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How many weeks is considered preterm?
<37-38
How many weeks is considered extremely preterm?
<28 weeks
How many weeks is considered very preterm?
28 to <32 weeks
How many weeks is considered moderate to late preterm?
32 to <37 weeks
Risk factors for premie birth?
maternal age <19 years, >40 years
high BP after 20 weeks
premature rupture of placenta
race/ethnicity (African American higher risk)
low socioeconomic status
use of drugs/smoking
Autonomic signs of stability?
pink color
regular respiration
stable digestion
Autonomic signs of stress?
pale
mottled
flushed
gasping
tachypnea
hiccups
yawning
sneezing
spitting up
Motor signs of stability?
smooth movements
controlled posture
clasping of hand
hand to mouth
Motor signs of stress?
jerky movements
minimal movement
weak/flaccid
arching
finger/toe splaying
State signs of stability?
well defined sleep states
focused alertness
some facial expressions
State signs of stress?
diffuse sleep with twitching
gaze aversion
weak cry
fussing
How does muscle tone develop after birth for premature babies?
<28 weeks: flaccid
32-35 weeks: LE tone develops
35-37 weeks: UE tone develops
36-40 weeks: trunk tone develops
**develop from bottom to top (normally develop top to bottom when born full term)
little or no physiologic flexion
African heritage: higher tone
Asian and Native American: lower tone
How do reflexes develop after birth for premature babies?
present at 28 weeks PCA
not easily elicited
first seen in LE then UE
orderly sequence
may see toe walking with automatic walking
How does PROM vary for premature babies when compared to full term?
More flexibility
Less likely to have contractures
How does active movement vary for premature babies when compared to full term?
large, gross movements
disorganized
variable
How does premature birth impact resting posture?
very influenced by gravity
UE and LE abduction
UE and LE ER
rotation of cervical spine
retracted scapula
influence on skull shape
still going through ossification
need to be rotated to avoid flat spots
Premature birth tactile system
begins development at conception
constant NICU procedures
less responsive to touch
may lack the ability to respond to pain
Tactile system infant responses
increase BP
increase HR
increase intracranial pressure or startle
Development of vestibular system
one of first to develop in utero
womb provides stimulation
slow rocking = promote calming
fast stimulation = increases alertness
Development of olfactory and gustatory systems
taste buds being to mature at 13 weeks
24 weeks: swallows 1L amniotic fluid/day
NICU: endotracheal tubes, medications no constant practice
Development of auditory system
24 weeks: cochlea and peripheral sensory end organs are complete
28 weeks: hearing threshold = 40 db
Sound level 1
60-74 dB
arousal to discomfort
ordinary conversation = 60 dB
ringing phone = 65 dB
Sound level 2
81-96 dB
discomfort to damage
bubbling ventilator = 87 dB
closing portholes = 90 dB
Sound level 3
101-108 dB
damage to pain
subway train = 100 dB
setting bottle on isolate = 108 dBA
Auditory system infant responses
increased ICP
increased startle response
decreased sleep
decreased auditory discrimination
Development of visual system
least mature at term birth
22-24 weeks: major eye structures and pathways in place
<32 weeks: pupillary reflex absent, leads to fatigue
prefers human faces, tracks in arc
State organization stage order
deep sleep
light sleep
drowsy
quiet awake
active awake
crying
Full term state organization
sustained quiet awake states
transitions smooth
Preterm state organization
dominant sleep state
more motor during sleep
difficulty with changes between states
more restless and excitable
Intraventricular hemorrhage (IVH)
bleeding around lateral ventricles
most common brain lesions <32 weeks
due to the fragile nature of vasculature, hypoxia, or frequent swings in BP
grades I and II: minimal long-term deficits
grades III and IV: increase in long term deficits (more likely to develop CP)
Periventricular leukomalacia (PVL)
necrosis of white matter surrounding lateral ventricles
seen in <32 weeks GA, with cardiorespiratory issues
due to immature circulation, decreased oxygen
correlated with CP (spastic dip[legia)
>2 mm cysts at 1 mos, 95% predictive of CP
Bronchopulmonary dysplasia (BPD)
chronic lung disease-thickening of lung walls
