noncaucasian skin 3 slides color (2)

8/6/2019 Noncaucasian Skin 3 Slides Color (2)

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Heather Hettrick PT, PhD, CWS, MLT, FACCWS

Vice President Academic Affairs & EducationAmerican Medical Technologies

Prepared in Support of Advancing Excellence in Americas Nursing Homes

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American Medical Technologies 2

Disclaimer

The information presented herein is provided for educational

and informational purposes only. It is for the attendeesgeneral knowledge and is not a substitute for legal or medicaladvice. Although every effort has been made to provide

accurate information herein, laws change frequen tly and varyfrom state to state. The material provided herein is not

comprehensive for all legal and medical developments andmay contain errors or omissions. If you need advice regardinga specific medical or legal situation, please consult a medical

or legal professional. Gordian Medical, Inc. dba AmericanMedical Technologies shall not be liable for any errors or

omissions in this information.

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Objectives

Understand the basic physiology responsible

for skin pigmentation

Recognize normal dermatological variations in

black skin Describe the appropriate methods to perform

thorough skin/wound assessment in non-Caucasian skin

Recognize the signs and symptoms of skinbreakdown or pathology in non-Caucasian skin

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A&P Review of the Skin

Skin is the largest organ of the body

In a 150- pound person, the skin iscomprised of 18 square feet and weighsabout 12 pounds

The skin has three functional layers

Epidermis

Dermis

Hypodermis or sub-

cutaneous layer

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A&P: Layers of the Skin

Epidermis Five layers of cells (superficial to deep)

Functional components: Made up of tough, flattened cells of the protein keratin Cells provide barrier to injury, contaminants, light, re tain water Keratinocytes secrete protein keratin

Melanocytes produce melanin (pigment)

Basal and prickle cells regenerate epidermis, produce Vit D

Langerhans cells are a component of the immune system

Corneum

Lucidum

Granulosum

Spinosum

Basal

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Epidermis: Stratum Corneum

Protective layer Highlighted in green

Outermost layer withcells that aredesquamated and turnover every 30 days

Comprised of 15-20layers of non-nucleated keratinizedcells

From: trc.ucdavis.edu/.../ skin/epi0/epi4.htmlFrom: trc.ucdavis.edu/.../ skin/epi0/epi4.html


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Epidermis: Stratum Lucidum

Transparent layerfound mainly in thesoles and palms(i.e. thickepidermis)

Transitional layerthat is 1-5 layersthick


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Epidermis: Stratum Granulosum

Granular layer that is1-5 cells thick

Forms a waterproofbarrier that functions toprevent fluid loss

Synthesizeskeratonyaline which isthe precursor tokeratin


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Epidermis: Stratum Spinosum

This is the prickle cell layer This layer contains

desmosomes whichterminate in spiny

projections which hold thecells together and helpprotect the skin fromabrasion

Langerhans cells alsoprovide antigens to T-lymphocytes (immuneresponse)



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Epidermis: Stratum Germanitivum

Single cell layer

Provides germinalcells necessary for theregeneration of theepidermis

Contains melanocyteswhich are responsiblefor the pigment of theskin


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Basement Membrane

The epidermal-dermal junction- wherecells reside that are responsible for mitoticgrowth and epidermal regeneration occurs approximately every 30 days

Fibronectin is the major protein in thebasement membrane It is an adhesive glycoprotein (the glue that

holds it together)

Layers are lamina lucida and lamina densa Rete pegs (epidermal) attach with the

dermal papillae to support the epitheliumand dermis

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Layers of the Skin

The epidermis has an irregular shape, resemblingdownward, finger-like projections called rete ridgesor rete pegs (see next slide). The significance of this anatomical structure is that the

dermis has upward p rojections.

The upward and downward projections fit together, verymuch like a waffle iron. These protuberances connect,anchoring the epidermis to the dermis.

This bond also helps to prevent the epidermis from slidingback and forth across the dermis with normal movementand skin manipulation. In healthy young skin, the 2 layers of skin move as one. This is not

the case in elderly skin (skin over the age of 60!)

This is why shear and friction can cause skin tears in the elderly.


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Layers of the Skin

Note the dark pink fingerlike projections. These are theNote the dark pink fingerlike projections. These are the reteretepegs.pegs.

