Nancy Newman RN BSNContact Nancy Newman

@newmannk@courses.alverno.edu

Alverno CollegeApril 15, 2011

Delirium at End-of-Life: Assessment and Treatment When

Comfort is the Goal

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What is Delirium at End -of- Life

Learner Outcome

s

Causes of Delirium at End –of- Life

Case Study

Part One

Case Study

Part Four

Case Study

Part Two

Drug Toxicity

MentalAssessme

ntTools

Systemic Inflamma

tion

Case StudyPart Three

Interventions for drug

toxicity

Case Study Part

Seven

Metabolic Imbalanc

es

Spiritual Distress

Interventions

Other Nursing

Interventions

Case Study

Part Five

Case Study

Part Eight

Case Study

Part Six

Medications for

Delirium at End -of -

Life

Learner OutcomesThe learner will be able to assess and identify signs

and symptoms of delirium at end-of-lifeThe learner will be able to distinguish between

dementia and delirium at end-of-lifeThe learner will understand and identify the

physiology of known causes of delirium at end-of-life

The learner will be able to identify appropriate treatments/nursing interventions for delirium at end-of-life

The learner will be able to identify the impact of stress, genetics and aging on delirium at end-of-life

Do you want to review delirium at end- of-life?

If you don’t want to review delirium at end-of-life, click here to start case study

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What is delirium at end-of-life?

Delirium is an altered level of consciousness characterized by reduced attention and memory, perceptual disturbances (hallucinations and or delusions), incoherent speech, and altered sleep/wake cycles. (Weissman, Anbuel, & Hallenbeck, 2010, p. 56)

Delirium at end-of-life usually occurs in weeks to hours prior to death

Other terms for delirium at end-of-life include terminal agitation, terminal restlessness, and end-stage restlessness

Occurs in 25-85% of cancer patients prior to death (Blanchette, 2005, p.18)

Cause may never be confirmed. May be result of interaction between precipitating factors and other risk factors, and/or by the shut down of different body systems during the dying process (Blanchette, 2005, p. 18)

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What are common causes of delirium at end-of-life? Select answer(s)

Metabolic ImbalancesYes, you are very smart!

Hypercalcemia, hyponatremia, liver and renal failure may cause delirium at end-of-life.

MedicationsYes you are right! Drug

toxicity can cause delirium at end of life.

Brain MetastasisYes, you are right again!

History of Extreme Exercise

No, you are incorrect.

Other causes of delirium at end-of-lifeConstipationUrinary retentionSpiritual distressDyspneaUncontrolled painInfection

Hyperactive or Hypoactive?Hyperactive delirium is characterized by

increased arousal and agitation. Climbing out of bed, pulling out IV lines, foley catheters, picking at air.

Hypoactive delirium is characterized by the patient being more quiet, withdrawn, sleepy, mumbling speech.

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Delirium at end-of-life is NOT dementia “Dementia is a loss of mental ability

severe enough to interfere with normal activities of daily living, lasting more than six months, not present since birth, and not associated with a loss or alteration of consciousness ( THE FREE DICTIONARY BY FARLEX, 2011)”.

Frequently used mental assessment tools

Click on link for examples of frequently assessment tools to determine cognitive status.

Confusion Assessment Method (CAM/ICU)Richmond Agitation-Sedation ScaleMini- Mental Status Exam

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Case Study Part One

Mr. G. is an 80 yo male with stage IV lung cancer with metastasis to brain and bone and renal failure. He is a home hospice patient with a prognosis of 1-2 weeks. The patient and family have identified the goals of care as comfort and no aggressive treatment. He was admitted to the palliative care unit last night for pain control and restlessness. In report you hear that his wife reported that he had not slept the last 2 nights, c/o urge to urinate but only “goes a little bit each time”. He is newly confused with increasing agitation.

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Does Mr. G appear to have delirium at end- of-life or dementia? Select answer

DementiaSorry, try again.

Delirium at end-of-life

Yes, you are correct. Mr. has

had a rapid change in level of

consciousness

Case Study Part Two

You enter the patient’s room to do your assessment. Mr. G. has his feet over the side of the bed and is trying to get out of bed. His hospital gown is off. He has pulled out his IV. You greet Mr. G. and ask him where he is going. He states he has to go to the bathroom. When you try to help him put his gown on, he pushes you away and yells, “Get out of my room or I’ll call the police”.

