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angiosome, deep-tissue injury, pressure injury, pressure ulcer, vascular occlusion, wound care



  1. Yap, Tracey L. PhD, RN, WCC, CNE, FGSA, FAAN
  2. Alderden, Jenny PhD, APRN, CCRN, CCNS
  3. Lewis, MaryAnne BSN, RN, CWOCN
  4. Taylor, Kristen MSN, RN, CCRN-K
  5. Fife, Caroline E. MD


ABSTRACT: Compression of the soft tissue between a support surface and a bony prominence has long been the accepted primary mechanism of pressure injury (PrI) formation, with the belief that said compression leads to capillary occlusion, ischemia, and tissue necrosis. This explanation presupposes an "outside-in" pathophysiologic process of tissue damage originating at the local capillary level. Despite advances in prevention protocols, there remains a stubbornly consistent incidence of severe PrIs including deep-tissue injuries, the latter usually evolving into stage 4 PrIs with exposed bone or tendon. This article presents just such a perioperative case with the aim of providing further evidence that these more severe PrIs may result from ischemic insults of a named vessel within specific vascular territories (labeled as angiosomes). Pressure is indeed a factor in the formation of severe PrIs, but these authors postulate that the occlusion occurred at the level of a named artery proximal to the lesion. This vascular event was likely attributable to low mean arterial pressure. The authors suggest that the terminology proposed three decades ago to call both deep-tissue injuries and stage 4 PrIs "vascular occlusion pressure injuries" should be the topic of further research and expert consensus.