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Layers of the Skin

Dermis Two layers of irregular connective tissue

Papillary layer- anchors dermis to epidermis Reticular layer- contains dense, deep accessory organs

Functional components of the dermis: hair follicles

nerve endings (pain, heat, cold, touch, pressure) lymph vessels (remove excess fluid, store protein) capillaries (supply nutrients and O2, remove water and

waste) collagen (bulk, strength, support) elastin and reticulin (extensibility, integrity)

sweat glands sebaceous glands (sebum, controls pH, antibacterial and

antifungal effects)

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Layers of the Skin

Subcutaneoustissue Functional components:

adipose or fat connective and elastic tissue

insulate, support, cushion and

store energy

Adipose tissueAdipose tissue


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Functions of the Skin

Dynamic organ continuously engaged in biologicaland biochemical activity

Protection Temperature regulation

Fat and water storage

Vitamin D synthesis

Excretion of waste

Cosmesis

Touch/sensation

Trauma and damage to the skin can lead to functional impairments

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Stats and Information

80% of the worlds population consists of individuals withpigmented skin

Skin pigmentation continuum: light ivory, deep brown,black, yellow to olive, light pink to dark, ruddy pink, andred (Baranoski & Ayello 2004)

The population of the US is ~ 29% non-Caucasian

By 2050, it is projected 48% of the US population will benon-Caucasian

Ethnic skin is defined as non-Caucasian darker skin types(Fitzpatrick IV, V, VI phototypes)

Asians, Africans, Afro-Caribbeans, African Americans,Aborigines, Native Americans, and Hispanics

General categories (not all inclusive)

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Fitzpatricks Skin Phototypes

Phototype Sunburn &Tanning Hx

ImmediatePigmentDarkening

DelayedTanning

ConstitutiveColor

UV-A MED(mJ/cm2)

UV-B MED(mJ/cm2)

I Burns easilyNever tans

None None Ivory White 20-35 15-30

IIBurns easily

Tans min withdifficulty

Weak Min to weak White 30-45 25-40

III Burns modTans mod anduniformly

Definite Low White 40-55 30-50

IV Burns minTans mod andeasily

Moderate Moderate Beige-Olive,

lightly tanned

50-80 40-60

V Rarely burnsTansprofusely

Intense

(brown)

Strong,

intense brown

Moderate

brown ortanned

70-100 60-90

VI Never burnsTansprofusely

Intense (dark

brown)

Strong,

intense brown

Dark brown or

black

100 90-150

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Pigmentation

Normal skin color or tone is composed of fourbiochromes: Melanin (brown)

Carotenoids (yellow; exogenous from diet; foundin subcutaneous tissue) Oxyhemoglobin (red; concentration and state of

oxygenation of hemoglobin) Reduced hemoglobin (blue; presence of other

pigments)

The total amount of melanin is the principledeterminant of skin color Constitutiveskin color designates a genetically

determined level of cutaneous melanin, in theabsence of exogenous or endogenousinfluences

Faculativeskin color designates an inducedlevel of increased epidermal melanin contentdue to solar radiat ion, hormones, and otherenvironmental factors (Pathak 1985)

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www.gnxp.com


Pigmentation

The cutaneous pigment melanin isproduced by melanocytes

Studies of human skin revealed nosignificant differences in the actualnumber of melanocytes (Szabo 1969)

Racial differences in skin color are attributedto differences in the rate at whichmelanosomes are produced and melanizedin melanocytes and then transferred,

distributed and degraded in keratinocytes

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Pigmentation

The biosynthesis of

melanin occurs within

the metabolic unit of the

melanocyte, the

melanosome The melanocyte, an

exocrine cell, resides in

the basal layer (or

stratum germanitivum)

of the epidermis and inthe matrix portion of the

hair bulbFrom: trc.ucdavis.edu/.../ skin/epi0/epi4.htmlFrom: trc.ucdavis.edu/.../ skin/epi0/epi4.html


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Assessment


Assessment Basics

Visual inspection of the skin is not sufficient byitself; must use all senses Look, listen (to the patient/family), touch and smell

To accurately detect skin changes in patients,visual assessment must be followed by athorough physical assessment of thewound/problem area and its surrounding skin Minimal skin assessment:

Color, temperature, moisture, turgor, presence of intactskin or open areas

Minimal wound assessment: Thorough patient exam, etiology or wound type, wound

characteristics Location, size, depth, exudate, and tissue type


Skin Assessment Components

DERMATOLOGICALFromHettrickH, In Myers B. Wound Management Principles and Practice, PrenticeHall, 2008.

