Other Risk Factors for Foot Ulcers

Other Risk Factors for Foot Ulcers

Biomechanical Aspects The neuropathic foot does not ulcerate spontaneously. It is the combina-

tion of neuropathy and trauma that results in tissue breakdown. The trauma required to ulcerate the neuropathic foot can take several different forms.

Sometimes it is a single event such as standing on a nail, but more frequently it occurs as repeated minor trauma such as unperceived shoe rubbing to the toes or increased pressure beneath the metatarsal heads during walking. A number of studies have clearly demonstrated that dynamic plantar foot pres- sures are elevated in diabetic neuropathy and especially in patients with a history of plantar ulceration. More importantly, a prospective study has shown that elevated plantar pressures are predictive of ulceration, with 17% of patients with high foot pressures developing plantar ulcers during a 30-month follow- up period, whilst no plantar ulcers developed in patients with normal pressures. The presence of callus (produced in response to pressure) may exacerbate the problem both by acting as a foreign body and by increasing plantar pressures. Amongst those with diabetic neuropathy, the presence of callus is a strong and important predictor of subsequent ulceration at the site of the callus. The simple removal of the callus significantly reduces foot pressures, and presumably, therefore, also reduces the risk of ulceration.

Most studies on foot pressure have simply looked at the highest instanta- neous pressure measured during a single foot step. However, evidence from in vitro studies indicates that the rate of increase of applied pressure is more important than the peak pressure achieved in causing cellular damage. If this Most studies on foot pressure have simply looked at the highest instanta- neous pressure measured during a single foot step. However, evidence from in vitro studies indicates that the rate of increase of applied pressure is more important than the peak pressure achieved in causing cellular damage. If this

The main cause of increased pressure is thought to be the alteration in foot shape resulting in prominent metatarsal heads. Atrophy of the intrinsic muscles of the foot (predominantly plantar flexors of the toes) alters the flexor/ extensor balance at the metatarso-phalangeal joints and causes clawing of the toes, and prominence of the metatarsal heads.

A further contributing factor to elevated plantar pressure is limited joint mobility. Glycosylation of collagen results in thickening and cross-linking of collagen bundles. This is manifested clinically as thick, tight, waxy skin and restriction of joint movement. Limited joint mobility of the subtalar joint alters the mechanics of walking and is strongly associated with high plantar pressure.

Other Long-Term Complications Patients with retinopathy and nephropathy have been shown to have an

increased risk of foot ulceration and amputation. The pathogenic mechanisms by which other complications lead to ulceration and amputation are not entirely clear, but visual impairment makes it more difficult for patients to identify a lesion at an early stage, and tissue repair is slow in nephropathy, because of oedema, the frequent co-existence of macrovascular disease and immunological abnormalities. Thus, such patients must always be regarded as being at high risk.

Previous Foot Ulceration Several studies have confirmed foot ulceration is more common in those

patients with a past history of ulceration or amputation and in patients with

a poor social background. Diabetes Control

Poor glycaemic control as measured by HbA 1c , fasting and even a single random blood glucose is a strong risk factor for subsequent amputation. Chronic hyperglycaemia increases the risk of developing complications such as neuropathy, and impairs the wound healing capacity, thus setting the scene for ulceration and amputation.

Ethnicity Lower extremity amputation rates have been shown to be high amongst

several groups of American Indians and may be as much as 4 times greater several groups of American Indians and may be as much as 4 times greater

be higher amongst Black than Europid people with diabetes. Studies in the UK have shown lower incidences of amputation and foot ulceration in the Asian than the White population. The reasons for different amputation rates among different ethnic groups are unclear. Access to health care (ranging from detection and early treatment of diabetes to availability of specialized foot services) is likely to be important, but biological variation between ethnic groups may also play a role.

Cardiovascular Factors Evidence would suggest that hypertension is probably a moderately impor-

tant risk factor for amputation, but neither lipid abnormalities nor surprisingly smoking predict amputation.

Behavioural/Psychological Factors Despite the fact that causal pathways to ulceration are well recognized

(predominantly involving neuropathy and PVD), and many high-risk patients receive education on footcare, ulceration remains common. It has been sug- gested that denial of risk is the main reason for this and indeed extreme denial has been reported in some foot ulcer patients. However, in our own prospective study of psychological factors in foot ulceration, measures of denial have failed to predict ulceration. In contrast, neuropathic patients developing ulcers showed a more negative attitude to the feet, and their belief in the efficacy of advice (as provided in footcare education) was lower than that of patients who did not develop ulcers.

Wound Healing Slow wound healing and increased susceptibility to infection increase the

problems of foot ulceration and may predispose to amputation. A number of inherent immunological abnormalities have been documented in diabetes and these may explain the increased infection rates that are seen in postoperative wounds of diabetic patients. Amongst other abnormalaties, neutrophil function is impaired, with abnormalities of adherence, chemotaxis, phagocytosis and killing ability, and these may be partly due to ascorbic acid transport defects.

Microcirculation and Endothelial Dysfunction Diabetes is associated with microcirculatory abnormalities, which are ac-

centuated in the presence of long-term complications, including diabetic neu- ropathy. Typically, in the neuropathic foot, resting skin blood flow is elevated, but there is a marked blunting of the hyperaemic reserve, and of the postural vasoconstriction that should reduce limb blood flow on standing. The vasodila-

Table 1. Foot ulcer risk factors and relevant measurement techniques; all people with diabetes should be screened for these risk factors annually

Risk factor

Screening method

Abnormal result indicating increased risk of foot ulceration

Neuropathy Vibration perception Greater than 25 V at the great toe threshold 1 Pressure perception

Insensitivity to a 10-gram monofila- threshold 1 ment on the plantar surface of the foot Clinical examination 1 Absent ankle reflexes or sensory loss

Peripheral vascular disease Clinical examination Less than 2/4 palpable foot/ankle pulses Doppler pressures 1 Systolic ankle pressure less than 90% of brachial pressure

Previous foot lesion Self-report 1 Previous ulcer or amputation 1 Screening methods that have been shown to predict subsequent foot ulceration.

tory response is mediated by both endothelium-dependent and endothelium- independent mechanisms, both of which appear to be impaired in neuropathy. Whilst the direct causal connection between these abnormalities and foot ulceration is attractive, since a failure to respond appropriately to tissue injury could lead to chronic ulceration, the possible association is as yet untested.

Another related factor which may be important in the development of ulceration is capillary fragility. Recent work has shown the presence of micro- haemorrhages in the feet of neuropathic patients with a history of ulceration. As haemorrhage into callus commonly precedes ulceration, this may be an important finding.