RENAL OSTEODYSTROPHY - DNB Orthopaedics MS Orthopedics MRCS Exam GUIDE - Orthodnb.com

DNB Orthopaedics  MS Orthopedics  MRCS Exam GUIDE - Orthodnb.com

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Wednesday 14 November 2018

RENAL OSTEODYSTROPHY

RENAL OSTEODYSTROPHY



  • comprises a continuum of diseases ranging from low turn over bone disease like osteomalacia – to high turn over disease like 20hyperparathyroidism
Pathology
  • renal disease – PTH -Vit D axis is deranged – hydroxylation to form 1,25 dihydroxy VitD decreased – impairs calcium absorption in gut – increased calcium excretion – hypocalcemia – effect of PTH on kidney decreased
  • impaired renal clearance – hyperphosphatemia
High turnover form
  • hyperphosphatemia – secondary hyperparathyroidism – increase bone resorption
  • osteitis fibrosa – fibrous tissue accumulates in bone
  • osteoblast activity increases – osteoid is woven – increased turnover
  • bone pain, brown tumors, ulcers
  • classic salt and pepper skull, soft tissue calcification, osteopenia next to osteosclerosis, erosions of phalangeal tuft, distal clavicle
  • children – metaphyseal and epiphyseal changes – rickets like
  • unlike rickets – premature genu valgum, SCFE common
  • epiphyseal slippage also in distal femoral or proximal tibial
Low turnover form
  • due to Al toxicity in aluminum contaminated water in dialysis
  • also Al in phosphate binders to prevent hyperphosphatemia and 20hyperparathyroidism
  • Al deposited along mineralization front – impair calcification of osteoid – decrease in number of osteoblasts
  • histologically – excessive osteoid (unmineralized collagen)
  • prevented by use of CaCO- to buffer high phosphate in blood
Symptoms
  • patients rarely have one extreme form of disease – mixed pattern is common
  • bone pain, muscle weakness, skeletal deformities, ectopic calcification, growth retardation
  • ectopic calcification – more in adults - periarticular
  • skeletal deformities – children both axial and appendicular – adult mostly axial esp. in Al toxicity
  • children up to 4yrs – resembles Vit D deff rickets
  • 4- 10yrs – bowing of tibia and femur, genu valgum, SCFE
Amyloidosis
  • complication of long term renal disease
  • CTS most common presenting syndrome
  • pathologic fracture
  • scapulohumeral periarthritis
  • arthritis of MCP, IP, shoulder, hand, wrist, knee
  • bone cysts – femoral head, acetabulam, humerus, radius, carpal bone, tibial plateau, pubis – resembles brown tumor
  • no adequate treatment options
Treatment
  • primary treatment of renal osteodystrophy – restriction of phosphorous intake in diet to 400-800 mg/day
  • PO4 binding antacids
  • Calcium supplements as CaCO3 – increases available Ca for absorption and also act as PO4 binders
  • Ca supplements given only when PO serum level fall to 6.5mg/dl – to minimize risk of extra skeletal calcification
  • Vit D derivatives – Oral calcitriol (0.25 to 1.5microgm/day) – improve muscle strength, decrease bone pain, growth increase in ureamic children – risk of hypercalcemia
  • 20 hyperparathyroidism – surgery – in case of persistent hypercalcemia, intractable pruritus, progressive ectopic calcification, severe skeletal pain/ fractures
  • Al toxicity – chelator deferoxamine – only in symptomatic Al toxicity cases
  • Pinning for SCFE
  • bracing or osteotomy in bowing of long bones
  • pseudofractures causing bone pain – weight restriction and analgesics
  • rule out fractures – treat fractures accordingly
  • surgery for CTS
  • Arthroplasty only cemented – high incidence of prosthesis loosening
  • surgery planning – r/o clotting abnormalities, anemia, arteriovenous fistula, infections

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