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Is Mr. G. exhibiting signs of hyperactive or hypoactive delirium ? Select answer

Hyperactive delirium

Yes you are correct

Hypoactive delirium

Sorry, try again

Case Study Part Three

You ask Mr. G. if he needs to go to the bathroom. He says “yes “ and you help him to the bathroom. He voids 50 ml of urine. You assist him back to bed. You ask him if he is having any pain. He denies pain, but winces every time he moves in the bed. You revise your question and ask Mr. G. if he is comfortable. He shakes his head “no”. You notice that Mr. G.’s arms are twitching intermittently.

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According to Mr. G.’s case study what are potential causes of his delirium at end-of-life ? Select answer(s)

UTIYou are right again. The

symptoms of urinary urgency and frequency

could be due to infection

DyspneaIncorrect. Mr. G. has not complained of dyspnea.

You are correct that dyspnea can cause

terminal restlessness

Urinary retentionYes, you are correct, he has urinary urgency and

frequency

Brain MetastasisYou are correct. Mr. G. does have lung cancer with brain metastasis

Case Study Part Four

You quickly review Mr. G.’s admission note and medication list. He has been taking morphine SR 60 mg every 12 hours. In the last 24 hours he has had liquid morphine IR 20 mg orally every 2 hours. You remember that Mr. G.’s arms were twitching. He has no history of seizures.

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You remember that drug toxicity can cause delirium at end-of-life

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Morphine is commonly prescribed at end of life for pain and dyspnea“The principal actions of therapeutic value

of morphine are analgesia and sedation (i.e., sleepiness and anxiolysis). The precise mechanism of the analgesic action is unknown. However, specific CNS opiate receptors for endogenous compounds with opioid-like activity have been identified throughout the brain and spinal cord and are likely to play a role in the expression of analgesic effects” (Drugs.com, 2011).

Morphine-what happens when it is metabolized?

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Morphine is metabolized by the liver.The plasma morphine metabolites are:

Morphine-6-glucuronide (M6G) which binds to mu opioid receptor sites and provides analgesia and sedation

Morphine-3-glucuroinide (M3G) M3G does not appear to have any analgesic properties, nor does it bind to mu opioid receptors. It can cause neuroexcitation, hyperalgesia, allodynia, myoclonus, and terminal agitation (Maluso-Bolton, 2000, p. 12)

To review drug metabolism click here

Some morphine metabolites may lead to delirium at end-

of-life

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(Tierney, 2008)

Morphine metabolism in the liver

Morphine

UGT1A1

M-6-GProvides

analgesia, sedation

UGT2B7

UGT1A1

UGT2B7

M-3-G Causes

neuroexcitation and

restlessnes

s

Normorphine

Liver Cell

Note. From “Pathway- Codeine and Morphine Pathway” (PK) by PHARMGKB. Copyright 2006. Adapted with permission from PharmGKB and Stanford University.

Which morphine metabolite can lead to delirium at end-of-life ? Select answer

M-6-GNo, M-6-G

provides pain relief and sedation

M-3-G Yes, M-3-G can

cause neurotoxicity

and restlessness

Factors that may affect morphine metabolism Age. Morphine metabolites are excreted by the kidney. Renal

function declines with age. “Numerous cross-sectional studies have documented a steady, age-related decline in total renal blood flow of approximately 10% per decade after 20 years of age…(Porth & Matfin, 2009, p. 44)”.

Gender. Some studies have found that morphine has a longer onset and offset in women (Sarton et al., 2000, p. 1253) One study found that elderly women have higher levels of morphine metabolites than elderly men, and a reduced renal clearance.(Wittwer & Kern, 2006,p. E350)

Genetic mutations of the genes of the mu opioid receptor sites may increase or decrease the effectiveness of morphine metabolism. Mutations may cause patients to require a higher dose and/or have increased side effects. Studies continue. (Ross, et al., 2005) (Fujita, et al., 2010)

Interventions

Opioid rotation (changing to a different opioid, i.e.. morphine to hydromorphone) hydration or dose reduction

Renal failure can increase accumulation of morphine metabolites. Hydromorphone or other opioids would be a better choice of medication for patients with renal failure

ALL treatment is based on therapeutic goals for patient and family and how close pt is to death. The benefit of treatment should outweigh the burden of treatment

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Case Study Part Five

The home hospice nurse had recommended lorazepam 0.5-1 mg po every hour prn for restlessness. The wife stated she gave him 2 doses of lorazepam and he had become more agitated with each dose. She thinks he is allergic to lorazepam.

