Our contemporary understanding of the aetiology of pressure ulcers/pressure injuries

Abstract

In 2019, the third and updated edition of the Clinical Practice Guideline (CPG) on Prevention and Treatment of Pressure Ulcers/Injuries has been published. In addition to this most up-to-date evidence-based guidance for clinicians, related topics such as pressure ulcers (PUs)/pressure injuries (PIs) aetiology, classification, and future research needs were considered by the teams of experts. To elaborate on these topics, this is the third paper of a series of the CPG articles, which summarises the latest understanding of the aetiology of PUs/PIs with a special focus on the effects of soft tissue deformation. Sustained deformations of soft tissues cause initial cell death and tissue damage that ultimately may result in the formation of PUs/PIs. High tissue deformations result in cell damage on a microscopic level within just a few minutes, although it may take hours of sustained loading for the damage to become clinically visible. Superficial skin damage seems to be primarily caused by excessive shear strain/stress exposures, deeper PUs/PIs predominantly result from high pressures in combination with shear at the surface over bony prominences, or under stiff medical devices. Therefore, primary PU/PI prevention should aim for minimising deformations by either reducing the peak strain/stress values in tissues or decreasing the exposure time.

Keywords: aetiology; pressure injury; pressure ulcer; risk.

FIGURE 1

A, A schematic description of the vicious cycle of cell and tissue damage in pressure ulcers/injuries (PUs/PIs), resulting from sustained mechanical deformations (the triggering event), which inflicts the primary, direct deformation damage (first damage event), then leading to secondary inflammatory‐oedema related damage (second damage event), and finally to tertiary ischaemic damage (third damage event). B, Each of these three factors contributes to the cumulative cell and tissue damage, which develops in an escalated manner as a result of the added contributions of the above factors. Of note, while it is likely that the ischaemic damage follows from the inflammatory damage as visualised here, ischaemia per se may also be present prior to the onset of the PU/PI vicious cycle (eg, due to a persistent peripheral vascular disease), or develop independently from, or concurrently with the inflammation (eg, as a result of a thrombotic event in a patient with coronavirus disease 2019). In contrast, localised inflammation may follow from or intensify because of an existing ischaemic condition, especially when reperfusion is allowed (eg, immediately after repositioning). Accordingly, the process of accumulation of tissue damage over time in a forming PU/PI as described here is likely, but is not necessarily a linear one (particularly with regard to the order of the inflammatory and ischaemic damage phases)

FIGURE 2

Tolerance behaviour of soft tissues subjected to sustained mechanical loads formulated by Linder‐Ganz et al. and Gefen et al. based on experimental data from animal and tissue‐engineered models, respectively (marked “Gefen curve”), compared with the historical Reswick and Rogers pressure‐based damage threshold proposed for sitting and recumbent patients in the 1970s