Clinical Update on Nursing Home Medicine: 2015

Clinical Update on Nursing Home Medicine: 2015

JAMDA 16 (2015) 911e922 JAMDA journal homepage: www.jamda.com Updates from the AMDA Meeting Clinical Update on Nursing Home Medicine: 2015 Barbara ...

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JAMDA 16 (2015) 911e922

JAMDA journal homepage: www.jamda.com

Updates from the AMDA Meeting

Clinical Update on Nursing Home Medicine: 2015 Barbara J. Messinger-Rapport MD, PhD, FACP, CMD a, Angela Sanford MD b, John E. Morley MB, BCh b, *, Julie K. Gammack MD, CMD b a b

Section of Geriatric Medicine, Cleveland Clinic, Cleveland, OH Division of Geriatric Medicine, Saint Louis University School of Medicine, St Louis, MO

a b s t r a c t Keywords: Disease management frail elders heart failure pneumonia mild cognitive impairment meaningful activities in the nursing home anticoagulation atrial fibrillation multiple chronic conditions clinical guidelines

This is the ninth yearly update on clinical care in the nursing home. Topics covered this year are disease management in frail elders, heart failure, pneumonia, mild cognitive impairment, meaningful activities in the nursing home, atrial fibrillation, and anticoagulation. Ó 2015 AMDA e The Society for Post-Acute and Long-Term Care Medicine.

Disease Management in Frail Elders Older adults in long-term care (LTC) are typically frail. Most have experienced geriatric conditions such as falls and urinary incontinence, as well as diseases such as hypertension (HTN), chronic obstructive pulmonary disease (COPD), heart failure (HF), diabetes (DM), atrial fibrillation (AF), and osteoporosis (OP). Although clinical guidelines exist for each chronic condition, guidelines typically have not accounted for the multiple concurrent conditions, or the advanced age and shortened life expectancy of frail elders. Adherence to evidence-based clinical guidelines in patients with multiple conditions can lead to polypharmacy as well as contradictory and potentially dangerous prescribing.1 Prescription use for this population already reflects multimorbidity, with more than 70% of LTC residents receiving 9 or more medications.2 In testimony to the challenge of adapting single-condition guidelines to older patients with multimorbidity, a 2015 “app” called “MCC GEMS” was developed to guide clinicians with a patient-centered approach. However, chronic disease-management guidelines published within the past 2 years are starting to incorporate age and vulnerability, and thus have more applicability to frail patients. The topics in this review, culled from recent literature and professional society recommendations, were chosen because they include guidance that

may influence disease management of frail elders. Topics in this review include updates on current recommendations for managing HTN, hyperlipidemia, and chronic HF. An update from the 2014 Guideline on NoneST-Segment Elevation Myocardial Infarction (NSTEMI) is included for prognostication as well. Hypertension The Eighth Joint National Committee (JNC 8) made 9 evidence-based recommendations for managing high blood pressure (BP), with only one specifically addressing adults 60 years and older.3 JNC 8 recommends that antihypertensive therapy should be initiated at 150/90 mm Hg in this age group to reduce BP to less than that value (grade A recommendation; ie, strong). If treated systolic BP (sBP) is lower than 140 mm Hg without adverse effects, it may be sustained (grade E recommendation; ie, based on expert opinion).3 The new guideline is appropriately more relaxed for older adults than the previous recommendation of lower than 140/90. However, it does not specifically identify the “young-old” who may be in their 60s and early 70s and who may benefit from more aggressive BP targets. The “old-old,” defined loosely as over 75 or 80 years, are more likely to be frail. The risk of adverse cardiovascular events may rise in the latter group when sBP is lower than 130 or diastolic BP is lower than 60 mm Hg.4,5 Hyperlipidemia

The authors declare no conflicts of interest. * Address correspondence to John E. Morley, MB, BCh, Division of Geriatric Medicine, Saint Louis University School of Medicine, 1402 S. Grand Boulevard, M238, St Louis, MO 63104. E-mail address: [email protected] (J.E. Morley). http://dx.doi.org/10.1016/j.jamda.2015.09.001 1525-8610/Ó 2015 AMDA e The Society for Post-Acute and Long-Term Care Medicine.

The 2013 American College of Cardiology/American Heart Association (ACC/AHA) cholesterol guideline6 advocates using a new cardiovascular disease risk calculator. This calculator estimates the

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10-year risk for atherosclerotic cardiovascular disease (ASCVD), based on data from multiple community-based populations and applicable to African American and non-Hispanic white men and women 40 through 79 years of age. Primary prevention with a statin is encouraged for those with a 10-year risk of 7.5% or higher. The tool generated controversy from the moment it was announced, and may overestimate ASCVD risk by 67% in women and 86% in men.7 Additionally, the tool excludes the population 80 years and older, those most often encountered in LTC. However, the guideline does offer new recommendations for adults 75 years and older, emphasizing optimization of tolerability and reduction in polypharmacy. Additionally, the focus is on statin intensity rather than specific lowdensity lipoprotein (LDL) targets. This guideline discourages use of multiple drugs to lower cholesterol, specifically deemphasizing the adjunctive use niacin, ezetimibe, and fenofibrate for this purpose alone. Emphasis on Tolerability For the old-old (in general, older than 75 years), the guideline recommends reassessing statin choice and intensity according to pain, tenderness, stiffness, cramping, weakness, and fatigue (class IIa recommendation [“reasonable”], level of evidence B [“limited”]). Also recommended is reassessment of statin choice and intensity for patients older than 75 or for those taking multiple medications, drugs that alter metabolism, and conditions requiring complex medications (class IIa, level of evidence C [“very limited”]). For patients with confusion, statin and nonstatin causes should be considered as potential etiologies (class IIb [“consider”], level of evidence C). Of note, recent evidence suggests that the confusion thought to be associated with statin use may be more of a finding in older adults due to their cerebrovascular conditions rather than the drug itself.1 Initiating high-intensity statin therapy is not recommended by the guideline for those older than 75; however, continuing such treatment is reasonable for patients already undergoing and tolerating the therapy for an appropriate indication. Initiation of moderate-intensity statin therapy in this age group is recommended for those with either clinical atherosclerotic cardiovascular disease or an LDL-cholesterol (LDL-C) level of at least 190 mg/dL. For patients older than 75 without atherosclerotic cardiovascular disease, LDL-C less than 190 mg/dL, or with DM, no specific guidance is provided. In these groups, statin therapy may be initiated, continued, or intensified (class IIb, level of evidence C). Reasonable Sodium Restriction Although sodium restriction has been standard practice in HF for decades, restricting sodium in the elderly was given only a IIa (“reasonable”) classification, based on level C (very limited) evidence.8 Strong evidence exists that middle aged and young-old adults with HF (with preserved or reduced ejection fraction) should reduce their sodium intake by approximately 1 g per day or aim for a mean 24-hour urinary sodium excretion of approximately 2.3 g per day. However, little evidence exists to support a specific long-term target intake, and no evidence exists for “old-old” patients. Given the lack of evidence for feasibility or benefit for very low sodium intake, the “2-g sodium diet” may not be a blanket recommendation for all patients with HF. Rather, sodium restriction can be individualized to the response of the individual, optimizing medication use and liberalizing diet to prevent sarcopenia and nutritional deficits. Heart Failure Aldosterone antagonists have been recommended for moderate-tosevere HF (New York Heart Association [NYHA]9 III-IV) for some time.

ACC/AHA guidelines issued in 2013 also recommend them for mild HF (NYHA II).8 The Eplerenone in Patients with Systolic Heart Failure and Mild Symptoms (EMPHASIS) trial10 randomized 2737 patients, median age 69, with NYHA II HF and an ejection fraction of no more than 35% to receive the aldosterone antagonist eplerenone (up to 50 mg daily) or placebo, in addition to recommended therapy. The trial was stopped early after a median follow-up of 21 months when the treatment group was found to have a significantly lower risk of cardiovascular death or hospitalization for HF or for any cause. Of note and concern to older adults, or those of any age with even mildly impaired renal function: hyperkalemia occurred in 11.8% of the eplerenone group versus 7.2% in the placebo group (P < .001). The high frequency of hyperkalemia in the placebo group may have been due to concomitant use of angiotensin-converting enzyme inhibitors. Caution with the use of either of the existing aldosterone antagonists in older adults is needed due to higher prevalence of renal impairment than younger adults. Caution With Digoxin Use of digoxin has been recommended in patients with HF with reduced ejection fraction (HFrEF) to reduce hospitalization,8 but more recent publications have raised questions regarding its safety and purported efficacy. One prospective study followed 2891 patients, mean age 69 years, with newly diagnosed HFrEF over 2.5 years, with 529 patients prescribed digoxin. The digoxin group had a higher rate of death (14.2 vs 11.2 per 100 patient-years) and HF-related hospitalization (28.2 vs 24.4 per 100 person-years).11 The study was unable to determine if the digoxin level influenced the results, because approximately 30% of participants had no digoxin level drawn, and an additional 27% had only one level drawn during the time period of the study. For those with measured blood levels, the mean digoxin level for men was 0.83 ng/mL and 1.12 ng/mL for women. Risks and benefits of this particular medication should be weighed carefully. Tension Between Guidelines The higher threshold for HTN treatment and the lower threshold for statin therapy create tension between guidelines, and between guidelines and epidemiological data. For example, the ACC/AHA ASCVD risk calculator predicts a 10-year risk of less than 7.5% in a 67-year-old woman without DM and with a favorable lipid profile, if sBP is 147 mm Hg. However, if the patient’s BP is 148 or 149 mm Hg and all the other variables were the same, the JNC 8 would not recommend initiating antihypertensives to reduce the risk of cardiovascular complications, but the ACC/AHA guidelines (Figure 1) would recommend preventive statin therapy for that purpose due to the effect of the BP value on the risk calculator. Tension also exists between HTN guidelines and epidemiological data on HF. Multiple studies demonstrate a reduction in HF incidence with HTN treatment. A 70-year-old man whose systolic BP is 140 mm Hg has an approximate 15% lifetime risk of HF. If his sBP were 160 mm Hg, his lifetime HF risk is more than 50%.12 If his sBP were 149, his lifetime risk of HF is between 15% and 50%, but the JNC 8 criteria do not recommend antihypertensive therapy to reduce the risk of cardiovascular complications. Another example of tension between a guideline and epidemiological data is the incidence of white matter disease (WMD) burden and BP targets over time. The burden of WMD may be associated with the presence and degree of cognitive impairment. A longitudinal study of adults 80 years and older with a mean Folstein of 25.8 had the lowest burden of WMD when systolic targets were between 140 and 160 mm Hg.13 So an 80-year-old man may appear to tolerate an antihypertensive keeping his sBP at 130, but may develop more WMD

