Diabetic Foot

Dr. Narender
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Diabetic Foot
Any foot pathology that results directly from diabetes or its long term complications ( Boulton 2002) The foot of a diabetic patient that has the potential risk of pathologic consequences including infection, ulceration and or destruction of deep tissues associated with neurologic abnormalities, various degrees of peripheral vascular disease and/or metabolic complications of diabetes in the lower limb
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Diabetic Foot
Diabetic foot ulcer Diabetic foot infections Charcot Joints

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Epidemiology
DM is the largest cause of neuropathy 50% patients dont know that they have diabetes Foot ulcerations is most common cause of hospital admissions for Diabetics Expensive to treat, may lead to amputation and need for chronic institutionalized care

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Pathophysiology
Combination of factors
Neuropathy Peripheral arterial disease Abnormal foot biomechanics Delayed wound healing

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Diabetic Neuropathy
Microvascular complication Occlusion of vasa nervosum Can be
Sensory / motor/ autonomic Mono / poly / radiculopathy

Most commonly distal symmetric sensory neuropathy

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Neuropathy
Sensory Neuropathy
Loss of touch and temperature Minor trauma goes unnotices

Disorders of proprioception
Abnormal weight bearing Callus formation, ulceration

Motor and sensory neuropathy

Abnormal foot biomechanics Structural changes
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Neuropathy
Autonomic neuropathy
Anhidrosis in lower limbs Drying of feet Fissure formation

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Altered biomechanics
Abnormal weight bearing Fixed foot deformities
Hammer toe Claw toe Prominent metatarsal heads Charcots joints

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Hammer Toes

Claw Toes

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Hallux Valgus

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Other factors
Impaired wound healing
Does not allow resolution of fissures and minor injuries Increased chances of infection

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Peripheral arterial disease

30 times more prevalent in diabetics Diabetics get arteriosclerosis obliterans or lead pipe arteries Calcification of the media Often increased blood flow with lack of elastic properties of the arterioles Not considered to be a primary cause of foot ulcers
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Causal Pathways for Foot Ulcers

Neuropathy % Causal Pathways Neuropathy: Minor trauma: Deformity: 78% 79% 63%

Deformity

Minor Trauma
- Mechanical (shoes) - Thermal - Chemical

Behavioral

Poor self-foot care

ULCER

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Risk Factors for Diabetic Foot

Male Sex DM > 10 years duration Peripheral neuropathy Abnormal foot structure Peripheral arterial disease Smoking H/O previous ulceration / amputation Poor glycemic control
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EVALUATION OF A PATIENT WITH DIABETIC FOOT

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Examination
Vascular Examination
Palpation of pulses Skin/limb colour changes Presence of edema Temperature gradient Skin changes
Atrothy Abnormal wrinkling Absence of hair Onychodystrophy

Neurological examination
Vibration perception Light pressure Light touch Two point discrimination Pain Temperature perception Deep tendon reflexes Clonus Babinski test Romberg test
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Venous filling time

Examination
Dermatological
Skin appearance Calluses Fissures Nail appearance Hair growth Ulceration/infection/ gangrene Interdigital lesions Tinea pedis Markers of diabetes

Musculoskeletal
Biomechanical abnormalities Structural deformities Prior amputation Restricted joint mobility Tendo Achilles contractures Gait evaluation Muscle group strength testing Plantar pressure assessment
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Investigations
Blood investigation
FBS, PPBS HbA1C Complete blood counts ESR RFT Urinalysis Wound / blood culture
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Imaging
Plain X-rays
Osteomyelitis Fractures Dislocations Osteolysis Structural foot abnormalities Arterial calcification Tissue gas
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X rays

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Vascular evaluation
Non invasive evaluation
Doppler segmental pressure and waveform analysis Ankle brachial pressure index Toe blood pressure Transcutaneous CO2 Laser doppler velocimetry

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Interpretation of ABI
Interpretation ABI Normal 0.90-1.30 Mild obstruction 0.70-0.89 Moderate obstruction 0.40-0.69 Severe obstruction <0.40 Poorly compressible >1.30 2 to medial calcification
*Poor ulcer healing with ABI < 0.50 **Further vascular evaluation needed Page 29

