Quality Indicators for the Care of Dementia in Vulnerable Elders [PDF]

Dementia, defined as an acquired, persistent impairment in two or more cognitive areas (e.g., frontal executive function

0 downloads 3 Views 110KB Size

Recommend Stories


Toolkit for Dementia Care
If you want to become full, let yourself be empty. Lao Tzu

Developing quality indicators for in-patient post-acute care
Learn to light a candle in the darkest moments of someone’s life. Be the light that helps others see; i

(MSE) in dementia care
Stop acting so small. You are the universe in ecstatic motion. Rumi

Dementia Care
Be who you needed when you were younger. Anonymous

Dementia in New Zealand: improving quality in residential care
If you want to go quickly, go alone. If you want to go far, go together. African proverb

Free Training in Dementia Care Dementia Care Essentials
Don’t grieve. Anything you lose comes round in another form. Rumi

Selecting Indicators for the Quality of Cardiac Care at the Health Systems Level in OECD Countries
Ego says, "Once everything falls into place, I'll feel peace." Spirit says "Find your peace, and then

creating excellence in dementia care
Life isn't about getting and having, it's about giving and being. Kevin Kruse

Idea Transcript


Quality Indicators for the Care of Dementia in Vulnerable Elders Denise G. Feil, MD, MPH, w Catherine MacLean, MD, PhD,wz § and David Sultzer, MD w

Key words: dementia; cognitive screening; quality indicators; health care

D

ementia, defined as an acquired, persistent impairment in two or more cognitive areas (e.g., frontal executive function, language, memory)1 is a leading cause of disability in older adults. Alzheimer’s disease (AD) comprises 55% to 77% of all dementias, whereas vascular dementia (VaD) is the second most common dementia, comprising 15% to 25% of all dementias.2 Although the prevalence of AD is only 2% of persons aged 60 to 64, it rises to approximately 40% in those aged 80 and older.3 The need for dementia care will increase significantly in the next few decades because of the rapid growth of the oldest age groups in the U.S. population.4 The 4.5 million persons with AD in 2000 will almost triple, to 13.2 million by 2050. The cohort aged 85 and older with AD will more than quadruple, to 8.0 million.5 Dementia is the most common reason for placement of older adults in nursing facilities, and the demands for nursing home care will also likely quadruple in this group aged 85 and older.6 Furthermore, in California, the costs of nursing home care for AD are projected to triple by 2040.7 A number of quality indicators (QIs) present new opportunities to forestall cognitive decline and reduce disability and nursing home admission during the course of dementia. Early recognition of cognitive impairment and dementia, followed by intervention, can offer patients and caregivers the opportunity for better quality of life. This article presents a set of indicators to assess the quality of care of patients with dementia. The target patient population is vulnerable elders (VEs), defined as persons aged 65 and older who are at risk for death or functional decline. From the Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, California; wDavid Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California; zRAND Health, Santa Monica, California; and §Programs in Clinical Excellence, WellPoint Inc., Thousand Oaks, California. Address correspondence to Denise G. Feil, MD, MPH, West Los Angeles VA Medical Center, Bldg. 500 3-South, 116-AE, 11301 Wilshire Boulevard, Los Angeles, CA 90073. E-mail: [email protected] DOI: 10.1111/j.1532-5415.2007.01335.x

JAGS 55:S293–S301, 2007 r 2007, Copyright the Authors Journal compilation r 2007, No claim to original US government works

The QIs proposed here do not incorporate exclusions for cases of advanced dementia, which is handled in Assessing Care of Vulnerable Elders (ACOVE) in a uniform fashion across the set of QIs. Refer to ‘‘Application of Assessing Care of Vulnerable Elders-3 Quality Indicators to Patients with Advanced Dementia and Poor Prognosis’’ for exclusions due to advanced dementia or poor prognosis.

METHODS A total of 357 articles were considered in this review: 24 identified using a Web search, 94 through reference mining, and 224 through the ACOVE-3 literature searches. Fifteen additional articles were included after peer review. RESULTS Of the 22 preliminary QIs, the expert panel process judged 16 to be valid (see the QIs on pages S464–S487 of this supplement). Six indicators were rejected, and the expert panel added one QI. The literature summaries that support each of the indicators judged to be valid in the expert panel process are described. Cognitive and Functional Screening 1. IF a VE is new to a primary care practice or inpatient service, THEN there should be a documented assessment of cognitive ability and functional status. 2. ALL VEs should be evaluated annually for changes in memory and function. Supporting Evidence No direct evidence was found that screening for dementia improves clinical outcomes, although medical,8–11 behavioral,12 and social13 interventions early in dementia improve clinical outcomes and provide indirect evidence in support of screening. In addition, early diagnosis may allow patients and families to plan for the future. Cognitive screening tests generally provide better results in populations with a higher risk of dementia, such as VEs.14,15 Examples include the Blessed OrientationMemory-Concentration Test, which is briefer than the Mini-Mental State Examination (MMSE) and performs similarly. Additional tests that are shorter than the MMSE include the 7-Minute Screen, the Memory Impairment Screen,14 and the Mini-Cog,16 which adds a three-item recall to the clock drawing task.

0002-8614/07/$15.00

S294

FEIL ET AL.

The clock drawing test takes several minutes to complete and has better cross-cultural validity than the MMSE. It adds a dimension of executive function and visuospatial function that is missing from some screening tests. In a sample of poorly educated, non-English speakers, the clock drawing test detected dementia with higher sensitivity than the MMSE (85% vs 46%).17 Informant-based questionnaires make use of the caregiver’s observations; can be completed in the waiting room; and improve sensitivity, specificity, and cross-cultural validity of dementia screening. Examples include the Functional Activities Questionnaire, which provides high sensitivity and specificity (90%) and cross-cultural applicability,14,18 and the Informant Questionnaire on Cognitive Decline in the Elderly, which is also highly reliable.19 No evidence was found that screening translated into improvements in clinical outcomes, although the American Academy of Neurology (AAN) recommends specific cognitive screening in ‘‘patient populations with an elevated prevalence of cognitive impairment either due to age or presence of memory dysfunction.’’14,15 The U.S. Preventive Services Task Force,18 the AAN,15 and Kaiser Permanente20 did not support screening asymptomatic individuals for dementia. A systematic review of nine guidelines and consensus statements found that none addressed frequency of cognitive testing. No statement or guideline outlined a procedure to assess the course of cognitive deterioration after the initial cognitive screening.21

Clinical Cognitive Evaluation 3. IF a VE screens positive for dementia, THEN a physician should document an objective cognitive evaluation that tests two or more cognitive domains, BECAUSE a clinical cognitive evaluation will diagnose dementia more precisely by excluding patients without dementia and identifying dementia subtypes. Supporting Evidence The cognitive evaluation identifies deficits in cognitive domains such as attention, memory, language, visuospatial skills, and executive function. The pattern of deficits can help to diagnose a specific dementia type, which can in turn guide treatment. The cognitive evaluation also helps to identify false positives from dementia screening tests and can separate dementia from milder forms of cognitive impairment such as age-associated memory impairment or mild cognitive impairment. Semistructured or structured clinical cognitive evaluations can be performed by combining clinical and neuropsychological assessments. Instruments with generally high sensitivities and specificities for detecting AD include the MMSE with the clock drawing test and the Mattis Dementia Rating Scale, which has a sensitivity of 98% and a specificity of 97%.22 Interview-based techniques, which require an informant, have generally high sensitivities and specificities when scales are applied to populations that are at risk for dementia because of older age or memory loss.14 Examples include the Blessed Roth Scale,23 the Clinical Dementia Rating (CDR) Scale,24 and the Informant Questionnaire on

OCTOBER 2007–VOL. 55, NO. S2

JAGS

Cognitive Decline in the Elderly in combination with an objective measure.25 The AAN specified that neuropsychiatric batteries ‘‘should be considered useful’’ or ‘‘interview-based techniques may be considered in identifying patients with dementia when administered to a population at increased risk of cognitive impairment,’’ 14 such as to VEs. This QI does not require formal cognitive testing; it requires only an objective assessment of individual cognitive domains.

