1. MSK Ortho 2 Flashcards
2 most commonly affected joints in OA:
1) Knee
2) Hip
Local risk factors for hip OA:
Local Hx of trauma
Anatomical abnormalities
Muscle weakness
Joint laxity
High impact sports
Genetic?
Clinical features of OA of the hip:
Pain in the groin area, or lateral hip / deep buttock
Antalgic gait
Trendelenburg gait
Fixed flexion deformity
Painful passive movement and reduced ROM
DDx for OA of the hip:
Sciatica
NOF#
Trochanteric bursitis
Gluteus medius tendinopathy
Management of hip OA:
Conservative efforts as in all OA cases; pain control, lifestyle measures, physio.
Definitive = arthroplasty or hemiarthroplasty. Posterior approach is most common (risk of sciatic nerve injury and dislocation), followed by anterolateral (risk of damage to gluteal nerve).
Designed to last 15-20 years.
AVN of the hip usually starts asymptomatic and then progresses to pain in the affected joint. List 4 causes of AVN of the hip:
Long term steroid use
Alcohol excess
Trauma
Chemotherapy
Pathophysiology of AVN of the hip:
The medial circumflex artery (branch of profunda femoris) is responsible for the majority of blood supply to the hip joint. Damage can result in avascular necrosis as there is little input from any other arteries e.g. the lateral circumflex.
Investigations and findings for AVN of the hip:
Plain x-ray; may show nothing initially. Osteopenia and microfractures, then progression to collapse of the articular surface and the crescent sign.
MRI is scan of choice.
What causes the ‘crescent sign’ on x-ray, and where is it most often seen?
A sign of osteonecrosis.
Trabeculae failure, leading to subchondral fracture.
It is most often seen in the femoral and humeral heads.
What does SUFE stand for, and who usually presents with it?
Slipped Upper Femoral Epiphysis
Children, 10-15 year old males, more common in obesity.
Describe the innervation of the hip.
Sciatic, femoral and obturator nerves.
The same innervation as the knee, which is why pain can be referred between these two joints.
What is the classic treatment for DDH, and how does it help?
Pavlik harness
Holds the femoral head in the acetabular fossa and promotes proper development of the hip joint.
Common clinical features of DDH in younger children (3):
Limited hip abduction
Limb length discrepancy (affected = shorter)
Asymmetrical gluteal or thigh skin folds
What is the problem in SUFE, and what is the timing of presentation?
Postero-inferior displacement of the femoral head epiphysis.
Can present following trauma, or chronic, persistent symptoms.
Clinical features of SUFE:
Hip, groin, medial thigh or knee pain
Loss of internal rotation of the leg in flexion
Bilateral in 20%
Which investigations are diagnostic for SUFE?
AP and lateral ‘frog leg’ x-ray views.
Shows widening of the physis at the proximal affected femur.
Management of SUFE:
Internal fixation - cannulated screw inserted into the centre of the epiphysis.
DDH is a spectrum of disorders that includes mild dysplasia, subluxation and dislocation of the hip. What are some risk factors for this condition?
Female
First born
Positive FHx
Breach position
Oligohydramnios - low levels of amniotic fluid lead to increased intrauterine pressure
Incorrect swaddling techniques
Clinical signs of DDH in an older child / teenager:
Gait abnormalities - waddling / limping
Osteoarthritis
Hip pain
The diagnosis of DDH is based on clinical examination and imaging. List 3 imaging modalities and describe the instances in which they would be performed.
US = <4-6 weeks
Plain x-ray (AP + lateral frog leg) = >4-6 weeks
CT/MRI if surgical planning / other imaging is inconclusive.
What 3 factors inform the treatment of DDH?
Patient’s age
Severity
Underlying risk factors
List 3 types of treatment for DDH:
Pavlik harness
Closed reduction
Open reduction
+ regular monitoring, clinical examination and imaging for all
Which children with DDH are treated with a Pavlik harness?
<6 months with reducible dislocations or mild/mod dysplasia
Which children with DDH are treated via closed reduction and spica casting?
6 months to 2 years, or if Pavlik fails.
Closed reduction is done under GA, and then a spica cast is applied.
