218 - Fractured hip Flashcards
what is an intracapsular hip fracture?
proximal to intertrochanteric line
- femoral head fracture - rare hip dislocations in young
- femoral neck fractures - associated with osteoporosis/malacia in elderly can lead to avascular necrosis of femur head (medial & lateral curcumflex arteries). classification I - incomplete, II - impacted (complete, not displaced), III - partially displaced, IV - completely displaced or comminuted (shattered)
what is an extracapsular hip fracture?
involving or distal to intertrochanteric line (TyI non-displaced, TyII displaced
- trochanteric - avulsion of greater/lesser trochanter from femur by muscle in children & young athletes
- intertrochanteric - elderly & women with osteoporosis
- Subtroachanteric - young adults in high energy trauma & elderly in falls with osteoporosis
what is FRAX scoring?
10 year fracture risk assessment
what is total hip replacement?
For intracapsular fractures - acetabulum replaced, cartilage removed, femur head prosthesis inserted into reshaped femur with cement. FOr sever comminution & severely degenerated joints
what is hemiarthroplasty?
most common for intracapsular fractures - acetabulum kept, head of femur removed and replaced with prosthesis. For patients where risk of AVN is high & older patients who are too unwell for 2nd op
how is pinning/canulated screws used in hip fracture?
multiple pins/screws drilled across fracture to hold bone together. for simple neck of femur and young patients with no osteoporosis. risk of AVN must be low
how is dynamic hip screws & plate used in hip fracture?
Extracapsular fractures - compression screw drilled into medulla of neck.head of femur and attached to plate on shaft. risk of AVN must be low
what is the definition of a fracture, dislocation & subluxation?
- fracture - loss of continuity of substance of a bone due to physical force
- dislocation (luxation) - complete loss of contact between articulating surfaces of a joint
- subluxation - partial dislocation - still some contact between articular surfaces but joint no longer congruous
what is the epiphyseal, metaphyseal, diaphyseal levels of bones?
- Epiphyseal - end section
- metaphyseal - neck of bone
- diaphyseal - shaft/mid section of bone
what is varus and valgus deformation of bone?
- varus - distal part towards midline
* valgus - distal part away from midline
what are the requirements for good fracture healing?
controlled micromovement (stimulates repair) and fracture haematoma (provides stem cells)
what are the stages of fracture healing?
- inflammation immediately - fracture haematoma forms containing fibrin clot, platelets, monocytes then later fibroblasts, osteoprogenitors
- soft callus - over weeks when pan& swelling goes - osteoid formed by fibroblasts to produce weak join between fragments. Mast cells, mphages clear debris
- hard callus -weeks/monts - osteoblasts mineralise osteoid into disorganised woven bone incr. stiffness & endochondral/membranous bone forming
- remodelling- months/yrs - woven bone slowly converted to lamellar bone and, excessive callus removed & medullary canal reformed
what are the ads & disads of internal fixation of fractures?
needed if gross movement likely, direct bone healing but disperses fracture haematoma
what should be done in x-rays for fractures?
2 views right angles, 2 joints above & blow fracture, 2 occasions (apparent after, 2 limbs to compare
what are the 3 elements to fracture management?
- reduction - realign bones (closes or open when accurate reduction req & in nerve damage)
- retention - to stabalise either no operative (strappings/sling, plaster, traction) or internal fixation in displaced inta articular fractures, multiple injury, path fractures
- rehabilitation -stop stiffness & start weight bearing
what are some complications of fractures?
- malunion, delayed union, non union (after 6mths, hypertrophic good blood supply but insuff stability & atrophic non union no cellular activity)
- joint stiffness *AVN (bone death due to infarction), *myositis ossificans (calcification of soft tissue)
- infection, nerve damage, vascular damage (arteries -pain, pale, paraesthesia, pulselessness, cold venous -swelling haematoma)
- compartment syndrome - muscle swelling with a closed osseofascial compartment causing ↑P, ischemia & infarction of tissues. Signs - out of proportion pain to injury & passive stretch, pins & needles, pulseless
- visceral trauma
what is a pathological fracture?
fracture occuring following min stress through abnormal bone - tumours primary myeloma sec mets from breast, bronchus, prostate, kidney,thyroid
infection, osteoporosis/malacia, pagets, osteogenesis imperfecta
what is a stress fracture?
due to fatigue - repeated freq forces in normal bone - athletes
what do open fractures req?
washout and debridement within 6 hours & stabilisation
how are the bones of children different?