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10-year risk of ASCVD for 67 yo Caucasian woman, total cholesterol 130 mg/dL, HDL 55 mg/dL, non-diabeƟc 8.2% 5.9%

6.3%

6.8%

7.3%

8.7%

9.2%

7.7%

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preventive interventions. The guidelines also have not reconciled tensions between complementary guidelines, such as cholesterol and BP management, or between BP management and clinical data on HF. Additionally, it would be a shame if providers interpreted the caution with statins and confusion to apply across the board to all older adults, given the potential of statins to reduce vascular complications and influence the white matter disease burden in a beneficial way to protect cognition in vulnerable elders. Diagnosis and Management of Pneumonia in the LTC Setting

130

135

140 145 150 155 Systolic Blood Pressure

160

165

Fig. 1. Calculations derived from the 2013 ACC/AHA guidelines and 10-year risk pool calculator.

than he would at a slightly higher sBP. In fact, sBP of 150 may actually optimize his cognitive function. Finally, the association of statins with confusion has been made in case series but not consistently in large studies. In a case-controlled study of 295 community-dwelling older adults, there was no overall effect of statin exposure on cerebral structure indices. However, in the lowest tertile of cognition, with a mean Modified Mini-Mental State score of 86 (lower end of normal in this population), statinexposed elders had a lower white matter disease burden than those not exposed to statins.14 This finding suggests (but does not prove) a benefit to statins in vulnerable elders, as cognitive impairment is associated with the white matter burden. In another study, statins were associated with a slower rate of decline in cognitive function in older adults.15 NSTEMI Guidelines In an era when the incidence of acute myocardial infarction is declining and use of biomarkers is rising, most myocardial infarctions are NSTEMI rather than STEMI.16 The NSTEMI is defined by a rise and fall of biomarkers during a symptomatic episode. There are 5 categories of NSTEMIs described in the guideline. More than 95% of persons present with either type I (acute coronary syndrome causing a plaque rupture) or type II (an imbalance between demand and supply during an acute medical or surgical condition). The type of NSTEMI is determined clinically. Type II is more likely to be seen in functionally impaired elders, particularly those with lower body mass index and multiple comorbidities. The 1-year prognosis of type II NSTEMI is lower than that of type I, 76.1% versus 91.4%. The guidelines for type I NSTEMI contain general recommendations for older adults (Tables B and C in the guideline16) but no specific guidelines for type II. Despite the absence of recommendations, this guideline does address the importance of differentiating between the type of NSTEMI both in terms of direction of care and prognosis.

Background Nursing homeeacquired pneumonia (NHAP), which can be used interchangeably with the term “nursing homeeassociated pneumonia,” is defined simply as pneumonia that occurs in a resident of a nursing home (NH) or LTC facility. First described in 1978, it is one of the most common infections in the LTC setting18 and one of the most common reasons for sending a LTC resident for hospitalization.19 NHAP falls in the spectrum of community-acquired pneumonia (CAP) and health careeassociated pneumonia (HCAP), and includes aspiration pneumonia (Figure 2). Many medical specialties and societies consider NHAP to be synonymous with HCAP, but this is not always the case. HCAP is technically defined as pneumonia that occurs in a patient previously hospitalized for 2 or more days in the previous 90 days, a resident of an NH, a patient who frequents a hemodialysis unit, or anyone who has received intravenous antibiotics or chemotherapy in the previous 30 days. The hallmark of HCAP is the increased risk of multidrug-resistant pathogens and the need for broadened antibiotic coverage. The problem with the definition of HCAP and its inclusion of NH residents is that it necessitates treatment with broad-spectrum intravenous antibiotics, but not every NH resident requires this intensive of antibiotic coverage to get well. This level of coverage is not always feasible or practical to undertake in the LTC setting, nor is it always necessary. In many instances, NHAP more closely resembles CAP and can be treated as such with favorable outcomes. Pathogens and Risk Factors One distinguishing factor between NHAP, CAP, and HCAP is the etiologic agents associated with each. A study conducted in NH facilities in Hong Kong by Ma et al,20 evaluating the most common

Conclusion Newer guidelines are slightly more “geri-centric” than previous versions, and providers may appropriately find justification in some practices that they were already doing, such as following lessstringent guidelines for BP management, and prescribing less-potent statins and lower doses of digoxin. Additionally, the guidelines allow providers to reduce polypharmacy and streamline cholesterol management to the drugs most strongly associated with clinical benefit: the statins. Frustratingly, the guidelines still do not differentiate between the robust elder and the frail elder, despite the heterogeneity of older adults. Highly functioning elders live longer lives than lower-functioning elders17 and may be candidates for more intensive

Fig. 2. Spectrum of NHAP. PNA, pneumonia.

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pathogens isolated in patients diagnosed with pneumonia, found that among the bacterial cases of pneumonia, Streptococcus pneumoniae was most common, followed by Pseudomonas, Haemophilus influenza, and last, methicillin-resistant Staphylococcus aureus. The prevalence rate of atypical bacterial pathogens was found to be approximately 10%,20 which varies largely from the prevalence of approximately 40% to 50% in community dwellers with CAP.21 Viral and bacterial causes were about equally predominant, with respiratory syncytial virus, followed by the parainfluenza viruses, metapneumovirus, and influenza A and B being most common, respectively. Interestingly, no etiologic agent was found in 31.5% of cases, which the authors concluded may represent cases of aspiration pneumonitis or pneumonia. In general, NH residents are more likely than communitydwelling elders to be colonized with gram-negative rods and multidrug-resistant pathogens, but less likely so than hospitalized patients or those with true HCAP. It is also important to keep in mind that S pneumoniae is the most common infectious agent across all settings.20e22 Risk factors for development of pneumonia in NH residents include relative immobility and frequent bedbound status, cognitive impairment, poor oral hygiene, and medications that decrease gastric acid secretion, including the commonly prescribed proton pump inhibitors and H2 blockers. Contrary to what was once believed, feeding tubes also increase risk for the development of pneumonia, particularly aspiration pneumonia. In the NH, patients’ heads are often not adequately elevated while they are receiving feedings, which leads to increased likelihood of aspiration of gastric contents. Additionally, cognitive or neurological impairment can result in impaired swallow reflexes or dysphagia, frequently resulting in aspiration of oropharyngeal contents. Staff factors in the NH, including hand hygiene and vaccination status, also augment resident risk. Diagnosis It is not usually possible to distinguish among viral, bacterial, or aspiration pneumonia/pneumonitis clinically and patient-specific risk factors should guide diagnostic reasoning. Unfortunately, however, this can lead to overtreatment, particularly in cases of viral pneumonia, which does not respond to antibiotics. In one study, there were no differences in the clinical appearances of pneumonia caused by atypical bacterial pathogens versus those from other pathogens.20 In some cases, aspiration pneumonia may be distinguishable by chest radiograph, with infiltrates in the distribution of the right middle or lower lung lobes being the most common due to the orientation of the right main stem bronchus. However, aspiration pneumonia may be located in either lung or bilaterally, depending on the position of the patient during the aspiration event. Aspiration pneumonitis occurs when there is aspiration of sterile gastric contents and results in an acute chemical injury to lung parenchyma without bacterial infection and is manifested on chest radiograph by bilateral infiltrates.23 Viral pneumonia is most common during the winter months, but can occur year-round. Specifically, respiratory syncytial virus season starts in mid-September and lasts approximately 26 weeks, ending in March, and overlaps with influenza season, which usually begins in late November and continues for an average of 12 weeks into February. To be of further nuisance, viral pneumonia can predispose to or evolve into bacterial pneumonia, particularly in those with weakened immune systems, such as NH residents. Pneumonia can be more difficult to diagnose in NH residents than in persons who reside in the community, as NH residents are often frailer at baseline and may not exhibit typical symptoms. In general, clinical findings of fever higher than 38 degrees Celsius, cough with or without purulent sputum, tachycardia, tachypnea, and hypoxia may be suggestive of pneumonia. Leukocytosis may be found on laboratory assessment. Frail, elderly individuals often only display nonspecific

