Anemia and its impact on function in nursing home residents: What do we know?

C E A R T I C L E

Anemia and its impact on function in nursing home residents:What do we know?Valerie K. Sabol, PhD, CRNP (Assistant Professor)1, Barbara Resnick, PhD, CRNP, FAAN, FAANP (Professor)1,Elizabeth Galik, PhD, CRNP (Assistant Professor)1, Ann Gruber-Baldini, PhD (Associate Professor)2, PatriciaGonce Morton, RN, PhD, CRNP, FAAN (Associate Dean for Academic Affairs)1 & Gregory E. Hicks, PT, PhD(Assistant Professor)3

1 Organizational Systems and Adult Health, University of Maryland School of Nursing, Baltimore, Maryland2 Division of Gerontology, Department of Epidemiology and Preventive Medicine, University of Maryland School of Medicine, Baltimore, Maryland3 Department of Physical Therapy, University of Delaware, Newark, Delaware

KeywordsAnemia; elderly; physical function;

long-term care (LTC).

CorrespondenceValerie K. Sabol, PhD, CRNP,

Organizational Systems and Adult Health,

University of Maryland School of Nursing,

655 W. Lombard Street, 3rd Floor,

Baltimore, MD 21201-1579.

Tel: 410-706-7806;

Fax: 410-706-0344;

E-mail: [email protected]

Received: June 2008;

accepted: August 2008

doi:10.1111/j.1745-7599.2009.00471.x

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Abstract

Purpose: To provide the advanced practice nurse (APN) information on theprevalence and causes of anemia in elderly nursing home (NH) residents, inorder to affect diagnostic and management strategies that may help improvephysical function and mobility outcomes.Data Sources: Literature review of current peer-reviewed research articles.Conclusions: In the United States, the prevalence of anemia increases withadvancing age, and are reported to be much higher among older NH residentsthan among community-dwelling older adults. Causes of anemia among theelderly are often multifactorial. Older individuals with anemia, including mildanemia and even low normal level, have demonstrated lower muscle strength,physical function, mobility, and increased morbidity and mortality outcomes.Implications for Practice: Given the potentially significant relationshipbetween anemia and physical performance outcomes among NH residents,gaining a better understanding will help guide future evidence-based careby allowing the APN an opportunity to tailor both medical and restorativecare interventions. Because anemia is a potentially modifiable condition,intervention may preserve, limit, or reverse functional impairment and/ordisablement, and allow for maximal functional independence.

Introduction

Definition of anemia

Anemia is not a disease, but rather a sign of an

underlying illness. It is defined as any condition in

which the number of red blood cells (RBCs), the

amount of hemoglobin, and/or the volume of RBCs is

less than normal. More specifically, the World Health

Organization (WHO) defined anemia for women as a

hemoglobin (Hgb) level less than 12 g/dL, and for men,

a Hgb level less than 13 g/dL (WHO, 1968). These

values are measured concentrations, rather than absolute

measurements, and thus interpretation should include

evaluation of individual factors. For example, changesin plasma volume may skew concentration values;therefore, comparison of baseline and/or previous Hgblevels is useful when evaluating trends and thereby aidsin interpretation of findings.

Prevalence of anemia in the elderly

Hgb levels are noted to decline with age (Ania,Suman, Fairbanks, Rademacher, & Melton, 1997; Beghe,Wilson, & Ershler, 2004; Ershler et al., 2005), and theprevalence rates of anemia (as per WHO criteria) fornoninstitutionalized individuals 65–74 years of age are

Journal of the American Academy of Nurse Practitioners 22 (2010) 3–16 © 2010 The Author(s) 3Journal compilation © 2010 American Academy of Nurse Practitioners

Impact of anemia on function in NH residents V.K. Sabol et al.

7.8% for men and 8.5% for women; for those in the75–84 age category prevalence rates increase to 15.7%for men and 10.3% for women (Balducci, 2003; Begheet al.; Brill & Braumgardner, 2000; Guralnik, Eisenstaedt,Ferrucci, Klein, & Woodman, 2004). Among those whoare 85 years of age and older, the prevalence rates ofanemia are 26.1% for men and 20.1% for women(Balducci, 2003; Beghe et al.; Brill & Braumgardner;Guralnik et al.). Among all age groups there is a slightlyhigher prevalence of anemia in men when compared towomen, although these gender differences are generallyrelated to the two different cut points for defining anemiain men and women (Guralnik et al.). Multiple studieshave noted an almost threefold increase in the prevalenceof anemia among elderly African Americans compared toCaucasians, nonblack Hispanics, and Asian Americans(Denny, Kuchibhatla, & Cohen, 2006; Zakai et al., 2005).Anemia among community-dwelling non-Hispanic blacksaged 65 or older was 27.8%, which again is nearly threetimes more prevalent than elderly Caucasians (27.8%vs. 9%, respectively; Gaskell, Derry, Moore, & McQuay,2008; Guralnik et al.).

In nursing home (NH) settings the prevalence of anemiahas increased over time. In the 1999 National NursingHome Survey (NNHS) summary (Jones, 2002), only 2.4%of NH residents were reported as having a diagnosis ofanemia (ICD-9 codes 280–284; Department of Healthand Human Services [DHHS], 1989). More recently, theCenters for Medicare and Medicaid (CMS) indicated thatthe prevalence rate among elderly NH residents wasmuch higher, with a national average of 26.5% (Centersfor Medicare and Medicaid Services). Additionally,prevalence rates of anemia among NH residents havebeen consistently reported to be approximately 50%(Artz et al., 2004; DeMaria, Ripamonti, Sandri, Ceretti,& Ferrantini, 2005; Resnick, Sabol, Galik, & Gruber-Baldini, in review; Robinson et al., 2007). These extremevariations in prevalence may be because of differencesin indirect (i.e., chart history, billing codes) and directmeasurement (i.e., Hgb laboratory data) methods.

