Paediatics Flashcards
What age to paediatric physios typically see?
Up to the age of 21
Where do peds physios work?
hospitals, clinics, treatment centers, schools and homes
*focus on treatment in childs environment
What is the goal of peds physio?
Optimize partiicpation
What is the APGAR scale?
used to assess newborn’s health, physical condition, need for immediate medical care
done 1 minute after birth, 5 minutes, and 10 minutes if the other was bad
scored 0-10, 0-3 = severely depression, 4-6=moderately depressed, 7-10 = excesslent
(low score= medical attention (ventilation), remains low = increased risk of neurological complications
see chart in book for scoring
Activity
Pulse
Grimace
Appearance
Respiration
When do the lungs finish development?
32 weeks gestation
*before that - not enough surfactant to keep lungs open (harder to pull apart) = increased risk of atelectasis
What is infant respiratory distress syndrome
type II alveolar cells typically produce surfactant, if this doesn’t happen, decrease surface tension = atelectasis = distress
How do you classify the gestational age at extremely preterm, very preterm, moderate to late preterm, term birth?
extremely preterm - less than 28 weeks
very preterm: 28-32 weeks
moderate to late preterm: 32-37 weeks
term birth: 37 weeks (typically 38-41 weeks)
What is preterm birth?
birth of a viable infant that occurs at fewer than 37 weeks of gestation
If combined with low-birth weight - significantly increases the risk for neuro impairments
What is adjusted age and how do you calculate it?
based on 40 week gestation timeline
chronological age (weeks since birth) - number of weeks born prematurely (prior to 40 weeks gestation) = adjusted age
*this is the age that you should compare to child’s development - should catch up by the age of 2
What are neonatal reflexes?
Involuntary response to a stimulus and appear during neonatal period that become integrated by the end of infancy (to the higher center controls)
can’t achieve milestones if these don’t do away
What is the onset, integration, stimulus and response for ATNR reflex?
Onset - 20 weeks gestation
Integration - 5 months
Stimulus - turning head
Response - extension on UE and LE on side the face is turned to
What is the onset, integration, stimulus and response for rooting reflex?
Onset - 28 weeks gestation
Integration - 3 months
Stimulus - lightly stroking perioral area
Response - movement of head and lips towards that stimulus
What is the onset, integration, stimulus and response for suck-swallow reflex
Onset - 28 weeks gestation
Integration - 5 months
Stimulus - touch inside of mouth
Response - rhythmic sucking and swallowing
What is the onset, integration, stimulus and response for palmar grasp reflex
Onset - 28 weeks gestation
Integration - 7 months
Stimulus - pressure against palm of hand
Response - flexion of fingers
What is the onset, integration, stimulus and response for flexor withdrawal reflex
Onset - 28 weeks gestation
Integration - 2 months
Stimulus - Noxious stimulus to bottom of foot
Response - extension of toes, DF, hip and knee flexion on stimulus side
What is the onset, integration, stimulus and response for crossed extension reflex
Onset - 28 weeks gestation
Integration - 2 months
Stimulus - noxious stimulus to bottom of foot
Response - flexion of LE on stimulated side and extension and adduction of LE on contralateral side
What is the onset, integration, stimulus and response for galant (trunk incurvation) reflex
Onset - 28 weeks gestation
Integration - 3 months
Stimulus - stroke paravertebral skin in prone
Response - incurving of trunk towards stimuluated side
What is the onset, integration, stimulus and response for moro reflex?
Onset - 28 weeks gestation
Integration - 5 months
Stimulus - sudden head drop backwards
Response - extension and abduction of UE with opening of hands and crying, may be followed by flexion and adduction of UE
What is the onset, integration, stimulus and response for positive support reflex?
Onset - 35 weeks gestation
Integration - 2 months
Stimulus - feet in contact with floor or surface
Response - bilateral leg extension to support weight
What is the onset, integration, stimulus and response for stepping reflex?
Onset - 37 weeks gestation
Integration - 4 months
Stimulus - supported upright with feet in contact with firm surface
Response - rhythmic high stepping movements
What is the onset, integration, stimulus and response for Landau reflex?
Onset - 4-5 months after full term delivery
Integration - 24 months
Stimulus - supported in prone with hands under thorax
Response - head, neck, back, and LE extension
What is the onset, integration, stimulus and response for STNR reflex?
Onset - 4 -6 months after full term delivery
Integration - 12 months
Stimulus - flexion or extension of cx spine
Response - flexion cx spine = UE flexion, LE extension, extension Cx = opposite
What are the gross motor development milestones?
