This author shares a story of a pressure ulcer that occurred during an unrelated surgery and theorizes that some pressure ulcers are due to angiosomal ischemia and not localized pressure.
You can’t get the right prevention in place if you have the wrong pathophysiology. An experience with my son’s lower extremity pressure injury had me question whether some pressure injuries are not actually due to localized pressure.
In August of 2017, Hurricane Harvey dumped 52 inches of rain on Houston, turning the fourth largest city in America into a literal island. However, with our house above water, I was selfishly focused on something else. My 22-year-old son had long been scheduled for major maxillofacial surgery to correct a congenital jaw problem, and to my surprise, the hospital called to say his case was still on. I wasn’t too worried because, except for the jaw issue, he’s a completely healthy young man on no medications. That morning we managed to get to the hospital (no easy feat), he walked into the pre-op area and his 5-hour surgery started a couple of hours later.
To keep my mind occupied during his surgery, I spent the time writing up the case of a stage 4 buttock pressure ulcer that had developed in the ICU a few months earlier. The evidence was overwhelming that it was a vascular event; specifically, an infarction of the angiosomes that supplied the buttock cheeks. Angiosomes are three-dimensional blocks of tissue, supplied by a named vessel, that typically traverse from the bone to the skin. Plastic surgeons use “maps” of angiosomes to plan flaps for reconstruction, so I was studying the angiosomal maps in the plastic surgical literature while I waited for my son to get out of surgery.
After 5 hours, they brought him to his room with his jaw wired shut, which naturally prevented him from talking. In recovery, he’d been handed a clipboard so he could communicate. He showed me the note he wrote in answer to the question, “Are you hurting anywhere?” It read, “My heel hurts. What did they do to my heel?”
There were foam dressings over his heels, which have become the standard to prevent “pressure injuries.” I had to remove the foam pad over the left heel to inspect it. Under the foam dressing, there was a triangular area of non-blanching erythema on the lateral heel. I started checking the skin on the rest of his body and found a round area of non-blanching erythema over the right lateral malleolus, except unlike the left lateral heel, the right malleolar area was painless (see Figure 1).
When the surgeon arrived, I said, “You had to turn him from side to side during the procedure, didn’t you?” The surgeon almost laughed. “No, for this surgery, it’s imperative that the patient remain supine the entire time. It’s really important that they not move at all.”
I showed the surgeon the pressure injuries on his lateral heel and ankle. “That’s a mystery,” he said. “There were wedges under the back of his ankles, and he was never turned to either side.”
After getting my son settled, I sat down to think. What mechanism could be responsible for pressure ulcers on the left lateral heel and right lateral ankle in a healthy patient who was confirmed to have remained supine for a 5-hour operation, and who had walked into the hospital immediately prior to surgery? I’d been writing up that case of the buttock infarction so a textbook illustration of the angiosome map was open on my computer.
There was the answer, as plain as the nose on my face.
How Angiosomes Factor Into Pressure Injuries
For 30 years I have been trying to explain “stage 1 pressure ulcers” to myself. It wasn’t what we called them that troubled me—I could not figure out what they were. According the available literature, among patients with an intact nervous system, the majority of stage 1 pressure injuries are painful, and furthermore the pain is neuropathic in character.1 Neuropathic pain simply can’t be explained by local “outside to inside” pressure.
Although my son had just undergone a massive maxillofacial operation, it was the excruciating pain in his lateral heel for which he needed morphine. The pain, which had to be coming from the sural nerve, persisted for weeks event though visible changes to the skin resolved in 3 or 4 days. Furthermore, the pattern of erythema was a perfect triangle. There is only one thing that could cause persistent neuropraxia and an area of discoloration with straight borders, and that is something that impacts a vascular territory. The calcaneal branch of the posterior tibial artery emerges laterally between the Achilles and the peroneal tendons. It is easy to understand how the vessel could be compressed within the Achilles.
We are all aware of angiosomes thanks to the work of Attinger, whose cadaveric studies have revealed these vascular patterns in the extremity.2 The skin blood supply is divided into anatomical vascular territories defined by the perimeter of the choke arteries, which arise from the source vessel. On the extremity angiosomes appear as “sectors,” (as they do in the photo of my son) but may follow a neurological dermatome on the torso. Figure 2 is a picture of a stage 1 pressure injury on the buttock that follows a dermatomal pattern.