Identifying causes of anemia

There are many contributing causes to anemia,although these generally fall under the major categoriesof nutritional deficiency (i.e., iron, cobalamin, folate),iron deficiency because of acute or chronic blood loss,anemia of chronic disease (ACD), and anemia of chronickidney disease (anemia of CKD).

Nutritional deficiencies

Aging is associated with a progressive decline in thedigestion and absorption of nutrients related to decreased

gastric and intestinal secretions, motility, nutrient absorb-ing surface area, and splanchnic circulation (Caruso& Silliman, 2008). Additionally, age-related changes inreduced olfaction and taste may cause a physiologicanorexia that affects nutritional choices and intake.Subsequently, 34% of the cases of anemia among theelderly are related to nutritional deficits, either throughinadequate dietary intake and/or reduced absorption ofthe nutrients necessary for erythropoiesis, a regulatedprocess of RBC production (Beghe et al., 2004; Guralniket al., 2004).

Iron deficiency anemia

Inadequate iron dietary intake and/or inadequate ironabsorption from a variety of medical conditions can lead toiron deficiency anemia (IDA). Among NH residents, 40%of anemia cases are classified as IDA (Artz et al., 2004;Chen & Cook-Newell, 1989; Kalchthaler & Tan, 1980).IDA occurs from two main mechanisms: (a) inadequateintake and/or absorption of iron and/or (b) acute orchronic loss of iron, typically through gastrointestionalbleeding that exceeds an individual’s ability to absorbenough iron and replace losses. IDA related to poordietary intake, however, is relatively uncommon inelderly NH residents compared to other populations(i.e., children, adolescents, and women of childbearingage; Clark, 2008; Looker, Dallman, Caroll, Gunter, &Johnson,1997). Conversely, anemia as a result of bloodloss is prevalent among NH residents (Artz et al.; Begheet al., 2004; Eisenstaedt, Penninx, & Woodman, 2006).Normally, after the RBC completes its life cycle, ironcontained within the RBC is extracted and stored in theliver and spleen to be recycled for future RBC production.

Iron loss from acute and/or chronic blood loss

Normally, after the RBC completes its life cycle, ironcontained within the RBC is extracted and stored inthe liver and spleen to be recycled for future RBCproduction. During episodes of acute and/or chronicbleeding, when iron is unable to be recycled andexisting stores are depleted, IDA may develop (Smith,2000; Umbreit, 2005). Additional diagnostic workup(i.e., endoscopy) may be indicated to identify a bleed-ing source and/or rule out underlying disease processes.Premature destruction or hemolysis of RBCs by eitherimmune (i.e., autoimmune, drug-induced reactions) ornonimmune pathways (i.e., congenital defects, acquiredinfections, mechanical destruction) may also cause IDAto develop. Functional iron deficiency may develop incases where iron stores may be adequate, but inflamma-tory processes impair metabolism of available iron stores(Jongen-Lavrencic et al., 1997; Nordstrom et al., 1997).For example, circulating concentrations of hepcidine, a

4

V.K. Sabol et al. Impact of anemia on function in NH residents

glycoprotein synthesized in the liver that is stimulatedby the presence of inflammatory cytokine interleukin-6(IL-6), may impair duodenal absorption of iron andrelease of recycled iron from macrophages (Andrews,2004; Ferucci et al., 2005; Nemeth et al., 2004). Helicobac-ter pylori related (corpus) gastritis is also another possiblecause of IDA, as the organism may impair iron absorption(Choi, 2006).

Cobalamin (vitamin B12) and folate nutritionaldeficiency

It has been estimated that approximately 5.9%–15% ofcommunity-dwelling older adults over the age of 65 haveanemia related to cobalamin (vitamin B12) deficiency and6.4% have anemia related to folate deficiency (Guralniket al., 2004). Although cobalamin and folate deficiencieshave been noted among NH residents, the prevalencerates of anemia as a result of these nutrient deficiencieshave been estimated to be lower at less than 5%, whichis thought in large part to be because of the wide use ofmultivitamin supplementation in NHs (Artz et al., 2004;Chernetsky, Sofer, Rafael, & Ben-Israel, 2002; Guralnik,Ershler, Schrier, & Picozzi, 2005).

Cobalamin deficiency among older adults is thoughtto be primarily related to age-related changes in gastricatrophy and decreases in acidic gastric secretions, pepsin,and intrinsic factor (IF), required for its digestion andabsorption in the terminal portion of the ileum (Sipponen,Laxen, Huotari, & Harkonen, 2003). Malabsorption ofcobalamin is also thought to be related to the chronic useof H2 receptor antagonists, and proton pump inhibitors,which reduces the acidity of gastric acids necessary forcleaving cobalamin from dietary proteins and otherfood sources (Andres, Noel, & Abdelghani, 2003).Other possible factors include chronic use of biguanides(metformin), chronic alcoholism, gastric surgery or gastricreconstruction, partial pancreatic exocrine failure, andautoimmune disorders (i.e., Sjogren’s syndrome; Andreset al., 2004). Although some studies have reported dietarydeficiency of cobalamin among older adults (i.e., strictvegan diets, chronic malnutrition), it is not until hepaticreserves of cobalamin are depleted that insufficient dietaryintake will result in symptomatology (Andres et al.). Itremains prudent, however, to obtain a thorough socialand dietary history prior to a new NH admission to allowfor early diagnosis and intervention as necessary.

Clinical manifestations of cobalamin deficiency caninclude a spectrum of hematologic (i.e., pancytopenia),neurologic (i.e., peripheral neuropathy, paresthesias,impaired vibration, proprioception, balance, and gait),and psychiatric (i.e., impaired memory, irritability,depression, acute psychosis, and dementia) sequelae(Oh & Brown, 2003). With the exception of neurologic

abnormalities, these symptoms are mimicked by folatedeficiency (Smith, 2001). Consequently, timely symptomrecognition and intervention in B12 deficiency is criticalas there may be a time-limited window of less than6 months before central nervous system symptomsbecome irreversible (Carmel, 2000; Martin, Francis,Protech, & Huff, 1992). This is particularly importantbecause large doses of folic acid can correct the anemiacaused by B12 deficiency (Hoffbrand, 2008). Folic acid,however, cannot reverse the neurologic sequelae of B12deficiency if left untreated, and therefore it is criticalto correctly diagnose the specific nutrient deficiencyand provide directed supplementation. Finally, becausefolate deficiency is often associated with excessivealcohol consumption and malnutrition, screening isparticularly important upon NH admission and may allowfor additional supportive interventions beyond folatesupplementation.