Medication Review 4. IF a VE screens positive for dementia, THEN the physician should review the patient’s medications (including over the counter) for any that may be associated with mental status changes, BECAUSE medications can increase cognitive, physical, or functional disability; hasten decline; or necessitate institutionalization. Supporting Evidence Rates at which drugs are inappropriately prescribed in elderly people range from a high of 40% of nursing home patients to 21.3% of community-dwelling patients.26 Inappropriate drug use or polypharmacy is associated with poor health outcomes, such as risk of hospitalization, nursing home placement, and mortality.27–29 Many prescription drugs may contribute to delirium in a vulnerable older patient, but drugs with anticholinergic and antihistaminic properties, corticosteroids, anti-Parkinson’s agents, opioids, and sedatives or sleep medications are the most commonly implicated.30 Furthermore, adding a new medication to a long-standing regimen may result in drug–drug interactions that affect their metabolism and contribute to new mental status changes.28,31 Alcohol intake may also contribute alone or interact with medications to alter mental status in elderly people.32 A number of guidelines emphasize the importance of reviewing patients’ medications to identify those that may be associated with mental status changes.32 The American Psychiatric Association (APA) Guidelines for Dementia Care recommend medication review to identify polypharmacy-induced dementia.33 Medication Adjustment 5. IF a VE screens positive for dementia and is taking medications that are commonly associated with mental status changes in older people, THEN the physician should discontinue or justify continuing these medications, BECAUSE removing or decreasing medications that affect cognition can improve cognitive status and function in VEs. Supporting Evidence Drugs are reported to be responsible for delirium in 11% to 30% of hospitalized patients, and these drugs may worsen preexisting cognitive impairment.30 In VEs, medicationinduced cognitive impairment is more likely to be a concern, because these patients are older and more likely to experience delirium from their medications; they are also more medically ill and thus more likely to be taking numerous drugs, which may add to their risk for cognitive impairment.30,34

JAGS

OCTOBER 2007–VOL. 55, NO. S2

The APA Guidelines for Dementia Care recommend medication review to identify polypharmacy-induced dementia.33

Neurological Examination 6. IF a VE is newly diagnosed with dementia, THEN a physician should perform a neurological examination that includes evaluation of gait, motor function, and reflexes, BECAUSE positive findings on a neurological examination may identify treatable conditions that cause or exacerbate cognitive impairment or that provide further evidence in support of a dementia subtype. Supporting Evidence No direct evidence has shown that physical and neurological examinations lead to clinical improvement in patients with dementia, although the physical and neurological examination may help to identify medical conditions that, when treated, reverse or improve cognitive impairment.35 Furthermore, focal neurological findings from a neurological examination may suggest a dementia with neurological signs such as VaD, frontal temporal dementia, Parkinson’s disease, or dementia with Lewy bodies. In contrast, the general neurological exam is usually normal in early AD.36 The diagnosis of dementia type can inform treatment. From a review of guidelines and consensus statements in 2000,21 all nine guidelines and consensus statements, including the AAN, Veterans Affairs (VA), American Medical Association (AMA), and National Institutes for Health (NIH),21 recommend a neurological examination. Laboratory Testing 7. IF a VE is newly diagnosed with dementia, THEN a complete blood count, thyroid testing, electrolytes, liver function tests, glucose, blood urinary nitrogen, serum B12, and a syphilis test should be performed, BECAUSE abnormalities in these laboratory tests may identify common and treatable conditions that can manifest as and contribute to cognitive impairment. Supporting Evidence One of the major purposes of laboratory tests is to identify potentially reversible causes of cognitive impairment. Two meta-analyses on ‘‘reversible dementias’’ found rates of 13.2% and a range of 0% to 37.5%.2,37 In VEs who have already undergone cognitive evaluation, a laboratory screening may reveal few reversible cases but may identify comorbid conditions that exacerbate the patient’s existing dementia. For instance, vitamin B12 deficiency is common in older persons,38 and a number of studies show a relationship between cognition and B12. A 7-year observational study of dietary intake of folate and B12 showed that subjects with a higher intake of B12 had a slower rate of cognitive decline.38 Five published guidelines and four consensus statements for dementia recommend complete blood count and thyroid testing as a part of the dementia examination.14,20,21 Seven guidelines and consensus statements recommend liver function tests, electrolytes, calcium, and glucose (updated Canadian Conference on Dementia

DEMENTIA QUALITY INDICATORS FOR VULNERABLE ELDERS

S295

(CCD) Guidelines do not recommend liver function tests), whereas six guidelines and consensus statements recommend blood urea nitrogen to test renal function.21 Nine published guidelines and consensus statements recommended B12 testing, whereas three guidelines21,20,40and the updated CCD Guidelines did not include B12 testing for dementia evaluation. Neurosyphilis presents with cognitive deficits that can persist in up to 77% of treated patients.41 The epidemiology of syphilis has changed significantly in the United States, and current Centers for Disease Control and Prevention reports document increasing rates in several demographic groups.42,43 Five published guidelines and consensus statements including the NIH and the American Association for Geriatric Psychiatry (AAGP) recommend routine syphilis serology testing. The AMA and the AAN recommends syphilis screening only for targeted individuals. The AAN recommends syphilis screening only if the patient ‘‘has some specific risk factor or evidence of prior syphilitic infection, or resides in one of the few areas in the United States with high numbers of syphilis cases.’’43 Neuroimaging is another test recommended in many guidelines, because it can aid in diagnosing specific types of dementias and uncover other causes of cognitive deficits such as tumor, subdural hematoma, stroke, and normal pressure hydrocephalus.44,45 The expert panel judged that neuroimaging of all VEs who are newly diagnosed with dementia should not be set as a minimum standard of clinical care, because numerous conditions in VEs could preclude clinicians from ordering neuroimaging tests. The AAN supports neuroimaging at least once in the course of a dementia evaluation. 15,46,47 Other guidelines support targeted neuroimaging.21,48

HIV Testing 8. IF a VE is newly diagnosed with dementia and has risk factors for human immunodeficiency virus (HIV), THEN HIV testing should be offered, BECAUSE HIV is a communicable disease, and treatment of HIV can potentially slow the rate of or reverse cognitive impairment. Supporting Evidence HIV-related dementia is more common in older adults (aged 50 years) than younger adults (aged 20–39) with HIV, although it is unrelated to duration of HIV-1 infection,49,50 and few of these patients fall into the VE age group. In a study of 16 cognitively impaired patients receiving highly active antiretroviral therapy for 45 months, two no longer met the criteria for AIDS dementia, and nine (56%) no longer met the criteria for cognitive impairment,50 suggesting that treatment can reverse cognitive impairment, although it is unclear whether this outcome applies to VEs. Nonetheless, treatments exist that can potentially improve cognition, and HIV dementia is more prevalent in older adults with HIV than in younger adults with HIV. Four guidelines support targeted screening for HIV.21 The Swedish Consensus on Diseases recommends routine HIV testing as a part of the dementia evaluation, whereas the NIH, the AMA, the VA, and the AAN recommend HIV testing only in targeted populations.21

S296

FEIL ET AL.