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Lorazepam may have paradoxical side effectsLorazepam may increase agitation or

cognitive deficits

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Medications for hypoactive delirium at end-of-life

Haloperidol PO/IV/SQ 0.5-6 mg every 4-12 hours prn.

Add benzotropine 0.5-1 mg IV (PO TID) for extra pyramidal symptoms (EPS)

Use olanzopine 2.5-5 mg po if continued EPS(Derby & O’Mahony, 2006)

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Medications for hyperactive delirium at end-of-lifeHaloperidol IV/PO/SQ 2-10 mg every 4-12 hours

prn.Add benzotropine 0.5-1 mg IV (PO TID) for extra

pyramidal symptoms (EPS)Add lorazepam 0.5-2 mg every 4 hours for

sedation prnChange lorazepam to chlorpromazine 25-50 mg

IV every 4-12 hours if increased sedation is needed

Change lorazepam to olanzapine if regimen is not tolerated or if EPS are an issue

(Derby & O’Mahony, 2006)

Select the interventions you would perform

Medicate with haloperidol.

Yes, you are correct. Haloperidol is the primary agent for treating terminal

restlessness.

Contact the physician to check on changing

opioidsYes, you are correct.

Mr. G. has renal failure.

Medicate with lorazepam.

No you are incorrect. Lorazepam would be

given only if haloperidol is ineffective.

Contact the physician to check on reducing the dose of

pain medication.No, Mr. G.’s pain is not well controlled.

You wouldn’t want to reduce the dose.

Case Study Part Six

Mr. G. is calmer since you have medicated him with haloperidol and hydromorphone. He allows you to continue your assessment. When you assess his abdomen you find that his abdomen is slightly distended and firm. You can palpate his bladder. Mr. G. mumbles, “I have to go to the bathroom,” as you palpate his abdomen. Mr. G.’s wife reported his last b.m. was 5 days ago.

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Which interventions are appropriate for Mr. G.? Select answer(s)

Insert a foley catheter.

No, do a bladder scan first to ensure

he needs a foley catheter.

Pre-medicate for a rectal exam.

Yes, you should pre-medicate for the

exam.

Turn the bed alarm on.Yes, the bed alarm

should be on. Mr. G. is a fall risk due to his

confusion.

Perform a bladder scan.

Yes, a bladder scan will validate the need for a foley catheter.

Case Study Part Seven

The bladder scan revealed 500 mls urine. You inserted a foley catheter. He had a b.m. after you gave him a suppository. Mr. G. is calmer. You go to lunch and come back to find Mr. G. is restless again. His bed alarm is going off almost continuously. You enter Mr. G.’s room to find him pulling at his gown. He is halfway out of the bed. You are calm and reassuring as you assist him to lay down. You ask him where he is trying to go. Mr. G. replies, “The priest, the priest…” over and over.

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Spiritual or Existential Distress

“ Spiritual distress is an expression of profound disharmony in the person’s belief or value system that threatens the meaning of his or her life (Nursing Care Plans, 2010) ”.

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Click on the pictures below to find nursing interventions to help Mr. G.

Call the

chaplain

Offer to pray with

the patient

Ask his wife

about his spiritual beliefs

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Case Study Part Eight

You told Mr. G.’s wife that he seemed to be asking for a priest. Mrs. G replied that she knew he hadn’t been to church in a long time. She thought he would like to see a priest. You contacted the chaplain department and a priest visited Mr. G. the next day. Mr. G. is on scheduled haloperidol and hydromorphone. He is comfortable and peaceful as he nears the end of his life. His goals of care are being met.

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Palliative sedation/Terminal sedation“Terminal sedation is the use of

pharmacological agents to induce sedation to unconsciousness in order to relieve intractable suffering” (Moluso-Bolton, T. .2000,p.18).

