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
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
3
Q
What is the aetiology of OA?
A
-
Abnormal forces on normal cartilage
- Force = load/unit area
- Increase Load = Obesity
- Decrease contact area= Subluxation/ankle diastasis
-
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
-
Age
4
Q
Describe the pathology of OA?
A
-
Collagen network damaged
- disorganised and loosened
-
Loss of Proteoglycan
- leach from matrix
- decrease chondroitin: keratin
- **Increase H20 **
- as result of above, H20 content increases
-
Cartilage swells
- less stiff and more prone to damage
- increase permeability
-
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
-
__Cartilage damage
- attempt repair
- hypermetabolic state
-
Subchondral bone
- increase force transmitted to bone
- -> mechanical strain on overlying cartilage
- percipitates cartilage degeneration
-
Subchondral cysts
- ?caused by stress fx, focal avn, synovial fluid pumps thru cracks
-
Osteophytes
- Result of pizoelectric forces on abnormal bone
- increase surface area of joint
5
Q
What is the presentation of OA?
A
- Joint pain
- often worse in mane
- Swelling
- Stiffness
O/E
- decreased rom
- Malalignment
- effusion
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)
- WB views of joint
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
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
-
NSaids/tramadol
- 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
-
Arthroscopic debridement
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
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
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
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%
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
-
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
-
Rotational osteotomy
- Only for small lesions <50% in which lesion can be rotated away from WB surface
- thru intertrochanteric region
- success 60-90%
-
Curettage and bone graft thru trapdoor technique
- pre collapse
- trap door thru cortex of femoral neck -> access necrotic bone of femoral head
-
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
-
Total hip replacement
- young py with crescent sign/ more adv collapse
-
Total hip resurfacing
- adv disease small djd, adequate bone stock
-
Hip arthrodesis
- in v young pts in a labour intensive occupation
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
15
Q
What are the forms of adult hip dysplasia?
A
- Dsyplasia that was previously tx
- dysplasia that was not tx
- if left untx-> early OA
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%
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
- femoral head
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
