VOL: 99, ISSUE: 42, PAGE NO: 70
Maria Mousley, MSc, BSc, DpodM, is chief podiatrist in diabetes care, Northampton Primary Care Trust
Diabetes is a multisystem disorder that affects the wound healing process.
Diabetes is a multisystem disorder that affects the wound healing process. Physiological changes in tissues and cells may delay healing and complications of diabetes also have an impact. Given these factors, it is important for health care teams working across the acute community interface to manage diabetic wounds effectively.
Implications for healing
Diabetes has implications for acute and chronic wound healing (Mulder et al, 1998). Type 2 (non-insulin dependent) diabetes continues to increase in incidence and is more prevalent in older patients (Cruickshank, 1997), in whom age-related skin changes already negatively impact on the healing process.
Complications resulting from type 1 (insulin dependent) and type 2 diabetes include neuropathy and ischaemia, which may lead to foot ulceration (Boulton et al, 1999). Patients with unhealed ulcers have an increased risk of infection, and lower-limb amputation is usually preceded by foot ulceration (Frykberg et al, 2000).
Maintaining normoglycaemia (normal blood sugar levels) is important as hyperglycaemia has been correlated with impaired wound healing (Senior, 2000). In order to optimise wound-healing potential, patients should be encouraged to achieve target levels for glycated haemoglobin (HbA1c). The target for glycated haemoglobin is 7.2 per cent in type 1 diabetes (Diabetes Control and Complications Trial Research Group, 1993). For people with type 2 diabetes, the target is similar at 7 per cent (United Kingdom Prospective Diabetes Study Group, 1998). Patients need to be actively involved in this process and require information and support from health care teams.
Obesity is often a characteristic of type 2 diabetes (Jung, 1997) and patients with obesity are not always well nourished. Nutritional assessment of these patients is therefore an important part of their wound management. Taking a dietary history biochemical analysis, including albumin levels, may provide useful information to assess nutritional status (Williams, 2002).
Delayed wound healing may be a challenging postoperative problem in patients with obesity due to one or more factors:
- Obesity increases the risk of infection;
- Adipose tissue has a relatively insufficient nutritive blood supply;
- Obesity increases tension on newly oppositioned wound edges (Pudner, 2000).
Diabetic peripheral neuropathy affects sensory, motor and autonomic function.
Sensory neuropathy is the single most important risk factor for the development of diabetic foot ulceration (Reiber et al, 1999), as the patient’s pain perception is altered or absent.
Motor neuropathy results in increased pressure on the foot. The small muscles of the foot become atrophied, which leads to an imbalance between the extensor and flexor tendons (Boulton et al, 1999). The resulting clawed toes can cause back pressure across the metatarsal heads, and this is a common site for the development of foot ulceration.
Prevention of ulceration through education has been shown to be effective (Mason et al, 1999). Patients need to adopt behaviours such as examining their feet daily for minor changes that may signal ulceration. Appropriate footwear is extremely important and all patients who develop neuropathic foot ulcers should be referred to their local diabetic foot team for assessment of footwear requirements (Frykberg et al, 2000).
When neuropathic ulcers are free of infection they have a granulating wound bed. However, autonomic neuropathy (affecting the autonomic nervous system) leads to arteriovenous shunting. This compromises the blood supply to the capillary plexus of the foot and leads to a corresponding delay in healing (Boulton et al, 1999).
Management of neuropathy - It is not possible to control for microcirculatory factors associated with neuropathy, so clinicians need to utilise other skills. Sharp debridement and pressure relief have been recommended for treatment of neuropathic foot ulcers (Mason et al, 1999). Sharp-debridement techniques require specialist training. Pressure relief can be provided by pressure-relieving casts.
Various ready-made pressure-relieving devices are now available, such as Aircast walkers, and these offer patients a greater degree of choice within their treatment plan. The devices are usually provided by local diabetic foot teams and so early referral is important in order to optimise care for patients with neuropathic foot ulcers. Compliance with the non-weight bearing regimen impacts greatly on patients’ quality of life (Brod, 1998), and they may benefit from additional psychological support at this time.
