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Lifespan > Pediatrics Test 1: Lecture 1 > Flashcards

Pediatrics Test 1: Lecture 1 Flashcards

1
Q

when/how do skeletal muscles develop in childhood

A

most skeletal mm fibers present at birth and all are present by 12 months

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2
Q

what cells are important for skeletal mm development and what happens if these cells are impaired somehow

A

satellite cells

allow mm to build and regenerate

some progressive conditions do not allow these cells to regenerate/restore and thus it is important to know this when treating these pts (i.e. you can’t make the mm grow no matter how much exercise)

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3
Q

important things to note about mm development

A

mm fibers susceptible to internal and external forces; development and experiences w/i first year can matter

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4
Q

what happens with spastic mm

A

spastic mm are smaller and more susceptible to contractures

mm do not keep up with growing bone and sarcomeres overstretch

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5
Q

do type I or type II mm fibers atrophy/hypertrophy with various conditions

A

inconclusive of which fibers are involved in which conditions

with CP type II is lost (fast acting) compared to type I but research is still ongoing

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6
Q

when does bone development progress most rapidly and what does this indicate for premies

A

more rapid in prenatal period

by birth diaphyses are almost ossified

premature = osteopenia common

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7
Q

what determines if bone growth is complete and when does this happen

A

epiphyseal plate is ossified, diaphyses and epiphyses are joined, and growth of bone length is considered complete

timing varies with each bone; most are fully ossified by 20 years

after they have ossified PT can no longer change bone structure

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8
Q

when does the skull fully close/fuse

A

18 months

cant wear helmet after

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9
Q

what determines the joint structure/shape in development

A

basic structures formed during 6th - 7th week of gestation

final shape develops through early childhood under influence of different forces of movement and compression

forces need to be PROPER to develop normally (i.e. toe walker could be problematic from wrong forces)

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10
Q

what is bone functional adaption

A

bone shape can be changed after initial development

process uses resorption of old or mature bone and formation of new bone to determine its shape

bone structure adapts in response to mechanical forces that are placed on bone (when therapists can impact bone structure)

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11
Q

how does bone development differ in kids with CP

A

they do not get as much pressure through the hip via musculature

babies all have shallow acetabulum; is they dont have the right forces then the hip remains shallow/unstable

joint is unstable and not stressed enough to form properly

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12
Q

how might a brachial plexus injury affect bone development

A

GH joint doesn’t get proper forces w/o mm

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13
Q

why might a premature infant have an extended posture

A

less movement in womb

more “floppy”/extended posture from lack of mm development

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14
Q

full term baby body/spinal alignment at birth

A

kyphotic = normal at birth

PPT at birth

if baby is 6 months and still not extending spine or have an anterior pelvic tilt may need to have looked at by a doctor; babies should be pushing up while prone and extending at this point

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15
Q

MSK issues that may occur with adults with CP

A

scoliosis
hip dislocation
cervical neck dislocation
contracture
arthritis
patella alta (mm not pishing patella into groove and it dislocates)
overuse syndrome
nn entrapment
fx

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16
Q

children with CP typically have what type of impairments

A

delays with walking

ROM limitations

atypical muscular pull/spasticity

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17
Q

why are hip subluxation/dislocation common with kids with CP

A

hip is shallow/unstable at birth

kids with CP do not have strong ABD/EXT mm

adduction and flexion mm often override others and pull hip out of joint

this is why it is crucial that kids stand and get compression through the joint

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18
Q

what has happened to the incidence of pathological hip conditions in recent years

A

increasing

i.e. legg calve perthes and slipped capital femoral epiphysis

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19
Q

examples of rotational/angular problems of the bone

A

in toeing

blounts disease

patella alta

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20
Q

what is blounts disease

A

abnormal tibial growth

excessive varus at knees past 2 years old

may need to be referred to orthopedist

treatment = staple growth plate on 1 side to normalize growth

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21
Q

at birth the femur is in more anteversion; what causes this to decrease to more normal ranges