Anemia of chronic disease and/or inflammation

Among community-dwelling older adults, approxi-mately 32% of anemia cases are related to chronic diseasestates (20%), renal failure (8%), or both (4%; Guralniket al., 2004). For elderly NH residents, the prevalence ofACD has been estimated to range from 13% (Artz et al.,2004) to 66% (Chernetsky et al, 2002). Again, theseextreme variations in prevalence may be a result of dif-ferences in indirect and direct measurement of anemia,and perhaps because ACD is often a diagnosis of exclusion,which may alter prevalence reporting methods.

ACD is immune-driven and has also been called ‘‘ane-mia of chronic inflammation’’; it has been associatedwith acute and chronic infections (i.e., viral, bacterial,parasitic, fungal), autoimmune inflammatory states (i.e.,rheumatoid arthritis, systemic lupus erythematosus, andconnective-tissue diseases, vasculitis, sarcoidosis, inflam-matory bowel disease), malignancy (i.e., hematologic andsolid tumor), chronic rejection after solid organ transplan-tation, and CKD and inflammation (Weiss & Goodnough,2005). Complicating diagnosis and management of under-lying ACD pathology include the frequency of acuteexacerbations of chronic disease states, the frequencyof acute events (i.e., infections surgical procedures), andthe existence of multiple comorbid disease states com-mon in many older adults. Additionally, management ofanemia related to a single disease state may be just aschallenging as managing anemia thought to be related tomultiple, comorbid disease states, particularly if diseaseexacerbations or event occurrences are frequent and offerlittle, if any, recovery time.

The central feature of ACD is the dysregulation ofiron homeostasis. Increased concentrations of inflam-matory cytokines (i.e., tumor necrosis factor-α [TNF-α],

5


interferon-γ [IFN-γ ], interleukin-1β [IL-1β], and IL-6),are thought to not only increase ferritin synthesis caus-ing hypoferremia but also to cause an increased uptakeand retention of iron by macrophages and hepatocytes,thereby limiting its availability for erythropoiesis (Torti &Torti, 2002). Additionally, these inflammatory cytokinesare thought to suppress erythropoietin (EPO) production,blunt the response to existing EPO levels by interactingwith EPO receptors and by possibly contributing to adecreased erythrocyte life span (Penninx et al., 2004;Weiss & Goodnough, 2005). The increased levels ofthese inflammatory markers may in part explain the linkbetween inflammation and subsequent physical decline.In cases of initially unexplained anemia, myelodysplas-tic syndrome is one of the most common findings afterfurther diagnostic workup (Guralnik et al., 2004).

Anemia of CKD

The link between CKD and anemia is well estab-lished (Hsu, McCulloch, & Curhan, 2001). Recent reportsfrom the third National Health and Nutrition Examina-tion Survey (NHANES III) indicate that approximately11% of individuals (over 19 million) in the generalU.S. population have CKD, defined as an estimatedglomerular filtration rate (GFR) of 60 mL/min/1.73 m2

as determined by the four-variable Modification ofDiet in Renal Disease (MDRD) equation (Coresh,Astor, Greene, Eknoyen, & Levey, 2003): GFR = 186 ×(creatinine)−1.154 × age−0.203 × 1.212 (if African Ameri-can) × 0.742 (if female).

Serum creatinine levels alone are poor indicators ofrenal function, and the MDRD predictive formula ispreferred over the Cockcroft–Gault formula (Cockcroft& Gault, 1976) and even 24-h urine collections, whichmay overestimate GFR by as much as 16% and 19%,respectively (Levey et al., 1999). Approximately 50%of NH residents with CKD (Stage 3 or greater, GFR<60 mL/min/1.73 m2) have anemia (Kazmi et al., 2001;McClellan et al., 2004), and it has been estimated thatresidents with CKD were more likely to have anemia thanthose without CKD (64.9% with CKD vs. 55.7% withoutCKD, odds ratio [OR] = 1.47, 95% confidence interval[CI] = 1.33–1.63; Robinson et al., 2007). Additionalstudies have reported that of the 36%–48% of elderlyNH residents identified as anemic, a wide range(10%–43%) was noted for those individuals who also hadCKD, suggesting nonlinear trends between the degree ofCKD and the degree of anemia (Artz et al., 2004; Garget al., 2004; Robinson et al., 2007).

In addition to the aforementioned dysregulation of ironhomeostasis of ACD, the effects of renal insufficiencysuch as decreased EPO production and accumulatinguremic toxins are thought to be additional contributing

factors toward anemia of CKD (Eschbach, 2002; Weiss &Goodnough, 2005). Also, declining serum testosteronelevels may be an important consideration for oldermen with CKD as testosterone is thought to enhanceethryopoiesis by increasing EPO secretion from thekidneys (Weber, Walsh, Peters, & Spivak, 1991). Usingdata from the Invecchiare in Chianti study (InCHIANTIstudy or Aging in the Chianti Area, Tuscany, Italy),Ferrucci et al. (2006) found that low testosterone levelswere associated with anemia in both men and women,and were also predictive of anemia in nonanemicindividuals over the following 3 years.