When is open reduction considered for the treatment of DDH?
Children older than 2 or if closed reduction hasn’t worked.
+/- pelvic or femoral osteotomies
Describe the Salter-Harris fracture classification system:
I-V
‘SALTR’ mnemonic
I; fracture passes all the way through growth plate, not involving bone. ‘Slipped’
II; passes through most of the growth plate and up into the metaphysis. 75%, most common. ‘Above’
III; fracture plane passes along some of the growth plate and then down into the epiphysis. ‘Lower’
IV; through metaphysis, growth plate and epiphysis. ‘Together/transverse’
V; crush type injury, no displacement of growth plate but injury by compression. Worst prognosis. ‘Rammed’
https://radiopaedia.org/articles/salter-harris-classification?lang=gb
What are the 2 structures that are at risk of damage in a supracondylar distal humerus fracture?
Brachial artery
Anterior intraosseous nerve
4 types of clubfoot:
‘CAVE’
Cavus
Adductus
Varus
Equinuus
What is the official name for clubfoot?
Talipes equinovarus
Around 50% of cases are bilateral
What are some associated conditions of talipes equinovarus?
Spina bifida
Cerebral palsy
Edward’s syndrome (trisomy 18)
Oligohydramnios
Arthrogryposis
What is the mainstay of treatment of clubfoot and what is the relapse rate?
Serial casting using the Ponseti method
+ night-time braces until the child is 4 years old
The relapse rate is 15%
What does the Ponseti method consist of and what is it used for?
Correction of clubfoot
Manipulation and progressive casting, starting soon after birth. Usually corrects the deformity in 6-10 weeks.
An Achilles tenotomy is required in 85% of cases but can be done with local anaesthetic.
What are the 2 most common primary malignant tumours of bone in children?
Osteosarcoma (most common)
Ewing’s sarcoma (2nd)
5 common causes of a limping child:
Transient synovitis
Perthe’s
DDH
SUFE
Septic arthritis
Features of Ewing’s sarcoma (age, distribution, x-ray findings, translocation, clinical findings):
Age 5-15 ish
Pelvis and long bones (femur most common)
Severe pain, ?fever, ESR + LDH elevated
t(11:22) translocation
X-ray = onion skin appearance (periostitis), moth eaten
Features of osteosarcoma (age, distribution, x-ray findings, genetics, predisposing, clinical findings):
Metaphyseal region of long bones prior to epiphyseal closure usually (femur>tibia>humerus)
X-ray = Codman’s triangle and sunburst pattern
Rb gene mutation, a/w retinoblastoma
Predisposing factors = Paget’s DOTB, radiotherapy (termed ‘secondary’)
Age 10-25
What are the top 5 primary tumours that metastasise to bone?
Lung
Prostate
Thyroid
Kidney
Breast
LP Thomas Knows Best
Which parts of the skeleton often present with pain when associated with a metastatic lesion?
Spine
Pelvis
Hips
Long bones
Symptoms associated with MSK malignancy in adults i.e. red flag symptoms:
Night pain
Weight loss
Unremitting pain
Non-traumatic joint or limb pain
3 most common primary bone tumours (in order):
Osteosarcoma
Ewing’s sarcoma
Chondrosarcoma
What is the common presentation of an osteosarcoma?
Metaphyseal region of bone e.g. around the knee
Limping child (more common in children!)
Progressive swelling around the knee / limb
Night pain
3 most common soft tissue sarcomas:
Liposarcoma
Leiomyosarcoma (smooth muscle)
GI stromal tumours
List 5 non-malignant tumours of bone and soft tissue (OOOEL):
Osteochondroma (cartilage capped bony projections, most common)
Osteoma (skull, a/w Gardner’s syndrome / FAP)
Osteoid osteoma (osteoblasts, femur + tibia)
Enchondroma (cartilage)
Lipoma (fat tissue, superficial or deep)
Investigations for suspicious bone / soft tissue lesions:
XR
Bloods inc bone profile, calcium, ALP, TFTs etc
CT to show size of lesions
MRI for soft tissue lesions
Biopsy for definitive diagnosis
Definition of osteoporosis:
A syndrome associated with low BMD and microarchitectural deterioration of bone tissue leading to increased risk of fractures.