Depression Screening 9. IF a VE has newly diagnosed dementia, THEN he or she should be screened for depression during the initial evaluation period, BECAUSE the recognition and treatment of depression will improve symptoms of dementia. Supporting Evidence Depression occurs in 25% of dementia patients and is an independent risk factor for early institutionalization.52 Sertraline was effective in reducing depressive symptoms in AD and improving behavioral disturbances and activities of daily living.53 Five guidelines (National Institute of Neurological and Communicative Disorders and Stroke and Alzheimer’s Disease and Related Disorders Association Work Group (NINCDS), AMA, VA, AAN, U.S. Agency for Health Care Policy and Research)21 and two consensus statements (Swedish and Canadian)21 recommend routine depression assessment with or without additional psychiatric assessment of patients with dementia. For depression, the AAN provides a guideline on the treatment of depression with antidepressants.54 Cholinesterase Inhibitor Discussion 10. IF a VE has been diagnosed with mild to moderate AD, mild to moderate vascular dementia, or Lewy body dementia, THEN there should be a documented discussion with the patient or caregiver about cholinesterase inhibitor (AChI) treatment, BECAUSE these agents have been shown to slow the progression of cognitive and functional decline. Supporting Evidence In most studies of patients with mild to moderate AD, AChIs (donepezil, galantamine, rivastigmine) improved cognitive skill measures and functional abilities over the 6-month to 1-year trial period.8–10,55–58 Some studies also showed improvement in behavior and mood. Overall, clinical improvement is modest, and response varies across individuals. Side effects of AChI treatment may include diarrhea, nausea, and vomiting. These effects are dose related and occur most commonly during initial dose titration. Persons with more advanced AD may also respond to AChIs.59–61 The Food and Drug Administration (FDA) recently approved donepezil for severe AD.62 For the most severely impaired or medically ill patients, ethical and quality-of-life concerns enter more prominently into the decision-making process of prescribing AChIs. Patients with VaD may benefit from AChIs. In one study, donepezil treatment led to improved cognitive and global function in those with VaD.63 Although one review63 suggests that the data are not strong enough to guide treatment, and the FDA has not included VaD as a treatment indication, the Cochrane Collaboration review64 suggests that 3- and 6-month data from two large-scale, randomized, controlled, double-blind, parallel-group trials on possible and probable VaD are sufficient to demonstrate efficacy of donepezil in this patient population. The drug was also well tolerated in this group. Patients with Lewy body dementia, a condition marked by a substantial cholinergic deficit, may also benefit from AChI treatment, with improved function and behavior and

OCTOBER 2007–VOL. 55, NO. S2

JAGS

reduced psychosis.65–67 In addition, the FDA recently approved rivastigmine for the treatment of mild to moderate dementia associated with Parkinson’s disease.68 The Accreditation Council for Continuing Medical Education expert consensus statement on AChIs supports this drug class as the first-line treatment for AD, mixed dementia, VaD, and dementia with Lewy bodies.69 The American Geriatrics Society (AGS) Clinical Practice Committee14 supports AChIs for mild to moderate AD but suggests a small average benefit. The AAN does not support dementia treatment with AChIs because of the modest treatment effect size.54 The 2006 AAGP Position Statement supports the efficacy of AChIs and recommends consideration in mild to moderate AD.70 Memantine, a medication with a different mechanism of action from AChIs, has also been shown to be effective in some patients with dementia. Randomized, controlled trials support memantine’s modest efficacy in measures of cognition and function in patients with moderate to severe AD,71 an indication for which it is FDA approved, although the expert panel determined that a discussion about memantine was not appropriate for an ACOVE QI, because they judged that it would not be considered poor care not to have this discussion with every caregiver and VE with dementia.

Stroke Prophylaxis 11. IF a VE has mild to moderate vascular or mixed dementia, THEN he or she should receive stroke prophylaxis, BECAUSE vascular risk factors and comorbid cerebrovascular disease can worsen cognitive impairment and increase mortality. Supporting Evidence Few clinical trials have been conducted on the cognitive benefit of stroke prophylaxis in patients with dementia and cerebrovascular disease, but because it is known that those who develop poststroke dementia have greater risk of subsequent stroke than those who do not develop dementia,72 stroke prophylaxis should be instituted when clinically indicated. Proactive control of risk factors and stroke prevention in the early stage of poststroke dementia may help maintain cognitive skills and quality of life.73 Specific cerebrovascular risk factor treatment, such as with antihypertensives, lipid-lowering agents, and aspirin, may prevent cognitive decline, but more evidence is needed.74–76 Although some epidemiological studies suggest that lipid-lowering agents may reduce the risk of developing AD and VaD, other prospective cohort studies have shown no effect on risk reduction.77 One study suggested that, in patients with AD, treatment with statins led to improvement on some clinical measures,78 although effects were modest in this preliminary study, and additional data are needed. In a community-based study of subjects aged 85 and older, the calcium channel antagonist nitrendipine prevented cognitive decline better than all other blood pressure–lowering agents combined.79 These results suggest that the effect on cognition may be mediated through calcium channels rather than blood pressure. No consensus statements or guidelines address control of vascular risk factors for patients with dementia. The 2006 AAGP Position Statement on AD supports manage-

JAGS

OCTOBER 2007–VOL. 55, NO. S2

ment of associated vascular brain disease and vascular risk factors and, in those with significant brain vascular disease, recommends that low-dose aspirin therapy or, if appropriate, other forms of anticoagulation be considered to potentially prevent worsening of dementia. They do not support statin treatment for AD but suggest that it may hold promise for prevention of AD.

