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Incontinence-associated dermatitis

Incontinence-associated dermatitis
Literature review current through: Jan 2024.
This topic last updated: Oct 24, 2023.

INTRODUCTION — Incontinence-associated dermatitis (IAD) is a specific type of irritant contact dermatitis caused by prolonged contact of the skin with urine and/or feces and friction [1]. IAD causes discomfort, itching, and pain and can result in increased burden of care, disruption of daily activities and sleep, and reduction in quality of life.

This topic will discuss the clinical presentation, diagnosis, and management of IAD. Irritant contact dermatitis in adults and vulvar dermatitis are discussed separately. Pressure ulcers are also discussed separately.

(See "Irritant contact dermatitis in adults".)

(See "Vulvar dermatitis".)

(See "Clinical staging and general management of pressure-induced skin and soft tissue injury".)

EPIDEMIOLOGY — The prevalence of IAD varies across countries, health care settings, and patient populations. A prevalence of approximately 4 to 6 percent has been estimated among residents of nursing homes and patients who are hospitalized, but rates as high as 20 to 50 percent have been reported in long-term acute care settings [2-6]. The prevalence is highest among patients with limited mobility.

Patients with fecal or dual incontinence have a higher risk of developing IAD than those with urinary incontinence alone [4,7]. Additional independent risk factors for the development of IAD include older age, female sex, higher body mass index (BMI), increased friction or shearing of skin, dementia, functional impairment, diabetes, immobility, liquid stools, smoking, not using diapers, and perineal neuropathies or nerve trauma [5,7-10].

PATHOGENESIS — IAD is a subset of moisture-associated skin damage, where skin breakdown occurs as a result of prolonged exposure to moisture and irritants, including urine, stools, wound drainage, or other bodily fluids [11,12]. The mechanism of skin injury involves both chemical and physical irritation [1,13,14]:

The acidic pH of the skin surface (the "acid mantle") is a key regulator of the skin barrier function. Urease-producing bacteria from the perineum or urinary tract convert urea in urine into ammonia, which is alkaline [15]. Increase in skin pH results in disruption of the epidermal barrier, increased skin permeability, and inflammatory changes. In patients with fecal incontinence, lipolytic and proteolytic enzymes from feces can contribute to skin damage and inflammation [16]. Alteration of the skin microbiota and bacterial or fungal colonization are additional contributing factors.

Friction and skin shearing from repositioning and prolonged immobility can exacerbate symptoms. Frictional injury can also occur with clothing, diapers, or bed and chair surfaces.

Experimental studies have shown that skin changes of IAD develop rapidly, with increase of transepidermal water loss and appearance of erythema occurring after a few hours of exposure to urine [17].

CLINICAL PRESENTATION — IAD initially presents with persistent erythema and edema, without skin breakdown, involving the perianal area, buttocks, genitalia, upper thigh, and skin folds between genitalia and thighs [3]. The borders of the erythematous areas are typically irregular.

In patients with lightly pigmented skin, the involved skin appears pink or red (picture 1A). In patients with darkly pigmented skin, the areas of involvement may appear purple, dark red, or lighter or darker than the underlying skin tone (picture 1B). In more severe cases, vesicles, bullae, and erosions may develop along with signs of secondary infection (figure 1) [1,13]. The surrounding skin may appear macerated. Areas of discoloration can be noted at sites of previously healed lesions.

Symptoms include itching, stinging, burning, and pain.

COMPLICATIONS

Secondary infection – Colonization and secondary infection with bacteria and yeasts are common complications. Clinical signs of infection include presence of satellite pustules, scaling, or purulent exudate.

Pressure ulcers – Patients with IAD are at increased risk of developing pressure ulcers in the sacral area [18]. The presence of deep red or purplish, nonblanchable erythema with demarcated borders associated with pain suggests early-stage, pressure-induced skin and soft tissue injury.

In a review of over 5000 patients in acute care facilities in the United States, 17 percent of patients with IAD had facility-acquired pressure injury in the sacral area, and 4 percent had full-thickness pressure injury [7]. Immobility and dual incontinence were independently associated with increased risk of pressure skin injury in the sacral area.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS — The diagnosis of IAD is based on the clinical presentation and concurrent history of urinary and/or fecal incontinence. The Ghent Global Incontinence-Associated Dermatitis Categorization Tool (GLOBIAD) is a simple and widely used tool to assess severity (figure 1) [13].