due to long term mechanical ventilation, RDS, PH, infection
long term outcomes vary (depends on how long they have been on oxygen)
Respiratory distress syndrome (RDS)
respiratory failure due to lung immaturity and decreased surfactant
seen in 20% of all preterm infants
first 1-2 days
see increased respiratory rate, grunting, retractions, cyanosis
precursor to BPD
treat with surfactant can help avoid chronic changes
Patent ductus arteriosus (PDA)
occurs when ducts arteriosus fails to close
ductus arteriosus allows blood to bypass circulation to lungs, closes 10-15 hours after birth
see murmurs, increase HR, respiratory distress
may resolve on own
Necrotizing enterocolitis (NEC)
acute inflammation and necrosis of immature intestine
etiology unknown
possibly due to infection, toxins, injury to GI tract
see bloody stools, vomiting bile or blood, apnea, lethargy, temperature instability
Gastroesophageal reflex (GER)
movement of gastric contents into esophagus and above
due to relaxation of lower esophageal sphincter
see irritability, apnea (if severe), failure to thrive (if severe)
usually resolves with maturation
Retinopathy of prematurity (ROP)
abnormal growth of blood vessels in immature retina
due to increased oxygen concentration, hypoxia, IVH, sepsis, RDH
may lead to blindness if severe
treatments: laser surgery, cryotherapy, injection of Avastin, glasses
Methods to improve outcomes for extreme premies
steroids
surfactant
antenatal magnesium sulphate
delayed cord clamping
family bonding
APGAR assessment
appearance, pulse, grimace, activity, respiration
assesses HR, respiratory effort, reflex irritability, tone, color
scored 0-2 (2 best)
assessed at birth and 5 minutes
<6: resuscitation
8-10: typical
Neonatal behavioral assessment scale (NBAS)
Brazelton
assesses neurobehavioral function of those full term 37-48 weeks PCA and supplemental items for premies
30-45 min administration with extensive training
Assessment of preterm infant behavior (APIB)
assessment of neurobehavioral functioning of high-risk infant 32 weeks PCA and above
1-3 hours with intensive training
Neonatal Neurobehavioral Exam (Morgan)
assesses neurobehavioral status of infants 32-42 weeks PCA
items: tone/motor patterns, reflexes, behavioral responses
5-20 min administration
lack standardization
Neurological assessment of preterm and full-term newborn infant (Dubowitz)
documents the gestational age of preterm infants’ neurological maturation
used with full-term infants to 3rd day of life or with preterm infant who tolerates handling
quick
performed by physician
Test of infant motor performance (TIMP)
assess infants functional motor behavior
34 weeks PCA to 4 months corrected age
24-45 min
training required
developed by pT
high interrater reliability
Harris infant neuromotor test (HINT)
assesses low or high risk infants 2.5 to 12.5 months
discriminates between those low and high risk delay at ages 4, 5, 7, 8 months
higher test-retest, intra-rater and inter-rater reliability
Prechtl’s assessment of general movements (GMA)
observation of general movement patterns that being early in fetal life (5 weeks)
video tape for 3-5 min
specialized training
predictive of CP, administered before 5 months corrected age
Hammersmith infant neurological examination (HINE)
assess children 2-24 months
good interrater reliability
specialized training
predictive value for CP, type, severity
Alberta infant motor scale (AIMS)
assesses term to 18 months or until indep ambulation, premie or full term
motor development measurement for infants at risk for delay
focuses on milestones
valid, reliable, norm references
predicts motor delays
NICU PT interventions
positioning
sensory stimulation/environmental controls
feeding
gross motor development
education
splinting
PT interventions after DC
gross motor delay and differences in quality of movement
developmental intervention, positioning, sensory stimulation, splinting, education
Cystic fibrosis etiology
autosomal recessive disorder
multisystem disease
characterized by chronic bacterial infection of the airways
mutation in the genes that encode the CF transmembrane conductance regulator protein (CFTR)
chromosome 7: 3-bp deletion is most common
abnormality in a membrane chloride channel: results in altered chloride transport and water flux across the apical surface of epithelial cells
Cystic fibrosis pathophysiology
