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z S15 HEHI 4 > pediatric musculoskeletal > Flashcards

pediatric musculoskeletal Flashcards

1
Q

developmental dysplasia of the hip: previously known as…

A

congenital dislocation of the hip

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2
Q

developmental dysplasia of the hip

A

abnormal development of the hip
- maternal hormones can lead to transient lax hips

  • FYI 80% female, 50% first born
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3
Q

developmental dysplasia of the hip: contributing factors

A
  • frank breech
  • maternal hormones
  • parent, sibling with DDH: 5X likelihood
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4
Q

frank breech

A

buttocks presenting part with hips acutely flexed and knees extended

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5
Q

degrees of DDH (list)*

A

preluxation
subluxation
dislocation

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6
Q

preluxation*

A

MILD degree of ddh

femoral head remains in acetabulum (is in contact with it) but is displaced

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7
Q

subluxation

A

degree of ddh; incomplete dislocation

largest %

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8
Q

dislocation

A

most severe form of ddh

femoral head loses contact with acetabulum

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9
Q

ddh: diagnosis when

A

ideally made in neonatal period (tx w/in 2 mo = highest success rate)

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10
Q

ddh assessment techniques for diagnosis (list)

A
  • ortolani test
  • barlow test
  • galeazzi sign
  • trendelenburg sign
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11
Q

ortolani test

A

diagnostic tool for ddh

apply forward pressure form behind trochanter during full abduction (careful, can do damage)

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12
Q

barlow test

A

diagnostic tool for ddh

apply pressure from front during adduction

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13
Q

galeazzi sign

A

diagnostic tool for ddh

shortened limb on affected side

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14
Q

trendelenburg sign

A

diagnostic tool for ddh

as patient bears weight on affected hip, pelvis tilts downward on the normal side instead of upward

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15
Q

ddh: classic signs (list)

A
  • asymmetric gluteal folds
  • limited hip abduction
  • unequal knee height
  • lordosis/waddling gait
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16
Q

ortolani and barlow disappear after…

A

2-3 months (most reliable within this time period)

ddh

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17
Q

most sensitive test after ortolani/barlow disappear

A

after 3 months, limited hip abduction

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18
Q

ddh: therapeutic management goal

A

obtain and maintain safe, congruent position of the hip joint to promote normal development

begin ASAP! early intervention = favorable outcome

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19
Q

pavlik harness

A

therapeutic management of ddh; hip in controlled flexion and abduction: use pavlik harness

  • 0-6 months of age
  • worn continuously for ~5mo
  • dynamic splinting (adjust for growth)
  • not rigid
  • 95% effective
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20
Q

spica cast

A

therapeutic management of ddh; used when hip unable to be reduced/remain aligned properly and when pavlik ineffective

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21
Q

ddh: therapeutic management - 0 to 6 mo

A

pavlik harness or spica cast

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22
Q

ddh: therapeutic management - 6 to 18 mo

A
  • traction in prep for surgery
  • surgery for closed/open reduction
  • then spica cast 2-4 mo
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23
Q

ddh: therapeutic management - older child

A

hip correction much more difficult, surgery much more involved

after 4 years: very difficult
after 6 years: poor outcome

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24
Q

club foot

A

deformity of ankle and foot

  • talipes equinovarus (tev) most common, 95%
  • males affected 2x more than females
  • bilateral 50% cases
  • family tendency
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25
Q

talipes equinovarus

A

most common form of club foot: 95%

  • talipes: involves ankle, foot
  • equino: heel is elevated like horse (plantar flexion)
  • varus: fixed inversion (turned in)
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26
Q

club foot: diagnosis

A

readily apparent at birth

increased chance of ddh with tev!!!!

27
Q

club foot: therapeutic management (list)

A 
serial casting
surgical correction (if casting is ineffective)
28
Q

serial casting

A

therapeutic management of club foot

  • tx begins in newborn period
  • allows for gradual stretching
  • cast changed q few days 1-2 weeks, then q 1-2 weeks
  • usually casted for 8-12 weeks
29
Q

pmss

A

p ulse
m obility
s ensation
s kin

cast considerations

30
Q

kyphosis

A

abnormal increase in convex curve of thoracic spine

31
Q

lordosis

A

accentuation of lumbar curve

32
Q

scoliosis

A

lateral curvature + spinal rotation + thoracic hypokyphosis

  • most common spinal deformity
  • adolescent females 7:1
  • genetic component but not fully understood
33
Q

idiopathic scoliosis

A

no apparent cause

34
Q

congenital scoliosis

A

associated with neuromuscular disorders

35
Q

scoliosis: clinical manifestations

A

most noticeable during preadolescent growth spurt

36
Q

scoliosis: diagnosis*

A

screening assessment (view at hip height)

