Musculoskeletal Flashcards
RFs for DDH? (2)
FH
Breech
Presentation of DDH?
- Usually at screening
- Otherwise limp or abnormal gait
- Asymmetry of skinfolds around hip
- Limited abduction of hip
- Shortening of affected leg
Management of DDH?
- If suspected→ specialist orthopaedic opinion
- USS quantifies degree of dysplasia and whether there is subluxation or dislocation
- If USS abnormal – infant may be placed in splint/harness
- → Keep hip flexed and abducted for several months
- Progress monitored by USS or XRay
- Splinting must be done expertly as necrosis of femoral head is potential complication
- In most cases → resolves
- Surgery required if conservative measures fail
What is torticollis?
Flexion, extension or twisting of muscle in neck that allows neck to move beyond its normal position
–> IE twisted neck
Most common sites of osteomyelitis? (2)
Distal femur
Proximal tibia
(Yet any bone can be affected)
Most common pathogen in osteomyelitis?
S. Aureus
Others: strep, H influezae
Clinical features of osteomyelitis?
- Markedly painful, immobile limp (pseudoparesis)
- Acute febrile illness
- Swelling and v tender over infected site
- Moving limb→ v painful
- May be sterile effusion of adjacent joint
- May be more insidious in infants
- → Swelling/ reduced limb movement 1st sign
- Occasionally multiple foci – disseminated staph or HIB
Ix for osteomyelitis?
Bloods:
- Cultures – usually positive
- FBC – WBC raised
- CRP/ ESR – raised
Imaging:
- XRay – initially normal except soft tissue swelling, at 7-10d subperiosteal new bone formation and localized bone rarefraction become visible
- USS – may show periosteal elevation
- MRI – allows identification of infection (subperiosteal pis and purulent debris in bone)
- Radio-nuclide bone scan→ helpful if site of infection unclear
Treatment of osteomyelitis?
- Immediate parenteral abx
- → For several wks to prevent bone necrosis, chronic infection, limb deformity and amyloidosis
- Abx IV until clinical recovery and acute-phase reactants back to normal
- Then oral therapy for several weeks
- Aspiration/surgical decompression of subperiosteal space
- → If atypical or imunodeficient
- Surgical drainage if no rapid response to abx
- Affected limb rested in splint and subsequently mobilized
Presenting sx of subacute osteomyelitis?
- Mild/moderate localised pain
- → Usually exacerbated by unusual physical activity
- Night pain common → relieved by aspirin
- Minimal loss of function
- Localised tenderness, occasionally + warmth, redness and soft tissue swelling
What age is septic arthritis most common?
<2y
Most common pathogen in septic arthritis?
S. Aureus
Presentation of septic arthritis?
- Erythematous, warm, acutely tender joint
- Reduced ROM
- Acutely unwell, febrile child
- Infants often hold limb still (pseudoparesis, pseudoparalysis) and cry if it is moved
- Joint effusion may be detectable in peripheral joints
- Diagnosis of septic arthritis of hip esp difficult in toddlers, as joint well covered by subcutaneous fat
- → Initial presentation may be limp or pain referred to knee
Ix for septic arthritis?
Bloods:
- FBC – increased WBC
- CRP/ESR – raised
- Blood cultures
Imaging:
- USS – helpful to identify effusion
- XR – exclude trauma and other bony lesions
- In septic arthritis- initially normal except widening of joint space and soft tissue swelling
- Bone scan
- MRI – may demonstrate adjacent osteomyelitis
Other:
- Aspiration of joint space under USS for culture = definitive investigation
- Ideally done immediately (unless sig delay in giving abx)
Treatment of septic arthritis?
- Prolonged course abx – initially IV
- Washing out joint/ surgical drainage if no rapid resolution or joint is deep seated (eg hip)
- Joint initially immobilized in functional position
- Subsequently must be mobilized to prevent deformity
Most common locations of fractures?
- Distal forearm – 22.7%
- Hand, phalanges – 18.9%
- Carpal-metacarpal – 8.3%
- Clavicle – 8.1%: immobilise with a sling for 4-6 weeks
- Ankle – 5.5%
Ie in gen upper extremities
Most common subtype of JIA?
Oligoarthritis (4 or less joints)
- Knee, ankle, wrist most common
- Onset 1-6y
S+S of JIA?
Sx:
- Gelling (stiffness after rest)
- Morning joint stiffness + pain
- If young → intermittent limp, deterioration in behavour/mood or avoidance of activities
- If systemic sx present → consider sepsis/ malignancy
Signs:
- Initially may only be minimal swelling
- Subsequently → swelling of joint due to fluid, inflammation and in chronic proliferation of synovium and swelling of periarticular soft tissues
> 6w
Conditions associated with JIA? (6)
Chronic anterior uveitis (20%) - eyes Flexion contractors of joints Growth failure Constitutional problems (e.g. anaemia, delayed puberty) Osteoporosis Amyloidosis (v rare)
Management of JIA? (5)
NSAIDs and analgesics Joint injections Methotrexate Corticosteroids Cytokine modulators
Most common form of arthritis in childhood?