symptoms, such as weakness, altered mental status, increased confusion, delirium, or poor appetite, necessitating a more thorough workup to reveal the underlying cause. Although laboratory work can be useful, the chest radiograph is considered the primary diagnostic tool and will reveal a radiographic infiltrate that is new or progressing in patients with NHAP. Rapid antigen tests of respiratory secretions, such as nasopharyngeal swabs, can quickly rule out respiratory syncytial virus and influenza. Although sputum cultures are very helpful in tailoring antibiotic regimens, they are often difficult to obtain in the NH. An acceptable sputum culture should reflect lower respiratory flora rather than oral flora, as indicated by the presence of neutrophils and absence of epithelial cells in the specimen, and requires the patient to be able to follow directions so as to produce an adequate specimen. Growth of polymicrobial organisms on sputum culture points toward an aspiration event rather than typical bacterial pneumonia, which may be a helpful diagnostic consideration. Urine samples can be collected for urinary antigen testing for S pneumoniae, and Legionella spp, but again, these specific tests may not always be available at all LTC facilities. Treatment Treatment for NHAP is based on patient-specific risk factors and suspected (or proven) etiology. There are few evidence-based treatment guidelines available for NHAP, but there are some consensus statements that were developed using evidence-based treatment guidelines developed for CAP and HCAP. It has been suggested that empiric antibiotic therapy be given if any of the following are present: a fever higher than 101.5 degrees Fahrenheit, sBP lower than 90 mm Hg or 20 mm Hg less than baseline, oxygen saturations less than 90% on room air, heart rate greater than 130 beats per minute, or respiratory rate greater than 30 breaths per minute.24 For patients who are stable, but have probable pneumonia, the decision to start empiric antibiotic treatment can be placed on hold until a chest radiograph has resulted. However, it is important to note that early initiation of antibiotic treatment is ideal, as studies in other settings (ie, emergency departments) have shown improvement in morbidity and mortality with initiation of antibiotics within 8 hours of emergence of symptoms.25 Randomized-controlled trials evaluating specific antibiotic choices for NHAP are nonexistent and thus antibiotic choice is determined by risk factors for specific pathogens, knowledge of local patterns of antibiotic resistance, and pathogen prevalence. It is also helpful to know what medications are readily available in the NH “emergencydispense” kit, as this will aid in faster administration for the initial dose. In general, in patients who can tolerate oral medications, antibiotics should be given in pill form rather than intravenously, as the bioavailability of the most common oral antibiotics is fairly good. Additionally, intravenous antibiotics should be reserved for patients in whom multidrug-resistant pathogens are suspected. Antibiotic choice is further guided by history of recent administration, as the risk of resistant pathogens is higher in patients who have received antibiotics in the past 90 days. If patients rapidly improve after antibiotic initiation, antibiotic therapy can be stopped after a 7-day course. With regard to specific antibiotic choices, there are 3 regimens that have been agreed on based on expert opinion and consensus (Figure 3). There is no evidence in the LTC setting that any one of these regimens is superior to the other. The first and simplest is an antipneumococcal fluoroquinolone (ie, levofloxacin, moxifloxacin) that is used as monotherapy and can be given daily or less, depending on renal function. The second regimen is a high-dose beta-lactam/ beta-lactamase inhibitor (ie, amoxicillin/clavulanate) plus a macrolide (ie, azithromycin). The final regimen is a second- or third-generation cephalosporin (ie, cefuroxime, cefpodoxime, ceftriaxone) plus a macrolide.24,26 One study that evaluated prevalence rates of atypical

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Fig. 3. Recommended antibiotic regimens for NHAP.

bacterial pathogens in NHAP revealed their low prevalence and also low mortality (no patients with infections caused by atypical pathogens died even when they received no antibiotic coverage for atypical pathogens, whereas the overall mortality rate in the study from NHAP of other etiologies was 14.8%).20 Based on this and other studies, it is not beneficial to place patients on monotherapy directed solely against atypical pathogens (ie, macrolide monotherapy).22 Viral pneumonia is most definitely overtreated in the NH setting because it is often impossible to distinguish viral from bacterial etiologies clinically. It is also difficult to tell whether a patient has improved because of initiation of antibiotics or because of the progression of time (ie, the virus has “run its course”). A population-based analysis of 381 NHs over 4 years found that during each study year, influenza was associated with an average of 28 hospitalizations, 147 courses of antibiotics, and 15 deaths per 1000 residents. Respiratory syncytial virus yielded similar results: an average of 15 hospitalizations, 76 courses of antibiotics, and 15 deaths per 1000 residents.27 Obtaining timely rapid influenza and respiratory syncytial virus nasopharyngeal swabs before empiric antibiotic treatment may eliminate some of the antibiotic overprescribing that occurs in residents with viral pneumonia. When Should We Hospitalize? The mean daily cost of hospitalization for patients with NHAP was estimated at $420 per day in 1998 and it is quite conceivable that this figure has increased exponentially in the past 15 years. It was also estimated that the same patient could remain in the NH and undergo similar treatment for only $138 per day.28 There is always concern about hospitalizing frail, elderly NH patients, as hospitalization has been shown to lead to adverse outcomes, such as delirium, pressure ulcers, and decline in functional status.29 When are the hospitalization benefits worth the risks and does hospitalization improve morbidity and/or mortality from NHAP? There are a few studies that have been done comparing 30-day mortality rates of patients with NHAP who are hospitalized with those who remain in the NH, and these have found similar or even decreased mortality rates for those patients who are treated in the NH.28 Only residents with a respiratory rate of greater than 40 breaths per minute had decreased mortality rates when treated in the hospital versus the NH.30 Additionally, of those patients treated in the NH, there was a significant decrease in functional decline than those treated in the hospital. These results should be interpreted with caution, as residents who are sent to the hospital are likely more ill and unstable in comparison with those who remain in the NH.

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Given the considerable monetary benefit and possible overall morbidity/mortality benefit to treat patients in the facility, it must be acknowledged that there are several inherent barriers that may prevent acutely ill residents from receiving adequate care in the NH. First, there is the difficulty in obtaining antibiotics, often from off-site pharmacies, quickly. Second, there is the issue of inadequate staffing, as the staff-to-patient ratio is often quite low, particularly on LTC wards (as opposed to skilled nursing wards) and acutely ill patients need more intensive nursing. And third, there is often poor documentation of patients’ advanced directives or wishes to remain in the NH should they become sick.30 Dr Evelyn Hutt and colleagues24,31 have done extensive work in developing guidelines for evidencebased management of NHAP and has proposed that residents with 2 or more of the following should be sent to the hospital: oxygen saturation less than 90% on room air; sBP lower than 90 mm Hg or 20 mm Hg lower than baseline; respiratory rate greater than 30 breaths per minute or 10 breaths per minute above baseline; requiring supplemental oxygen of 3 L per minute greater than baseline; presence of uncontrolled COPD, congestive HF, or DM; unresponsiveness if previously conscious; or new-onset or increased agitation. For NH residents with only 1 of the critical findings, the decision to hospitalize should be based on the facility’s ability to provide frequent measurement of vitals, prompt access to laboratory draws and results, parenteral hydration, and presence on licensed nurses in the facility. The Pneumonia Severity Index (PSI) or Pneumonia Outcomes Research Team (PORT) score is a scale that predicts 30-day survival and assists in determining whether or not an outpatient would benefit from inpatient treatment of pneumonia. Although helpful in the outpatient setting, it is not useful in the NH, as the criteria are not all obtainable in that setting (ie, arterial blood gases) and more than 85% of NH residents are automatically classified as high risk given their age and living situation.32 Mehr et al32 developed a similar risk-prediction model specifically for NHAP and residents of LTC facilities, using 8 variables to assign points and calculate a 30-day mortality risk. These variables include serum urea nitrogen, white blood cell count, absolute lymphocyte count, heart rate, sex, body mass index, activities of daily living, and change in mood.32 It is unique in that it does not use some measures that are common to other models, such as respiratory rate or oxygen saturation. Putting the risk-prediction model into practice, Mehr et al32 found that 30% of residents in the study with low mortality risk scores were hospitalized for NHAP, indicating that overhospitalization for this condition is of concern. Interestingly, Hutt et al31 developed a comprehensive, multifaceted treatment approach for NHAP to see if hospitalization rates could be decreased and found that at study initiation, compliance with guidelines recommending that stable patients remain in the NH for treatment was fairly high (84%); however, compliance with guidelines recommending hospitalization for critically ill residents was poor (8.7%). These 2 studies indicate that hospitalization rates vary greatly among LTC facilities, depending on the level of care, staffing, and ancillary services available to the NH. Prevention It is widely accepted that influenza and pneumococcal vaccinations of both NH residents and staff prevent infection and reduce mortality. Unfortunately, LTC facility staff vaccination rates are often suboptimal and are among the lowest in any health care setting. The Centers for Disease Control and Prevention (CDC) reported in 2012e2013 a LTC facility staff vaccination rate of 59%, which is poor in comparison with the 83% of hospital staff who received influenza vaccinations that year. Similarly, in one study, 99% of NHs offered influenza vaccinations to residents, 86% offered vaccinations to staff, but the vaccination rate was 83% for residents and only 46% for staff.33 Why are these vaccination rates so dismal when we know that influenza in the NH is

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responsible for 7300 resident deaths annually? A CDC survey of nonvaccinated health care workers found that only 34.2% agreed with the statement “influenza is a serious threat to my health” and 40% thought the vaccine could cause influenza.34 Staff are also reluctant to receive vaccinations because of fear of needles, concern for vaccination side effects, desire to avoid medications, and the erroneous belief that they are not at risk of contracting the flu.35 Although influenza vaccination rates for residents are subpar, pneumococcal vaccination rates are far more dismal and average 50% in many facilities.33 To complicate this ongoing issue, the CDC changed their recommendations regarding pneumococcal vaccinations in 2014. Previously, a 1-time vaccination with the 23-valent pneumococcal polysaccharide vaccine (PPSV23 or Pneumovax) was recommended in patients after the age of 65. Now, it is recommended that adults older than 65 first receive the 13-valent pneumococcal conjugate vaccine (PCV13, or Prevnar), which was previously reserved only for children, and within 6 to 12 months after the initial shot, receive a Pneumovax vaccination.36 These 2 vaccinations together expand coverage against additional serotypes of S pneumoniae and increase protection against pneumococcal infections in already susceptible individuals. Conclusion NHAP remains a leading cause of morbidity and mortality in the NH. There are few evidence-based guidelines available in terms of management and treatment and it is often challenging for the clinician to determine whether a patient should be hospitalized or remain in the NH for treatment. Pneumococcal and influenza vaccinations for both NH staff and residents greatly decrease risk of severe infection in this vulnerable elderly population. Mild Cognitive Impairment The recent International Association of Gerontology and Geriatrics (IAGG) consensus conference has called for case finding for cognitive impairment for all persons older than 70 years seeing health professionals.37 Although there was some dissent, based on the shortage of trained health care professionals to handle a marked increase in persons diagnosed with early cognitive impairment, there was an overwhelming majority in favor of either case finding or even screening. The major reason to support case finding is physicians need to be aware if a person is cognitively impaired to allow them to appropriately treat their patient. Other reasons include that there are a number of treatable causes of early cognitive impairment and new studies have suggested a number of preventive measures that slow the rate of cognitive decline. A number of relatively short tests, such as the St Louis University Mental Status (SLUMS) examination38e40 and the Montreal Cognitive Assessment (MOCA)41,42 are available to detect mild cognitive impairment. The recently validated Rapid Cognitive Screen (RCS) takes only 2.5 minutes to perform and also identifies mild cognitive impairment.43 This test appears ideally suited for a primary care situation and is included as part of the Rapid Geriatric Assessment (RGA).44 The Brief Interview for Mental Status (BMS) used in the Minimum Data Set 3.0 does not detect mild cognitive impairment.45 It is particularly important to monitor cognitive function in persons entering an NH, as there is often a decline in cognitive function following institutionalization.46 Persons who show such a decline need to be carefully evaluated for delirium and reversible causes of cognitive decline.47e50 Care dependency and decline in cognition are major reasons for institutionalization and thus reversal of these problems may allow return to home.51 Reversible causes of early cognitive decline include drugs with anticholinergic activity and polypharmacy52e56; depression57e59;