Clinical consequences of anemia

Anemia is thought to impact a variety of out-comes, including physical functioning, mobility, andcardiovascular-related morbidity and mortality. Themechanism by which anemia impacts physical func-tion and mobility is not well defined, but is thought tobe because of the limited numbers of RBCs available,and hence their diminished oxygen-carrying capacityand decreased oxygen-delivery to the muscles (Dodd,Powers, Brooks, & Crawford,1993). Both anemia andanemia associated with CKD have been associated withlower muscle strength and poorer physical performance(Cesari et al., 2004; Chaves et al., 2005; Chaves, Ashar,Guralnik, & Fried, 2002; Ouslander et al., 2005; Penninxet al., 2003, 2004, 2005), disability and falls (Penninxet al., 2004, 2005), and increased morbidity and mor-tality (Denny, Kuchibhatla, & Cohen, 2006; Nissenson,Goodnough, & Dubois, 2003; Zakai et al., 2005). In addi-tion, there is some evidence that older adults with Hgblevels >12.0 gm/dL have better health outcomes such asbetter hand grip strength, knee extensor strength, abil-ity to rise from a chair, standing balance, and walkingspeed compared to those with Hgb levels <12.0 gm/dL(Chaves et al., 2002; Penninx et al., 2003, 2004). AmongNH residents, however, no differences in impairmentin functional activities were noted during chart review(DeMaria et al, 2005; Landi et al., 2007). In some samples,however, trends suggest that function is more impairedin those with anemia, particularly when the anemia isassociated with CKD (DeMaria et al., 2005; Resnick et al.,in review).

There is mounting evidence to suggest that anemia andanemia of CKD adversely affect the cardiovascular sys-tem (Astor, Coresh, Heiss, Pettitt, & Sarnak, 2006; Go,Chertow, Fan, McCullough, & Hsu, 2004; London, 2003;Mann, Gerstein, Pogue, Bosch, & Yusuf, 2001; O’Riordan& Foley, 2000). Mild anemia is often asymptomatic, butduring periods of activity or exercise, anemia may mani-fest itself in the form of tachycardia, palpitations, dyspnea

6


on exertion, and fatigue (Adamson & Longo, 2008). Thiscompensatory tachycardia places an additional strain onthe myocardial cells, particularly for those elderly individ-uals with preexisting comorbid conditions and/or reducedcompensatory mechanisms, which may further exacer-bate tissue hypoxia and fatigue (Caruso & Silliman, 2008).In cases of severe anemia, symptoms may occur even atrest and may cause intolerance to any form of activityand/or exercise, which may promote deconditioning andfurther functional decline.

Both anemia and CKD were found to be independentrisk factors for death among patients with heart failureand after myocardial infarction (McClellan, Flanders,Langston, Jurkovitz, & Presley, 2002). In severe heartfailure, severity of anemia was predictive of mortality(Komajda et al., 2006; Langston, Presley, Flanders, &McClellan, 2003; Mozaffarian, Nye, & Levy, 2003),and treatment interventions to correct anemia in renalpatients have been shown to reverse mild left ventriculardilation (Sikole, Polenakovic, Spiroska, Polenakovic, &Masin, 2002; Steinberg, Wexler, & Iaian, 2002; Tsakiris,2000). These findings suggest that early targeted medicaland restorative care therapies could be very beneficialto elderly NH residents in helping to attain and/ormaintain physical function and mobility.

Diagnosis of anemia

In light of the relatively mild and typically insidiousonset of anemia, coupled with symptom presentationthat is often associated with many other disease states, theclinical significance of anemia among the elderly is oftennot recognized, evaluated, and/or managed appropriately(Guralnik et al., 2004). In a study (Izaks, Westendorp,& Knook, 1999) that evaluated Hgb concentration, 10-year survival, and primary cause of death among 755community-dwelling elders (aged 85 years and older),it was noted that anemia in older persons was notbecause of aging itself, but rather was associated with poorhealth status and/or underlying disease. Subsequently, itwas recommended that elderly individuals classified asanemic (as per WHO criteria) but without evidence ofovert clinical disease should receive further diagnosticevaluation and treatment consideration.

Taking careful medical, dietary, and psychosocial histo-ries, and performing a comprehensive physical examina-tion, can help identify underlying disease and potentialcauses of anemia (Table 1). For example, discovery ofpertinent positive review of system complaints such asanosmia (loss of sense of smell), dysgeusia (altered senseof taste), dysphagia (difficulty swallowing), or odynopha-gia (painful swallowing), or poor dentition or loose and/orill-fitting dentures may prove invaluable in terms of

preventing malnutrition-related anemias (Sabol, 2004).More general complaints, such as anorexia, early satiety,fatigue, and shortness of breath, may further impact nutri-tional choices and intake patterns, and may be the initialpresentation of underlying disease. Complaints of dizzi-ness, dyspnea on exertion, palpitations, peripheral edema,and orthopnea may be indicative of congestive heartfailure and anemia-related hypoxia. Changes in mentalstatus or mood, and physical complaints of paresthesiasand changes in sensation, proprioception, and gait, may bepresenting symptoms of cobalamin deficiency (Dharmara-jan, Adiga, & Norkus, 2003; Hoffbrand, 2008). As always,it is prudent to review all prescribed, over-the-counter,and herbal medications known to cause anemia-relatedside-effects or interactions (i.e., aspirin, nonsteroidal anti-inflammatory drugs, prednisone). Finally, physical exam-ination should be individually tailored and systematicallyorganized to progress from a global to a more focusedexamination, as advanced clinical judgment warrants.Weight loss, muscle wasting (i.e., bitemporal muscles,proximal extremity muscle mass, hand intrinsic mus-cles), subcutaneous tissue loss, and edema are importantgeneral malnutrition observations (Hoffbrand, 2008).

Laboratory evaluation

It is the recommendation by the National KidneyFoundation-Kidney Disease Outcome Quality Initiative(NKF-KDOQI) that diagnostic workup should be initiatedwhen Hgb levels are less than 13.5 gm/dL for men and lessthan 12.0 gm/dL for women (NKF-KDOQI, 2006), andadditional diagnostic workup should be determined by theindividual’s history, clinical presentation, and likelihoodof disease (Tangalos, 2006). Table 2 outlines first- andsecond-order laboratory testing that may be helpful inidentifying different types of anemia.

