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full term infant
39 0/7- 40 6/7
preterm infant
<37 weeks
late preterm: still at risk for complications
-34-36.6 weeks
-physical characteristics
-physiologically and metabolically immature
-interventions and nsg care
very perterm: 28-32 weeks
extremely preterm: <28 weeks
post term
42+ weeks
chronological age
how old based on delivery date
corrected age
how old should be based on EDD
28 weeks at 6 months old, so 12 weeks = 3 months
birth weight
classification based on gestational age
SGA: small for gestational age; <10%
LGA: large for gestational age; >90%
AGA: appropriate for gestational age
low birth weight (LBW): <2500grams
very low birth weight (VLBW): <1500grams
extremely low birth weight (ELBW): <1000grams
smaller they are, more at risk for complications
intrauterine growth restriction (IUGR)
failure to grow normally while in uterus
vascular impairment, decreased placental perfusion, decreases supply of glucose and oxygen to fetus
symmetric IURG: long-term exposure so more detrimental ; early in pregnancy.
asymmetric IUGR: occurs later in pregnancy, head continues to grow
preterm characteristics
poor muscle tone
large head compared to rest of body
minimal subcutaneous/white fat; at risk for skin tears; shift weight
thin red and translucent skin
nipples and areola barely noticeable
vernix abundant
lanugo none in extremely preterm then to abundant
plantar creases absent in less than 32 weeks
pinnae of ears soft and flat with recoil, lack cartilage
female/male not developed
skin: protectants
physiologic immaturity
adaptation struggles
increased complications; decrease surfactant = compromised respiratory
bathing consideration; could stress them out
position considerations; skin breakdown
erythema toxicum; normal newborn rash. newborns don’t get this so if have a rash = infection
preterm infant - pain
signs for pain in preterm infants; VS changes, color change, may cry, grimace, furrow brow but depends on what baby can do
consequences of pain; brain hemorrhage
nsg considerations: holding, skin to skin, suck, give meds
preterm infant - stress
lack ability to select, control, and properly process stimuli
easily exhausted by environment stimuli; lights, touch
easily exhausted by routine activities
overstimulation
short term effects: apnea, increased O2 consumption, alterations in O2 sat, HR variability, altered nutrition, altered growth, sleep disturbances, increased ICP (brain hemorrhages)
long term effects: montor development, coordination of movement, and adaptive behaviors
stress limiting interventions
schedule care: follow infant cues, cluster care
reduce stimuli: ear muffs, private rooms/cover incubators, low voice tone, low lights
promote rest
promote motor development: nesting to promote flexed positioning, position changes
NIDCAP: newborn individualized developmental care and assessment program: promote individualized relationship-based care involving family members to decrease stress
preterm infant - thermoregulation
increased risk of cold stress
5-6 times more likely to lose body heat than an adult; less subcutaneous fat, less flexion of extremities, thinner skin, blood vessels closer to surface, decreased ability to vasoconstrict
cold stress is fatal to preterm infants
artificial means of thermoregulation: kangaroo care (skin to skin), radiant warmer, incubator
preterm infant - immune system
preterm infants increased risk for infection
-decreased IgG from mother
-decreased IgA from breast milk (limited intake)
-thin skin and easily damaged
management of sepsis in preterm infant; same as full term
preterm infant - cardiac
preterm infants are at an increased risk for delay of fetal shunts closing
PDA: increased pulmonary blood flow, pulmonary edema, decreased lung compliance, left sided volume overload, left side enlargement
treatment: medications (indomethacin or ibuprofen); surgical closure
preterm infant - respiratory
preterm infant at risk
-immature lungs; can give mom steroids if know is going to happen; 7 days prior to delivery
-lack surfactant; can give artificial surfactant
-poor cough reflex
-narrow airway passages
-weak respiratory muscles
assessment: resp rate, tachy/bradycardia, periods of apnea (stop breathing 20 sec or more), retractions, labored, accessory muscle use, see-saw breathing, nasal flaring, grunting, lung sounds
blood gases; most accurate way to assess oxygenation
pulse oximetry
chest xray: atelectasis? something else?