problems with hearing and vision49,60,61; metabolic disorders, such as hypothyroidism, DM, and vitamin B12 deficiency62e67; normalpressure hydrocephalus68; tumors and other space-occupying lesions63; infections with excess cytokine production69,70; AF71,72 and brain ischemia due to small infarcts73e75; and sleep apnea.76,77 The recent Finnish geriatric study demonstrated that a combination of a Mediterranean diet together with exercise and brain games can markedly slow the aging-related decline in mental function, thus maintaining brain health.78 Other studies have supported the role of exercise in improving thought process38,79e82; the increased utilization of fruits, vegetables, and olive oil83e85; and brain games.86 Maintaining vitamin D levels also appears to maintain cognitive function.87e89 This combinational therapy should be offered to all persons demonstrating cognitive decline. There is evidence for cognitive stimulation therapy either alone, or in combination with exercise, improving mental function in mild to moderate dementia.87,90e92 SAIDO has a similar effect93 and there is also some support for reminiscence therapy in persons with early cognitive dysfunction.94,95 Researchers are beginning to focus on cognitive frailty as an important condition to be aware of in persons with early cognitive impairment.37,96e99 These are persons who have a physical frailty phenotype100e106 along with cognitive impairment (CDR 0.5). They appear to be at increased risk for falls99,107e111 and more rapid functional decline.96,98 Meaningful Activities in the NH A recent editorial in the Journal highlighted the paucity of truly meaningful activities that are carried out in nursing homes.112 This was recently confirmed in a study by Ouden et al113 that demonstrated that between 7 AM and 11 PM residents were observed in inactivities between 45% and 77% of the time. To be meaningful, an activity needs to either engage the brain or be a physical activity. These are activities that have been shown to delay cognitive decline (vide supra) or physical decline.114e119 They are also activities that may reduce disruptive behaviors.120e123 In general, it is felt that in end-stage dementia, most meaningful activities are physical in nature, whereas in mild to moderate dementia, a combination of physical and mental activities would seem to be ideal. A review has supported the concept that function-focused care approaches is safe and efficacious.124 Function-focused activities that are fun include music and dance therapy.125,126 Interactions with animals (such as dogs, birds, and other species) and gardening have been 2 well-established sets of meaningful activities in the NH.127,128 More recently, interacting with robotic animals, such as Paro the seal and Aibo the dog, also have been successful.129e135 Playing a variety of games from the ever-popular Bingo to card games, mahjong, and Monopoly can all be stimulating. Writing postcards to God (the God-card) has been considered a way to allow residents to express their spirituality.136 Other physical activities can include fencing, martial arts, and yoga. As discussed in detail in the previous section, cognitive stimulation and reminiscence therapy represent important activities that can enhance an older person’s function. To successfully increase meaningful activities in the NH and improve resident function requires an increased focus on the importance of the activities director and an increase in activity staff. Finally, although self-evident, if the role of NHs is to enhance the function of residents, physical restraints should not be used.137 Unfortunately, they are still common in many parts of the world.138 The IAGG NH committee has called for more research to improve quality of care for NH residents.139,140 Certainly there is a need to increase our knowledge on the effectiveness of meaningful activities to enhance quality of life.

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Anticoagulation in the Elderly: Venous Thromboembolism Prophylaxis, Atrial Fibrillation, and New Oral Anticoagulants In the post-acute/LTC (PA/LTC) setting, clinicians are regularly challenged to initiate, maintain, and modify the anticoagulation medications based on new and chronic conditions that place residents at higher risk for thrombosis and bleeding. The older adult population is at higher risk for both thrombotic and bleeding events due to a higher burden of acute and chronic diseases, hospitalizations, immobility, falling, renal impairment, infections, and malignancy. Balancing the bleeding and thrombosis risk when selecting the treatment that maximizes benefit and minimizes risk is challenging. In 2012, the American College of Chest Physicians (ACCP) published the ninth edition of the Antithrombotic Therapy and Prevention of Thrombosis Guidelines, replacing the 2008 edition with a 968-page document that includes 600 recommendations. The 41-page executive summary provides an organized review of the most pertinent recommendations.141 Although this guideline does not highlight separately the elderly or PA/LTC populations, some recommendations do reference age or site-of-care delivery. This guideline references the group of medications referred to as New Oral Anticoagulants (NOAs); however, based on the timing of publication relative to the Food and Drug Administration (FDA) indication for use, only 2 of the 3 currently available NOAs are referenced in that chapter. When considering all of the potential thrombotic conditions, this series of guidelines highlights prevention and treatment of both venous and arterial thrombotic conditions, as categorized in Table 1. In 2014, the AHA, in collaboration with the ACC and Heart Rhythm Society, published a “Guideline for the Management of Patients with Atrial Fibrillation.”142 This 126-page document updated the previous 2006 and 2011 guidelines with a full review of the NOA medications. Only 2 paragraphs specifically discuss the elderly as a special population with AF. The NOAs are discussed in this report; however, only in the context of AF. With the development of the NOA group of medications, there are now many FDA-indicated choices for anticoagulation of AF and venous thromboembolism (VTE) prophylaxis and treatment (Table 2). The route of administration, monitoring, dosing range, cost, and use in renal insufficiency must all be carefully considered and individualized to the patient. All of the NOAs carry the FDA warning of increased risk of stroke when discontinuation occurs without bridging to another form of anticoagulant. With the exception of warfarin, all of the FDAindicated medications carry the warning of greater risk of spinal and epidural hematoma in the setting of central nervous system procedures. There are many important changes to anticoagulation management published in the 2012 ACCP guidelines. Some specifically guide care in the PA/LTC setting. As many patients come to PA/LTC after hospitalization for an acute medical or surgical condition, the posthospital use of VTE prophylaxis must be addressed by the PA/LTC provider. The 2012 guidelines suggest that after major orthopedic surgery, the use of low molecular weight heparin (LMWH) is the

Table 1 Indications for Anticoagulation Therapy Prevention

Treatment

Cardiovascular disease Cerebrovascular disease Peripheral arterial disease VTEdsurgical patient VTEdorthopedic patient VTEdmedical patient

Acute coronary syndrome Cerebral vascular accident Acute limb ischemia Deep vein thrombosis Pulmonary embolism Atrial Fibrillation Cardiac thrombosis Cardiac valve replacement

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preferred treatment and should be continued for up to 35 days. For hospitalized patients, risk stratification for VTE is suggested through the use of the Caprini score.143 A score of 3 or more points on this scale conveys a high risk (6% or more) of symptomatic VTE. Age of 75 years or older is assigned a point value of 3 on this scale. For the nonorthopedic surgical patients, VTE prophylaxis can end at the time of hospital discharge with the exception of those who have cancer and are at high risk based on Caprini score. This group should receive 4 weeks of additional VTE prophylaxis with LMWH. For the nonsurgical (medical) patient, VTE prophylaxis can end at the time of hospital discharge. Although it is recognized that immobility increases the risk of VTE in acutely ill individuals, studies in the PA/LTC population have not demonstrated that chronically immobile individuals have higher rates of VTE or require long-term VTE prophylaxis. A multivariate analysis of LTC residents did not find immobility to be a factor in the development of VTE compared with a control population. In this same study, recently hospitalized post-acute residents were at higher risk for VTE if admitted needing “extensive or total assistance” with ambulation compared with an ambulatory population.144 The 2012 ACCP guidelines do not recommend the routine use of thromboprophylaxis in chronically immobilized persons residing at home or at an NH. An additional important change in the ACCP 2012 guidelines is the anticoagulation choice in AF based on the CHADS2 risk scoring method in which 1 point is assigned for Congestive HF, HTN, Age 75 years or older, or DM, and 2 points are assigned for a history of Stroke.145 For a score of 0 points, no anticoagulation or antiplatelet therapy is recommended. Oral anticoagulation therapy is recommended rather than antiplatelet therapy for a CHADS2 score of 1 or more points (Table 3). The guidelines go further to suggest that the NOA group is preferred over adjusted-dose vitamin K antagonist (VKA) therapy. The 2014 AHA guidelines suggest use of a modified CHADS2 scoring method called the CHADS2-VASc, which assigns 1 additional point for a history of Vascular disease, 1 point for Age between 65 and 74 years, and 1 point for female (Sex). Data suggest that these additional factors allow more accurate risk stratification, especially in those who might otherwise be labeled as low risk in the original CHADS2 method.146 The AHA guidelines suggest no anticoagulation for a score of 0 points, antiplatelet therapy versus no anticoagulation for a score of 1 point, and anticoagulation rather than antiplatelet therapy for a score of 2 or more points. Both NOA and VKA therapy are recommended as appropriate anticoagulant choices. The use of anticoagulation for older adults with AF is much lower than would be predicted based on the CHADS2 or CHADS2-VASc scores. Studies reveal that less than 50% of the PA/LTC population with AF is prescribed oral anticoagulation.147,148 A significant concern in older adults is the risk of bleeding with the use of anticoagulation with either antiplatelet or other therapies. Several risk assessment tools have been developed to assess bleeding risk, and often include factors such as age, previous bleeding, HTN, and chronic kidney disease. The most commonly referenced tools are the HEMORR2HAGES (Hepatic or Renal Disease, Ethanol Abuse, Malignancy, Older Age, Reduced Platelet Count or Function, Re-Bleeding, Hypertension, Anemia, Genetic Factors, Excessive Fall Risk and Stroke), ATRIA, and HAS-BLED which were all developed to predict bleeding risk in AF.149e151 The HAS-BLED tool is thought to be the better predictor of bleeding and a simpler tool to apply.152,153 This tools assigns one point each for HTN (sBP >160 mm Hg), Abnormal kidney function (creatinine >2.3 mg/dL), abnormal liver function (bilirubin, aspartate transaminase, alanine transaminase 2 times normal), history of Stroke, history of Bleeding, history of Labile international normalized ratio on warfarin, Elderly (age >65 years), Drug use, and excessive alcohol use. Using the predicted bleeding and thrombosis rates predicted with HAS-BLED and CHADS2-VASc (Table 4), it is possible to create a graph