A

femoral head, neck, and greater trochanteric areas are made of pliable cartilage and attached to rigid osseous diaphysis

as infant develops, normal torsional forces about this point of fixation cause a decrease in anteversion

if important hip motions like ER and ABD are not obtained (i.e. like with walking), proper forces are not present to help develop the hip and decrease anteversion

walking is delayed = infantile torsion does not decrease as it should; with conditions like CP want to intervene early

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22
Q

torsion vs version

A

torsion = head and neck relative to condyles

version = position of head of femur in acetabulum relative to frontal plane (anteversion- head is more anterior in acetabulum, retro - head is more posterior)

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23
Q

at birth how much anteversion is present at birth and what does this decrease to

A

40-60 degrees anteversion at birth

resolves to 15-20 deg with proper forces

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24
Q

angle of inclination at birth vs after development

A

at birth = 150 deg (coxa valga)

2-3 years old = decreases to ~130 deg

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25
Q

what does anteversion of the femur present like

A

persistent in toeing pattern

common with kids who do not get proper forces

CP - causative factor for hip instability

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26
Q

when does genu varus present a cause for concern

A

as an infant, physiological bowing is normal

if still present around 2-6 years

varum/torsion generally normalizes by 12-24 months

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27
Q

if there is still excessive bowing of the knees at 1-2 years old, what are some factors that may be contributing

A

medial knee capsule tightness b/c of interuterine position

coxa valga of femur

lateral hip RT contracture

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28
Q

normal tibia external torsion

A

about 5 deg as newborn

increases by about 20 deg by adolescence

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29
Q

describe the typical newborn foot

A

flexible

newborn talocrural joint rests in DP and may have PF limit resulting from intrauterine posture (especially in the last 2-3 months of gestation)

forefoot and rearfoot rest in inversion when non-weightbearing and eversion with supported weight bearing

if not flat/flexible could be a bigger issue

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30
Q

lateral border of the foot should look like what

A

straight regardless of weight bearing

if curved, could be metatarsal abductus due to intrauterine positioning and may need bracing to correct

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31
Q

typical developing children have flat feet for how long

A

4-5 years

usually do not treat flat foot unless there is pain, tripping, or no arch

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32
Q

when does longitudinal arch develop

A

develops over the forst 10 years of life

start seeing development around 4

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33
Q

things to keep in mind with a peds MSK exam

A

keep a consistent and logical sequence

want a detailed hx (including birth story)

restructure as needed due to child’s participation level

must have a knowledge of peds cases to know what to look for

understand exam procedures appropriate for age and condition

want exam in natural environment if possible

want to keep kid engaged

want to create family centered POC and goals

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34
Q

what to know about observation, ROM, and strength for a general peds assessment

A

ovservation - observe child playing spontaneously or assist if needed

ROM - assess for limitations, contractures, or excessive motion

strength - can estimate strength from skills a child can perform like riding tricycle, getting up from floor with half kneel, pull to sit, lift head in prone, climbing stairs or others; can use dynamometer at 3 or 4 or MMT

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35
Q

how do kids with JIA often align their legs

A

ER for greater comfort

may also have leg length discrepancy

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36
Q

kids with CP have an increase likelihood of what type of malalignment as they age

A

rotational malalignment between tibia and femur

i.e. hip IR and outtoeing

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37
Q

rotational abnormalities are common in kids with what

A

JIA and CP

especially when ambulatory

force across the knee is dramatically increased

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38
Q

what is a common side effect of disuse in children with severely limited movement such as those with CP, spina bifida, or arthrogryposis

A

adverse effects such as delaying ossification centers and bone reabsorption

fx risk increases as well

also occurs with other conditions that cause demineralizaton (i.e. on chemo or corticosteroids)