Describe integrity Edema Review sensory status

Moisture Atrophic changes Turgor/texture

Observe nail composition/hair quality

Look/feel color and temperature variations Observe skin folds Gerontodermatological changes Inquire about allergies and previous medical history Callus Assess vascular status

Lesions (rashes, scars, bruising, hemosideran, nevi, etc.)


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O: observe skin folds

Look for breakdown, yeast/fungal infections, foreign

objects G: gerontodermatological changes

Normal skin changes with aging

Risks: skin tears, bruising, senile purpura, pressureulcers

I: inquire about allergies and past medical history

Are findings exogenous or endogenous in nature

C: callus

Indicates area(s) of high pressure or repetitivestress/trauma



A: assess vascular status

Look, listen, touch

Color changes

Doppler

Palpate pulses, capillary refill, ABI (ankle brachialindex)

L: lesions (rashes, scars, bruising, hemosideran, nevi, etc.)

Document location(s), describe presentation, formulateworking clinical diagnosis

Denote anything unusual or suspicious, and what may bea normal dermatological variant for the individual


Normal Variations in Black Skin

Futchers (Voigts) line Sharp demarcation between darkly pigmented and lightly pigmented skin in the

upper extremity

Follows spinal nerve distribution

Midline hypopigmentation Line of hypopigmentation over the sternum Lessens with age

Nail pigmentation Diffuse nail pigmentation or linear dark bands on the nail

May appear brown, blue, or blue-black

Oral pigmentation Oral mucosa appears blue to blue-gray Gingivae may also be affected

Palmar changes Creases may be hyperpigmented

May contain hyperkeratotic papules or pits in the creases

Plantar changes Hyperpigmented macules may vary in color and distribution May present with irregular borders

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The following slides contain photosused with permission from Merit

Publishing. Special thanks to CoyleConnolly and Joseph Bikowski,

authors of Dermatological A tlas ofBlack Skin 2006.


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www.nature.com/.../n4/thumbs/4812611f6th.jpg

Gingival Hyperpigmentation:Symmetrical discoloration usually of

anterior gingivaCertain drugs (antimalarials,phenothiazine) and heavy metals cancause oral pigmentationAddisons disease, Peutz Jeghers

syndrome and hemochromatosis shouldalso be consideredBenign condition

www.darkgums.com/images/showki_beforemelanin1.jpg



Palmoplantar Hyperpigmentation:

Due to localized hypermelanosisPolymorphous brown macules withsharp or indistinct borders

Creases on the palms often present withhyperpigmentation and may contain

hyperkeratotic papules or pits

Photo reproduced with permission from Merit Publishing



Photo reproduced with permission from Merit Publishing

Idiopathic Guttate Hypomelanosis:AKA Disseminate Lenticular Leucoderma

involves small, white, irregularly shaped maculesprimarily on the anterior lower extremitiesUnknown etiology; benign

Macules range in size from 2-6 mmMore common in women over the age of 40Histologica lly, there is a decrease in thenumber of melanocytes


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Abnormal Variations

Pigmentary skin disorderscan cause emotional distress andsocial stigma Disorders are the result of altered melanin production Most common pigmentary disorders are albinism, vitiligo,

melasma, ephilis (freckles), and lentigo (liver spots)

www.patient.co.uk/images/dis127.jpgwww.medscape.com


Abnormal Variations

Vitiligo Vitiligo is a pigmentary problem

that appears in all races andaffects up to 1% of the generalpopulation.

The lesion is a maculardepigmentation (loss ofmelanocytes) with distinctborders on the face, neck,axillae, and extremities.

The etiology is unknown,although it appears to beinherited.

It has also been found to bemore prevalent in people withthyroid disease, perniciousanemia, and diabetes mellitus.

Vitiligo is a chronic disease witha highly variable course.

Melasma Melasma is an acquired light or

brown hyperpigmentation thatpresents most frequently on theface.

It is commonly associated withexposure to sunlight, pregnancy,or ingestion of oralcontraceptive hormones;however, many cases areidiopathic.

Melasma may disappearspontaneously after thecessation of oral c ontraceptivesor childbirth, but it may returnwith subsequent pregnancies.

Because sun exposure canexacerbate the condition,patients should use sunblocksor sunscreens.


How Does This Impact Wound

Management? Thorough history and physical exam should reveal

normal/abnormal dermatological conditions

Early detection of skin lesions is a top priority

This can be problematic in darker pigmented individuals

Erythema and/or blanching are not reliable indicators


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How Does This Impact Wound

Management?