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Table 2 Commonly Used Anticoagulants for Thrombotic Prevention and Treatment Medication

FDA Indication

Dosing Range

Route

Chronic Kidney Disease Dosing

Dabigatran

Nonvalvular AF Treatment of VTE Nonvalvular AF Treatment of VTE VTE prophylaxis knee/hip Nonvalvular AF Treatment of VTE VTE prophylaxis knee/hip Nonvalvular AF Treatment of VTE VTE prophylaxis Mechanical/bioprosthetic valves Acute coronary syndrome Treatment of VTE VTE prophylaxis Unstable angina Myocardial infarction Treatment of VTE in cancer VTE prophylaxis Unstable angina Acute coronary syndrome Treatment of VTE VTE prophylaxis Unstable angina Myocardial infarction VTE prophylaxis hip surgery

75e150 mg bid

Oral

10 mg qde15 mg bid

Oral

Cr Cl* <15 not indicated Cr Cl 15e30: 75 mg bid Cr Cl < 15 not indicated Cr Cl 15e30: 15 mg daily

2.5e10 mg bid

Oral

ESRD on hemodialysis: unclear Cr Cl < 30: unclear; 2.5 mg bid

Daily

Oral

Cr Cl < 30: caution

40 mg qde1 mg/kg bid

SC

Cr Cl < 30: caution

5000e18,000 units qd (weight-based)

SC

Cr Cl < 30 not indicated

2.5 mge10 mg qd

SC

Cr Cl 30e50: caution Cr Cl < 30 not indicated

15 mg bid

SC

Cr Cl 30e60: 5 mg bid Cr Cl < 30: 1.7 mg bid

Rivaroxaban

Apixaban

Warfarin

Enoxaparin

Dalteparin

Fondaparinux

Desirudin

bid, twice a day; ESRD, end-stage renal disease; qd, every day; SC, subcutaneous. *Creatinine clearance in mL/min.

that may assist clinicians and patients in visually identifying which risk is higher: bleeding versus thrombosis (Figure 4). A history of falling is not an element in 2 of these 3 validated bleeding risk assessment instruments and the risk of fall-associated bleeding may be overestimated by clinicians if not using a validated risk assessment method. In a database analysis of all fall-related hospitalizations in those age 65 or older, there was a higher rate of intracranial hemorrhage in warfarin users; however, no difference in mortality or other injuries in the anticoagulated group.154 Another study of elders presenting to the emergency department after falling did not find an increased risk of intracranial hemorrhage in the anticoagulated group.155 In the landmark AF trials of the 3 FDA-indicated NOAs (rivaroxaban, apixaban, dabigatran), adults older than 75 accounted for only one-third of the study participants. It is estimated that approximately 50% of individuals with AF are older than 75. In the trials of NOA for other thrombotic conditions, older adults often accounted for fewer than 25% of study participants. The PA/LTC population was not represented in these trials, and most studies excluded participants with a creatinine clearance of less than 30 mL/min. To better understand the outcomes of the NOA in older adults, a meta-analysis of the elderly subgroups of the 10 largest clinical trials was performed.156 More than 25,000 individuals were represented in this study; however, pooling of data was problematic for some outcomes, as the study design, clinical indication, and comparison medication often differed across these trials. The data did show that

Table 3 ACCP Recommendations for AF Anticoagulation Using CHADS2 Score CHADS2 Score, Points

2008 Recommended Therapy

2012 Recommended Therapy

0 1 2þ

Either aspirin or no therapy Either aspirin or oral anticoagulation Oral anticoagulation

No therapy Oral anticoagulation Oral anticoagulation

major bleeding events were not different between the NOA and the control agents and occurred at a rate of 5% to 7%. For AF, thrombotic events were similar between the treatment and control groups for rivaroxaban and apixaban. Thrombotic events were reduced in the dabigatran elderly subgroup, with an odds ratio of 0.75 (95% confidence interval 0.58e0.96) based on approximately 7000 individuals. For VTE outcomes, interpretation of results for NOA treatment was difficult, as the comparison group in many cases was a placebo, aspirin, or cessation of conventional medication after a short treatment period. Data suggest that extended use of NOAs reduces VTE events compared with alternate and short-term treatment regimens. A key challenge for practitioners is deciding whether to use an NOA or warfarin for long-term management of AF. Examining the data from elderly subgroups of the key original studies can be helpful; however, these studies did not include the frail, PA/LTC, or populations with renal impairment. Using data from the ARISTOTLE (Apixaban in Comparison with Warfarin in Patients with Atrial Fibrillation and Valvular Heart Disease: Findings from the Apixaban for Reduction in Stroke and other Thromboembolic Events in Atrial Fibrillation) trial of apixaban compared with warfarin, fewer bleeding and thrombotic events were

Table 4 Stroke or Bleeding Event Rate Based on HAS-BLED and CHADS2-VASc Scores Score

Bleeding Rate, % per year

Stroke Rate, % per year

0 1 2 3 4 5 6 7 8 9

1.1 1.0 1.9 3.7 8.7 9.1 Unknown Unknown Unknown Unknown

0 1.3 2.2 3.2 4 6.7 9.8 9.6 6.7 15.2

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Fig. 4. Stroke and bleeding risk using HAS-BLED and CHADS2-VASc scores.

seen with apixaban in those older than 65.157 In the group older than 75, those individuals who received a reduced “renal dose” of apixaban did not have different bleeding or thrombotic outcomes compared with the traditional dose. The ROCKET AF (Rivaroxaban Once-Daily, Oral, Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and embolism Trial in Atrial Fibrillation) study of rivaroxaban versus warfarin for AF was analyzed for bleeding and thrombotic outcomes in the group older than 75.158 The incidence of bleeding and stroke was the same in both groups. No data for renal insufficiency were reported in this study. Two studies of dabigatran versus warfarin in the elderly have analyzed bleeding and thrombosis rates in older adults with AF. The first study was an elderly (age 75þ) subgroup analysis of the RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) trial comparing traditional-dose dabigatran (150 mg), a lower dose of dabigatran (110 mg) that is not clinically available, and warfarin.159 The dabigatran 150-mg dose had fewer stroke events and similar bleeding events when compared with warfarin; however, there were more gastrointestinal bleeding events in both the 150- and the 110-mg groups compared with warfarin. Stroke rates were similar in the 110mg dabigatran and warfarin groups. A lower dabigatran dose (75 mg), which is available and is generally used in those with impaired renal function or high risk of bleeding, was not studied in RE-LY. A separate analysis of dabigatran outcomes related to renal function was performed and suggested no trends in bleeding or thrombosis rates by creatinine clearance.160 Unfortunately, fewer than 20% of participants in this study had a creatinine clearance of less than 50 mL/min and no analysis was performed in those with creatinine clearance less than 30 mL/min. The second study of dabigatran versus warfarin in older adults (age 65þ) did include the 75-mg dose. This Medicare database analysis included more than 134,000 individuals with AF who filled at least 1 prescription of dabigatran or warfarin between 2010 and 2012.161 It is notable that more than 50% of both the warfarin and dabigatran groups filled only a single month of the prescribed medication during the study period. Fewer than 10% of participants in either group had a HAS-BLED score higher than 3. Outcomes of bleeding and thrombotic events were identified. In the 75-mg dabigatran group, there was no difference in stroke or all-cause bleeding events compared with warfarin. There was a lower rate of intracranial hemorrhage with dabigatran than with warfarin and no difference in gastrointestinal bleeding. In the 150-mg

group, there was a lower rate of stroke and intracranial bleeding than warfarin but a higher rate of other bleeding events. Results based on renal function were not reported in this study. In summary, new clinical guidelines have been published to guide treatment of thrombotic conditions. Three NOAs are available for use in AF and VTE treatment/prevention. Scoring tools can assist clinicians in assessing bleeding and thrombosis risk in older adults. With the exception of high-dose dabigatran and gastrointestinal bleeding, most data suggest that the NOAs have similar or reduced bleeding risk when compared with warfarin or alternate antithrombotic medications. Most data suggest that the NOAs have equal or improved thrombotic benefit compared with warfarin. Data on the benefit and safety in the PA/LTC setting and in those with renal dysfunction (creatinine clearance <30 mL/min) are still lacking. References 1. Dumbreck S, Flynn A, Nairn M, et al. Drug-disease and drug-drug interactions: Systematic examination of recommendations in 12 UK national clinical guidelines. BMJ 2015;350:h949. 2. Centers for Medicare and Medicaid Services. Available at: http://www.cms. gov/Research-Statistics-Data-and-Systems/Computer-Data-and-Systems/MDS PubQIandResRep/index.html. Accessed July 13, 2015. 3. James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: Report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA 2014;311:507e520. 4. Cooper-DeHoff RM, Gong Y, Handberg EM, et al. Tight blood pressure control and cardiovascular outcomes among hypertensive patients with diabetes and coronary artery disease. JAMA 2010;304:61e68. 5. Aronow WS, Fleg JL, Pepine CJ, et al. ACCF/AHA 2011 expert consensus document on hypertension in the elderly: A report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. J Am Soc Hypertens 2011;5:259e352. 6. Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013;63: 2889e2934. 7. DeFilippis AP, Young R, Carrubba CJ, et al. An analysis of calibration and discrimination among multiple cardiovascular risk scores in a modern multiethnic cohort. Ann Intern Med 2015;162:266e275. 8. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA Guideline for the Management of Heart Failure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013;62:e147ee239. 9. Ahmed A. A propensity matched study of New York Heart Association class and natural history end points in heart failure. Am J Cardiol 2007;99: 549e553.