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39
Q

standing programs show improvements in bone density under what parameters

A

standing between 60-90 min, 5 days a week

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40
Q

standing programs show improvements in hip stability under what parameters

A

60 min/day when positioned between 30 and 60 deg ABD

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41
Q

effectiveness of weightbearing with adaptive devices

A

good

impact through bones is best even if only partial WBing

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42
Q

interventions for MSK disorders

A

strengthening exercises in various conditions

botox

stretching

bracing

supported standing/walking

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43
Q

what type of strengthening has no negative effect of duchens muscular dystrophy

A

submaximal concentric contraction

avoid eccentric

aquatic exercise is also safe and beneficial

none of these will stop the progession but it can have other benefits

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44
Q

benefits of botox in kids/when it is used/how it works

A

good for spasticity; works at NMJ and inhbits firing of nn

used when ROM is important for certain activities

research is looking at starting it younger to promote better mm development of kids with mm disorders

recent research also notes that it should not be used in certain joints to increase flexibility

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45
Q

stretching benefits for different types of stretching

A

short term improvements with normal mm with short term stretches

neuro compromised mm (i.e. CP) need a more prolonged stretch to see improvements

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46
Q

common peds disorders involving bone

A

fxs

greenstick fx

epiphyseal fx

osteogenesis imperfecta

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47
Q

S&S to screen for abuse

A

children under 3 that are fx prone

premature kids

developmental disabilities

low socioeconomic status

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48
Q

epiphyseal fxs can cause what types of secondary problems and how prominent are they

A

can cause problems with bone growth, limb length discrepancy, etc

20% of all fxs in kids

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49
Q

what is osteogenesis imperfecta

A

genetic collagen problem that causes weak bones

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50
Q

4 types osteogenesis imperfecta

A

type I = mild

type II = perinatal; lethal; child will not survive

type III = severe/progressive; multiple fxs at birth

type IV = moderately severe

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51
Q

what is duchenne muscular dystrophy

A

most common muscular dystrophy

fatal/progressive weakness of skeletal and respiratory mm

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52
Q

what causes duchenne muscular dystrophy and what demographics obtain this disease

A

genetic; recessive defect in X chromosome; males

lack of dystrophin protein production that is needed for mm regeneration

can run in families

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53
Q

life expectancy for DMD

A

most dont live past 30

kids usually walk until middle school

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54
Q

5 stages of DMD

A

1 = pre-symptomatic
2 = early ambulation
3 = late ambulation
4 = non-ambulatory
5 = late non-ambulatory

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55
Q

what might you first see with an undiagnosed DMD child

A

delayed milestones

usually around 3 years; can dx as early as 18 months

clumsy, walk on toes, motor regression, gowers sign

pseudohypertropy in calf = toe walk to stabilize b/c proximal mm are more affected

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56
Q

what happens with kids as DMD progresses

A

develop scoliosis; can have sx intervention

cardiac/respiratory mm affected (eventually fatal)

some do tendon lengthening to keep feet flat

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57
Q

DMD treatment

A

corticosteroids to decrease inflammation in mm

genetic treatment being worked on now

PT - QOL is major emphasis; decide goals, PT, aquatics, active ex, standing programs, etc

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58
Q

what is spinal mm atrophy

A

group of autosomal recessive disorders

mutation or deletion of survival motor neuron 1 (SMN1) gene

characterized by degeneration of anterior horn cells of SC, mm atrophy, absent DTRs, and widespread weakness

sensation/cognition not generally impaired

occurs in 1 of every 10000 live births

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59
Q

4 types of SMA

A

1 = severe; death by 2 years

2 = moderate; most common; weakness around 7-18 months; progressive

3 = mild; after first 18 months

4 = adult onset

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60
Q

S&S of SMA

A

hypotonia
absent reflexes
hip sublux
scoliosis
increased club foot
dysphagia
GI dysfunction

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61
Q

PT focus for SMA

A

depends with child/type

want to maintain and improve:
balance
respiratory mm
mobility

62
Q

what is ideopathic toe walking

A

diagnosis of exclusion; kid walks on toes with no known reason/pathology

can be intermittent or constant

30-42% considered genetic

63
Q

treatment for idiopathic toe walking

A

want to intervene early

if they havent stopped by 2.5-3 years old they probably will not

articulating AFO - prevents kid from going into toes

casting advised if they toe walk >25% of time and have <10 deg ROM with knee ext

PT = strengthen, stretch, balance, ambulation, auditory therapy

sx is last resort to increase ROM and prevent toe walk

64
Q

what is elhers danlos syndrome

A

heterogeneous group of disorders

characteristics: hyper-extensibility, ligament laxity, tissue fragility, delayed wound healing, atrophic scarring, and bruising/bleeding

