Gerontological Advanced Practice Nurses Association

OFFICIAL SECTION OF THE OFFICIAL SECTION OF THE

Gerontological Advanced Practice Nurses Association

The Evolution of the GNP-NCGNPthe Second Decadedthe 1990s

Kathleen Fletcher, RN, MSN, GNP,APRN-BC, FAAN, and

Laurie Kennedy Malone, PhD, GNP-BC, FAANP

In 1991, National Conference of GerontologicalNurse Practitioners (NCGNP) celebrated its firstdecade of progress in Rochester, Minnesota. Witha growth in membership from 25 to 292, thegrowth and accomplishments of the organizationwere dramatic during the first 10 years, and theparticipants celebrated the past, reveled in themoment, and planned for the future. The seconddecade of NCGNP history (1990e2000) wouldprove to be no less remarkable.

The early 1990s reflected significant growth ofadvanced practice nursing (APN) programs andorganizations (nurse practitioners [NP] and clini-cal nurse specialist [CNS]) in the United Statesand greater clarity and understanding of the roleand unique contributions of APNs. Although NPprograms primarily prepared the APN in primaryand specialty care, the CNS preparation was fo-cused on populations of patients and improvingcare largely through consultation and educationof care providers. Recognizing that therewas con-siderable overlap in these respective roles, rolemergerwasdiscussed in the literature andat nurs-ing organizational forumsdincluding NCGNP.

Nationally a new organization was formed, theAmerican College of Nurse Practitioners (ACNP),in an attempt to bring some cohesiveness and leg-islative muscle to the growing number of NP spe-cialty organizations. Looming on the horizonwere legislative and reimbursement issues influ-encing NP practice. We were honored that oneof our own, Norma Small, was elected as presi-dent of the National Alliance of Nurse Practi-tioners (NANP). In early 1990, NCGNP decidednot to belong to the ACNP but to continue mem-bership in the NANP for legislative support.

NCGNP was increasingly being recognized fortheir expertise in the care of elders. The OmnibusBudget Reconciliation Act (Nursing Home Re-form) had been passed in 1987, requiring thatnursing homes decrease the use of physical andchemical restraints, and NCGNP was called

Geriatric Nursing, Volume 33, Number 3

upon by HCFA and NCNHR to help lead theway in restraint reduction. In 1995, the ANA in-vited NCGNP to be represented on an expertpanel to revise the Scope and Standards of Geron-tological Nursing and for the first time the role ofthe APN in gerontological nursing was includedin the second edition of this publication.

Following the lead of NCGNP leaders of the firstdecade, members continued to disseminate theirexpertise in geriatric best practices through publi-cation. The second edition of Towards Healthy

Aging (Ebersole and Hess) was released in 1998,and a new publication, Management Guidelines

for Gerontological Nurse Practitioners (Kennedy-Malone and Fletcher and Plank), in 1999.

As NCGNP exerted its influence nationally, theorganization continued to thrive. The bylaws ofthe organization were streamlined and modified.As membership in NCGNP and vendor sponsor-ship of NCGNP grew, the organization estab-lished a contingency fund to provide for greaterfinancial stability. Acceptance of diversity was re-flected in a revised philosophy statement.

Still, NCGNP was experiencing growingpainsdby 1994 membership was approaching400. Although financial records were computer-ized, the hours for the part-time administrativeassistant in the Central Office in Fort Collins, Col-orado, were increased, and a fax and copier werepurchased, it was difficult for the all-volunteerboard of GNPs to continue to keep up with needs.NCGNP was fined by the IRS for a late filing oftaxes, appealed, and thanks to “fancy footwork”by our leaders at the time, the IRS waived the fee.

The late 1990s marked one of the most monu-mental events in the history of the NP movementand the NCGNP. The collective legislative effortsof the NCGNP, the NANP, and the ACNP wererewarded when President Clinton signed theBudget Consolidation Act in 1997. Medicare reim-bursement for NP’s was now a reality. NCGNPentered the internet age with the launching ofits first web page in 1998.

