Abstract and Introduction
Abstract
Background. The evaluation and treatment of heel pressure injuries are a significant and expensive sequela of the aging population. Although the workup of patients with lower extremity tissue loss usually involves an assessment of the arterial blood flow by means of noninvasive vascular testing, the results may be misleading in patients with heel pressure injuries when the ankle-brachial index (ABI) does not provide direct information about perfusion of the rearfoot. The objective of this retrospective, observational investigation was to determine if noninvasive vascular testing provides accurate and reliable results in patients with heel pressure injuries.
Materials and Methods. A retrospective chart review of 67 consecutive inpatients with 75 heel decubitus ulcerations was performed.
Results. At least 1 noncompressible ankle artery was observed in 35 (46.67%) of the 75 feet. When at least 1 compressible vessel was present, allowing for calculation of an ABI (n = 49 feet), it was based on the posterior tibial artery in 23 (46.94%) feet and on the anterior tibial artery in 26 (53.06%) feet. In total, of the 75 feet with heel pressure injuries that underwent noninvasive vascular testing, a compressible posterior tibial artery allowing for calculation of an ABI as a direct measure of heel perfusion was observed in only 23 (30.67%) feet.
Conclusions. The results of this study suggest noninvasive vascular testing may be inaccurate and unreliable in the majority of patients with heel pressure injuries.
Introduction
The evaluation and treatment of pressure injuries are a significant and expensive sequela of the aging population.[1–6] Specific to the lower extremity, this is particularly true in people who are nonambulatory, those who are bedridden for any period of time, and in the presence of certain comorbidities including diabetes mellitus and peripheral arterial disease.[7–11] Part of the initial clinical workup of any patient with lower extremity tissue loss usually involves an assessment of the arterial blood flow by means of noninvasive vascular testing (ankle-brachial index [ABI] and pulse volume recording).[12–15] Although these are primarily screening tests for peripheral arterial disease, abnormalities should prompt a formal vascular evaluation, potentially including angiography.
Unfortunately, however, such screening tests may be misleading in patients with heel pressure injuries when the ABI does not provide direct information about perfusion of the rearfoot. By convention, the ABI represents a mathematical ratio with the systolic pressure in the brachial artery as the denominator and the systolic pressure of an ankle artery as the numerator (the higher value of the anterior tibial artery [ATA] or posterior tibial artery [PTA] is used).[13–15] Figure 1A demonstrates a patient with single-vessel arterial runoff through the ATA without any direct or indirect inflow to the heel. It is likely the ABI would be calculated based on the ATA in this situation, and it might even appear normal, even though the heel is ischemic. This concept may be best described by the so-called "orphan heel syndrome," in which the only arterial inflow to the foot is via the ATA, essentially leaving the plantar rearfoot in an ischemic zone.[16]
Figure 1.
Three angiograms demonstrate situations involving heel tissue loss in which noninvasive vascular testing and the ankle-brachial index (ABI) may be misleading. (A) A patient with only anterior tibial artery runoff into the foot without any direct or indirect perfusion of the heel. Because the ABI ratio is conventionally calculated using the higher of the anterior tibial or posterior tibial artery values, it is possible a normal pressure and ratio could be calculated based on the anterior tibial artery, even though there is no perfusion to the heel; (B) a patient with antegrade flow through the anterior tibial and peroneal arteries. The primary flow to the heel is likely via the peroneal artery, which is not generally measured with ABI; and (C) a patient with only peroneal artery single-vessel runoff, which would not likely be measured with the ABI.
Vascularization to the heel is possible through the dorsalis pedis artery, but only indirectly via collateralization and the vascular arch in the proximal first intermetatarsal space.[17–19] Recent investigations[20–23] lend some support to direct revascularization of lower extremity tissue loss, indicating that the healing potential of heel ulcerations may be better assessed with measurement of pressure of the PTA as opposed to the ATA.
Further, Attinger et al[24] have described the arterial supply to the heel, with the angiosome theory as a redundant dual inflow via the posterior tibial and peroneal arteries. Measurement of the peroneal artery is not included in calculation of the ABI, although the peroneal artery is the infrapopliteal vessel most likely to be spared of chronic obstructive atherosclerotic disease.[25,26] Figure 1B demonstrates a clinical situation in which the primary arterial flow to the heel is likely through the peroneal artery, but where the ABI would conventionally be calculated based on the ATA. Figure 1C represents a patient with only single-vessel runoff through the peroneal artery. It is unclear what information, if any, the ABI would provide in this situation given the lack of measurement of the peroneal artery pressure in the formula.
Finally, a high percentage of patients with diabetes have peripheral arterial calcification, which may contribute to false elevation of ABI pressure measurements and interpretation.[27–29] The presence of medial arterial calcific sclerosis leads to vessel incompressibility and renders the results of noninvasive testing inaccurate and unquantifiable.
In lieu of these potential complicating factors, this work investigates the accuracy of the ABI with respect to heel pressure injuries. The specific objective of this retrospective, observational investigation was to determine if noninvasive vascular testing provides accurate and reliable results in patients with heel pressure injuries.
Wounds. 2017;29(2):51-55. © 2017 HMP Communications, LLC