abnormalities in the CFTR protein makes epithelial cells impermeable to chlorine, which results in
dehydration results in thick, viscous mucous gland secretions causing mechanical obstruction
obstruction in the lungs predisposes the lung to infection and causes atelectasis with hyperinflation
in pancreas, mucous blocks the channels that carry important enzymes to the intestines to digest food, preventing the body from properly processing/absorbing nutrients
CF genetic screening in prenatals
Genetic counseling: CF carriers can be identified (70% effective — mutated DF508)
DNA analysis of oocytes
CF genetic screening in newborns
genetic screening: gene on chromosome 7
37 states
½ of all infants present with failure to thrive and/or respiratory failure
CF sweat test values
gold standard for diagnostic test
normal = 40 mEq/L
abnormal NaCl > 60 mEq/L for those under 20 years
abnormal NaCl > 80 for those over 20 years
**positive test may not be diagnostic by itself
CF pancreatic elastase-1 (EL-1)
marker of severe exocrine pancreatic insufficiency
measured in feces
can be used to rule out CF if normal
CF sweat test part 1
pilacarpine is applied to leg or arm
electrode placed over the chemical
weak electric current applied to initiate sweating
CF sweat test part 2
skin is cleared
sweat is collected on filter paper, plastic coil, or gauze
sent to lab after 30 min
measure amount of chloride in sweat
CF lung function tests
used to monitor lung function in people with CF
performed in those 6+
CF in infancy symptoms
failure to thrive
compromised respiratory system
**milder presentation likely if diagnosed in adulthood
CF clinical features
salty taste when kissed
bulky, frothy and foul-smelling stools
hyperglycemia
rectal prolapse
poor nutrition and weight loss
chronic cough and purulent sputum production
barrel chest, pectus carinatum, and kyphosis
hypoxia, clubbing, cyanosis
reduced oxygen-carbon dioxide exchange
exacerbation of pulmonary disease
liver disease
infertility
amenorrhea
muscle pain
excessive kyphosis, neck and back pain
clubbing
increased incidence of Crohn’s and ischemic bowel disease
What causes the salty taste when kissed in pts with CF?
increased sodium and chloride concentrations in sweat
What causes bulky, frothy and foul smelling stools in pts wit CF?
blocked pancreatic ducts
impairing nutrient digestions and absorption
What causes hyperglycemia in pts with CF?
pancreatic damage affecting beta-cells
CF-related diabetes
What causes rectal prolapse in pts with CF?
intestinal obstruction
thickened, dried or impacted stools
What causes poor nutrition and weight loss in pts with CF?
malabsorption
early satiety
increased utilization of calories
What causes barrel chest in pts with CF?
chronic pulmonary infection
hyperinflation due to retained mucous
CF prognosis
no cure
respiratory failure is the leading cause of death
diagnosis in adulthood generally due to milder presentation
more than 50% live into adulthood
males better prognosis than females
What do GI symptoms at diagnosis of CF indicate?
good clinical course
What do pulmonary symptoms at diagnosis of CF indicate?
clinical deterioration
CF medical management
oriented toward alleviating symptoms
pulmonary intervention
pharmacotherapy
nutrition high calorie diet
gene therapy
transplantation
double lung
heart lung
liver
supplemental oxygen
CF medications
digestive tract medications (Creon, Pancreaze, Zenpep)
vitamins (A, D, E and K)
reflux medications (Zantac, proton pump inhibitors - prevacid, prilosec)
laxatives (Lactulose, MiraLax, Actigall)
mucolytics and bronchodilators
corticosteroids
antibiotics
Role of PT in CF patients
chest PT/breathing activities
exercise
education
pain management
Chest PT/breathing activities for CF
percussion and postural drainage
flutter device, incentive spirometer
pursed lip breathing, active cycle of breathing techniques, segmental breathing
Exercises for CF
includes strengthening, stretching, aerobic and endurance components
UE: arm aerobic exercise, arm ergometry or free weights
LE: walking, jogging, rowing, cycling and swimming
stretching of chest
Education for CF
drink fluids to avoid dehydration
avoid triggers that increase mucus production
teach family techniques for chest clearance
use of devices
importance to do all of these techniques to get the best outcomes
What is osteogenesis imperfecta?
