Incontinence Associated Dermatitis

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Incontinence Associated Dermatitis

Incontinence Associated

Dermatitis

Mikel Gray, PhD, FNP, PNP, CUNP, CCCN, FAANP, FAAN

Professor & Nurse Practitioner

University of Virginia Department of Urology


Functions of the Skin

Thermoregulation

Sensory organ/

communication

Immune functions; acts as a

first line of defense

Vitamin D metabolism

Barrier against toxins in

external environment and

against fluid & electrolyte

loss from internal

environment

Burns T et al. Textbook of Dermatology, 2004. Mass: Blackwell Science.

Figure: Verdier-Sevrain

S, Bonte F. Journal of Cosmetic Dermatology 2007; 6:75.


Barrier Function: The Bricks

Corneocytes (keratinocytes)

– Anucleated cells filled with

keratin & other molecules created

by breakdown of filaggrin

– Collectively referred to as natural

moisturizing factor (NMF)

– Surrounded by cornified

envelope (corneodesmosomes(

corneodesmosomes)

that degrade as they move to

surface of skin

– 20% content is H 2 0

Verdier-Sevrain

S, Bonte F. J Cosmetic Dermatology 2007; 6:75.

Gray M. American Journal of Clinical Dermatology 2010; 11(3): 201.

Figure:

http://www.bioskinregeneration.com/wrinkles/skin.j

pg


Moisture Barrier:

Natural Moisturizing Factor (NMF)

NMF contains various hygroscopic molecules 1 :

– Amino acids 40%

– pyrrolidone carboxylic acid 12%

– Lactate 12%

– Urea 7%

NMF levels ↓ by:

– Repeated washing with soaps or detergents 2

– Low humidity (


Skin’s s Moisture Barrier:

The Mortar (Lipid Matrix)

Primary components 1 :

– Ceramides 50%

– Cholesterol 23%

– Free fatty acids 15%

– Organized in lamellar arrangement as bi-layers with

water; stores water needed for adequate hydration and

slows water passage

Lipid Matrix ↓ by:

– Age 2

– Seasonal effects 1

– Atopy 2

1. Verdier-Sevrain

S, Bonte F. Journal of Cosmetic Dermatology 2007; 6:75.

2. Rogers J et al. Archives in Dermatologic Resarch 1996; 288: 756.

3. Chamlin SL et al. Archives in Dermatology 2001; 137: 1110.


Moisture Barrier:

Additional Factors

Aquaglyceroporin AQP3 1

– Membrane protein that forms water channels across

cell facilitating transport of water, urea, glycerol

within epidermis but preventing excessive loss via SC

– Expressed from the granulosum to just below the SC

Tight Membrane Junctions 2

– Water gradient steepest at junction or stratum

corneum and stratum granulosum

– TMJ comprises transmembrane proteins that control

skin permeability

1. Verkman AS, Mitra American J Physiology Renal Phys 2000; 278: F13.

2. Madara JL. Annual Review of Physiology 1998; 60: 143.


Moisture Barrier:

Vulnerable at the

Extremes of Life

Neonates: less efficient moisture barrier,

especially in premature infants 1

– More hydrophobic than older infants; result is

dryer more brittle skin 2

– TEWL ; ; skin capacitance

Cornification begins about GW 20

– Full-term skin contains 10-20 layers of SC, skin

in premature baby has 2-32

3 layers of SC

– Ability to regenerate skin cells considerable

1. Lund C et al. JOGNN 1999; 28(3): 241.

2. Matsumoto T et al. Journal of Dermatology 2007; 34: 447.


Moisture Barrier

Vulnerable at the Extremes of

Life

Aging Skin: gradual decline

in barrier function

– Thickness

– NMF content

– hydration

– TEWL

Comparatively slow to

regenerate

.


Water

Adverse Effects of

Urine on Skin

– skin hardness, rendering it more susceptible

to friction and erosion 1-3

– Compromises barrier function of skin 4

permeability to pathogenic species

permeability to irritants in urine or stool

– Effects exacerbated by presence of occlusive

device such as warp around incontinence

brief

brief

1. Berg W et al. Pediatric Dermatology 1986; 3: 102.

2. Leyden JJ et al. Archives of Dermatology 1977; 113: 1678.

3. Gray M. Journal of WOC Nursing 2004; 31(1 Suppl):S2-9.

4. Zimmerer RE et al. Pediatric Dermatology 1986; 3: 95.


Ammonia

Adverse Effects of

Urine on Skin

– From urine itself; ammonia also produced by

conversion of urea in presence of certain bacteria,

such as Corynebacterium and fungal species such

as candida albicans 1-3

– Especially with double UI & FI

– No direct evidence ammonia damages intact skin;

