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Biomechanics of the Diabetic Foot Robert G. Frykberg, DPM, MPH Robert G. Frykberg, DPM, MPH Chief, Podiatry Section Chief, Podiatry Section Carl T. Hayden VA Medical Carl T. Hayden VA Medical Center Center Phoenix, AZ USA Phoenix, AZ USA

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Biomechanics of the Diabetic Foot

Robert G. Frykberg, DPM, MPHRobert G. Frykberg, DPM, MPHChief, Podiatry SectionChief, Podiatry Section

Carl T. Hayden VA Medical CenterCarl T. Hayden VA Medical CenterPhoenix, AZ USAPhoenix, AZ USA

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Diabetes Mellitus

Neuropathy Vascular Disease

Trauma

MOTOR SENSORY AUTONOMIC MICROVASCULAR MACROVASCULAR

Weakness Loss of Protective Anhidrosis Structural: AtherosclerosisAtrophy sensation Dry skin, Fissures Capillary BM Decreased Sympathetic thickening Deformity tone Functional: Ischemia (Altered blood flow A-V shuntingAbnormal stress regulation) Increased blood flow Neuropathic edema High plantar pressure

Callus formation

Reduced nutrient capillary blood flow Osteoarthropathy

AmputationAmputation DIABETIC FOOT ULCERATION

Impaired Response to Infection

RGF

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Causal Pathways to Foot Ulcers

63%

77% 78%

Neuropathy

Deformity

Trauma

From: Reiber et al: Diabetes Care 22:157-162, 1999

Critical Triad in >63% of causal pathways

High Plantar Foot Pressures

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Altered Biomechanics in Diabetes• Biomechanical abnormalities / structural

deformities are most frequently a consequence of Neuropathy

• Altered gait patterns can result in unsteady gait with increased plantar foot pressures for longer durations (pressure-time integrals)

• Combination of foot deformity and neuropathy increases the risk of ulcer

• Limited Joint Mobility (ankle, STJ, great toe) will also lead to higher plantar pressures and ulcers

Van Schie 2005Cavanagh 1996

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Contributing Factors to the Abnormal Mechanics of the Diabetic Foot

Diabetes Mellitus

Neuropathy Structural Deformity Gait Abnormalities LJM Mononeuropathy Primary (idiopathic) Foot drop Collagen glycosylation Polyneuropathy Secondary Equinus reduced mobility Sensory Muscle atrophy Intrinsic muscle reduced shock absorption Motor Equinus atrophy increased pressures Autonomic Amputations Clawtoes Charcot Amputations

Abnormal BiomechanicsAbnormal BiomechanicsHigh Plantar PressuresHigh Plantar PressuresNeuropathic UlcerationNeuropathic Ulceration

Van Schie 2005Zimny 2004Frykberg 1995

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Classification of Diabetic Neuropathy

Generalized Symmetric Polyneuropathies– Acute Sensory– Chronic Sensorimotor– Autonomic

Focal and multifocal neuropathies– Cranial – Truncal– Focal limb– Proximal motor (amyotrophy– Coexisting CIDP

Boulton, Malik et al: Diabetes Care, 2004Boulton, Vinik, et al: Diabetes Care, 2005

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Andersen et al: 2004Andersen et al: 2004

Intrinsic Muscle Atrophy

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Bus et al: Diabetes Care, 2002Bus et al: Diabetes Care, 2002

Intrinsic Muscle Atrophy

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Common Foot Deformities in Diabetes

• Hammertoes (Clawtoes)• Bunions (hallux valgus)• Prominent metatarsal heads (pes cavus)• Charcot arthropathy• Partial foot amputations• Equinus (Achilles contracture)• Foot drop

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STRUCTURAL DEFORMITY•Primary (idiopathic) Pes cavus, pes planus, hallux valgus, hammertoes, forefoot deformities Deformities, pressure points, calluses precede neuropathy.•Secondary "intrinsic minus foot"- clawtoes, pes cavus, depressed metatarsals. Loss of intrinsic muscle stability with long flexor over-dominance. Anterior crural atrophy (Ant. Tib.,EHL) - weakness, foot drop Equinus deformity- triceps surae dominance, post. tibial, long flexors Charcot deformity - rocker bottom, Lisfranc subluxation, MTP subluxation•Iatrogenic

Post amputation: digital, ray, TMA, Lisfrancs, Choparts, SymesFrykberg 1995

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AMPUTATIONS IN THE FOOTCONSEQUENCES

Structural alterations

Reduced contact areas

Increased plantar pressures

Altered function

Altered gait

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STRUCTURAL DEFORMITY

Frykberg et al: J Foot Ankle Surg 2006

Any deformity can lead to high plantar Pressures and subsequent ulceration in the Neuropathic Foot