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Treatment in the actively dying patient

Remember, ALL treatment is based on therapeutic goals for patient and family and how close pt is to death. The benefits of treatment should outweigh the burden of treatment.

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Some interventions assist to “de-stress” patient and familySome of the symptoms of terminal

restlessness may indicate the “fight or flight” response of the sympathetic nervous system has been activated

Many nursing non-medication interventions assist to activate the relaxation response of the parasympathetic nervous system (PNS)

“The PNS slows the heart rate, stimulates GI function, promotes bowel and bladder elimination, and contracts the pupil, protecting from excessive light during periods when visual function is not vital to survival” (Porth & Matfin, 2009, p. 1216).

Click on items to find additional nursing interventions

Oxygen to decrease dyspnea

Fan to decrease dyspnea

Frequent Orientati

on

Decrease stimuli, but leave a light

on Gentle touch or light massage

Encourage family to

visit/stay with patient

Reassure the family and

answer questions

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Metabolic imbalances that may cause delirium at end-of-life

Hypercalcemia- Calcium >10.5 mg/dL Due to bone metastasis, dehydration,

certain cancersHyponatremia- Serum sodium <136 meq/LDue to disease process or from side effects

of some diuretics (Blanchette, 2005, p. 20)Note -No lab work was done on Mr. G due to

his short prognosis and goals of care

Common metabolic imbalances that can affect delirium at end-of-life

Hypercalcemia

Serum calcium> 10.5 mg/dL

Caused by bone metastasis, dehydration, certain cancers

Main neurological symptoms due to decreased neuromuscular excitability

Muscle weakness personality change, cognitive dysfunction, disoriented, incoherent speech, coma(National Cancer Institute, n.d.)

Treatment with rehydration, biophosphonates(biophosphonate accumulates in bone and inhibit osteoclast-mediatated bone resorption)(Cleveland Clinic, 2011)

Hyponatremia

Serum sodium < 136 meq/L

May be caused by disease process and dehydration

Main symptoms due to cerebral edema

Fatigue, confusion, decreased consciousness, hallucinations, convulsions, coma, restlessness, (Medline Plus,2011)

Treatment may include rehydration (dependent on cause), fluid restriction, medications dependent on underlying disorder(GlobalRPH.com,n.d.)

*No bloodwork was done on Mr.. due to short prognosis and goals of care

Pathophysiology of malignant hypercalcemia

Osteolytic hypercalcium results from bone destruction by tumor

“Humoral hypercalcemia is mediated by circulating factors secreted by malignant cells without evidence of bony disease.[8,9] It is believed that hypercalcemia results from the release of factors by malignant cells that ultimately cause calcium reabsorption from bone [4]” (National Cancer Institute, 2011).

Humoral hypercalcemiaMalignant

cells

Secrete PTHrP into circulation

Binds with skeletal and

renal receptors

Increases calcium reabsorption from the bone into the blood

Hypercalcemia

Which factors can cause hypercalcemia? Select answer (s)

Bone MetastasisYes, you are correct.

DehydrationYes, you are correct.

Drinking a glass of milk daily

Sorry, try again.

CancerYes, you are correct.

Click on red boxes to see pathophysiology of hyponatremia

Decreased sodium in ECF

Causes water to move into ICF by osmosis

Increased ICF causes swelling in

cell

Edema in brain cells cause

cerebral edema

Cerebral edema causes most of the

symptoms of hyponatremia

The impact of systemic inflammation on delirium at end-of-life

Systemic inflammation may occur when delirium at end-of-life is precipitated by infection

The acute-phase of the inflammatory response includes symptoms of “anorexia, somnolence, and malaise, probably because of the actions of IL-1 and TNF on the central nervous system”( Porth & Matfin, 2009, p.389)

The elderly are at higher risk. Recent studies have shown that with ageing and some forms of pathology there is an “exaggerated CNS response to stress and inflammation results” ( MacLullich, 2008).

Increase in IL-2 and TNF affects the central nervous system and results in somnolence,

malaise, and anorexia

INFECTION

Inflammatory response is

initiatedInflammatory response progresses to systemic inflammatory response

Acute-phase response with increased release of IL-2, TNF

being produced

References Blanchette,H. (2005). Assessment and treatment of terminal

restlessness in the hospitalized adult patient with cancer. MEDSURG Nursing, 14 (1), 17-23.

