korsakoff’s psychosis. This is a chronic memory disorder caused by severe deficiency of
thiamine (vitamin B1). Thiamine is essential for glucose use and axonal conduction. The
damaged liver impairs the body’s ability to store thiamine, and low levels restrict the
brain from carrying signals and generating enough energy to function properly.
Wernicke’s encephalopathy often precedes Korsakoff’s psychosis, with symptoms like
confusion, staggering, stumbling, lack of coordination, and abnormal involuntary eye
movements. This is an acute episode. If it develops into Korsakoff’s psychosis, the
patient will have problems learning new information, the inability to remember recent
events, and long-term memory gaps (Xiong, 2015).
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John Doe survives a rocky course of hepatic encephalopathy and near-renal
failure. After 27 days, including a week in the ICU, he is discharged to a drug and alcohol
rehabilitation facility. He is employed as a longshoreman; fortunately, his insurance
covers his month of in-house rehabilitation.
When caring for patients going through alcohol withdrawal, the priority nursing
intervention is safety. These patients are at a high fall risk because of their changes in
neurological status, high risk for seizures, sympathetic overdrive and withdrawal
symptoms, and poor nutritional status. They should be closely monitored and re-oriented
appropriately. Medications can be given to prevent seizures, but must be carefully
administered to prevent addiction and overdose. More research should be done to
investigate the most beneficial diets for this population in terms of protein and sodium
restrictions. Electrolyte and vitamin supplements are a crucial part in their recovery
process too because an adequate balance is necessary for proper functioning. After
ensuring the patient is safe and stable, it is important to provide education on the
multitude of effects that alcohol has on the body and what they can do to change their
lifestyles to prevent further hospitalizations related to alcohol.
The patient should be given education and resources on how to quit drinking to
prevent further lasting effects on the body. Although hepatic encephalopathy is an acute
complication, alcoholism is a chronic disease and should be treated as such. There are
some medications that can help with addiction like Disulfiram (Antabuse) that gives
unpleasant side effects when consumed in combination with alcohol. It will condition to
patient to refrain from drinking because negative side effects like flushing, nausea,
tachycardia, and chest pain will occur if it is taken with alcohol. This medication will
NURSING CARE FOR HEPATIC ENCEPHALOPATHY
require follow-ups and counseling to ensure medication compliance. As nurses, we can
also give referrals to support groups like Alcoholics Anonymous and Smart Recovery.
This will allow alcoholics to openly share and listen to others’ journeys related to
alcoholism, providing them with a support system and assuring them that they are not
alone in their struggle. Lastly, it is important to remember that alcoholism is a disease
and should be treated like one. Even though it is easy to pass harsh judgments and
assume John Doe did this to himself, we must be unbiased and provide care to him like
we would to any other sick patient.
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References
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Xiong, G. L. (2015, August 19). Wernicke-Korsakoff Syndrome. Retrieved
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