Caregiver Support and Patient Safety 12. IF a VE with dementia has a caregiver, THEN the patient or caregiver should be given information on dementia diagnosis, prognosis, and associated behavioral symptoms; home occupational safety; and community resources, BECAUSE the patient’s nursing home placement can be delayed and quality of life for the caregiver can be improved through educational interventions and comprehensive support and counseling. Supporting Evidence Three randomized, controlled studies and three intervention studies on cognitive behavioral education, counseling, and support of caregivers and families reduced caregiver stress and depression, reduced patient behavioral disturbances, and delayed institutionalization.13,80–84 Multidimensional treatment is the most effective intervention and has a bigger effect than treating caregiver burden and depression alone, which has an incidence of 48%.85 The AAN Evidence-Based Review54 guidelines support providing education and support services to family caregivers to improve caregiver satisfaction and delay time to nursing home placement. The 2006 AAGP Position Statement70 and the Alzheimer’s Association and AGS Consensus Statement86 recommend establishing a close working relationship with the family caregiver and providing ongoing education about the patient’s course of illness and needs, providing community and other resources, referring to a support group to diminish caregiver distress, and referring to the caregiver’s primary provider for depression evaluation if indicated. Behavioral Symptoms of Dementia 13. IF a VE has dementia, THEN he or she should be screened annually for behavioral symptoms of dementia, BECAUSE these symptoms increase patient morbidity; contribute to physical injury, and may increase the risk of early nursing home admission, caregiver burden, and depression. Supporting Evidence Behavioral symptoms include physical aggression, screaming, restlessness, agitation, wandering, culturally inappropriate behaviors, sexual disinhibition, hoarding, cursing, and shadowing. Additional symptoms include anxiety, depressed mood, apathy, psychosis, hallucinations, and delusions.87,88 Up to 90% of nursing home patients were found to have one or more behavioral symptoms.89 Behavioral symptoms often reflect patient distress and can contribute to physical injury90–92 and need for institutionalization.92,93

DEMENTIA QUALITY INDICATORS FOR VULNERABLE ELDERS

S297

Scales that measure these symptoms include the Neuropsychiatric Inventory,94 the Neurobehavioral Rating Scale,95 the Cohen-Mansfield Agitation Inventory,96 and the Behavioral Pathologic Rating Scale for AD.97 Two guidelines (VA, NINCDS), one consensus statement (Canadian),21 and the 2006 AAGP Position Statement on AD70 recommend assessment for psychosis. 14. IF a VE with dementia has behavioral symptoms, THEN specific target symptoms should be documented and behavioral interventions instituted first or concurrently with pharmacotherapy, or if treating first with a pharmacological intervention, then severe symptoms or safety concerns should be present and documented, BECAUSE targeted treatment provides optimal benefits and minimizes risks to the dementia patient. 15. IF a VE with dementia and behavioral symptoms is newly treated with an antipsychotic, THEN there should be a documented risk–benefit discussion, BECAUSE individual perceptions of risk and benefit may differ, and for some, the risks may outweigh the benefits of treatment.

Supporting Evidence The most common behaviors in mild to moderate dementia include depression, irritability, sleep disturbance, agitation, and anxiety.69,98 Depression is prevalent in 25% of patients with dementia and is an independent risk factor for early institutionalization.52,53 The most common behavioral problems in moderate to severe dementia include agitation, aggression, sleep disturbance, sundowning, wandering, restlessness, irritability, disinhibition, and delusions. Hallucinations and delusions in AD manifest in half of patients by the fourth year of diagnosis.98,99 A review of 43 papers that met the authors’ criteria for patients with ‘‘one or more difficult behaviors’’ found that most studies using a psychosocial approach demonstrated a ‘‘beneficial effect.’’100 Other interventions that showed some statistical improvement included environmental adjustments (adapting, simplifying, or enriching the physical surroundings), activity programs, music and language programs, massage and aroma therapy, light therapy, multidisciplinary teams, and caregiver education studies.100 In patients with marked agitation, behavioral interventions may be insufficient, and pharmacological treatment may be necessary. Identifying specific target symptoms and monitoring the treatment effect is essential, but the efficacy and effectiveness of pharmacological treatment for behavioral symptoms in dementia has recently been challenged. A multisite study of 421 outpatients with AD and behavioral problems or psychosis compared the effectiveness of atypical antipsychotics with that of placebo based on time to medication discontinuation. Olanzapine and risperidone were more effective than placebo (measured according to fewer discontinuations due to lack of efficacy) but not when combined with results showing earlier discontinuation due to side effects in the antipsychotic treatment groups.101 Results from a meta-analysis of pharmacotherapy for neuropsychiatric symptoms in dementia led the authors to conclude that atypical antipsychotic medications are only modestly effective for psychosis or agitation in dementia.102 In addition to modest efficacy and effectiveness, atypical antipsychotic treatment for behavioral disturbances in

S298

FEIL ET AL.

dementia may also have higher health risks in this patient population. Recent meta-analyses indicate that there may be greater risk for stroke103 and mortality104 with antipsychotic treatment. The typical antipsychotics may have a similar greater risk of death,105 although results from meta-analyses need to be interpreted with caution and are not definitive proof of risks from antipsychotics. These are post hoc analyses of combined studies in which study trial selection can be subjective and there can be methodological differences across studies, although results may provide hypotheses for designing prospective studies to test these results. AChIs and memantine may improve behavioral symptoms in some patients,71,106,107 and in one randomized, controlled trial, the patients’ caregivers also demonstrated a reduction in their distress.108 The antidepressants citalopram and trazodone show some evidence of efficacy for psychosis and agitation,109,110 whereas studies of mood stabilizers are inconsistent in their findings.102 Kaiser Permanente20 recommends nonpharmacological and pharmacological treatment of depression and psychosis in dementia and pharmacological treatment of depression and behavioral symptoms of dementia. The AAN recommends pharmacological treatment as standard treatment of agitation or psychosis when environmental manipulation fails and recommends atypical over typical antipsychotics. For depression, the AAN provides a guideline on the treatment of depression with antidepressants.54 The AAGP Consensus Statement86 describes in detail nonpharmacological and pharmacological treatment options for depression and agitation in dementia. The 2006 AAGP Position Statement on AD recommends the involvement of a physician with specific expertise in the pharmacological treatment of behavioral problems and psychosis in AD.70

Driving 16. IF a VE has newly diagnosed dementia, THEN (consistent with state law) the patient should be advised not to drive a motor vehicle, should be referred to the Department of Motor Vehicles to test driving ability, or should be referred to a driver’s safety course that includes assessment of driving ability, BECAUSE patients with dementia are at greater risk of motor vehicle accidents, which increases risk of disability and death to the patient and others. Supporting Evidence Persons with dementia are 2.5 to 4.7 times as likely to be involved in a motor vehicle accident as age-matched controls.111 Standard medical evaluations do not identify older adults who are at greater traffic safety risk. A meta-analysis examined the relationship between specific cognitive tests and driving ability as measured using on-road and non-road tests.111 Global neuropsychological functioning and performance in each major cognitive domain were associated with driving ability, but these studies did not identify the cognitive severity at which an individual is no longer safe to drive.112 Some individuals with early-stage dementia have been shown to be unsafe on driving tests,98,113–115 but not all individuals in this group are at risk, and further testing of driving abilities by departments of motor vehicles is rec-

OCTOBER 2007–VOL. 55, NO. S2

JAGS

ommended.116,117 The AAN recommends that individuals with a CDR of 1.0 and higher pose a significant traffic safety risk and should strongly consider discontinuing driving. For those with a CDR of 0.5, clinicians should reassess dementia every 6 months because of the high likelihood of further cognitive decline.116 Three published dementia guidelines from the APA, the AAGP/Alzheimer’s Association/AGS, and one expert reviewer also support restriction or revocation of driving privileges for patients with dementia.33,86,118 Laws for each state may differ, and some states require the physician to report those with dementia and functional impairment to the Department of Motor Vehicles for evaluation and review of driving privileges.

