Pediatrics Test 1: Lecture 1 Flashcards
when/how do skeletal muscles develop in childhood
most skeletal mm fibers present at birth and all are present by 12 months
what cells are important for skeletal mm development and what happens if these cells are impaired somehow
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)
important things to note about mm development
mm fibers susceptible to internal and external forces; development and experiences w/i first year can matter
what happens with spastic mm
spastic mm are smaller and more susceptible to contractures
mm do not keep up with growing bone and sarcomeres overstretch
do type I or type II mm fibers atrophy/hypertrophy with various conditions
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
when does bone development progress most rapidly and what does this indicate for premies
more rapid in prenatal period
by birth diaphyses are almost ossified
premature = osteopenia common
what determines if bone growth is complete and when does this happen
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
when does the skull fully close/fuse
18 months
cant wear helmet after
what determines the joint structure/shape in development
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)
what is bone functional adaption
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)
how does bone development differ in kids with CP
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
how might a brachial plexus injury affect bone development
GH joint doesn’t get proper forces w/o mm
why might a premature infant have an extended posture
less movement in womb
more “floppy”/extended posture from lack of mm development
full term baby body/spinal alignment at birth
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
MSK issues that may occur with adults with CP
scoliosis
hip dislocation
cervical neck dislocation
contracture
arthritis
patella alta (mm not pishing patella into groove and it dislocates)
overuse syndrome
nn entrapment
fx
children with CP typically have what type of impairments
delays with walking
ROM limitations
atypical muscular pull/spasticity
why are hip subluxation/dislocation common with kids with CP
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
what has happened to the incidence of pathological hip conditions in recent years
increasing
i.e. legg calve perthes and slipped capital femoral epiphysis
examples of rotational/angular problems of the bone
in toeing
blounts disease
patella alta
what is blounts disease
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
at birth the femur is in more anteversion; what causes this to decrease to more normal ranges
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
torsion vs version
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)
at birth how much anteversion is present at birth and what does this decrease to
40-60 degrees anteversion at birth
resolves to 15-20 deg with proper forces
angle of inclination at birth vs after development
at birth = 150 deg (coxa valga)
2-3 years old = decreases to ~130 deg
what does anteversion of the femur present like
persistent in toeing pattern
common with kids who do not get proper forces
CP - causative factor for hip instability
when does genu varus present a cause for concern
as an infant, physiological bowing is normal
if still present around 2-6 years
varum/torsion generally normalizes by 12-24 months
if there is still excessive bowing of the knees at 1-2 years old, what are some factors that may be contributing
medial knee capsule tightness b/c of interuterine position
coxa valga of femur
lateral hip RT contracture
normal tibia external torsion
about 5 deg as newborn
increases by about 20 deg by adolescence
describe the typical newborn foot
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
lateral border of the foot should look like what
straight regardless of weight bearing
if curved, could be metatarsal abductus due to intrauterine positioning and may need bracing to correct
typical developing children have flat feet for how long
4-5 years
usually do not treat flat foot unless there is pain, tripping, or no arch
when does longitudinal arch develop
develops over the forst 10 years of life
start seeing development around 4
things to keep in mind with a peds MSK exam
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
what to know about observation, ROM, and strength for a general peds assessment
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
how do kids with JIA often align their legs
ER for greater comfort
may also have leg length discrepancy
kids with CP have an increase likelihood of what type of malalignment as they age
rotational malalignment between tibia and femur
i.e. hip IR and outtoeing
rotational abnormalities are common in kids with what
JIA and CP
especially when ambulatory
force across the knee is dramatically increased
what is a common side effect of disuse in children with severely limited movement such as those with CP, spina bifida, or arthrogryposis
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)
standing programs show improvements in bone density under what parameters
standing between 60-90 min, 5 days a week
standing programs show improvements in hip stability under what parameters
60 min/day when positioned between 30 and 60 deg ABD
effectiveness of weightbearing with adaptive devices
good
impact through bones is best even if only partial WBing
interventions for MSK disorders
strengthening exercises in various conditions
botox
stretching
bracing
supported standing/walking
what type of strengthening has no negative effect of duchens muscular dystrophy
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
benefits of botox in kids/when it is used/how it works
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
stretching benefits for different types of stretching
short term improvements with normal mm with short term stretches
neuro compromised mm (i.e. CP) need a more prolonged stretch to see improvements
common peds disorders involving bone
fxs
greenstick fx
epiphyseal fx
osteogenesis imperfecta
S&S to screen for abuse
children under 3 that are fx prone
premature kids
developmental disabilities
low socioeconomic status
epiphyseal fxs can cause what types of secondary problems and how prominent are they
