DEPARTMENTS: LETTERS TO THE EDITOR
It was with great interest that we read Dr Levine’s commentary1 published in the March 2019 issue of Advances in Skin & Wound Care reflecting on the pressure injury (PI) classification system published by Shea2 in 1975. It is indeed very important to know the historical background to better understand our current PI definitions, classifications, debates, and future developments.3–6 It is also important to report Shea’s historical classification as accurately as possible to capture its intended meaning.
Shea described the grade I pressure sore as involving “an acute inflammatory response involving all soft tissue layers…. The dilatation of blood vessels and accumulating edema fluid secondary to ischemia cause a thickening and distortion of all tissue layers between the surface and the underlying bone.”2 From this, Shea did not consider a grade I to involve only “…superficial soft tissue layers….”1 It is true that he did describe observable cutaneous clinical signs such as induration and erythema, but he clearly regarded all soft tissues as being affected. Similarly, he described a grade II pressure sore as a more-advanced stage of inflammation and damage involving all layers but with the visible skin defect limited to the epidermis and dermis. Shea’s proposed “closed pressure sore” aligns with his comments that all tissue layers are involved in each manifestation of PI. Although the clinical appearance of a closed pressure sore differs from other grades, Shea commented that it is “…caused by the same pathologic process.”2 In other words, he never regarded PIs as simply a top-down process from the skin surface later reaching deeper layers.
Why is it important to be aware of this detail? Later classifications such as those introduced by the International Association for Enterostomal Therapy7 or by the National Pressure Ulcer Advisory Panel8 defined grade/stage I and II PIs as affecting only the epidermis and/or dermis. This has helped contribute to the incorrect idea of the top-down pathogenesis of PIs that was widely accepted for many years. This assumption has since been challenged,9–11 but in fact, the currently accepted “bottom-up” development was never a new idea. As early as 1942, Groth12 demonstrated in his doctoral thesis that PIs start in the deeper soft tissues under intact skin.
There are many other differences between Shea2 and more recent PI classifications. For instance, the concept of full-thickness skin loss is often related to damage within subcutaneous fat, muscle, or tendon rather than being limited to the layers of the epidermis and dermis as suggested by Shea.5 This example demonstrates that the careful study of historical evidence is critical to avoid possible detours. A major challenge in previous and current PI classification is that diagnoses are made based on the clinical signs of visible tissue involvement within the injury. Tissue damage deeper in the tissues, often invisible to the clinician, cannot be evaluated and is therefore ignored during decision-making. As long as alternative imaging or other measurement techniques are not routinely used to assist PI classification, this challenge will remain for those in clinical practice.
1. Levine JM. Historical perspective on pressure injury classification: the legacy of J. Darrell Shea. Adv Skin Wound Care 2019;32(3):103–6.
2. Shea JD. Pressure sores: classification and management. Clin Orthop Relat Res 1975(112):89–100.
3. Kottner J, Sigaudo-Roussel D, Cuddigan J. From bed sores to skin failure: linguistic and conceptual confusion in the field of skin and tissue integrity. Int J Nurs Stud 2019;92:58–9.
4. Ayello EA, Levine JM, Langemo D, Kennedy-Evans KL, Brennan MR, Gary Sibbald R. Reexamining the literature on terminal ulcers, SCALE, skin failure, and unavoidable pressure injuries. Adv Skin Wound Care 2019;32(3):109–21.
5. Edsberg LE, Black JM, Goldberg M, McNichol L, Moore L, Sieggreen M. Revised National Pressure Ulcer Advisory Panel pressure injury staging system: revised pressure injury staging system. J Wound Ostomy Continence Nurs 2016;43(6):585–97.
6. Bader D, Schoonhoven L. What's in a name? J Tissue Viability 2016;25(4):191–2.
7. Dermal wounds: pressure sores. Philosophy of the IAET. J Enterostomal Ther 1988;15(1):4–17.
8. Pressure ulcers prevalence, cost and risk assessment: consensus development conference statement—The National Pressure Ulcer Advisory Panel. Decubitus. 1989;2(2):24–8.
9. Berlowitz DR, Brienza DM. Are all pressure ulcers the result of deep tissue injury? A review of the literature. Ostomy Wound Manage 2007;53(10):34–8.
10. Kottner J, Balzer K, Dassen T, Heinze S. Pressure ulcers: a critical review of definitions and classifications. Ostomy Wound Manage 2009;55(9):22–9.
11. Sibbald RG, Krasner DL, Woo KY. Pressure ulcer staging revisited: superficial skin changes & Deep Pressure Ulcer Framework©. Adv Skin Wound Care 2011;24(12):571–80.
12. Groth KE. Klinische Beobachtungen und experimentelle Studien über die Entstehung des Decubitus. Uppsala: Almqvist&Wiksell; 1942.
Thank you for reading my article. The topic of PI staging is one that incites passion in practitioners and wound scientists. I wholeheartedly agree with your observation that Shea might have indeed considered deeper injury in PI pathogenesis and that “bottom-up” genesis is not a new idea. Unfortunately, subsequent classification definitions relied specifically upon visual depth, as you stated. I appreciate the citation of Groth’s doctoral thesis and would love to see a copy in English if available.
—Jeffrey M. Levine, MD, AGSF, CMD
Icahn School of Medicine at Mount Sinai
New York, New York