brittle bone disease
disorder of collagen synthesis leads to recurrent fractures and deformation
Causes of osteogenesis imperfecta
most inherit from parent (autosomal dominant inheritance)
25% of cases caused by genetic mutation occurring spontaneously
Osteogenesis imperfecta pathophysiology
due to defect in collagen synthesis
more than 150 mutations identified (all affecting genes that code for type 1 collagen)
type 1 collagen: major structural component in ECM of bone, skin and tendons
mutated genes instruct body to make too little type 1 collagen or abnormal polypeptide chains that cannot form the triple helix of type 1 collagen
Type 1 osteogenesis imperfecta collagen production
reduced by 50%
Type 2 osteogenesis imperfecta collagen production
reduced by 80%
Diagnostic tools for osteogenesis imperfecta
DNA testing
prenatal ultrasound
fetal 3D CT scan
human chorionic villus biopsy
DEXA: low bone mineral density
x-ray films
Type 1 osteogenesis imperfecta
most common
mildest clinically
two types
A: teeth are normal
B: dentinogenesis imperfecta is a feature (abnormal tooth development)
grayish-blue sclerae at birth
mild to mod bone fragility
osteopenia
mild femoral bowing at birth
generalized ligamentous laxity with joint hypermobility
50% develop hearing loss by teens
Type 2 osteogenesis imperfecta
most severe form
lethal: mainly due to pulmonary complications from rib and vertebral fractures
severe bone fragility
at birth, short limbs, small chests, and soft skulls
sclerae dark blue or gray
intrauterine fractures common
respiratory and swallowing problems
Type 3 osteogenesis imperfecta
severe form
usually result of new mutations
fractures and deformities from utero
large skull (upper portion), triangular face
dentinogenesis imperfecta
blue to pale blue sclerae
healing is impaired
severe osteopenia
severe disorganization of growth plate structure
progressive kyphoscoloiosis
early onset hearing loss
very short stature
lifespan may be shortened due to respiratory conditions
Type 4 osteogenesis imperfecta
moderate form
diagnosis can be made at birth but often occurs later
normal birth weight and length
two subsets
A: normal dentition
B: dentinogenesis imperfecta (majority)
slightly gray sclerae
moderate bone fragility
mild femoral bowing at birth
osteopenia occurs with aging
scoliosis
mild bone angulation
child might not fracture until walking
Osteogenesis imperfecta prognosis
Types I and IV: milder course, normal lifespan
Type II: most severe, 90% die in first few weeks
Type III: mortality related to cardiorespiratory failure stemming from kyphoscoliotic deformity
significant risk also exists of basilar invagination of the skull and intracranial bleeding
Osteogenesis imperfecta clinical features
brittle bones
joint hypermobility
thin skin
weak muscles
diffuse osteoporosis
shortened stature
multiple recurrent fractures
blue sclerae
deformed teeth
deafness
hernias
easy breathing
excessive sweating
scoliosis
pectus deformity
osteogenesis imperfecta metabolic defects
elevated serum
pyrophosphate
decreased platelet aggregation
osteogenesis imperfecta cardiovascular complications
aortic and mitral valve insufficiency
aortic dissection
Reasons for delayed development of motor skills in osteogenesis imperfecta
poorly developed muscles
hypermobility of joints
multiple fxs requiring immobilization
osteogenesis imperfecta medical management
no cure
manage fractures
promote function and independence
osteogenesis imperfecta fractures
most heal well
short-term immobilization
prevention important
treatment options
surgery
medications
healthy lifestyle
PT
osteogenesis imperfecta medications
biphosphonate drugs: slows loss of bone, does not build new bone
growth hormones
stem cell therapies
anti-sclerostin antibody
current antibody studies
osteogenesis imperfecta healthy lifestyle
adequate intake of calcium (maintain bone density), vitamin C (promote healing)
large doses not recommended
avoid smoking, alcohol, caffeine, steroid medications
can affect bone density
genetic counseling
Role of PT in osteogenesis imperfecta
protective handling and positioning
strengthening
adaptive equipment
ambulation
post-surgery
aquatics
education/prevention
Type 1 osteogenesis imperfecta ambulation
majority of children ambulate either as functional or household ambulators
50% walk without any type of AD as community ambulators
Type 3 osteogenesis imperfecta ambulation
½ are dependent on power mobility, with only 27% becoming household ambulators
Type 4 osteogenesis imperfecta ambulation
26% are community ambulators and 57% are household ambulators
What are the best predictors of ambulatory status?
disease type
ability to sit by 9 or 10 months of age