respiratory support
nasal canula
oxygen hood
continuous positive airway pressure (CPAP): deliver constant PEEP, keep alveoli open and prevent collapsing
high frequency ventilation: decrease volume and pressure → decreases damage and trauma to lungs. 300-400 breaths/min
NAVA: mutually assisted ventilatory assistance. NG tube/catheter placed into stomach that has signal that picks up signal from diaphragm and tells when to breathe
respiratory - nsg interventions
positioning: HOB up, prone, side lying
suction when necessary
-small air passages; edema caused from suctioning can cause further narrowing
-weak/absent cough reflex
-as needed suctioning and gentle
-can cause trauma and edema
preterm infant complication - apnea of prematurity
apnea of prematurity: “spontaneous pausing in breathing”, typically last longer than 20 seconds
why? immature inspiratory center in brain, immature chemoreceptors and neuroregulators
s/s oxygen destaturation, bradycardia
treatment: maintain neutral thermal environment (NTE), monitor O2 sats; maintain >92%, monitor HR, RR all the time, tactile stimulation, artificial ventilation, medications (caffeine citrate)
long-term: 37-38 weeks corrected age
respiratory distress syndrome (RDS)
caused by insufficient surfactant
-alveoli collapse on expiration, decreasing lung function
-surgactant deficiency → atelectasis → hypoxia → acidosis
incidence increases with decreasing gestational age
risk factors: prematurity, perinatal asphyxia, c section without labor, multiple births, male, cold stress, maternal diabetes
antenatal steroids: decrease risk
surfactant
decreases surface tension and makes breathing easier
keeps alveoli open on expiration
RDS s/s
tachypnea, nasal flaring, cyanosis, retractions, accessory muscle use, grunting, diminshed breath sounds, crackles, acidosis, elevated CO2 in and decreased O2
diagnositic tests: diagnosis supported by chest xray (see atelectasis, decrease lung volumes), ABGs (decreased pH, decrease PaO2, increase PaCO2)
RDS nsg considerations
monitor vital signs (RR, HR, BP, O2 sats)
monitor blood glucose
assess and report changes in infant status
monitor for complications; PDA and BPD
monitor blood gases; acid-base balance
provide NTE
provide nutrition
O2 sats:
full term: >95%
preterm: 85-90%
RDS treatment and management
pulmonary surfactant administration
lucinactant: first FDA approved artificial surfactant
poractant alfa (curosurf)
calfactant (infasurf)
reduces morbidity and mortality
decreases risk of BPD
ventilation/oxygenation supportive treatment; CPAP most common
sodium bicarb; changes pH from acidic → alkalotic
IV fluids
antibiotics
pulmonary surfactant - poractant alfa
artificial lung surfactant
action: reduces the surface tension, and improvement in lung compliance and respiratory gas exchange
dosage: intratracheally, weight-based dosage
adverse reactions: bradycardia, hypotension, endotracheal tube blockage, and oxygen desaturation
nsg considerations: assist, monitor, and collaborate with respiratory therapy
bronchopulmonary dysplasia (BPD)
aka chronic lung disease; need for supplemental O2 at 36 weeks
RDS can lead to BPD
patho: immature lungs; result of lung injury caused by mechanical ventilation and O2, acidosis, inflammation. leads to decreased lung compliance, inflammation, and oxygen dependency, barotrauma/volutrauma
babies on high frequency ventilation have lower chance than mechanical ventilation
easier gestation at birth → high pressure from ventilator to get aveoli to expand → more damage to bronchioles and cilia → inflammation, atelectasis, edema, airway hyperreactivity
BPD risk factors
extreme prematurity and need long term ventilation or increased O2 concentration
<32 weeks
1/3 of VLBW infants
prolonged mechanical ventilation
high oxygen concentrations
infection/inflammation
BPD s/s
persistent oxygen requirement
inability to wean off respiratory support and O2
respiratory distress
wheezing
respiratory acidosis due to CO2 retention
increased secretions
bronchospasms
possible pulmonary edema
BPD diagnosis
clinical signs and symptoms
chest X-rays: show serous fluid with generalized hyperinflation, atelectasis, interstitial thickening, cardiomegaly
28 days on O2 support; with inability to wean off
BPD management
prevention steroids to mom
assessment: VS, respiratory status, fluid status (strict I&O, daily weight)
chest physiotherapy (CPT)
suction as needed
positioning; prone to open space
supportive treatments
possible discharge on O2; weaning off
increased risk for respiratory infections into childhood
preterm infant - fluid and electrolytes
preterm infants at higher risk of imbalances because:
-immature kidney function
-increased water loss through skin and lungs
-physiologic diuresis
nutritional needs based on gestational age but also individualized
-fluid overload; edema, weight gain
-fluid deficit; dehydration s/s
-lab draw; increased concentration
preterm infant - nutrition
preterm infants have immature ingestion, digestion, and absorption
feeding difficulties include: immature suck/swallow reflexes, lack of coordination, weak suck, low tone, fatigue/exhaustion can’t complete oral feedings, lack of muscle development, bradycardia/desats
digestion difficulties include: decreased GI motility, immature gut colonization, prolonged gastric emptying, difficulty absorbing saturated fats and lactose, lack gastric acids needed for digesting products
feeding progression of a preterm infant
NPO at birth
clear IV fluids
TPN/intralipids for long term
-includes glucose, amino acids, lipids, electrolytes
-start as soon as possible
-effects of long term use: infections
gavage feedings (NG or OG): enteral feeds started ASAP