The differential diagnosis of IAD includes the following:

Pressure ulcers – IAD is often confused with (stage I or II) pressure ulcers (table 1). The finding of deep red or purplish, nonblanchable erythema with demarcated borders in the sacral area associated with pain suggests early-stage, pressure-induced injury. Additional clinical features that help in differentiating IAD from pressure ulcers are summarized in the table (table 2). (See "Clinical staging and general management of pressure-induced skin and soft tissue injury".)

Allergic contact dermatitis – Allergic contact dermatitis (picture 2A-B) should be considered, with possible exposures including topical medicaments, preservatives, and fragrances [19]. (See "Clinical features and diagnosis of allergic contact dermatitis".)

Intertrigo and other intertriginous dermatitis – Intertrigo and other forms of intertriginous dermatitis should be considered in the differential diagnosis of IAD. The latter include inverse psoriasis (picture 3) and seborrheic dermatitis. Moreover, in patients with psoriasis involving other areas of the body, the irritative and traumatic aspects of IAD increase the risk of superimposed psoriasis due to Koebner phenomenon. (See "Intertrigo" and "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Inverse (intertriginous) psoriasis'.)

Lichen sclerosus – Some studies suggest urinary incontinence may be more common in female patients with lichen sclerosus. Patients should be examined for the typical white, atrophic plaques involving the vulva and perianal skin (picture 4A-B). (See "Vulvar lichen sclerosus: Clinical manifestations and diagnosis".)

MANAGEMENT — Management of incontinence and careful skin hygiene and protection are the mainstays of treatment and prevention of IAD [1,20-22]. A structured skin care regimen is especially indicated for patients with limited mobility and in patients in long-term care settings. Secondary skin infections should be assessed and treated.

Structured skin care regimen – An example of a structured skin care regimen is outlined below [22]:

Frequent examination of the perineal skin to assess the presence of IAD.

Prompt, gentle cleansing of urine and feces from the skin using soap-free and preservative-free, mild, liquid cleansers. Leave-on cleansers may be preferred to products that need to be rinsed off. Premoistened wipes designed for incontinence are an alternative, but care should be taken to avoid common allergens in wipes (including fragrances, preservatives, and surfactants) that could trigger allergic contact dermatitis. Methylisothiazolinone, a commonly used preservative in moistened wipes, may cause superimposed allergic contact dermatitis, particularly in a region, such as this, with abrogated barrier function [23]. Washing with water and regular soaps that have an alkaline pH should be avoided, as they can worsen the irritant effect of urine and stools on the skin. Vigorous washing and rubbing of skin should also be avoided. Normal saline can be used to clean open wounds.

Carefully patting the skin dry after cleansing or washing using a soft cloth without rubbing.

Hydrating and protecting the skin by applying moisturizers or barrier creams that have a low irritant or allergenic potential (eg, petroleum jelly, silicone-based products, soft zinc oxide creams). Creams are generally preferred to ointments and should be gently applied (without rubbing) on the affected areas in a thin layer. An excess of moisturizers can promote skin maceration. Commercial and formulated products available by prescription can be very helpful after irrigation, cleansing, and drying affected areas. These products typically contain combinations of zinc oxide, anhydrous lanolin, Burow's solution, silicon preparations, and polymer films [24].

Exuding lesions may benefit from the application of zinc oxide-based creams, films, lotions, or sprays.

Erosions or ulcerations should be covered with nonadherent dressings.

There is a paucity of high-quality studies evaluating the efficacy of different skin care measures for the treatment and prevention of IAD. A systematic review of 13 clinical trials including 1295 patients who were incontinent for urine, feces, or both and were residents in a nursing home or hospitalized found that structured skin care regimens consisting of gentle skin cleansing and application of moisturizing and protective topicals were more effective for the treatment and prevention of IAD than the use of soap and water [25]. However, the included studies were generally of low quality and showed considerable heterogeneity in the type of skin care products used, skin care procedures, and outcome measurement.