Management of anemia

Nutritional deficiencies

Management of anemia is variable and usuallydepends on the underlying etiology (Table 3). Fornutritional deficiency anemia, the treatment focus ison supplementing the diet with the nutritional elementthat is deficient (i.e., cobalamin and/or folate), whichis typically safe and relatively inexpensive. Subjectivereports of symptom improvement, RBC indices, andserum cobalamin and/or folate levels are key clinicalmarkers to evaluate treatment progress (Zarowitz, 2006).In cases of IDA, the gold standard of treatment is200 mg/day of elemental iron, which is available invarying concentrations through supplementation withferrous salts (Zarowitz, 2006). Supplementation of iron

7

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ski,

Del

Gia

cco,

Alle

n,St

able

r,&

Lind

enb

aum

,199

8)•

Ifse

rum

cob

alam

inis

abov

e40

0p

g/m

L,

scre

enin

gat

5-ye

arin

terv

als

upto

the

age

of65

,an

dth

enan

nual

lyth

erea

fter

,

isre

com

men

ded

(Dha

rmar

ajan

&N

orku

s,

2003

)

8

V.K. Sabol et al. Impact of anemia on function in NH residentsTa

ble

1C

ontin

ued

Com

mon

anem

ias

Rev

iew

ofsy

stem

sP

hysi

cale

xam

Dia

gnos

ticte

sts

Inte

rpre

tatio

n

•M

ayha

veot

her

asso

ciat

edau

toim

-

mun

ed

isea

ses

with

spec

ific

dia

g-

nost

icev

alua

tion

(i.e.

,rh

eum

atoi

d

arth

ritis

)

• Fol

ate

Sim

ilar

toID

ASi

mila

rto

IDA

•M

CV

•M

CH

C

•Se

rum

cob

alam

in•

Fola

te

•H

omoc

yste

ine

•M

ethy

lmal

onic

acid

•El

evat

ed(m

acro

cytic

)•

Nor

moc

hrom

ic

•N

orm

al•

Dec

reas

ed•

Elev

ated

•N

orm

al

Chr

onic

dis

ease

and

/or

infla

mm

atio

n•

Mye

lod

ysp

last

icsy

ndro

me

•Sy

stem

icin

flam

mat

ory

and

infe

ctio

usd

isor

der

s•

Neo

pla

sms

•C

hron

icliv

erd

isea

se

•En

doc

rine

dis

ord

ers

Sim

ilar

toID

A,b

utsy

mp

tom

s

may

be

rela

ted

toun

der

lyin

g

dis

ease

pro

cess

Sim

ilar

toID

A,b

utsy

mp

tom

s

may

be

rela

ted

toun

der

lyin

g

dis

ease

pro

cess

•Si

mila

rto

IDA

,b

utad

diti

onal

dia

g-

nost

icla

bs

are

dis

ease

-sp

ecifi

c

inco

nsul

tatio

nw

ithhe

mat

olog

ist

and

/or

onco

logi

st

• Ane

mia

ofC

KDM

ayb

eas

ymp

tom

atic

,or

may

rep

orto

nly

sym

pto

ms

rela

ted

toun

der

lyin

gch

roni

cd

isea

se

(usu

ally

dev

elop

sym

pto

ms

with

in1

–2m

onth

sof

onse

tof

illne

ss,a

ndco

inci

des

with

dis

ease

seve

rity

)

Fatig

ue

Shor

tnes

sof

bre

ath

Loss

ofap

pet

ite/w

eigh

tlos

s

Sim

ilar

toID

A,b

utp

hysi

cale

xam

find

ings

are

pri

mar

ilyth

ose

of

the

und

erly

ing

dis

ease

pro

cess

•H

gb•

MC

V•

MC

HC

•R

etic

uloc

yte

coun

t•

Ferr

itin

•Se

rum

iron

•TI

BC

•Tr

ansf

erri

n

•Tr

ansf

erri

nsa

tura

tion

per

cent

age

•C

RP

•C

reat

inin

e

•R

arel

yd

rop

sto

<10

g/d

Lan

d/o

rco

rrel

ates

with

seve

rity

ofco

nditi

on•

Dec

reas

ed/n

orm

al

•N

orm

ochr

omic

•D

ecre

ased

•El

evat

ed/n

orm

al(in

diff

eren

tiatin

gb

etw

een

IDA

and

AC

D,

this

test

isth

em

ost

usef

ul;

resu

ltsm

ayb

esk

ewed

,how

ever

,with

liver

inju

ryor

chro

nic

infe

ctio

n/in

flam

mat

ion)

•D

ecre

ased

/nor

mal

•D

ecre

ased

/nor

mal

•D

ecre

ased

•D

ecre

ased

•El

evat

ed

•Fo

rG

FRca

lcul

atio

n•

Pan

cyto

pen

iam

ayb

eno

ted

ifin

flam

mat

ory

orin

fect

ious

pro

cess

aC

obal

amin

defi

cien

cyis

defi

ned

by

ase

rum

conc

entr

atio

nle

ssth

an15

0p

mol

/Lon

two

sep

arat

eoc

casi

ons

ora

seru

mco

bal

amin

leve

l<15

0p

mol

/Lan

da

tota

lser

umho

moc

yste

ine

leve

l>13

μmol

/L,o

r

am

ethy

lmal

onic

acid

leve

l>0.

4μm

ol/m

Lin

the

abse

nce

ofre

nalf

ailu

reor

fola

tean

dB

6d

efici

ency

(And

res

etal

.,20

04).

