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Mgmt Test 3 - OB > Care of High-Risk Newborns > Flashcards

Care of High-Risk Newborns Flashcards

1
Q

Why are preemies more susceptible to hypothermia?

A

Lack of white fat to keep them insulated
Lack of brown fat, (develops at 28-30 weeks)
Babies don’t shiver (which normally produces heat)
Immature CNS, immature temp regulator in the brain (H1=hypothalamus)
Greater surface area (premature infants don’t flex)
Thin skin - blood vessels are closer to the surface of the skin (losing heat/vasoconstriction)

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2
Q

more than 1/3 of all infant deaths are related to preterm T or F

A

True

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3
Q

Causes related to high risk infants

A 
Substance abuse
Diabetes
Teen Moms
Illness (sepsis)
Multiple pregnancies
Unknown
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4
Q

What will we see in a baby experiencing hypothermia

A 
Changes in feeding behavior
lethargic or irritable (change from norm)
respiratory difficulty
hypoglycemia
mottled/pale appearance
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5
Q

what happens in cold stress

A

baby has decreased body temp
babies need to increase metabolic rate to produce heat; using up a lot of glucose and oxygen, resulting in hypoglycemia and resp. distress
babies are increasing their caloric & oxygen use - which they need just to sustain life
non-shivering thermogenesis
vasoconstriction

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6
Q

trt/prevention of hypothermia/thermo-regulation

A

kangaroo care (skin to skin)

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7
Q

signs of respiratory distress

A 
grunting
nasal flaring
retractions
cyanosis (lips)
see-saw respiration's (chest goes down, belly goes up)
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8
Q

A serious complication of hypothermia

A

cold stress

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9
Q

Respiratory Distress Syndrome (RDS) is a

A

lung disorder affecting preterm infants

insufficient surfactant production

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10
Q

RDS is found in this population more often

A 
big babies (born to diabetic moms) - insulin blocks cortisol, cortisol is involved in surfactant production
male babies - androgen's (male hormones) inhibit surfactant production
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11
Q

incidence and severity of RDS is reduced by giving

A

Maternal steroids - maternal betamethazone, acts as cortisol in the baby to get surfactant production going

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12
Q

S/S of RDS appear within

A

at birth or within the first 6 hours - quickly

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13
Q

treatment for AOP

A

caffeine - IV loading dose, then PO

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14
Q

Rate of death from RDS went from 100 - 10% of babies after surfactant trt was found T or F

A

true - considered golden treatment

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15
Q

ROP retinopathy of prematurity cause

A

Blood vessels in the eye become injured; still grow, abnormally, can rupture causing a leak and bleed, scar tissue forms which actually puts traction on retina, causing cause retinal detachment and blindness.
Don’t know the exact range; prolonged oxygen/ventilation support can put them at an increased risk and cause ROP

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16
Q

condition which inhibit/interferes with surfactant production

A

birth asphyxia

c-section

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17
Q

treatment of RDS

A

surfactant replacement therapy through ET tube, intubate them

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18
Q

two complications of oxygen therapy/ventilation support

A

retinopathy of prematurity

chronic lung disease

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19
Q

treatment of CLD (chronic lung disease)

A

supportive/palliative
antibiotics (prn)
broncho-dilators
provide support for parents as well

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20
Q

With IVH, patients are likely to develop

A

developmental delays

neurological abnormalities

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21
Q

Intraventricular (IVH) hemorrhage cause

A

because blood vessels are fragile they will rupture/burst; we will see bleeding in the brain
any hypoxic injury to the brain (systolic)
fluctuations in BP
fluctuations in cerebral blood flow

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22
Q

over the course of 2 years, having had CLD, what can you expect

A

chronic respiratory/lung infections

pneumonia’s

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23
Q

s/s of CLD (chronic lung disease)

A

tachycardia

resp acidosis

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24
Q

CLD prevention

A

maternal steroids -beta methadone
decreases inflammation in airways
minimize exposure to oxygen/ventilation

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25
Q

Screening/mgmt of IVH

A

day 7 ultrasound
oxygen/ventilation therapy

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26
Q

stage 4 IVH will present with

A

neurological abnormalities

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27
Q

what causes fluctuation in blood flow in IVH patients

A

crying
diaper changing
oxygen/ventilation support

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28
Q

prevention of IVH

A

maternal steroids - beta methazone

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29
Q

when will we s/s of IVH

A

within 72 hours birth; otherwise no evidence of a problem

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30
Q

Nursing interventions for IVH

A 
cluster care
minimum to care for these patients
measure head circumference
observe for chg in neurological status
elevate head 30* - decreasing intracranial pressure
parental support
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31
Q

if a baby has symptoms with IVH what would they be

A 
lethargy
poor muscle tone
respiratory deterioration w/apnea or cyanosis(hypo glycemia/thermia)
seizures (last sign)
decreased reflexes
tenting/bulging fontanel
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32
Q

complication of IVH

A

hydrocephalus (water on the brain); requires a shunt

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33
Q

what is NEC

A

infection of the intestines - gas forming bacteria invade intestinal wall; pockets form in intestine as well as food those areas of intestine begin to die
sepsis/systemic infection can occur

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34
Q

what causes nec

A

unknown -
immature GI system?
hypoxia - lack of air to the belly?
feeding too much, to soon?

