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Lifespan > The High Risk Infant > Flashcards

The High Risk Infant Flashcards

1
Q

how do you high risk defined

A

high probability of developmental delay
high rate of mortality and morbidity

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2
Q

what is high risk classified by (3)

A

birth weight
gestational age
physiological status

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3
Q

what determines the setting of care

A

medical stability
level of care needed

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4
Q

what are the 4 levels of Neonatal care

A

1 - well-baby nursery
- capacity for emergency resuscitation
- expectation that infant requires little monitoring and is on way of going home

2 - special care nursery
- more monitoring available

3 - NICU
- critically ill

4 - regional NICU
- speciality centers

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5
Q

who is a developmental follow up clinic most appropriate for

A

levels 2-4 of neonate care
- level 1 still might need

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6
Q

who is appropriate for inpatient rehab

A

if can’t go home right away

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7
Q

why can asphyxia or hypoxia-ischemia happen

A

d/t placental insufficiency or umbilical asphyxiation

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8
Q

what are risks for morbidity & mortality of an infant (8)

A

prematurity
LBW, SGA
IUGR
RDS, BPD
metabolic
- hypoglycemia -> significant risk
multiple births
genetic syndromes & dz
neonatal abstinence syndrome

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9
Q

what is IUGR

A

intrauterine growth retardation
- infant born significantly low in wt, length, and head circumference

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10
Q

why can multiple births inc risk for morbidity and mortality

A

defined amt of space
can compromise fetus and inc risk of premature delivery and mortality

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11
Q

how can disparities in health and healthcare affect risk for morbidity and mortality

A

racial inequities in pregnancy related mortality

black women 2x likely to deliver VLBW infant
preterm birth 50% higher in black women

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12
Q

what is FTG

A

38-41wks

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13
Q

what is pre-term gestational age

A

<37wks

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14
Q

what is post-term gestational age

A

> 42wks

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15
Q

what is normal birth weight at 40wks

A

~6lbs

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16
Q

what is low BW

A

~5.5lbs

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17
Q

what is very low BW

A

</= 3.3lbs

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18
Q

what is extremely LBW and when is this normal

A

<2lbs
normal BW for 24wks gestation

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19
Q

what are 4 common related complications associated w prematurity

A

pulmonary (IRDS & BPD)
CNS (IVH, PVL)
GI (NEC)
hemotological (hyperbilirubinemia)

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20
Q

what multisystem path are premature infants at risk for

A

cardiopulmonary
CNS
GI
primary sensory

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21
Q

what are 4 general characteristics of premature infants (<37wks)

A

physiological flexion
- absent or diminished
reflexes (rooting, suck swallow)
- absent or diminished
immaturity - physio & behavior
pain sensitivity

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22
Q

why is the premature infant more sensitive to pain

A

by 20-24wks gestation: pain pathways, cortical and subcortical centers of pain perception, and neurochemical system associated w pain transmission are functional

not until 36-40wks gestation that pain modulatory tracts which inhibit pain via serotonin and norepinephrine are functional

= heightened sensitivity

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23
Q

what is the risk of poor management of the premies’ heightened sensitivity to pain

A

can lead to prolonged structural and functional changes

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24
Q

what are components for pain management

A

clustering care
sucrose
developmental supportive care

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25
Q

what are 4 risk factors for developing IRDS

A

prematurity
- CP system immature
LBW
low APGAR
need for neonatal transport
- from community hospital bc not able to provide care

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26
Q

what are 3 causes of IRDS

A
  1. significant pulmonary immaturity
  2. no/insufficient surfactant
  3. ventilation/perfusion mismatch
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27
Q

why is it common for no/insufficient surfactant in premies

A

surfactant starts being produced at 26-29wks but not chemically mature -> doesn’t start to function until 34wks

28
Q

why is a ventilation/perfusion mismatch sometimes seen in premies

A

surfactant not doing its job -> inc surface tension -> alveolar collapse & atelectasis -> inc pulmonary artery pressure -> ventilation perfusion mismatch

29
Q

when does uncomplicated IRDS resolve

A

w/i 3-4 days

30
Q

what are interventions that may be utilized with IRDS

A

supplemental O2
- mechanical vent
- ECMO

surfactant replacement therapy

31
Q

what are the benefits of surfactant replacement therapy for IRDS

A

dec morality
dec air leak
dec chronic lung dz in premies w IRDS

32
Q

what is the pathophys of bronchopulmonary dysplasia (BPD) - 3

A

interstitial fibrosis
alveolar collapse
smooth ms hypertrophy

33
Q

what is a common dx to follow a dx of BPD

A

chronic lung dz of infancy

34
Q

what is the dx criteria for BPD (3)

