Msk Disorders Flashcards
How common is developmental dysplasia of the hip? What is included in DDH?
5/100
Dislocated hips - other acetabular dysplasia (where femoral head is in position but acetabulum is shallow)
Screening of DDH ? Manoeuvres called? Why are they unhelpful tests as the baby gets older?
Screened at birth and at 6 weeks
Barlow’s / ortolani’s
Contractures form
What are the warning signs (features) of DDH
Delayed walking
painless limp
Waddling gait
What two features are common in babies and do not represent DDH? How common?
Asymetrical skin creases -30% of all infants
Hip clicks - 10%
How is a diagnosis of DDH made?
uss is diagnostic
Femur may be shortened - Allis sign
O/e - limited abduction
What level of hip abduction should be achieved by children? Up to what age?
Supine children should be able to abduct a flexed hip fully until 2 years old
Why are X-Ray’s not useful for diagnosis of DDH
Femoral head doesn’t ossify until 4/12 (becomes useful then)
Management of DDH in
How often does a harness for DDH have to be worn? How often is it adjusted?
Constantly
Every 2 weeks
What happens if there is accelerated degenerative changes in DDH?
Open surgery
Often have total hip replacement in early adult life
What is (legg-calve-) perthes disease ? What happens? How long does it take?
Osteonecrosis of the skeletal head prior to skeletal maturity.
Idiopathic ischemia -> avascular necrosis at the upper femoral epiphysis with flattening and fragmentation of the femoral head.
Revascularisation & reossification occur and growth resumes (may not be normal)
3-4 years
Risk factors leg-calve-perthes disease?
Males 5:1
Family Hx
Features / presentation of leg clave perthes disease
- insidious* onset of lump (+/- hip pain) between 3 and 12 years -> pain may be felt in hip, thigh or knee
- Abduction and rotation are limited O/E*
Diagnosis of legg calve perthes
Hip X-ray - shows decreased height (flattening) and increased density of femoral head
Can you have more than one hip affected in LCP disease
Bilateral in 20%
Management in LCP disease if
Prognosis is good
Bracing with analgesia & mild activity restriction
Prognosis / Management of LCP in older children / more than 1/2 femoral head involved
Permanent deformity in 40% with early degenerative arthritis/
Several surgical options
What is transient synovitis often called
Irritable hip
Usual course of transient synovitis
Self limiting. Common esp in children 2-12yrs following viral URTI
Features of transient synovitis ? O/e?
Sudden onset hip pain (NON AT REST), limp and refusal to weight bare on affected side.
Limited abduction / rotation in otherwise well afebrile child
What is the key differential to transient synovitis ? When should this be queried ?
Septic arthritis
Febrile with pain at rest & refusal to even move affected joint
Why do you investigate transient synovitis ? What do you use to make a diagnosis?
To exclude septic arthritis Acute phase reactants - CRP, WBC, ESR (only *mildly raised*) Blood cultures - should be *-ve* X-ray hip - normal Hip USS - may be small effusion
Management of transient synovitis
Supportive - bed rest and analgesia
Should resolve spontaneously in 2 weeks
What is slipped upper femoral epiphysis (SUFE)
Displacement of the epiphysis of the femoral head posterio-inferiorly
When does SUFE most commonly occur? In who?
10-15 (usually occurs around growth spirt / minor trauma)
Male (black / obese)
Delayed skeletal maturation & endocrine disorders
Family Hx
Presentation of SUFE ? O/e?
limp or with referred hip / knee pain
O/e - restricted abduction & internal rotation of hip
Diagnosis / treatment of SUFE
Hip X-ray (may require frog leg lateral view)
Surgical - usually pin fixation
2 common knee disorders (male / female)
Osgood - schlatter (physically active males)
Chondromalacia patellae - adolescent females
When should back pain be referred ?
