Download to read offline
Uploaded byRem Kulung
Dio bh
This document discusses diabetes and its effects on the orthopedic system, with a focus on the diabetic foot. It covers the pathophysiology of diabetes and how it can lead to complications like neuropathy, vasculopathy, and immunopathy. These complications increase the risk of issues like diabetic foot ulcers and Charcot arthropathy. The document outlines treatments for various conditions like total contact casting, antibiotics, and surgery. It also describes classifications of diabetic foot ulcers and Charcot arthropathy to help guide treatment decisions.
More Related Content
Dio bh
- 1. Bhadra Hamal Orthopaedic Resident NAMS, BirHospital DIABETES IN ORTHOPAEDICS-DIABETIC FOOT
- 2. ď¨ Diabetes mellitus- refersto 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 ď¨Retinopathy(nonproliferat ive/proliferative) Macular edema ď¨ Neuropathy Sensory and motor (mono- and polyneuropathy) ď¨ Autonomic Nephropathy ď¨ Angiopathy: ď¨ Coronary artery disease ď¨ Peripheral arterial disease ď¨ Cerebrovascular disease ď¨ Gastrointestinal (gastroparesis, diarrhea) ď¨ Genitourinary (uropathy/sexual dysfunction) ď¨ Dermatologic ď¨ Infections ď¨ Cataracts ď¨ Glaucoma ď¨ Periodontal disease ď¨ MUSCULOSKELE TAL
- 5. DIABETIC FOOT ď¨ AncientEgyptian prostheses of big toe ď¨ Lancet 2000;356:2176-79
- 6. Risk factors forDiabetic foot ď¨ NEUROPATHY ď¨ VASCULOPATHY ď¨ IMMUNOPATHY
- 7. NEUROPATHY ď¨ Different metabolicpathways activated by excess glucose- reactive oxygen species(ROS) ie, nitric oxide, hydrogen peroxide, advanced glycosylation end products such as HbA1c ď¨ ROS cause damage by causing nerve ischemia affecting protein and cell lipids and injuring nuclear material leading to increased apoptosis
- 8. ď¨ Advanced glycosylationend products, by binding cellular receptors decrease the cells ability to detoxify itself ď¨ Nerve myelinization can be affected, along with injury to nerve ion channel which decrease conduction velocity ď¨ Microvascular disease also damage nerves
- 9. ď¨ When largesensory fibres are affected protective sensation can be lost ď¨ Small fibres afferent neuropathy can lead to increased pain generation ď¨ Motor neuropathy can cause claw toes â ulcerations over bony prominences ď¨ When sympathetic nervous system is affected ,skin becomes dry and scaly-cracks in skin- invasion by bacteria
- 10. VASCULOPATHY ď¨ Advanced glycosylationend products can damage vascular endothelium leading to microthrombosis and capillary obstruction,also increase LDL which cause atherosclerosis ď¨ Vascular tone loss due to Reactive oxygen species(ROS)
- 11. IMMUNOPATHY ď¨ Defects inleucocyte response to infection ie,problems with chemotaxis, adherence, impaired fibroblast proliferation, phagocytosis,and intracellular killing ď¨ Impaired growth factor 80% increased risk of cellulitis Four fold risk of osteomyelitis Double risk of sepsis and death from infection
- 12. ď¨ DELAYED BONEHEALING ď¨ Collagen synthesis is decreased ď¨ Biomechanical strength of fracture callus is lower in diabetics ď¨ Decreased cellular proliferation at fracture site and decreased mechanical stiffness
- 13. DIABETIC ULCER PATHOPHYSIOLOGY ď¨ Sensoryneuropathy- loss of sensation ď¨ Motor neuropathy- claw toes bony prominences make skin vulnerable to breakdown ď¨ Achillies contracture-(due to disorganisation of tendon fibres and calcification within tendon) increased forefoot pressure forefoot ulceration ď¨ Peripheral arterial disease- ischemia
- 14. Wagner classification ď¨ Grade0- skin at risk ď¨ Grade 1- superficial ulcer ď¨ Grade 2- exposed tendon and deep structures ď¨ Grade 3-deep ulcer with abscess or osteomyelitis ď¨ Grade 4-partial gangrene ď¨ Grade 5- more extensive gangrene
- 17. TREATMENT ď¨ NONOPERATIVE TOTAL CONTACTCASTING (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.
