976 Total number of patients surveyed

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1 Incontinence Associated Dermatitis in the Person with Inflammatory Bowel Disease Mikel Gray, PhD, FNP, PNP, CUNP, CCCN, FAANP, FAAN Professor & Nurse Practitioner University of Virginia Department of Urology Objectives v Define Incontinence Associated Dermatitis (IAD) and its epidemiology v Identify persons with Inflammatory Bowel Disease who are at risk for IAD v Discuss the etiology and pathophysiology of IAD focusing on the adverse effects of stool in contact with the skin v Review the assessment of IAD v Describe options for prevention and treatment 1

2 Definition: Incontinence Associated Dermatitis (IAD) v Irritation and inflammation associated with exposure to stool or urine v Often accompanied by erosion of the skin v Sometimes accompanied by secondary cutaneous infection (ie: candidiasis) v Etiology and pathophysiology distinct from pressure ulceration 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. 2

3 Epidemiology of IAD v 95% of 44 ICU patients with incontinence (n=44) 1 v MDS mined data suggests at least 5.7% prevalence from 10, 217 residents in 31 states 2 v 3.4% incidence in 981 residents on IAD prevention program (over 14 days) v Median (range) time to onset 13 days v 39% still had IAD after 2 weeks 1. Peterson, AACN NTI abstract, Bliss DZ et al. Nursing Research 2006; 55(4): 243. IAD Risk in Persons with IBD v Prevalence of fecal incontinence higher in parous women with IBD as compared to those without IBD 1 v Onset of FI associated with vaginal delivery; caesarean section may be protective v Prevalence of daytime FI from 5%-11% and nighttime FI from 12%-21% 21% within first 1-2 decades after IPAA 2 v Meta-analysis analysis of 43 observational studies with 9317 subjects found mild FI in 17% and severe FI in 3.7% 3 1. Ong JPL et al. Inflammatory Bowel Disease 2007; 13(11): Hahnloser D et al. British Journal of Surgery 2007; 94(3): Hueting WE et al. Digestive Surgery 2005; 22(1-2): 2): 69. 3

4 Physiology: Skin s Moisture Barrier Prevents MASD v Stratum corneum: avascular, keratinocytes or corneocytes v Lipid matrix: : slows movement of water & electrolytes v Water: : hydrates corneocytes v ph: : (range ) 5.9) acid mantle v Bacterial flora: : compete with pathogens to prevent infection v Temperature: : regulates permeability Barrier Function: The Bricks v 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) that degrade as they move to surface of skin ~20% content is H 2 0 Verdier-Sevrain S, Bonte F. Journal of Cosmetic Dermatology 2007; 6:75. Figure: g 4

5 Moisture Barrier: Natural Moisturizing Factor (NMF) v Natural Moisturizing Factor contains various hygroscopic molecules 1 : Amino acids 40% pyrrolidone carboxylic acid 12% Lactate 12% Urea 7% v NMF levels by: Repeated washing with soaps or detergents 2 Low humidity (<10%), UV exposure 3 Age 4 1. Verdier Atopy 5 1. Verdier-Sevrain S, Bonte F. Journal of Cosmetic Dermatology 2007; 6: Caspers PJ et al. Journal Investigative Dermatology 2001; 116: Katagari C et al. Journal of Dermatologic Sci 2003; 31: Horii et al. British Journal of Dermatology 1989; 121: Matsumoto T et al. Journal of Dermatology 2007; 34: 447. Skin s Moisture Barrier: The Mortar (Lipid Matrix) v 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 v Lipid Matrix by: Age 2 Seasonal effects 1 Atopy 2 1. Verdier-Sevrain S, Bonte F. Journal of Cosmetic Dermatology 2007; 6: Rogers J et al. Archives in Dermatologic Resarch 1996; 288: Chamlin SL et al. Archives in Dermatology 2001; 137:

6 Moisture Barrier: Additional Factors v 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 v 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: F Madara JL. Annual Review of Physiology 1998; 60: 143. Adverse Effects of Stool on Skin v 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 u TEWL & ph udamage exacerbated when bile salts present uvisible damage ONLY when occlusion present uevidence of damage present after 12 days 1. Atherton DJ Eur Academy Dermatology Venereology 2001; 15 (Supp1): Gray M. Journal of WOC Nursing 2004; 31(1 Suppl):S Anderson PH et al. Contact Dermatitis 1994; 30(3): Buckingham KW, Berg RW. Pediatric Dermatology 1986; 3(2):