oral feeding (bottle/breast)
preterm infant feeding considerations
dietary needs
goal: simulate a growth pattern similar to what would have occurred in utero
weight gain: goal is 15 grams/day
monitor caloric intake and volume intake
feeding readiness: determined by behavioral state; gag present, rooting, alert state for 10+ minutes, tolerate handling
feeding tolerance
gastric aspirates if gavage feeding
regurgitation
vomiting
abdominal assessment: palpate(non tender, soft), auscultate(normoactive), distention, loops, measure abdominal girth every feed
necrotizing enterocolitis (NEC)
inflammation of intestinal tract that may lead to cellular death of intestinal mucosa
cellular death/ischemia → peristalsis stops → food/gas builds up → localized bacterial infection → septicemia
mortality 40%
contributing factors: prematurity, history of hypoxia, feedings
necrosis, perforation, peritonitis
prevention: breast milk is benefit, feeding slowly, minimize hypoxia
NEC s/s
GI symptoms/feeding intolerance
-abdominal distention
-increased gastric residuals
-decreased bowel sounds
-bowel loops
-vomiting
-bile stained residuals/emesis
-tender abdomen
-discolored abdomen
-occult blood
activity changes
-apnea
-bradycardia
-irritability
-lethargy
temperature intability
hypotension
shock
suspicion of NEC
abdominal xray: dilation of bowel, free air (perforation)
laboratory findings: leukopenia, metabolic acidosis, anemia, electrolyte imbalances
NEC treatment/management
prevention: probiotics, breastmilk, slow increase in feeding volume and calorie concentration
treatment/management:
-based on severity
-medical management: bowel rest, gastric decompression, antibiotics, parenteral nutrition
-surgical intervention; bowel resection
NEC nsg consideration
encourage mothers to provide breastmilk
monitor s/s; early subtle signs
measure abdominal girth
administer IV fluids
parenteral nutrition
monitor I&O; risk for third spacing
position infant on the side
monitor for feeding intolerance when recovering and feeds restarted
preterm infant - neurologic
nervous system underdeveloped
fragile blood vessels
immature regulation of cerebral blood flow
short-term and long-term neurologic deficits: intellectual and learning disabilities, cerebral palsy
magnesium sulfate administration antenatal reduces risk of cerebral palsy in preterm infants
intracranial hemorrhage
intraventricular hemorrhage (IVH), periventricular hemorrhage, germinal matrix hermorrhage
antenatal steroid administration linked to prevention of IVH
most occur in first 72 hours
30% of infants <1500 grams
intracranial hemorrhage increased risk
rapid changes in BP (high or low); from IV fluids, position changes (keep head midline, move slowly)
asphyxia
respiratory distress requiring mechanical
elevated of fluctuating cerebral blood
rapid blood volume expansion
hypercarbia
anemia
hypoglycemia
IVH
grade 1-4
diagnosis: cranial US
American academy of neurology recommend that all infants born <30 weeks receive US at DOL 7-14. repeat screening at 36-40 weeks corrected age
s/s are variable: lethargy, poor muscle tone, bradycardia, weak suck/feeding difficulties, uneven posture/reflexes/movements, deterioratoin of respiratory status, apnea, drop in hematocrit bc bleeding, hyperglycemia, tense fontanel, seizures
IVH outcomes
can depend; may not have outcomes. long term outcomes: seizures, intellectual disabilities, cerebral palsy
nsg considerations:
-avoid situations that cause changes in cerebral blood flow
-minimize handling, reduce environmental stimuli, minimize pain
-minimize deep suctioning
-developmental care
-monitor for s/s of IVH
-daily head circumference
-monitor Neuro status
-family support
-provide supportive care
-administer medications for seizures if warranted
periventricular leukomalacia (PVL)
cause:
-lack of oxygen or inflammation in the periventricular area of brain
-white matter damage
-cysts develop in damaged area
s/s: generally none
outcomes: motor disorders, delayed mental development, coordination problems, vision impairments, cerebral palsy
retinopathy of prematurity (ROP)
injury to blood vessels in eye leading to growth of new blood vessels that develop abnormally
67% of infants <1250 grams
contributing factors
-high levels of O2 administration; allows blood vessels to grow rapidly → grows incorrectly
-prolonged ventilation
-acidosis
-sepsis
-shock
-IVH
-fluctuating blood oxygen levels
ROP screening
screening:
<1500 grams
<32 weeks
>32 weeks with unstable clinical course
1st exam at 4-6 weeks old
exam: dilated eye and look at vessels behind eyes
treatment: laser surgery, anti-vascular endothelial growth factor (anti-VEGF) injection into eye that stops blood vessel growth, cryosurgery or reattachment of retina
RPO nsg considerations
oxygen administration decreases
parent education about follow up
swaddling during exam
mydriatic eye drops: dilate eyes
preterm infant - discharge planning
often go home before due date
education early on: normal vs abnormals to look for, med admin, feeding
“rooming in”: parents stay and take care day and night at hospital
consistent weight gain
maintaining temperature in open crib
feeding without cardiopulmonary compromise
stable cardiopulmonary function
required testing prior to discharge
carseat evaluation; monitor status for 90 mins
immunizations given
metabolic screening completed
hearing screen
eye exam as needed
nutritional risks performed
appropriate treatment plans completed
2 individuals who can feed and car for infant demonstration
CPR education
medication administration education
operate needed equipment
home evaluation
social work/family evaluation
primary care follow up
other follow up appointment