probably aggravates already compromised skin 1

– Alkaline urine may provoke or exacerbate

inflammation 2

1. Leyden JJ et al. Archives of Dermatology 1977; 113: 1678.

2. Atherton DJ Eur Academy Dermatology Venerology 2001; 15 (Supp1): 1.

3. Berg W et al. Pediatric Dermatology 1986; 3: 102.


Adverse Effects of

Stool on Skin

Fecal enzymes

– Protease & lipase potentially break down both

principal elements of moisture barrier 1,2

– In vivo evidence shows that exposure to

digestive enzymes in human skin led to 3

TEWL

pH

Visible Visible damage only when occlusion present

Evidence Evidence of damage present after 12 days

1. Atherton DJ Eur Academy Dermatology Venerology 2001; 15 (Supp1): 1.

2. Gray M. Journal of WOC Nursing 2004; 31(1 Suppl):S2-9.

3. Anderson PH et al. Contact Dermatitis 1994; 30(3): 152.


Pathophysiology

Use of absorptive containment devices

– Exacerbate overhydration by promoting

perspiration & retaining urine and stool; with

padding alone:

TEWL TEWL increases 3-43

4 fold within days

COCO 2

emission increases > 4 fold

pH pH increases from 4.4 to 7.1 (without(

incontinence)

1. Grove GL et al. Clinical Problems in Dermatology 1998; 26:183

2. Zimmerer RE et al. Pediatric Dermatology 1986; 3: 95.

3. Zhai H et al. Skin Research & Technology 2002; 8:13.


IAD: Pathophysiology

Urine/ Stool and Skin Flora

– Flora of skin near groin usually

colonized with staphylococcus

epidermidis & diphtheroids such as

Corynebacterium

– Contains few gram negative bacilli

– Candida albicans found in stool of infants

with diaper dermatitis, but not infants

without dermatitis

Leyden JJ et al. Archives of Dermatology 1977; 113: 1678.


Beekman D et al. Journal of Advanced Nursing 2009; 65(6): 1141.


Definition:

Incontinence Associated Dermatitis

(IAD)

Irritation and inflammation

associated with exposure to stool

or urine

Often accompanied by erosion of

the skin

Sometimes accompanied by

secondary cutaneous infection

(ie: candidiasis)

Etiology and pathophysiology

distinct from pressure ulceration

Photograph courtesy Linda

Bohacek


IAD as One Form of

Moisture Associated Skin Damage (MASD)

– Intertrigo: : inflammation in skin folds related to

perspiration, friction and bacterial/ fungal

bioburden

– Periwound maceration: : skin breakdown from

wound exudate, related to volume,

constituents or exudate & bacterial bioburden

– IAD: : urine, stool, containment device,

secondary cutaneous infection –fungal or

bacterial

1. Gray M et al. Journal of Wound, Ostomy & Continence Nursing 2007; 2

34(2):134.


Prevalence in Acute Care

976

Total number of

patients surveyed

35% had

Foley catheter

(deemed continent)

20.3% (198)

prevalence of

incontinence

urine or stool

• 27% had IAD

• 33% had a pressure

ulcer

• 18% had a probable

fungal Infection

21% had more than 1 type of injury

Junkin J, Selekof J. IAD prevalence in acute care. WOCN National Conference, June 2006

Minneapolis, MN.


Prevalence in Acute Care

N = 608

33% had

Foley catheter

(deemed continent)

19.7% (120)

prevalence of

incontinence

urine or stool

• 42.5% perineal skin injury

• 20% had IAD

• 21.7% had PU

• 10% had a probable

fungal Infection

Junkin J, Selekof J. Journal Wound, Ostomy & Continence Nursing 2007; 34(3): 260.

.


Prevalence & Incidence

in Critical Care Setting

95% of 44 ICU patients with incontinence

(n=44) 1

MDS mined data suggests at least 5.7%

prevalence from 10, 217 residents in 31 states 2

3.4% incidence in 981 residents on IAD

prevention program (over 14 days)

Median (range) time to onset 13 days

39% still had IAD after 2 weeks

1. Peterson, AACN NTI abstract, 2007.

2. Bliss DZ et al. Nursing Research 2006; 55(4): 243.


Etiology: Pressure Ulcers

Pressure

Shear

Pressure + Shear

Histopathologic Analysis of PU: ischemia 1

1. Houwing RH et al. SKINmed 2007; 6(3): 113.


Etiology: IAD

Histopathologic Analysis of IAD: inflammation 1

1. Houwing RH et al.

SKINmed 2007; 6(3): 113.


