Diabetic Foot

A dry, scaly, swollen, clumsy limb that the patient dissociates from the rest of the body because of the loss of sensory feedback

Pathophysiology

• Breakdown of the skin
• Stems from diminished sensation from neuropathic disease
• Trauma from unappreciated local stress on feet
• Autonomic neuropathy dries and cracks skin, exposing to infection
• Autonomic neuropathy impedes normal reactive hyperemia
• Motor neuropathy affects intrinsic muscles leading to deformities and bony prominences which predispose to ulceration

Exacerbated by diabetic co-morbid conditions:

• Peripheral atherosclerosis impedes oxygen delivery to distal tissue
• Compromised microvasculature diminish likelihood of wound helaing
• Nephropathy leading to peripheral edema, stasis
• Retinopathy causing inability to see and care for feet

Physical Exam:

• Inspection of skin, hair growth, perfusion, pulses, color
• Bony prominences
• Metatarsal heads
• Dorsum of proximal interphalangeal joints
• Medial arch in Charcot foot (see below)
• Neurologic exam
• Light touch, Pin-prick, Vibration, Proprioception

Vascular exam:

• Palpation of pulses
• Determination of Ischemic Index
• Brachial artery blood pressure ¸ dorsalis pedis and posterior tibial arteries blood pressure
• Normal = 1, Index >0.45 – 90% of ulcers will heal
• Limitation of Ischemic Index is inability to determine pressure calcified and sclerotic lower extremity vessels

Grade 3 Ulcer, exposed metatarsal head, presumed osteomyelitis	Early neuropathic arthropathy with dislocation of first and second metatarsocuneiform articulations, but without significant bony

Treatment of diabetic ulcers:

A multidisciplinary team approach to treatment is crucial, involving a dietician, endocrinologist, infectious disease specialist, vascular surgeon, orthopaedic surgeon, diabetic nursing specialist, orthotist, prosthetist, and podiatrist

Dependent on determining if the ulcer is:

• primarily neurotrophic or ischemic
• localized or heralds a deep abscess
• osteomyelitis or pyarthrosis is absent or present

Neuropathic Arthropathy – Charcot Foot

Etiology:

** Diabetes

Also - Hansen Disease, Neurosyphiis, Paraplegia, Alcoholism, Syringolmelia, Myelodysplasia

Hypothesized Pathophysiology:

1. Loss of autonomic control of vasculature

Increased blood flow 5 times normal

Results in osteopenia

2. Combined with somatic sensory loss of pain and proprioception

3. Minor injury (often unnoticed) with resulting localized warmth and swelling out of proportion to injury

4. Eventual bony dissolution and loss of structural integrity, collapse deformity

A & B, Acute inflammatory stage: swelling and loss of arch, warm, dry, and nontender and had midfoot crepitance. C, dissolution of bone at Lisfranc articulation. D profound collapse deformity. E and F, 3 years later.

Treatment:

Inflammatory stage:

• Characterized by acute, warm, swollen foot
• Immobilization is key
• Non-weightbearing cast until all signs of inflammation resolve

(Often inflammatory stage progresses to collapse deformity prior to presentation)

Early deformity:

• Subluxation of tarsometatarsal joint without significant soft-tissue or bony destruction
• Closed, percutaneous pinning or open reduction internal fixation (vs arthrodesis) followed by cast immobilization and non-weightbearing
• Late deformity:
  Padding of bony prominences, custom orthothotics,