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We read with interest the March 2021 case report, "Angiosomal Vascular Occlusions, Deep-Tissue Pressure Injuries, and Competing Theories: A Case Report," by Yap et al. The authors are to be congratulated on publishing an important article. We agree that anatomy, in particular angiosomes, greatly contributes to how tissue dies via various mechanisms. In this context, pressure injuries largely progress from the inside to the outside with muscular ischemia occurring prior to integument ischemia, whereas for moisture-associated skin damage and other epidermal/dermal causes of skin failure, the mechanism is reversed, starting with skin breakdown. As we pointed out in a recent publication,1 although the mechanisms are different, the resultant tissue death still occurs. Nevertheless, some caveats are in order.


Anatomy is complex, even more so when considering associated anatomic variants and pathologies. For any given area of tissue, the associated angiosome may be fed by more than one source artery, and the effective perfusion is also mediated by cutaneous perforators, both intramuscular and septal. The body possesses compensatory mechanisms that Taylor and Palmer2 and Taylor et al3 describe as collateral "choke vessels" that interconnect many adjacent angiosomes, as well as the "angiosome tree," an apt description.


We agree that kinking of the arterial vessels directly supplying the musculature is one mechanism that leads to muscle death and the most likely overt cause.3 However, in Figure 1 in their article, Yap et al describe kinking of the source vessel when it enters the angiosome. We would like to note that a "source vessel" never perforates muscle other than at the hilum. The vessels that we call perforators (perforating branches) traverse toward the muscle and skin (muscular and septal perforators). Although it is possible that an entire source vessel can kink, kinking of the various individual perforating vessels seems more common. De Bruijn et al4 show internal iliac artery aneurysm leading to buttock tissue ischemia. The size of the injured area will likely define the extent of the ischemic event.


Figure 2 in the article by Yap et al seems to depict a deep tissue injury that has progressed from muscular loss to frank skin loss and not a true deep-tissue injury as described. While depicting the end pathway progressing from arterial kinking, muscular ischemia, and ultimately integument death, it seems to show the injury later in the process. We feel that, in concept, this is why the sacrum tends to be the site of ischemic insult after shock compared with the lateral portion of the buttocks. Whether it is the actual source vessel or the perforating vessels that are being compressed is likely case dependent. The perforating vessels can be imagined (again, in Figure 2) to be on the right superior buttock. This corresponds with the superior sacral perforator.


The plantar heel is also another common area of integument failure, despite having two angiosomes supplied by different source arteries with substantial perforator crossover. Many comorbid factors, including macroarterial and microarterial disease, diabetes, chronic hypoxia/reperfusion injury, impaired nutrient supply, growth factor abnormalities, and chronic inflammation, can adversely affect angiosome perfusion. In addition, severe neuropathy itself can contribute to skin capillary shunting, with local infection a contributing factor as well.5-7


Hypotension also can be a contributing factor to the initiation of integument failure as pointed out by the authors of another case study by Fife and Gkotsoulias,8 which we were negligent in not reporting in our article.1 However, a mean arterial pressure of 60 mm Hg or below by itself is not usually the prime cause of integument death. At least a second intrinsic or extrinsic factor is required to cause progression to tissue death. In this case described by Fife and Gkotsoulias,8 there was an associated neuropraxia associated with the injury in the perfusion pattern of the peroneal angiosome of the heel.


Finally, the overlying factor that is not discussed is time. Vascular compromise and tissue death occur via known temporal ischemic times for various tissues. Deficits in nursing care can lead to eventual tissue death via different mechanisms, although not all tissue death seems to be associated with deficiencies in care. As we develop a better understanding of the underlying pathologic process, we can begin to understand the means of prevention. Further, we agree that not all tissue death of the sacrum or heels is either a pressure injury or an avoidable pressure injury. There is a pathway that leads to integument failure.


Further study is needed to better elucidate the various processes and better define the mechanisms of pressure, moisture, and terminal ulcers.


-Michael Bain, MD, MMS


-Junko Hara, PhD


Hoag Memorial Hospital Presbyterian, Newport Beach, CA


-Marissa Carter, PhD, MA


Strategic Solutions, Inc, Bozeman, MT




1. Bain M, Hara J, Carter MJ. The pathophysiology of skin failure vs. pressure injury: conditions that cause integument destruction and their associated implications. Wounds 2020;32:319-27. [Context Link]


2. Taylor GI, Palmer JH. The vascular territories (angiosomes) of the body: experimental study and clinical applications. Br J Plast Surg 1987;40:113-41. [Context Link]


3. Taylor GI, Corlett RJ, Shymal CD, Ashton MW. The anatomical (angiosome) and clinical territories of cutaneous perforating arteries: development of the concept and designing safe flaps. Plast Reconstr Surg 2011;127:1447-59. [Context Link]