9


Table 2 Basic laboratory data for anemia

First-order laboratory testing

Complete blood count (CBC)

• RBC count (Hgb, hemocrit, reticulocyte count)

• RBC indices (mean cell volume [MCV], mean cell hemoglobin [MCH], mean cell hemoglobin concentration [MCHC], RBC distribution width [RDW])• White blood cell count (WBC; cell differential, nuclear segmentation of neutrophils)• Platelet count

• Cell morphology (anisocystosis [cell size], poikilocytosis [cell shape])

Second-order laboratory testing

Iron supply studies

• Serum iron

• Serum ferritin• Total iron binding capacity (TIBC)• Transferrin

• Transferrin saturation percentage

Reticulocyte count

• A reticulocyte (immature RBC) count is a measure of evaluating bone marrow function and erythropoietic activity in response to anemia

• A normal response to anemia would be an elevated reticulocyte count

Nutrition-related anemias

• Macrocytic (MCV >100 fL) anemias such as cobalamin and folate deficiency, reflect abnormal RBC maturation, and can be evaluated by checking

serum cobalamin and folate levels• The red cell folate concentration may be more reliable than serum folate levels (Smith, 2000)• Serum methylmalonic acid and homocysteine levels may be more reliable as these tests measure vitamin tissue stores; both methylmalonic

acid and homocysteine are elevated in cobalamin vitamin deficiency, but in folate deficiency, only homocysteine levels are elevated (Adamson

& Longo, 2008)

Iron deficiency anemia

• Microcytic (MCV <80 fL) anemias reflect reduced iron availability, heme synthesis, or globin production• Iron <60 μg/dL; ferritin <15 ng/mL; TIBC >400 μg/dL; transferrin saturation percentage <16% (Balducci, 2003)

(a) If hemolysis is suspected, check for damaged RBCs on a peripheral smear (i.e., RBC fragments, spherocytes), bone marrow response

with elevated reticulocyte counts, and biochemical evidence of RBC destruction (i.e., increased unconjugated bilirubin, increased

lactate dehydrogenase [LDH], and decreased/absent haptoglobin)

(b) If bleeding is suspected, a reticulocyte count and fecal occult blood test are indicated; additional workup to identify the site of bleeding

may include endoscopy (Smith, 2000)

Anemia of chronic disease

• MCV is normocytic/microcytic• Iron <60 μg/dL; ferritin >100 ng/mL; TIBC <250 μg/dL; transferrin saturation percentage <20% (Balducci, 2003)

• C-reactive protein (CRP) or IL-6 assays, are nonspecific inflammatory markers• Myelodysplastic syndrome

(a) Evidence of pancytopenia, with immature WBCs or nucleated RBCs on a peripheral smear (Smith, 2000)

(b) In cases of unexplained and/or severe anemia, a bone marrow biopsy may be recommended, and a discussion with the NH resident

and/or proxy is critical to determine if they are interested and/or willing to go for this invasive diagnostic workup

• Alcoholism and hepatic disease

(a) History and physical presentation of jaundice and/or hepatosplenomegaly, additional liver function studies are indicated

• Hypothyroidism

(a) History and physical presentation of thryoid dysfunction is suspected, a thyroid stimulating hormone (TSH) test is indicated

10


Table 2 Continued

Anemia of CKD

• Serum creatinine and/or calculate GFR (Coresh et al., 2003)• Serum EPO, although may have limited clinical utility• CBC peripheral smear may show Burr cells (Smith, 2000)

• Check urine for proteinuria and/or albuminuria. However, not all individuals with CKD will have protein or albumin in his or her urine, so care

must be taken with diagnostic interpretation (Snyder & Pendergraph, 2005)

that exceeds requirements or when body stores arenormal may cause organ damage as a result of irontoxicity. In order to minimize the risk of iron overload,the NKF-KDOQI guidelines (2006) recommend serumferritin levels not to exceed 800 ng/mL and transferrinsaturation percentage not to exceed 50%. If symptomaticiron overload occurs, administration of deferoxamine(desferal) or phlebotomy may be indicated. Treatmentof IDA may also include parenteral iron therapy andblood transfusion. Parenteral iron has newer and saferformulations. As a result of its safety profile, theNKF-KDOQI guidelines (2006) recommend iron sucrosefor those elderly individuals with anemia of CKD(not receiving dialysis) and for those receiving eitherperitoneal dialysis or hemodialysis (Aronoff et al., 2004).Blood transfusions, which can be done in an outpatientsetting, are the most invasive and most expensive formof iron replacement, and carry a higher risk of adversereactions than other forms of replacement. Moreover, thephysical and emotional stress of transferring to anothersite for blood transfusion and the associated fatigue withthe long procedure is something that many older adultsdo not desire.

ACD and CKD

Management of ACD is disease-specific and may beparticularly complex, especially if there are multiplechronic disease states to consider. It may be necessary tocoordinate care among multiple specialists in hematology,oncology, nephrology, and/or others. Despite low serumiron levels in ACD, iron stores are often adequate. Asa result of the potential risk for iron overload, ironsupplementation for low Hgb levels without furtherdiagnostic workup and evaluation is inappropriate, andoften contraindicated (Weiss & Goodnough, 2005). Soleconsideration of serum iron levels can be diagnosticallymisleading, and may erroneously suggest that if levelsare low, iron supplementation is needed. Rather, theinflammatory-mediated macrophage sequestration ofiron in ACD is thought to be a ‘‘host defense mechanism’’against invading microbial pathogens and neoplastic cellsthat require iron for growth and metabolism (Weinberg,1999). Serum ferritin levels that are normal or high

(>100 ng/dL) are diagnostically suggestive of ACD, andindicate that iron stores are adequate. However, therehave been some studies suggesting that iron therapy inACD for specific disease states may offer some benefit.For example, iron therapy for ACD associated withrheumatoid arthritis and end-stage renal disease mayinhibit the formation of TNF-α, and reduce overall diseaseactivity (Kaltwasser, Kessler, Gottschalk, Stucki, & Moller,2001; Weiss et al., 2003). Additionally, individuals withACD associated with inflammatory bowel disease havedemonstrated improved Hgb levels with parenteral ironadministration (Gasche et al., 2001). Finally, in caseswhere ACD and IDA coexist, iron therapy is indicated,and should also be considered for individuals who havebeen identified with a functional iron deficiency thatis unresponsive to erythropoietic stimulating proteins(ESP), which are discussed in the next section (Weiss& Goodnough, 2003). These studies highlight not onlythe importance of identifying the underlying etiology ofACD in order to appropriately target therapies but alsothat treatment itself is beneficial.

