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