IAD & Pressure Ulcers

Most experts believe that IAD impairs skin’s

tolerance for pressure/ shear

Ongoing debate & controversy reflects lack of

knowledge of underlying mechanisms…in in one

study subepithelial moisture differentiated

erythema and stage I PU; higher SEM predicted

greater likelihood of erythema/stage I PU 1

FI and double incontinence strongly associated

with PU risk, mixed evidence concerning UI

alone 2-6

1. Jensen BB. Journal of Wound, Ostomy and Continence Nursing, 20092

(in pres).

2. Maklebust J & Magnan MA Advances in Wound Care 1994; 7(6): 25.

3. Gunninberg L. Journal of Wound Care 2004; 13(7): 286.

4. Fader M et al. Journal of Clinical Nursing 2003; 12(3):374.

5. Berlowitz DR et al. Journal of the American Geriatrics Society 2001; 49(7):866

7):866-71. 71.

6. Narayan S et al. Jounal of WOCN 2005; 32(3): 163.


IAD: Screening begins with CNA

or Non-professional care provider


IAD:

Diagnosis

Relies solely on

inspection

– Inflammation (bright

red) in persons with

light skin tones

– IAD located in skin fold

or underneath

containment device,

borders are poorly

demarcated & irregular

– Surface of skin may

“glisten” owing to

serous exudate


IAD: Diagnosis in persons with

Darker Skin Tones

Inflammation not readily

apparent (ie: not bright

red); often presents as

area of

hyperpigmentation or

subtle red tone

Hypopigmented areas

with chronic

inflammation

Pattern of skin damage

does not vary


IAD: Diagnosis

Inspect Skin Folds

– Opposing skin surfaces trap

& harbor moisture

– Warm moist environment

encourages bacterial and

fungal colonization,

overgrowth and infection

– Friction occurs as skin folds

rub against one another


IAD: Diagnosis

Assess for skin

erosion

– Partial thickness

erosion occurs with

IAD

– Necrotic tissue:

eschar or slough, full

thickness damage

indicates pressure

ulceration


IAD: Diagnosis

Look for secondary

cutaneous infection,

especially candidiasis

– Opportunistic infection with

candida albicans

– Thrives in warm, moist

environment & damages

stratum corneum

– Seen in 18% of one group of

976 acute care inpatients 1

Junkin J, Selekof J. IAD prevalence in acute care. WOCN National l Conference, June 2006 Minneapolis, MN.


IAD: Diagnosis

Suspect PU when wound

is

– Over bony prominence

– Full thickness

– Necrotic tissue is present

– Skin is dark to purplish

red

Images: http://www.lhsc.on.ca/wound/p_chart.htm


Differentiate IAD from

Pressure Ulceration

Gray M et al. Journal of Wound, Ostomy and Continence Nursing 2007; 07; 34(2): 134.


IAD and its Severity

Instrument

Designed and validated by WOC nurses and

their faculty

2 WOC nurses established initial face validity

Content and criterion validity via 9 WOC nurses

in North Central Region of WOCN

Interrater reliability via 247 WOC nurses

attending 2007 National Conference

Descriptive, ranks severity allowing longitudinal

assessment; responsiveness has not yet been

tested

Borchert K et al. Journal of Wound, Ostomy and Continence Nursing 2010; 37(5): 527.


IAD and its Severity

Instrument

Borchert K et al. Journal of Wound, Ostomy and Continence Nursing 2010; 37(5): 527.


IAD and its Severity

Instrument

Borchert K et al. Journal of Wound, Ostomy and Continence Nursing 2010; 37(5): 527.


IAD and its Severity

Instrument

Borchert K et al. Journal of Wound, Ostomy and Continence Nursing 2010; 37(5): 527.


Clinical Evidence: How do we

Prevent and Treat IAD?

Structured skin care

regimen based on

available evidence and

followed routinely

Lyder, Journal of Enterostomal Therapy Nursing 1992

Hunter et al., Journal of Wound, Ostomy and Continence Nursing 20032

Zehrer et al., OWM 2004

Bale et al., J Tissue Viability 2004

Bliss, et al., Journal of Wound, Ostomy and Continence Nursing 20062


IAD: Prevention & Treatment


IAD: Cleanse

When frequent bathing necessary, current

evidence suggests….

– Gentle cleansing: NO scrubbing 1,2

– Select a cleanser with pH close to acid mantle of skin

– Select product that minimizes potential irritants,

scents, etc.

– Towel drying has been found to compromise

moisture barrier, consider no-rinse formulation for

frequent bathing 2

1. Gray M et al. Journal of Wound, Ostomy & Continence Nursing 2007; 2

34(2):134.