Before adolescence - ?significant pathology
Causes of back pain in adolescence
Muscle spasm / soft tissue injury
Schearmann’s disease
Spondylolisthesis / spondylolisis
Tumours
Usual cause of muscle spasm / soft tissue injury
Sports
What is shearmanns disease ? Features?
Osteochonditis (avascular necrosis of ossification centre) of lower thoracic vertebrae)
Localised pain, tenderness, kyphosis
Usual location of spondylo- things ? What happens if there is anterior shift of the vertebral body?
L4/5
*lower back pain exacerbated by bending backwards (spondylisthesis)
What is scoliosis ? How many children affected?
Lateral deformity of the spine with rotational deformity
4%
How is scoliosis classified ? Egs?
Vertebral abnormalities (eg. Ostegenesis imperfecta / hemivertebra) Neuro muscular (eg. Polio / cerebral palsy) Mischellaenous (eg. Idiopathic (most common) / dysmorphic syndromes)
What is hemivertebra
Lack of formation of one half of the vertebral body
How can you demonstrate rotation in scoliosis
Child bends forwards - rib hump noted
When does idiopathic scoliosis occur ? Who is it more common in ?
85% in adolescence
Females with FHx
Management of various idiopathic scoliosis
Mild - none
Moderate - brace
Severe - surgery
What is torticollis also called? Who is it usually in? What is the usual cause? Prognosis?
Wry neck - head turned persistently to one side
Common, self limiting in young children (often with URTI)
sternomastoid tumour
Usually resolves in 1 year
What is osteomyelitis
Infection of the metaphysis of long bones - any bone can be affected
When can osteomyelitis cause septic arthritis
When joint capsule is inserted distal to the epiphysis (eg. The hip)
Usual cause of osteomyelitis
Haematogenous spread
Can occur directly from infected wound
Usual pathogen in osteomyelitis ? Neonates?
Staph aureus (group B strep and E.coli in neonates)
What disease has an increased risk of osteomyelitis and which types
Staphylococcal & salmonella osteomyelitis
In Sickle cell disease
Features of osteomyelitis
Painful and immobile limb (pseudoparesis) in a febrile child
O/e - erythermatous, warm, swollen, and very tender
How does osteomyelitis present in infants
More insidious, swelling and decreased limb movements
Investigations in osteomyelitis
Acute phase reactants raised - CRP, ESR, WCC
Blood cultures - +ve in 50%
X-rays - takes 7-10 days
What to do if +ve blood cultures in osteomyelitis
Joint aspiration for M, C & S
What is seen on X-ray 7-10 days after infection? What can be done initially?
Subperiosteal elevations & localised decreased density.
Radionuclide scans can be used to elicit a likely site of infection (as there is increased uptake)
Treatment of osteomyelitis
IV Abx until there is clinical recovery & acute phase reactants normalise followed by oral therapy for several weeks.
Surgical drainage if unresponsive to Abx
Complications of osteomyelitis
Septic arthritis, growth disturbance & limb deformity (if epiphyseal plate infected)
What is septic arthritis ? Vs OM more common?
Infection of the joint space
Yes it’s more common
What can septic arthritis lead to ?
Disability and bone destruction
Usual age for septic arthritis? Origin? How many joints? Usual cause?
Features of septic arthritis
Painful joint -> limp, irritability, refusal to bear weight
Limb is held rigid (pseudoparesis) with tenderness and varying degrees of swelling / warmth
Investigations for septic arthritis
Elevated acute phase reactants
Aspiration of joint for M, C & S
USS - can show effusions
X-rays - exclude trauma & other bony lesions
Management of septic arthritis
Early and prolonged IV Abx
Surgical drainage - if recurrent or hip affected
What is the most common childhood arthritis
Reactive
What are the features of reactive arthritis
Transient joint swelling
Usual cause of reactive arthritis ? Other causes?
Bacterial - salmonella, shigella, campylobacter, versilsia
Viral - rubella, parvovirus B19, influenza, herpes, cozsackie
What is juvenile idiopathic arthritis
Children and adolescents with persistent joint swelling >6 weeks in the absence of infection or any other defined cause
What are the types of JIA? What is the classification according to ?
