Fig. 8.1
Cross section of the skin
In addition to establishing individual uniqueness, the skin serves several key functions in protecting the body from injury and disease. These include maintenance of body temperature, protection from the environment, and synthesis of vitamin D. The sensatory function of the skin affords further protection. The skin consists of three layers: epidermis, dermis, and subcutaneous (see Fig. 8.2):
Epidermis : the outermost layer of the skin is responsible for the biomechanical barrier function of the skin. The top layer of the epidermis, known as the stratum corneum (SC) , is composed of layers that are continuously renewed and contains between 15 and 20 layers of flattened skin cells called corneocytes. Corneocytes comprise keratinocytes, cells filled with a tough fibrous, insoluble protein, known as keratin, which is resistant to change in temperature and pH [1]. Excessive skin surface moisture can cause overhydration of the keratinocytes and disruptions of the intercellular lipid bilayers. As a result, the corneocytes swell and the thickness of the SC increases leading to breakdown. Increased skin pH will lead to more swelling of the SC, causing the skin to be more permeable and compromising the skin barrier function. In addition to appropriate pH, SC function depends on water. The primary water source of the SC lies deep down in the subcutaneous tissue and it has to move to the surface to hydrate the upper layers. SC architecture is key to this water migration. The structure of both the corneocytes and the lipid layers of the SC combine to both move and maintain moisture that contributes to the skin’s physical barrier property and elasticity [2]. The lipid layers provide a moisture barrier but also function to regulate the entry of topical skin products into the SC when applied externally. Inside the corneocytes, the lipid substance, the Natural Moisturizing Factor (NMF) also helps to regulate SC hydration. NMF, made up of amino acids and salts, is produced in direct relationship to external humidity. Finally, maintenance of the SC architecture requires normal turnover of cells by desquamation. Desquamation is orchestrated by enzymes and is water dependent. Corneocytes over-accumulate on the skin when the water content is less than 10% or when skin continuity is breached [3].
Dermis : lies directly beneath the epidermis, is the second layer of skin and contains both blood vessels and nerve endings as well as proteins like collagen and elastin. The latter provide support and elasticity. This layer also contains macrophages and lymphocytes, cells important in the protection from invading organisms.
Subcutaneous (SubQ) or hypodermis : lies under the epidermis and dermis. It is several millimeters thick and is composed primarily of connective tissue, blood vessels, and fat. It attaches the dermis to underlying structures and promotes an ongoing blood supply to the dermis for regeneration. The hypodermis is primarily adipose (fat) tissue that provides a cushion between skin layers, muscles and bones. It stores fat for energy, provides insulation for temperature control, and aids in protection through its soft cushioning effect.
Fig. 8.2
Layers of the skin
Definitions
Incontinence exposes the skin to moisture, digestive enzymes, microorganisms, and alkalinizes skin pH; these conditions are thought to alter skin integrity and precipitate dermatitis. Individuals with severe intractable urinary incontinence (UI) and/or fecal incontinence (FI) are often immobile and at major risk for skin breakdown. Historically, a variety of terms have been utilized to describe skin conditions in the perineal area including: diaper rash, perineal dermatitis, perianal rash, contact dermatitis, irritant dermatitis, moisture maceration injury and heat rash [4, 5]. The universal term currently used for skin damage resulting from exposure to stool and/or urine is incontinence associated dermatitis (IAD) [1, 6]. IAD is defined as a skin inflammation, manifested as redness with or without blistering, erosion, or loss of the skin barrier function that occurs when urine or stool comes into contact with perineal or perigenital skin. IAD describes the primary clinical manifestation caused by exposure of the skin to urine and stool (inflammation), and identifies the source of the inflammation as UI and/or FI [1, 7]. Moisture must be present and the erythema is superficial (partial thickness skin loss). According to a 2015 Cochrane Collaboration review [4, 5], IAD is sometimes accompanied by bullae with serous exudates or secondary cutaneous infection. IAD can range in severity from erythema with or without loss of skin integrity to infection. Erosion or denudation of superficial layers is generally associated with more advanced or severe cases [1].
