OSTEOARTHRITIS

1. EPIDEMIOLOGY
 Frequency of OA
o Asians: knees > hips
o Caucasians: hips > knees
 OA of hands & knees: F > M
 OA of hips: M > F

2. ETIOLOGY
 Primary
o Genetic, endocrine, metabolic
o Increased frequency with age
o Primary changes of cartilage matrix
 Secondary
o Anatomical defects and trauma
o Disease: Crystal deposition disease, type 2 collage defect, rheumatic disorder
o Increase mechanical stress in articular surface

3. RISK FACTORS
 Joint dysplasia
 Trauma
 Occupation – repetitive stress type
 Obesity
 Family history

4. CLINICAL FEATURES
 Middle aged patient
 Family history of OA

 Mechanical pain
 Stiffness
 Swelling
 Deformity – varus
 Loss of function

5. INVESTIGATION
 X-ray
o Narrowing of joint space
o Subchondral sclerosis
o Subchondral cyst
o Osteophyte formation
o Evidence of previous disorders (congenital defects, old #, RA) may be present

6. MANAGEMENT
a) Conservative
o Non-pharmacological
 Lifestyle modification
  Reduce weight
 Non-weight bearing exercise
 Avoid climbing stairs
o Pharmacological
 Non-selective
 NSAIDs – avoid in old age (if want to use, must + PPI)
 Mefenemic acid, voltaren
 Selective
 Celecoxib
 Glucosamine supplement
 Intraarticular injection of hyaluronic acid compound

b) Operative
 Therapeutic arthroscopy
 Joint debridement
 Realignment osteotomy
 Knee arthroplasty
 Arthrodesis (fusion of joint)

7. TYPES
 Polyarticular OA
o DIPJ of hands (Heberden’s nodes) – most common
o PIPJ of hands (Bouchard’s nodes)
o 1st CMCJ
o 1st MTPJ
o Knees
o Hips
o Cervical and lumbar facet joints
 Monoarticular OA – in weight bearing areas
 OA of unusual sites
o Shoulder
o Elbow
o Wrist
o ankle
8. DDX
 Ankylosing spondylitis
 Rheumatoid arthritis
 Gout

9. COMPLICATIONS
 Capsular herniation – Baker’s cyst
 Loose bodies
 Rotator cuff dysfunction – OA of acromioclavicular joint
 Spinal stenosis – hypertrophic OA of lumbar apophyseal joint
 Spondylolisthesis – destructive OA of apophyseal joint (L4/L5)
 OBSTETRICAL BRACHIAL PLEXUS INJURY
1. ETIOLOGY
 Excessive traction on brachial plexus during childbirth
o Upper root injury (Erb’s palsy) – overweight babies with shoulder
dystocia at delivery
o Complete plexus injury (Klumpke’s palsy) – after breech delivery of
smaller babies

2. CLINICAL FEATURES
 Floppy or flail arm soon after delivery
 Further examination will define type of BPI

ERB’S PALSY KLUMPKE’S PALSY

 Injury of C5, C6 and
(sometimes) C7
 Paralysis of abductors and
external rotators of
shoulder, and forearm
supinators
 Arm is held to the side,
internally rotated and
pronated
 Complete plexus injury
 Less common, but more
severe
 Arm is flail and pale; all
finger muscles are paralyzed
 There may also be
vasomotor impairment and
ipsilateral Horner’s
syndrome
3. INVESTIGATION
 X-ray – to exclude # of shoulder or clavicle

4. MANAGEMENT
 Paralysis may recover completely
o Erb’s palsy often recover spontaneously – indicator: return of biceps
activity by 3rd month
 Paralysis may improve and then remain static
o A total lesion may partially resolve, leaving the infant with either an
upper (Erb’s) or a complete (Klumpke’s) root syndrome which is
unlikely to change
 Paralysis may remain unaltered
o More likely with Klumpke’s palsy (especially if presented with
Horner’s syndrome)

5. TREATMENT
 Physiotherapy is applied to keep the joints mobile while waiting for recovery
 Consider surgery if there’s no biceps recovery by 3 months
o If roots not avulsed, excise the scar and bridge the gap with free sural
nerve-grafts
o If roots are avulsed, do nerve transfer
 Subscapularis release + tendon transfer
 Older children: rotation osteotomy of humerus