Diabetic Foot

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

Diabetic Foot Diabetic foot ulcer Diabetic foot infections Charcot Joints

Epidemiology DM is the largest cause of neuropathy 50% patients don’t 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

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

Diabetic Neuropathy Microvascular complication Occlusion of vasa nervosum Can be Sensory / motor/ autonomic Mono / poly / radiculopathy Most commonly distal symmetric sensory neuropathy

Neuropathy Sensory Neuropathy Disorders of proprioception 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

Neuropathy Autonomic neuropathy Anhidrosis in lower limbs Drying of feet Fissure formation

Altered biomechanics Abnormal weight bearing Fixed foot deformities Hammer toe Claw toe Prominent metatarsal heads Charcot’s joints

Hammer Toes Diabetic motor neuropathy leads to atrophy of the intrinsic musculature of the foot with consequent dorsiflexion of the proximal phalanx to form a hammer toe. Dorsiflexion of the middle phalanx and a flexion contracture of the distal phalanx convert the hammer toe into a claw toe. Note the increasingly prominent metatarsal heads with these two deformities. These deformities result in areas of high pressure and subsequent callus formation over the metatarsal head and the tip of the toe when walking, and over the distal end of the proximal phalanx from shoe gear. [PATRICK AND TED: I DO NOT HAVE PERMISSION TO USE THIS DIAGRAM IN A MONOGRAPH THAT IS FOR SALE, AND I DOUBT IT WILL BE GRANTED BY THE AMERICAN DIABETES ASSOCIATION. DO YOU HAVE ARTISTS TO DRAW A SIMILAR PICTURE?] Claw Toes

Hallux Valgus Hallux valgus deformities are more common in persons with diabetes and result in high pressure points from shoe gear at the distal end of the proximal phalanx. [PATRICK AND TED: FROM SAME REFERENCE, NO PERMISSION]

A marked Hallux valgus deformity and early hammer-toe deformities from diabetic motor neuropathy. Note the areas of persistent erythema over pressure points on the first MTP joint and on the dorsum of the proximal phalanges. This patient requires a modification of shoe gear to relieve pressure and prevent callus and ulcer formation.

Severe hammer and claw-toe deformities. There are areas of persistent erythema on the dorsum of the fourth and fifth toes. The consequences of the ill-fitting shoe gear have now progressed to marked callus formation at the peak of the hammer toe deformities on the dorsum of the second and third toes.

Diabetic motor neuropathy has resulted in hammer and claw-toe deformities and very prominent metatarsal heads on the plantar surface of the foot. Excessive pressure on the metatarsal heads and inadequate shoe gear have resulted in marked callus build-up that is further accelerated by the dry skin. The patient is at high risk for ulceration at these sites. Ted: Can we remove background and put neutral color or blue background instead so foot shows up better?

This patient has a pes cavus or high plantar arch deformity that has resulted in pressure points and callus formation over the heels, metatarsal heads, and along the medial aspect of the great toe. Extensive callus increases the subcutaneous pressure immediately beneath the callus and can result in a subcutaneous hemorrhage, the so-called “pre-ulcer.” Note the extensive nail pathology. Ted: Can you provide a color background?

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

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

Causal Pathways for Foot Ulcers Neuropathy % Causal Pathways Neuropathy: 78% Minor trauma: 79% Deformity: 63% Behavioral ?  Deformity  Minor Trauma - Mechanical (shoes) - Thermal - Chemical Poor self-foot care ULCER

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

Evaluation of a patient with diabetic foot

Examination Vascular Examination Neurological examination Palpation of pulses Skin/limb colour changes Presence of edema Temperature gradient Skin changes Atrothy Abnormal wrinkling Absence of hair Onychodystrophy Venous filling time Neurological examination Vibration perception Light pressure Light touch Two point discrimination Pain Temperature perception Deep tendon reflexes Clonus Babinski test Romberg test

Examination Dermatological Musculoskeletal 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

Investigations Blood investigation FBS, PPBS HbA1C Complete blood counts ESR RFT Urinalysis Wound / blood culture

Imaging Plain X-rays Osteomyelitis Fractures Dislocations Osteolysis Structural foot abnormalities Arterial calcification Tissue gas

X rays

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

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

Vascular evaluation Invasive evaluation Arteriography MR angiography CT angiography

Classification of Diabetic Foot ulcers

Wagner’s 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

Wanger’s stage 0

Wanger’s Stage 0

Classification Type 1, type 2

Classification Type 3

Type 4

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

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

Risk stratification for ulcer risk Risk Level Foot Ulcer %/yr 3: Prior amputation Prior ulcer 28.1% 18.6% 2: Insensate and foot deformity or absent pedal pulses 6.3% 1: Insensate 4.8% 0: All normal 1.7%

Treatment Attention to other risk factors Glycemic control Smoking Hypertension Dyslipidemia Glycemic control

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

Treatment Offloading Debridement Wound dressing Antibiotics Revascularisation Amputation

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

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

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

Treatment Wagner 4-5 Amputation ? level

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

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

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

Wound care products Topical agents Saline Detergents/antiseptics Povidone iodine Chlorhexidine Hypochlorite Topical antibiotics Bacitracin, neomycin Mupirocin, poly B SSD, mafenide Enzymes Papain urea collagenase

Wound care products Growth factors Autologoud PRP PDGF VEGF FGF Autologoud PRP Bioengineered tissues Apligraft Dermagraft

Wound care Adjunctive modalities Hyperbaric oxygen Ultrasound therapy Vacuum assisted closure

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

Charcot Foot Neurotraumatic Neurovascular 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

Charcot Foot

Classification Eichenholtz 1 – acute inflammatory process Often mistaken for infection 2 – coalescing phase 3 – reconstructive

Classification Location Atrophic or hypertrophic Forefoot, midfoot (most common) , hindfoot Atrophic or hypertrophic Radiographic finding Little treatment implication

Treatment Immobilisation Stress reduction Bisphosphonates Surgery Exostectomy Arthodesis

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