Restraints 17. IF a VE with dementia is physically restrained in the hospital, THEN the target behavioral disturbance or safety concern justifying the use of restraints should be documented in the medical record and communicated to the patient, caregiver, or guardian, BECAUSE this will promote the appropriate use of restraints and allow identification and correction of inappropriate use of restraints. Supporting Evidence Restraints should be used only when less-restrictive measures have proven ineffective. There are no clinical or observational trials to support the use of restraints for protection of the patient from injury.119 Some studies show an increase in the number of falls when patients are restrained.120–123 In one study, two of the top three indicators that determine restraint use were nursing staff attitudes toward restraint use and the number of behavioral disturbances.124 Two educational intervention studies demonstrated that education had an effect on restraint use.125,126 Thus, restraints are often unnecessarily used, they do not decrease and may possibly increase the risk of injury, and education interventions may positively influence their appropriate use. This indicator is based upon evidence-based protocols from the University of Iowa Gerontological Nursing Interventions Research Center Research Development and Dissemination Core,127,128 the University of California at Los Angeles Medical Center Standards of Care for inpatients,129 the State Operations Manual written by the Department of Health and Human Services,130 the American Medical Directors Association and the American Health Care Association,131 the AGS,132 the Council on Scientific Affairs of the AMA,133 and the recommendations of the AAN Ethics and Humanities Subcommittee.134 The University of Iowa Gerontological Nursing algorithm for restraint use states that, if there is no potential for patient self-injury or injury to others, restraints should not be applied.128 ACKNOWLEDGMENTS We recognize the support of Patricia Smith, who provided technical assistance. This manuscript and its content reflect the views of Dr. MacLean and have not been reviewed or endorsed by her employer, WellPoint Inc.

JAGS

OCTOBER 2007–VOL. 55, NO. S2

Financial Disclosure: The ACOVE project was supported by a contract from Pfizer Inc to RAND. Catherine MacLean has received research funding from the Department of Veterans Affairs, the Arthritis Foundation, and the Agency for Healthcare Research and Quality. She is now employed by WellPoint Inc. David Sultzer reports having received research support from Forest Laboratories and Pfizer; consulting fees from Eli Lilly and Novartis; and lecture fees from Astra-Zeneca, Bristol-Myers Squibb, Forest Laboratories, and Pfizer. Denise Feil has nothing to disclose. Author Contributions: Denise Feil was involved in the study concept, literature review, analysis of data to determine appropriate QIs, and preparation of manuscript. Catherine MacLean was involved in study concept and design, review, and writing and editing of the manuscript. David Sultzer was involved in study concept, literature review, manuscript preparation, and edits. Sponsor’s Role: The funding source had no role in the design, analysis, or interpretation of the study or in the preparation of the manuscript for publication.

REFERENCES 1. Cummings JL, Cole G. Alzheimer disease. JAMA 2002;287:2335–2338. 2. Clarfield AM. The decreasing prevalence of reversible dementias: An updated meta-analysis. Arch Intern Med 2003;163:2219–2229. 3. Small GW. Alzheimer’s disease and other dementing disorders. In: Kaplan HI, Sadock BJ, eds. Comprehensive Textbook of Psychiatry, 6th Ed, Vol. 2. Baltimore, MD: Williams and Wilkins, 1995, p 2562. 4. Aevarsson O, Svanborg A, Skoog I. Seven-year survival rate after age 85 years: Relation to Alzheimer disease and vascular dementia. Arch Neurol 1998;55:1226–1232. 5. Hebert LE, Scherr PA, Bienias JL et al. Alzheimer disease in the US population: Prevalence estimates using the 2000 census. Arch Neurol 2003;60: 1119–1122. 6. Hendrie HC. Epidemiology of dementia and Alzheimer’s disease. Am J Geriatr Psychiatry 1998;6(2 Suppl 1):S3–S18. 7. Fox PJ, Kohatsu N, Max W et al. Estimating the costs of caring for people with Alzheimer disease in California: 2000–2040. J Public Health Policy 2001;22:88–97. 8. Ritchie CW, Ames D, Clayton T et al. Metaanalysis of randomized trials of the efficacy and safety of donepezil, galantamine, and rivastigmine for the treatment of Alzheimer disease. Am J Geriatr Psychiatry 2004;12:358–369. 9. Winblad B, Engedal K, Soininen H et al. A 1-year, randomized, placebocontrolled study of donepezil in patients with mild to moderate AD. Neurology 2001;57:489–495. 10. Rogers SL, Farlow MR, Doody RS et al. A 24-week, double-blind, placebocontrolled trial of donepezil in patients with Alzheimer’s disease. Donepezil Study Group. Neurology 1998;50:136–145. 11. Doody RS, Geldmacher DS, Gordon B et al. Open-label, multicenter, phase 3 extension study of the safety and efficacy of donepezil in patients with Alzheimer disease. Arch Neurol 2001;58:427–433. 12. Ayalon L, Gum AM, Feliciano L, Area´n PA. Effectiveness of nonpharmacological interventions for the management of neuropsychiatric symptoms in patients with dementia. Arch Intern Med. 2006;166:2182–2188. 13. Mittelman MS, Ferris SH, Shulman E et al. A family intervention to delay nursing home placement of patients with Alzheimer disease. A randomized controlled trial. JAMA 1996;276:1725–1731. 14. AGS Clinical Practice Committee. Guidelines abstracted from the American Academy of Neurology’s Dementia Guidelines for early detection, diagnosis, and management of dementia. J Am Geriatr Soc 2003;51:869–873. 15. Petersen RC, Stevens JC, Ganguli M et al. Practice parameter:: Mild cognitive impairment (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56:1133–1142. 16. Borson S, Scanlan JM, Watanabe J et al. Improving identification of cognitive impairment in primary care. Int J Geriatr Psychiatry 2006;21:349–355. 17. Borson S, Brush M, Gil E et al. The clock drawing test: Utility for dementia detection in multiethnic elders. J Gerontol A Biol Sci Med Sci 1999;54A: M534–M540.

