Paeds Flashcards
APGAR scale
quick evaluation of new borns health + need for immediate medical care
administered 1 min and 5 mins after birth
score 0-10: 4-6 moderately depressed >6 excellent, <4 severely depressed
score 0-2 for muscle tone, heart rate, grimace (reflex), appearance, respiration
risks of births 28-32 weeks after gestation
undeveloped lungs, no surfactant yet
Asmmetrical tonic neck reflex integration age
5 months
stimulus : head turning
response : extension of UE and LE to side the face is turned to
moro reflex integration age
5 months
stimulus : sudden head drop backwards
response : extn and abd of UE with opening of hands and crying
landau reflex integration age
24 months (2 years)
stimulus : supported in prone with hands under thorax
response : head, neck, back, LE extension
Symmetrical tonic neck reflex integration age
12 months
stimulus : flexion or extn of cervical spine
response : cervical spine flexion causes UE flexion and LE extn
response : cervical spine extension causes UE extn and LE flexion
gross motor development milestone - roll prone to supine
3 months
gross motor development milestone - roll supine to prone
6 months
gross motor development milestone - head control
4 months
gross motor development milestone - standing
9 months
gross motor development milestone - stair climbing (step-to)
18-20 months
gross motor development milestone - reciprocal stair climbing
3 years
floppy infant syndrome
global hypotonia and decreased antigravity strength
supine position: baby limbs collapse against gravity “frog leg position”
= legs fully abducted and externally rotated, arms flaccid beside head
rag doll posture in ventral suspension
head lag on pull to sit
down syndrome
extra 21st chromosome
normal milestones but delayed later
features: flat nose, narrowed eyes, small mouth/jaw, protruding tongue
risks: ligamentous laxity and global hypotonia, respiratory problems, congenital heart conditions
Cerebral Palsy
disorder of movement development and posture resulting in activity limitation due to NON-PROGRESSIVE disturbances that occurred in the developing fetal or infant brain
perinatal = after birth, prenatal=before birth
Cerebral Palsy definition (CP)
disorder of movement development and posture resulting in activity limitation due to NON-PROGRESSIVE disturbances that occurred in the developing fetal or infant brain
perinatal = after birth, prenatal=before birth
diagnosis based on clinical presentation and history
Cerebral Palsy
disorder of movement development and posture resulting in activity limitation due to NON-PROGRESSIVE disturbances that occurred in the developing fetal or infant brain
perinatal = after birth, prenatal=before birth
CP risk factors
prematurity - reduced lung development, reduced blood flow to brain
infection
trauma
infarction
developmental defects
atypical intrauterine growth (low/high birth weight)
multiple gestation (twins, etc)
placental pathology
CP classification by impairment (area affected)
hemiplegia - one side of the body affect
diplegia - legs more affected than the arms
quadriplegia - arms, legs, trunks all affected
asymmetrical diplegia - legs more affected than arms and one side of the body is more affected is more affected than the other
CP presentation of impairment - spastic
most common type of CP
velocity-dependent resistance to passive elongation
positive UMN signs
signs/symptoms: diplegia (common), scissoring gait, toe walking, adductor + plantar flexor spasticity
CP presentation of impairment - dyskinetic (3 types)
ataxic: movement disorder with intention tremor, lack of muscle control, poor coordination of voluntary movements
most don’t need gait aid but may have less balance
athetosis: slow, continuous, writhing movements (choreo = quick/jerky )
affects distal extremities and mouth
difficulty maintain stable posture, significant gross motor limitations
dystonic: involuntary sustained or intermittent muscle contractions leading to repetitive movements, abnormal fixed posture, disordered tone
damage to thalamus and basal ganglia
triggered by voluntary movements
significant gross motor function limitations and high metabolic demand
mixed: combo of dyskinetic and spastic
different assessment tools for CP
GMFM-88 or GMFM-66
gross motor function classification system (GMFCS)
modified ashworth scale
modified tardieu scale
solid AFO for CP
blocks knee hyperextension
blocks ankle movement at talocrual and subtalar joint
used after surgery, excessive DF, correctible equinus
hinged AFO for CP
allows for controlled amount of ankle DF while limiting PF
limits movement at subtalar joint, trains foot flat for stance phase
reduces knee hyperextension
used for true and correctible equinus, drop foot, subtalar OA
ground-reaction AFO for CP
blocks movement at subtalar and limits subtalar joint
increases knee extension
used for jump gait, crouch gait, weak quads, over lengthened calf muscles
true equinus
calf spasticity
hip in extension
knee in extension
ankle in plantar flexion
jump gait
hip flexor, hamstring and calf spasticity
hip in anterior pelvic tilt and flexion
knee in flexion
ankle in plantar flexion
crouch gait
hip and hamstring spasticity
hip in excessive flexion
knee in excessive flexion
ankle in excessive DF
Duchenne Muscular Dystrophy
genetic disorder leading to progressive weakening and muscle degeneration causing activity limitation and participation restriction
Duchenne Muscular Dystrophy
genetic disorder leading to progressive weakening and muscle degeneration causing activity limitation and participation restriction
DMD etiology and epidemiology
mutation of dystrophin gene on the X chromosome
inherited in X-linked recessive pattern
carrier = MOTHER, 25% chance son affected, 25% daughter carrier
MALES, 20-30 year life expectancy
elevated CK levels in bloods, muscle biopsy or genetic testing
DMD disease progression
typically age 2-5 presentation - early milestone achieved, then more apparent with gross milestones (running, jumping)
LE > UE
PROXIMAL > DISTAL
muscles of the eyes, face, speech, swallowing, sphincter not involved!
DMD signs/symptoms
gowers sign/maneuver - pushing off thighs, climbing up legs
waddling gait - wide stance, bilat. glute weakness, circumduction
pseudohypertrophy of calves - increased fat deposits, connective tissue
lumbar hyperlordosis - progressive weakness hips, knee extensors
wide stance with external rotation of LE
toe walking - weak DF, foot drop
weakness in abdominals (belly protrudes)
DMD complications
cardio-resp muscle weakness and reduced function (70% deaths)
cardiomyopathy - impaired strength, under constant stress from constant contractions leading to death
impaired cognitive function
OBESITY - dietary intake»_space; energy expenditure
GI constipationfrom reduced mobility
increased lordosis (ambulation) and scoliosis (non-ambulation)
DMD PT interventions
AVOID aggressive strengthening! (no eccentrics) wont recover well
stretching and ROM exercises for contractures
gait training - dont correct gait!
education re: overexertion and energy conservation
breath stacking, assistive cough, incentive spirometer
sliding board transfers
osteogenesis imperfecta (brittle bone disease)
genetic congenital bone disorder affecting bone formation, bone strength, and structure of other tissues (fragile bones)
affects type 1 collagen
osteogenesis imperfecta characteristics
frequent #’s (reduces after puberty)
bone deformity and bone pain
low bone density
short stature
scoliosis
ligament laxity
muscle weakness
fatigue
cardiac and resp. issues
dental, vision and hearing problems
osteogenesis imperfecta interventions
goals: minimize #’s, enhance independent function, and promote health
# care, strengthening (swimming, aquatherapy), aerobic conditioning, assistive devices, surgery (ORIF, correct bone deformities, spine stability)
osteogenesis imperfecta treatment cautions! **
never push/pull on limb
if # suspected, minimize handling of limb
handle babies with care - lift with one hand under glutes/legs and other under shoulder, neck and head
don’t lift from armpits
support infants in variety of positions to promote strengthening
