This article provides a timely reminder that incontinence-associated dermatitis (IAD) affects patients of all ages. Urinary incontinence affects 25 million Americans,1 and fecal incontinence affects between 2% and 10% of community-dwelling adults.2 Epidemiologic studies have found that more than 50% of elders residing in long-term care facilities suffer from urinary incontinence and that 20% have double urinary and fecal incontinence. As many as 54% of those managed in long-term care may experience an injury of the perineal skin,1 and IAD was found in 18% of incontinent adult patients in acute care facilities.3 Although most IAD studies have focused on the neonate population, it is a growing problem in the geriatric population. The need to protect the skin from irritants has been demonstrated for some time and is widely accepted by WOC nurses as a standard of care. The economics of staffing shortages and an increase in the elder population raises the risk for damage to the skin barrier that can lead to moisture-associated skin damage with its associated risk for secondary cutaneous infection or pressure ulceration.

Multiple factors contribute to the risk for IAD, including moisture, friction, dermal colonization, the type of incontinence (urine vs stool and stool consistency), and tissue tolerance.4 Excessive saturation of the skin from constant exposure to stool and/or urine prevents it from effectively acting as a barrier. Compromise of the skin's moisture barrier, when coupled with ongoing exposure to irritants, creates an environment that promotes increased colonization with bacterial and fungal species, leading to erythema and an increased risk of cutaneous infection, especially in the immunocompromised patient.1,5

Once skin becomes oversaturated, it tends to drag more when it comes in contact with other surfaces, resulting in friction and denudation of superficial layers of the skin. In the pediatric population, friction is often caused by rubbing of clothing or diapers, and in the elderly population, immobility may lead to friction between the skin and bed linens. Maceration, along with the skin changes and the more relaxed papillary ridges securing the layers of skin, also increases the risk for shear and more severe damage.4

Urinary and fecal incontinence are both responsible for skin damage, each creating an opportunistic environment for the other. Skin damage in the patient with urinary and fecal incontinence is rapid. The increased moisture of urinary incontinence alone can elevate the risk of friction damage and alter the pH level of the skin. This elevated pH affects the barrier qualities of the skin. With the addition of fecal incontinence, the combination of fecal bacteria and urea from urine changes the pH of the skin to alkaline, eliminating the acidic barrier of the skin from protecting against bacterial invasion.1,5

When selecting an IAD treatment, multiple patient- focused and product-focused factors should be considered.6,7 Assessment should address the etiology of perineal skin damage, and contributing factors, such as overall skin health, systemic illness, nutrition, and immunocompromise. Attention is then turned to cleansing and protection of the skin from further damage. Perineal washes contain surfactants and reduce bacterial overgrowths; caution should be used against scented cleansers that may serve as irritants to damaged skin. Moisture barriers were intended to protect from moisture exposure, so they work well against urinary incontinence but may not stand the test against harsh, frequent, and liquid stools. Products containing zinc oxide and dimethicone may serve as a more effective barrier in these cases, but it is no secret that the removal and reapplication process may be more challenging, and care must be taken to avoid further erosion. In cases of high-output diarrhea, the clinician may consider pouching of the anorectal area or use of a bowel management system.

Some clinicians suggest a more aggressive approach to manage those high-risk patients with perineal dermatitis associated with erosion. Ointments containing balsam of Peru, along with a barrier product, seem to provide a healing environment in addition to barrier protection.8 This combination has shown good results in the adult population, but no research is available in the pediatric population. Although a more advanced therapy may be associated with increased costs, the cost of fecal and urine containment devices to contain the incontinence in addition to antibiotic therapies for skin infections would be far more cost effective.

Regardless of the patient population or setting, it is clear that the skin cannot tolerate continued exposure to urine or fecal enzymes. The best treatment is always prevention. At the sign of exposure, a strictured skin regimen, based on principles of routine cleansing, moisturization, and application of a skin protectant, is implemented. It is critical that the skin protectant selected is able to withstand the irritant that it is providing a barrier against. Considerations of the patient's health, nutritional, and overall skin status influence a decision to initiate more aggressive management. Once erosion has occurred in a compromised population, more aggressive management is clearly indicated.

As demonstrated in the case examples presented by Ratliff and Dixon, perineal skin damage will occur with exposure to urine and feces, but damage can be halted with the selection of a barrier that is well suited for the insulting agent and the risk factors associated with the affected population. Prevention is most often possible, but treatment is essential for patient comfort and safety once skin damage has occurred.

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