Collaborations with other organizations contin-ued though the late 1990s. The Hartford InstituteofGeriatricNursing formedaGerontologicalNurs-ing Consortium recognizing the need for discus-sion and partnerships between the nursingorganizations that had a focus on older adults,

235

and NCGNP was invited to the table with the Na-tional Gerontological Nursing Association(NGNA) and the National Association of Directorsof Nursing in Long Term Care (NADONA). Duringthis time, NCGNP started forming relationshipswith allied interprofessional groups such as theAmerican Medical Directors Association (AMDA)and the American Society of Consulting Pharma-cists (ASCP). In 1998, a representative fromNCGNP, Laurie Kennedy-Malone who was at thattime serving as president of the organization, wasinvited to testify at a publicmeeting held by the In-stitute of Medicine in preparation for the report“Improving the Quality of Long-TermCare,” whichwas published in 2001. She emphasized the needfor all nurses employed in long-term care to haveeducational preparation in gerontological nursingand the vital role that GNPs play in managing thecare of residents in long-term care.1

Internally, at NCGNP this was a time of growth,strategic planning, and change.Membership com-prised more than 600, and a 3-year strategic planwas created. Citing geographic and communica-tion issues, the board decided tomove the centraloffice to Washington, DC, and a new administra-tive assistant was hired. At the end of the seconddecade, NCGNP began to explore contracting formanagement and web development services.

In 2001, the 20th anniversary of NCGNP wascelebrated in one of our favorite conference loca-tions: San Francisco. It occurred just 1 week afterthe tragic events of the September 11 terroristattacks, and the nation was still stunned, mourn-ing, and fearful. A few speakers cancelled at thelast minute, but the California planning commit-tee did a masterful job finding expert replace-ments. Demonstrating the commitment to the

236

organization, 78% of the registered participantsattended a highly successful 20th conferenceand helped shape the future of our organizationas we moved into our third decade.

Reference

1. Kennedy-Malone L. A NCGNP pioneer inlegislation/reimbursement. Geriatr Nurs 2007;28:232.

Gerontological Advanced PracticeNurses Associationd31st Annual

Conference will be heldSeptember 19-22, 2012

in Las Vegas, NV

� Relevant general, in-depth focus, and con-current sessions designed to offer choiceand variety

� Interactions with leading industryrepresentatives

� Peer-conducted research presented as inter-activeposter sessionsandoral presentations

� APRN Consensus Model� Beers Criteria� Transitional Care� Dementia� Osteoporosis� Pharmacology Updates� Advanced Wound Care

Please got to www.GAPNA.org to register orfor more details.

Geriatric Nursing, Volume 33, Number 3

CC Wound Identification

Differentiating Types of Ulcers: Arterial,

Venous, Diabetic, & Pressure

Lisa Byrd, PhD, FNP-BC, GNP-BCGerontologist Assistant Professor of NursingUniversity of Mississippi Medical Center

Jackson, MS

An ulcer, is an ulcer, is an ulcerdNOT TRUE.Not all ulcers are the same, nor can they be treatedin the samemanner. There are someulcers that re-sult from pressure, but an ulcer may also becaused by peripheral vascular disease/venous sta-sis, arterial insufficiency, or complications of dia-betes including peripheral neuropathy. Elderlyindividuals have many normal aging changes aswell as changes due to chronic disease that pre-dispose them to development of ulcers on lowerextremities. Ulcerations on lower extremities cancause pain, lead to infection, increase cost ofcare, decreasequalityof life, andeven lead todeathof a frail elder. It is imperative to determine thecause of an ulcer to assist in resolving the problem.

An ulcer is a separation in the layers of the skinthat fails to heal and may be accompanied by in-flammation. Some ulcers begin as skin tears oras a reaction to something the person has comein contact with. Other ulcers result from chronicdisease in elders, including peripheral vasculardisease and peripheral arterial disease. Thewound may or may not be painful and may havedifferent colors from red to pink to brown oreven black. It may be warm to touch or cool. As-sessing the individual’s health status as well asthe ulcer itself will usually answer the questionof the cause of the ulcer, which will help deter-mine the best plan of care.

Anatomy of the Skin in an Aging Individual

Several changes occur in the skin of older indi-viduals during the normal aging process: the der-mis becomes 20% thinner with less subcutaneousfat; there are fewer dermal blood vessels, evi-denced by pallor and cooler skin; collagen syn-thesis is decreased, which results in slowerwound healing; elastin fibers diminish in numberand diameter, leading to loss of stretch and resil-ience; the vascular supply to hair bulbs andglands results in loss of spontaneous sweatingin the presence of heat and altered thermoregula-tion; the ability to retain moisture decreases

Geriatric Nursing, Volume 33, Number 3

because of diminished dermal proteins causingthe skin to become drier; vascular hyperplasialeads to more pronounced varicosities, benigncherry angiomas, and venous stars; the dermal-epidermal junction flattens and dermal papillaeand epidermal rete cells (which anchor the skinlayers) become flatter making skin tear easier;and nerve endings decrease with the reductionin sensation ability.1,2