2. Voegeli D. Journal of Wound, Ostomy & Continence Nursing 2008; ; 35(1).


Moisturize

Three categories

– Humectants attract water to the skin

– Emollients replace lipids to stratum corneum;

designed to smooth skin surface

– Occlusives act to protect skin from exposure

to moisture and potential irritants; vary in

their ability to maintain skin hydration

– Some prefer emollient based on clinical

considerations, no research available to verify

or refute


Protect

Skin Protectants should

– Act as a “moisture barrier”, , protecting skin from

deleterious effects of exposure to irritants and

excess moisture

– Maintain hydration and favorable skin’s s normal

transepidermal water loss (TEWL)

– Avoid maceration when left on for prolonged

period of time

– Options

Ointment based skin protectants

Liquid acrylates (marketed as a skin barrier)

Gray M. Skin Protectants in the Treatment of Irritant Dermatitis In: Sek CK. Advances in Wound

Care, Volume 1. New Rochelle, NY: Mary Ann Liebert, , Inc.


Protect

Ointment based skin

protectants

– Petrolatum: : blend of

castor seed oil &

hydrogenated castor

oil

– Dimethicone: : silicone

based oil

– Zinc Oxide: : white

powder, mixed with

cream or ointment

base


Clinical Evidence

Petrolatum

– Good protection against irritant

– Avoided maceration

– Modest skin hydration

Dimethicone

– Variable protection against irritant

– Modest protection against maceration

– Good skin hydration

Zinc Oxide

– Good protection against irritant

– Did not avoid maceration

– Poor skin hydration

Hoggarth A et al. OWM 2005; 51(12): 30.


Protect

Skin barriers (polymer acrylate)

– Non-alcohol preferred

Less pain

Less drying

No different when compared to ointment based

skin protectants in one robust RCT (powered for

economic rather than efficacy outcomes)

Bliss DZ et al. Journal of Wound, Ostomy & Continence Nursing 2009; 09; 35 (2).


Cleanse, Moisturize & Protect:

Single Step Approach

Disposable Bathing

Cloth: : Cleanses &

moisturizes

Shield Cloths: : Tailored

cloths, cleanse

(chlorhexidine

gluconate), moisturize

(glycerine, aloe),

protect (3%

dimethicone)


Hospital

vs.

Washcloth Disposable

Washcloth


Preventive Skin Care

Typical Protocol

– Routine daily cleansing &

moisturization for all

patients

– For Incontinent and High

Risk Patients

Cleanse, Cleanse, moisturize &

protect daily and after

each major incontinent

episode


IAD: Treatment

Establish or continue structured

program based on “cleanse,

moisturize & protect”, , consider

changing skin protectant

Minimize exposure to irritants

(Aggressively manage UI or FI)

Treat secondary cutaneous

infections

Allow skin to heal or apply

protectant with active ingredients

designed to promote healing


IAD: What about

Dressings

Topical Dressings

– Hydrocolloids

– Thin film dressings

Act as barrier to urine & stool

Promote moist environment

for wound healing

Can be combined with topical

treatments


Dressings:

Practical Concerns

Topical Dressings

– Maintaining adherence

significant challenge

– Skin surfaces complex

– Borders often roll when

ointments or

moisturizing products

have been applied

– Undermining of urine

or stool may occur


IAD Treatment

Aluminum sulphate or acetate (Burow’s

Solution) with Stomahesive powder:

– Applied as compress; causes protein

precipitation & has antimicrobial properties

– Exerts drying & soothing effect; followed by

application of moisture barrier

– Often used when dermatitis complicated by

extensive erosion and serous exudate


IAD: Treatment

BCT Agents

– BCT Ointment (Xenaderm)

Balsam Peru, Castor Oil, Trypsin in

ointment base

Applied to dermatitis twice daily or with

major cleansing

Goal is to combine skin protectant

with active ingredients that promote

wound healing


IAD Treatment:

Secondary Complications

Candidiasis

– Topical antifungals are effective for the

treatment of cutaneous infections

– Effective agents include the polyene

antibiotics, azoles and the allylamines 1

– Resistance to antifungals is emerging, careful

monitoring of research literature is essential

1. Evans E & Gray M, Journal of Wound, Ostomy & Continence Nursing 2003; ,30(1).


Conclusion

IAD is a prevalent and clinically relevant

condition,

Relationship to PU risk poorly understood,

etiology appears distinct, some

pathophysiologic mechanisms shared

Structured skin regimen key to prevent &

treat

Principles of skin regimen: cleanse,

moisturize & protect

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