Part 6: Detection and Prevention of Foot Problems in Type 2 Diabetes

Part 6: Detection and Prevention of Foot Problems in Type 2 Diabetes Part 6: Detection and Prevention of Foot Problems in Type 2 Diabetes

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10.07.2015 Views

Section 3: Diabetes Foot ProblemsIssueIs foot deformity or a previous amputation a risk factor for ulceration or amputation?RecommendationPeople with diabetes who have had a previous amputation are at high risk of ulceration andfurther amputation and therefore require regular and frequent reviewPeople with diabetes should be assessed regularly to detect foot deformities including:• Hallux deformities• Hammer or claw toes• Callus• Charcot’s footEvidence Statements• A previous amputation is a risk factor for ulceration and further amputationEvidence Level III-2• Foot deformity is a risk factor for ulceration, especially in people with neuropathyEvidence Level III-2• Callus is a risk factor for ulceration, especially in people with neuropathyEvidence Level III-226

Background – Foot Deformity and Previous Amputation as RiskFactors for Ulceration and AmputationMechanical factors play a critical role in the aetiology of neuropathic foot ulcers(Cavanagh et al, 1996; Mayfield et al, 1998). Alterations in the normal biomechanicsof the foot result from alterations in foot structure and non-enzymatic glycosylationwhich alters foot tissue properties. These combine to increase plantar pressure, aconsistent finding in people with diabetes, which has been associated with increasedrisk of ulceration (Veves et al, 1992). Plantar pressures are difficult to measure in aroutine practice setting as sophisticated technology is required, however callus, a signof increased foot pressure, is more predictive of ulceration than increased plantarpressure alone (Mayfield et al, 1998).Plantar pressures during walking and standing in the normal foot are sufficient toocclude capillary blood flow and it has been suggested that local reflexes includingthe hyperaemic response are abnormal in people with neuropathy and that capillaryfragility may be greater in people with diabetes (Cavanagh et al, 1996). People whohave lost protective sensation may not appreciate increasing damage to the foot due toincreased pressure and continue to traumatise the same tissue (Mayfield et al, 1998).Causes of increased plantar pressures in people with diabetes include increased bodymass (however this contributes less than 14% of variance in peak plantar pressure),changes in posture, gait, soft tissues and bone structure. Limited joint mobility occursin the absence of neuropathy but only becomes a risk for ulceration with the loss ofprotective sensation. Glycosylation of soft tissues is thought to predispose to theexcess callus formation seen in people with diabetes in response to abnormal plantarpressures. Bony deformities caused by motor neuropathy, hammer toe or claw toedeformity are present in up to half of all people with diabetes (Mayfield et al, 1998).Foot deformity is a major contributor to increasing foot pressures. Foot deformities inpeople with diabetes range from minor abnormalities in joint mobility to the severedeformity seen in advanced Charcot’s foot. A previous amputation, particularly aminor amputation, frequently results in abnormal plantar pressures and increases therisk of subsequent amputation.Callus is a diffuse hyperkeratotic area which develops in response to shear stresses,usually in proximity to a bony prominence (Reiber et al, 1999). Callus is not only asign of increased foot pressures but also contributes to further increase plantar footpressures by acting as a foreign body and predispose to the formation of ulcersbeneath such lesions.Reducing plantar pressures is the basis of treating foot ulcers and preventingulceration in at risk feet (Cavanagh et al, 1996). Several measures have been shown toreduce abnormal pressures, protect the foot from external trauma and reduce theformation of callus and ulcers. Conservative management of increased plantarpressures involves debridement of callus and footwear modification.27