Assessing and treating secondary infections – Skin swabs and potassium hydroxide preparations for microscopic examination and culture should be performed if there are clinical signs of secondary bacterial or fungal infection. Topical antiseptics (eg, povidone iodine), topical antibiotics (eg, mupirocin cream), or topical antimycotics can be used for superficial, localized infections. Severe skin infections require systemic antibiotics or antifungals. (See "Acute cellulitis and erysipelas in adults: Treatment".)

The management of urinary and fecal incontinence in adults are discussed separately. (See "Female urinary incontinence: Treatment" and "Urinary incontinence in men" and "Fecal incontinence in adults: Management" and "Fecal incontinence in adults: Etiology and evaluation".)

PROGNOSIS — With appropriate skin care, IAD symptoms may improve in a few days, with resolution in one to two weeks.

SUMMARY AND RECOMMENDATIONS

Risk factors and pathogenesis – Incontinence-associated dermatitis (IAD) is a common, specific type of moisture-associated skin damage caused by prolonged contact of the skin with urine or feces. The risk of IAD is especially high for patients with fecal or dual incontinence. Older age, female sex, diabetes, and immobility are additional risk factors. (See 'Epidemiology' above and 'Pathogenesis' above.)

Clinical presentation – IAD presents with persistent erythema; edema; and in severe cases, bullae or erosions on the perianal skin, buttocks, and genitalia (picture 1A-B). Colonization and secondary infection with bacteria and yeasts are common complications. (See 'Clinical presentation' above and 'Complications' above.)

Diagnosis – The diagnosis of IAD is generally obvious, based on clinical presentation and history of urinary and/or fecal incontinence. The Ghent Global Incontinence-Associated Dermatitis Categorization Tool (GLOBIAD) is a simple and widely used tool to assess severity (figure 1). IAD must be differentiated from stage I and II pressure ulcers (table 2). (See 'Diagnosis and differential diagnosis' above.)

Management – For all patients with IAD, we suggest a structured skin care regimen that includes gentle, soap-free and preservative-free skin cleansing and moisturizer or barrier cream protection rather than usual care (Grade 2C). Soap-free, leave-on cleansers may be less irritating than products that need to be rinsed off. Moisturizers or barrier creams that have a low irritant or allergenic potential (eg, petroleum jelly, silicone-based products, soft zinc oxide creams) should be used for skin protection. (See 'Management' above.)