The general management of anemia of CKD includestreatment of reversible causes of renal dysfunction,preventing or slowing the progression of renal disease,and treatment of the complications associated withrenal dysfunction to prevent further renal deterioration(NKF-KDOQI, 2006). ESP such as recombinant humanerythropoietin (rHuEPO) (i.e., epoetin-α, epoetin-β,epoetin-γ ) and novel erythropoiesis stimulating proteins(NESP; i.e., darbepoetin-α), stimulate the proliferation oferythroid progenitors into reticulocytes and subsequentdifferentiation into erythrocytes, and are recommendedfor individuals with end-stage renal disease and for thosewho are classified as predialysis (Adamson & Longo, 2008;NKF-KDOQI, 2006). Recommended target goals for Hgblevels range between 11 and 12 gm/dL as the upperlimits for both men and women as adverse cardiovascularand mortality outcomes have been observed at higherHgb levels (Food and Drug Administration [FDA], 2007;NKF-KDOQI, 2007; Strippoli, Craig, Manno, & Schena,2004). Effective treatment with EPO or darbepoetin-αrequires adherence to recommended treatment andmonitoring guidelines (ARANESP, 2003; FDA; NKF-KDOQI, 2006; PROCRIT, 2000, Revised 2008). Finally,

11


Tab

le3

Man

agem

ento

fcom

mon

anem

ias

amon

gel

der

lyN

Hre

sid

ents

Com

mon

anem

ias

Man

agem

ent

Spec

ialc

onsi

der

atio

ns

Nut

ritio

nald

efici

enci

es• I

ron

defi

cien

cyan

emia

Ora

l(Za

row

itz,2

006)

•Fe

rrou

ssu

lfate

325

mg

tab

let

(eac

hta

ble

tco

ntai

ns60

mg

ofel

emen

tali

ron)

,titr

ate

toth

ree

times

dai

ly•

Ferr

ous

gluc

onat

e30

0m

gta

ble

t(e

ach

tab

let

cont

ains

35m

gof

elem

enta

liro

n),t

itrat

eto

five

times

dai

ly

•Fe

rrou

sfu

mar

ate

325

mg

tab

let

(eac

hta

ble

tco

ntai

ns

107

mg

ofel

emen

tali

ron)

,titr

ate

totw

otim

esd

aily

Giv

eon

emp

tyst

omac

hto

incr

ease

abso

rptio

n

Vita

min

Che

lps

enha

nce

iron

abso

rptio

n

Ap

ositi

vere

spon

seto

atr

ialo

fora

lthe

rap

yw

illre

sult

ina

mod

estr

etic

uloc

ytoi

sin

5–7

day

s.

Ifre

ticul

ocyt

osis

doe

sno

tocc

ur,i

tis

nece

ssar

yto

re-e

valu

ate

iron

rep

lace

men

tthe

rap

y,

and

/or

the

dia

gnos

is

Par

ticul

arca

resh

ould

be

take

nto

calc

ulat

eth

eam

ount

inea

chd

osag

ein

ord

erto

rep

lace

iron

stor

es;d

epen

din

gon

the

caus

eof

iron

defi

cien

cy,t

reat

men

tcan

cont

inue

for

3–6

mon

ths

until

iron

stor

esar

ere

stor

ed,o

rev

enin

defi

nite

ly,i

fthe

und

erly

ing

etio

logy

ofan

emia

rem

ains

orp

rogr

esse

sin

seve

rity

(i.e.

,CKD

)

Inth

eab

senc

eof

ble

edin

g,re

com

men

dat

ions

have

bee

nm

ade

toav

oid

iron

rep

lace

men

taft

er

6m

onth

sb

ecau

seof

pot

entia

lsid

e-ef

fect

s(F

ick,

Coo

per

,Wad

e,M

acle

an,&

Bee

rs,2

003)

Sub

ject

ive

rep

orts

ofsy

mp

tom

imp

rove

men

t,an

dse

rum

ferr

itin

(>10

0ng

/mL)

and

tran

sfer

rin

satu

ratio

np

erce

ntag

ele

vels

(>20

%)ar

eke

ycl

inic

alm

arke

rsto

eval

uate

trea

tmen

t

pro

gres

s(N

KF-K

DO

QI,

2006

)

Pri

orto

iron

dex

tran

adm

inis

trat

ion,

use

25m

gan

aphy

lact

icte

std

ose

over

5m

in,a

nd

pre

med

icat

ew

ithac

etam

inop

hen,

hyd

roco

rdis

one,

and

dip

ehen

hyd

ram

ine

(Zar

owitz

,200

6)P

aren

tera

l(Za

row

itz,2

006)

•Ir

onsu

cros

e20

mg/

mL

•Ir

ongl

ucon

ate

12.5

mg/

mL

•Ir

ond

extr

an50

mg/

mL

•B

lood

tran

sfus

ion

•Te

std

osin

gfo

rp

aren

tera

liro

nsu

cros

eor

iron

gluc

ose

isno

tre

com

men

ded

(Zar

owitz

,200

6)

•Ea

chm

illili

ter

oftr

ansf

used

blo

odp

rovi

des

1.0

mg

ofir

on•

Mon

itor

for

acut

ere

actio

ns,i

nfec

tions

,vol

ume

over

load

,and

syst

emic

iron

over

load

•Ty

pic

ally

don

eas

anou

tpat

ient

pro

ced

ure,

may

need

top

rem

edic

ate

with

acet

amin

ophe

n,

hyd

roco

rdis

one,

and

dip

ehen

hyd

ram

ine

•Tr

ansf

usio

nas

soci

ated

with

low

ersh

ort-

term

mor

talit

yra

team

ong

eld

erly

ind

ivid

uals

with

acut

em

yoca

rdia

linf

arct

ion

ifth

ehe

mat

ocri

twas

less

than

30%

orlo

wer

onho

spita

lad

mis

sion

(Wu,

Rat

hore

,Wan

g,R

adfo

rd,&

Krum

holz

,200

1)

