In the November 2015 issue of Advances in Skin & Wound Care, an excellent article by Delmore et al1 was published: “Differentiating a Pressure Ulcer from Acute Skin Failure in the Adult Critical Care Patient.” Several important, plausible statements were made in the article, such as the following:
- Experts agree that the occurrence of a pressure ulcer (PrU) differs from an ulcer due to acute skin failure (ASF).
- Thus, it is plausible in the critical care population that many of the ulcers that develop are often classified as PrUs but could represent manifestations of ASF. However, lack of diagnostic criteria to define ASF impedes this conclusion.
- It is plausible that some clinical situations that result in an unavoidable PrU may be better categorized as ASF because of the pathophysiologic changes inherent in ulcer development.
I essentially agree with the statements above by Delmore et al.1 Over the years, the wound care community’s interprofessional teams, including nurses, physicians, physician assistants, physical and occupational therapists, registered dietitians, and pharmacists, have attempted to get their arms around the definition and etiology of ASF as it relates to PrUs. Such examples include SCALE (Skin Changes at Life’s End)2 and Kennedy Terminal Ulcer.3,4 I believe our use of the term “skin failure” should be able to document that the skin as a generalized organ is actually failing, and we are convinced that we are not dealing with a PrU. Oftentimes, clinicians may diagnose a skin breakdown in the patient with critical end-stage disease as a result of ASF, yet there is rarely any other sign of skin failure other than over a bony prominence. Pressure ulcers have been defined more clearly and staged by the National Pressure Ulcer Advisory Panel.5
Acute skin failure in the dermatological literature differs from that discussed in the wound care literature. Two common dermatological definitions are (a) “Interference with skin function as a result of damage or loss of large areas of skin resulting in loss of barrier function, hemodynamic problems, impaired thermal regulation, and metabolic, endocrine, and hemodynamic changes”6; and (b) “skin failure” is a loss of normal temperature control with inability to maintain the core temperature and failure to prevent loss of fluids, electrolytes, and protein, with resulting imbalance and failure of the mechanical barrier to penetration of foreign materials.”7 Examples of ASF in the dermatological literature include Stevens-Johnson syndrome, necrotizing fasciitis, toxic epidermal necrolysis, graft-versus-host disease, pemphigus, and epidermolysis bullosa. These types of ASFs demonstrate actual failure of the skin, which appears randomly over the body, indicating that the skin as an organ is truly failing. There is no relationship to pressure or bony prominences.
A wound management definition of ASF was given by Langemo and Brown8 in 2006. They stated, “Acute skin failure is an event in which skin and underlying tissue die because of hypoperfusion concurrent with a critical illness.” This definition only addresses hypoperfusion as a cause of skin failure. My objection to this definition is that, clinically, it is extremely rare to see skin fail with breakdown from hypoperfusion alone. In 2012, in another wound management article by White-Chu and Langemo,9 “Skin Failure: Identifying and Managing an Underrecognized Condition,” the authors state that “Pressure ulcers and skin failure are not the same. Skin failure occurs without the presence of pressure and/or shear.” This is a very important point! The authors do note that a PrU can occur over an area of skin failure; however, I would suspect this would be rare, especially having a single area of ASF over a bony prominence without other signs of skin failure elsewhere on the body.
I believe there is general agreement that when a patient develops multisystem organ failure and hypoperfusion, the skin becomes extremely susceptible to PrUs. In most of these cases, if a patient does develop a skin breakdown, it is typically over a bony prominence, including a Kennedy Terminal Ulcer, which may actually be a PrU. Seeing other areas of skin breakdown, as one sees in true skin failure, is rare in my clinical experience. If the skin as an organ is actually failing, we would expect to see various areas of “skin failure” on the body and not just over bony prominences. As a result, accurately defining skin failure is critical from a diagnostic, quality, and legal point of view, as well as how it relates to avoidable and unavoidable PrUs.
The conclusion of Delmore et al’s1 article includes the statement, “Although the concept of the unavoidable PrU is gaining wider acceptance with improved understanding of the events that contribute to these ulcers emerging, the concept of ASF remains an enigma.” By agreeing upon a coherent definition, we will make significant progress.
In summary, I believe the time has come for the wound care, dermatological, and clinical community to create a uniform definition and diagnostic criteria for “skin failure” that will bring clarity to this difficult condition.
1. Delmore B, Cox J, Rolnitzky L, Chu A, Stolfi A. Differentiating a pressure ulcer from acute skin failure in the adult critical care patient. Adv Skin Wound Care 2015; 28: 514–24.
2. Sibbald RG, Krasner DL, Lutz J. SCALE: Skin Changes at Life’s End: final consensus statement: October 1, 2009. Adv Skin Wound Care 2010; 23: 225–36.
3. Kennedy KL. The prevalence of pressure ulcers in an intermediate care facility. Decubitus 1989; 2(2): 44–5.
4. Yastrub DJ. Pressure or pathology: distinguishing pressure ulcers from the Kennedy terminal ulcer. J Wound Ostomy Continence Nurs 2010; 37: 249–50.
6. Isaac F. Acute Skin Failure. Gulf Journal Of Dermatology 2004; 11(2): 14–5.
7. Irvine C. Skin failure—a real entity: discussion paper. J R Soc Med 1991; 84: 412–3.
8. Langemo DK, Brown G. Skin fails too: acute, chronic and end-stage skin failure. Adv Skin Wound Care 2006; 19: 206–11.
9. White-Chu EF, Langemo D. Skin failure: identifying and managing an underrecognized condition. Ann Long Term Care 2012; 20(7): 28–32.