Reactive arthritis
Clinical features of reactive arthritis?
- Transient joint swelling (usually <6w)
- → Often ankles or knees
- Usually follows (or rarely accompanies) extraarticular infection
- Fever is low grade
Causes of reactive arthritis?
- Enteric bacteria often cause in children • Salmonella • Shigella • Campylobacter • Yersinia are
- Or viral infections
- STIs in adolescents (chlamydia, gonococcus)
- Mycoplasma and Borrelia burgdorferi (Lyme disease)
- Rheumatic fever and poststreptococcal rare in developed countries but frequent in developing countries
Treatment of reactive arthritis?
- None
- Or NSAIDs
- Complete recovery anticipated
Causes of polyarthritis? (7)
Infection (septic arthritis, reactive arthritis)
IBD
Vasculitis (HSP, kawasaki)
Haematological disorders (haemophilia, SC)
Malignancy (leukaemia, neuroblastoma)
Connective tissue disorders(JIA, SLE etc)
CF
What is Perthe’s disease?
Avascular necrosis of capital femoral epiphysis of femoral head
–> - Due to interruption of blood supply followed by revascularization and reosification over 18-36m
Age of Perthe’s disease?
5-10y
Presentation of Perthe’s disease?
- Insidious
- Onset of limp, or hip or kne pain
- May initially be mistaken for transient synovitis
- Bilateral in 10-20%
Ix for Perthe’s disease?
- XR both hips (inc frog views)
- Early signs = increased density in femoral head → subsequently becomes fragmented + irregular
- If initial XR normal – repeat if sx persist
- Bone scan + MRI can be helpful
Treatment of Perthe’s?
- <50% head affected → only bed rest + traction may be needed
- If more severe/late → femoral head must be covered by acetabulum to act as mould for re-ossifying epiphysis
- → Achieved by maintaining hip in abduction with plaster or calipers or performing femoral or pelvic osteotomy
What is a slipped upper femoral epiphysis?
Fracture through growth plate (in metaphysis) that → slippage of underlying end of femur (epiphysis)
–> Displacement of femoral head poster-inferiorly
Age is SUFE most common?
10-15y (adolescent growth spurt)
- Obese boys most common
Presentation of SUFE?
- Limp or hip pain - may be referred to knee
- Onset may be acute, following minor trauma or insidious
- Examination shows restricted abduction and internal rotation of hip
Management of SUFE?
- Surgical
- Usually with pin fixation in situ
Probable diagnoses (2) Febrile, toxic looking infant, irritability with nappy changing - Restricted joint range)
Septic arthritis
Osteomyelitis
Probable diagnoses (2) Sudden limp in otherwise well, young child - Unilateral restricted hip movement
Transient synovitis of hip joint
Perthe’s disease
Probable diagnosis
Hip pain in obese adolescent boy
- Unilateral hip restriction
Slipped upper femoral epiphysis
Probable diagnosis
Joint pain, stiffness and restriction, loss of joint function
- Persistent joint swelling and loss of ROM
JIA
What metabolic changes does Vit D deficiency lead to?
Low serum Ca
- –> secretion of PTH and normalises serum Ca but demineralises bone
- PTH causes renal losses of phosphate → low serum phosphate levels
- → Further reducing potential for bone calcification
What is rickets?
Rickets signifies failure in mineralisation of growing bone or osteoid tissue
- Due to vit D deficiency
Causes of rickets? (3)
Nutritional
Malabsorptive (CF, coeliac, pancreatic insufficiency)
Drugs (e.g. anti-epileptics)
Clinical manifestations of rickets?
- Earliest sign = pingpong ball sensation of skull (craniotabes) elicited by pressing firmly over occipital or posterior parietal bones
- Misery
- FTT/short stature
- Frontal bossing of skull
- Delayed closure of anterior fontanelle
- Delayed dentition
- Rickety rosary
- Harrison sulcus
- Expansion of metaphyses (esp wrist)
- Bowing of weightbearing bones
- Hypotonia
- Seizures (late)
Blood test abnormalities in rickets? (5)
- Serum Ca low or normal
- Phosphorus low
- Plasma alkaline phosphatase activity greatly increased
- 25hydroxyvitamin D may be low
- PTH elevated
What is skeletal dysplasia?
Heterogenous group of >200 disorders characterised by abnormalities of cartilage and bone growth
