1. Bhadra Hamal
Orthopaedic
Resident
NAMS, Bir Hospital
DIABETES IN
ORTHOPAEDICS-DIABETIC
FOOT

2.  Diabetes mellitus-
refers to a group of common metabolic
disorders that share the phenotype of
hyperglycemia
Diagnosed by symptoms of diabetes and a two
hour plasma glucose >11.1mmol/l
(200mg/dl)and a fasting glucose>7.0mmol/l
(126mg/dl)(WHO criteria)

3. Complications of diabetes
 Retinopathy(nonproliferat
ive/proliferative)
Macular edema
 Neuropathy Sensory
and motor (mono- and
polyneuropathy)
 Autonomic Nephropathy
 Angiopathy:
 Coronary artery disease
 Peripheral arterial
disease
 Cerebrovascular disease
 Gastrointestinal
(gastroparesis,
diarrhea)
 Genitourinary
(uropathy/sexual
dysfunction)
 Dermatologic
 Infections
 Cataracts
 Glaucoma
 Periodontal disease
 MUSCULOSKELE
TAL

5. DIABETIC FOOT
 Ancient Egyptian
prostheses of big
toe
 Lancet
2000;356:2176-79

6. Risk factors for Diabetic foot
 NEUROPATHY
 VASCULOPATHY
 IMMUNOPATHY

7. NEUROPATHY
 Different metabolic pathways activated by
excess glucose- reactive oxygen
species(ROS) ie, nitric oxide, hydrogen
peroxide, advanced glycosylation end
products such as HbA1c
 ROS cause damage by causing nerve
ischemia affecting protein and cell lipids and
injuring nuclear material leading to increased
apoptosis

8.  Advanced glycosylation end products, by
binding cellular receptors decrease the cells
ability to detoxify itself
 Nerve myelinization can be affected, along
with injury to nerve ion channel which
decrease conduction velocity
 Microvascular disease also damage nerves

9.  When large sensory fibres are affected protective
sensation can be lost
 Small fibres afferent neuropathy can lead to
increased pain generation
 Motor neuropathy can cause claw toes –
ulcerations over bony prominences
 When sympathetic nervous system is affected
,skin becomes dry and scaly-cracks in skin-
invasion by bacteria

10. VASCULOPATHY
 Advanced glycosylation end products can
damage vascular endothelium leading to
microthrombosis and capillary obstruction,also
increase LDL which cause atherosclerosis
 Vascular tone loss due to Reactive oxygen
species(ROS)

11. IMMUNOPATHY
 Defects in leucocyte response to infection
ie,problems with chemotaxis, adherence,
impaired fibroblast proliferation,
phagocytosis,and intracellular killing
 Impaired growth factor
80% increased risk of cellulitis
Four fold risk of osteomyelitis
Double risk of sepsis and death from infection

12.  DELAYED BONE HEALING
 Collagen synthesis is decreased
 Biomechanical strength of fracture callus is
lower in diabetics
 Decreased cellular proliferation at fracture site
and decreased mechanical stiffness

13. DIABETIC ULCER
PATHOPHYSIOLOGY
 Sensory neuropathy- loss of sensation
 Motor neuropathy- claw toes bony
prominences make skin vulnerable to
breakdown
 Achillies contracture-(due to disorganisation
of tendon fibres and calcification within
tendon) increased forefoot pressure
forefoot ulceration
 Peripheral arterial disease- ischemia

14. Wagner classification
 Grade 0- skin at risk
 Grade 1- superficial ulcer
 Grade 2- exposed tendon and deep structures
 Grade 3-deep ulcer with abscess or osteomyelitis
 Grade 4-partial gangrene
 Grade 5- more extensive gangrene

17. TREATMENT
 NONOPERATIVE
TOTAL CONTACT CASTING (TCC) is the standard
of care because it reduces plantar loads better
than a well molded shoe cast
GOAL of total contact casting is the relief of
pressure by distributing stresses over a large
surface area

