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Reconstruction FRCS > Joint disease > Flashcards

Joint disease Flashcards

OA ostenecrosis/AVN of the hip Adult hip dysplasia

1
Q

What is OA?

A
  • A degenerative disease of synovial joints that causes progressive loss of articular cartilage
  • may lead to
    • pain
    • ligamentous laxity
    • joint deformity
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2
Q

What is the epidemiology of OA?

A
  • > F
  • Incidence increase with age, 75% at 70, 15% 40- >50% have symptoms
  • Risk factors
    • obesity
    • trauma
    • occupation- hard labour
    • muscle weakness
    • Female
    • age
    • Genetics
    • Race- some asian populations lower risk
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3
Q

What is the aetiology of OA?

A
  1. Abnormal forces on normal cartilage
    • Force = load/unit area
    • Increase Load = Obesity
    • Decrease contact area= Subluxation/ankle diastasis
  2. Normal forces on abnormal cartilage
    • Age
      • cartilage more stiff/less strong/elastic
      • hypocellular
      • decrease H20 content
    • Increase stiffness
      • ochronosis/CPPD/HA deposition
    • Increase softness
      • Chronic inflammation
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4
Q

Describe the pathology of OA?

A
  1. Collagen network damaged
    • disorganised and loosened
  2. Loss of Proteoglycan
    • leach from matrix
    • decrease chondroitin: keratin
  3. **Increase H20 **
    • as result of above, H20 content increases
  4. Cartilage swells
    • less stiff and more prone to damage
    • increase permeability
  5. Chondrocyte damage
    • IL-1/ TNF aplha/IL-6 released from synovium & chondrocytes
    • IL-1 important mediator of matrix metalloproteinases- Plasmin/Stromeylsin
    • collagenase breaks down collagen
  6. _​_Cartilage damage
    • attempt repair
    • hypermetabolic state
  7. Subchondral bone
    • increase force transmitted to bone
    • -> mechanical strain on overlying cartilage
    • percipitates cartilage degeneration
  8. Subchondral cysts
    • ?caused by stress fx, focal avn, synovial fluid pumps thru cracks
  9. Osteophytes
    • Result of pizoelectric forces on abnormal bone
    • increase surface area of joint
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5
Q

What is the presentation of OA?

A
  • Joint pain
    • often worse in mane
  • Swelling
  • Stiffness

O/E

  • decreased rom
  • Malalignment
  • effusion
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6
Q

What is seen on imaging of OA?

A
  • xray
    • WB views of joint
      • joint space narrowing
      • osteophytes
      • subchondral sclerosis
      • subchondral cysts
      • Eburnation of bone ( chnage in exposed subchondral bone to ivory)
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7
Q

What is seen on histology of OA?

A
  • Loss of superifical chondrocytes
  • Replication & breakdown of tidemark
  • fissuring
  • cartilage destruction with eburnation of subchondral bone
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8
Q

What is the tx of OA

A
  • Non operative
    • NSaids/tramadol
      • AAOS guidleines strongly recommended
    • weight loss
      • arthritis and BMI >25- moderate recommeded
    • Exercise programme/Physio
      • supervised and home best results
      • benefits lost after 6 months if exercises stopped- strongly recommended
    • bracing - no recommendation
    • Corticosteriod injections- not for or against
    • Viscoelastic joint injections- not recommended
  • Operative
    • Arthroscopic debridement
      • with menisceal symptoms
    • HIgh tibial osteotomy
      • young pt with unicompartmental disease
    • Unicompartmental knee replacement
      • isolated unicompartment OA
    • Total joint replacement
      • ​adv disease
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9
Q

What is Osteonecrosis of the hip?

A
  • aka AVN
  • accounts for 10% of THR
  • M>F
  • Av age of presentation 35-50
  • bilateral hips involved 80% of time
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10
Q

What are the risk factors of osteonecrosis of the hip?