Vascular evaluation
Invasive evaluation
Arteriography MR angiography CT angiography

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CLASSIFICATION OF DIABETIC FOOT ULCERS

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Wagners Classification
0 Intact skin (impending ulcer) 1 superficial 2 deep to tendon or ligament 3 - deep abscess, osteomyelitis 4 gangrene of toes or forefoot 5 gangrene of entire foot

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Wangers stage 0

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Wangers Stage 0

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Classification Type 1, type 2

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Classification Type 3

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Type 4

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Treatment
Prevention
Identification of high risk patients Patient education
Careful selection of foot wear Daily inspection of feet Daily foot hygiene
Keep foot clean, moist

Avoidance of self treatment of foot abnormalities and high risk behavior ( walking barefoot) Prompt consultation with health care provider Orthotic shoes and devices Callus management Nail care
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Identifying at risk patient

History:
Prior amputation or foot ulcer Peripheral artery disease (PAD)

Exam:
Insensate Foot deformities Absent pulses Prolonged venous filling time Reduced ABI Pre-ulcerative cutaneous pathology
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Risk stratification for ulcer risk

Risk Level 3: Prior amputation Prior ulcer 2: Insensate and foot deformity or absent pedal pulses 1: Insensate 0: All normal Foot Ulcer %/yr

28.1% 18.6%

6.3%

4.8% 1.7%

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Treatment
Attention to other risk factors
Smoking Hypertension Dyslipidemia

Glycemic control

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Treatment
Plantar surface of the foot is the most common site Ulcer may be
Primarily neuropathic a/w surrounding cellulitis/ ostemyelitis

Cellulitis without ulceration may occur

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Treatment
Offloading Debridement Wound dressing Antibiotics Revascularisation Amputation

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Treatment
Wagner 0-2
Total contact cast Distributes pressure and allows patients to continue ambulation Principles of application
Changes, Padding, removal

Antibiotics if infected

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Treatment
Wagner 0-2
Surgical if deformity present that will reulcerate
Correct deformity exostectomy

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Treatment
Wagner 3
Excision of infected bone Wound allowed to granulate Grafting (skin or bone) not generally effective

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Treatment
Wagner 4-5
Amputation
? level

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Indications for Amputation

Uncontrollable infection or sepsis Inability to obtain a plantar grade, dry foot that can tolerate weight bearing Non-ambulatory patient Decision not always straightforward

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Treatment
After ulcer healed
Orthopedic shoes with accommodative (custom made insert) Education to prevent recurrence

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Wound Care products

Dressings
Gauze pads Transparent films Hydrogels Foam Hydrocolloid Alginate Collagen dressing Antimicrobial dressings
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Wound care products

Topical agents
Saline Detergents/antiseptics
Povidone iodine Chlorhexidine Hypochlorite

Topical antibiotics
Bacitracin, neomycin Mupirocin, poly B SSD, mafenide Papain urea collagenase

Enzymes

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Wound care products

Growth factors
PDGF VEGF FGF

Autologoud PRP Bioengineered tissues

Apligraft Dermagraft
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Wound care
Adjunctive modalities
Hyperbaric oxygen Ultrasound therapy Vacuum assisted closure

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Charcot Foot
More dramatic less common 1% Severe non-infective bony collapse with secondary ulceration Two theories
Neurotraumatic Neurovascular

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Charcot Foot
Neurotraumatic
Decreased sensation + repetitive trauma = joint and bone collapse

Neurovascular
Increased blood flow increased osteoclast activity osteopenia Bony collapse Glycolization of ligaments brittle and fail Joint collapse

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Charcot Foot

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Classification
Eichenholtz
1 acute inflammatory process
Often mistaken for infection

2 coalescing phase 3 reconstructive

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Classification
Location
Forefoot, midfoot (most common) , hindfoot

Atrophic or hypertrophic
Radiographic finding Little treatment implication

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Treatment
Immobilisation Stress reduction Bisphosphonates Surgery
Exostectomy Arthodesis

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THANK YOU

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