Diabetic Foot

Neuropathic/ neuroischemic foot ulcer leads to 85% of non-traumatic amputation

Pathology:
1) PVD:
- atherosclerosis of medium sized vessels,
- microangiopathy of small & digital vessels,
- skin & nail atrophic changes
- painful ischemic ulcers
2) Peripheral neuropathy:
Prevalence for peripheral neuropathy: 50%, increase with diabetes duration
● Sensory neuropathy (defined as 1/2 + 3/4 or 3+4, from Joint Asia Diabetes Evaluation Program)
○ Sx: [1]Burning sensation, [2]numbness (Gloves and stocking)
○ Light touch: cotton wool
○ Vibration: 128Hz tuning fork
○ Affect proprioception
○ Easy to have skin injury and painless ulcer due to loss of protective sensation
○ Neurothesiometer - [3] vibration sensitivity threshold (VPT)
■ inability to feed 25volts vibration --> 7.7x risk of developing foot ulcer
○ [4]Semmes-Weinstein nylon monofilament: 10g
○ Neurotip: sharp sensation
○ Neuropen: combine 10g monofilament & neurotip in a pen-like device
○ Hot & cold metal rods or water-filled test tubes
○ Tendon reflexes (ankle & knee)
○ Neuropathy symptom score (duration, day/night, site, relieving factors)
○ Neuropathy disability scores (light touch, temp, reflexes, vibration)
● Motor neuropathy
○ Clawed toes with intrinsic muscle wasting due to reduced counteraction against
long flexors; also reduced fullness on dorsum between toes
○ High arched feet - r/o congenital & hypermobile foot
○ ?Altered gait typically show unsteadiness & a high stepping gait ~ a drop foot gait
○ claw/ hammer toe--> distal plantar fat-pad displacement
■ exposure submetatarsal heads to elevated pressure during gait
● Autonomic neuropathy
○ Dry skin (denervation of sweat glands)
○ Strong, easy-to-feel bounding foot pulses (loss of sympath. vasoconstriction)
○ Dilated dosral veins
○ Warm feet
○ Postural hypotension

Classification
1. Low risk foot
2. High risk foot
3. ulcerated foot
 4. cellulitic foot
5. necrotic foot
6. amputated foot

Presentation
1. Ulcers +/- infections
2. Gangrene (dry/ wet)
3. Charcot joint (neuroarthropathy)

1. Foot ulcer
Ulcer depth classification:
Grade I: subcutaneous ulcer
Grade II: ulcer deep to joint capsule or tendon
Grade III: ulcer down to bone or joint

Lifetime foot ulcer risk in diabetes: 15%

● High-risk foot risk factors:
○ Previous ulcers or amputation
○ deranged biomechanics
○ trauma (poor footwear)
○ Neuropathy
○ PVD
○ Low socio-economic status

Factors inhibiting ulcer healing: TIME

1. Non viable tissue
2. Presence of inection of inflammation
3. Moisture imbalanace
4. Failure of Edges or Epithelialisation to take place (in which the germinal layer of
epidermis migrates across the granulation tissue to form a new layer of epidermal cells)

Wound control
1. Surgical debridement (necrotic tissue) +/- skin graft (e.g. free vascularized rectus
abdominal free flap)
2. Biological debridement (maggot??????)
3. Dressings: protect from trauma, absorb exudates, reduce infection
4. Orthotic & shoe-wear care (weight lifting)

DM ulcer + Infection
Clinical diagnosis
Indicators of infection in DM foot ulcers
1. ulcer base yellowish/ grey
2. blue discoloration of surrounding tissues
 3. fluctuance/ crepitus on palpation
4. prurulent exudates
5. sloughing of ulcer and surrounding tissues
6. sinuses with undermined or exposed bone
7. odour
8. wound breakdown
9. delayed healing
Polymicrobial infection
● 3-5 species
● frequently incl. Pseudomonas, peptostreptococcus, bacteriodes, clostridium
Management
1. Microbiological control: wide-spectrum antibiotics, iv for deep infection
2. Wound control: surgical debridement
3. vascular control: revascularization
4. Mechanical control: bed-rest/ non-weight bearing walking
5. metabolic control: hyperglycemia/ DKA
6. Consider immediate hospitlization

2. Diabetic gangrene
The walls of small arteries are infiltrated by polymorphs leading to occlusion of lumen by septic
embolus (EMERGENCY!)
e.g. Deep sepsis and osteomyelitis; septic vasculitis --> big toe necrosis
Dry necrosis
2ry to a severe reduction in arterial blood supply without bacterial infection e.g. acute ischemia,
severe chronic ischemia, embolization
● Open amputation
○ debridement
○ revascularization

Necrotizing fasciitis
● Relatively rare but potentially life-threantening
● More common in diabetic than non-diabetic patients
● Streptococcus pyogenes (GAS), enter body through long-standing chronic wounds
Treated immediately:
● A/B: benzylpenicillin for GAS; clindamycin, gentamicin, MTZ for polymicrobials
● Aggressive debridement +/- skin graft
● ??hyperbaric oxygen