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35
Q

prevention of NEC

A

breast-milk (formula w/probiotics)

maternal betamethazone

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36
Q

s/s of nec

A

abdominal distention- loops of bowel can be seen
respiratory distress - diaphragm pushing against lungs
spitting up feedings

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37
Q

NEC mgmt

A 
stop feedings immed - call physician (iv nutrition)
antibiotics
decompress belly
surgery may be necessary - ostomy?
long-term gi problems
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38
Q

birth asphyxia - what is it

A

lack of oxygen/increased carbon dioxide in blood

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39
Q

hypoxia vs asphyxia

A

hypoxia - lack/decreased amt of oxygen

asphyxia - increased carbon dioxide (acidosis)

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40
Q

what does asphyxia cause

A

ischemia to organs

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41
Q

possible causes of asphyxia

A

insufficient surfactant
maternal fxrs (htn, infection)
placental fxrs (insufficient, abruption, previa)
fetal fxrs (congenital anomalies, cord problems, prematurity)
Stress puts baby at risk for asphyxia

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42
Q

birth asphyxia manifestations

A

rapid breaths then nothing (resuscitating when nothing is happening)
rapid fall in HR
gasping
loss of consciousness

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43
Q

what do we want to prevent (goal) for birth asphyxia

A

prevent further brain damage - secondary cell death

44
Q

intervention to prevent secondary cell death to the brain in birth asphyxia

A

therapeutic hypothermia - controlled cooling w/cap or blanket
decreasing biological processes - metabolism
must be done within 6hrs of birth
must be 36 weeks in utero
cooled for 72hours
must slowly increase their temperatures (seizures if done too fast)
34-35*C
babies are monitored w/EEG, iv fluids, sedation
helps mild to moderate cases, not much improvement for significantly impaired cases

45
Q

other complications w/birth asphyxia

A

hypo-thermia/tension/glycemia
feeding problems
seizures
fluid/electrolyte imbalances

46
Q

nursing care for birth asphyxia

A

sedation
ventilation
parental support

47
Q

difference between transient tachypnea and respiratory distress syndrome is

A

TTN - really called wet lung amniotic fluid leftover in lungs (wet lung), usually resolves on its own in 12-72 hrs
RDS - surfactant problem

48
Q

transient tachypnea of the newborn (TTN) cause

A

amniotic fluid leftover in lungs (wet lung), resolves on its own in 12-72 hs

49
Q

risk fxrs for TTN

A

male babies
c-section w/o labor (labor process pushes fluid along)
maternal diabetes/asthma

50
Q

most common respiratory problem seen in NICU

A

TTN - transient tachypnea of the newborn

51
Q

population affected w/TTN

A

term

late pre-term

52
Q

if a babies respiratory rate is greater than 60 will we feed them?

A

NO. IV fluids/continue checking xrays

53
Q

Meconium Aspiration Syndrome MAS is caused by a stress event such as asphyxia/hypoxia - anal sphincter relaxes causing release of stool, baby aspirates meconium in utero or at birth. t or f

A

true

54
Q

what is MAS

A

meconium fluid enters lungs during fetal life or at birth

55
Q

what does MAS result in

A

obstruction of airway (meconium is thick/tarry)

infection/inflammation of the airway

56
Q

nursing intervention for MAS

A

gives lung rest/support (oxygen/ventilation)
npo
Viagra (helps w/vaso-dilation of lungs)-off label use

57
Q

last resort trt for MAS

A

extra corpral membrane oxygenation (ecmo) heart/lung bypass machine

58
Q

hyperbillirubinemia can cause

A

brain damage

59
Q

positive direct coombs test

A

monitors bilirubin levels
direct = babies test - not moms
(+) = maternal antibodies were found on babies RBCs;
moms blood cells were attacking babies antigens (rh incompatibility/hemolytic disorders)

60
Q

1 cause of hyperbilirubinemia

A

HEMOLYTIC FXRS - Rh incompatibility; sometimes ABO

61
Q

causes of hyperbilirubinemia

A

hemolytic fxrs (#1 cause)
infection
hypoxia
diabetic mom

62
Q

pathological vs physiologic hyperbilirubinemia

A 
TIMING
Pathological (disease process going on) - appears in 1st 24 hrs - acidosis seen a lot (interferes w/ blood/brain barrier) - picks up albumin - no albumin to conjugate the bilirubin 
Physiologic - after 24hrs of birth - norm RBC process (breaking down) fetus has to make more RBC  then is needed extrautero - babies breaking down its fetal hemoglobin the byproduct is bilirubin
63
Q

conjugated vs un-conjuguated bilirubin

A 
Conjugated = good - liver makes bilirubin water soluble, excrete through urine/stool
Un-conjugated = bad - toxic - bilirubin builds up - give albumin (trt)
64
Q

kernicteris

A

chronic brain damage from hyperbilirubinemia (jaundice on the brain)

65
Q

byproduct of RBC is

A

bilirubin

66
Q

hyperbilirubinemia can lead to what acute and chronic conditions?