• Cob

alam

in(v

itam

inB

12)

B12

load

ing

do

se(O

h&

Bro

wn,

2003

)

Ora

l

1000

–200

0m

cg/d

ayfo

r1

–2w

eeks

Par

ente

ral

100

–100

0m

cgd

aily

orev

ery

othe

rd

ayfo

r1

–2w

eeks

B12

mai

nte

nan

ced

ose

(Oh

&B

row

n,20

03):

Ora

l

1000

–200

0m

gd

aily

for

life

•In

crea

sed

ieta

ryB

12in

take

ifm

alno

uris

hed

and

/or

stri

ctve

gan

die

t

•O

ralB

12ha

sb

een

show

nto

have

equa

leffi

cacy

toth

atof

par

ente

rali

njec

tions

;how

ever

,hig

h

oral

dos

esar

ene

eded

bec

ause

ofth

eva

riab

leab

sorp

tion

ofor

alB

12in

doe

sof

500

mcg

or

less

(Kuz

min

skie

tal.,

1998

;Oh

&B

row

n,20

03)

•In

tran

asal

app

licat

ion

ofhy

dro

xoco

bal

amin

resu

lted

infa

stab

sorp

tion

and

sust

aine

din

crea

se

ofb

asel

ine

cob

alam

inco

ncen

trat

ions

(Slo

t,M

erku

s,V

anD

even

ter,

&Ty

tgat

,199

7)

12


Tab

le3

Con

tinue

d

Com

mon

anem

ias

Man

agem

ent

Spec

ialc

onsi

der

atio

ns

Par

ente

ral

100

–100

0m

cgev

ery

mon

thor

once

ever

y3

mon

ths

for

life

Intr

anas

al

500

mcg

wee

kly

for

life

•In

tran

asal

rout

eis

cont

rain

dic

ated

for

thos

ew

ithna

sald

isea

ses

orfo

rth

ose

rece

ivin

got

her

med

icat

ions

sim

ulta

neou

sly

inth

esa

me

nost

ril(

Dha

rmar

ajan

&N

orku

s,20

03)

• Fol

ate

•In

crea

sed

ieta

ryfo

late

inta

keif

mal

nour

ishe

d•

Fola

te1

mg

oral

lyun

tilH

gbno

rmal

ized

;dos

eca

nb

eup

to

3m

gp

erd

ayif

need

ed(S

mith

,200

0)

•R

esp

onse

isus

ually

seen

with

in1

–2w

eeks

oftr

eatm

ent;

mon

thly

follo

w-u

pun

tilH

gb

norm

aliz

ed

•V

itam

inC

help

sco

nver

tfo

late

toits

activ

efo

rm

Ane

mia

ofch

roni

cd

isea

se

orin

flam

mat

ion

•M

anag

emen

tis

dis

ease

-sp

ecifi

can

dm

ayre

qui

resy

mp

-

tom

atic

trea

tmen

t

•H

emat

olog

y/on

colo

gyco

nsul

tatio

nm

ayb

ein

dic

ated

Ane

mia

ofC

KDG

ener

alan

dsp

ecifi

cm

anag

emen

tsho

uld

follo

wth

e

NKF

/KD

OQ

IClin

ical

Pra

ctic

e(N

KF-K

DO

QI,

2006

)

Gui

del

ines

,and

any

sub

seq

uent

clin

ical

upd

ates

Trea

tmen

tofr

ever

sib

leca

uses

ofre

nald

ysfu

nctio

n(i.

e.,h

ypov

olem

ia,h

ypot

ensi

on,i

nfec

tion,

nep

hrot

oxic

med

icat

ions

)

Pre

vent

ing

orsl

owin

gth

ep

rogr

essi

onof

rena

ldis

ease

(i.e.

,red

uctio

nin

pro

tein

excr

etio

nto

less

than

500

–100

0m

g/d

ay,r

educ

tion

inb

lood

pre

ssur

eto

less

than

130/

80m

mH

g,

mon

itori

ngp

otas

sium

and

crea

tinin

ele

vels

with

in3

–5d

ays

ofin

itiat

ion

ofan

giot

ensi

n

conv

ertin

gen

zym

ein

hib

itor

[AC

E-I]

and

angi

oten

sin

rece

pto

rb

lock

er[A

RB

]med

icat

ion

ther

apy)

Trea

tmen

toft

heco

mp

licat

ions

asso

ciat

edw

ithre

nald

ysfu

nctio

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13


effective treatment also requires sufficient iron storesand typically requires iron supplementation (Table 3).Subjective reports of symptom improvement, along withimprovement in Hgb, ferritin, and transferrin saturationpercentage trends are key clinical markers to evaluatetreatment progress (NKF-KDOQI, 2006).

Summary

Despite reported high prevalence rates among theelderly, anemia is often an unrecognized and/or under-treated clinical diagnosis. Causes of anemia among theelderly are often multifactorial and generally includenutritional deficiencies, anemia of chronic disease and/orinflammation, and anemia of CKD. Failure to identifyand evaluate anemia could lead to delayed diagnosis ofpotentially treatable conditions. Given prior research andtrends, and the potentially significant impact of anemiaon cardiovascular disease, physical performance, mobil-ity, morbidity, and mortality outcomes among elderlyNH residents, gaining a better understanding of anemiamay allow the APN to tailor both medical and restora-tive care interventions for elderly NH residents. Suchinterventions may be able to limit or reverse functionalimpairment and/or disablement, and allow for maximalfunctional independence.

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Anemia and its impact on function in nursing home residents: What do we know?