65
Q

primary interventions for ehlers danlos

A

PT

interventions based on severity to maximize flexibility, strength, and independence with precautions as needed for joint instability

66
Q

characteristics of JIA (previously juvenille rheumatoid arthritis)

A

unknown origin
occurs before 16 yrs
7 main categories

67
Q

most common JIA types seen by PT

A

systemic, oligoarthritis, and polyarthritis

68
Q

pathophysiology of JIA

A

inflammation leads to capsule hypertrophy, irregular bone growth, altered growth, chronic joint instability , osteoporosis, and contractures

69
Q

JIA treatment

A

modalities
strenfth
ROM
posture
endurance
joint protection
activity modification

**must modify treatment when there is active inflammation

can do a splint to support

70
Q

what is hemophilia

A

lack of clotting proteins (A, B, C types)

bleed easy from minor trauma

inflammation or bleeding in jts causes destructive changes with thickening of synovial tissue and breakdown of cartilage narrowing the joint space, and contractures

71
Q

PT intervention for hemophilia

A

ROM
strength
adaptive aides
splints

often just see when there is an acute injury

avoid trampolines, karate, heavy weights, etc

with infants and toddlers you dont want to limit activities but you do want to prevent bleeds

72
Q

structural vs nonstructural scoliosis

A

structural = curve of spine fixed; due to vertebrae structure

nonstructural = flexible; some spine straightening; due to position, mm imbalance, limb discrepancy, neuropathy, etc

73
Q

when to screen for nonstructural scoliosis

A

CP
down syndrome
spina bifida

74
Q

types/age ranges for idiopathic scoliosis

A

infantile = <3 years
juvenille = 3-10 years
adolescent = 10 years to bone maturity

75
Q

scoliosis treatment

A

bracing
exercise (strength, flexibility, respiratory mm, stretching)

sx fusion

76
Q

when does scoliosis require sx

A

if cobbs angle > 45 deg

T/S is compressing organs

77
Q

C curve vs S curve

A

C curve = starts in T/S

S curve = 1 curve in T/S and another secondary curve

78
Q

cobbs angle of what denotes scoliosis

A

> 10 deg

79
Q

what is adams fwd bend test

A

standing fwd bend

compare shoulder height

leg length discrepancy? pelvic obliquity?

80
Q

what S&S with scoliosis should be referred to physician

A

excessive kyphosis
P!
mm spasm
HS tightness
P! w/ SLR

could be a pinched nn

81
Q

what is done to stabilize scoliosis in growing kids

A

growing rods

connect to vertebrae on top and bottom of the curve; not all vertebrae

use a magnet to extend rod as the kid grows

get a fusion once skeletally mature

82
Q

what is a progressive scoliosis curve

A

sustained increase of 5 degrees or more on two consecutive examinations within 4-6 month intervals

83
Q

what are the main factors (6) that influence the probability of progression in skeletally immature pt

A
  1. younger the pt at diagnosis the greater the chance of progression
  2. double curve pattern vs single curve
  3. lower the rissner sign (bone maturity; lower risser is more likely to progress)
  4. curves are larger at initial presentation
  5. female pt
  6. curves develop before menarche
84
Q

congenital scoliosis curves are caused by

A

anomalous vertebral development in utero

85
Q

normal kyphosis range

A

from T5-T12

20-40 deg between vertebral segments

86
Q

spinal kyphosis can occur due to

A

trauma
congenital conditions
neuromuscular
post traumatic (i.e. tuberculosis)
scheuermann disease (most common; due to poor posture; only in kids)

