Presentation is loading. Please wait.

Presentation is loading. Please wait.

Nancy Newman RN BSN Contact Nancy Newman Alverno College April 15, 2011 Delirium at End-of-Life: Assessment and Treatment.

Similar presentations

Presentation on theme: "Nancy Newman RN BSN Contact Nancy Newman Alverno College April 15, 2011 Delirium at End-of-Life: Assessment and Treatment."— Presentation transcript:

1 Nancy Newman RN BSN Contact Nancy Newman Alverno College April 15, 2011 Delirium at End-of-Life: Assessment and Treatment When Comfort is the Goal All Images are Microsoft Clip Art

2 Navigation To move to next slide select To return to previous slide select To return to the Menu slide select

3 Menu Navigation What is Delirium at End -of- Life Learner Outcomes Causes of Delirium at End –of- Life Case Study Part One Case Study Part Four Case Study Part Two Drug Toxicity Mental Assessment Tools Systemic Inflammation Case Study Part Three Interventions for drug toxicity Case Study Part Seven Metabolic Imbalances 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

4 Learner Outcomes The learner will be able to assess and identify signs and symptoms of delirium at end-of-life The learner will be able to distinguish between dementia and delirium at end-of-life The 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

5 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 studyhere Microsoft Clip Art

6 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) Microsoft Clip Art

7 What are common causes of delirium at end-of-life? Select answer(s) Metabolic Imbalances Yes, you are very smart! Hypercalcemia, hyponatremia, liver and renal failure may cause delirium at end-of-life. Medications Yes you are right! Drug toxicity can cause delirium at end of life. Brain Metastasis Yes, you are right again! History of Extreme Exercise No, you are incorrect.

8 Other causes of delirium at end-of-life Constipation Urinary retention Spiritual distress Dyspnea Uncontrolled pain Infection

9 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. Microsoft Clip Art

10 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)”.

11 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 Scale Mini- Mental Status Exam Microsoft Clip Art

12 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. Microsoft Clip Art

13 Does Mr. G appear to have delirium at end- of-life or dementia? Select answer Dementia Sorry, try again. Delirium at end-of-life Yes, you are correct. Mr. has had a rapid change in level of consciousness

14 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”. Microsoft Clip Art

15 Is Mr. G. exhibiting signs of hyperactive or hypoactive delirium ? Select answer Hyperactive delirium Yes you are correct Hypoactive delirium Sorry, try again

16 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. Microsoft Clip Art

17 According to Mr. G.’s case study what are potential causes of his delirium at end-of-life ? Select answer(s) UTI You are right again. The symptoms of urinary urgency and frequency could be due to infection Dyspnea Incorrect. Mr. G. has not complained of dyspnea. You are correct that dyspnea can cause terminal restlessness Urinary retention Yes, you are correct, he has urinary urgency and frequency Brain Metastasis You are correct. Mr. G. does have lung cancer with brain metastasis

18 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. Microsoft Clip Art

19 You remember that drug toxicity can cause delirium at end-of-life Microsoft Clip Art

20 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” (, 2011).

21 Morphine-what happens when it is metabolized? Microsoft Clip Art

22 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 herehere Some morphine metabolites may lead to delirium at end-of-life Microsoft Clip Art (Tierney, 2008)

23 Morphine metabolism in the liver Morphine UGT1A1 M-6-G Provides analgesia, sedation UGT2B7 UGT1A1 UGT2B7 M-3-G Causes neuroexcitation and restlessness Normorphine Liver Cell Note. From “Pathway- Codeine and Morphine Pathway” (PK) by PHARMGKB. Copyright 2006. Adapted with permission from PharmGKB and Stanford University.

24 Which morphine metabolite can lead to delirium at end-of-life ? Select answer M-6-G No, M-6-G provides pain relief and sedation M-3-G Yes, M-3-G can cause neurotoxicity and restlessness

25 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)

26 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 Microsoft Clip Art

27 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. Microsoft Clip Art

28 Lorazepam may have paradoxical side effects Lorazepam may increase agitation or cognitive deficits Microsoft Clip Art

29 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) Microsoft Clip Art

30 Medications for hyperactive delirium at end-of-life Haloperidol 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 prn Change 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)

31 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 opioids Yes, 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.

32 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. Microsoft Clip Art

33 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.

34 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. Microsoft Clip Art

35 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) ”. Microsoft Clip Art

36 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 All images on this page are Microsoft Clip Art

37 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. Microsoft Clip Art

38 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). Microsoft Clip Art

39 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. Microsoft Clip Art

40 Some interventions assist to “de- stress” patient and family Some 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).

41 Click on items to find additional nursing interventions Oxygen to decrease dyspnea Fan to decrease dyspnea Frequent Orientation 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 All images on this page are Microsoft Clip Art

42 Metabolic imbalances that may cause delirium at end-of-life Hypercalcemia- Calcium >10.5 mg/dL Due to bone metastasis, dehydration, certain cancers Hyponatremia- Serum sodium <136 meq/L Due 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

43 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) HyponatremiaSerum 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 (,n.d.) *No bloodwork was done on Mr.. due to short prognosis and goals of care

44 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).894

45 Humoral hypercalcemia Malignant cells Secrete PTHrP into circulation Binds with skeletal and renal receptors Increases calcium reabsorption from the bone into the blood Hypercalcemia

46 Which factors can cause hypercalcemia? Select answer (s) Bone Metastasis Yes, you are correct. Dehydration Yes, you are correct. Drinking a glass of milk daily Sorry, try again. Cancer Yes, you are correct.

47 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

48 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).

49 Increase in IL-2 and TNF affects the central nervous system and results in somnolence, malaise, and anorexia INFECTION Inflammatory response is initiated Inflammatory response progresses to systemic inflammatory response Acute-phase response with increased release of IL-2, TNF being produced

50 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 docrinology/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. (2011). Retrieved March 27, 2011 from Ely, E. (2007). CAM/ICU Worksheet. (2007). Retrieved March 27, 2011 from

51 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 MedlinePlus. (2011). Retrieved April 5,2011 from Mini-Mental Status Exam. (n.d.). Retrieved March 27, 2011 from

52 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 althProfessional/page1 National Cancer Institute. (n.d.). Retrieved April 5, 2011 from althProfessional/page3 Nursing Care Plans. (2010). Retrieved March 29, 2011 from cfm?plan=50

53 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 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

54 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 Weissman, D., Anbuel, B., & Hallenbeck, J. Palliative care: A resource guide for physician education, 4 th 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.

Download ppt "Nancy Newman RN BSN Contact Nancy Newman Alverno College April 15, 2011 Delirium at End-of-Life: Assessment and Treatment."

Similar presentations

Ads by Google