TO THE EDITOR:

I read with great interest the View From Here article, "Incontinence-Associated Dermatitis; Progress, Promises, and Ongoing Challenges," by Mikel Gray, Laurie McNichol, and Denise Nix in the March/April 2016 edition of JWOCN, pp. 188-192. I thoroughly enjoyed the excellent historical review, the detailed current understanding of incontinence-associated dermatitis (IAD) pathology, as well as the challenges of building the evidence for the concept of IAD.

The purpose of my letter is to commend you for this excellent article and to reply to the Implications for Research section in the article. As stated in the section, "Perhaps the most important question is the need to increase our knowledge and skills in the differentiation of IAD and pressure ulcers" (p. 191). I feel that another piece of the puzzle is being overlooked, especially concerning etiology of skin injury pathology on the lower posterior torso and thighs. Specifically, the recognition of friction (sliding) as another possible etiology of skin injury, distinct from pressure and moisture, should be considered.

I know the concept of friction injury is very new, with little scientific publication.1 Most of us remember when deep-tissue injury and moisture-associated skin damage (MASD) were relatively unknown. As the evidence increases related to various etiologies of skin/tissue damage (medical adhesive-related skin injury, skin tears, MASD, IAD, infectious, vascular and neuropathic-related skin/tissue damage), we need to advocate for our patients so that the correct diagnosis(es) can be identified and the most effective treatments can be implemented.

An accurate physical assessment and patient history, including moisture exposure, activity, and mobility, are critical to begin the differential diagnosis of these particular wound types (pressure, moisture, friction).

I offer the following comments to succinctly assist with this differential diagnosis:

* The current theory of the etiology of pressure ulcer development is ischemia caused by tissue load (pressure) and internal tissue deformation (shear force). The understanding is that muscle is much more susceptible to ischemia than skin, so damage is deeper first.2 In a nutshell, think of "bottom-up damage" (my emphasis). Development of a pressure ulcer/injury is very much related to immobility.

* Moisture alone does not "cause" measurable open wounds or ulcers. Otherwise, we would not be able to spend a day at the beach or pool, or soak in the tub for an hour. Simply put, moisture contributes to erosion by altering the "brick and mortar" makeup of the skin layers. If the source of moisture is something other than water or physiologic serum (eg, feces, urine, wound drainage), those chemicals/irritants add to the erosive power of the trapped moisture, cause inflammation, and could lead to an infectious process. Chronic moisture exposure (and inflammation) places affected skin and underlying tissues at risk for damage from pressure and friction forces that can lead to ulceration. Moisture damage most often occurs first in the perineal skinfolds/creases (or deep skinfolds, surrounding wounds, fistula, or ostomies) exposed to urine/feces.3

* The current theory of etiology of friction injury is the "slip and stick principle." Friction and sliding are not the same; they are opposite. Friction force is the "brakes" to sliding. It is the force that stops the sliding, and it peaks just before the slide begins; this is the point of greatest damage to the skin and soft tissues below. The force is abrasive. Think of this as "top-down damage." Damage can extend into full-thickness ulcerations with acute or chronic sliding forces (especially if moisture and/or inflammation are involved, but do not have to be present), and often these full-thickness ulcers/wounds "appear to look like" pressure ulcer/injuries, especially in places that we have attributed to pressure ulcer/injury formation in the past (eg, bilateral gluteal and posterior thigh areas). Friction injury damage is very much related to impaired mobility (different than immobility). Friction injury can occur acutely and typically present as blisters or erythematous, rough and/or moist, abraded patches; patients can be admitted with chronic friction injury that are often diagnosed as pressure ulcer/injuries when they are located on the gluteal or posterior thigh areas (not directly over bony prominences).4

I thank you very much for the opportunity to expand on the possible etiologies of skin/tissue damage, especially in the posterior lower torso, buttocks, and thigh regions. I encourage our colleagues to continue to develop the etiologic concepts of skin vulnerability in these areas to aid with differential diagnosis.

Sincerely,

Christine T. Berke, MSN APRN-NP,

CWOCN-AP, AGPCNP-BC

Nebraska Medicine

Omaha

[email protected]

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