920

B.J. Messinger-Rapport et al. / JAMDA 16 (2015) 911e922

10. Zannad F, McMurray JJ, Krum H, et al. Eplerenone in patients with systolic heart failure and mild symptoms. N Engl J Med 2012;364:11e21. 11. Freeman JV, Yang J, Sung SH, et al. Effectiveness and safety of digoxin among contemporary adults with incident systolic heart failure. Circ Cardiovasc Qual Outcomes 2013;6:525e533. 12. Lloyd-Jones DM, Larson MG, Leip EP, et al. Lifetime risk for developing congestive heart failure: The Framingham Heart Study. Circulation 2002;106: 3068e3072. 13. Peng J, Lu F, Wang Z, et al. Excessive lowering of blood pressure is not beneficial for progression of brain white matter hyperintensive and cognitive impairment in elderly hypertensive patients: 4-Year follow-up study. J Am Med Dir Assoc 2014;15:904e910. 14. Nadkarni NK, Perera S, Hanlon JT, et al. Statins and brain integrity in older adults: Secondary analysis of the Health ABC study. Alzheimers Dement; 2015 12 Jan [Epub ahead of print]. 15. Steenland K, Zhao L, Goldstein FC, Levey AI. Statins and cognitive decline in older adults with normal cognition or mild cognitive impairment. J Am Geriatr Soc 2013;61:1449e1455. 16. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;127:e362ee425. 17. Walter LC, Covinsky KE. Cancer screening in elderly patients: A framework for individualized decision making. JAMA 2001;285:2750e2756. 18. El Solh A, Akinnusi M, Alfarah Z, et al. Effect of antibiotic guidelines on outcomes of hospitalized patients with nursing home-acquired pneumonia. J Am Geriatr Soc 2009;57:1030e1035. 19. Muder R, Aghababian R, Loeb M, et al. Nursing home-acquired pneumonia: An emergency department treatment algorithm. Curr Med Res Opin 2004;20: 1309e1320. 20. Ma H, Ip M, Hui E, et al. Role of atypical pathogens in nursing home-acquired pneumonia. J Am Med Dir Assoc 2013;14:109e113. 21. Irfan M, Farooqi J, Hasan R. Community-acquired pneumonia. Curr Opin Pulm Med 2013;19:198e208. 22. Sakoda Y, Ikegame S, Ikeda-Harada C, et al. Retrospective analysis of nursing and healthcare-associated pneumonia: Analysis of adverse prognostic factors and validity of the selection criteria. Respir Investig 2014;52:114e120. 23. Marik P. Aspiration pneumonitis. N Engl J Med 2001;344:655e671. 24. Hutt E, Kramer A. Evidence-based guidelines for management of nursing home-acquired pneumonia. J Fam Pract 2002;51:709e716. 25. Meehan T, Fine M, Krumholz H, et al. Quality of care, process, and outcomes in elderly patients with pneumonia. JAMA 1997;278:2080e2084. 26. Mills K, Nelson C, Winslow R, et al. Treatment of nursing home-acquired pneumonia. Am Fam Physician 2009;79:976e982. 27. Ellis S, Coffey C, Mitchel E, et al. Influenza-and respiratory syncytial virusassociated morbidity and mortality in the nursing home population. J Am Geriatr Soc 2003;51:761e767. 28. Kruse R, Mehr D, Boles K, et al. Does hospitalization impact survival after lower respiratory infection in nursing home residents? Med Care 2004;42: 860e870. 29. Fried T, Mor V. Frailty and hospitalization of long-term stay nursing home residents. J Am Geriatr Soc 1997;45:265e269. 30. Dosa D. Should I hospitalize my resident with nursing home-acquired pneumonia? J Am Med Dir Assoc 2006;7:S74eS80. 31. Hutt E, Ruscin M, Linnebur S, et al. A multifaceted intervention to implement guidelines did not affect hospitalization rates for nursing home-acquired pneumonia. J Am Med Dir Assoc 2011;12:499e507. 32. Mehr D, Binder E, Kruse R, et al. Predicting mortality in nursing home residents with lower respiratory tract infection. JAMA 2001;286:2427e2436. 33. Zadeh M, Bridges C, Thompson W, et al. Influenza outbreak detection and control measures in nursing homes in the United States. J Am Geriatr Soc 2000;48:1310e1315. 34. Advisory Committee on Immunization Practices; Centers for Disease Control and Prevention (CDC). Immunization of health-care personnel: Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep 2011;60:1e45. 35. Daugherty J, Blake S, Grosholz J, et al. Influenza vaccination rates and beliefs about vaccination among nursing home employees. Am J Infect Control 2015; 43:100e106. 36. Ask the Experts: Diseases & Vaccines. Pneumococcal Vaccines (PCV13 and PPSV23). Immunization Action Coalition. Centers for Disease Control and Prevention. Available at: http://www.immunize.org. Accessed August 19, 2015. 37. Morley JE, Morris JC, Berg-Weger M, et al. Brain Health: The importance of recognizing cognitive impairment: An IAGG consensus conference. J Am Med Dir Assoc 2015;16:731e739. 38. Tariq SH, Tumosa N, Chibnall JT, et al. Comparison of the Saint Louis University mental status examination and the mini-mental state examination for detecting dementia and mild neurocognitive disorderda pilot study. Am J Geriatr Psychiatry 2006;14:900e910. 39. Cummings-Vaughn LA, Chavakula NN, Malmstrom TK, et al. Veterans Affairs Saint Louis University Mental Status examination compared with the Montreal Cognitive Assessment and the Short Test of Mental Status. J Am Geriatr Soc 2014;62:1341e1346. 40. Cao L, Hai S, Lin X, et al. Comparison of the Saint Louis University Mental Status Examination, the Mini-Mental state examination, and the Montreal

41.

42. 43.

44. 45. 46.

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.

Cognitive Assessment in detection of cognitive impairment in Chinese elderly from the geriatric department. J Am Med Dir Assoc 2012;13:626e629. Liew TM, Feng L, Gao Q, et al. Diagnostic utility of Montreal Cognitive Assessment in the fifth edition of Diagnostic and Statistical Manual of Mental Disorders: Major and mild neurocognitive disorders. J Am Med Dir Assoc 2015;16:144e148. Cruz-Oliver DM, Morley JE. Early detection of cognitive impairment: Do screening tests help? J Am Med Dir Assoc 2010;11:1e6. Malmstrom TK, Voss VB, Cruz-Oliver DM, et al. The Rapid Cognitive Screen (RCS): A point-of-care screening for dementia and mild cognitive impairment. J Nutr Health Aging 2015;19:741e744. Morley JE. Rapid Geriatric Assessment. J Am Med Dir Assoc 2015;16:808e812. Saliba D, Buchanan J, Edelen MO, et al. MDS 3.0: Brief interview for mental status. J Am Med Dir Assoc 2012;13:611e617. González-Colaço Harmand M, Meillon C, Rullier L, et al. Cognitive decline after entering a nursing home: A 22-year follow-up study of institutionalized and noninstitutionalized elderly people. J Am Med Dir Assoc 2014;15:504e508. Voyer P, McCusker J, Cole MG, et al. Feasibility and acceptability of a delirium prevention program for cognitively impaired long term care residents: A participatory approach. J Am Med Dir Assoc 2014;15:77.e1e77.e9. Rockwood K. Making delirium prevention acceptable in nursing homes. J Am Med Dir Assoc 2014;15:6e7. Cruz-Oliver DM, Malmstrom TK, Roegner M, et al. Cognitive deficit reversal as shown by changes in the Veterans Affairs Saint Louis University Mental Status (SLUMS) examination scores 7.5 years later. J Am Med Dir Assoc 2014;15:687. e5e687.e10. Yevchak AM, Han JH, Doherty K, et al. Impaired arousal in older adults is associated with prolonged hospital stay and discharge to skilled nursing facility. J Am Med Dir Assoc 2015;16:586e589. Afram B, Stephan A, Verbeek H, et al. Reasons for institutionalization of people with dementia: Informal caregivers reports from 8 European countries. J Am Med Dir Assoc 2014;15:108e116. De Souto Barreto P, Vellas B, Morley JE, Rolland Y. The nursing home population: An opportunity to make advances on research on multimorbidity and polypharmacy. J Nutr Health Aging 2013;17:399e400. Sino CG, Sietzema M, Egberts TC, Schuurmans MJ. Medication management capacity in relation to cognition and self-management skills in older people on polypharmacy. J Nutr Health Aging 2014;18:44e49. Onder G, Liperoti R, Foebel A, et al. Polypharmacy and mortality among nursing home residents with advanced cognitive impairment: Results from the SHELTER study. J Am Med Dir Assoc 2013;14:450.e7e450.e12. Moga DC, Carnahan RM, Lund BC, et al. Risks and benefits of bladder antimuscarinics among elderly residents of Veterans Affairs community living centers. J Am Med Dir Assoc 2013;14:749e760. Morley JE. Anticholinergic medications and cognition. J Am Med Dir Assoc 2011;12:543e543.e1. Chen MH, Li CT, Tsai CF, et al. Risk of subsequent dementia among patients with bipolar disorder or major depression: A nationwide longitudinal study in Taiwan. J Am Med Dir Assoc 2015;16:504e508. Saliba D, DiFilippo S, Edelen MO, et al. Testing the PHQ-9 interview and observational versions (PHQ-9-OV) for MDS 3.0. J Am Med Dir Assoc 2012;13: 618e625. Thakur M, Blazer DG. Depression in long-term care. J Am Med Dir Assoc 2008; 9:82e87. Yamada Y, Vlachova M, Richter T, et al. Prevalence and correlates of hearing and visual impairment in European nursing homes: Results from the SHELTER study. J Am Med Dir Assoc 2014;15:738e743. Jupiter T. Cognition and screening for hearing loss in nursing home residents. J Am Med Dir Assoc 2012;13:744e747. Dominguez LJ, Bevilacqua M, Dibella G, Barbagallo M. Diagnosing and managing thyroid disease in the nursing home. J Am Med Dir Assoc 2008;9:9e17. Krause D, Roupas P. Effect of vitamin intake on cognitive decline in older adults: Evaluation of the evidence. J Nutr Health Aging 2015;19:745e753. Luo L, Yang M, Hao Q, et al. Cross-sectional study examining the association between metabolic syndrome and cognitive function among the oldest old. J Am Med Dir Assoc 2013;14:105e108. Blasko I, Hinterberger M, Kemmler G, et al. Conversion from mild cognitive impairment to dementia: Influence of the folic acid and vitamin B12 use in the VITA cohort. J Nutr Health Aging 2012;16:687e694. Mooradian AD, Morley JE, Korenman SG. Endocrinology in aging. Dis Mon 1988;34:393e461. Arvanitakis Z, Wilson RS, Bennett DA. Diabetes mellitus, dementia, and cognitive function in older persons. J Nutr Health Aging 2006;10:287e291. Siraj S. An overview of normal pressure hydrocephalus and its importance: How much do we really know? J Am Med Dir Assoc 2011;12:19e21. Michaud M, Balardy L, Moulis G, et al. Proinflammatory cytokines, aging, and age-related diseases. J Am Med Dir Assoc 2013;14:877e882. Banks WA, Farr SA, La Scola ME, Morley JE. Intravenous human interleukin1alpha impairs memory processing in mice: Dependence on blood-brain barrier transport into posterior division of the septum. J Pharmacol Exp Ther 2001;299:536e541. Ampadu J, Morley JE. Heart failure and cognitive dysfunction. Int J Cardiol 2015;178:12e23. Hui DS, Morley JE, Mikolajczak PC, Lee R. Atrial fibrillation: A major risk factor for cognitive decline. Am Heart J 2015;169:448e456.