have periosteum membrane (thicker & metablolicallt active), more collagen so elastic and porous but weak, epiphyseal plates open (weakness)
what is a green stick fracture?
under torsion - outer cortex pulled apart and inner bends due to elasticity but remains intact. can re displace once swelling reduceds
what is a buckle/torus fracture?
crushing fracture
what is osteoporosis?
a predisposition to skeletal fractures caused by a reduction in total/regional bone mass as calcium hydroxyapatite (makes bone rigid) is reduced. Bone mass decreases after 30-35 yrs (remodelling occurs but lose more). Fractures occur commonly at hip, vertabrae, wrist (colle’s fracture - hands spread on fall). F>M
what are the risk factors for osteoporosis?
- family history
- early menopause (progesterone causes ↑osteoblast activity). In younger women due to oestrogen deficiency *sedementary lifestyle (no weight bearing)
- smoking & excess alcohol
- low Ca2+ omtale & sun exposure (↓ vit D)
- medications - thyroxine & steroids
- caucasian *slender build
what conditions can cause osteoporosis?
osteomalacia, osteogenesis imperfecta, myeloma, renal failure and endocrine disorders:
- ↑ PTH / hyperparathyroidism - ↑ [Ca2+] in blood due to ↑resorption
- ↑ Calcitonin/hyperthyroidism - C cells of thyroid produce excess calcitonin ↓[Ca2+] in blood so less available for deposition
- cushings - cortisol suppresses osteoblasts & bone growth factors ↓bone deposition
- ideopathic hypercalciuria
what investigations should be done on px with suspected osteoporosis?
- investigate for disorders causing 2ry osteoporosis
- Dual energy X-ray Absorpitometry (DEXA) scan - T score is standard deviations from mean peak value for a young adult - normal <-1 indicates bone loss faster than for age
what pharmacological treatments are available for the treatment of osteoporosis?
- Ca & vit D (↑Ca & PO4 absorp from gut) supplements
- anti-resorptive therapy - bisphosphonates (alendronate, zolendronate) encourage osteoclast apoptosis but causes adynamic bone (↑fractures as ↓ bone remodelling) & can be used for 5 year periods only
- prodeposition therapy - Selective estrogen receptor modulator SERM (raloxifene) mimics progesterone action on osteoblasts ↑ activity. Slight ↑risk of thrombosis
- Recombinant PTH (Teriparatide) once daily injection ↑ serum Ca stimulates osteoblast activity more than clasts
- Strontium Ranelate - ↑bone formation ↓resorption
what is osteomalacia/rickets (children)?
impaired mineralisation ( low calcium hydroyapatite) of normal osteoid tissue. ↑ osteoids to counter low mech strength - 2ry cause of osteoporosis
what causes osteomalacia?
- vit D deficiency - ↓vit D causes ↓Ca absorp in GIT ↓ reabsorp in kidneys
- abnormal vit D deficiency - cant convert D2/3 to DGCCF due to renal/liver disease or drugs
- hypophosphatemia - PO4 req for hydroyapatite. low conc. causes ↑ bone resorption
- mineralisation inhibitors - biphosphonates, Al, F
- congentital causes in rickets - hypophosphatemic (↓renal PO4 reabsorption), 1alpha hydroxylase deficiency in osteoblasts (↓mineralisation), vit D resistance
what are the signs and symptoms of osteomalacia?
- bone pain and deformity esp in long bones & pelvis
- fractures
- myopathy and weakness
- growth retardation in rickets
what investigations can be carried out for osteomalacia and what are the treatments?
- urine - ↓Ca2+ & ↑PO4
- Bloods - ↓Ca2+ & PO4, ↑Alkaline phosphotase (osteoclast activity), ↓vit D, ↑ serum PTH
- X-rays - looser’s zones - pseudofractures
- treat underlying cause & vit D supplements - oral D2/3 require good renal function
what is pagets disease?
disorder of bone remodeling as ↑osteoclast resorption followed by ↑ bone formation leading to disorganised woven bone (weaker, larger, more vascular, compresses nerves). Signs/symptoms - deep constant boring pain worse on weight bearing and path fractures & deformities (frontal bossing), sciatica, cauda equina
what investigations and management for pagets?
- bloods - ↑alkaline phosphotase (osteoclast activity)
- x-ray -lessions & cortical thickening
- bone scan - incr. uptake
- bisphosphonates encourage osteoclast apoptosis
