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Heel pressure ulcers and ankle brachial pressure index measurement

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VOL: 101, ISSUE: 04, PAGE NO: 47

Julia Graham, RGN, community staff nurse/vascular link nurse, Arran War Memorial Hospital, Lamlash, Isle of Arran


I practise in a remote rural area in the community and act as a wound care link nurse with a specialist interest in vascular nursing. In the past nine months I have seen two patients who were discharged from hospital with an isolated pressure ulcer on one of their heels. Both patients had asymptomatic undiagnosed PVD with reduced ABPI measurements of 0.8 and 0.75 (Royal College of Nursing, 1998). Both lesions had delayed healing of four months and six months respectively.

A wound is generally considered to be non-healing if it fails to respond to conservative therapy in 4-12 weeks (Santilli and Santilli, 1999). There is no literature comparing healing rates of pressure ulcers on heels with normal arterial circulation and those associated with impaired arterial blood flow.

The RCN (1998) guideline on leg ulcers does not refer to heel and foot ulcers. However, patients with established PVD have an increased risk of an extensive full-thickness injury occurring and it could be argued that patients with heel pressure ulcers should therefore have their ABPI measured. However, patients with heel ulcers are classified as having a 'pressure ulcer', and much of the literature aimed at pressure ulcer assessment does not mention measuring ABPI before planning management.

Pressure ulcer assessment
Parish et al (1983) defined a pressure ulcer as 'a lesion on any skin surface that occurs as a result of pressure and includes reactive hyperemia as well as blistered, broken or necrotic skin'. The European Pressure Ulcer Advisory Panel (EPUAP) (1999) also includes in its definition shear, friction forces and/or a combination of all three causes.

Any patient who is at risk of developing a pressure ulcer should have a risk assessment performed. This formal approach determines whether or not there is a risk that tissue damage will occur. There are several risk assessment scales available. Flanagan (1993) describes some of the more commonly used ones, and evaluates their application to clinical practice.

If a pressure ulcer develops, the patient will require a full holistic assessment incorporating her/his medical and social history, the condition of the wound and those factors that may delay healing. There are several national clinical guidelines available to assist with the assessment and planning of care (National Institute for Clinical Excellence, 2001; EPUAP, 1999). The RCN (2003) has established an implementation guide and protocol that can assist with implementing the national guidelines.

A pressure ulcer should be classified and graded by appearance and depth. The purpose of this is to achieve a consensus of common language for describing and documenting the extent of tissue damage. EPUAP (1999) has adapted the four-grade pressure ulcer classification, and this is being disseminated throughout Europe.

Heel ulcers
There are many potential sites where pressure ulcers can develop, but ulcers that develop on heels, particularly in isolation, require special consideration. Heel pressure ulcers are the second most common type of pressure-related ulcers (Calianno, 2000). They occur because of prolonged pressure over a small contact area where there are high local pressures, which can compromise blood flow, resulting in localised tissue necrosis (Cameron, 1999). Common extrinsic and intrinsic risk factors are listed in Box 1.

Peripheral vascular disease: There are a number of risk factors associated with PVD. These include ageing, smoking, raised cholesterol, and diseases such as diabetes mellitus, heart disease, hypertension and cerebrovascular accident. A patient presenting with a heel ulcer, particularly grade 3 or 4, with any of the above risk factors may have PVD.

According to Burdette-Taylor and Kass (2002), a 'lack of sufficient blood flow to the lower extremity is the single component that, if not addressed immediately, can lead to an ulcer and possibly an amputation'. They provide extensive assessment guidelines for heel pressure ulcers that include pressure ulcer assessment techniques and non-invasive arterial assessment (Box 2).

Burdette-Taylor and Kass (2002) also recognise that ABPI should be measured, and that if the result indicates PVD (index <0.8) the="" patient="" should="" be="" referred="" to="" a="" vascular="" surgeon.="">

The guideline of the Registered Nurses Association of Ontario (2002) recommends that vascular assessments, including ABPI measurements, should be used to rule out arterial disease and to determine therapy for individuals who develop pressure ulcers on their lower limb.

British guidelines identify that vascular disease is a risk factor for the development of pressure necrosis, but do not identify the significance of measuring ABPI and the relevance of an index of <0.8. (crest="" 1998;="" nice,="" 2001;="" rcn,="" 2003).="" the="" best="" practice="" statement="" of="" the="" nursing="" and="" midwifery="" practice="" development="" unit="" (2002)="" does="" not="" mention="" pvd="" as="" being="" an="" important="" risk="" factor.="">

Diabetes: Diabetes is a major risk factor for heel pressure ulcers because it is frequently associated with PVD. Arteriosclerosis tends to affect the distal vessels, which are less amenable to revascularisation (Springett, 2000; Foster and Edmonds, 2001). These authors identify the role of PVD in the development of foot ulcers and the relevance of measuring ABPI.

However, ABPI measurements are not always accurate in patients with diabetes because these patients may have calcification of the main blood vessels to the foot, which results in inaccurate results (Gibbons et al, 1995). In this case, toe pressures provide more accurate assessment of the distal circulation, as pedal blood vessels are not affected by calcification. This supports a consensus statement that toe pressures should be used to assess the arterial status of the diabetic foot where calcification of arteries may be a problem (Vowden et al, 1996).

Treatment: Treatment should aim at preventing heel pressure ulcers. This can be achieved by: maintaining good skin condition; repositioning the patient at regular intervals to ensure that prolonged pressure on the heels is minimised; and providing appropriate equipment to prevent damage, particularly in patients identified as being at risk (NICE, 2001; Burdette-Taylor and Kass, 2002).

Patients with arterial disease with an ABPI of below 0.8 are at risk of developing pressure ulcers on the heel, which can be extremely painful and difficult to heal. Those with an index below 0.5 and ulceration are considered to have critical limb ischaemia (Beard, 2001), in which case referral to a vascular specialist is indicated for further investigation using Duplex scanning and /or angiography. This will establish the degree of underlying ischaemia and whether corrective surgery is needed.

The NICE (2004) guidelines for type 2 diabetes and foot ulceration indicate that a foot at high risk of ulceration should be referred to a specialist within 24 hours. Debridement of a heel ulcer is a major clinical decision because the evidence supporting its use is limited and the outcomes unpredictable.

Conclusion: Patients with PVD have significant intrinsic risk factors that are known to delay wound healing. Arterial leg ulcers tend to develop tissue necrosis and/or slough, which is slow to separate (Bale et al, 2000). Patients with this type of leg ulcer would have an ABPI measurement performed routinely. On this basis it would seem logical that an ABPI measurement should be included in an assessment for heel pressure ulcers, particularly when tissue necrosis is present. Unfortunately, there is no research-based evidence to support this practice; a formal study is required to establish if ABPI measurement should be included in heel pressure ulcer assessment.

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