4. De Bruijn MT, Verbelen T, Kralt CP, van Baal CG. An internal iliac artery aneurysm causing sudden buttock ischemia and nerve root compression. J Vasc Surg Cases 2015;1(2):151-3. [Context Link]


5. O'Neal LW. Surgical pathology of the foot and clinicopathologic correlations. In: Levin and O'Neal's The Diabetic Foot. Bowker JH, Pfeifer MA, eds. 7th ed. Philadelphia, PA: Mosby Elsevier; 2007:367-401. [Context Link]


6. Marso SP, Hiatt WR. Peripheral arterial disease in patients with diabetes. J Am Coll Cardiol 2006;47:921-9. [Context Link]


7. Jorneskog G. Why critical limb ischemia criteria are not applicable to diabetic foot and what the consequences are. Scan J Surg 2012;101:114-8. [Context Link]


8. Fife CE, Gkotsoulias E. On the origin of intraoperative pressure injury: an angiosomal theory of pressure injury formation. Adv Wound Care (New Rochelle) 2019;8:580-4. [Context Link]

In response:


We are thrilled that your comments concern the specific way the anatomy of the vasculature impacts the development of pressure injuries, rather than whether this is a valid mechanism! Thank you for your helpful explanation regarding the anatomy of the perforating vessels, which would seem to explain much about the clinical presentation of severe pressure injuries.


We agree that by the time we first encountered the patient, skin necrosis had already begun so that "deep tissue injury" was not an accurate description. We assume you agree that the skin changes commonly referred to as "deep tissue injuries" likely precede the tissue necrosis associated with severe pressure injuries, even though they may not be observed at that stage. One of the points we hoped to make with this case report was that the anatomic location of the vascular occlusion had to be proximal to, and somewhat distant from, the area of tissue necrosis on the buttock. Buttock injuries cannot be attributable to compression between a support surface and underlying bone; thus, the current "outside-in" explanation is insufficient, nor could such pressure injuries occur at the level of the capillaries.


Similarly, the only explanation for the "stage 1" heel pressure injury described by Fife and Gkotsoulias8 is a vascular occlusion proximal to the visible tissue injury. That case report suggests that (1) the skin changes called "stage 1" pressure injuries likely represent ischemia-reperfusion injuries (a new explanation for stage 1 injuries), and (2) the occlusion of a named vessel had to be the mechanism for these stage 1 pressure injuries because the left lateral heel and right lateral ankle were affected simultaneously in the absence of any local pressure to either side. The only explanation is that they were both attributable to the temporary occlusion of the supply vessels proximally. In other words, the injury was not at the capillary level and not right over the visible skin changes.


Please note that the article by Fife and Gkotsoulias8 was published in October 2019, nearly a year before your excellent article on the angiosomal mechanism of pressure injuries1 and thus could not have referenced your work. We regret that our case report was already in press when your article became available, and published in March for inclusion in the journal issue dedicated to pressure injuries; the timing prevented us from referencing your article, which is an important contribution to the discussion on mechanisms and which also would have been of great help to us.


We agree that many factors (systemic and local) determine the extent of tissue injury, particularly on the lower extremity. It is overly simplistic to diagnose all necrotic heel lesions as simply "pressure injuries" (largely considered iatrogenic and preventable) when peripheral arterial disease and diabetic neuropathy may significantly contribute to the ischemic process.


Thank you for emphasizing that not all tissue deaths on the sacrum or heels represent "avoidable" pressure injuries. We would like to emphasize that "avoidable" and "unavoidable" are regulatory terms with payment implications, whereas "unpreventable" more accurately describes lesions that cannot be averted because of overwhelming medical and/or physiologic conditions.2


We completely agree that further study is needed to understand the vascular ischemic process(es) involved in severe pressure injuries. Hopefully, this discussion will lead to a new approach to "prevention." If occlusion of either the artery or vein supplying the angiosome is the final pathway for most severe pressure injuries, then current mitigation strategies are not targeting the right processes.


We are pleased that our case report could provide a clinical demonstration of the mechanism you proposed in your 2021 article. If our article succeeds in getting more plastic surgeons and vascular experts engaged in a discussion of angiosomal anatomy as it relates to pressure injury formation, then it has served its purpose.


-Tracey L. Yap, PhD, RN, WCC, CNE, FGSA, FAAN


Jenny Alderden, PhD, APRN, CCRN, CCNS


MaryAnne Lewis, BSN, RN, CWOCN


Kristen Taylor, MSN, RN, CCRN-K


Caroline Fife, MD


Authors of "Angiosomal Vascular Occlusions, Deep-Tissue Pressure Injuries, and Competing Theories"