B.J. Messinger-Rapport et al. / JAMDA 16 (2015) 911e922 73. Ogama N, Sakurai T, Shimizu A, Toba K. Regional white lesions predict falls in patients with amnestic mild cognitive impairment and Alzheimer’s disease. J Am Med Dir Assoc 2014;15:36e41. 74. Morley JE. White matter lesions (leukoaraiosis): A major cause of falls. J Am Med Dir Assoc 2015;16:441e443. 75. Gudmundsson P, Olesen PJ, Simoni M, et al. White matter lesions and temporal lobe atrophy related to incidence of both dementia and major depression in 70-year-olds followed over 10 years. Eur J Neurol 2015;22. 781e788.e49ee50. 76. Resnick HE, Phillips B. Documentation of sleep apnea in nursing homes: United States 2004. J Am Med Dir Assoc 2008;9:260e264. 77. Onen F, Onen H. Obstructive sleep apnea and cognitive impairment in the elderly. Psychol Neuropsychiatr Vieil 2010;8:163e169. 78. Ngandu T, Lehtisalo J, Solomon A, et al. A 2-year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): A randomized controlled trial. Lancet 2015;385:2255e2263. 79. Lam LC, Chau RC, Wong BM, et al. A 1-year randomized controlled trial comparing mind body exercise (Tai Chi) with stretching and toning exercise on cognitive function in older Chinese adults at risk of cognitive decline. J Am Med Dir Assoc 2012;13:568.e15e568.e20. 80. Fiatarone Singh MA, Gates N, Saigal N, et al. The study of mental and resistance training (SMART) studydresistance training and/or cognitive training in mild cognitive impairment: A randomized, double-blind, double-sham controlled trial. J Am Med Dir Assoc 2014;15:873e880. 81. Burzynska AZ, Wong CN, Voss MW, et al. Physical activity is linked to greater Moment-to-Moment variability in spontaneous brain activity in older adults. PLoS One 2015;10:e0134819. 82. Farag I, Howard K, Hayes AJ, et al. Cost-effectiveness of a home-exercise program among older people after hospitalization. J Am Med Dir Assoc 2015;16:490e496. 83. Martinez-Lapiscina EH, Clavero P, Toledo E, et al. Virgin olive oil supplementation and long-term cognition: The PREDIMED-NAVARRA randomized, trial. J Nutr Health Aging 2013;17:544e552. 84. Shah R. The role of nutrition and diet in Alzheimer disease: A systematic review. J Am Med Dir Assoc 2013;14:398e402. 85. Farr SA, Price TO, Dominguez LJ, et al. Extra virgin olive oil improves learning and memory in SAMP8 mice. J Alzheimers Dis 2012;28:81e92. 86. Anderson K, Grossberg GT. Brain games to slow cognitive decline in Alzheimer’s disease. J Am Med Dir Assoc 2014;15:536e537. 87. Brouwer-Brolsma EM, Dhonukshe-Rutten RA, van Wijngaarden JP, et al. Cognitive performance: A cross-sectional study on serum vitamin D and its interplay with glucose homeostasis in Dutch older adults. J Am Med Dir Assoc 2015;16:621e627. 88. Morley JE. Dementia: Does vitamin D modulate cognition? Nat Rev Neurol 2014;10:613e614. 89. Brouwer-Brolsma EM, van de Rest O, Tieland M, et al. Serum 25-hydroxyvitamin D is associated with cognitive executive function in Dutch prefrail and frail elderly: A cross-sectional study exploring the associations of 25-hydroxyvitamin D with glucose metabolism, cognitive performance and depression. J Am Med Dir Assoc 2013;14:852.e9e852.e17. 90. D’Amico F, Rehill A, Knapp M, et al. Maintenance cognitive stimulation therapy: An economic evaluation within a randomized controlled trial. J Am Med Dir Assoc 2015;16:63e70. 91. Loraine J, Taylor S, McAllister M. Cognitive and physical stimulation therapy. J Am Med Dir Assoc 2014;15:140e141. 92. Berg-Weger M, Tebb S, Henderson-Kalb J, et al. Cognitive stimulation therapy: A tool for your practice with persons with dementia? J Am Med Dir Assoc 2015;16:795e796. 93. Kawashima R, Hiller DL, Sereda SL, et al. SAIDO learning as a cognitive intervention for dementia care: A preliminary study. J Am Med Dir Assoc 2015;16:56e62. 94. Wingbermuehle C, Bryer D, Berg-Weger M, et al. Baseball reminiscence league: A model for supporting persons with dementia. J Am Med Dir Assoc 2014;15:85e89. 95. Van Bogaert P, Van Grinsven R, Tolson D, et al. Effects of a SolCos model-based individual reminiscence on older adults with mild to moderate dementia due to Alzheimer disease: A pilot study. J Am Med Dir Assoc 2013;14:528.e9e528.e13. 96. Malmstrom TK, Morley JE. The frail brain. J Am Med Dir Assoc 2013;14: 453e455. 97. Nishiguchi S, Yamada M, Fukutani N, et al. Differential association of frailty with cognitive decline and sarcopenia in community-dwelling older adults. J Am Med Dir Assoc 2015;16:120e124. 98. Kelaiditi E, Cesari M, Canevelli M, et al. Cognitive frailty: Rational and definition from an (I.A.N.A./I.A.G.G.) International consensus group. J Nutr Health Aging 2013;17:726e734. 99. Woods AJ, Cohen RA, Pahor M. Cognitive frailty: Frontiers and challenges. J Nutr Health Aging 2013;17:741e743. 100. Morley JE, Vellas B, van Kan GA, et al. Frailty consensus: A call to action. J Am Med Dir Assoc 2013;14:392e397. 101. Morley JE. Frailty screening comes of age. J Nutr Health Aging 2014;18: 453e454. 102. Shimada H, Makizako H, Doi T, et al. Combined prevalence of frailty and mild cognitive impairment in a population of elderly Japanese people. J Am Med Dir Assoc 2013;14:518e524.

