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Paeds > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

RFs for DDH? (2)

A

FH

Breech

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2
Q

Presentation of DDH?

A
  • Usually at screening
  • Otherwise limp or abnormal gait
  • Asymmetry of skinfolds around hip
  • Limited abduction of hip
  • Shortening of affected leg
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3
Q

Management of DDH?

A
  • 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
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4
Q

What is torticollis?

A

Flexion, extension or twisting of muscle in neck that allows neck to move beyond its normal position
–> IE twisted neck

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5
Q

Most common sites of osteomyelitis? (2)

A

Distal femur
Proximal tibia
(Yet any bone can be affected)

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6
Q

Most common pathogen in osteomyelitis?

A

S. Aureus

Others: strep, H influezae

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7
Q

Clinical features of osteomyelitis?

A
  • 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
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8
Q

Ix for osteomyelitis?

A

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
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9
Q

Treatment of osteomyelitis?

A
  • 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
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10
Q

Presenting sx of subacute osteomyelitis?

A
  • 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
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11
Q

What age is septic arthritis most common?

A

<2y

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12
Q

Most common pathogen in septic arthritis?

A

S. Aureus

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13
Q

Presentation of septic arthritis?

A
  • 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
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14
Q

Ix for septic arthritis?

A

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)
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15
Q

Treatment of septic arthritis?

A
  • 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
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16
Q

Most common locations of fractures?

A
  • 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

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17
Q

Most common subtype of JIA?

A

Oligoarthritis (4 or less joints)

  • Knee, ankle, wrist most common
  • Onset 1-6y
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18
Q

S+S of JIA?

A

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

19
Q

Conditions associated with JIA? (6)

A 
Chronic anterior uveitis (20%) - eyes
Flexion contractors of joints
Growth failure
Constitutional problems (e.g. anaemia, delayed puberty)
Osteoporosis
Amyloidosis (v rare)
20
Q

Management of JIA? (5)

A 
NSAIDs and analgesics
Joint injections
Methotrexate
Corticosteroids
Cytokine modulators
21
Q

Most common form of arthritis in childhood?

A

Reactive arthritis

22
Q

Clinical features of reactive arthritis?

A
  • Transient joint swelling (usually <6w)
  • → Often ankles or knees
  • Usually follows (or rarely accompanies) extra­articular infection
  • Fever is low grade
23
Q

Causes of reactive arthritis?

A 
-	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
24
Q

Treatment of reactive arthritis?

A
  • None
  • Or NSAIDs
  • Complete recovery anticipated
25
Q

Causes of polyarthritis? (7)

A

Infection (septic arthritis, reactive arthritis)
IBD
Vasculitis (HSP, kawasaki)
Haematological disorders (haemophilia, SC)
Malignancy (leukaemia, neuroblastoma)
Connective tissue disorders(JIA, SLE etc)
CF

26
Q

What is Perthe’s disease?

A

Avascular necrosis of capital femoral epiphysis of femoral head
–> - Due to interruption of blood supply followed by revascularization and reosification over 18-36m

27
Q

Age of Perthe’s disease?

A

5-10y

28
Q

Presentation of Perthe’s disease?

A
  • Insidious
  • Onset of limp, or hip or kne pain
  • May initially be mistaken for transient synovitis
  • Bilateral in 10-20%
29
Q

Ix for Perthe’s disease?

A
  • 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
30
Q

Treatment of Perthe’s?

A
  • <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
31
Q

What is a slipped upper femoral epiphysis?

A

Fracture through growth plate (in metaphysis) that → slippage of underlying end of femur (epiphysis)

–> Displacement of femoral head poster-inferiorly

32
Q

Age is SUFE most common?

A

10-15y (adolescent growth spurt)

- Obese boys most common

33
Q

Presentation of SUFE?

A
  • 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
34
Q

Management of SUFE?

A
  • Surgical

- Usually with pin fixation in situ

35
Q 
Probable diagnoses (2)
Febrile, toxic looking infant, irritability with nappy changing 
- Restricted joint range)
A

Septic arthritis

Osteomyelitis

36
Q 
Probable diagnoses (2)
Sudden limp in otherwise well, young child
- Unilateral restricted hip movement
A

Transient synovitis of hip joint

Perthe’s disease

37
Q

Probable diagnosis
Hip pain in obese adolescent boy
- Unilateral hip restriction

A

Slipped upper femoral epiphysis

38
Q

Probable diagnosis
Joint pain, stiffness and restriction, loss of joint function
- Persistent joint swelling and loss of ROM

A

JIA

39
Q

What metabolic changes does Vit D deficiency lead to?

A

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
40
Q

What is rickets?

A

Rickets signifies failure in mineralisation of growing bone or osteoid tissue
- Due to vit D deficiency

41
Q

Causes of rickets? (3)

A

Nutritional
Malabsorptive (CF, coeliac, pancreatic insufficiency)
Drugs (e.g. anti-epileptics)

42
Q

Clinical manifestations of rickets?

A
  • 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)
43
Q

Blood test abnormalities in rickets? (5)

A
  • Serum Ca low or normal
  • Phosphorus low
  • Plasma alkaline phosphatase activity greatly increased
  • 25­hydroxyvitamin D may be low
  • PTH elevated
44
Q

What is skeletal dysplasia?

A

Heterogenous group of >200 disorders characterised by abnormalities of cartilage and bone growth

Paeds (15 decks)

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