For an ulcer to heal, the ulcer must receive anadequate amount of blood and nutrients. Mea-suring circulation in the lower extremity isimportant to assess the body’s ability to healproperly. Normal ankle-brachial index (ABI) isa reliable, noninvasive method to measureperipheral tissue perfusion. A normal ABI is0.9 to 1.1. Lower ABI values can be an indicatorof atherosclerosis and arterial disease.2

Arterial Ulcers

Arterial ulcers account for approximately 10%of lower extremity ulcers.3 They are caused by im-paired arterial blood flow to the lower extremity,the leg and foot. Impairment in blood flow leads todeprivation of oxygen to the tissue, resulting in is-chemia, necrosis, and skin death. Arterial leg ul-cers are caused by poor blood circulation asa result of narrowed arteries due to arteriosclero-sis, and fatty deposit builds up inside the arteries.The limited blood supply causes the tissues in theextremities to be starved for oxygen and nutri-ents, leading to break down and formation of anulcer. Elders with arterial leg ulcers often sufferfrom intermittent claudication. This causescramplike pains in the legswhenwalking becausethe legmuscles donot receive enoughoxygenatedblood. The leg may be thin, shiny, with minimalhair (or hairless). Pulsesmay be diminished or ab-sent. The ABI may be less than 0.9dthe lower thenumber, the more severe the circulation problem(there may be falsely elevated ABI in certain indi-viduals with severe arterial disease). Toenailsmay be yellow and thick. Arterial ulcers are com-monly locatedon the toes, lateralmalleolus, or an-terior leg and rarely above the knee. The ulcerresulting from arterial insufficiency is usuallypainful with the pain increasing when the extrem-ity is elevated. Pain may also increase with activ-ity or exercise. Arterial ulcersmay be pale in coloror may be dark evenmaroon, brown, or black andusually have little or no drainage. Arterial ulcersoften have a “punched-out” appearance-may

237

Table 1.Compare and Contrast of Different Types of Lower-Extremity Ulcers

Ulcer Arterial Venous Diabetic/Neuropathic Pressure

Location � Lower extremities, most

commonly toes, lateral

malleolus, or anterior leg

� Rarely above the knee

� Usually appear on the lower

extremity: lower leg, medial

malleolus

� Rarely occurs above the

knee

� Generally appear on the

plantar surface of the foot,

over the heels, and over the

metatarsal heads

� Over a bony prominence;

on the lower extremity,

common sites are the

greater trochanter, between

the knees, lateral or medial

malleolus, heels, and

proximal joint of the first

or fifth toes

ExtremityAppearance

� Lower extremities cool to

touch and hairless legs

� Skin is pale, shiny, taut,

and thin

� Often thickened, yellow

nails secondary to fungal

infections

� Pulses are decreased or

absent

� Capillary filling may be

.20 seconds

� ABI\0.8

� Edema may be present

� Pulses are normal or

decreased

� Capillary filling may be

\5 seconds

� ABI 0.8e1.0 (unless

concomitant arterial disease)

� Varicose veins may be

present

� Hemosiderin staining

(brownish pigment changes

in the skin due to deposition

of red blood cells)

� Lipodermatosclerosis

(thickening of the skin; loss

of elasticity in the gaiter

area)

� Dry, warm, cracked, fissured

skin, thickened nails

� Usually no edema is present

� Extremity may be atrophic,

and contractures may be

present

� Pulses may be normal

unless peripheral vascular/

arterial disease is present

� ABI 0.8e1.0 (unless con-

comitant disease present)

Appearance � Punched-out appearance

� Wound edges are smooth

� Ulcers usually in the lower

leg or foot

� Periwound skin is pale

� Wound bed contains bright

red granulation tissue

� Shallow

� Superficial

� Irregular shape

� Size may vary

� Periwound may be

macerated (whitish/moist

appearance)

� Temperature is normal or

mildly warm

� Wound bed contains beefy

red granulation tissue or has

ruddy appearance

� Round, punched-out

appearance

� Minimal to no exudate

� Wound margins are round

with occasional periwound

calluses, dry, or cracked

� Contributing factor may be

pressure

� Ulcer may be secondary to

peripheral neuropathy or

arterial insufficiency and

poor microvascular

� Begin as nonblanchable

erythema and can progress

to full thickness to the

underlying muscle and

tendons

� Eschar may be present (ma-

roon, dark brown, or black)