A

Acute - Billirubin Encephalopathy (jaundice of the brain)
Chronic - Kernicterus - neurological abnormalities/developmental delays
This can be prevented

67
Q

trt for bilirubin

A 
photo-therapy (protect babies eyes/groin)
increased feeds (urine and stool excretion)
in extreme cases exchange transfusions (remove babies unconguated blood, & replace it, along with albumin)
68
Q

most common bacterial causing infection in the newborn

A

group B strep

69
Q

Sepsis onset

A

early - s/s within the first 24 hrs of life - worse prognosis
late - after 1st week of life

70
Q

risk fxr for sepsis (infection)

A

> 18hr ruptured membranes
foul smelling fluid
preemies
maternal infection (group B)

71
Q

sepsis (infection) characteristics

A

hypothermia (early sign)
resp problems
seizures (late sign) - shock

72
Q

trt for sepsis (infection)

A 
iv antibiotics
supportive care (ventilated)
73
Q

hypoglycemia classification

A

40

74
Q

hypoglycemia can cause

A

brain damage; brain uses glucose for fuel

75
Q

hypoglycemia risk fxrs

A

prematurity/late preterm/postmaturity
prematurity - don’t have glycogen stores
post-maturity -they had to use glycogen due to placental insufficiency

76
Q

normal blood glucose for a term baby

A

50-90; less than 40 classify hypoglycemia

77
Q

early s/s of hypoglycemia

A

jittery/tremors (most common)
resp. difficulty
low temp

78
Q

late s/s of hypoglycemia

A

seizures
coma
resp. distress

79
Q

most common early sign of hypoglycemia

A

jittery/tremors

80
Q

prevention of hypoglycemia

A

monitor (glucose)

early feeds

81
Q

if s/s of hypoglycemia continue, treat with

A

IV glucose (dextrose)

82
Q

risk fxrs for infants of diabetic mothers

A

prematurity
hypoglycemia
asphyxia
resp distress

83
Q

mgmt of hypoglycemia

A

on moms end - control diabetes so baby isn’t affected
monitor glucose
feed early
monitor complications

84
Q

neonatal abstinence syndrome (NAS) is

A

drug exposed babies showing signs of withdrawal

85
Q

method to score babies (around feeding times)

A

Finnegan Score Sheet for NAS (tool to determine if treatment is needed for withdraw)

86
Q

characteristics of NAS

A 
resp problems
irritable - inconsolable
hyperthermia
sneezing (3x's in a row)
diaper rash (constant stools)
87
Q

medications for withdrawal (babies)

A

oral morphine

phenobarbital (due to poly drug use)

88
Q

nursing care for NAS

A 
cluster care
encourage feedings
once they sleep - try to allow them to get an hours rest
injury prevention
involve parents (non judgmental)
89
Q

what is Gastroschisis***

A

abdomen doesn’t fully close/fuse
organs are outside the abdomen
this does NOT involve the cord
congenital abdominal anomaly

90
Q

Gastroschisis can be dx when

A

in utero

91
Q

Gastroschisis begins/happens when

A

at the 6th week gestation

92
Q

Gastroschisis nursing mgmt

A

prevent infection/injury to organs
apply warm sterile dressings
wrap in plastic for protection

93
Q

trt for gastroschisis

A

silo - gravity pulls organs into stomach area slowly (can take days for this to happen)

94
Q

what is omphalocele ***

A

pt with omphalocele have other anomalies (trisomy…)

intestines/organs are housed IN the umbilical cord

95
Q

omphalocele trt

A

same as gastroschisis (silo)

96
Q

congenital diaphragmatic hernia (cdh) where would you hear bowel sounds

A

chest

97
Q

congenital diaphragmatic hernia (cdh) where would you hear heart sounds

A

shifted over - more left

98
Q

congenital diaphragmatic hernia (cdh) occurs when

A

there is an opening in the diaphragm, the intestines travel into the chest cavity
left lung doesn’t grow to the optimal level

99
Q

s/s of cdh

A 
respiratory distress (only 1 lung is functioning properly)
barrel chest (aveoli hyper-stimulated)
100
Q

s/s of MAS

A

barrel chest (aveoli hyper-stimulated)

101
Q

mgmt of cdh

A

oxygen/ventilator
ecmo (extracorporeal membrane oxygenation)
surgery (when stable)

102
Q

best position for cdh baby

A

affected side - left side

103
Q

babies are at risk for what later in life if on ecmo

A

stroke

104
Q

treatment on ecmo is usually no longer than

A

2 weeks

gives lungs a rest to allow the other lung to grow

105
Q

Glucose protocol

A

usually every hr/1st 4 hrs; every 4hrs/x’s 2

Mgmt Test 3 - OB (7 decks)

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