3. Charcot foot
Clinical diagnosis, no specific diagnostic test
● Features
○ hot, erythematous swollen foot
○ after long walking
○ extensive bone destruction
 ○ proper blood circulation
● Not infection
● Common in neuropathy
● Vascular calcification common on X-ray
Treatment:
Immobilization and weight-sparing (takes a long time before inflammatory process settles down)
From acute phase --> quiescent phase: 18 mo, watch out for deformity during this period
(plaster if needed)

Clinical Assessment
● site of ulcer
● underlying bony prominence/ foot deformity
● severity of infection
● peripheral pulse & circulation
● Neuromuscular examination
● Septic?
Investigations
● Blood taking: WBC, ESR, Glu
● Wound swab of ulcers for culture
● XR foot: r/o osteomyelitis
● Doppler USG: assess vascular status

Overall management - Multidisciplinary approach

● Glycaemic & BP control
● Appropriate footwear
● Orthotic prescription
● Risk factors screening, esp. neuropathy, ischemia, deformity
● Patient centered education: ?Home monitoring

● Orthotic prescription:
○ factors to be considered:
■ 1) Deformity: significant if foot shape deviated from normal mechanical
alignment & support (e.g. rigid pes cavus); not significant if minor (hallux
valgus, hammer toes)
● hammer toes: flexion of PIP, hyperextension of MTP & DIP c.f.
mallet toe: flexion of DIP
● Bunion: enlargement of bone or tissue around the joint at the
base of the big toe (metatarsophalangeal joint).The big toe
(hallux) may turn in toward the second toe (angulation), and the
tissues surrounding the joint may be swollen and tender
● Rocker-hammer foot (?Charcot’s foot)
■ 2) Ambulatory status: occupationally active or sedentary?
■ 3) Biochemical analysis: Ankle J, subtalar J, mid-tarsal J, MTRJ to restore
pressure re-distribution
 ■ 4) Neuropathic status: prevent shear & friction force
■ 5) Ischemic status: prevent pressure ischemia
■ 6) Environment: prevent allergy, moisture
○ Foot orthosis materials e.g. high-density plastazole on firm support/ multi-layer
insole with Scaphoid+MT pads & orthotic shoe
■ supportive function
■ accommodation of deformities
■ relieve excessive plantar pressure
■ reduce shear pressure
■ limitation of ROM
■ rocker if necessary
● Role of Home monitoring
○ ulceration on sole if often caused by repetitive trauma at pressure points
○ early identification with hand-held infrared skin thermometer may detect raised
skin temperature

Chronic ischemic foot

● Features
○ Skin & nail atrophic changes: nail dystrophy/ hypokeratotic, shinny/ thin skin,
absent toe hair
○ Cold skin temperature
○ absent pulses
○ ischemic pain
○ ischemic ulcer
○ toes/ foot gangrene
● PVD is more comon in T2DM
● PVD is the single most likely cause of lower extremity amputation
● occurs in a younger age compared with people without diabetes
● Neuroischemia is common (45% of DM foot)
● c.f. Acute limb ischemia:
○ 5’P’s: Pain, paraesthesia, pallor, paralysis, pulselessness
○ Causes::
■ Lower limb trauma --> vessel injury
■ Compartment syndrome
■ Embolization: atrial emboli (AF), AAA, infective emboli
● Vascular assessment
○ Identify symptoms & examine signs of ischemia
○ Palpate pulses (dorsalis pedis, post tibial, popliteal, femoral)
○ Hand-held doppler to locate non-palpated pulses (esp. waveform analysis:
biphasic/ monophasic)
○ Buerger’s test - elevation & dependency
■ also differentiate from infection because redness decreases more in
Charcot foot than septic foot
○ Toe pressure
 ○
ABPI:
■ >1.3 - suggestive of arterial calcification, test results unreliable
■ 0.8-1.3: normal
■ 0.5-0.79: significant arterial disease
■ <0.5: critical limb ischemia
○ Transcutanenous oximetry
● Management
○ Stop smoking, life-style modification
○ Good control of other associated medical co-morbities: HT. DM, IHD
○ Keep lower limbs warm
○ Medical Tx: Aspirin, oxpentifylline (Trental)
○ Development of ulcer/ gangrene: prevention of infection
○ Orthropedic intervention: debridement, amputation for foot ulcer/ gangrene if
conservative treatment failed

Some notes:
Inspection:
● Skin: Healed ulcers with thickened scars & fissure, callus in the plantar surface of midfoot/ chronic ulcer: no
surrounding erythema; changes on plantar surface --> related to foot wear?
● Muscle: clawed toes, reduced fullness on dorsum between toes
● Bone
● Joint: pes cavus (high arched feet that does not flatten with weight bearing), hallux valgus, hammer toes
● Mass
- tight tendon achilles due to glycosylation of collagen
so reduced ROM (Normally dorsiflexion: 25deg, plantarflexion: 35deg
- flex pt’s knee to futher dorsiflex the ankle (because relax gastronecmius)