� The ulcer may be warm to

touch except in points with

necrotic tissue

� Tunneling and undermining

may be present

238Geriatric

Nursing,

Volum

e33,

Num

ber3

�Infections/cellulitiscommon

�Oftenrecurrentulcerations

circulation,inadequate

bloodglucosecontrol,and/

orlackofsensation

�Periwoundmaybe

nonblanchable

erythema

orindurated

�Derm

atitisis

common

surroundingapressure

ulcer

Drainage

�Ulcers

usuallyhaveminim

al

drainage

�Oftencopiousdrainage

�Usuallyminim

alorno

drainageunlessedema

presentdueto

vascular

disease

�Drainagemaybecopious

Pain

�Pain

worsenswhen

extremityis

atrest

�Pain

worsenswhen

extremityis

elevatedand

canberelievedbylowering

thelegbelow

heart

level

�Pain

decreaseswith

danglingleg-gravity;flow

ofbloodhelpsrelievepain

�Pain:mildto

moderate

�Dull,achinglegpain

or

heaviness

�Pain

maydecreasewith

elevationorcompression

�Maybepainlessdueto

the

individual’sinabilityto

sensepain

unlessperipheral

neuropathywithchronic

pain

ispresent

�Individuals

withintact

sensory

nervesusually

experiencepain

inthearea

oftheulcer

�Stage1ulcers

maypresent

astenderness

ABI5

ankle-brachialindex.

Sources:LondonHealthScienceCentre(2012);MacNair

(2012);Myers(2004);Baranowski&

Ayello(2008).

Geriatric Nursing, Volume 33, Number 3

have a raised edge with a sunken in center or holein the center of the ulcer. Arterial ulcers on thelower extremities can be difficult to manage andslow to heal due to their poor circulation.2,4

Venous Ulcers

Amajority of lower extremity ulcers are venousulcers accounting for up to70%of all lowerextrem-ity ulcers (5). Venous leg ulcersmay develop in thepresence of edema in the legs. In healthy legs,edema is not present, but in older individualswith peripheral vascular disease, there are ana-tomic changes resulting in fluid accumulation inthe feet and lower legs. Anatomy of the vascularsystem in the lower legs is as follows: superficialanddeepvein systemsareconnected toeachotherby veins that have 1-way valves to ensure thatblood flows from the superficial veins to thedeep system. Improperly functioning valves maydevelop with age-related changes, causing thevalves to become thin and weak. This may causeblood to flow from the deep veins back out tothe superficial onesda major cause of varicoseveins. The problem is aggravated by the effectsof gravity, which allows blood to pool in the lowerleg. Often, individuals with peripheral vasculardiseasehave concurrent arterial disease,which in-creases the problems of ulcer development andslows the healing process.4 Walking or exercising,the calf muscles assist in pumping venous bloodbackup toward the heart, against gravity. Ambula-tion and exercise helps to control fluid and pres-sure in the legs and reduces the risk of venousulcers. Most venous stasis ulcers occur belowthe knee, primarily found on the inner part of theleg, just above the ankle, and may affect 1 orboth legs. Pulses and the ABI may be normal ordecreased if there is concurrent arterial disease.Venous ulcers are often located on the lower leg,especially the medial malleolus and rarely abovethe knee. They usually have an irregular borderwith a red or ruddy wound bed and possibly a yel-low coat over the bed. These wounds often havecopious drainage and can become infected easily.The area around the wound or periwound area isoften mottled or whitish in appearance. Painmay be mild to moderate and is usually relievedby elevating the leg. Management includes properassessment andmanagement on an ongoing basis.A wound bed does need to be moist to heel butabedwith excessivedrainagewill not heal rapidly.Drying the wound bed with excessive drainage

239

and preventing or treating secondary infections isthe mainstay of management. Compression to as-sist in diminishing edema will also assist in thehealing process unless concomitant arterial dis-ease is present.