Must use all your senses

LOOK

What is normal for the individual?

Compare area to surrounding skin or contralateral sideif applicable

Is the area in question a site of previous injury/scar?

LISTEN

Is the individual complaining of pain, itching or othersensory changes?

TOUCH

Is the area warmer/cooler?

Is the area firm/boggy?


Assessment Considerations

Inflammation- normal response to tissue injuryor insult and integral to microbial resistance

Triggered by endogenous and exogenous mediators

which results in localized vasodilation and increasedblood flow to area

Signs of inflammation:

Erythema, heat, edema and pain

Changes in skin color and temperature aredue to the inflammatory process

Failure to detect/observe may increase the risk of apatient developing a PrU or wound infection



Erythema- change in usual skin color due to dilation ofsuperficial capillaries Mediated by polymorphonuclear leukocytes, monocytes

and macrophages Occurs from time of insult to 2-5 days post injury

Color is a proven indicator of a physiological response toinjury and a good indicator of a Stage I PrU (Lyder 1991) In non-Caucasian skin, erythema is difficult to detect

Light pigmentation erythema is bright or dark red Dark pigmentation erythema presents as a darkening of

patients natural skin tone

Caregivers who are not of the same ethnic background aspatients may be less sensitive to slight changes in skincolor (Lyder 1991)

Use of a pen light can assist with skin color changeobservations


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Palpation is useful to assess skin

temperature, edema and turgor ofsuspected damaged areas



Skin Temperature- usually warm to the touch

Warmer than usual could be sign of inflammation,

and/or indicator of infection or pressure damage

Pale and cool skin may be sign of poor perfusion

or ischemia and may indicate the end stage of non-

blanching erythema

An increase or decrease in skin temperature isusually detectable by touch (palpation)

Could also use a digital infrared thermometerto objectively assess local skin temperature

Compare adjacent tissues; contralateral side



Edema- one of the physiological signs ofinflammation; also indicative of heart, liver andkidney failure, and venous insufficiency

Shiny, taut skin or pitting impressions in the skinadjacent to any wound but within 4 cm of the wound

margin indicates edema

With finger, press firmly within 4 cm of wound margin,wait 5 seconds, observe for any indentation (Gardner & Frantz 2004)

Edema and induration occur because pressure causes

separation in the skin layers and allows interstitial fluid

to accumulate

Both are good indicators of tissue damage


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Turgor- should quickly return to its

original state Slow return may indicate dehydration or

effects of aging

Soft tissues may indicate underlyinginfection

Tense tissues may indicate lymphedemaand/or cellulitis


Guidelines for Identifying Stage I PrU

NPUAP- National Pressure UlcerAdvisory Panel

Intact skin with non-blanchable redness of alocalized area usually over a bony prominence.Darkly pigmented skin may not have visibleblanching; its color may differ from the surroundingarea. The area may be painful, firm, soft, warmer or

cooler as compared to adjacent tissue. May bedifficult to detect in individuals with dark skin tones.May indicate at risk persons (a heralding sign ofrisk).



EPUAP- European Pressure UlcerAdvisory Panel

Non-blanchable erythema of intact skin.

Discoloration of the skin, warmth, edema,induration or hardness may also be used asindicators, particularly on individuals withdarker skin.


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NICE- National Institute for Clinical

Excellence Healthcare professionals should be aware of

the following signs which may indicateincipient pressure ulcer developmentinthose with darkly pigmented skin: purplish,bluish, localized areas of skin; localized heatwhich is tissue becomes damaged (this is trueregarding inflammatory changes in the skin) isreplaced by coolness; localized edema andlocalized induration.


Blanch Test

When gentle pressure is exerted on the skin,blood is temporarily forced out of the area,causing skin to appear white instead of pink Blanch test differentiates healthy skin from damaged

skin that is non-blanching erythema

In darkly pigmented skin the presence of melanin willensure that the clinician will be unable to see theevacuation of blood, followed by the refill; only themelanin will be visible (Matas 2001)

A more accurate way to detect non-blanchingerythema is to use clear glass or a plastic discto assess whether discoloration blanches ornot (Halfens 2001)


Basic Skin Care Considerations

Wash and clean skin with an emollientantibacterial soap and warm water

Pat dry all skin surfaces including

between the toes and under skin folds Apply moisturizers after bathing or

showering to remoisturize and lubricatethe skin

Maintain appropriate hair and nail care


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Black skin can sometimes appear ashy when itbecomes dry Ashiness describes the slate-gray appearance that

the scales of the stratum corneum impart to skinwhen superimposed on dark-colored skin

