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Transcript of Dio bh
Bhadra Hamal Orthopaedic Resident NAMS, Bir Hospital
DIABETES IN ORTHOPAEDICS-DIABETIC FOOT
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)
Complications of diabetes
Retinopathy(nonproliferative/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 MUSCULOSKELETAL
DIABETIC FOOT
Ancient Egyptian prostheses of big toe
Lancet 2000;356:2176-79
Risk factors for Diabetic foot
NEUROPATHY
VASCULOPATHY
IMMUNOPATHY
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
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
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
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)
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
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
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
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
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
TOTAL CONTACT CASTING
Removable diabetic boots
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
TREATMENT
OPERATIVE Indications for urgent surgical
intervention -necrotising infections -gangrene -deep abscess-Incision and drainage with thorough
debridement-Complete excision of infected bone
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
CHARCOT ARTHROPATHY
HISTORY Prof Jean-Martin Charcot (1825-1893) French Neurologist and
professor of anatomical pathology
First described in
patient with Tabes dorsalis
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
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
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
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 seen on radiographs.
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
TREATMENT
NONOPERATIVE- Orthotics: custom-molded orthotics
that accommodate the deformity, resist progression
-Total contact casting with protected weight bearing
DRUGSBisphosphonate -may reduce bone turnover in charcot arthropathy and help with pain reliefCalcitonin decrease bone turnover
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
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
REFERENCES
Campbell’s operative orthopaedics-12th edition
Apley’s System of Orthopaedics and Fractures- 9th edition
Review of orthopaedics ,Miller-6th edition
Internet