7 Adverse Effects of Stool on Skin v Stool Consistency Overwhelming clinical experience suggests that liquid stool more damaging than solid (formed) stool Diarrhea emerged as risk factor in multivariate analysis of 532 children managed by diapers 1 Diversion of stool in SICU unit for patients with FI & diarrhea incidence of skin damage from 43.0% to 12.5% 2 1. Adalat S, Wall D, Goodyear H. Pediatric Dermatology Pediatric Dermatology 2007; 24 (5): Benoit R & Watts CA. Journal Wound, Ostomy & Continence Nursing 2007; 34(2): 163. Pathogenic Factors v Candida albicans Found in stool, skin and diaper in 2 groups of infants with incontinence associated (nappy) dermatitis 1,2 Both studies reported absence in comparison cohorts without skin damage Oral thrush emerged as risk factor for incontinence associated dermatitis in multivariate analysis of 532 infants and children in diapers 3 1. Rebora A, Keyden JJ. British Journal of Dermatology 1981; 105(5): Goklap AS et al. Tropical & Geographical Medicine 1990; 42(3): Adalat S, Wall D, Goodyear H. Pediatric Dermatology Pediatric Dermatology 2007; 24 (5):

8 Pathophysiology of IAD IAD: Diagnosis v Relies solely on inspection Inflammation (bright red) in light skinned persons IAD located in skin fold or underneath containment device, borders are poorly demarcated & irregular Surface of skin may glisten owing to serous exudate 8

9 IAD: Diagnosis in persons with Darker Skin Tones v Inflammation not readily apparent (ie: not bright red); often presents as area of hyperpigmentation or subtle red tone v Hypopigmented areas with chronic inflammation v Pattern of skin damage does not vary IAD: Diagnosis v 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 9

10 IAD: Diagnosis v Assess for skin erosion Partial thickness erosion occurs with IAD Necrotic tissue: eschar or slough, full thickness damage indicates pressure ulceration IAD: Diagnosis v 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 1. Junkin J, Selekof J. IAD prevalence in acute care. WOCN National Conference, June 2006 Minneapolis, MN. 10

11 Differentiate MASD from Pressure Ulceration Gray M et al. JWOCN 2007; 34(2). Clinical Evidence: Prevention and Treatment v Structured skin care regimen should be defined based on available evidence and followed routinely (Lyder, J ET Nurs 1992; Hunter et al., JWOCN 2003; Zehrer et al., OWM 2004; Bale et al., J Tissue Viability 2004; Bliss, et al., JWOCN 2006) 11

12 IAD: Prevention & Treatment IAD: Cleanse v 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; 34(2): Voegeli D. Journal of Wound, Ostomy & Continence Nursing 2008; 35(1). 12

13 Cleanse v Incontinence skin cleansers ph Balanced designed to maintain the acid mantle of perineal skin Many are no rinse (avoids need to towel dry) Require less time than basin cleansing with soap and water Many contain emollients or humectants to preserve lipid barrier, thus combining 2 steps into a single action Moisturize v 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 13

14 Protect v 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 normal transepidermal water loss (TEWL) Avoid maceration when left on for prolonged period of time Options u Ointment based skin protectants u Liquid acrylates (marketed as a skin barrier) Protect v 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 14

15 Protect v Petrolatum Good protection against irritant Avoided maceration Modest skin hydration v Dimethicone Variable protection against irritant Modest protection against maceration Good skin hydration v Zinc Oxide Good protection against irritant Did not avoid maceration Poor skin hydration 1. Hoggarth A et al. OWM 2005; 51(12): 30. Protect v Skin barriers (polymer acrylate) Non-alcohol preferred u Less pain u Less drying v 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; 35 (2). 15

16 Cleanse, Moisturize & Protect: Single Step Approach v Disposable Bathing Cloth: Cleanses & moisturizes v Shield Cloths: Tailored cloths, cleanse (chlorhexidine gluconate), moisturize (glycerine, aloe), protect (3% dimethicone) IAD: Treatment v Establish or continue structured program based on cleanse, moisturize & protect v Minimize exposure to irritants (Aggressively manage UI or FI) v Treat secondary cutaneous infections v Allow skin to heal or apply protectant with active ingredients designed to promote healing 16

17 IAD Treatment v 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: Candidiasis v 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). 17

18 Conclusion v IAD is an increasingly recognized and clinically relevant condition associated with FI and urinary incontinence v Patients with IBD are at increased risk for FI and associated sequelae, including IAD v Prevention and treatment of IAD is based on a structured skin care regimen that employs principles of cleanse, moisturize and protect 18

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