Roll - 3-6 months
Head control - 4months
Sit - 6 months
Crawl - 8-9 months
Cruising - 9 months
Standing - 9 months
Walking - 10-15 months
Stair climbing - 18-20 months
running - 2 years
kick a ball - 3 years
skipping 5 years
What are common tests / measures for development scales
Alberta Infant Motor Scale - 0-18 months, motor skills
Bayley Scales of infant development (BSID) - 1-42 months, mental, motor, behaviour scales
Peabody development motor scale (PDMS-2) - 0-60 months (5 years), fine and gross motor skills
Bruininiks-oseretsky tests for motor performance (BOT-2) - 4-21 years, fine and gross motor skills - will follow longitudinally
use if 4 (even if overlap - to be able to track longitudinally
Also for activity and participation - PEDI, SFA, CHAC, PTSIB (same as CTSIB but peds)
What is the Alberta Infant Motor Scale?
0-18 months, observational and performance based on what the child does in different positions. 0-58 scoring.
screen for motor delays and direct rehab towards that - no indication of future performance
* not appropriate for child with CP
5th percentile for developmental delay (i.e., downs), same trajectory but happens later
How do you classify a developmental delay?
a child <5 years of age who is delayed by >1.5 SD in at least one of the following:
-ADLs and self help
-Cognition
-Motor and sensory function
-Social- emotional function
-Speech / language / communication
What is floppy infant syndrome?
global hypotonia and decrease antigravity strength - leads to dev delay
frog leg position in supine - abducted and fully externally rotated - arms are flaccif beside
Rag doll in ventral suspension
head lag on pull to sit
In womb - typically run out of space so develop flexor tone but premature babies don’t get this - so they need to work on it. whereas typically work on extension out of womb.
What is down syndrome?
Genetic disorder caused by faulty cell divison resulting in an extra 21st chromosome
mild dev delay and mild to mod cognitive disability
distinict facial feature
-narrow eyes
-flattened nose
-small mouth and jaw
-protruding tongue
Increased risk for specific medical condition
-congenital heart malformations
-respiratory problems
-hearing and visual impairments
-ligamentous laxity and global hypotonia - careful with manipulation and mobilizations
*increased risk of SC injury cause transverse lig for AA is lax)
What is cerebral palsy?
Group of permanent disorders of development and movement and posture - non-progressive disturbances that occur in developing fetal or infant brain
motor can be accompanied by sensation, perception, cognition, communication, behaviour by epilepsy and secondary MSK problems
happen peri-natal or post-natal before 2 years
What are the risk factors of CP?
1 - prematurity - ventilation issues (decreased O2), PVL (white matter disorder) = spastic diplegia
2- atypical intrauterine growth (low - increased infection, high - materal diabetes birth weight)
3- infection (in-utero or post-natal)
4- infarction (increased risk of moms obese, older age, family Hx)
5- developmental defect (lissencephaly - flattened brain, microcephaly - small brain)
6- mutilple gestation
7- placental pathology
8- trauma (prenatal, perinatal (e.g., cord around throat), early postnatal - drop, shaken baby)
*more common in males, spastic more common
How do you diagnose CP?
No genetic or metabolic tests
based on clinical presentation and history
Imaging may be used to confirm
How do you classify CP?
impairment
-anatomic distribution (hemiplegia, diplegia, quadruplegia)
-type (spastic, dyskinetic, mixed)
Functional
-GMFCS
*NOT MUTUALLY EXCLUSION - helps communicate impairments and research
Describe the classification by impairment
Hemiplegia - one side of body
Diplegia - legs more than arms
Quadriplegia - arms, legs and trunk
Asymmetrical diplegia - legs more affected than arms, one side is more than other
Describe spastic CP
velocity dependent resistance to passive elongation
damage to cortex or white matter to and from sensorimotor cortex
most common type, diplegia most common
positive UMN signs
get scissoring gait (adductor spasticity), toe walking (PF spasticity)
Describe dyskinetic CP?
Ataxic
-movement disorder characterized by intention tremor, lack of muscle control, poor coordination of voluntary movements
-can walk without gait aid - may have balance difficulty
Athetosis
-movement disorder characterized by slow, continuous involuntary writhing movements
-common in distal extremity and mouth
-difficult to maintain stable position
-significant limitation in gross motor function
-postural instability as legs turn in too
-Chorea; movements are more rapid and jerky
Dystonic:
-damage to thalamus (relay center) and basal ganglia (pudemen and caudate)
-dystonia: involuntary muscle contractions leading to repetitive movements, abnormal fixed postures and disordered tone
-typically patterned and may include twisting or tremulous movements
- dystonic posturing - co-contraction of muscles causing a sustained abnormal posture
-triggered by voluntary movements
-limitations in gross motor function and fatigue due to high metabolic demand
Describe mixed CP
combo of spastic and dyskinetic
diffuse injury to motor cortex and basal ganglia
What is the gross motor function classification system?