The current version of the ICD-10 contains codes for “diaper dermatitis ” (skin damage in infants and toddlers prior to toilet training), but not IAD [8]. A diagnostic code is needed to describe this skin condition in adults. IAD is costly, painful and, for the most part, preventable [9].
IAD is considered part of a broader group of skin conditions that are referred to as “moisture-associated skin damage” (MASD) [4, 5]. MASD is considered an umbrella term that describes the spectrum of damage that can occur as a result of the prolonged exposure of a patient’s skin to various sources of moisture (urine or stool, perspiration, wound exudate, mucus, or saliva) [6, 10]. But, IAD is the preferred term as it identifies the problem directly with the UI and/or FI and not with other conditions (such as perspiration or wound exudate) [8]. In addition to IAD, other skin conditions are also seen which include erythema, maceration, intertrigo and pruritus ani, as well as secondary bacterial, and/or fungal infections (see Table 8.1).
Table 8.1
Common incontinence-associated skin conditions
Skin problem | Picture | Definition | Appearance, signs, symptoms |
|---|---|---|---|
Erythema |  | • Inflammatory response of the skin caused by dilation and congestion of the capillaries | • Presents as a red, macular rash that may be sensitive and tight • Edema may be present • May have increased skin temperature from the inflammation |
Maceration |  | • Superficial erosion of the skin from overhydration due to prolonged exposure to moisture (e.g., urine, liquid stool) • Areas include perineal skin, abdominal and breast folds, tube sites, between toes and fingers, and skin surrounding wound sites | • White appearance of the skin with a very soft, sometimes “soggy” texture • Moisture barriers and/or absorbent dressings should be used on all areas at risk for maceration and on maceration that occurs around wound edges |
Intertrigo |  | • Partial-thickness skin loss that occurs on opposing skin surfaces as a result of perspiration, friction, and maceration • Inflammatory condition of skin folds, induced or aggravated by heat, moisture, maceration, friction and lack of air circulation • At-risk patients includes those who are obese, have impaired mobility or have diabetes | • Erythema, superficial line erosions at base of gluteal fold and circular erosions between buttocks |
Pruritus ani |  | • Inflammation of the peri-anal area directly related to perineal hygiene that includes overzealous wiping or cleansing of the anal area • Can also occur as a generalized pruritus in patients with systemic diseases such as liver or renal failure | • Bouts of intense peri-anal itching and chronic scratching causing linear lesions • Often misdiagnosed as IAD |
Secondary skin infections | |||
Bacterial |  | • Caused by numerous microorganisms, particularly the bacteria Staphylococcus epidermidis • Occurs when balance between the host and microorganisms is altered | • Occur following a break in the skin, as a secondary infection to already damaged skin or as a sign of a systemic disease • These infections irritate and inflame the skin, decreasing its ability to be an effective barrier • If FI exists, may develop bacterial infections from Gram negative organisms |
Candida albicans or Candidiasis (fungi, yeast) |  | • Most common opportunistic skin infection that results from a warm, moist environment (e.g., perineum, groin and thigh folds) • Penetrates the compromised epidermis and damages SC • More often seen in those who are obese, have diabetes, are on long-term antibiotic therapy, and/or have AIDS | • Characterized by a bright to dull red central area with peripheral red pustules that can develop into secondary lesions of papules if damaged by friction or shearing • Skin is usually very erythematous and pruritic and may be tender and very itchy • In darkened skin, the central area may appear as darkened skin. It has an erythematous base that may itch or burn • Spread of the lesions is inhibited when it reaches dry skin |
According to the National Pressure Injury Advisory Panel [11], a pressure injury is defined as “localized damage to the skin and/or underlying soft tissue usually over a bony prominence or related to a medical or other device. The injury can present as intact skin or an open ulcer and may be painful. The injury occurs as a result of intense and/or prolonged pressure or pressure in combination with shear. The tolerance of soft tissue for pressure and shear may also be affected by microclimate, nutrition, perfusion, co-morbidities, and condition of the soft tissue” [11]. Consequently, the location of the impaired integrity and distribution of the breakdown are important considerations in determining diagnosis and developing a subsequent treatment plan.
