More Evidence for Angiosomal Ischemia in This Report
It’s finally out! The follow-up to the paper published previously about the angiosome theory of pressure injury! Pass this around freely because it was published Open Source.
It has never made sense that external compression of capillaries could infarct a large muscle. It’s also puzzled me that severe pressure ulcers nearly always follow the anatomical distribution of vascular “angiosomes,” three-dimensional blocks of tissue supplied by a named artery and vein.
Since the risk factors for severe pressure injuries are mostly hemodynamic in nature, it stands to reason that the key to their formation lies in the vasculature. This patient had the infarction of the fleshy part of the buttocks after several hours of hypotension following coronary artery surgery. I know you have seen similar events, yet the fleshy part of the buttocks do not lie over a bony surface, so how could it happen?
Since his sternum was also breaking down, we made the unusual decision to surgically debride the area before it finished demarcating, in order to apply NPWT and thus reduce wound colonization. Intraoperatively it was obvious that the muscle had infarcted, and there were hematomas on either side of the sacrum, some distance from the visible skin damage, along the distribution of the vessels that supply the buttocks. The obvious conclusion is that the arteries supplying the buttock had thrombosed.
If you haven’t taken gross anatomy, this may not make sense. However, the vessels that supply the buttock come from the abdominal aorta and to get to the backside of the body, they have to pass through the pelvis, exiting the gluteal muscles via some really tight junctions. Some of these vessels are called “perforators,” because they have to pass through the muscle fascia. The weight of a heavy body on those muscles and the vessels that perforate them could result in occlusion of either the arterial or the venous supply to the tissue block. It’s very possible the problem that causes these is occlusion on the venous side, as this is a low pressure zone. It would explain why a low albumin is a powerful risk factor for deep tissue injury. It would also account for why the injuries are so “messy” – not the pale ischemia of an arterial infarction, but the very messy tissue damage caused by engorgement of a vein with subsequent arterial inflow obstruction.
At last, I feel I finally have an explanation for the death of muscles in a predictable pattern in severe DTIs/Stage 4. I think this also explains “stage 1” pressure injuries, which are ischemia reperfusion injuries. I talk about this in a previous case report. The backstory is that I was working on the write-up for the buttock infarction to keep myself busy while waiting for my son to come out of surgery. I had the angiosome “map” open on my computer when my son was brought to his room with several stage 1 pressure injuries. His left lateral foot and right lateral ankle pressure injuries were on areas that had never experienced pressure in the operating room. The only explanation is that they were caused by the wedge at the back of the leg occluding arterial supply to the lateral heel and ankle. That’s when it hit me that both stage 1 and DTIs/Stage 4 lesions were ischemic events – with stage 1 being recoverable ischemia reperfusion events (without tissue necrosis) and DTI/Stage 4 being unrecoverable vascular events.
This idea is not new. More than three decades ago, visionary clinician Roberta Abruzzese suggested that severe decubitus ulcers (the term used at the time) be termed “vascular occlusion ulcers.” She saw the obvious.
I will be posting more about this concept and its implications.