focus on what the child CAN do
5 levels
-0-2
-2-4
-4-6
-6-12
-12-18
scale stably after age of 2
classified based on method of mobility
*see chart for scale
How do you do an assessment of CP
Motor function
-GMFM 88
-GMFM 66
*gold standard, 88 also validated for Downs
*can also use TUG for CP
-these are observational for gross motor function from 5months - 16 years
-appropriate for children whos motor skills are below or equal to a 5 year old without any motor disabilities
-high score is better
-dimensions - lying/rolling, crawling/kneeling, sitting, standing, walking/running/jumping
Spascity
-Modified ashworth scale
-modified tardieu scale
What are the interventions for CP
adress impairments
-bone development/deformity - hip dysplasia (esp GMFCS 5), scoliosis (?LLD - do in sitting), torsions
-balance
-coordination.
-motor planning
-ROM (flexbility, contractures)
-strength
-tone
-spasticity
Adress participation restrictions
-transfers, gait, stairs
-sports
-plauy
PT
-educaiton
-stretching
-exercise- strength, ROM, balance and coordaiont
-splinting
-orthosis
-assistance/ adaptive device - crutches, walkers, standaers, w/c
-gait, transfers and functional
What AFOs are commonly used for CP
solid AFO
-blocks all ankle at talocrural and subtalar
-rocker bottom
-limits knee extension movement (decreased hyperextension)
-Indications - post-surgery / botox, excessive DF, correctable equinois, dropp foot, increased med/lat stability
-*DO NOT USE FOR CROUCH GAIT. OR FIXED FOOT
Hinged AFO
-allows for controlled movement of ankle DF while still limting PF
-facilitates progression to foot flat position in early stance
-limits movement at subtalar
-limits knee extension moment (decrease knee hyperextension)
-Indications: correctable equinois, drop foot, knee hyperextension, subtalar OA
-DO NOT USE FOR CROUCH GAIT. OR FIXED FOOT OR BOTOX/LENGTHENING
Ground reaction AFO (GRAFO)
-blocks talocrural and limits subtalar
-provides knee extension moment (increase knee extension)
-DO NOT USE FOR DIXED KNEE FLEXION
-Indications: weak quads, overlengthening calf muscles, increase knee extension
What is the medical intervention for CP?
Bony realignemnt (osteotomy and fusion)
-botox - spasticity - lasts 3 months
-intrathecal baclofen - spastcity
-selective dorsal rhizotomy - spasticity
-serial casting - ROM
-ST (muscles and tendons) lengthening and tendon transfers - ROM
-percutaneous muscle/tendon release - ROM
-reconstruction - hip
What is the gait pattern for CP?
-true equinos - hip ext, knee ext, foot PF (calf spasticity)
- jumping = ant pelvic tilt, hip flex, knee flex, PF (hip flexor, hams and calf spasticity)
-crouch - increased hip flexion, knee flexion and DF (lengthened calf - over looked hip/knee)
What is Duchenne Muscular Dystrophy?
genetic disorder characterized by progressive weakening and degeneration
Due to mutation of the dystrophin gene - inherited in x-linked recessive pattern (1/3 arise from new genetic mutation)
M>F - live to 20-30s
How do you diagnose DMD?
Genetic testing
Creatine kinase
Muscle biopsy findings
What is the typical progression of DMD?
clinical signs apparent between 2-5 years
-early milestones achieved
-more apparent with higher level gross motor activiites (running, jumping)
progressive muscle wasting and weakness
-lower –> upper
– run, walk, standing, T/F with legs difficult
-Proximal –> distal
–quads, DF
-muscles of face, eyes, speech, swallowing, and spincter not involved
What are the S + S of DMD?
Waddling gait.- wide stances, shift CoG over and circumduct
Gower’s maneuver - used arms to push up to stand
Pseudohypertrophy of calves - enlargement due to fat deposits and connective tissue
Lumbar hyperlordosis - because weakness hip/knee (cog forward), weak abs, knees in hyperextension for stability
Wide stance with external rotation of LE - to increased Bos Don’t change this
Toe walking - DF weak (gastroc tight)
What are the associated problems with DMD?
Cardio-respiratory function - weakness in muscles = decrease resp function, cariomyopathy = impaired strength/structure, under stress from constant contractions
Congitive - 30% non-progressive impairments
Obesity - dietary intake >energy expenditure, steroid therapy
GI system - constipation and impaction due to decrease motility
Spine - increased lordosis, increased scoliosis (w/c) - sometimes get surgery
What is the management for DMD?
