Preventing pressure ulcers occurring on the heel
01/09/12 | Pressure ulcers | Joyce Black
Pressure ulcers are defined as localised injury to the skin and/or underlying tissue, usually over a bony prominence, as a result of pressure, or pressure in conjunction with shear. An important change to this definition is the elimination of friction as a cause of pressure ulcers. Patients can develop friction injury to the heel from the constant movement of the heel on their bed linen. The change to this definition stems from an understanding that frictional forces are superficial and lead to heat in the tissues, producing serum-filled blisters; friction does not involve pressure. Shear forces — the combination of pressure and movement — can and do lead to pressure ulcers.
In a large, cross-sectional survey focusing on pressure ulcer prevalence (104,266 patients), heel pressure ulcers were found to occur in 18.2% of cases. This number may seem lower than past estimates of heel ulcer prevalence - however, in this study pressure ulcers in 25 anatomical sites were recorded and ulcers that in the past were attributed to the heel were in fact shown to be located on other sites on the lower limb.
Earlier data from a similar cross-sectional survey on heel ulcers, this time with fewer patients (85,838), recorded prevalence ranging from 23-28.9% and incidence ranging from 23.6-26.1%. The heel is the most common site for deep tissue injury (DTI) and this area of the foot accounts for 41% of all DTIs.
COST AND SIGNIFICANCE
The cost of pressure ulcers is thought to be high, although no specific data on the cost of heel pressure ulcers could be found. General pressure ulcer prevention was estimated to cost $54.66 per day in acute care settings in the US. The model used by Padula did not include specific prevention methods or devices for heel pressure ulcers. The cost of pressure ulcer treatment in the UK was estimated at £1.4bn to £2.1bn. In 2012, US medical insurance claims comprised 394,699 cases of pressure ulcers that were treated at a cost of $8,730 per case, totalling $3.5bn. It is important to note that these costs related only to treatment submitted for payment.
Mortality data on patients with pressure ulcers on the heels are also not reported separately. Brown reported on 74 patients at end of life with full thickness pressure ulcers (16.2% were on the heel). The 180-day mortality rate for these patients was 68.9%, with an average of 47 days from the ulcer onset to death.
Healing times for heel ulcers are long, in many cases over a year. Some of the delays in healing can be attributed to underlying comorbid problems including poor arterial flow to the leg, diabetic neuropathy, continued use of tobacco and difficulty maintaining pressure relief on the heel for the length of time needed to heal the ulcer. Morbidity, that is to say amputation, for heel ulcers with osteomyelitis or critical limb ischaemia is also common. In one study, 11% of patients with ischaemic heel ulcers and gangrene required amputation, compared with a group of patients with ulcers on other aspects of the foot.
Similarly, Han and Ezquerro reported that 42% of 43 patients (18 patients) with heel ulcers required leg amputation due to persistent infection or non-healing wounds.
The heel is at increased risk of ulceration due to its posterior prominence and lack of padding over the calcaneus. Gefen found that the pressure on the fat pad of the heel when positioned at 90 degrees to the leg during bedrest is higher than when the foot is turned onto the side. Pressure can be applied to the heel during bedrest, and pressure can be higher if the heel is resting in a 'hammock' at the foot of the bed. Hammocks develop when the material of the mattress does not support the heel on the bed leaving the heel hanging in the mattress cover. This intense pressure can lead to ulceration and pain. Shear forces on the heel occur when the patient slides down in bed.
The hyperaemic response to pressure loading on the heel does not differ from other tissue. However, the heel is a unique bony prominence and with aging the number of capillaries are reduced, the amount of soft tissue padding over the calcaneus decreases and blood flow at rest to the heel is relatively low.
Owing to the unique anatomy of the heel and impaired ability to reperfuse (restoration of the blood flow to a previously ischaemic tissue or organ), the heel is a common site for deep tissue injury pressure ulcers[11,1]. Salcido et al correlated the relative risk of deep tissue injury of the heel to the relatively small radius of the calcaneus and thin, overlying tissue.
Co-morbid diseases also can impair arterial inflow and when patients are hospitalised vasoconstriction from medications, hypovolemia or pain can further reduce arterial inflow. Arterial blood flow to the heel is supplied by the lateral and medial plantar artery and the medial calcaneal branch of the posterior tibial artery [Fig 1]. Differences in blood flow to the heel were seen in patients with ankle-brachial indices lower than 0.8. Blood flow, via transcutaneous oxygen levels to the heels, was tested in patients who underwent hip-replacement surgery and had elastic support stocking and sequential compression devices on the legs. Transcutaneous oxygen levels were lower in both heels, and more so in the operative limb during periods of pressure loading and when pressure was removed (unloading).
IDENTIFYING HIGH RISK PATIENTS
The Braden Scale for detecting pressure ulcer risk has not been shown to consistently identify patients at risk of pressure ulcers on the heels. The National Database of Nursing Quality Indicators (NDNQI) and a study by Walsh and Plonczynski focusing on hospital-acquired pressure ulcers found that they predominantly occur in patients who are at low to mild risk on the Braden assessment tool.
Unique intrinsic risk factors for pressure ulcers on the heels include diseases that impair sensation in the heel (such as diabetic neuropathy, stroke, nerve block after surgery, analgesia), conditions that reduce blood flow to the leg (ie peripheral vascular disease, vasopressive medications) and lower limb weakness (such as hip fracture, total knee replacement) are the most common.
Low serum albumin levels were also seen in the patients with pressure ulcers on the heels. The calcaneus of the heel is prominent, extending into the mattress of the bed. Some patients have sharp posterior calcanei, thin soft tissue padding and heavy feet making them at higher risk, similarly, a 0.8 ankle brachial pressure index (ABI) provides high sensitivity and adequate specificity to predict pressure ulcer development on the heel.
It is recommended that nursing staff use a general pressure ulcer risk assessment tool and add risk factors unique to heel ulcers, including poor blood flow to the legs, neuropathy and lower limb weakness. Poor blood flow to the leg can be identified by a history of cardiovascular or peripheral vascular diseases with claudication and/or physical examination findings of thin, hairless legs, thick toenails, delayed capillary refill times, and/or absent pulses in the foot. Neuropathy can be assessed formally via Semmes-Weinstein monofilament testing or tested generally by asking the patient about pain in the legs or the ability to feel hot bath water, tight shoes or injury to the foot.
Neuropathy develops along with the other end-organ damage seen with diabetes, so if the patient is receiving dialysis or treatment of retinal damage, they probably have neuropathic changes in the feet. Inability to move the leg is tested by asking the patient to move his/her leg in bed - if the patient cannot or will not do so due to pain, the leg should be considered immobile.