921

103. Abellan van Kan G, Rolland YM, Morley JE, Vellas B. Frailty: Toward a clinical definition. J Am Med Dir Assoc 2008;9:71e72. 104. Woo J, Yu R, Wong M, et al. Frailty screening in the community using the FRAIL scale. J Am Med Dir Assoc 2015;16:412e419. 105. Woo J, Leung J, Morley JE. Comparison of frailty indicators based on clinical phenotype and the multiple deficit approach in predicting mortality and physical limitation. J Am Geriatr Soc 2012;60:1478e1486. 106. Gardiner PA, Mishra GD, Dobson AJ. Validity and responsiveness of the FRAIL scale in a longitudinal cohort study of older Australian women. J Am Med Dir Assoc 2015;16:781e783. 107. Morley JE. Is it possible to prevent injurious falls? Eur Geriatr Med 2014;5: 75e77. 108. Morley JE, Rolland Y, Tolson D, Vellas B. Increasing awareness of the factors producing falls: The mini falls assessment. J Am Med Dir Assoc 2012;13: 87e90. 109. Halil M, Cemal Kizilarslanoglu M, Emin Kuyumcu M, et al. Cognitive aspects of frailty: Mechanisms behind the link between frailty and cognitive impairment. J Nutr Health Aging 2015;19:276e283. 110. Dartigues JF, Amieva H. Cognitive frailty: Rational and definition from an (I.A.N.A./ I.A.G.G.) international consensus group. J Nutr Health Aging 2014;18:95. 111. Buchman AS, Bennett DA. Cognitive frailty. J Nutr Health Aging 2013;17: 738e739. 112. Morley JE, Philpot CD, Gill D, Berg-Weger M. Meaningful activities in the nursing home. J Am Med Dir Assoc 2014;15:79e81. 113. Ouden MD, Bleijlevens MH, Meijers JM, et al. Daily (in)activities of nursing home residents in their wards: An observation study. J Am Med Dir Assoc 2015;16:963e968. 114. Nishiguchi S, Yamada M, Tanigawa T, et al. A 12-week physical and cognitive exercise program can improve cognitive function and neural efficiency in community-dwelling older adults: A randomized controlled trial. J Am Geriatr Soc 2015;63:1355e1363. 115. Valenzuela T. Efficacy of progressive resistance training interventions in older adults in nursing homes: A systematic review. J Am Med Dir Assoc 2012;13: 418e428. 116. Colberg SR, Somma CT, Sechrist SR. Physical activity participation may offset some of the negative impact of diabetes on cognitive function. J Am Med Dir Assoc 2008;9:434e438. 117. Rolland Y, Abellan van Kan G, Vellas B. Physical activity and Alzheimer’s disease: From prevention to therapeutic perspectives. J Am Med Dir Assoc 2008;9:390e405. 118. Weening-Dijksterhuis E, de Greef MH, Scherder EJ, et al. Frail institutionalized older persons: A comprehensive review on physical exercise, physical fitness, activities of daily living, and quality-of-life. Am J Phys Med Rehabil 2011;90: 156e168. 119. Cheng ST, Chow PK, Song YQ, et al. Mental and physical activities delay cognitive decline in older persons with dementia. Am J Geriatr Psychiatry 2014;22:63e74. 120. Cohen-Mansfield J, Libin A, Marx MS. Nonpharmacological treatment of agitation: A controlled trial of systematic individualized intervention. J Gerontol A Biol Sci Med Sci 2007;62:908e916. 121. Ballard C, Brown R, Fossey J. Brief Psycho-Social Therapy (BPST) for the treatment of agitation in Alzheimer’s disease (The CALM-AD trial). Am J Geriatr Psychiatry 2009;17:726e733. 122. Cohen-Mansfield J, Werner P. Management of verbally disruptive behaviors in nursing home residents. J Gerontol A Biol Sci Med Sci 1997;52: 369e377. 123. Kolanowski A, Litaker M, Buettner I, et al. A randomized clinical trial of theory-based activities for the behavioral symptoms of dementia in nursing home residents. J Am Geriatr Soc 2011;59:1032e1041. 124. Resnick B, Galik E, Boltz M. Function focused care approaches: Literature review of progress and future possibilities. J Am Med Dir Assoc 2013;14: 313e318. 125. Li HC, Wang HH, Chou FH, Chen KM. The effect of music therapy on cognitive functioning among older adults: A systematic review and meta-analysis. J Am Med Dir Assoc 2015;16:71e77. 126. Vankova H, Holmerova I, Machacova K, et al. The effect of dance on depressive symptoms in nursing home residents. J Am Med Dir Assoc 2014; 15:582e587. 127. Rosher RB, Robinson S. Impact of the Eden Alternative on family satisfaction. J Am Med Dir Assoc 2005;6:189e193. 128. Afonso C, Graça P, Kearney JM, et al. Physical activity in European seniors: Attitudes, beliefs and levels. J Nutr Health Aging 2001;5:226e229. 129. Bemelmans R, Gelderblom GJ, Jonker P, de Witte L. Effectiveness of Robot Paro in intramural psychogeriatric care: A multicenter quasi-experimental study. J Am Med Dir Assoc 2015;16:946e950. 130. Robinson H, MacDonald B, Kerse N, Broadbent E. The psychosocial effects of a companion robot: A randomized controlled trial. J Am Med Dir Assoc 2013; 14:661e667. 131. Michel JP, Franco A. Geriatricians and technology. J Am Med Dir Assoc 2014; 15:860e862. 132. Banks WA. Artificial emotions: Robots caring for the elderly. J Am Med Dir Assoc 2013;14:635e636. 133. Bemelmans R, Gelderblom GJ, Jonker P, de Witte L. Socially assistive robots in elderly care: A systematic review into effects and effectiveness. J Am Med Dir Assoc 2012;13:114e120.e1.

922

B.J. Messinger-Rapport et al. / JAMDA 16 (2015) 911e922

134. Lattanzio F, Abbatecola AM, Bevilacqua R, et al. Advanced technology care innovation for older people in Italy: Necessity and opportunity to promote health and wellbeing. J Am Med Dir Assoc 2014;15:457e466. 135. Banks MR, Willoughby LM, Banks WA. Animal-assisted therapy and loneliness in nursing homes: Use of robotic versus living dogs. J Am Med Dir Assoc 2008; 9:173e177. 136. Morley JE, Sanford AM. The God card: Spirituality in the nursing home. J Am Med Dir Assoc 2014;15:533e535. 137. Tolson D, Morley JE. Physical restrains: Abusive and harmful. J Am Med Dir Assoc 2012;13:311e313. 138. Bleijlevens MH, Gulpers MJ, Capezuti E, et al. Process evaluation of a multicomponent intervention program (EXBELT) to reduce belt restraints in nursing homes. J Am Med Dir Assoc 2013;14:599e604. 139. Tolson D, Rolland Y, Andrieu S, et al. International Association of Gerontology and Geriatrics: A global agenda for clinical research and quality of care in nursing homes. J Am Med Dir Assoc 2011;12:184e189. 140. Rolland Y, Tolson D, Morley JE, Vellas B. The International Association of Gerontology and Geriatrics (IAGG) nursing home initiative. J Am Med Dir Assoc 2014;15:307e308. 141. Guyat GH, Alk EA, Crother M, et al, for the American College of Chest Physicians Antithrombotic Therapy and Prevention of Thrombosis Panel. Executive Summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012;141:7Se47S. 142. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation 2014;130:2071e2104. 143. Caprini JA, Arcelus JI, Reyna JJ. Effective risk stratification of surgical and nonsurgical patients for venous thromboembolic disease. Semin Hematol 2001;38:12e19. 144. Leibson CL, Petterson TM, Smith CY, et al. Rethinking guidelines for VTE risk among nursing home residents: A population-based study merging medical record detail with standardized nursing home assessments. Chest 2014;146: 412e421. 145. Gage BF, Waterman AD, Shannon W, et al. Validation of clinical classification schemes for predicting stroke: Results from the National Registry of Atrial Fibrillation. JAMA 2001;285:2864e2870. 146. Lip GY, Nieuwlaat R, Pisters R, et al. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: The Euro Heart Survey on Atrial Fibrillation. Chest 2010;137:263e272. 147. Ghaswalla PK, Harpe SE, Slattum PW. Warfarin use in nursing home residents: Results from the 2004 National Nursing Home Survey. Am J Geriatr Pharmacother 2012;10:25e36. 148. Bahri O, Roca F, Lechani T, et al. Underuse of oral anticoagulation for individuals with atrial fibrillation in a nursing home setting in France:

149.

150.

151.

152.

153.

154.

155.

156.

157.

158.

159.

160.

161.

Comparisons of resident characteristics and physician attitude. J Am Geriatr Soc 2015;63:71e76. Fang MC, Go AS, Chang Y, et al. A new risk scheme to predict warfarinassociated hemorrhage: The ATRIA (Anticoagulation and Risk Factors in Atrial Fibrillation) Study. J Am Coll Cardiol 2011;58:395e401. Gage BF, Yan Y, Milligan PE, et al. Clinical classification schemes for predicting hemorrhage: Results from the National Registry of Atrial Fibrillation (NRAF). Am Heart J 2006;151:713e719. Pisters R, Lane DA, Nieuwlaat R, et al. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: The Euro Heart Survey. The Euro Heart Survey. Chest 2010;138:1093e1100. Apostolakis S, Lane DA, Guo Y, et al. Performance of the HEMORR 2 HAGES, ATRIA, and HAS-BLED bleeding risk-prediction scores in nonwarfarin anticoagulated atrial fibrillation patients. J Am Coll Cardiol 2013;61:386e387. Roldán V, Marín F, Fernández H, et al. Predictive value of the HAS-BLED and ATRIA bleeding scores for the risk of serious bleeding in a “real-world” population with atrial fibrillation receiving anticoagulant therapy. Chest 2013;143:179e184. Pieracci FM, Eachempati SR, Shou J, et al. Use of long-term anticoagulation is associated with traumatic intracranial hemorrhage and subsequent mortality in elderly patients hospitalized after falls: Analysis of the New York State Administrative Database. J Trauma 2007;63:519e524. Gangavati AS, Kiely DK, Kulchycki LK, et al. Prevalence and characteristics of traumatic intracranial hemorrhage in elderly fallers presenting to the emergency department without focal findings. J Am Geriatr Soc 2009;57: 1470e1474. Sardar P, Chatterjee S, Chaudhari S, et al. New oral anticoagulants in elderly adults: Evidence from a meta-analysis of randomized trials. J Am Geriatr Soc 2014;62:857e864. Halvorsen S, Atar D, Yang H, et al. Efficacy and safety of apixaban compared with warfarin according to age for stroke prevention in atrial fibrillation: Observations from the ARISTOTLE trial. Eur Heart J 2014;35:1864e1972. Halperin JL, Hankey GJ, Wojdyla DM, et al. Efficacy and safety of rivaroxaban compared with warfarin among elderly patients with nonvalvular atrial fibrillation in the rivaroxaban once daily, oral, direct factor Xa inhibition compared with vitamin K antagonism for prevention of stroke and embolism trial in atrial fibrillation (ROCKET AF). Circulation 2014;130: 138e146. Eikelboom JW, Wallentin L, Connolly SJ, et al. Risk of bleeding with 2 doses of dabigatran compared with warfarin in older and younger patients with atrial fibrillation. Circulation 2011;123:2363e2372. Hijazi Z, Hohnloser SH, Oldgren J, et al. Efficacy and safety of dabigatran compared with warfarin in relation to baseline renal function in patients with atrial fibrillation: A RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) trial analysis. Circulation 2014;129:961e970. Graham DJ, Reichman ME, Wernecke M, et al. Cardiovascular, bleeding, and mortality risks in elderly medicare patients treated with dabigatran or warfarin for nonvalvular atrial fibrillation. Circulation 2015;131:157e164.