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[horizontal ellipsis]. 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 "[horizontal ellipsis]superficial soft tissue layers[horizontal ellipsis]."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 "[horizontal ellipsis]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.

References