Pathophysiology of osteoporosis:
Irregulation of bone remodelling, imbalance between bone formation and bone resorption.
Osteoclastic activity takes weeks, but blasts takes months.
Increased clastic activity, decreased blastic activity.
Outline the categories of osteoporosis:
Primary
Type I = postmenopausal
Type II = senile
Secondary
Risk factors for osteoporosis that reduce bone density:
Oestrogen deficiency in females
Androgen def in males
Endocrine diseases e.g. diabetes, hyperthyroidism, hyperparathyroidism
Malabsorption e.g. Crohn’s, UC, coeliac, chronic pancreatitis
CKD
CLD
COPD
Immobility
Low BMI
Risk factors for osteoporosis independent of BMD:
Age
Oral steroids
Smoking
Alcohol (>3 units/day)
Prev. fragility fracture
Rheumatological conditions e.g. RA
Parental Hx of hip#
Management of osteoporosis:
Lifestyle modifications e.g. calcium + vitD, falls assessment, weight bearing + muscle strengthening exercises
Pharmacological therapy reserved for 10yr risk >1% or T-score <2.5
Bisphosphonates
Denosumab
Raloxifene (SERM)
Terliparatide (activates blasts > clasts)
HRT (only early postmenopausal due to breast cancer and CV risk)
Most common sites of osteoporotic #s:
Hip
Spine
Wrist
MOA of bisphosphonates + side effects:
Adheres to hydroxyapatite and inhibits osteoclasts, reducing bone resorption.
Upper GI side effects e.g. oesophagitis.
Careful monitoring required in CKD4+5
MOA of denosumab + side effects:
Monoclonal antibody, anti-resorptive agent that increases BMD. Only used in severe.
Dysuria
Cellulitis
Osteonecrosis of the jaw
Describe how glucocorticoid use induces osteoporosis:
Induces a high turnover rate initially.
Prolonged use leads to reduced-turnover rate with a net loss due to reduced synthesis by osteoblasts.
Increased fracture risk is evident within 3 months of 10mg prednisolone OD.
Which non-osteoporotic causes of fragility fractures should be excluded before commencing osteoporosis treatment:
Metastatic disease
Paget’s Disease of the Bone
Myeloma
Osteomalacia
Exclude vitD deficiency and inadequate calcium intake.
What is osteomalacia + most common cause?
Qualitative bone disorder due to ineffective mineralisation of osteoid.
Can occur before or after skeletal maturity (Rickets vs osteomalacia)
Most common cause is vitamin D deficiency.
Describe the lab results that differentiate osteomalacia and osteoporosis:
Osteomalacia:
Low calcium
Low vitamin D
Low serum phosphate
High ALP
High PTH
Osteoporosis:
biochemically normal inc calcium, phosphate, ALP, PTH etc
Treatment of osteomalacia:
Replacement of missing components e.g. vitamin D, calcium, calcitriol (synthetic D3), phosphate
Surgical correction in some cases
Investigations required to exclude secondary causes of osteoporosis:
TFTs
FBC
U+Es inc calcium, creat, phosphate
LFTs
Vitamin D
Serum testosterone and prolactin
Protein immunoelectrophoresis and urinary BJP
Vitamin-D dependent causes of osteomalacia:
Low UV exposure
Low oral intake
Low absorption e.g. cystic fibrosis, chronic pancreatitis, coeliac disease, gastrectomy
Defective vitD metabolism:
CYP450 inducers increase metabolism of vitD
Anticonvulsants
HPB disease
Renal disease
Alcoholism
Hypophosphataemia
Clinical features of osteomalacia:
Pain in bones and muscles (unlike osteoporosis which is asymptomatic until fragility fracture)
Proximal muscle weakness
Fractures
Trefoil pelvis - loss of pelvic volume
Biconcave vertebral fractures
Pathophysiology of Paget’s disease of the bone:
Disorder of bone remodelling, starts with increased osteoclast activity.
