Diabetics in Orthopedics

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  • 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
  • 4. DIABETIC FOOT Ancient Egyptian prostheses of big toe Lancet 2000;356:2176-79
  • 5. Risk factors for Diabetic foot NEUROPATHY VASCULOPATHY IMMUNOPATHY
  • 6. 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
  • 7. 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
  • 8. 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
  • 9. 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)
  • 10. 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
  • 11. 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
  • 12. 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
  • 13. 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
  • 14. 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
  • 15. TOTAL CONTACT CASTING
  • 16. Removable diabetic boots
  • 17. 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
  • 18. TREATMENT OPERATIVE Indications for urgent surgical intervention -necrotising infections -gangrene -deep abscess -Incision and drainage with thorough debridement -Complete excision of infected bone
  • 19. 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
  • 20. CHARCOT ARTHROPATHY HISTORY Prof Jean-Martin Charcot (1825-1893) French Neurologist and professor of anatomical pathology First described in patient with Tabes
  • 21. 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
  • 22. Clinical Features Foot swelling Redness Numbness Pain not a chief complaint (if present, less than expected) CRT usually normal Infected charcots joint warm & red
  • 23. 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
  • 24. 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
  • 25. 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
  • 26. 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
  • 27. 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
  • 28. TREATMENT EXOSTECTOMY-remove bony prominences causing ulceration. It should be done only if it doesnt lead to further instability ARTHRODESIS-indicated for deformity correction and for instability AMPUTATION- last resort
  • 29. REFERENCES Campbells operative orthopaedics-12th edition Apleys System of Orthopaedics and Fractures- 9th edition Review of orthopaedics ,Miller-6th edition Internet