Osteoarthritis Flashcards
What is the etiology of OA?
Primary (idiopathic): usually polyarticular
- DIPJ (Herbeden’s nodes), PIPJ (Bouchard’s nodes), 1st CMCJ, 1st MTPJ, knees, hip, facet joints
Secondary – usually in weight bearing joints eg knees
- Pre-existing joint damage - trauma, inflammatory arthritis, AVN, CPPD
- Metabolic disease - eg acromegaly, cartilage calcification
- Systemic disease: haemophilia (causing recurrent haemarthrosis), Hbopathies eg sickle cell, neuropathic arthropathy (Charcot joint)
What are the risk factors for OA?
Non-modifiable
- ↑ age, gender: polyarthritis OA W>M, esp post menopausal (post-menopausal women tend to develop OA in DIPJ/PIPJ)
- Hypermobility: increased joint motion and reduced stability
- Trauma: intra-articular #, meniscal and ligament tears
- Congenital joint dysplasia (eg acetabular dysplasia for hip OA)
- Other co-morbidities (systemic disease causing jt damage)
- Family Hx (eg nodal, generalized OA)
- *Modifiable
- **Obesity
- Occupation (eg heavy labour)
- Sport (eg repetitive use and injury)
How is the progression of OA like?
Early OA is rarely symptomatic (unless joint effusion present)
- Advanced radiological and pathological OA not always symptomatic
- Radiological OA is usually progressive (but not inevitably) –> stepwise or continual, may have improvement (ie repair is possible)
Flare-ups may be due to inflammation (↑ ESR, CRP)
- Focal synovitis –> due to fragments of shed bone or cartilage
Axial involvement in OA
- Later in disease course, patients may show radiographic OA changes (eg osteophytosis), commonly cervical & lumbar spine (weight bearing areas)
- May not be symptomatic
- Eg neck pain may be due to other causes (eg pain of the trapezius), even though cervical spine shows OA changes
What are the is the hx to ask in a patient with OA?
HOPC
- Short-lived morning stiffness (<0.5-1hr)
- Pain worsening with movement and relieved by rest
- Functional limitation: premorbid vs now, restriction in recreational and jobe scopes
- Deformity: varus > valgus
- Instability
Causes: previous trauma, occupational/competitive contact sports hx, BMI, associated conditions
Previous treatment tried
Social hx: type of housing, lift landing, squatting toilet
GI bleed risk (affects Mx decision to start LT NSAIDS)
- Previous BGIT, PUD
- NSAIDs use: dose and duration
- Concurrent corticosteroids and warfarin use
- Age >60yo
- Renal dysfunction
What are the sign of OA?
- Joint crepitus (disruption to articular surfaces)
- Restricted movement
- Bony enlargement (osteophytes)
- +/- Joint effusion, variable inflammation
- Bony instability, muscle wasting
What is the ddx of OA?
Referred pain from hip/back if knee pain -> TRO neurogenic /vascular claudication
V- AVN (bone collapse and deformity but articular cartilage still preserved)
I – inflam jt conditions eg RA
T – trauma
A – AI
M – gout, pseudogout
Infective – SA
N – bone pain, red flags
Nodal OA
- Epidemiology & associations
- Initial presentation
- Clinical progression
Epidemiology & associations
- Often seen in post-menopausal women
- Familial tendency
- Polyarticular hand OA a/w slightly ↑ frequency of OA at other sites (knee, spine, hip)
Initial presentation
- Joints of the hand usually affected one at a time over several years
- Commonly the DIPJs, PIPJs, 1st CMCJ
- Painful onset, a/w tenderness, swelling, inflammation, impairment of hand function
- At this stage: enthesitis may be seen on MRI, may use intra-articular corticosteroids
Clinical progression
- After months to years, bony swellings may develop
- Bouchard’s nodes (PIPJs) and Heberden’s nodes (DIPJs)
- ‘Squared hand’ of OA : 1st CMC prominence (lat. surface, fixed adduction of thumb)
- There is associated stiffness, deformity, poor grip (esp. for PIPJ OA)
- X-ray: marginal osteophytes, joint space narrowing
Knee OA
- Epidemiology & associations
- Clinical features
Epidemiology & associations
- Women > men
- A/w obesity, previous trauma, meniscal and ACL/PCL tears
- Ask about BMI
- Ask about previous injury, sports and occupation
Clinical features
- Generally bilateral (unless is due to trauma)
- Strongly a/w nodal OA of hand in elderly women, or as part of generalized OA (NGOA)
- Medial compartment most affected: varus deformity (bow-legged)
- Often have retropatellar OA
- MRI show bone marrow lesions, which predict disease progression and eventual joint replacement
Hip OA
- What are the 2 clinical subgroups?