  • adam’s position, WEARING ONLY UNDERGARMENTS*, view from behind
  • see: asymmetric shoulder height, hip height, abnormal scapular shape
  • suspected? definitive tests required; even mild refer to ortho
37
Q

scoliosis: therapeutic management (list)

A
  • observation
  • bracing + exercise
  • spinal fusion
38
Q

bracing

A

therapeutic management of scoliosis; can halt/slow progression until skeletal maturity (non-curative)

  • worn 16-23 hours a day initially
  • adherence is an issue
  • exercise used in conjunction (increase muscle strength of spine, abdomen)
39
Q

spinal fusion

A

therapeutic management of scoliosis; correction of severe curve that doesn’t respond to bracing
- significant pain, possible respiratory compromise (atelectasis)

40
Q

scoliosis spinal fusion: mobility considerations

A 
day of surgery: log roll q2' (no twisting/bending!!)
pod 1: elevate HOB, sit at side of bed
pod 2: sit in chair for 1' x2
pod 3: ambulate 3x
- turn q2
41
Q

osteomyelitis

A

acute or chronic bone infection usually caused by bacteria, can lead to bone destruction, abscess formation, and dead bone

boys > girls

42
Q

osteomyelitis: etiology

A
  • exogenous source (puncture wound, open fracture, surgical contamination)
  • hematogenous source (bloodborne bacterium)
43
Q

osteomyelitis: clinical manifestations

A
  • severe pain
  • limited movement
  • fever
  • restlessness, irritability
44
Q

osteomyelitis: diagnostic eval

A
  • hx sx
  • leukocytosis
  • increased esr
    + blood culture, joint aspirate culture
  • x-ray: changes evident only after 2-3 weks
45
Q

leukocytosis

A

increased wbc

46
Q

osteomyelitis: therapeutic management

A
  • IV abx for at least 4 weeks

- followed by oral antibiotics

47
Q

septic arthritis

A

bacterial infection of the joint, usually hematogenous spread

  • staph aureus most common causative agent
  • most common joints affected: knees, hips, ankles, elbows
48
Q

septic arthritis: most common causative agent

A

staph aureus

49
Q

septic arthritis: most common joints affected

A

hips, knees, ankles, elbows

50
Q

septic arthritis: clinical manifestations

A

severe joint pain
swelling, tissue warmth, erythema
systemic illness may be present (fever, malaise, ha, n/v, irritability)

51
Q

septic arthritis: diagnosis

A
  • joint aspiration!

- early xray only reveals soft tissue involvement (but important for baseline)

52
Q

septic arthritis: treatment

A
  • IV abx based on gram stain 3-4 wks
  • adequate, timely drainage of infected synovial fluid
  • immobilization of joint (pain control)
  • pain management

after 5 days tx, begin PT. extensive PT allows maximum functioning

53
Q

muscular dystrophy

A

genetic, gradual, progressive degeneration of muscle fibers

  • progressive weakness, wasting of skeletal muscles
  • variable: age of onset, rate of progression, muscle groups affected
54
Q

duchenne muscular dystrophy

A

most severe, most common, most aggressive type of md

  • x linked inheritance
  • death usually by 30
55
Q

duchenne muscular dystrophy: clinical manifestations

A
  • onset between 3 to 5 years
  • usually lose ambulation ability by 12
  • cause of death usually respiratory tract infection or cardiac failure (all muscles affected!)
56
Q

duchenne muscular dystrophy: diagnostic eval

A
  • elevated serum cpk enzymes
  • muscle biopsy
  • gower sign
57
Q

gower sign

A

classic presentation of dmd; difficulty rising from sittin

58
Q

cpk enzyme

A

creatine phosphokinase: enzyme found mainly in the heart, brain, and skeletal muscle.

elevated serum levels in dmd

59
Q

duchenne muscular dystrophy: therapeutic management

A

NO CURATIVE TREATMENT

- genetic counseling (think of pregnancy spacing, sons)

60
Q

osteogenesis imperfecta*

A

characterized by bone fragility, fractures, deformity, blue sclera*, hearing loss, discolored teeth; autosomal dominant

most common osteoporosis syndrome in children; usually normal lifespan!

61
Q

blue sclera: think…

A

osteogenesis imperfecta!

62
Q

osteogenesis imperfecta: therapeutic management

A

primarily supportive!!

  • strengthen muscles = prevent contractures
  • light resistance exercise
  • handle carefully (fracture prevention)
  • limited benefit from pharm
  • family support!
63
Q

osteogenesis imperfecta: therapeutic management

A

primarily suppotive!!

  • strengthen muscles = prevent contractures
  • light resistance exercise
  • handle carefully (fracture prevention)
  • limited benefit from pharm
  • family support!

z S15 HEHI 4 (7 decks)

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