Cleveland Clinic. (2011). Retrieved April 9, 2011 from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/endocrinology/hypercalcemia/#cesec30

Derby, S., & O’Mahony, S. (2006). Elderly patients. In Betty R. Ferrell & Nessa Coyle (Eds.), Textbook of palliative nursing (pp. 635-657 ). New York, New York: Oxford University Press.

Drugs.com. (2011). Retrieved March 27, 2011 from

http://www.drugs.com/pro/morphine-sulfate.html Ely, E. (2007). CAM/ICU Worksheet. (2007). Retrieved March

27, 2011 from

http://www.mc.vanderbilt.edu/icudelirium/docs/CAM_ICU_worksheet.pdf

References Fujita, K., Ando, Y., Yamamoto, Y., Miya, T., Endo, H., Sunaawa, Y.,

et al. (2010). Association of UGT2B7 and ABCB1 genotypes with morphine-induced adverse drug reactions in Japanese patients with cancer. Cancer Chemotherapy Pharmacology, 65, 251-258.

MacLullich, A., Ferguson, K.,Miller, T., De Rooij,S., &Cummingham, C. (2008). Unravelling the pathophysiology of delirium: A focus on the role of aberrant stress responses. Journal of Psychosomatic Research, 65, 229-238.

McCauley,D. (n.d.). Hyponatremia. Retrieved April 5, 2011 from

http://www.globalrph.com/hyponatremia.htm MedlinePlus. (2011). Retrieved April 5,2011 from

http://www.nlm.nih.gov/medlineplus/ency/article/000394.htmlMini-Mental Status Exam. (n.d.). Retrieved March 27, 2011 from

http://www.nmaging.state.nm.us/pdf_files/Mini_Mental_Status_Exam.pdf

References

Moluso-Bolton, T. (2000). Terminal agitation. Journal of Hospice and Palliative Nursing, 2 (1), 9-20.

National Cancer Institute. (2011). Retrieved April 5, 2011 from http://www.cancer.gov/cancertopics/pdq/supportivecare/hypercalcemia/HealthProfessional/page1

National Cancer Institute. (n.d.). Retrieved April 5, 2011 from http://www.cancer.gov/cancertopics/pdq/supportivecare/hypercalcemia/HealthProfessional/page3

Nursing Care Plans. (2010). Retrieved March 29, 2011 from http://www1.us.elsevierhealth.com/MERLIN/Gulanick/Constructor/index.cfm?plan=50

References Ross,J., Rutter, D., Welsh, K., Joel, S., Goller, K., Wells, A.,et al.

(2005). Clinical response to morphine in cancer patients and genetic variation in candidate genes. The Pharmcogenomic Journal,5, 324-336.

Porth, C., & Matfin, G. (Eds.). (2009). Pathophysiology: concepts of altered health states. Philadelphia: Lippincott Williams & Wilkins.

Richmond Agitation/Sedation Scale. (n.d.). Retrieved March 27, 2011 from

http://www.mc.vanderbilt.edu/icudelirium/docs/RASS.pdf Sarton, E.,Olofsen, E., Romberg, R., den Hartigh J., Kest, B.,

Nieuwenhuijs, D, et al. (2000). Sex differences in morphine analgesia: An experimental study in healthy volunteers. Anesthesiology, 93 (5) 1245-1254.

THE FREE DICTIONARY BY FARLEX. (2011). Retrieved March 23, 2011 from

http://medical-dictionary.thefreedictionary.com/dementia

References

Thorn C., Klein, T., & Altman, R. (2009). Codeine and morphine pathway. Pharmacogenet Genomics ,19 (7), 556-558.

Tierney, K. (2008,September 12). Drug metabolism. [Video file]. Retrieved from http://www.youtube.com/watch?v=2uehdqZzKEM&feature=related

Weissman, D., Anbuel, B., & Hallenbeck, J. Palliative care: A resource guide for physician education, 4th Edition. Medical College of Wisconsin, 2010.

Wittwer,E., Kern, S. (2006). Role of morphine’s metabolism in analgesia: Concepts and controversies. American Association of Pharmaceutical Scientists Journal, 8 (2), E348-E352.