A
  • AS IT GRIPS​ 3c’s
  • Alcohol >4000ml/wl
  • Steriods
    • >20mg/day
    • often bilateral
  • Idiopathic
    • incidence of hypercoagulability
    • etoh related to hypercoagulability
  • Trauma
    • Displaced subcapital
    • dislocation
  • Gout, Gauchers disease
  • Rheumatoid arthritis, Radiation
  • Infection (CMV/HIV/Rubella), increase lipids, Inflamation ( arthritis)
  • Pancreatitis
  • SLE, Sickle cell, Smoking
  • Chronic renal failure, Chemotherapy, Caisson’s disease
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11
Q

What is the pathophysiology of idiopathic avn and traumatic avn?

A

Intravascular coagulation

  • coagulation of intraossoeus microcirculation->
  • Venous thrombosis->
  • Retrograde arterial occulsion->
  • Intraosseous hypertension->
  • decreased blood flow to humeral head->
  • AVN of femoral head->
  • Chondral fx and collapse

Traumatic avn

  • disruption to medial femoral circumflex artery
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12
Q

What is the classification system of AVN?

A

Ficat classification 1958

  • Stage 0= normal xray/normal MRI/ Bone scan- non painful
  • Stage 1= normal xray, abnormal MRI/bone scan- painful hip
  • Stage 2
    • cystic/sclerosis xray
    • Abnormal MRI/Bone scan
  • Stage 3
    • Cresent sign ( subchondral collapse)
    • Abnormal MRI/Bone scan
  • Stage 4
    • Flattening of femoral head
    • Abnormal MRI/Bone scan
  • Stage 5
    • Narrowing of joint
    • Abnormal MRI/Bone scan
  • ​Stage 6
    • Advanced degenerative changes
    • Abnormal MRI/Bone scan

​​Steinberg further divided extent of head involved into

  • A= Mild <15%
  • B= Moderate 15-20%
  • C= Severe >30%
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13
Q

What is the tx of AVN of hip?

A

Non operative

  • Bisphosphonates
    • precollapse - Fiscat 0-2
    • alendronate prevents femoral head collapse in AVN with subchondral lucency
      • other studies show no benefit

Operative

  1. core decompression with/ wout bone grafting
    • early avn before subchondral collapse
    • traditional method
      • drill a 8-10 mm hole thru subchondral necrosis
    • Alterntative method
      • pass a 3.2mm pin into the lesion 2/3 times for decompression
      • relieves intraoeeous hypertension = less pain
      • stimulates a healing process thru angiogenesis
  2. Rotational osteotomy
    • Only for small lesions <50% in which lesion can be rotated away from WB surface
    • thru intertrochanteric region
    • success 60-90%
  3. Curettage and bone graft thru trapdoor technique
    • pre collapse
    • trap door thru cortex of femoral neck -> access necrotic bone of femoral head
  4. Vascularised Free- fibular graft
    • pre and collapse avn
    • remove necrotic area with large core hole
    • fibular strut graft placed under subchondral bone to prevent collapse ot tamp up with small areas of collapse
    • success 80% at 5-10 yrs, less with pts >40 yrs
  5. Total hip replacement
    • young py with crescent sign/ more adv collapse
  6. Total hip resurfacing
    • adv disease small djd, adequate bone stock
  7. Hip arthrodesis
    • ​​in v young pts in a labour intensive occupation
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14
Q

What is adult hip dysplasia?

A
  • Is a disorder of abnormal development or dislocation of the hip secondary to capsular laxity and mechanical factors
  • dysplasia attributable to a 1/3rd of hip OA
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15
Q

What are the forms of adult hip dysplasia?

A
  1. Dsyplasia that was previously tx
  2. dysplasia that was not tx
    • if left untx-> early OA
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16
Q

What is the pathoanatomy of adult hip dysplasia?

A
  • Acetabular anteversion is most common factor
17
Q

Name the classification of adult hip dysplasia?

A
  • **Crowe **classification
  • Hartofilakidis classification
18
Q

Describe the Crowe classification?