Common practice to use petrolatum and other heavyoils and greasy substances to abolish it (lanolin,vegetable oils, waxes)

This can lead to acne acne cosmetica/pomade acne

Recommended to use products that containsqualane (Montagna et al, 1993)



Use a lift sheet to move and turn patients

Do not drag patients

Use transfer techniques that prevent friction orshear

Pad bedrails, wheelchair arms, and legsupports

Support dangling arms and legs with pillows orblankets

Teach family members appropriate handlingtechniques



Use air mattress and wheel chair/geri-chair cushions

Use pillows to assist with positioning and pressure redistribution

Do NOT use donut shaped devices

Head of bed should not be higher than 30

Unless indicated by physician

Side lying position should be 30

Not directly on greater trochanter

Support with pillows

Watch for catheter lines, IV lines, and foreign objects in bed

Potential sources of pressure

Off Load heels so they do not touch the bed

Free floating concept


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Differential Diagnosisand Photo Gallery


Differential Diagnosis

dermatlas.med.jhmi.edu/derm/display.cfm?Image...

What could this be?

1. Bruise2. Deep tissue injury3. Mongolian spot

4. Tattoo ink


Differential Diagnosis

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What is this?1. Closed PrU

2. Hypopigmented skin3. Acute burn

4. Erythema


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Clinical Presentation Comparison

Unstageable yet probable Stage III or Stage IV sacral pressure ulcer in dark skin(left) and light skin (right). Note the difference in the appearance of the periwound

(area within 4 cm of the wound margin) .


Post-Inflammatory Hyper/Hypopigmentation

Black skin may respond to trauma orinflammatory disease by either an increase ordecrease in pigmentation (dyschromia)

Many of these pigmentary alterationsnormalize over time When a wound resurfaces it is closed. It is only truly

healedwhen the maturation phase is complete andscar tissue is mature

This can take up to two or more years in someindividuals Immature scar: red, raised, rigid

Mature scar: pale, planar, pliable



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Resolving or healing pressure ulcers. Because scar tissue is present (hypopigmented

areas) , these were at least Stage III or Stage IV sacral pressure ulcers. Darkpigmented skin when wounded, results in significant yet temporary pigmentarychanges. The areas appear pink (hypopigmented) and the margins/periwound appear

hyperpigmented while the tissues are healing. Near normal pigmentation may returnover time. It begins with small purple-brown /hyperpigmented macules that expand

filling the hypopigmented area.

Macules of re-pigmentation


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Note the periwound hyperpigmentation reaction to the inflammation. This can

be very difficult to differentiate from suspected deep tissue injury.



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Note characteris tics of the wound margin and periwound area (4 cm beyond margin).Hyperpigmentation is present due to the inflammatory response. Difficult to determine

if tissue is bruised, infected or suspected deep tissue injury.



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From the photo, it is very

difficult to determine whatis viable versus nonviable

tissue on this person.

This is why clinicians cannotrely on visual cues alone in dark

pigmented individuals.Thorough skin and woundassessment must involve:

TouchingFeeling

AskingSmelling


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Sickle Cell Ulcer

Venous Ulcer

Visually, these two ulcers present similarly, however

the etiologies are very different.

10% of African Americans are heterozygous for the

sickle cell gene.Of those with the disease, 25-75% develop sickle cellulcers.

They typically arise from vaso-occlusion, traumaand infection and tend to have a high propensity for

colonization.The ulcers are common at the malleoli, and patientsfrequently present with multiple ulcerations

unilaterally or bilaterally.Severe pain is common and young male adults (10-

50) are most often affected.

Sickle Cell Ulceration

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Differential diagnosis: venous/arterial insufficiency

-Crusting nodules in the distal one third of the leg

-Absence of hair follicles, hyperpigmentation, and atrophy of subcutaneous fat

-Perisoteal thickening of underlying bone is associated with this pathology

American Medical Technologies



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www.patient.co.uk/showdoc/images/OM15a.jpg

Adverse drug reaction in dark skin (left) and

light skin (right). Note the difference in theerythematous response.


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www.jcn.co.uk/images/12-02-28-01.jpg

Maturing scar tissue on dark and light skin. Black individuals are 2-19 times morelikely to develop Keloids than their Caucasian counterparts. (Connolly, Bikowski 2006)


Hypertrophic scarHypertrophic scar-- scar tissue is raisedscar tissue is raisedand rigid yetand rigid yet confined to the boundariesconfined to the boundariesof the initial injury.of the initial injury.