Medical
steroids - increase risk of OP, weight gain, cataracts, slowing of physical growth
mechanical ventilation - BiPAP - 2 levels
surgery - scoliosis and spine stabilization, tendon release
PT
avoid agressive strengthening (esp eccentrics)
stretching / ROM
gait training
education on overexertion and energy conservation
respiratory exercises -breath stacking, assistive cough ,incentivee spirometer
transfer training
equipment selection
What is RA? Including etiology and epidemiology
Systemic inflam disease characterized by symmetrical polyarthritis - primarily a disease of the synovium
F>M, 3-45 onset which increases with age
autoimmune disease of unknown etiology - RF (antibodies that neutralize pathogen which attack normal tissue mistaken as foriegn) found in sera in 70%
-genetic basis
-high prevalence in smokers
What is the pathophys of RA?
Inflam of the synovium leads to joint effusion, pain, stiffness, loss of ROM - chronically leads to degradation of the articular cartilage
Synovial overgrowth of vascular granulation tissue (pannus) dissolves smooth cartilaginous surfaces - osteocytes and chondrocytes form
Joint surfaces become uneven
narrow of joint leads to pseudo-laxity
weakened joint capsule and ligaments - causes fraying of tendon sheath, ruptures = muscle imbalance
if advanced - tissue leads to adhesions, fibrosis or bony ankylosis (fusion) causing increasing immobility within the joint
What do the lab tests reveal in RA?
-acute phase reactants - increased C-reactive protein and erythrocyte sedimenation rate (ESR) - because active inflam
-autoantibodies present - RF (not all but usually more severe)
-complete blood count - RBC is decreased
-synovial fluid analysis - normal: transparent, yellowish, no clots, viscous. inflamed: cloudy, clots, less viscous
What do the radiographic findings reveal in RA?
-joint space - narrowed (uneven)
-bone - erosion, peri-articular osteopenia
-ST - rheumatoid nodules, swelling
What is the diagnostic criteria for RA?
*need at least 4
1. morning stiffness lasting at least 1 hour
2. ST swelling or fluid in at least 3 joints
3. at least one area swollen in wrist, MCP or PIP
4. Symmetrical arthritis
5. rheumatoid nodules
6. abnormal amounts of serum RF
7. erosions or bony decalcification on radiographs of the hand and wirst
What is the course of RA?
no cure, just manage disease
cycles of exacerbations and remission (<15 minutes of morning stiffness, no joint tenderness or effusion for at least 3 months)
What are the S + S for RA?
Systemic
Articular
Extra-articular
Impairments and complications - vascular, neurological, cardiopulmonary, ocular
What are the systemic S + S for RA?
morning stiffness - lasting >1 hour, generalized stiffness, progressively eases with movement, severity and duration of morning stiffness are directly related to degree of disease activity
Extreme fatigue - increased resting energy expenditure - due to chronic immune activation, leads to rheumatoid cachexia (loss of lean body mass as a result of RA) (also cause of deconditioning)
weight loss/loss of appetitive
fever
malaise
What are the articular S + S for RA?
bilateral and symmetrical pattern
effusion (swelling)
arthralgia (joint pain)
crepitus
deformity
loss of function
pseudo-laxity
eventually progresses to ankylosis/ fusion leading to immobility
What are the Cx S +S for RA?
Often involved
ROM limited in all planes (esp rotaiton)
C0/C1, C1/C2 and mid Cx - decreased ROM and potential instability
C1/C2 = life threatening - if transverse lig is lax = herniation of odontoid process into SC or C2 fractures into SC
If Cx neuro S +S - refer (MRI used to confirm)
What are the TMJ S +S for RA?
last joint involved
results in pain, swelling and limited ROM
can progress to ankylosis
What are the Shoulders S +S for RA?
GH, SC, AC involved
leads to distension and thinning of capsule and lig
joint surface erosion = shoulder instability and potential for shoulder subluxation
What are the elbows S +S for RA?
bilateral olecranon bursitis (in severe RA)
effusion between lat epicondyle and olecranon prominence
ulnar nerve entrapment
rheumatoid nodules
flexion contraction due to patient posturing
inflammation –> capsule and ligament distention and joint erosion –> instability
What are the wrists S +S for RA?
almost all RA patients
volar subluxation of wrist and hand on radius (piano key sign) –> may cause extensor tendon rupture
proximal row ulnar sublux, distal - radial –> loss of ulnar dev and compensatory ulnar drift of MCPs
carpal bone erosion
carpal tunnel syndrome common
decreased grasp and pinch strength
What are the MCP S +S for RA?
Commonly affected (almost ALL)
joint effusion
get zig zag effect
trigger finger - due to flexor tenosynovitis, friction with movement or tendon nodules
bunnel-littler test
-MCP in flexion/ extension with PIP flexion (limited both = capsule, limited in extension but not flexion = instrintic muscle tightness)