- What are the clinical features of both clinical subgroups?
Less common in Singapore
2 sub-groups (radiological): superior-pole hip OA and medial cartilage OA
1) Superior-pole (more common)
- Men > women, generally unilateral at presentation (both may be involved; disease is progressive)
- Joint space narrowing and sclerosis –> affects weight-bearing upper surface of femoral head and adjacent acetabulum
- If early onset -> a/w acetabular dysplasia or labral tears
2) Medial cartilage
- Women > men, usually bilateral, a/w hand involvement (NGOA – Nodal Generalised OA)
- More rapidly disabling
What are the clinical features of primary generalized OA?
- Rare, usually seen in combination w nodal OA
- Joints affected –> knee, 1st MTP, hip, intervertebral (spondylosis)
- Sudden and severe onset
- Female > male, strong familial tendency
- Periarticular ligamentous pathology may have important role
Crystal associated OA
- Epidemiology & associations
- Clinical features
Calcium pyrophosphate deposition in cartilage (chondrocalcinosis)
Clinical features
- Chronic arthropathy (pseudo-OA) in elderly women w severe chondrocalcinosis
- Knees (hyaline & fibrocartilage), wrists (TFCC) and shoulders
- X-ray: patchy linear calcification, osteophytes, cyst formation
What are the investigations conducted in patients with OA?
- ***WB XR of jt: V-LOSS (note: XR findings only in advanced OA)
- Minimally 2 views: Must be Weight Bearing!
- If PFOA, then skyline view x2
- V: Varus deformity (possibly valgus, but usually more a/w RA)
- L: Loss of joint space (mostly in med compartment) <5mm +- loose body
- O: Osteophyte formation
- S: Subchondral sclerosis
- S: Subchondral cysts
Bloods
- FBC (TWC TRO infection, Hb and plt for pre-op eval)
- ESR/CRP (may be slightly raised) – compared to inflamm arthritis
- RP LFT CXR ECG for pre-op eval
Joint aspiration (ONLY if there is painful effusion -> TRO septic and inflammatory arthritis)
- c/s, G stain, AFB
- Crystal tests
- Cytology
- Morphology and WCC
What is the management of OA?
Conservative
- Weight loss and exercises: ↑ strength and stability
- PT: strengthen muscle, improve mobility
- OT: offload w walking aids, soft soled shoes
Pharmacological
- 1st: Paracetamol
- 2nd: NSAIDS (caution in BGIT risk, add on PPI/H2RA) or COX 2
- 3rd: Intra-articular GC – avoid repeated injections into same joint. H&L injection = Hydrocortisone and Lignocaine
- 4th: intra-articular hyaluronate (visco-supplementation): Appears to help SOME people, will recommend if helps
- 5th: chronic opioids for severe pain, caution in elderly
- Glucosamine w chondroitin – no strong evidence, not recommended
Surgical
- Failure of conservative Mx, very symptomatic, fit for Sx
- Osteotomy (in young pts) – eg: high tibial osteotomy if knee
- Arthroplasty
o Total joint arthroplasty is definitive treatment
o Consider unicompartmental arthroplasty in knee if there is only medial compartment TFOA
- Arthrodesis (not commonly done anymore)