Oligoarthrits 4, systemic (Still’s disease), psoriatic arthritis, enthesitis
RF/HLA B27
Who gets affected by still’s disease ? Where does it affect? What are the other features ?
<5
hips, ankles, knees,
High fever, salmon pink rash, lymphadenopathy, myalgia, malaise
NO ARTHRITIS INITIALLY
Seen on investigations for still’s disease?
Anaemia on FBC
Neutrophilia
Increased acute phase reactants
Two types of polyarthrits and prognosis
RF -ve - good prognosis
RF +ve - Bad prognosis
RF -ve polyarthrits joints affected ? Ages?
All ages and all joints
typically (not always) spares MCP joints
Cervical spine and TMJ’s may be involved
Who is usually affected by RF +ve polyarthrits ? Which joints are affected? Other features?
Females >8
small joints of hands and feet (hip and knee also affected)
Early rheumatoid nodules in 10%, might be systemic vasculitis
Who is usually affected by oligoarthrits ? Type of arthritis ? Affecting?
*Girls
Investigations for oligoarthrits
Increased acute phase reactants
ANA (antinuclear antibodies) are almost always present
Associations with oligoarthrits
1/3 will develop chronic iridocyclitis (uveitis)
What happens if >4 joints are affected after 6/12 in oligoarthrits
Called ‘extended oligoarthrits ‘ - poor prognosis
Management of JIA
MDT
1- Physiotherapy to optimise joint mobility, prevent deformity and increase muscle strength
2- medication -analgesia and reduced inflammation (NSAIDs), systemic steroids for severe disease / severe uveitis, methotrexate used early to reduce joint damage
Egs of primary bone diseases
Achondroplasia, osteopetrosis, osteogenesis imperfecta
What is the cause of achrondroplasia
Autosomal Dominant
Chromosome 4
*fibroblase growth factor gene (FGFR3)
(Half are new mutations)
Clinical features of achondroplasia
Limbs - shortened (proximal>distal), bow legs (genu varum)
Neurological - hydrocephalus, delayed motor development, normal intelligence
Spine - short, lumbar lordosis, throacolumbar kyphosis
Ear - recurrent otitis media
What is the other name for osteopetrosis ? What is it?
Marble bone disease
Hyper density of bones due to osteoclasts dysfunction - deficient carbonic anhydrase - bones are very brittle
What is osteogenesis imperfecta often called ? What causes it? What are the characteristics?
Brittle bone disease
Group of disorders caused by mutations in type 1 collagen genes
fragile bones & frequent fractures
What are the normal genes for mutation in osteogenesis imperfecta
COL1A1 / 1A2 genes in 90%
Types of osteogenesis imperfecta
1- most common, autosomal dominant
2- lethal, usually multiple fractures before birth (often stillborn)
3- severe, progressively bone deformities, survival to adulthood rare
4 - moderate, bone fragility without other features of type 1
How does type 1 osteogenesis imperfecta present ?
Recurrent fractures, blue tinged sclerae, sometimes hearing loss
Management of osteogenesis imperfecta
BisPhosphonates - strengthens bone bit doesn’t areas underlying problem
What is rickets
Failed mineralisation of growing bones
What are the X-ray changes of rickets
Cupping of ends of bones
Splaying
Osteopenia
What are the clinical findings in rickets
Bow legs, wide wristed with delayed motor development due to associated myopathy
Rickettic rosary
What is rickettic rosary
Prominent knobs of bone at costochrondiral joints (ribs)
Causes of rickets
Vit d deficiency (nutritional, 1a-hydroxylase deficiency) Phosphate deficiency (usually due to poor renal absorption Calcium deficiency
What’s seen in bloods of rickets
Decreased - serum 25-OH vit D, phosphate
Increased - PTH, alkaline phosphatase
Treatment of rickets
Vitamin D- calcitriol
Calcium in infants