Differentiating IAD from pressure related partial-thickness skin loss can be particularly challenging for clinicians (see Table 8.2). Despite differences between IAD and pressure injury in both location and presentation, in many cases, patients in many cases may present with lesions of mixed etiology due to shared risk factors. The aging process itself predisposes the skin to an increased risk of both injury and infection.
Table 8.2
Differentiation between pressure injury and incontinence associated dermatitis
Assessment | Pressure injury | IAD |
|---|---|---|
Location | Typically bony prominences | Absorbent product areas Extreme cases may extend beyond containment product |
Tissue involvement | Partial to full thickness | Partial thickness |
Appearance | Varies from erythemic or ischemic epidermis to necrosis of deeper tissue layers and supportive structures | Diffuse borders Moist, shiny, taut, epidermis to shallow erosion(s) with exposed dermis |
Prevention | Offloading and protection from shear forces | Skin care regimen focusing on cleansing, moisturizing and protection from external irritants |
Complications | Necrosis of tissue and supportive structures, secondary infection, loss of function | Secondary bacterial/fungal infection Predisposition to pressure injury |
Risk factors | Immobility Incontinence Co-morbidity Impaired nutrition Impaired cognition Impaired sensory function | Immobility Incontinence Co-morbidity Impaired nutrition Impaired cognition GU/GI system factors Previous surgery Hormonal changes |
Etiology of Incontinence Associated Dermatitis
The relationship between incontinence and perineal skin breakdown comes from the presence of excessively moist or wet skin and the breakdown of the normal, healthy integrity of the skin. IAD is a “top-down” injury where the epridermis suffers superficial damage. The dermal injury caused by excessive moisture (see Fig. 8.3) itself is not entirely understood, but is believed to involve a complex cascade of events that can act upon one another in a self-perpetuating cycle as depicted in Fig. 8.4. Potential sources include UI and/or FI, liquid stool, frequent washes, poorly ventilated containment or a bodyworn occlusive product (e.g., external catheter, absorbent product or bed pad, penile clamp), and skin occlusion. Continued exposure to potential sources is a direct factor in skin breakdown, and the median time to onset of IAD can range from 4 to 13 days after this exposure. Other risk factors for IAD include poor skin condition, secondary to diabetes, etc., compromised mobility, pain, cognitive impairment, poor nutritional status, inability to perform personal hygiene, and critical medical status [4, 5].
Fig. 8.3
Dermal injury caused by moisture
Urea in urine is decomposed by bacteria to ammonia, a highly irritating substance. The perineal skin does not tolerate being wet for long periods of time, and the wetness destroys the natural barriers for the skin’s protection against destructive agents such as urine.
Normally, the SC, sebaceous gland secretions and the skin’s immune system furnish protection against aqueous, chemical, bacterial, and viral pathogens [1]. In addition to keratin in the SC, sebum, an oily substance secreted by the sebaceous glands, provides both moisturizing and water resistance protection to the skin. Sebum also maintains the natural mildly acidic pH of skin from 4 to 6 which retards the growth of microorganisms [9]. As discussed, IAD can range from mild inflammatory changes in the skin to infection. Figures 8.5 and 8.6 depict mild to severe IAD. Frequent and prolonged contact with moisture can precipitate inflammation by facilitating the passage of irritants into the skin, leading to dermatitis [13]. Urinary and/or fecal incontinence can be detrimental to the delicate pH balance. The natural acidic pH of the skin ranges between 4 and 6.8 with a mean of 5.5. The skin pH range is referred to as the “protective acid mantle.” Perspiration can increase the pH from 7.0 to 7.5, while urine and feces can increase pH to 8 or greater. Ammonia is alkaline and, therefore, raises the pH of the skin when it is in prolonged contact with urine or feces. If the skin becomes more alkaline, its ability to inhibit bacterial growth is compromised [14]. Fecal incontinence can cause dermal and epidermal erosion (see Fig. 8.7). Numerous integumentary changes occur over time, including diminished elasticity, decreased in the number and function of sweat glands, and a reduced collagen.