18. TOTAL CONTACT CASTING

20.  Removable diabetic boots

21. TREATMENT
 Negative pressure wound treatment with vacuum
assisted closure
 Hyperbaric oxygen treatment
overall healing rate 76% compared with 48% without
the use of it
 Extracorporeal shockwave treatment
helpful for healing of chronic ulcer
 Antibiotic treatment-if infected
deep culture obtained after debridement; superficial
swab often yield contaminants

22. TREATMENT
 OPERATIVE
 Indications for urgent surgical intervention
-necrotising infections
-gangrene
-deep abscess
-Incision and drainage with thorough
debridement
-Complete excision of infected bone

23. TREATMENT
 Osteomyelitis of metatarsal head
-metatarsal head resection
 If osteomyelitis involve more than metatarsal
head
-ray resection
 Osteomyelitis of calcaneum secondary to ulcer
-partial calcanectomy
 Achilles lenghtening
-to decrese plantar pressure

24. CHARCOT ARTHROPATHY
 HISTORY
Prof Jean-Martin
Charcot
(1825-1893)
French Neurologist and
professor of anatomical
pathology
First described in
patient with Tabes

25. CHARCOT ARTHROPATHY
 Diabetes – most common cause
 Others - syphilis, syringomyelia, alcoholism,
stroke, congenital insensitivity to pain, spinal cord
or peripheral nerve injury, and spina bifida
 Loss of autonomic control of the vasculature 
High resting blood flow  Osteopenia, combined
with somatosensory loss of pain and
proprioception  multiple small mechanical
insults unrecognized by the patient which set the
stage for bony dissolution and loss of structural
integrity, followed by a collapse deformity

27. Clinical Features
 Foot swelling
 Redness
 Numbness
 Pain – not a chief complaint (if present, less
than expected)
 CRT – usually normal
 Infected charcot’s joint – warm & red

28.  Radiographs
Early neuropathic arthropathy – joint widening
and stress fractures
Progressive and late stages – further
destruction and multiple joint involvement are
seen.
 Technetium bone scan is positive

30. CLASSIFICATION-EICHENHOLTZ
“I CAN HOLDS”
Stage 0: No radiographic changes, marked warmth and swelling
after injury
Stage 1: Fragmentation. Erythema, warmth and swelling
of the extremity, with subluxation/dislocation of joints
and bony debris and fragmentation of subchondral
bone.
Stage 2: Coalescence. Decreased erythema, warmth and
swelling of the extremity, with absorption of fine debris,
new bone formation, and coalescence of larger
fragments.
Stage 3: Consolidation. Resolution of swelling; however,
residual deformity is present, with remodeling of bone

31. Anatomical classification-
BRODSKY
 Type 1: Involvement of the
tarsometatarsal joints.
 Type 2: Involvement of the Chopart
and subtalar joints.
 Type 3A: involvement of the ankle
 Type 3B: involvement of the calcaneus
 Type 4 :involvement of multiple regions
 Type 5: involvement of forefoot

32. TREATMENT
 NONOPERATIVE
- Orthotics: custom-molded orthotics
that accommodate the deformity, resist
progression
-Total contact casting with protected
weight bearing
DRUGS
Bisphosphonate
-may reduce bone turnover in charcot
arthropathy and help with pain relief
Calcitonin
decrease bone turnover

33.  OPERATIVE
-surgery required for approx
25% patients with charcots
arthropathy
GOAL
-Deformity correction and
stabilisation to create/maintain
a braceable, infection free foot
and ankle

34. TREATMENT
 EXOSTECTOMY-remove bony prominences
causing ulceration. It should be done only if it
doesn’t lead to further instability
 ARTHRODESIS-indicated for deformity
correction and for instability
 AMPUTATION- last resort

35. REFERENCES
 Campbell’s operative orthopaedics-12th edition
 Apley’s System of Orthopaedics and Fractures- 9th
edition
 Review of orthopaedics ,Miller-6th edition
 Internet