Accuracy of the Ankle-brachial Index in the Assessment of Arterial Perfusion of Heel Pressure Injuries

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. 

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).^13-15Figure 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

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 al²⁴ 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. 

Following approval by the institutional review board, the authors performed a retrospective chart review of consecutive inpatients with 1 heel pressure injury per extremity, except for the 9 patients with bilateral ulcerations. Initially, a search of International Classification of Diseases, Ninth Revision diagnostic codes (as this was the version the authors used at the time) was performed for inpatient consultations at a single facility over a 1-year period (January 1, 2014 to December 31, 2014). Diagnosis codes used in the search included 707.07 (decubitus ulcer heel), 707.10 (unspecified ulceration of the lower limb), 707.14 (chronic ulceration of heel or midfoot), 785.4 (unspecified gangrene), 892.0/1/2 (open wound foot), 730.07 (acute osteomyelitis of the ankle or foot), and 730.17 (chronic ulceration of the ankle or foot). The electronic medical record was subsequently reviewed for study inclusion criteria, which consisted of patients with physical examination findings consistent with pressure injuries of the heel with consultation by the foot and ankle surgery service at Temple University Hospital (Philadelphia, PA). Extracted patient information included age, gender, laterality of tissue loss, specific described location of tissue loss (posterior, posterior-medial, posterior-lateral, plantar, or undocumented), presence of diabetes, presence of end-stage renal disease, history of vascular surgery consultation, history of lower extremity surgical intervention, history of major limb amputation, and available noninvasive vascular testing results. 

The authors specifically examined the noninvasive vascular testing results for evidence of arterial calcification (defined as reporting of noncompressible ATA and/or PTA) and whether the reported ABI was calculated based on the ATA or the PTA. 

Data were stored in a password-protected personal computer for subsequent statistical analysis.  All statistical analyses were performed using Statistical Analysis Systems software, version 9.2 (SAS Institute Inc, Cary, NC). Descriptive statistics were calculated and consisted of the mean, standard deviation (SD), range, and frequency count.  

Ninety-two pressure injuries in 83 patients met inclusion criteria. Of the 83 patients, 36 (43.37%) had right-sided ulcerations, 38 (45.78%) had left-sided ulcerations, and 9 (10.84%) had bilateral lesions. The mean ± SD (range) age was 60.47 ± 15.18 years (28–90 years). Forty-three (51.81%) patients were male, and 40 were female. Seventy-nine (95.18%) patients had a history of diabetes, and 20 (24.10%) patients had a history of end-stage renal disease. The location of the ulceration was described as plantar in 29 (31.52%) of 92 feet, posterior in 20 (21.74%) feet, posterior-lateral in 17 (18.48%) feet, posterior-medial in 5 (5.43%) feet, and was undocumented in 21 (22.83%) feet.  

An ABI was performed on 67 (80.72%) patients, whereby 75 (81.52%) of the 92 affected feet were included. A vascular surgery consultation was obtained on 37 (44.58%) patients with an angiogram procedure in 12 (14.46%) patients. Of the 83 patients, 32 (38.55%) underwent any type of vascular or podiatric procedure during their admission, and 8 (9.64%) were subjected to major limb amputation during their admission.

In terms of the specific ABI findings, at least 1 noncompressible ankle vessel was observed in 35 (46.67%) of the 75 affected feet. Both the ATA and PTA were noncompressible in 26 (34.67%) feet, only the PTA was noncompressible in 6 (8%) feet, and only the ATA was noncompressible in 3 (4%) feet. No digital pressure reading was observed in 36 (48%) feet.  

When at least 1 compressible ankle artery was observed, allowing for calculation of an ABI (n = 49 feet), it was based on the PTA in 23 (46.94%) feet and on the ATA in 26 (53.06%) feet.  

The results of this investigation provide health care professionals working with heel pressure injuries clinically relevant information that has the potential to affect medical decision making. Based on the results, the authors conclude that noninvasive vascular testing may be inaccurate and unreliable in the majority of patients with heel pressure injuries. Testing may be inaccurate based on evidence of noncompressible vessels providing no quantitative information or potentially falsely elevated results in at least 46.67% of feet. Further, in patients with compressible vessels, testing may be an unreliable measure of heel perfusion because more than 50% of the time the ABI was calculated based on the ATA (and not a direct measure of heel perfusion). Out of all 75 feet with heel pressure injuries that underwent noninvasive vascular testing, a compressible PTA allowing for calculation of an ABI as a direct measure of heel perfusion was observed in only 23 (30.67%) feet. When ordering and interpreting noninvasive vascular testing, physicians are encouraged to consider the angiosome and direct arterial supply to an area of tissue loss as opposed to a more general measure of foot perfusion. 

As with any scientific investigation, critical readers are encouraged to review and assess the study design and results to reach their own conclusions, while the preceding represents the authors’ conclusions based on the data. 

In addition, all investigations have limitations, and this study had several. First, data were collected from a limited number of subjects within an urban environment, and therefore results may not be representative of a broader population sampling. Second, this work defined the presence of arterial calcification as a noninvasive vascular testing that reported noncompressibility. Arterial calcification may also manifest as an elevated ABI (as opposed to simply noncompressible) or be visible on plain film radiographs. However, lowering the threshold for the diagnosis of arterial calcification by either of these 2 means would have likely made the study’s results more sensitive and decreased accuracy results even further. Finally, this work made no attempt to associate findings with clinical outcomes and instead only attempted to provide observational descriptive statistics. A prospective investigation of the effect of inaccurate ABIs on specific outcomes may represent an interesting avenue for future investigation.  

The results of this investigation provide original data on the potentially inaccurate and unreliable nature of noninvasive vascular testing in the evaluation of heel pressure injuries. The authors hope the results increase the body of knowledge on evaluation and treatment of lower extremity tissue loss and lead to future investigations on the topic.  

From the Temple University Hospital Podiatric Surgical Residency Program, Philadelphia, PA; and Department of Podiatric Surgery, Temple University School of Podiatric Medicine, Philadelphia, PA

Address correspondence to:
Andrew J. Meyr, DPM, FACFAS
Temple University School of Podiatric Medicine 
Department of Surgery
8th at Race Street
Philadelphia, PA 19107
ajmeyr@gmail.com 

Disclosure: The authors disclose no financial or other conflicts of interest.