DEMENTIA QUALITY INDICATORS FOR VULNERABLE ELDERS

S299

18. U.S. Preventive Services Task Force. Screening for Dementia: Recommendations and Rationale (AHRQ Publication no. 03-520A). Rockville, MD: Agency for Healthcare Research and Quality, 2003. 19. Jorm AF. The informant Questionnaire on Cognitive Decline in the Elderly (IQCODE): A review. Int Psychogeriatr 2004;16:274–293. 20. Kaiser Permanente Care Management Institute’s Dementia Guidelines Workgroup. Guidelines for the Diagnosis and Management of Dementia in Primary Care. Care Management Institute Kaiser Permanente, 2004. 21. Beck C, Cody M, Souder E et al. Dementia diagnostic guidelines: Methodologies, results, and implementation costs. J Am Geriatr Soc 2000;48: 1195–1203. 22. Monsch AU, Bondi MW, Salmon DP et al. Clinical validity of the Mattis Dementia Rating Scale in detecting Dementia of the Alzheimer type. A double cross-validation and application to a community-dwelling sample. Arch Neurol 1995;52:899–904. 23. Blessed G, Tomlinson BE, Roth M. Blessed-Roth Dementia Scale (DS). Psychopharmacol Bull 1998;24:705–708. 24. Juva K, Sulkava R, Erkinjuntti T et al. Usefulness of the clinical dementia rating scale in screening for dementia. Int Psychogeriatr 1995;7:17–24. 25. Fuh JL, Teng EL, Lin KN et al. The Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) as a screening tool for dementia for a predominantly illiterate Chinese population. Neurology 1995;45:92–96. 26. Liu GG, Christensen DB. The continuing challenge of inappropriate prescribing in the elderly: An update of the evidence. J Am Pharm Assoc (Wash) 2002;42:847–857. 27. Frazier SC. Health outcomes and polypharmacy in elderly individuals: An integrated literature review. J Gerontol Nurs 2005;31:4–11. 28. Perri M, Menon AM, Deshpande AD et al. Adverse outcomes associated with inappropriate drug use in nursing homes. Ann Pharmacother 2005;39: 405–411. 29. Klarin I, Wimo A, Fastbom J. The association of inappropriate drug use with hospitalisation and mortality: A population-based study of the very old. Drugs Aging 2005;22:69–82. 30. Moore AR, O’Keeffe ST. Drug-induced cognitive impairment in the elderly. Drugs Aging 1999;15:15–28. 31. Preskorn SH, Silkey B, Shah R et al. Complexity of medication use in the Veterans Affairs healthcare system: Part I: Outpatient use in relation to age and number of prescribers. J Psychiatr Pract 2005;11:5–15. 32. Patterson CJ, Gass DA. Screening for cognitive impairment and dementia in the elderly. Can J Neurol Sci 2001;28(Suppl 1):S42–S51. 33. Practice Guideline for the Treatment of Patients with Alzheimer’s Disease and Other Dementias of Late Life. American Psychiatric Association Guideline. Washington, DC: American Psychiatric Association, 1997. 34. Gray SL, Lai KV, Larson EB. Drug-induced cognition disorders in the elderly: Incidence, prevention and management. Drug Saf 1999;21:101–122. 35. Finkel SI, Woodson C. History and physical examination of elderly patients with dementia. Int Psychogeriatr 1997;9(Suppl 1):71–75. 36. Richards SS, Hendrie HC. Diagnosis, management, and treatment of Alzheimer disease: A guide for the internist. Arch Intern Med 1999;159:789–798. 37. Weytingh MD, Bossuyt PM, van Crevel H. Reversible dementia: More than 10% or less than 1%? A quantitative review. J Neurol 1995;242:466–471. 38. Pennypacker LC, Allen RH, Kelly JP et al. High prevalence of cobalamine deficiency in elderly outpatients. J Am Geriatr Soc 1992;40:1197–1204. 39. Seal EC, Metz J, Flicker L et al. A randomized, double-blind, placebocontrolled study of oral vitamin B12 supplementation in older patients with subnormal or borderline serum vitamin B12 concentrations. J Am Geriatr Soc 2002;50:146–151. 40. American Academy of Neurology. American Academy of Neurology guideline summary for clinicians: Detection, diagnosis and management of dementia [on-line]. Available at www.aan.com/professionals/practice/index. cfm Accessed February 13, 2004. 41. Timmermans M, Carr J. Neurosyphilis in the modern era. J Neurol Neurosurg Psychiatry 2004;75:1727–1730. 42. Centers for Disease Control and Prevention. Primary and secondary syphilisF United States, 2003–2004. MMWR Morb Mortal Wkly Rep 2006;55: 269–273. 43. Finelli L, Levine WC, Valentine J et al. Syphilis outbreak assessment. Sex Transm Dis 2001;28:131–135. 44. Petrella JR, Coleman RE, Doraiswamy PM. Neuroimaging and early diagnosis of Alzheimer disease: A look to the future. Radiology 2003;226: 315–336. 45. Zakzanis KK, Graham SJ, Campbell Z. A meta-analysis of structural and functional brain imaging in dementia of the Alzheimer’s type: A neuroimaging profile. Neuropsychol Rev 2003;13:1–18. 46. Knopman DS, DeKosky ST, Cummings JL et al. Practice parameter: Diagnosis of dementia (an evidence-based review). Report of the Quality Stan-

S300

47. 48.

49.

50.

51.

52.

53.

54.

55.

56. 57. 58. 59.

60.

61.

62.

63.

64. 65.

66. 67. 68.

69.

70.

71. 72. 73.

FEIL ET AL.