  1. Beele H, Smet S, Van Damme N, Beeckman D. Incontinence-Associated Dermatitis: Pathogenesis, Contributing Factors, Prevention and Management Options. Drugs Aging 2018; 35:1.
  2. Van Damme N, Van den Bussche K, De Meyer D, et al. Independent risk factors for the development of skin erosion due to incontinence (incontinence-associated dermatitis category 2) in nursing home residents: results from a multivariate binary regression analysis. Int Wound J 2017; 14:801.
  3. Gray M, Beeckman D, Bliss DZ, et al. Incontinence-associated dermatitis: a comprehensive review and update. J Wound Ostomy Continence Nurs 2012; 39:61.
  4. Kayser SA, Phipps L, VanGilder CA, Lachenbruch C. Examining Prevalence and Risk Factors of Incontinence-Associated Dermatitis Using the International Pressure Ulcer Prevalence Survey. J Wound Ostomy Continence Nurs 2019; 46:285.
  5. Bliss DZ, Mathiason MA, Gurvich O, et al. Incidence and Predictors of Incontinence-Associated Skin Damage in Nursing Home Residents With New-Onset Incontinence. J Wound Ostomy Continence Nurs 2017; 44:165.
  6. Boronat-Garrido X, Kottner J, Schmitz G, Lahmann N. Incontinence-Associated Dermatitis in Nursing Homes: Prevalence, Severity, and Risk Factors in Residents With Urinary and/or Fecal Incontinence. J Wound Ostomy Continence Nurs 2016; 43:630.
  7. Gray M, Giuliano KK. Incontinence-Associated Dermatitis, Characteristics and Relationship to Pressure Injury: A Multisite Epidemiologic Analysis. J Wound Ostomy Continence Nurs 2018; 45:63.
  8. Van Damme N, Clays E, Verhaeghe S, et al. Independent risk factors for the development of incontinence-associated dermatitis (category 2) in critically ill patients with fecal incontinence: A cross-sectional observational study in 48 ICU units. Int J Nurs Stud 2018; 81:30.
  9. Jiang H, Shen J, Lin H, et al. Risk factors of incontinence-associated dermatitis among critically ill patients: A systematic review and meta-analysis. Front Med (Lausanne) 2023; 10:1146697.
  10. Kottner J, Blume-Peytavi U, Lohrmann C, Halfens R. Associations between individual characteristics and incontinence-associated dermatitis: a secondary data analysis of a multi-centre prevalence study. Int J Nurs Stud 2014; 51:1373.
  11. Black JM, Gray M, Bliss DZ, et al. MASD part 2: incontinence-associated dermatitis and intertriginous dermatitis: a consensus. J Wound Ostomy Continence Nurs 2011; 38:359.
  12. McNichol L, Bliss DZ, Gray M. Moisture-Associated Skin Damage: Expanding Practice Based on the Newest ICD-10-CM Codes for Irritant Contact Dermatitis Associated With Digestive Secretions and Fecal or Urinary Effluent From an Abdominal Stoma or Enterocutaneous Fistula. J Wound Ostomy Continence Nurs 2022; 49:235.
  13. Beeckman D, Van den Bussche K, Alves P, et al. Towards an international language for incontinence-associated dermatitis (IAD): design and evaluation of psychometric properties of the Ghent Global IAD Categorization Tool (GLOBIAD) in 30 countries. Br J Dermatol 2018; 178:1331.
  14. Doughty D, Junkin J, Kurz P, et al. Incontinence-associated dermatitis: consensus statements, evidence-based guidelines for prevention and treatment, and current challenges. J Wound Ostomy Continence Nurs 2012; 39:303.
  15. Kohta M, Koyanagi H, Inagaki Y, et al. Selective detection of urease-producing bacteria on the genital skin surface in patients with incontinence-associated dermatitis. Int Wound J 2023; 20:3289.
  16. Mugita Y, Minematsu T, Nakagami G, Sanada H. Influence of digestive enzymes on development of incontinence-associated dermatitis: Inner tissue damage and skin barrier impairment caused by lipidolytic enzymes and proteases in rat macerated skin. Int Wound J 2018; 15:623.
  17. Phipps L, Gray M, Call E. Time of Onset to Changes in Skin Condition During Exposure to Synthetic Urine: A Prospective Study. J Wound Ostomy Continence Nurs 2019; 46:315.
  18. Koloms K, Cox J, VanGilder CA, Edsberg LE. Incontinence Management and Pressure Injury Rates in US Acute Care Hospitals: Analysis of Data From the 2018-2019 International Pressure Injury Prevalence (IPUP) Survey. J Wound Ostomy Continence Nurs 2022; 49:405.
  19. Warshaw EM, Kimyon RS, Silverberg JI, et al. Evaluation of Patch Test Findings in Patients With Anogenital Dermatitis. JAMA Dermatol 2020; 156:85.
  20. Zhang X, Wang X, Zhao X, Zhang Y. A Structured Skin Care Protocol for Preventing and Treating Incontinence-associated Dermatitis in Critically Ill Patients. Adv Skin Wound Care 2022; 35:335.
  21. Dissemond J, Assenheimer B, Gerber V, et al. Moisture-associated skin damage (MASD): A best practice recommendation from Wund-D.A.CH. J Dtsch Dermatol Ges 2021; 19:815.
  22. Beeckman D. Incontinence-associated dermatitis: Moving prevention forward. Proceedings from the Global IAD Expert Panel. Wounds International 2015. https://woundsinternational.com/consensus-documents/incontinence-associated-dermatitis-moving-prevention-forward/ (Accessed on September 27, 2023).
  23. Gardner KH, Davis MD, Richardson DM, Pittelkow MR. The hazards of moist toilet paper: allergy to the preservative methylchloroisothiazolinone/methylisothiazolinone. Arch Dermatol 2010; 146:886.
  24. Zehrer CL, Lutz JB, Hedblom EC, Ding L. A comparison of cost and efficacy of three incontinence skin barrier products. Ostomy Wound Manage 2004; 50:51.
  25. Beeckman D, Van Damme N, Schoonhoven L, et al. Interventions for preventing and treating incontinence-associated dermatitis in adults. Cochrane Database Syst Rev 2016; 11:CD011627.
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