Patients with diabetes may have peripheral vascular disease (PVD), which usually coexists with neuropathy. When this occurs feet are described as neuroischaemic. Recently the incidence of neuroischaemic ulceration has become predominant in diabetic foot clinics (Oyibo et al, 2002). Diagnosis of a neuroischaemic ulcer in primary care is based on palpation of pedal pulses. Failure to detect either dorsalis pedis or posterior tibial pulses in a patient presenting with foot ulceration indicates that an early referral to a vascular consultant is required.
Ankle brachial pressure indices (ABPI), used to assess arterial blood flow to the lower limbs, are of limited value in assessing PVD in diabetes (Boulton et al, 1999). Calcification of blood vessels in the ankle, which makes them difficult to compress, can lead to falsely elevated ABPI (see p62).
Vascular units offer advanced technologies, such as duplex ultrasound that accurately map the site and length of arterial occlusion prior to angioplasty or arterial reconstruction.
Peripheral vascular disease may affect the smaller blood vessels of the lower limb in patients with diabetes (Table 1). Research has identified changes in the microvasculature that alter its nutritional and thermoregulatory function and delays wound healing (Flynn and Tooke, 1995).
Following bypass surgery for treatment of PVD, surgical wounds should be closely monitored for clinical signs of infection. Dehiscence in a graft site may lead to occlusion of the new vessel and subsequent limb amputation.
Ischaemic ulcers are often caused by ill-fitting footwear and frequently occur where foot and footwear make contact, for example, at a bunion joint, the tip of the big toe or underneath nails. Pressure on ischaemic tissue causes blanching and a subsequent hyperaemic (reddening) response as the tissue tries to reperfuse.
Management of ischaemic wounds
Reperfusion is compromised in ischaemic tissues and the red mark of hyperaemia will proceed to tissue necrosis, which initially presents as a shallow ulcer. The wound bed may appear as a pale granulation tissue or with indolent yellow slough. Pressure relief with correctly fitting footwear is important in the management of ischaemic wounds. Comprehensive wound management also involves controlling for factors that influence the course of atherosclerosis: hyperglycaemia; hypertension; hyperlipidaemia and smoking (Camm, 1990).
Following surgery, patients with diabetes are at higher risk of wound infections as their immune response may be compromised (Mulder et al, 1998). Detecting infection is usually based on clinician assessment using the signs of inflammation. However, the response to infection may be subdued in diabetic foot disease, due to the underlying pathophysiology. This means infection is difficult to detect (Table 2).
Berendt and Lipsky (2003) recommend that the presence of any two signs of infection signifies its presence in the diabetic foot.
Wound infections are commonly polymicrobial (International Working Group on the Diabetic Foot, 1999). It is important to identify the invading pathogen and initiate specific antibiotic therapy. Deep wound swabs and, if possible, locally debrided wound tissue will provide optimum samples for wound cultures. Local prescribing policies and any uncertainty regarding choice of antibiotic should be discussed with the microbiologist.
There is no consensus on the ideal dressing in diabetes. The principles of moist wound healing are generally followed. This is good practice for uncomplicated acute surgical wounds. However, chronic diabetic wounds must be monitored for infection every one to two days, so dressings designed for optimum use over longer periods are not ideal.
Adhesive borders on modern dressings provide improved contact with the wound bed. However, care must be taken to avoid damaging surrounding skin on removal. Infected wounds produce increased exudate, so dressings’ exudate-handing capability should be considered - alginates are often useful.
All alginates have similar properties, but differences in manufacture affect the absorptive capabilities of various products. Those with needled fibres are dense and liable to form a fibrous mat in the presence of thick exudates. This obstructs drainage and can undermine neighbouring tissue. Use of alginates is best restricted to wounds exuding large amounts of thin exudate.
Silver preparations or cadexomer iodine dressings may be used to reduce bacteria in colonised or infected wounds (Schultz et al, 2003). However, dressings are not a replacement for systemic therapy for infection (Table 2). Bulky dressings are likely to increase intra-shoe pressures.
If a larger dressing is necessary patients should be offered footwear to accommodate it. This usually involves referral to a specialist team. Ultimately the aim is to provide a rationalised, evidence-based approach to wound care and dressing selection.
Diabetes is a complex disease that impacts on acute and chronic wound management. Education of patients within primary care can play a role in preventing complications. However, chronic diabetic foot ulcers present a clinical challenge. Physiological changes related to diabetes and its complications interact with extrinsic factors such as pressure relief. Optimum outcomes for patients require collaboration between skilled clinicians across primary and secondary care multidisciplinary teams.