Skin Assessment and Moisture-Associated Skin Damage

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skin assessment and moisture-associated skin damage

by the WoundSource Editors

The performance of an accurate and complete skin assessment is of utmost importance to obtaining and maintaining healthy skin. Understanding the structure and function of the skin is key to the differentiation of normal from abnormal findings. Having this baseline knowledge aids in determining the patient's level of risk, how skin is damaged, the impact of moisture on the skin, the resulting type of moisture-associated skin damage (MASD), and whether current skin care protocols are effective and adequate.

If an accurate skin assessment is not performed either for gathering baseline information or when a change in condition occurs, then the patient is not receiving the level of competent clinical care that should be given.1

Anatomy and Physiology of the Skin: Brief Overview

Healthy skin is tough, pliable, elastic, slightly moist, and well hydrated. The skin is the largest organ of the body, covering approximately 18 square feet and weighing about 12 pounds or up to 15% of total adult body weight. The skin requires approximately one-third of the circulating blood volume to sustain it. Normal skin temperature is approximately 92 degrees, whereas for most individuals core body temperature is 98.6 degrees Fahrenheit. 2 The skin is our outside armor and protects the body against microbes, toxins, and mechanical injury. The old adage "you can't see the forest for the trees" comes into play sometimes, causing the skin to take a second or latent place in the hierarchy during the head-to-toe assessment of the body's systems and perhaps many times goes unnoticed until changes occur either from damage or in response to aging. The skin also provides for sensation via nerve receptors, retention of water and other essential body fluids and nutrients within the skin, thermoregulation via circulation and sweating, excretion of toxic substances with sweat, synthesis of vitamin D in the presence of sunlight, immunological function mediated by Langerhans cells, and expression of emotion. 3

Human skin is divided into two primary layers. The epidermis is the outermost of the three main layers of the skin. The basal layer is composed of keratinocytes that lie at the base of the epidermis and migrate upward, where they eventually slough off at the outermost layer of the epidermis, known as the stratum corneum. The stratum corneum is enriched with a lipid matrix from the lamellar bodies. The barrier properties of the skin are enhanced by the intercellular lipids, corneocytes, amino acids, sebaceous secretions, and degradation products from corneal proteins besides lipids, and they keep the pH at an optimum level of 5.5. In simpler terms, this is the brick and mortar structure of the skin and our acid mantle. This acid mantle provides essentially a hostile environment for microorganisms and limits their ability to proliferate. For individuals under the age of 60 it takes approximately 30 days for a layer of epidermis to be replaced. For individuals over the age of 60 this process may take as long as 45 days. The epidermis is avascular, and it varies in thickness over the body, up to 1.5 mm on the palms of the hands and soles of the feet. 2,3

Differential Diagnosis of Types of Moisture-Associated Skin Damage

When completing a skin assessment, and it is determined that the individual has MASD, it is essential to use the clinical presentation information to differentiate among the four types of MASD and determine which one the individual has. These include: 1) incontinence-associated dermatitis or IAD; 2) intertriginous dermatitis, also called intertrigo or ITD; 3) peristomal moisture-associated dermatitis; and 4) periwound moisture-associated dermatitis. In all four the barrier property of the skin is impaired, and this allows irritants to penetrate the epidermis. These irritants disrupt the lipid matrix and essentially dissolve the brick and mortar structure or barrier property of the skin. At the same time, the acid mantle is disrupted, and the pH of the skin becomes more alkaline and conducive to bacterial proliferation and infection. 4 MASD manifests as mild erythema and inflammation to extensive and painful erosion complicated by bacterial and fungal infection. The cause is prolonged exposure to moisture and its contents, including urine, stool, perspiration, wound exudate, mucus, or saliva. 4,5

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Incontinence-Associated Dermatitis

The contaminants lending to IAD are urine and feces. IAD develops as a form of irritant dermatitis resulting from prolonged or chronic exposure to urine and/or stool, particularly liquid stool. These lesions are also often mistakenly labeled stage 1 or stage 2 pressure ulcers/injuries. 6 To differentiate, we must examine where, and how, the area presents itself. Additionally, we must ask whether it is diffuse over an area or isolated over a bony prominence. The latter would be more indicative of pressure-related injury and pressure injury is a bottom-up phenomenon, whereas IAD is a top-down phenomenon. 7 IAD occurs in the perineum, including the labial folds and vulva to the anus in women, and from the scrotum to the anus in men; groin, buttocks, gluteal cleft, and even extending down to the inner and posterior thighs. 8

Intertriginous Dermatitis

ITD is occasionally mistaken for pressure injury as well. ITD results from moisture accumulation between skin folds, especially in bariatric individuals, and the presence of friction between these opposing skin surfaces. 8 This can occur more often among persons with diabetes mellitus and those on bed rest. Any containment device or other medical device trapping moisture in a skin fold can contribute to ITD also. Some of the most common locations for ITD are the groin, the axilla, underneath the breast, and in the abdominal panniculus or pannus. Any individual with skin folds is at risk for ITD, and the importance of checking all skin folds cannot be understated. ITD can manifest with erythema, denudation, itching, oozing, or weeping. An alteration in the normal skin flora may also contribute to the overgrowth of Candida, for example, or another fungal infection or a bacterial overgrowth. 9

Peristomal Moisture-Associated Dermatitis

Peristomal moisture-associated dermatitis is an inflammation or erosion of the skin related to moisture from fecal, urinary, or chemical irritants beginning at the stoma skin junction, which can extend outward in approximately a four-inch radius. 10 The location of the stoma and the type and consistency of the effluent may increase the risk of peristomal skin breakdown. These factors may also affect prevention and treatment strategies. However, despite the utilization of various containment devices and strategies, in individuals with hyperactive bowels, diarrhea, or fistulas that connect the bowel and the skin, fecal effluent may leak out onto and erode peristomal skin. Determining which pouching system provides the best fit and maintaining a secure fit are the biggest challenges. Without accurate appliance fit and secure adherence, leakage of effluent can occur, resulting in erosion of the epidermis. This in turn can perpetuate the issue of not being able to maintain secure pouching post maceration.