A
  • Grade 1
    • prox displacement
    • Femoral head subluxation
  • Grade 2
    • Prox displacement 10-15%
    • femoral head subluxation 50-75%
  • Grade 3
    • prox displacement 15-20%
    • femoral head subluxtion 75-100%
  • Grade 4
    • prox displacement >20%
    • femoral subluxation >100%
19
Q

Describe the hartofilakidis classification?

A
  • Dsyplasia - Type A
    • femoral head within acetabulum despite some subluxation
    • segmental deficiency of superior wall
    • Inadequate true depth
  • Low dislocation - Type B
    • femoral head creates a false acetabulum superior to the true acetabulum
    • complete absence of superior wall
    • inadequate depth on true acetabulum
  • High dislocation- Type C
    • Femoral head is completely uncovered by true acetabulum, migrated superiorly & posteriorly
    • complete def of acetabulum
    • excessive anterversion on acetabulum
20
Q

What is the presentation of adult hip dysplasia?

A
  • Hip/groin pain esp in flexion
  • insidious in onset
  • O/E
    • increased internal rotation before arthritis sets in
      • due to increased femoral anterversion
    • decreased internal rotation may represent OA
    • increased ER with ambulation
    • positive impingment test= pain w passive flexion, IR and Adduction
21
Q

What is seen on imaging in adult hip dysplasia?

A
  • xray
    • femoral head
      • decreased sphericity
      • decreased Head: neck offset
    • Abn of pelvis
      • increased retroversion- cross over sign
      • acetbular protrusio
    • lateral centre edge angle
      • angle formed by a vertical line & a line conecting teh centre of the femoral head with the lateral edge of the acetabulum
      • <20 degrees assoc with dysplasia
22
Q

What is the tx for adult hip dysplasia?

A

Non operative

  • supportive measures- first line

Operative

  • Periacetabular osteotomy + femoral osteotomy
    • symptomatic dysplasia
    • congruent joint with gd joint space
    • concentrically reduces hip
    • Adv- delays THR/preserves ext rotators, provides hyaline cart coverage, post column remains intact
  • Salvage ostoeotomy Chiari/Shelf
    • Unreduced hip
    • pt with incongruent femoral head coverage + incongruent joint
  • Hip resurfacing
    • for crowe I or 2
  • THR
    • those with severe arthritis
      ​​
      *
23
Q

Describe the technique for a periacetbular ostoetomy in adult hip dysplasia?

A
  • Ganz, Bernese
    • multiple osteotomies in pubis, ilium, and ischium nr acetabulum
    • allow 3 d correction of acetabulum configuration
    • most challenging
    • complx rate high 15%
    • THR post this=> retroverted cup
24
Q

What is the technical aspects of a shelf osteotomy?

A
  • Goal is to increase the weight bearing surface by placing the extra-aticular buttress of bone over the subluxed femoral head
  • cover femoral head with fibrocartilage ( not articular cartilage)
  • Add bone to lateral aspect of acetabulum
  • depends on metaplastic ( fibrocartilage) for successful results
25
Q

What is the technical aspects of a chiari osteotomy?

A
  • Make a cut above acetabulum to scaitic notch and shift ilieum lateral beyond edge of acetabulum. Depends on metaplastic bone ( fibrocartilage) for successful results
26
Q

What are the considerations that need to be address in THR for adult dysplasic hip?

A
  • Aim to put acetabular cup in the centre of true acetabulum
  • This -> significant leg lengthening
  • may require femoral shortening
  • may need trochanteric osteotomy to imporve visualisation in crowe type 3/4
27
Q

Describe the complications of surgery in adult hip dysplasia?

A
  • **Sciatic n palsies **
    • 10X incidence 5-10%
    • lengthening leg > 4cm -> sciatic n palsy -> foot drop
  • Hip Dislocation
    • Increased risk post THR 5-10%
  • Periprosthetic femoral fx
  • infection

Reconstruction FRCS (17 decks)

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