can cause problems with bone growth, limb length discrepancy, etc
20% of all fxs in kids
what is osteogenesis imperfecta
genetic collagen problem that causes weak bones
4 types osteogenesis imperfecta
type I = mild
type II = perinatal; lethal; child will not survive
type III = severe/progressive; multiple fxs at birth
type IV = moderately severe
what is duchenne muscular dystrophy
most common muscular dystrophy
fatal/progressive weakness of skeletal and respiratory mm
what causes duchenne muscular dystrophy and what demographics obtain this disease
genetic; recessive defect in X chromosome; males
lack of dystrophin protein production that is needed for mm regeneration
can run in families
life expectancy for DMD
most dont live past 30
kids usually walk until middle school
5 stages of DMD
1 = pre-symptomatic
2 = early ambulation
3 = late ambulation
4 = non-ambulatory
5 = late non-ambulatory
what might you first see with an undiagnosed DMD child
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
what happens with kids as DMD progresses
develop scoliosis; can have sx intervention
cardiac/respiratory mm affected (eventually fatal)
some do tendon lengthening to keep feet flat
DMD treatment
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
what is spinal mm atrophy
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
4 types of SMA
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
S&S of SMA
hypotonia
absent reflexes
hip sublux
scoliosis
increased club foot
dysphagia
GI dysfunction
PT focus for SMA
depends with child/type
want to maintain and improve:
balance
respiratory mm
mobility
what is ideopathic toe walking
diagnosis of exclusion; kid walks on toes with no known reason/pathology
can be intermittent or constant
30-42% considered genetic
treatment for idiopathic toe walking
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
what is elhers danlos syndrome
heterogeneous group of disorders
characteristics: hyper-extensibility, ligament laxity, tissue fragility, delayed wound healing, atrophic scarring, and bruising/bleeding
primary interventions for ehlers danlos
PT
interventions based on severity to maximize flexibility, strength, and independence with precautions as needed for joint instability
characteristics of JIA (previously juvenille rheumatoid arthritis)
unknown origin
occurs before 16 yrs
7 main categories
most common JIA types seen by PT
systemic, oligoarthritis, and polyarthritis
pathophysiology of JIA
inflammation leads to capsule hypertrophy, irregular bone growth, altered growth, chronic joint instability , osteoporosis, and contractures
JIA treatment
modalities
strenfth
ROM
posture
endurance
joint protection
activity modification
**must modify treatment when there is active inflammation
can do a splint to support
what is hemophilia
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
PT intervention for hemophilia
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
structural vs nonstructural scoliosis
structural = curve of spine fixed; due to vertebrae structure
nonstructural = flexible; some spine straightening; due to position, mm imbalance, limb discrepancy, neuropathy, etc
when to screen for nonstructural scoliosis
CP
down syndrome
spina bifida
types/age ranges for idiopathic scoliosis
infantile = <3 years
juvenille = 3-10 years
adolescent = 10 years to bone maturity
scoliosis treatment
bracing
exercise (strength, flexibility, respiratory mm, stretching)
sx fusion
when does scoliosis require sx
if cobbs angle > 45 deg
T/S is compressing organs
C curve vs S curve
C curve = starts in T/S
S curve = 1 curve in T/S and another secondary curve
cobbs angle of what denotes scoliosis
> 10 deg
what is adams fwd bend test
standing fwd bend
compare shoulder height
leg length discrepancy? pelvic obliquity?
what S&S with scoliosis should be referred to physician
excessive kyphosis
P!
mm spasm
HS tightness
P! w/ SLR
could be a pinched nn
what is done to stabilize scoliosis in growing kids
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
what is a progressive scoliosis curve
sustained increase of 5 degrees or more on two consecutive examinations within 4-6 month intervals
what are the main factors (6) that influence the probability of progression in skeletally immature pt
- younger the pt at diagnosis the greater the chance of progression
- double curve pattern vs single curve
- lower the rissner sign (bone maturity; lower risser is more likely to progress)
- curves are larger at initial presentation
- female pt
- curves develop before menarche
congenital scoliosis curves are caused by
anomalous vertebral development in utero
normal kyphosis range
from T5-T12
20-40 deg between vertebral segments
spinal kyphosis can occur due to
trauma
congenital conditions
neuromuscular
post traumatic (i.e. tuberculosis)
scheuermann disease (most common; due to poor posture; only in kids)
what is congenital kyphosis
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
what is scheudermann disease
a rigid form of postural kyphosis
often neglected; develops in childhood due to poor posture
radiographic criteria for scheurmann disease
- anterior wedging of 5 deg or more for at ;east 3 or more continuous vertebrae
- narrowing of intervertebral disc space
- 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
scheurmann disease treatment
want to increase extension
increase flexibility and extensor strength
sports like volleyball and swim
when is hyperlordosis common in kids
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
what is spondylolisthesis
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
spondylolisthesis grades according to meyerding classification system
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
2 classifications of aquired leg length discrepancy
- direct (growth retardation)
- indirect (growth stimulation)
what is an apparent leg length discrepancy
due to things such as:
- spine alignment
- pelvic obliquity
- scoliosis
leg length discrepancy for 0-2cm difference
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
2-4 cm leg length discrepancy treatment
shoe lift
if lift is 3/8 inches or more it has to be added to sole of shoe and not the inside
2-6 cm leg length discrepancy treatment
epiphysiodesis, shortening
arrest growth on 1 side; delay it for a period
6-20 cm leg length discrepancy treatment