Background – <strong>Foot</strong> Deformity <strong>and</strong> Previous Amputation as RiskFactors for Ulceration <strong>and</strong> AmputationMechanical factors play a critical role <strong>in</strong> the aetiology <strong>of</strong> neuropathic foot ulcers(Cavanagh et al, 1996; Mayfield et al, 1998). Alterations <strong>in</strong> the normal biomechanics<strong>of</strong> the foot result from alterations <strong>in</strong> foot structure <strong>and</strong> non-enzymatic glycosylationwhich alters foot tissue properties. These comb<strong>in</strong>e to <strong>in</strong>crease plantar pressure, aconsistent f<strong>in</strong>d<strong>in</strong>g <strong>in</strong> people with diabetes, which has been associated with <strong>in</strong>creasedrisk <strong>of</strong> ulceration (Veves et al, 1992). Plantar pressures are difficult to measure <strong>in</strong> arout<strong>in</strong>e practice sett<strong>in</strong>g as sophisticated technology is required, however callus, a sign<strong>of</strong> <strong>in</strong>creased foot pressure, is more predictive <strong>of</strong> ulceration than <strong>in</strong>creased plantarpressure alone (Mayfield et al, 1998).Plantar pressures dur<strong>in</strong>g walk<strong>in</strong>g <strong>and</strong> st<strong>and</strong><strong>in</strong>g <strong>in</strong> the normal foot are sufficient toocclude capillary blood flow <strong>and</strong> it has been suggested that local reflexes <strong>in</strong>clud<strong>in</strong>gthe hyperaemic response are abnormal <strong>in</strong> people with neuropathy <strong>and</strong> that capillaryfragility may be greater <strong>in</strong> people with diabetes (Cavanagh et al, 1996). People whohave lost protective sensation may not appreciate <strong>in</strong>creas<strong>in</strong>g damage to the foot due to<strong>in</strong>creased pressure <strong>and</strong> cont<strong>in</strong>ue to traumatise the same tissue (Mayfield et al, 1998).Causes <strong>of</strong> <strong>in</strong>creased plantar pressures <strong>in</strong> people with diabetes <strong>in</strong>clude <strong>in</strong>creased bodymass (however this contributes less than 14% <strong>of</strong> variance <strong>in</strong> peak plantar pressure),changes <strong>in</strong> posture, gait, s<strong>of</strong>t tissues <strong>and</strong> bone structure. Limited jo<strong>in</strong>t mobility occurs<strong>in</strong> the absence <strong>of</strong> neuropathy but only becomes a risk for ulceration with the loss <strong>of</strong>protective sensation. Glycosylation <strong>of</strong> s<strong>of</strong>t tissues is thought to predispose to theexcess callus formation seen <strong>in</strong> people with diabetes <strong>in</strong> response to abnormal plantarpressures. Bony deformities caused by motor neuropathy, hammer toe or claw toedeformity are present <strong>in</strong> up to half <strong>of</strong> all people with diabetes (Mayfield et al, 1998).<strong>Foot</strong> deformity is a major contributor to <strong>in</strong>creas<strong>in</strong>g foot pressures. <strong>Foot</strong> deformities <strong>in</strong>people with diabetes range from m<strong>in</strong>or abnormalities <strong>in</strong> jo<strong>in</strong>t mobility to the severedeformity seen <strong>in</strong> advanced Charcot’s foot. A previous amputation, particularly am<strong>in</strong>or amputation, frequently results <strong>in</strong> abnormal plantar pressures <strong>and</strong> <strong>in</strong>creases therisk <strong>of</strong> subsequent amputation.Callus is a diffuse hyperkeratotic area which develops <strong>in</strong> response to shear stresses,usually <strong>in</strong> proximity to a bony prom<strong>in</strong>ence (Reiber et al, 1999). Callus is not only asign <strong>of</strong> <strong>in</strong>creased foot pressures but also contributes to further <strong>in</strong>crease plantar footpressures by act<strong>in</strong>g as a foreign body <strong>and</strong> predispose to the formation <strong>of</strong> ulcersbeneath such lesions.Reduc<strong>in</strong>g plantar pressures is the basis <strong>of</strong> treat<strong>in</strong>g foot ulcers <strong>and</strong> prevent<strong>in</strong>gulceration <strong>in</strong> at risk feet (Cavanagh et al, 1996). Several measures have been shown toreduce abnormal pressures, protect the foot from external trauma <strong>and</strong> reduce theformation <strong>of</strong> callus <strong>and</strong> ulcers. Conservative management <strong>of</strong> <strong>in</strong>creased plantarpressures <strong>in</strong>volves debridement <strong>of</strong> callus <strong>and</strong> footwear modification.27

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