Keloid scarKeloid scar-- scar tissue that extendsscar tissue that extendswellwell beyond the boundariesbeyond the boundaries of theof theinitial injury. This photo shows ainitial injury. This photo shows a

Keloid after an ear piercing.Keloid after an ear piercing.

Summary

Physiologically and histologically, few differencesbetween Caucasian and Non-Caucasian skin

Mostly rate of melanocyte production

Dark skin has unique normal dermatologicalvariations

Skin and wound assessment must be thoroughand comprehensive

Use all senses

As the population ages and as ethnic populationsincrease, awareness of normal and abnormal skinvariations is critical



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For more information about

this or other educationalactivities, please contact:

[email protected]


References

Alterescu V, Alterescu K. Etiology and treatment of pressure ulcers.Decubitus. 1988;1(1):28-35.

Baronoski S. Skin: the forgo tten organ. 16th Annual ClinicalSymposium of Advances in Wound Care. Lake Buena Vista Fl.September 2001.

Baronoski S, Ayello E. Wound Assessment. In Baronoski S, Ayello E(Eds) Wound Care Essentials. Practice Principles. Philadelphia PA:Lippincott, Williams, & Wilkens; 2004. p. 79-90.

Berardesca E, Maibach H. Ethnic skin: Overview of structure andfunction. J Am Acad Dermatol. 2003;48:s139-s142.

Bethell, E. Wound care for patients with darkly pigmented skin.Nursing Standard. 2005;20(4):41-56.

Connolly C, Bikowksi J. Dermatological Atlas of Black Skin. SurreyUK: Merit Publishing; 2006.

Fitzpatrick TB. Skin phototypes. 20th World Congress of Dermatology.Paris France. July 2002.

Gardner S, Frantz R. Wound Bioburden. In Baronoski S, Ayello E (Eds)Wound Care Essentials. Practice Principles. Philadelphia PA:Lippincott, Williams, & Wilkens; 2004. p. 91-116.


References

Halder R, Nootheti P. Ethnic skin disorders overview. J Am Acad Dermatol.2003;48:143-148.

Halfens RJ, Bouts GJ, Van Ast W. Relevance of the diagnosis stage I pressureulcer: an empirical study of the clinical course of stage I ulcers in acute care andlong-term care hospital populations. Journal of Clinical Nursing. 2001;10(6):748-757.

Lyder CH. Conceptualization of the stage I pres sure ulcer. Journal of ETNursing. 1991;18(5):162-165.

Lyder CH. Examining the inclusio n of ethnic minorities in pressure ulcerprediction studies. Journal of Wound, Ostomy, and Continence Nursing.1996;23(5):257-260.

Lyder CH. Is pressure ulcer care evidence based or evidence linked? Sciencesof Surfaces Meeting. Warwickshire UK. January 2005.

Lyder CH, Yu C, Stevenso n D, et al. Validating the Brad en Scale for theprediction of pressure ulcer risk in blacks and Latino/Hispanic elders: a pilotstudy. Ostomy/Wound Management. 19 98;44(3A Suppl):S42-S50.

Matas A, Sowa MG, Taylor V, et al. Eliminating the issue of skin color inassessment of the blanch response. Advances in Skin and Wound Care.2001;14(4):180-188.

McMichael A. A review of cutaneous disease in Af rican-American Patients.Dermatology Nursing. 1999;11(1):35-48.


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References

Montagna W, Prota G, Kenney J. Black Skin Structure and Function.San Diego CA: Academic Press Inc., 1993.

Pathak MA. A ctivation of the melanocyte system by ultraviolet radiatio n

and cell transformation. Ann New York Acad S cience. 1985;453:328-339. Projections of the resident population by race, Hispanic origin, and

nativity: middle series, 2006-2010. Washington, DC: PopulationsProjections Program, Population Division, US Census Bureau.

Projections of the resident population by race, Hispanic origin, andnativity: middle series, 2050-2070. Washington, DC: PopulationsProjections Program, Population Division, US Census Bureau.

Szabo GS, Gerald AB, Pathak MA, et al. Racial differences in the fateof melanosomes in human epidermis. Nature. 1969;222:1081-1082.

Taylor S. Skin of color: Biology, structure, function, and implications fordermatologic disease. J Am Acad Dermatol. 2002;46:S41-S62.

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noncaucasian skin 3 slides color (2)

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