lengthening that may or may not be combined with other procedures
if a leg length discrepancy is >20 cm, what is the treatment
fit for prosthetic
compensations common for those with leg length discrepancies
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
how to use a tape measure for leg length discrepancy
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
what is galeazzi sign of leg length discrepancy
look at kid in hooklying position and see if knees are in the same place
femoral head falls posterior with hip sublux/dislocation
transverse vs longitudinal deficiency types of congenital limb deficiency
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)
when does congenital limb deficiency form
at 2-6 weeks limb buds form in utero
at 3-8 weeks deletion occurs
what is hemimelia
absence or gross shortening of a bone
fibular hemimelia is most common
what is proximal femoral focal deficiency
PFFD
shortening or complete absence of femur
associated with problems like acetabular dysplasia
treatment options for congenital limb deficiency
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)
are upper or lower extremity deletions more common with congenital limb deficiency
upper
when to consider prosthesis for congenital limb deficiency
12-15 months
may use a prosthesis for certain tasks but still prefer remaining hand for sensory input for some tasks
what is arthrogyroposis multiplex congenita
collection of syndromes characterized by symmetric, congenital, non-progressive contractures of at least 2 joints
proposed cause of arthrogyroposis multiplex congenita
believed to result from decreased fetal movement and possible damage to anterior horn cells of SC
most common form of arthrogyroposis multiplex congenita
amyoplasia
deficient moration of mm tissue
mm are underdeveloped
joints have abnormal deformities/adhesions and abnormal skin folds
fatality rate of arthrogyroposis multiplex congenita
50% in infancy
90% of surviving infants have symmetrical involvement of multiple joints
arthrogyroposis multiplex congenita treatment
inclues PT/OT
casting for prolonged stretch
sx for soft tissue/bone deformities
do not want an aggressive stretch (would cause further inflammation/contractures)
JIA characteristics and proposed etiology
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
JIA encompasses what
all forms of arthritis that begin before 16 years old, persist for longer than 6 weeks, and are of an unknown cause
characteristics of oligoarticular JIA
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
characteristics of polyarticular JIA
2 subtypes - rheumatoid factor positive and rheumatoid factor negative
arthritis in 5 or more joints
up to 28% of kids with JIA
mostly girls
characteristics of systemic JIA
17% of cases
boys and girls
no preferential age for onset
intervention goal for JIA
want to give kids as great a chance as possible to function and participate in daily life
outcome for JIA
40-60% of pts have inactive disease or clinical remission
large improvements in functional outcome in recent years
cardinal S&S of JIA
inactivity stiffness, especially in AM
general demineralization, thinning/loss of articular cartilage, marginal erosions, and osteophytes with persistent disease
factors to increase risk of fx with JIA
nutricional deficits
low body weight
decreased PA
joint contractures with JIA generally result from
intraarticular adhesions and fibrosis of adjacent tendons
describe acute phase of JIA
periarticular mm of affected joints show spasm/hyperclonus- aka contraction deformity
subacute/chronic phases of JIA
mm atrophy and weakness more pronounced, especially near affected joints
can occur in distant areas too though and can persist long after arthritis remission
chronic inflammation associated with JIA causes what secondary concerns
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
retardation of growth with JIA is associated with what
extended periods of active disease
long term use of systemic steroids
accelerated growth may occur during remission if growth plates still open
common deficits in JIA and specific mm weakness common with JIA
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
acute vs subacute/chronic stage of JIA treatment focus
acute = maintain and restore joint function
subacute/chronic = restoration function and activities
arthritis PT joint management
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
shoe type for JIA kids
flexible sole
good arch support
high heel cup
if deformity - can get custom molded orthoses
what is developmental dysplasia
pathological hip instability
what is leg calve perthes
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
what is a slipped capital femoral epiphysis
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)
prone hip ext test
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
Ryders test
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
thigh foot angle test
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)
popliteal angle
assesses HS tightness
subtract knee flexion angle from 180 to get actual angle
SLR in supine; see how far knee can extend
blunt disease
refer to ortho if varus only in one knee or if it is severe in both
should not be bow legged past 3 years
conginetal talipees equinovarus (clubfoot)
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
treatment for mild vs severe clubfoot
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
what to look at when examining a kids foot (i.e. for flat foot)
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
congenital muscular torticollis presentation
unilateral tightness of SCM
may have mass in mm
etiology/factors contributing to development of CMT
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
histological changes associated with CMT
excessive fibrosis (in more severe cases)
hyperplasia
atrophy
can also have tightness in upper trap
early referral rate success for CMT
3-4 months has 99% rate of recovery with conservative treatment
what to look at in an exam for CMT pts
head
shoulder ROM
difficult birth?
some conditions cause CMT (i.e. GERD)
what is their normal positioning?
CMT treatment/age ranges
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
what is plagiocephaly
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