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The Role of High Plantar Pressures in Diabetic Foot Ulceration

• High plantar foot pressures are consistently detected in diabetic pts with neuropathy

• Boulton 1987, Veves 1992, Stess 1997, Shaw 1998• correlated with Limited Joint Mobility, plantar tissue

thickness, and plantar fascia thickness• Zimny 2004, Abouaesha 2001, D’Ambrogi 2003

• risk factor for foot ulceration• Fernando 1991 Lavery 1998 Frykberg 1998 Lavery 2003

• Racial variations are evident• Veves 1995 Frykberg 1998

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Predictive Value of Foot Pressure Assessment

• 24 month study of 1666 DM patients

• Mean age 69 yrs 50% male• Mean Duration DM 11.1 yrs• Mean Peak Plantar Pressure

86.6 N/cm2• VPT 22.5 volts• 263 (15.8%) had or developed

ulcer• Ulcer group had higher

pressures

95.5

85.1

75

80

85

90

95

100

N/cm

2Ulcer No Ulcer

Lavery LA, Armstrong, DG, et al, Diabetes Care 2003

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Pressure is a factor

Lavery LA, Armstrong, DG, et al, Diabetes Care 2003

Deformities IWGDF Foot Risk Categories

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Progressive Risk of Ulceration

5.114.3

18.8

55.8

0

10

20

30

40

50

60

Group 0 Group 1 Group 2 Group 3

No Neuropathy Neuropathy Neuropathy, PVD,And/ or Deformity

Hx Ulcer / Amp

Peters 2001IWGDF Foot Risk Classification

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GAIT DISTURBANCES Function of neuropathy, deformity, & LJM Abnormal loading patterns - earlier and longer Altered cadence - instability and limp Altered weight bearing sites –

Partial foot amputations - smaller area

Increased plantar pressures Susceptible to ulceration

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• Proximal muscle atrophy - thigh weakness• Anterior crural atrophy - dorsiflexor weakness• Intrinsic muscle atrophy - clawtoes; reduced toe loading• Foot drop - Anterior tibial, Extensor hallucis longus paresis• Equinus - Posterior group dominance; triceps surae• Structural deformities - Charcot, post amputations

GAIT ABNORMALITIESContributing Factors

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• A product of Nonenzymatic glycosylation of collagen – Also associated with retinopathy

• Decreased ankle and hallux motion• Restricted subtalar range of motion

– reduced shock absorption; – Increased vertical and shear forces – Increased peak plantar pressures

• Alone does not cause ulceration• With neuropathy, contributes to plantar ulceration

Limited Joint Mobility

Delbridge 1988Fernando 1991Zimny 2004

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0

10

20

30

40

50

60

70

VPT Ankle ROM 1st MTPROM

PTI

At-Risk DMControl DMNon-DM

The Role of Limited Joint Mobility in Diabetic Patients with an At-Risk Foot

Zimny, Schatz, Pfohl: Diabetes Care 27:942-946, 2004

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Zimny: Diabetes Care, 2004

There is a strong inverse correlation between joint mobility and PTI in diabetic patients

At-Risk Neuropathic patients have less joint mobility and higher PTI’s than control DM (non-neuropathic) patients

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Equinus Deformity• Achilles tendon contracture• Increases plantar forefoot

pressure• May increase risk for

ulceration• Present in ~ 40% of high-risk

patients• At 3x greater risk for

presenting with high plantar pressures

Barry DC et al, JAPMA, 1993Grant WP et al, JFAS, 1997Lavery, et al, Arch Intern Med, 1998Lavery, Armstrong, Boulton, JAPMA, 2002

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Equinus Deformity

• Diabetic population study San Antonio, TX n=1666

• 50% male Age ~ 69 yrs• Duration DM 11.1 yrs• VPT ~ 22.5• Equinus Prevalence 10.3%• Peak plantar pressure 86.6

N/cm2

Lavery, Armstrong, Boulton, JAPMA, 2002

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SUMMARY

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Biomechanics of The Diabetic Foot

Biomechanical alterations are a composite function of neuropathy, structural deformity, LJM, and associated gait disturbances

Neuropathy is a primary determinant

Early recognition, intervention, and prevention of deformity with high plantar pressures are crucial to the avoidance of ulceration

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You can observe a lot just by watching

Yogi BerraAmerican Baseball Player and Philosopher

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THANK YOU!

Robert G. Frykberg, DPM, MPHRobert G. Frykberg, DPM, [email protected]@med.va.gov

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