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Diabetic Foot.

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Presentation on theme: "Diabetic Foot."— Presentation transcript:

1 Diabetic Foot

2 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

3 Diabetic Foot Diabetic foot ulcer Diabetic foot infections
Charcot Joints

4 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

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

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

7 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

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

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

10 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

11 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]

12 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.

13 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.

14 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?

15 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?

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

17 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

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

19 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

20 Evaluation of a patient with diabetic foot


22 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

23 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

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

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

26 X rays

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


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

30 Vascular evaluation Invasive evaluation Arteriography MR angiography
CT angiography

31 Classification of Diabetic Foot ulcers

32 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

33 Wanger’s stage 0

34 Wanger’s Stage 0

35 Classification Type 1, type 2

36 Classification Type 3

37 Type 4

38 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

39 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

40 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%

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

42 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

43 Treatment Offloading Debridement Wound dressing Antibiotics
Revascularisation Amputation

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

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

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

47 Treatment Wagner 4-5 Amputation ? level

48 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

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

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

51 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

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

53 Wound care Adjunctive modalities Hyperbaric oxygen Ultrasound therapy
Vacuum assisted closure

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

55 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

56 Charcot Foot

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

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

59 Treatment Immobilisation Stress reduction Bisphosphonates Surgery
Exostectomy Arthodesis

60 Thank you

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