87
Q

what is congenital kyphosis

A

anomalies occur later during chondrification and ossification stages of embryonic period

most frequent defects = multiple hemivertebrae (44%), anterior segment defect (32%), and single hemivertebrae (18%)

usually needs sx intervention; without may progress to paraplegia or cardiac dysfunction

posterior spinal artherodesis can be safely completed in pts as young as 6 months

bracing does not help

88
Q

what is scheudermann disease

A

a rigid form of postural kyphosis

often neglected; develops in childhood due to poor posture

89
Q

radiographic criteria for scheurmann disease

A
  1. anterior wedging of 5 deg or more for at ;east 3 or more continuous vertebrae
  2. narrowing of intervertebral disc space
  3. kyphosis greater than 45 deg between vertebral segments T5-T12 coupled with compensatory cervical and/or lumbar hyperlordosis, uncorrected on active hyperextension and incongruent vertebral end plates with schmorl nodes
90
Q

scheurmann disease treatment

A

want to increase extension

increase flexibility and extensor strength

sports like volleyball and swim

91
Q

when is hyperlordosis common in kids

A

can occur with conditions that have weak abs

i.e. DMD or spina bifida

not using abs to stabilize; using lordosis for stability and locking out facets; stretches out trunk extensors

92
Q

what is spondylolisthesis

A

dysplastic and ischemic are most common types seen in peds

slippage of 1 vertebrae on the other

severity characterized by degree of slippage

common with gymnastics

93
Q

spondylolisthesis grades according to meyerding classification system

A

grade I (mild) = less than 25%; responds best to PT

grade II = 25-50%

grade III = 50-75%

Grade IV = 75-100%

Grade V = ptosis of cranial vertebrae

94
Q

2 classifications of aquired leg length discrepancy

A
  1. direct (growth retardation)
  2. indirect (growth stimulation)
95
Q

what is an apparent leg length discrepancy

A

due to things such as:
- spine alignment
- pelvic obliquity
- scoliosis

96
Q

leg length discrepancy for 0-2cm difference

A

no treatment generally at this point

if in an infant - hip dysplasia is possible and should refer

older kids = 1 cm could be a soft tissue abnormality, but more than 2cm refer out to be safe and check bones

97
Q

2-4 cm leg length discrepancy treatment

A

shoe lift

if lift is 3/8 inches or more it has to be added to sole of shoe and not the inside

98
Q

2-6 cm leg length discrepancy treatment

A

epiphysiodesis, shortening

arrest growth on 1 side; delay it for a period

99
Q

6-20 cm leg length discrepancy treatment

A

lengthening that may or may not be combined with other procedures

100
Q

if a leg length discrepancy is >20 cm, what is the treatment

A

fit for prosthetic

101
Q

compensations common for those with leg length discrepancies

A

if there is a contracture on the opposite (longer) side, they may try to shorten the limb

may use PF on short side to compensate and thus lose DF ROM

these types of stresses on back and knees lead to long term degenerative changes

102
Q

how to use a tape measure for leg length discrepancy

A

measure from ASIS to medial malleolus or tuberosity to medial malleolus (takes pelvic obliquity out of the equation)

can also use on an x-ray for more accuracy

103
Q

what is galeazzi sign of leg length discrepancy

A

look at kid in hooklying position and see if knees are in the same place

femoral head falls posterior with hip sublux/dislocation

104
Q

transverse vs longitudinal deficiency types of congenital limb deficiency

A

transverse = level at which the limb terminates

longitudinal = deficient bones proximal to distal (i.e. may be missing tibia/fibula but still have some foot bones)

105
Q

when does congenital limb deficiency form

A

at 2-6 weeks limb buds form in utero

at 3-8 weeks deletion occurs

106
Q

what is hemimelia

A

absence or gross shortening of a bone

fibular hemimelia is most common

107
Q

what is proximal femoral focal deficiency

A

PFFD

shortening or complete absence of femur

associated with problems like acetabular dysplasia

108
Q

treatment options for congenital limb deficiency

A

depends on numerous factors

limb lengthening

epiphysiodesis

amputation (to make functional and fit prosthesis)

rotationplasty (make ankle function as knee joint; residual ankle faces posterior)