My son had developed an ischemia reperfusion injury to his left lateral heel because the flow to an angiosome had been occluded temporarily, enough to injure the nerve and cause a reactive hyperemia of the area supplied by the vessel. On the left, the affected vessel had to be the lateral calcaneal artery. On the right side, it was the lateral malleolar artery that was affected, because that supplies an annular area right over the lateral malleolus.
With my son’s permission, I reviewed his anesthesia records. It’s typical to keep patients somewhat hypotensive to limit bleeding during facial surgery, but I wondered if his mean arterial pressure had dropped a bit too low. Records showed his vitals were reasonable and amazingly stable throughout the surgery. His hemoglobin was normal postoperatively. There was nothing in his records that would explain the pressure ulcers on his lateral heel and ankle.
What a Study Revealed About Pressure Injuries
Eight months after the operation, we went to visit Efthymios Gkotsoulias, DPM, and tried a little experiment with his very good arterial Doppler and a few colored pens.
We recreated the conditions of the operating room with wedges at his Achilles and reported our findings in Advances in Wound Care in an article we called, “On the Origin of Intraoperative Pressure Injury: An Angiosomal Theory of Pressure Injury Formation.”3
We used the Doppler to locate the exact position of the lateral calcaneal and lateral malleolar arteries and marked the anatomy on the lower legs with colored markers.3 Then we simulated his supine positioning in the operating room, placing a wedge at the back of the calf in the Achilles area. In this position, the feet naturally abduct laterally, which places the wedge at the posterior calf exactly at the juncture of the lateral calcaneal and/or the lateral malleolar arteries.
While we can’t prove that the positioning of the wedge is the culprit in the genesis of his pressure ulcers, it is the only explanation that makes logical sense given that direct pressure over the area couldn’t have occurred. We therefore postulate a vascular mechanism of pressure injury development.3
And now I finally agree with the term “pressure injury.” There’s no doubt that these stage 1 pressure events really were “injuries” because they were ischemia reperfusion (IR) injuries. These stage 1 pressure injuries most likely resulted from the occlusion of either the arterial outflow or the venous return of angiosomes. An IR injury is also the best explanation for the neuropathic pain that persisted for weeks on the left lateral heel.
This case suggests that at least some heel pressure injuries are not the result of localized pressure but rather angiosomal ischemia. We base our theory on the fact that the anatomical pattern of stage 1 pressure “injuries” frequently follow the distribution of a named vessel. We hypothesize that in this case, intraoperative positioning combined with mild permissive hypotension may have occluded blood flow to the relevant angiosomes, causing an ischemia reperfusion injury to the downstream tissues.
What This All Means
This little observation has big implications:
• If we are right about the mechanism, then not all pressure ulcers are due to local pressure.
• Foam pads on the heel cannot prevent an ischemia reperfusion injury caused by compression of vessels several centimeters away from the heel. Pads might prevent skin breakdown due to moisture or friction, but not IR injury.
• My hospital spends $500,000 per year on foam pads to prevent heel and buttock pressure ulcers. The hospital system spends nearly $5 million dollars a year on foam pads.
• We need to think of positioning through a new lens, which is the anatomical vascular supply to the angiosome of an at-risk area.
Caroline E. Fife is Chief Medical Officer at Intellicure Inc., The Woodlands, TX; executive director of the U.S. Wound Registry; medical director of St. Luke’s Wound Clinic, The Woodlands; and co-chair of the Alliance of Wound Care Stakeholders.
This article originally appeared at https://carolinefifemd.com/2019/08/21/yes-it-is-a-pressure-injury-an-ischemia-reperfusion-injury/.
1. Briggs M, Collinson M, Wilson L, et al. The prevalence of pain at pressure areas and pressure ulcers in hospitalised patients. BMC Nursing. 2013; 12(1):19.
2. Attinger CE, Evans KK, Bulan E, et al. Angiosomes of the foot and ankle and clinical implications for limb salvage: reconstruction, incisions and revascularization. Plast Reconstr Surg. 2006; 117(7 Suppl):261S-293S.
3. Fife CE, Gkotsoulias E. On the origin of intraoperative pressure injury: an angiosomal theory of pressure injury. Adv Wound Care. 2019; epub July 3.