Diabetic/Neuropathic Ulcers

Older individuals with diabetes are at specialrisk of developing foot ulcers due to a number ofthe complications of diabetes. Contributingcauses include 1) sensory, motor, and autonomicneuropathy; 2) peripheral vascular disease withpoor microvascular circulation; 3) repetitivetrauma, unperceived pressure, or friction/shear;and 4) poor control of blood glucose levels whichimpairs tissue healing. Peripheral neuropathy af-fects the sensory nerves responsible for detect-ing sensations including temperature or pain.Also affected are themotor nerves,which are re-sponsible for the contraction of muscles that maylead to minormuscle wasting. The consequenceis an imbalance of flexor and extensor musclesleading to foot deformities, such as claw toesor prominent metatarsal heads (the end of thelong foot bone that is closest to the toe joint).The deformities cause additional pressure

points prone to ulceration. Ulcerations in dia-betic individuals frequently occur at commonpressure points on the plantar (bottom) surfaceof the foot, such as at the hallux (first or bigtoe),metatarsophalangeal joint (the area betweenthe long bones in the foot and typically the big[first] or pinky [fifth] toe), or the heel. Ulcerationmay also occur on the side of the foot, typicallya result of poor-fitting footwear, or on the dorsum(top) of the foot, typically due to trauma. The baseof neuropathic ulcers will vary based on the indi-vidual’s circulation with coloration ranging fromreddish to brown or black. The wound marginsare usually well-defined, with a punched-appear-ance, and the surrounding skinmay often be thickand calloused. There may be undermining at theedge/border of thewound and possibly pockets ofinfection.A complication of a diabetic ulcermaybe a severe infection of the bone known as oste-omyelitis. The combination of ischemia and neu-ropathy can allow infection to advance rapidly.The diabetic ulcer itself is often painless unlessthere is also infection or an arterial componentto the ulcer. The limb will generally maintaina normal pulse unless there are additionalcirculatory problems.2 Effective management of

240

a neuropathic ulcer requires offloading or reduc-ing pressure on the affected area, paying closeattention to maintain proper circulation (keep

the individual ambulatory if possible-bedrest

is not indicated). Proper shoes or diabetic

therapeutic shoes may be used for preventionor to avoid recurrence as opposed to during treat-ment. If the ulcer does not resolve with conserva-tive measures, surgery to correct deformities inthe foot may be considered.

Pressure Ulcer/Decubitus Ulcer

Pressure ulcers are localized areas of tissuenecrosis that develop when soft tissue is com-pressed between a firm surface and the underly-ing bony prominence. When pressure on thetissue is greater than the intercapillary bloodpressure, blood flow is occluded and local tissueis deprived of oxygen, which leads to ischemiaand cell death. Frail elders have decreased elastincontent in their skin tissue as well as loss of der-mal vasculature and less subcutaneous fat pad-ding, and veins are more fragile and closer tothe skin surface. A pressure ulcer can developin less than 2 hours in an immobile elder.6 Woundhealing is slower in an older person, and thisproblem leads to pressure ulcers extremelyslow healing process or nonhealing ulcers in cer-tain frail elders who have multiple comorbidities.Pressure ulcers are often recurrent in an immo-bile person because, when an ulcer heals, thenew skin is only 80% tensile strength as normalskin tensile strength, and thus the skin is morefragile and more prone to breakdown. Shearingcan occur to skin when a force is applied parallelto the skin tissue. Usually the skin tear is in theshape of a tear drop. Undermining may be pres-ent.2 Malnutrition may be a contributing factorthat occurs in a significant number of immobilefrail elders. Pain may or may not be present be-cause many of the individuals who develop pres-sure ulcers have a decreased ability to sense pain.A pressure ulcer may begin as a nonblanchableerythema and progress to full thickness if notmanaged appropriately. Eschar may develop asthe skin becomes necrotic. Table 1 comparesand contrasts the different types of ulcers.

Wound Management

Ideally, the goal of ulcer management is com-plete wound healingdthe wound bed is

Geriatric Nursing, Volume 33, Number 3

Table 2.Management of Ulcers

Arterial Venous Diabetic/Neuropathi Pressure

� Moist dressings such as

hydrogels or hydrocolloids

� Debride necrotic tissue if

appropriate

� Moisturize skin surrounding

ulcer

� Avoid adhesives

� Avoid compression

� Reduce friction between toes

� Choose footwear that is able

to accommodate foot and

relieve pressure

� If nonhealing, consider referral

to wound specialist when

necessary

� If dry ulcers: Moist to moist

dressings and/or hydrogels/

hydrocolloids

� If drainage present: Calcium

alginate dressings or collagen

wound dressings

� If infection is present with

minimal drainage: antibiotic

ointment with foam dressing or

ointments containing silver such

as silver alginate

� If slough or eschar present:

consider debriding agents

� If edema present: consider

compression treatments such as

compression stockings,

multilayer compression wraps,

or wrapping an ACE bandage or

dressing from the toes or foot to

the area below the knee

� If nonhealing: consider synthetic

skin substitutes or refer to

wound specialist when

necessary

� Monitor periwound area and use

protective barrier cream when

maceration noted

� Control glucose levels

� If infected: manage with opical

antibiotic cream or silve algi-

nate or appropriate syst mic

antibiotics if necessary

� If callus or necrotic tissu is

present: consider debrid ment

with enzymatic ointmen or

mechanical debridemen

� Dependent on the prese tation

of the ulcer: followmana ement

suggestions for arterial/ enous

ulcers

� Refer to wound specialis when

necessary, especially if

suspicious of osteomye tis

� Offload pressure points

� Minimize shearing forces

� Use protective barrier cream

around wounds which have

drainage

� Moisturize dry skin

� If infected: manage with topical

antibiotic cream or silver algi-

nate or appropriate systemic

antibiotics if necessary

� If necrotic: consider debridement

when appropriate (may be

appropriate to leave intact eschar

on the heel if arterial disease

present)

� Dependent on the presentation

of the ulcer: followmanagement

suggestions for arterial/venous

ulcers

� Follow National Pressure Ulcer

Guidelines

� Refer to wound specialist when

necessary especially if

nonhealing

Myers, 2008; Baranoski & Ayello, 2008

Geriatric

Nursing,

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Num

ber3

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r

e

e

e

ts

t

n

g

v

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completely resurfaced with epithelium. The pro-cess to attain this goal is maintaining a moistwound bed that is clean, warm, and free of infec-tion to allow granulation tissue to grow from theedge inward and to protect the periwound area. Amoist wound heals 3 to 5 times faster than a drybed.4 A scab, a crusty wound bed, and escharare considered dry wound beds and usually re-quire removal to allow the new granulation tissueto be formed to heal the ulcer. The exceptionmaybe eschar on the heel in an individual with periph-eral vascular/peripheral arterial disease becausethis is considered a protective barrier of an areawith poor circulation and may be difficult to re-solve and heal properly.6 Exposed wounds areusually more inflamed, more painful, and more fi-brotic, thus dressings are usually encouraged topromote healing.4 Dressings should createa moist environment. If a wound is too wet, thedressing should absorb excess exudate, and ifthe wound is too dry, the dressing should add tothe moisture of the wound bed. The wound dress-ing should also provide thermal insulation withaims to maintain the wound bed at normal bodytemperature. Dressings should not be changedany more frequently than necessary becausedressing changes open the ulcer to the environ-ment and allow it to become cooler. It can takeup to 90 minutes to rewarm to the temperatureof the body and then begin to allow the woundto form granulation tissue and work toward thehealing process.7 Oxygenation also promotes

242

wound healing, and dressings that promote oxy-genation while preventing bacteria contamina-tion are ideal. Table 2 presents a basic reviewof dressing selections.

References

1. Ebersole P, Hess P, Luggen A. Towardhealthy aging: human needs and nursing re-sponse. 6th ed. St. Louis, KY: Mosby; 2004.p. 79-83.

2. Baranoski S, Ayello E. Wound care essen-tials: practice principles. 2nd ed. Philadel-phia: Lippincott Williams & Williams; 2008).

3. National Database of Nursing Quality Indica-tors. Other wound types and skin injuries.2012. Available at www.nursingquality.

org/NDNQIPRESSUREULCERTRAINING/

Module2/ArterialUlcers1.aspx. Cited March12, 2012.

4. Myers B. Wound management: principles andpractice. 2nd ed. NJ: Pearson Education; 2008.

5. Kesltrel Health Media. Neuropathic ulcersandwound care: symptoms, causes, and treat-ments. 2010. Available at www.kestrelhealth

info.com/blog/neuropathic-ulcers-and-wound-

care-symptoms-causes-and-treatments. CitedMarch 12, 2012.

6. London Health Science Centre. Venous sta-sis & arterial ulcer comparison; diabetic/neuropathic ulcers. 2012. Available at www.

lhsc.on.ca/Health_Professionals/Wound_Care/

venous.htm; http://www.lhsc.on.ca/Health_

Professionals/Wound_Care/diabetic.htm.Cited March 12, 2012.

7. MacNair P. Foot and leg ulcers. 2012. Avail-able at www.netdoctor.co.uk/diseases/facts/

footandlegulcers.htm. Cited March 11, 2012.

0197-4572/$ - see front matter

� 2012 Published by Mosby, Inc.

doi:10.1016/j.gerinurse.2012.03.010

Geriatric Nursing, Volume 33, Number 3