Fig. 8.5
Mild IAD Wound, Ostomy and Continence Nurses Society (2007). The WOCN image library [Image database]. Retrieved from http://images.wocn.org. In-text citation: (Mild Irritant Dermatitis; Wound, Ostomy and Continence Nurses Society 2007)
Fig. 8.6
Severe IAD Wound, Ostomy and Continence Nurses Society (2007). The WOCN image library [Image database]. Retrieved from http://images.wocn.org. In-text citation: (Severe Irritant Dermatitis; Wound, Ostomy and Continence Nurses Society 2007)
Fig. 8.7
Dermal and epidermal erosion secondary to fecal incontinence Wound, Ostomy and Continence Nurses Society (2007). The WOCN image library [Image database]. Retrieved from http://images.wocn.org. In-text citation: (Buttocks skin breakdown; Wound, Ostomy and Continence Nurses Society 2007)
Prevalence
Prevalence of IAD in hospitalized patients is 27% [1] and 43% for residents in skilled nursing facilities [1]. Incidence varies with population and care setting, ranging from 3.4 to 25% [1]. However, research regarding the prevalence of IAD and related moisture associated skin impairment has been wrought with the challenges from under-reporting, particularly due to embarrassment and stigma associated with UI and/or FI. Also, general perception and lack of understanding of the differences between IAD and pressure injury identification creates an additional are further hindrances.
Predisposing factors for IAD are also risk factors for development of a pressure injury. A 2012 multi-center investigation of 3,713 incontinent patients (mean age 81.2) in hospitals, nursing homes, and home care in Austria and the Netherlands reported an IAD prevalence of 6.1% and demonstrated there is a higher incidence of IAD in persons who have FI, moist perineal skin, higher BMIs, diabetes, and who need increased assistance in moving [15].
The development of IAD can have a considerable effect on patients physical and psychological well-being [12]. It can result in an “undue burden of care, loss of independence, disruption in activities, sleep, and reduced quality of life, worsening with frequency and quantity of soiling” ([8], p. 2).
Although IAD and pressure injuries may co-exist, especially in individuals who are both immobile and suffering from UI and FI, each of these conditions have distinct characteristics. Careful examination is crucial to making a precise diagnosis so that an individualized plan of care can be established.
Assessment
Symptoms of IAD include discomfort, pain, burning, itching, and/or tingling in the affected areas. Examination should include both inspection and palpation, and should be conducted frequently (e.g., every 8 hours (h)) on all patients with either UI and/or FI. Inspect perineal skin for excessive moisture, excoriation, and erythema or irritation. IAD presentation can range from erythema (with or without loss of skin) to cutaneous infection (such as candidiasis) [16]. In persons with light skin, erythema can be pink to red in color. Lesions may present as vesicles or bullae, papules, or pustules. The epidermis may or may not be intact. In cases where secondary infection is present, the appearance may include satellite pinpoint lesions, vesicles or erosion. Fecal incontinence, especially in high volumes, can be especially destructive and can result in erosion of the epidermis and dermis due to the presence of digestive enzymes (Table 8.2). The skin in the affected area may be warm. Inspection should be performed when removing clothing, protective pads, dressings, and/or containment devices.
Assessment of the perineal skin includes inspection of the sacrococcygeal, the gluteal cleft, the perianal, the buttocks, upper thighs, external genitalia and suprapubic areas (see Table 8.3). The skin will appear shiny and taut with redness and tenderness with diffuse borders, but limited to exposed areas (typically the buttocks, perineal, peri-genital, and peri-anal areas and skin folds of the groin, and upper thighs).
Table 8.3
Perineal skin examination
External perineal skin—women |
• Assess for rash, skin lesions, odor, and discharge |
• Separate the labia and visualize the urinary meatus, note any redness, inflammation, erythema ulceration, urethral or vaginal discharge, swelling, or nodules. Excoriations and maceration of the vulva may occur with constant wetness or may be secondary to infection
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