1362405083 diabetic neuropathy

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Diabetic Neuropathy in the Context of Diabetic Foot

Podiatry Workshop Kuala Lumpur 18 – 19 November 2K

Dr.Ashok Kumar DasDean, Director, Prof. and Head Dept. of Medicine, JIPMERPondicherry

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Diabetic Neuropathy in the Context of Diabetic Foot - 2

DFU - cause for more amputation than anyother pathology. Is it inevitable?

St. Vincent’s and Health 21 WHO Declarationhave called for reduction in amputation indiabetic foot.

Most contemporary and challenging issue

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“5-10% of all diabetic patients have foot ulceration of various degrees and about 1% undergo amputation”

“Diabetes accounts for upto 50% of non traumatic leg amputations”

“Of all the diabetic amputees about 50% will lose their life or their other leg by 3 years”

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Diabetic Neuropathy in the Context of Diabetic Foot

Foot ulcers result in *Morbidity * Mortality “Enormous health care expenditure” “Psychosocial problems”Paucity of data regarding prevalence of diabetic foot in India

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Neuropathy that is significant enough to cause foot ulceration may affect 40% of diabetic population especially elderly with type 2 diabetes.

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Indian Patients

Our major problem is neuropathic ulcer85 - 95 %, 10 – 15% vascular.

-younger patients -mean age of amputation earlier- number of amputations for

neuropathic ulcer

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Indian Context

Eminently preventableAmputation in a diabetic neuropathiculcer is deplorableNeed of the hour * Awareness/ education * Early identification of a high risk foot and its appropriate management

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Components of neuropathic foot transforming to diabetic foot - 1

A. Ulcerative diabetic neuropathic foot components

B. Non-ulcerative neuropathic pathologies in diabetic foot

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A. Components of ulcerative diabetic neuropathic foot - 2

1. Neuropathic foot and Neuroischaemic foot

2. Neuropathic foot deformitiesa. Clawed toesb. Pes cavusc. Hallux rigidus and valgusd. Hammer toee. Nail deformitiesf. Charcot foot

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A. Components of ulcerative diabetic neuropathic foot - 3

3. Neuropathic callus4. Neuropathic oedema5. Neuropathic ulcers

a. Callus ulcers b. Ulcer over the pressure

points on the solec. Decubitus ulcersd. Puncture wound ulcerse. Traumatic ulcers

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B. Non-ulcerative neuropathic pathologies in diabetic foot

1. Charcot FootAcute, chronic bone destruction

anddeformed diabetic foot and toes

2. Pathological fractures3. Diabetic painful neuropathy

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DN in context of diabetic foot - 1

Our job – look after “NDF at risk”A: Preventive measures

Treatment rapid and intensiveRestOff loadAntibioticsFoot wearPatient education

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DN in context of diabetic foot - 2

B. Metabolic control Hyperglycemia Hypertension Hyperlipidaemia Cessation of smoking

C. Deformity managementD. Callus managementE. Debridement and dry skin and fissure management

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DN in context of diabetic foot - 3F. Mechanical control

Off load, Off load, Off loadby rest, crutches, walkers, protective shoes,

heel protective pad, decrease plantar pressure by removal callus

G. The importance of callus removal in NFUdecrease plantar pressureknow full dimension of the ulcerdeep swabdrainage of exudate, removal of dead tissue

H. Infection controlI. Educational control

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Diabetic neuropathy Scope of the syndrome - 1

Three components of neuropathy: *sensory – painful, painless

*Motor*AutonomicAll contribute to diabetic foot ulcerationAsymptomatic neuropathy 35%

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Diffuse1. Distal symmetric sensorimotor polyneuropathy2. Autonomic neuropathy A.Sudomotor B.Cardiovascular C.Gastrointestinal D.Genitourinary

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Focal1.Cranial neuropathy2.Radiculopathy/plexopathy3.Entrapment neuropathy4.Asymmetric lower limb motor neuropathy- Diabetic amyotrophy

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Rather than acting in isolation neuropathyexerts

Its vicious effects in concert withangiopathy + immunopathy leading toinfections

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Neuropathic foot components

Neuropathic ulcer

Neuropathic joint

Neuropathic oedema

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Diabetic foot – Mechanisms - 1

Loss of pain sensation results inneuropathic injury due torepeated unrecognised traumainflicted in many different ways

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Loss of joint positon sense results in abnormal foot postureThis may lead to injury when the shoes are not properly selectedor during walking

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Motor Neuropathy* Weakness* Wasting of small intrinsic muscles of foot *Imbalance between the flexor and

extensor muscles

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Intrinsic deformity

Clawing of the toes Prominence of metatarsal headsFlattening of the arch

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Abnormal distribution of body weightWeight gets concentrated on smallerareas like metatarsal head and the heel.

Excess pressure loading of these areasfinally results in callus formation.

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Body weight in patients with plantar ulcerswas significantly greater than in thosewith neuropathy but no ulcer.