Other ostomy sites must be considered as well, including percutaneous gastrostomy tube insertion sites and tracheostomies. With gastrostomy tubes the potential for leakage of digestive enzymes and tube feeding around the insertion site exists. Patients with tracheostomies may develop skin issues related to perspiration, saliva, or sputum accumulation around the stoma, under the flange of the external cannula, or on the tracheostomy ties or dressing. 11

Periwound Moisture-Associated Dermatitis

With periwound moisture-associated dermatitis, wound exudate, which contains proteolytic enzymes, comes in contact with periwound skin for prolonged periods of time. The exudate of chronic wounds can exacerbate the problem because of a higher concentration of bacteria and its released histamines, as well as proteolytic enzymes known as matrix metalloproteases or MMPs. The lower the viscosity of wound exudate, the lower the protein content will be, hence a lower amount of proteolytic enzymes. 12 Prolonged exposure of periwound skin to the excessive moisture plus these enzymes leads not only to maceration, but also to excoriation, which Dowsett, Groemann, and Harding13 defined as an injury to the skin caused by trauma, chemical, or thermal burn. This excoriation can stem not only from the impact of the enzymes, but also from the physical scratching of the area by the patient because of associated irritation and itching. The skin is then more susceptible to pressure, shear, and friction as well, which can prevent the wound from closing. When the skin is moist, it is more susceptible to damage from pathogens. Skin damage may be exacerbated with the use of alkaline cleansers, soaps or detergents, aggressive cleaning, and inappropriate use of containment devices.

Prevention and Treatment of Moisture-Associated Skin Damage

Prevention and treatment of all types of MASD begin with a thorough assessment of the skin. Proper cleansing with gentle pH-balanced cleansers with gentle surfactants that protect the lipid profile of the skin should be done as soon as possible after soiling. Added benefit may be achieved with the use of no-rinse formulas that allow for cleansing without requiring additional friction. Cleansing should be followed by application of barrier products that protect the skin from subsequent episodes of prolonged exposure to moisture and other caustic agents. Emollients may also be used to aid in retaining moisture in the stratum corneum by rehydrating the corneocytes. This will also help prevent transepidermal water loss or TEWL. 4 Remembering the fundamentals of skin care and taking a structured approach to cleansing, moisturizing, and protecting the skin will not only aid in its repair, but also keep the skin intact and prevent breakdown. RE

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References
1. Holloway S, Jones V. The importance of skin care and assessment. Br J Nurs. 2017;14(22):1172-6.
2. Wysocki AB. Skin integrity. In: Bryant RA, Nix DP, eds. Acute and Chronic Wounds: Current Management Concepts. 5th ed. St. Louis, MO: Elsevier; 2016:1-25.
3. Man MQ, Lin TK, Santiago JL, et al. Basis for enhanced barrier function of pigmented skin. J Invest Dermatol. 2014;134(9):2399–2407. doi.org/10.1038/jid.2014.187.
4. Young T. Back to basics: understanding moisture-associated skin damage. Wounds UK. 2017;13(4):56-65.
5. Gray M, Black JM, Baharestani MM, et al. Moisture-associated skin damage: overview and pathophysiology. J Wound Ostomy Continence Nurs. 2011;38(3):233-41.
6. 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(10):1373-80. doi.org/10.1016/j.ijnurstu.2014.02.012.
7. Campbell JL, Gosley S, Coleman K, Coyer FM. Combining pressure injury and incontinence-associated dermatitis prevalence surveys: an effective protocol. Wound Pract Res. 2016;24(3):170-7.
8. Black JM, Gray M, Bliss D, et al. MASD part 2: incontinence-associated dermatitis and intertriginous dermatitis. J Wound Ostomy Continence Nurs. 2011;38(4):359-70. doi:10.1097/WON.0b013e31822272d9
9. Bryant RA. Types of damage and differential diagnosis. In: Bryant RA, Nix DP, eds. Acute and Chronic Wounds: Current Management Concepts. 5th ed. St. Louis, MO: Elsevier; 2016:82-108.
10. Gray M, Colwell JC, Doughty D, et al. Peristomal moisture-associated skin damage in adults with fecal ostomies: a comprehensive review. J Wound Ostomy Continence Nurs. 2013;40(4):389-99.
11. Woo KY, Beeckman D, Chakravarthy D. Management of moisture-associated skin damage: a scoping review. Adv Skin Wound Care. 2017;30(11):494-501. doi: 10.1097/01.ASW.0000525627.54569.da.
12. Voegeli D. Incontinence-associated dermatitis: new insights into an old problem. Br J Nurs. 2016;25(5):256-62.
13. Dowsett C, Groemann NM, Harding K. Taking wound assessment beyond the edge. Wounds Int. 2015;6(1):19-23.

The views and opinions expressed in this blog are solely those of the author, and do not represent the views of WoundSource, Kestrel Health Information, Inc., its affiliates, or subsidiary companies.

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