109
Q

are upper or lower extremity deletions more common with congenital limb deficiency

A

upper

110
Q

when to consider prosthesis for congenital limb deficiency

A

12-15 months

may use a prosthesis for certain tasks but still prefer remaining hand for sensory input for some tasks

111
Q

what is arthrogyroposis multiplex congenita

A

collection of syndromes characterized by symmetric, congenital, non-progressive contractures of at least 2 joints

112
Q

proposed cause of arthrogyroposis multiplex congenita

A

believed to result from decreased fetal movement and possible damage to anterior horn cells of SC

113
Q

most common form of arthrogyroposis multiplex congenita

A

amyoplasia

deficient moration of mm tissue

mm are underdeveloped

joints have abnormal deformities/adhesions and abnormal skin folds

114
Q

fatality rate of arthrogyroposis multiplex congenita

A

50% in infancy

90% of surviving infants have symmetrical involvement of multiple joints

115
Q

arthrogyroposis multiplex congenita treatment

A

inclues PT/OT

casting for prolonged stretch

sx for soft tissue/bone deformities

do not want an aggressive stretch (would cause further inflammation/contractures)

116
Q

JIA characteristics and proposed etiology

A

joint swelling, pain, and limited mobility

theory = autoimmune inflammatory disorder activated by an external trigger in a genetically predisposed host

viral or bacterial infection often preceds onset

117
Q

JIA encompasses what

A

all forms of arthritis that begin before 16 years old, persist for longer than 6 weeks, and are of an unknown cause

118
Q

characteristics of oligoarticular JIA

A

this type of onset is in 56% of children with JIA

usually girls 2-4. demonstrate low grade inflammation in 4 or fewer joints, most often the knee

119
Q

characteristics of polyarticular JIA

A

2 subtypes - rheumatoid factor positive and rheumatoid factor negative

arthritis in 5 or more joints

up to 28% of kids with JIA

mostly girls

120
Q

characteristics of systemic JIA

A

17% of cases

boys and girls

no preferential age for onset

121
Q

intervention goal for JIA

A

want to give kids as great a chance as possible to function and participate in daily life

122
Q

outcome for JIA

A

40-60% of pts have inactive disease or clinical remission

large improvements in functional outcome in recent years

123
Q

cardinal S&S of JIA

A

inactivity stiffness, especially in AM

general demineralization, thinning/loss of articular cartilage, marginal erosions, and osteophytes with persistent disease

124
Q

factors to increase risk of fx with JIA

A

nutricional deficits
low body weight
decreased PA

125
Q

joint contractures with JIA generally result from

A

intraarticular adhesions and fibrosis of adjacent tendons

126
Q

describe acute phase of JIA

A

periarticular mm of affected joints show spasm/hyperclonus- aka contraction deformity

127
Q

subacute/chronic phases of JIA

A

mm atrophy and weakness more pronounced, especially near affected joints

can occur in distant areas too though and can persist long after arthritis remission

128
Q

chronic inflammation associated with JIA causes what secondary concerns

A

increased synovial fluid production

stretches/weakening of joint capsule and adjacent structures - ligament laxity/jt instability

massive overgrowth of synovium (pann us)

inflammaotry enzymes released into synovial fluid

129
Q

retardation of growth with JIA is associated with what

A

extended periods of active disease

long term use of systemic steroids

accelerated growth may occur during remission if growth plates still open

130
Q

common deficits in JIA and specific mm weakness common with JIA

A

mm strength and aerobic capacity affected

specific mm impairments common:
- hip weakness - EXT and ABD
- Knee EXT weakness
- PF weakness
- shoulder weakness - ABD and FLX
- elbow weakness - FLX and EXT
- wrist weakness - EXT and grip

mm bulk, strength, and endurance should be examined at disease onset and monitored regularly