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Autonomic neuropathy - 1

* Damages the sympathetic innervation of lower limb

* This results in Decreased sweatingResults in dry skin fissures /

cracks Super added infection

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Autonomic neuropathy - 2

Opening of arteriovenous channels Warm skin ( misleadingly healthy )

Shunting of nutrients and oxygen fromthe tissues

Impaired vascular response to infection

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Autonomic neuropathyclassical signs

Dry skin with fissuring

Distended veins over the dorsum of footand the ankle

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Connective tissue changes

Hyperglycemia causes non enzymaticglycation of collagen and keratin Increase in cross linking Become rigid and inflexibleTissue break down in places where thereis high horizontal shear force

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Neuropathic ulcer

* Painless* Develops on pressure points (metatarsal

heads/heel)* Pulsations intact unless superadded

ischaemia is also present* Decrease in pain / temperature as also in the vibration perception * Punched out ulcer surrounded by callus

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Neuropathic (n) /Ischemic ulcer (i)

Site Pressure points (n) Sides / tips of toes (i)Pain --- ( n ) +++ ( i )Callus ++ ( n ) --- ( i )Pulse ++ ( n ) --- ( i )Abi > 1 ( n ) < .6 ( i )Healing ++ ( n ) --- ( i )

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Quantitative tests for neuropathic assessement - 1

1. Measurement of light touch sensation - Nylon monofilament (Semmes Weinstein)2. Measurement of thermal sensitivity - Marstock Thermode

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The advantage of the assessment with monofilaments or biosthesiometry is the detection of whether the patient has lost protective pain sensation that would render him susceptible to foot ulceration.

Nylon monofilaments test the threshold to pressure sensation

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Monofilament: This is a simple technique.When applied perpendicular to the foot itbuckles at a force of 10 gms

Areas to be tested include plantar aspectof big toe metatarsal heads of first, thirdand fifth and the plantar surface of heel.

Filament not to be applied over the callus

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Quantitative tests forneuropathic assessement - 4

1. Measurement of vibration *Biosthesiometer *Graduated tuning fork

2. Nerve conduction studies

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Management of Neuropathic Ulcer - 1

General measures

Specific measures

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Good glycemic control

Treatment of infections

Management of neuropathic oedema

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Management of Neuropathic Ulcer - 3All ulcers irrespective of their cause will

be slow to heal in presence of oedema, due impairment of local flow

Neuropathic oedema can be treated with DiureticsAce inhibitors Ephedrine ( 30 mg tds )D/d hypo albuminemia cardiac failure

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“Over 90% of predominantly neuropathiculcers will heal satisfactorily withconservative measures”

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“Key to the management is the relief ofpressure that caused the initial lesion”Pressure is off loaded most effectively byencasing the foot in a light plaster of pariscast.

*Total contact cast*Removable scotch cast boot, custom

made shoes etc.

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Preventing Neuropathic Foot Ulcers - 1

Regular inspection of foot - annuallyIdentification of high risk feet – 3 mo /

6moCareful choice of foot wearRegular chiropodyIntense education

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Preventing neuropathic foot ulcers - 2

“As little as one hour’s education provided by the podiatrist resulted in 70% reduction in amputations over the following 2 years . as compared with a control group who did not receive the advice”

Malone IM et al 1989

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Glycemic control and diabetic neuropathy

Diabetes control and complication trialshowed that intensive insulin therapyreduced the incidence of appearance of neuropathy by about 70%

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Intensive insulin treatment

Reduced the clinical appearance of overtneuropathy in patients with subclinicalneuropathy from 16% to 7% (57%reduction)

Reduced the risk of developing clinicallyovert diabetic neuropathy by 60% over fiveyears

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Neuropathic joint or Charcot arthropathy - 1

1868 French neurologist I.M. Charcot First described in tabesCan also be seen in leprosy, syringomyelia, hereditary sensory neuropathy, Charcot Marie Tooth disease etc

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Relatively rare Potentially devastating disorderLong standing diabetesDense peripheral neuropathyPeripheral vascular disease is typicallyabsent

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Sympathetic failure-- increased bloodflow due to arteriovenous anastomosis

Bone demineralisation (diabeticosteopenia)

Susceptibility to minor, recurrent fractures

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Painless disintegration of bone inresponse to trivial traumaCommon joints involved are

Tarso metatarsalMetatarso phalangealAnkle jointKnee joint

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Acute Charcot arthropathy may mimic infection

Chronic Charcot foot is classically described as ‘bag of bones’

(Gross destruction of joint surfaces and bone with effusion which is typically painless)

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Differentiation from osteomyelitis isdifficult* TC 99 Scan* Indium labelled white cell scan* MRI

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Early diagnosis and intervention are important to prevent deformity and loss of function

Treatment includes *long term immobilisation in a plaster of Paris

cast (for upto 1 year)*Charcot Restraint Orthotic Walker (crow) which

allows pressure to be off loaded *Pamidronate - tried as a new treatment of Charcot arthropathy

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Newer (experimental) measures for treating neuropathy are

Aldose reductase inhibitorsGamma linolenic acid Vasodialators (ace inhibitors /ca 2+ channel blockers)AminoguanidineNerve growth factors

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Management involves

Bed restPressure offloadingReduction of oedemaGlycemic controlMost important step is the early detectionof a high risk foot by simple tests / fewquantitative tests

1362405083 diabetic neuropathy

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