dards Subcommittee of the American Academy of Neurology. Neurology 2001;56:1143–1153. Cummings JL. Alzheimer’s disease. N Engl J Med 2004;351:56–67. Dementia Identification and Assessment: Guidelines for Primary Care Practitioners. Washington, DC: U.S. Department of Veterans Affairs and the University Health System Consortium, 1997. Valcour V, Shikuma C, Shiramizu B et al. Higher frequency of dementia in older HIV-1 individuals: The Hawaii Aging with HIV-1 Cohort. Neurology 2004;63:822–827. Valcour VG, Shikuma CM, Watters MR et al. Cognitive impairment in older HIV-1-seropositive individuals: Prevalence and potential mechanisms. AIDS 2004;18(Suppl 1):S79–S86. Tozzi V, Balestra P, Galgani S et al. Changes in neurocognitive performance in a cohort of patients treated with HAART for 3 years. J Acquir Immune Defic Syndr 2001;28:19–27. Dorenlot P, Harboun M, Bige V et al. Major depression as a risk factor for early institutionalization of dementia patients living in the community. Int J Geriatr Psychiatry 2005;20:471–478. Lyketsos CG, DelCampo L, Steinberg M et al. Treating depression in Alzheimer disease: Efficacy and safety of sertraline therapy, and the benefits of depression reduction: The DIADS. Arch Gen Psychiatry 2003;60: 737–746. Doody RS, Stevens JC, Beck C et al. Practice parameter: Management of dementia (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56: 1154–1166. Santaguida PS, Raina P, Booker L et al. Pharmacological Treatment of Dementia. Summary, Evidence Report/Technology Assessment No. 97. Rockville, MD: Agency for Healthcare Research and Quality (AHRQ), 2004. Birks JS, Harvey R. Donepezil for dementia due to Alzheimer’s disease. Cochrane Database Syst Rev 2006;(1):CD00119. Loy C, Schneider L. Galantamine for Alzheimer’s disease. Cochrane Database Syst Rev 2004;(4):CD001747. Birks J, Evans G, Iakovidou V et al. Rivastigmine for Alzheimer’s disease. Cochrane Database Syst Rev 2000;(4):CD001191. Feldman H, Gauthier S, Hecker J et al. Efficacy and safety of donepezil in patients with more severe Alzheimer’s disease: A subgroup analysis from a randomized, placebo-controlled trial. Int J Geriatr Psychiatry 2005;20: 559–569. Winblad B, Kilander L, Eriksson S et al. Donepezil in patients with severe Alzheimer’s disease: Double-blind, parallel-group, placebo-controlled study. Lancet 2006;367:1057–1065. Tariot PN, Cummings JL, Katz IR et al. A randomized, double-blind, placebo-controlled study of the efficacy and safety of donepezil in patients with Alzheimer’s disease in the nursing home setting. J Am Geriatr Soc 2001;49: 1590–1599. FDA Approves Expanded Use of Treatment for Patients With Severe Alzheimer’s Disease [on-line], October 13, 2006. Available at http://www.fda.gov/ bbs/topics/NEWS/2006/NEW01491.html Accessed December 1, 2006. Passmore AP, Bayer AJ, Steinhagen-Thiessen E. Cognitive, global, and functional benefits of donepezil in Alzheimer’s disease and vascular dementia: Results from large-scale clinical trials. J Neurol Sci 2005;229–230:141–146. Malouf R, Birks J. Donepezil for vascular cognitive impairment. Cochrane Database Syst Rev 2004;(1):CD004395. Edwards KR, Hershey L, Wray L et al. Efficacy and safety of galantamine in patients with dementia with Lewy bodies: A 12-week interim analysis. Dement Geriatr Cogn Disord 2004;17(Suppl 1):40–48. Fernandez HH, Wu CK, Ott BR. Pharmacotherapy of dementia with Lewy bodies. Expert Opin Pharmacother 2003;4:2027–2037. Wild R, Pettit T, Burns A. Cholinesterase inhibitors for dementia with Lewy bodies. Cochrane Database Syst Rev 2003;(3):CD003672 FDA Approves the First Treatment for Dementia of Parkinson’s Disease [online]. June 27, 2006. Available at http://www.fda.gov/bbs/topics/NEWS/ 2006/NEW01399.html Accessed December 1, 2006. Alexopoulos GS, Jeste DV, Chung H et al. The Expert Consensus Guideline Series: Treatment of dementia and its behavioral disturbances. Postgrad Med Spec Rep 2005, 1–111. Lyketsos G, Colenda CC, Beck C et al. Position Statement of the American association for geriatric psychiatry regarding principles of care for patients with dementia resulting from Alzheimer disease. Am J Geriatr Psychiatry 2006;14:561–573. Aereosa SA, Sherriff F, McShane R. Memantine for dementia. Cochrane Database Syst Rev 2005;(2):CD003154. Moroney JT, Bagiella E, Tatemichi TK et al. Dementia after stroke increases the risk of long-term stroke recurrence. Neurology 1997;48:1317–1325. Leys D, Henon H, Mackowiak-Cordoliani MA et al. Poststroke dementia. Lancet Neurol 2005;4:752–729.

OCTOBER 2007–VOL. 55, NO. S2

JAGS

74. Forette F, Seux ML, Staessen JA et al. The prevention of dementia with antihypertensive treatment: New evidence from the Systolic Hypertension in Europe (Syst-Eur) study. Arch Intern Med 2002;162:2046–2052. 75. Jonker C, Comijs HC, Smit JH. Does aspirin or other NSAIDs reduce the risk of cognitive decline in elderly persons? Results from a population-based study. Neurobiol Aging 2003;24:583–588. 76. Xiong GL, Benson A, Doraiswamy PM. Statins and cognition: What can we learn from existing randomized trials? CNS Spectr 2005;10:867–874. 77. Shobab LA, Hsiung GY, Feldman HH. Cholesterol in Alzheimer’s disease. Lancet Neurol 2005;4:841–852. 78. Sparks DL, Sabbagh MN, Connor DJ et al. Atorvastatin for the treatment of mild to moderate Alzheimer disease: Preliminary results. Arch Neurol 2005;62:753–757. 79. Trompet S, Westendorp RG, Kamper AM et al. Use of calcium antagonists and cognitive decline in old age. The Leiden 85-plus study. Neurobiol Aging in press. 80. Marriott A, Donaldson C, Tarrier N et al. Effectiveness of cognitivebehavioural family intervention in reducing the burden of care in carers of patients with Alzheimer’s disease. Br J Psychiatry 2000;176:557–562. 81. Brodaty H, Gresham M. Effect of a training programme to reduce stress in carers of patients with dementia. BMJ 1989;299:1375–1379. 82. Mittelman MS, Ferris SH, Steinberg G et al. An intervention that delays institutionalization of Alzheimer’s disease patients: Treatment of spousecaregivers. Gerontologist 1993;33:730–740. 83. Burns R, Nichols LO, Martindale-Adams J et al. Primary care interventions for dementia caregivers: 2-year outcomes from the REACH study. Gerontologist 2003;43:547–555. 84. Mohide EA, Pringle DM, Streiner DL et al. A randomized trial of family caregiver support in the home management of dementia. J Am Geriatr Soc 1990;38:446–454. 85. Cuijpers P. Depressive disorders in caregivers of dementia patients: A systematic review. Aging Ment Health 2005;9:325–330. 86. Small GW, Rabins PV, Barry PP et al. Diagnosis and treatment of Alzheimer disease and related disorders. Consensus statement of the American Association for Geriatric Psychiatry, the Alzheimer’s Association, and the American Geriatrics Society. JAMA 1997;278:1363–1371. 87. International Psychogeriatric Association. The BPSD Educational Pack. Skokie, IL: International Psychogeriatric Association, 2003. 88. Black W, Almeida OP. A systematic review of the association between the behavioral and psychological symptoms of dementia and burden of care. Int Psychogeriatr 2004;16:295–315. 89. Finkel SI, Costa e Silva J, Cohen G et al. Behavioral and psychological signs and symptoms of dementia: A consensus statement on current knowledge and implications for research and treatment. Int Psychogeriatr 1996;8(Suppl 3):497–500. 90. Coyne AC, Reichman WE, Berbig LJ. The relationship between dementia and elder abuse. Am J Psychiatry 1993;150:643–646. 92. Drinka TJ, Smith JC, Drinka PJ. Correlates of depression and burden for informal caregivers of patients in a geriatrics referral clinic. J Am Geriatr Soc 1987;35:522–525. 92. Gaugler JE, Kane RL, Kane RA et al. The longitudinal effects of early behavior problems in the dementia caregiving career. Psychol Aging 2005;20: 100–116. 93. Yaffe K, Fox P, Newcomer R et al. Patient and caregiver characteristics and nursing home placement in patients with dementia. JAMA 2002;287:2090– 2097. 94. Cummings JL, Mega M, Gray K et al. The Neuropsychiatric Inventory: Comprehensive assessment of psychopathology in dementia. Neurology 1994;44:2308–2314. 95. Sultzer DL, Levin HS, Mahler ME et al. Assessment of cognitive, psychiatric, and behavioral disturbances in patients with dementia: The Neurobehavioral Rating Scale. J Am Geriatr Soc 1992;40:549–555. 96. Cohen-Mansfield J. Conceptualization of agitation: Results based on the Cohen-Mansfield Agitation Inventory and the Agitation Behavior Mapping Instrument. Int Psychogeriatr 1996;8(Suppl 3):309–315, discussion 351–354. 97. Reisberg B, Auer SR, Monteiro IM. Behavioral pathology in Alzheimer’s disease (BEHAVE-AD) rating scale. Int Psychogeriatr 1996;8(Suppl 3): 301–308, discussion 351–354. 98. Paulsen JS, Salmon DP, Thal LJ et al. Incidence of and risk factors for hallucinations and delusions in patients with probable AD. Neurology 2000;54: 1965–1971. 99. Sink KM, Holden KF, Yaffe K. Pharmacological treatment of neuropsychiatric symptoms of dementia: A review of the evidence. JAMA 2005; 293:596–608. 100. Opie J, Rosewarne R, O’Connor DW. The efficacy of psychosocial approaches to behaviour disorders in dementia: A systematic literature review. Aust N Z J Psychiatry 1999;33:789–799.

