Paeds Flashcards by marie w

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

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risks of births 28-32 weeks after gestation

undeveloped lungs, no surfactant yet

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Asmmetrical tonic neck reflex integration age

5 months
stimulus : head turning
response : extension of UE and LE to side the face is turned to

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moro reflex integration age

5 months
stimulus : sudden head drop backwards
response : extn and abd of UE with opening of hands and crying

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landau reflex integration age

24 months (2 years)
stimulus : supported in prone with hands under thorax
response : head, neck, back, LE extension

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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

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gross motor development milestone - roll prone to supine

3 months

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gross motor development milestone - roll supine to prone

6 months

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gross motor development milestone - head control

4 months

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gross motor development milestone - standing

9 months

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gross motor development milestone - stair climbing (step-to)

18-20 months

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gross motor development milestone - reciprocal stair climbing

3 years

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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

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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

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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

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Cerebral Palsy definition (CP)

diagnosis based on clinical presentation and history

Cerebral Palsy

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 >> 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