After a consensus process with interactive discussion and voting, the National Pressure Ulcer Advisory Panel (NPUAP) announced the term pressure injury should replace pressure ulcer to “more accurately describe pressure injuries to both intact and ulcerated skin.”1 The rationale for the change is to clarify the distinction between “Stage 1 and Deep Tissue Injury as both described injured intact skin while other stages described open ulcers.”1 The consensus also included using Arabic as opposed to Roman numerals for staging.
As a participant of the NPUAP Consensus Conference, I am not certain the differences between Stage 1 and deep tissue injury have been clarified. As newly defined, Stage 1 pressure injury still focuses on skin changes, while deep tissue injury notes skin changes but acknowledges a likely change below the skin level that may manifest in deterioration of the deeper tissues. Pressure at the bone muscle interface is identified as a discriminating factor. A deep tissue injury could resolve without tissue loss or it could reveal tissue death of the deeper structures, resulting in a wound or “ulcer”. If the deep tissue injury resolved, would it be different from a Stage 1 ulcer where skin changes were observed? If partial-thickness skin loss was observed, would Stage 2 be different from the deep tissue injury in terms of how it developed or the forces applied to the injured area?
Does pressure injury start at the top (ie, the skin) and work down through tissues, or does it work from the bottom up? Although it may seem injury from pressure starts at the skin and progressively involves deeper tissues or starts deep with the muscle at the bone interface and works its way to involve the skin by loss of supporting structure, the proposed mechanism has not been clearly articulated. Some literature supports a bottom-up mechanism.2 Does that translate into a mechanism by which the muscle is impaired and damaged by pressure effects and that the other tissues also will show the effects of the pressure? Based on the tissues’ tolerance for pressure, will cellular death and tissue loss occur? Promising research3 in pressure injury identification looks at changes in subcutaneous tissues that may herald or predict ulcer development; for example, subepidermal moisture measured by impedance predicted erythema and Stage 1 pressure ulcer development. Does this finding indicate a top-down mechanism that can be halted once pressure is identified and relieved? Sharp and McLaws4 note current staging in Australia uses a top-down model similar to what is proposed in the NPUAP consensus statement. However, these authors acknowledge it is not well understood or used and they instead proposed an ischemia reperfusion injury or middle model.
As a practitioner reading through the literature, I appreciate that information on the mechanism and factors by which a pressure injury develops seems to be evolving. The importance of updating the concept of injury can’t be overlooked. The mechanism by which the pressure injury occurs will directly influence how it is treated and equally important, prevented. Both treatment and prevention will be assessed as to effectiveness or appropriateness in the manner by which the proposed therapy impacts on that mechanism.
Staging also becomes important in terms of patient care given the extent of injury and the tissues involved. With the current top-down staging system, injuries categorized as Stage 1 or Stage 2 may be undertreated or protected. When approval of therapy choices is stratified based on the visual assessment, the deeper structure that has been compromised could be missed. As an example, I consulted on a gentleman that had undergone a left hip disarticulation and developed a Stage 4 pressure ulcer over his right ishcial tuberosity. Because bone was exposed, an MRI was performed to assess for the presence of osteomyelitis. I was consulted because an abscess was diagnosed over the right lower sacrum. The patient had what was initially categorized as a Stage 2 pressure ulcer but with deeper tissue involvement. Ultrasound demonstrated deep tissue damage and inflammation of the fat and muscle with fluctuance,5 characteristics consistent with deeper tissue injury. This patient’s injury showed how the same pressure injury/episode in relatively the same area can evolve differently in terms of what could be seen with the naked eye using the current staging system. In the case of the Stage 4 ulcer, depth of tissue injury was accurately assessed and treated, but the Stage 2 lesion was more than superficial loss of epithelium and perhaps some dermis. The second injury was every bit as involved in terms of underlying structures as the Stage 4 with one exception: the skin was still intact over the deep tissue damage. The defect could be seen on the ultrasound images and tissue loss down to the bonecould be demonstrated.
Can patient care be improved with a different way to look at categorizing pressure injury, given there is more to assess than what the top-down staging system would suggest? This is something to consider when you are evaluating your next patient.