131
Q

acute vs subacute/chronic stage of JIA treatment focus

A

acute = maintain and restore joint function

subacute/chronic = restoration function and activities

132
Q

arthritis PT joint management

A

avoid - increases inflammation:
- heat
- prolonged stretch/PROM

Do:
- exercise
- cold
- occasional splinting
- aquatic/land exercise programs - decrease P!
- strengthen mm around jt (isometric during inflammation)
- WBing/ambulation

133
Q

shoe type for JIA kids

A

flexible sole

good arch support

high heel cup

if deformity - can get custom molded orthoses

134
Q

what is developmental dysplasia

A

pathological hip instability

135
Q

what is leg calve perthes

A

avascular necrosis of femoral head
(ages 3-7); loss of blood supply to growth plate

usually find if kid is limping; refer to ortho

if not severe case - more activity is good to increase blood flow; can resolve with therapy

if severe - may have to do sx

PT focus = ROM, strength, stretching, aquatic therapy

136
Q

what is a slipped capital femoral epiphysis

A

femoral epiphysis slides posterior in relation to femoral neck

increasing incidence with pediatric obesity

hip P! radiates down thigh/into groin

dont always need sx

PT = ROM, WBing, restrictions (avoid lots of jumping/high impact)

137
Q

prone hip ext test

A

easier than thomas test with young kids

stabilize lordosis of back

ext hip while child lays over edge of table

typical = 20-30 deg hip ext

138
Q

Ryders test

A

in sitting or prone

tests femoral torsion

leg in flexed position (knee)

hip in neutral

move hip, when greater trochanter is sticking out the most this is the position you are looking at

are they neutral or in more ante/retro torsion

139
Q

thigh foot angle test

A

prone

check tibial RT amount

use goni; calcaneus is fulcrum, line up arms with axis of foot and femur

a little IR is normal with growth (i.e. ~10 deg)

140
Q

popliteal angle

A

assesses HS tightness

subtract knee flexion angle from 180 to get actual angle

SLR in supine; see how far knee can extend

141
Q

blunt disease

A

refer to ortho if varus only in one knee or if it is severe in both

should not be bow legged past 3 years

142
Q

conginetal talipees equinovarus (clubfoot)

A

variation in severity

“packaging disorder” often times - womb position

breech babies have higher incidence

S&S = large arch, forefoot turns in, and calcaneus turns medial

143
Q

treatment for mild vs severe clubfoot

A

mild = bracing early on; cast then brace is common

severe = tendon lengthening to alogn foot

may also have to elongate medial foot ligaments and stabilize bones

may do a derotationalotomy where they break the tibia and place in more ER

144
Q

what to look at when examining a kids foot (i.e. for flat foot)

A

is it rigid? - could be bony problem

does arch form when you pull on big toe?

is there an arch when they stand on toes

if foot is only flat with WBing not super concerning

145
Q

congenital muscular torticollis presentation

A

unilateral tightness of SCM

may have mass in mm

146
Q

etiology/factors contributing to development of CMT

A

prenatal factors
- ischemic injury b/c abnormal vascular pattern
- head position in utero causing compartment syndrome
-intrauterine crowding/malpositioning
-mm rupture
- ineffective myositis
- hereditary factors

perinatal factors
-birth drauma
- breech presentations
- assisted deliveries

postnatal
- presence of hip dysplasia
- positional preference
- presence of deformational plagiocephaly

147
Q

histological changes associated with CMT

A

excessive fibrosis (in more severe cases)

hyperplasia

atrophy

can also have tightness in upper trap

148
Q

early referral rate success for CMT

A

3-4 months has 99% rate of recovery with conservative treatment

149
Q

what to look at in an exam for CMT pts

A

head
shoulder ROM
difficult birth?
some conditions cause CMT (i.e. GERD)
what is their normal positioning?

150
Q

CMT treatment/age ranges

A

3-4 months you just work on positioning

can get a helmet at 4 months if needed

helmet can only remain from 4-18 months

151
Q

what is plagiocephaly

A

flattening of head on one side

common with CMT

usually one side more than other

orthotist can use a CT or laser to look at a 3D view of the head

152
Q
A

Lifespan (6 decks)

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