Likely viral aetiology (paramyxovirus + genetic susceptibility)
3 Phases: lytic, mixed and sclerotic.
Common sites for Paget’s disease of the bone:
Femur
Tibia
Pelvis
Skull
Spine
Complications associated with Paget’s disease of the bone (8):
Deformity and pathological #
Osteoarthritis risk
Sensorineural (compression of CNVIII in internal auditory canal / loss of BMD in cochlear capsule) and conductive (fixation of middle ear ossicles) hearing loss
Neural compression - cranial nerve paresis
Malignant transformation (1% cases)
High output congestive cardiac failure - when bone involvement is >15%, rapid formation/resorption can lead to left to rigth shunting and decreased peripheral resistance
Hyperparathyroidism (10%)
Extramedullary haematopoeisis
Clinical features of Paget’s disease of the bone:
5% of patients are symptomatic
Older male
Bone pain (pelvis. lumbar spine, femur)
Isolated rise in ALP
Untreated = bowing of tibia, bossing of skull
Radiographic features of Paget’s (SKULL):
Osteoporosis circumscripta - large, well defined lytic lesions involving inner aspect of the outer table of the skull
Cotton wool appearance - mixed lytic and sclerotic lesions
Common sites for the development of AVN:
Hip number 1
Epiphysis of long bones at weight bearing joints e.g. knee, talus, humeral head
Scaphoid due to retrograde blood supply
Olecranon bursitis describes inflammation of the olecranon bursa. List 4 causes of this inflammation:
Infection (i/c patients. 90% S.aureus)
Trauma (direct / repetitive)
Rheumatoid arthritis
Gout
Clinical features of olecranon bursitis:
Non-septic = subacute onset of swelling over the olecranon process +/- tenderness +m erythema
Septic = more likely to have pain and fever. ?skin abrasion prevalent.
ASPIRATE for microscopy and culture if suspected.
Management of olecranon bursitis:
Conservative (non-severe symptoms and no infection): ice packs, elevation, activity modification, NSAIDs if mild pain.
Aspiration if significant bursal fluid accumulation causing discomfort.
Steroid injections if no response to conservative measures, but be aware of infection and tendon rupture risk.
Antibiotics if septic confirmed.
?Surgical
Clinical signs of RA in the hands:
Ulnar deviation
Z thumb
Extensor tendon rupture
Boutonniere deformity
Swan neck deformity
Rheumatoid nodules
What is a ganglion?
Common, benign, cystic swelling that arises from the synovial lining of joints or tendon sheaths.
What are the common sites for ganglion cysts + management?
Dorsal aspect of wrist
Volar aspect of wrist
Flexor tendon sheaths at base of fingers
Dorsal interphalangeal joints
Tarsal joints
Symptomatic / causing functional impairment: aspiration or surgery
Smith vs Colles fracture:
Colles = dorsal angulation of distal bone
Smith = volar angulation of distal bone
Describe Monteggia vs Galeazzi fracture dislocations:
‘Monty loses his head’
Monteggia = proximal ulnar fracture, radial head dislocation
Galeazzi = distal radial fracture, distal DRUJ dislocation
Which nerve is at risk of damage in a diaphyseal humeral fracture?
Radial nerve
Which nerve is at risk of damage in a distal radius fracture?
Median nerve compression
Prolapsed lumbar disc usually produces clear dermatomal leg pain associated with neurological deficits. Common to all is leg pain worse than back and worse on sitting.
What are L3 nerve root compression features?
Sensory loss over anterior thigh.
Weak hip flexion, knee extension and hip adduction.
Reduced knee reflex.
Positive femoral stretch test.
What are L4 nerve root compression features?
Sensory loss anterior aspect of knee and medial malleolus.
Weak knee extension and hip adduction.
Reduced knee reflex.
Positive femoral stretch test.
What are L5 nerve root compression features?
Sensory loss over the dorsum of the foot.
Weakness in foot and big toe dorsiflexion.
Reflexes intact.
Positive sciatic stretch test.
What are S1 nerve root compression features?
Sensory loss posterolateral aspect of leg and lateral aspect of foot.
Weakness in plantar flexion of foot.
Reduced ankle reflex.
Positive sciatic stretch test (reduced straight leg raise).
Most common causes of nerve root impingement in the spine?
Disc herniation
Spinal stenosis