- 20.
- 21. TREATMENT ď¨ Negative pressurewound treatment with vacuum assisted closure ď¨ Hyperbaric oxygen treatment overall healing rate 76% compared with 48% without the use of it ď¨ Extracorporeal shockwave treatment helpful for healing of chronic ulcer ď¨ Antibiotic treatment-if infected deep culture obtained after debridement; superficial swab often yield contaminants
- 22. TREATMENT ď¨ OPERATIVE ď¨ Indicationsfor urgent surgical intervention -necrotising infections -gangrene -deep abscess -Incision and drainage with thorough debridement -Complete excision of infected bone
- 23. TREATMENT ď¨ Osteomyelitis ofmetatarsal head -metatarsal head resection ď¨ If osteomyelitis involve more than metatarsal head -ray resection ď¨ Osteomyelitis of calcaneum secondary to ulcer -partial calcanectomy ď¨ Achilles lenghtening -to decrese plantar pressure
- 24. CHARCOT ARTHROPATHY ď¨ HISTORY ProfJean-Martin Charcot (1825-1893) French Neurologist and professor of anatomical pathology First described in patient with Tabes
- 25. CHARCOT ARTHROPATHY ď¨ Diabetesâ most common cause ď¨ Others - syphilis, syringomyelia, alcoholism, stroke, congenital insensitivity to pain, spinal cord or peripheral nerve injury, and spina bifida ď¨ Loss of autonomic control of the vasculature ďŽ High resting blood flow ďŽ Osteopenia, combined with somatosensory loss of pain and proprioception ďŽ 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 ď¨ Footswelling ď¨ Redness ď¨ Numbness ď¨ Pain â not a chief complaint (if present, less than expected) ď¨ CRT â usually normal ď¨ Infected charcotâs joint â warm & red
- 28. ď¨ Radiographs ď¤ Earlyneuropathic arthropathy â joint widening and stress fractures ď¤ Progressive and late stages â further destruction and multiple joint involvement are seen. ď¨ Technetium bone scan is positive
- 30. CLASSIFICATION-EICHENHOLTZ âI CAN HOLDSâ Stage0: 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
- 32. Anatomical classification- BRODSKY ď¨ Type1: Involvement of the tarsometatarsal joints. ď¨ Type 2: Involvement of the Chopart and subtalar joints. ď¨ Type 3A: involvement of the ankle ď¨ Type 3B: involvement of the calcaneus ď¨ Type 4 :involvement of multiple regions ď¨ Type 5: involvement of forefoot
- 33. TREATMENT ď¨ 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
- 34. ď¨ OPERATIVE -surgery requiredfor approx 25% patients with charcots arthropathy GOAL -Deformity correction and stabilisation to create/maintain a braceable, infection free foot and ankle
- 35. TREATMENT ď¨ EXOSTECTOMY-remove bonyprominences causing ulceration. It should be done only if it doesnât lead to further instability ď¨ ARTHRODESIS-indicated for deformity correction and for instability ď¨ AMPUTATION- last resort
- 36. REFERENCES ď¨ Campbellâs operativeorthopaedics-12th edition ď¨ Apleyâs System of Orthopaedics and Fractures- 9th edition ď¨ Review of orthopaedics ,Miller-6th edition ď¨ Internet
Editor's Notes
- #33Â type 1:This is the most common type and often leads to the rocker-bottom deformity and plantar ulcerations secondary to bony prominences in this area. Type 2:The second most common affected area, type 2 involvement also can lead to a rocker-bottom deformity with plantar flexion of the talar head. Marked varus/valgus of the hindfoot also can develop.