What is the pathophysiology of OA?
deterioration of articular cartilage due to local biomechanical factors and release of proteolytic and collagenolytic enzyme; occurs when cartilage catabolism > synthesis + loss of proteoglycans and water exposes underlying bone.
common site of OA involvement
hand (DIP, PIP, 1st CMC)
hip, knee,
1st MTP
L spine (L4-5, L5-S1)
risk factors of OA
genetic advance age obesity (knee OA) female trauma
sign of OA
pain is localised to joint, insidous onset, gradual and progressive with intermittent flares and remissions
jt line tenders, stress pain bony enlargement malalignment/ deformity limited ROM crepitus on passive ROM inflammation (mild) muscle atrophy
symptoms of OA
joint pain with motion, relieved with rest
short duration of stiffness (
common hand feature of OA
thumb squaring (CMC) heberden's nodes (DIP) bouchard's nodes (PIP) due to osteophytes -> enlargement of joints 1st MCP
is OA joint involvement symmetrical or asymmetrical?
asymetrical
hip and knee involvment feature of OA
hip =
- groin pain +/- dull or sharp pain in trochanteric area, internal rotation and abduction lost first
- radiate pain to anterior thigh
knee
- medial > lateral, narrowing
lumbar and cervical spine involvement in OA
common in L4-5 or L5-S1
degeneration of intervertebral discs and facet joints
reactive bone growth -> neurological impingement (sciatica/ neurogenic caludication)/ spondylolisthesis (displacement of vertebrae)
cervical spine = mid lower area (C5, 6)
radiographic hallmarks of OA
(LOSS)
loss of joint space
osteophyte formation
subcondral sclerosis
subcondral cysts
what are the investigation of OA
no specific lab test for OA - usually dx via clinical features and xray
test are performed to exclude other systemic disease that can cause pain, especially rheumatological disorders:
blood test
- haem: full blood count, erythrocyte sedimentation rate
- biochemical: baseline renal and liver function (if LT steroid is consider)
- immunological : rheumatoid factor, antinuclear antibody
radiological” anteroposterior and lateral view (joint below and above)
What are the treatment options of OA in hip?
non-surgical:
- lifestyle modifications: diet and exercise, weight loss (if appropriate)
- physiotherapy: some will respond to personalized exercise regimens which will improve symptoms and delay need for total hip replacement
- occupational therapy: fitting of suitable decies to aid mobility (eg. walk sticks/ frames) and practical advice on use
- analgesic therapy: use pain ladder begin with paractamol and NSAID (non steroidal anti inflammatories)
sx:
- osteotomy - bone cut to shorten or lengthen or change alignment
- arthroplasty - hip resurfacing or hip replacement
- arthrodesis - artificial anklyosis/ syndesis, artificial induction of jt ossificaiton between two bones via surgery
indications of total hip replacement for OA
instability
severe pain or disability not substantially relieved by extended course of non-surgical mx
- rest pain or pain with movement
- loss of mobility
what are the complication of total hip replacement
complications can be divided into intraoperative, immediate (24 hour), early (within 30 days) and late (later then 30 days).
intraoperative:
- # of acetabulum or femur
immediate:
- dislocation (due malalignment of prosthetic components)
early:
- deep vein thrombosis and pulmonary embolus
- sciatic nerve palsy (> common if posterior surgical approach to the hip joint)
- infection
- fat embolism syndrome
late:
- infection
- loosening (septic or aseptic)
- heterotopic ossification
- leg lenght discrepancy
- periprostehtic #
- thigh pain
how to prevent DVT post-op following total hip replacement?
DVT most common complication follow total hip replacement, peak 5-10 days post op. Prevent possible via measure:
- preoperative: thromboemoblic deterrent (TED) stokcing fitted preop
- perioperative: TED stockings, minimize sx length, compression boots and foot pumps
- postop: low dose/ low molecular weight heparin, early mobilization with physio
list the movement of hips, muscle groups and expected degree of movement
flexion: illiopsoas, rectus femoris, tensor fascia lata, quads, 140 degree
extension: gluteus maximus and hamstrings, 10 degree
abduction: gluteus medius and minimus 45 degree
adduction: adductors (longus brevis, magnus) 30 degree
internal rotation: gluteus medius, minimus, iliopsoas, 40 degree
external rotation: glutues maximus 40 degree
what are the xray changes of OA of the knee?
LOSS
- loss of jt space
- osteophyte formation
- subchondral sclerosis
- subchondral cyst
standing and weight bear view
commonly - tibiofemoral jt space dimished, usually medial > lateral
how to treat OA of knee?
non-surgical:
- lifestyle modifications: diet and exercise, include weight loss if appropriate
- physiotherapy: respond to personalized exercise reginmens that will improve symptoms or delay need for replacement + strengthening of quadriceps muscles is very important
- occupational therapy: fitting of suitable decies to aid mobility, practical advice on how to use them, elastic support by improve proprioception in unstasble knee
- medical: use pain ladder begin with paracetamol or NSAIDs
- intra-articular steroid injection - temp relief, but repeated injections -> progressive cartilage and bone destruction
- viscosupplementation: intra-articular injections of hyaluronic acid
sx:
- arthroscopic debridement and washout -> temp relief for younger patients as temp measure before arthroplasty (trim off osteophytes and meniscal tears)
- patellectomy -> (rare) for OA confined to patellofemoral jt only -> decrease extensor mechanism power -> if later total knee replace -> unpredicable pain
- realignment osteotomy -> use for young ( older with progresive jt destruction confined to one compartment
- arthrodesis - strong CI to arthroplast (eg. previous sepsis) or salvage procedure for failed arthropathy
what are the complication of total knee replacement
intraoperative - # of tibia/ femur
immediate - vascular injuries (superficial femoral, popliteal, genicular vessels)
early - DVT, PE, peroneal nerve palsy (1 [ercent), infeciton, fat emoblism syndrome
late - infection, loosening (septic/ aseptic), patellar instability/ #/ disruption of extensor mechanism, periprosthetic #
What are the causes of OA?
primary:
- idiopathic (most common)
secondary:
- post trauma, mechanical
- post inflammatory (RA), post infectious
- heritable skeletal disorders (scoliosis)
- endocrine disorders (acromegaly, hyperparathyroidism, hypothyroidism)
- metabolic disease (gout, pseudogout, hemochromatosis, wilson disease, ochronosis)
- neuroapthic (aka charcot joints) = diabetes, syphilis -> atypical jt trauma due to loss of proprioceptive senses
- avascular necrosis (eg. #, alcohol, steroids, gout, sickle cell)
- other (congenital)