JAGS

OCTOBER 2007–VOL. 55, NO. S2

102. Schneider LS, Tariot PN, Dagerman KS et al. Effectiveness of atypical antipsychotic drugs in patients with Alzheimer’s disease. N Engl J Med 2006; 355:1525–1538. 102. Sink KM, Holden KF, Yaffe K. Pharmacological treatment of neuropsychiatric symptoms of dementia: A review of the evidence. JAMA 2005;293: 596–608. 103. Schneider LS, Dagerman K, Insel PS. Efficacy and adverse effects of atypical antipsychotics for dementia: Meta-analysis of randomized, placebo-controlled trials. Am J Geriatr Psychiatry 2006;14:191–210. 104. Schneider LS, Dagerman KS, Insel P. Risk of death with atypical antipsychotic drug treatment for dementia: Meta-analysis of randomized placebocontrolled trials. JAMA 2005;294:1934–1943. 105. Wang PS, Schneeweiss S, Avorn J et al. Risk of death in elderly users of conventional vs. atypical antipsychotic medications. N Engl J Med 2005;353: 2335–2341. 106. Holmes C, Wilkinson D, Dean C et al. The efficacy of donepezil in the treatment of neuropsychiatric symptoms in Alzheimer disease. Neurology 2004;63:214–219. 107. Finkel SI. Effects of rivastigmine on behavioral and psychological symptoms of dementia in Alzheimer’s disease. Clin Ther 2004;26:980–990. 108. Gauthier S, Feldman H, Hecker J et al. Efficacy of donepezil on behavioral symptoms in patients with moderate to severe Alzheimer’s disease. Int Psychogeriatr 2002;14:389–404. 109. Pollock BG, Mulsant BH, Rosen J et al. Comparison of citalopram, perphenazine, and placebo for the acute treatment of psychosis and behavioral disturbances in hospitalized, demented patients. Am J Psychiatry 2002;159: 460–465. 110. Sultzer DL, Gray KF, Gunay I et al. A double-blind comparison of trazodone and haloperidol for treatment of agitation in patients with dementia. Am J Geriatr Psychiatry 1997;5:60–69. 111. Reger MA, Welsh RK, Watson GS et al. The relationship between neuropsychological functioning and driving ability in dementia: A meta-analysis. Neuropsychology 2004;18:85–93. 112. Duchek JM, Carr DB, Hunt L et al. Longitudinal driving performance in early-stage dementia of the Alzheimer type. J Am Geriatr Soc 2003;51: 1342–1347. 113. Uc EY, Rizzo M, Anderson SW et al. Driver route-following and safety errors in early Alzheimer disease. Neurology 2004;63:832–837. 114. Rizzo M, McGehee DV, Dawson JD et al. Simulated car crashes at intersections in drivers with Alzheimer disease. Alzheimer Dis Assoc Disord 2001;15: 10–20. 115. Brown LB, Ott BR. Driving and dementia: A review of the literature. J Geriatr Psychiatry Neurol 2004;17:232–240. 116. Dubinsky RM, Stein AC, Lyons K. Practice parameter: Risk of driving and Alzheimer’s disease (an evidence-based review): Report of the quality standards subcommittee of the American Academy of Neurology. Neurology 2000;54:2205–2211.

DEMENTIA QUALITY INDICATORS FOR VULNERABLE ELDERS

S301

117. Carr DB, Duchek J, Morris JC. Characteristics of motor vehicle crashes of drivers with dementia of the Alzheimer type. J Am Geriatr Soc 2000;48: 18–22. 118. Jarvik LF, Wiseman EJ. Checklist for managing the dementia patient. Geriatrics 1991;46:31–34, 39–40. 119. Wang WW, Moyle W. Physical restraint use on people with dementia: A review of the literature. Aust J Adv Nurs 2005;22:46–52. 120. Castle NG, Mor V. Physical restraints in nursing homes: A review of the literature since the Nursing Home Reform Act of 1987. Med Care Res Rev 1998;55:139–170, discussion 171–176. 121. McHutchion E, Morse JM. Releasing restraintsFa nursing dilemma. J Gerontol Nurs 1989;15:16–21. 122. Miles SH, Irvine P. Deaths caused by physical restraints. Gerontologist 1992; 32:762–766. 123. Innes EM, Turman WG. Evaluation of patient falls. QRB Qual Rev Bull 1983;9:30–35. 124. Karlsson S, Bucht G, Eriksson S et al. Factors relating to the use of physical restraints in geriatric care settings. J Am Geriatr Soc 2001;49: 1722–1728. 125. Testad I, Aasland AM, Aarsland D. The effect of staff training on the use of restraint in dementia: A single-blind randomised controlled trial. Int J Geriatr Psychiatry 2005;20:587–590. 126. Huizing AR, Hamers JP, Gulpers MJ et al. Short-term effects of an educational intervention on physical restraint use: A cluster randomized trial. BMC Geriatr 2006;6:17. 127. Hall GR. Research-Based Protocol: Alzheimer’s Disease and Chronic Dementing Illnesses. Iowa City, IA: University of Iowa Gerontological Nursing Interventions Research Center Research Development and Dissemination Core, 1996. 128. Ledford L, Mentes J. Research-Based Protocol: Restraints. Iowa City, IA: University of Iowa Gerontological Nursing Interventions Research Center Research Development and Dissemination Core, 1996. 129. UCLA Medical Center Standards of Care, Involuntary Physical Restraint. Policy No. 0030 Los Angeles, CA: UCLA Medical Center, 1998. 130. Department of Health and Human Services, Health Care Financing Administration State Operations Manual: Provider Certification. Washington, DC: U.S. Government Printing Office, 1995. 131. Dementia. Clinical Practice Guidelines. Columbia, MD: American Medical Directors Association, American Health Care Association, 1998. 132. American Geriatrics Society Position Statement: Guidelines for Restraint Use. New York, NY: The American Geriatrics Society, 1991. 133. Use of Restraints for Patients in Nursing Homes. Report 4 of the Council of Scientific Affairs (A-97). Chicago, IL: American Medical Association, 1997. 134. American Academy of Neurology Ethics and Humanities Subcommittee. Ethical issues in the management of the demented patient. Neurology 1996;46:1180–1183.

Smile Life

When life gives you a hundred reasons to cry, show life that you have a thousand reasons to smile

Get in touch

© Copyright 2015 - 2024 PDFFOX.COM - All rights reserved.