A
  1. mechanical vent - 1st wk of life
  2. (D) on O2 >28days
  3. persistent densities on chest XR
35
Q

what are dx findings via PFTs in BPD (3)

A

inc airway resistance
dec compliance
inc work of breathing

36
Q

what are interventions for BPD (3)

A

infection control* significant
hydration & nutrition
- critical for growth of healthy alveoli
respiratory support therapy
- CPT -> poor airway clearance, retention of secretions

37
Q

what is an important factor to consider with interventions for BPD

A

poor activity tolerance

38
Q

what is the overall goal/outcome of interventions for BPD

A

can outgrow BPD if facilitate new alveolar growth w good infection control and nutrition

39
Q

what are 3 signs of poor activity tolerance in a baby w IRDS

A

change in VS
poor feeding
- fatigue quickly
- need breaks
- not gaining wt
poor interaction

40
Q

what is considered activity for infants

A

revolves around feeding & interaction
- maybe early motor activity (ex: head control)

41
Q

what are the 3 main goals of PT in infants

A

improve activity, feeding, and interaction

42
Q

why do you commonly see CNS complications in premies

A

immaturity/anomalies of CVP will create inc vulnerability to altered states of HoTN or HTN, inc vulnerability to CNS damage

43
Q

what is periventricular leukomalacia (PVL)

A

areas of cellular necrosis in white matter, near lateral ventricle
- fluid filled cysts left behind

44
Q

what are 2 causes of PVL

A

trauma

hypoxia/ischemia to arterial supply to periventricular white matter

45
Q

what is PVL a sensitive marker for and why

A

sensitive marker for poor neurodevelopmental outcomes
- risk for CP inc

bc of location, along lateral ventricle near corticospinal tract

46
Q

what is intraventricular hemorrhage (IVH)

A

starts in subependymal layer (where glioblasts are formed) of germinal matrix
- may extend into intraventricular space

47
Q

what is IVH associated with (3)

A
  1. poor vascular autoregulation
  2. high metabolic activity of germinal matrix
  3. fragile endothelial walls of immature vasculature
48
Q

what does IVH have a direct relationship to

A

prematurity

49
Q

grades 1/2 vs 3/4 of IVH

A

1/2: mild and infants have good outcomes

3/4: much more significant w more bleeding
- 3: bleeding press on brain
- 4: bleeding invades brain

50
Q

what are 2 complications of IVHs

A

hydrocephalus
- obtructed flow of CSF
hypoxic/ischemic lesions

51
Q

how is IVH dx

A

head US, CT

52
Q

what is medical treatment for IVH (2)

A

stabilize hemodynamics
limit stim (acute phase)

53
Q

what is necrotizing enterocolitis (NEC)

A

acute inflammatory dz of bowel
- reflects immaturity of bowel to handle minor toxins and infections

54
Q

what are 3 factors for NEC

A

intestinal ischemia
infection
toxins

55
Q

what are signs/red flags for NEC (4)

A

vomiting
abdominal distention
bloody stools
change in respiratory status

56
Q

what are treatments for NEC

A

TPN
- gives gut time to rest
gastric suctioning
possible surgery
- remove necrotic tissue via temporary colostomy and later re-anatomize ends of colon

57
Q

what is hyperbilirubinemia

A

buildup of bilirubin in blood d/t immature liver
- leading to jaundice

58
Q

what are sx of hyperbilirubinemia (4)

A

lethargic
low tone
low feeding
low sucking

59
Q

what is the risk fo hyperbilirubinemia

A

kernicturus
- buildup of bilirubin in BG d/t weakened BBB

60
Q

what is the main treatment for hyperbilirubinemia

A

phototherapy
- can also be used prophylactically

61
Q

NAS vs NOWS

A

neonatal abstinence syndrome
- result of poly substance used

neonatal opioid withdrawal syndrome
- result of opioid use (prescription, methadone, heroin)

62
Q

what is NAS/NOWS caused by

A

prenatal exposure to opiates

rapid discontinuation at delivery w cutting of cord
-> significant inc in noradrenalin
-> ANS, CNS, & GI s/sx of withdrawal

63
Q

what are CNS (4), ANS (4), and GI (3) s/sx of withdrawal seen in NAS/NOWS

A

CNS:
- inc ms tone
- inconsolibility
- irritability
- high pitched cry

ANS
- sweating
- sneezing
- frequent yawning
- inc RR

GI
- poor feeding
- regurgitation/vomiting
- loose / watery stools

64
Q

what medical intervention is seen with NAS/NOWS

A

methadone/morphine
- dosing determined by q4hour assessment

65
Q

what does NAS/NOWS impacts in the infant’s development outcomes

A

neurobehavioral
language
motor systems

66
Q

what are long term outcomes in early stages of NAS/NOWS impacted by

A

polypharmacy exposure
SES

Lifespan (20 decks)

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