The Newborn at Risk: Birth
Related Stressors
Chapter 29
1) Newborn at Risk for Asphyxia
2) Care of the Newborn with Respiratory Distress
3) Transient Tachypnea of the Newborn (TTN)
4) Meconium Stained Amniotic Fluid
5) Newborn at Risk Cold Stress
6) Hypoglycemia
7a) Hyperbilirubinemia
7b) Hemolytic Disease of the Newborn
8) Newborn at Risk for Anemia
9) Newborn at Risk Polycythemia
10) Antibiotic Therapy
1
All InfantsNursing Care
-A, B, C’s
-NTE
-Early detection/treatment of hypoglycemia
-Support the family
2
• Nursing care
•
Should always include these
• How do you maintain a NTE?
•
- cap on head
•
- radiant heat source
•
- keep infant dry
•
- warm objects prior to contact with infant
•
- positioning of the infant (flexed posture)
• Early detection/treatment of hypoglycemia
3
1) Newborn at Risk for
Asphyxia
• Asphyxia is severe, prolonged hypoxia
• Can occur during antepartum, intrapartum,
or postpartum
• Causes respiratory, circulatory, and
biochemical changes
4
Risk Factors for Asphyxia
• Before and during labor
– Biophysical profile
– Fetal heart rate – nonreassuring
• Due to complications causing low O2
–
–
–
–
Low fetal scalp pH
Meconium stained fluid
Prematurity
Multiple gestation
5
• Biophysical profile
•
- fetal breathing movement
•
- fetal movement of body/limbs
•
- fetal tone
•
- amniotic fluid volume
•
- reactive FHR with activity
• FHR
•
- decreased variability
•
- normal FHR 110-160 baseline
•
- decelerations
• Scalp pH
•
- 7.25 or > considered normal
6
Risk Factors for Asphyxia
• At birth
–
–
–
–
–
–
–
Diffcult birth
Low cord pH - acidosis
APGAR
Male
SGA
Sepsis
Congenital heart/lung defects
7
03:05
Asphyxia
• Newborn may be unable to make the
transition to extrauterine circulation
• Reverts to fetal circulatory patterns
• pulmonary hypertension
• increasing hypoxia
• acidemia
• Requires intensive supportive care to reverse
8
Newborn at Risk
Asphyxia(R<60, start chest compressions)
Nursing care
•
•
•
•
Oxygen
IV fluids
May need newborn resuscitation (NRP)
Relate appropriate information to parents
9
5:35
2) Care of the Newborn
with Respiratory Distress
• Respiratory Distress Syndrome
– Prematurity
– Surfactant deficiency disease
– Transient Tachypnea of the Newborn
• Meconium Aspiration Syndrome
10
6:05
11
• How would we know that the infant has
high CO2, or is acidotic?
• ABG or Capillary Blood Gas (CBG)
• Normal PH = 7.30-7.40 after birth….
• Co2 arterial= 35-45 & capillary= 35-50
• Po2 on room air arterial = 50-80& capillary=
35-45
• Bicarbonate 19-22 arterial or capillary l
• Sao2 per pulse ox probe >90
– What would be normal for a cord pH……?
• Look it up!
12
Newborn at Risk
Respiratory Distress
• Respiratory distress syndrome (RDS) aka.
Hyaline membrane disease (HMD)
– ↓ surfactant
– Hypoxia
– Respiratory acidosis which can develop
• Into Metabolic acidosis
• RDS- indicates a failure to synthesize surfactant
• So who is at risk?
•
more frequent in caucasian
•
more frequent in males than females
•
prematurity
13
14
Newborn at Risk
Respiratory Distress
Nursing assessment, you’re going to see
– Respiratory – tachypnea, apnea (Normal is
30-60)
– Chest – retractions, grunting, nasal flaring
– Skin color – pallor, mottling, cyanosis
15
• Nursing Care Plan, page 744, Care of the Newborn with Respiratory
Distress
• Turn to
• Table 28-1, page 742 Clinical Assessment Associated with
Respiratory Distress
• Respiratory
•
- tachypnea (RR > 60) is the most frequent
•
and easily detected sign of respiratory distress
•
- apnea (bad sign)
•
sign of
•
-metabolic alterations
•
- CNS disease
•
-IVH
•
-sepsis
•
-prematurity
• Chest
•
work of breathing
•
-retractions
-grunting -nasal flaring
16
17
10:10
Newborn at Risk
Respiratory Distress
• Nursing Care
– Surfactant replacement
– Oxygen – ventilation (ex: oxy hood/tent)
– ABG’s monitored
– IV fluids/TPN (ex: Central lines)
– Cluster care
– Supportive care
18
12:18
3) Transient Tachypnea of
the Newborn (TTN)
• Failure to clear airways of lung fluid (in utero fluid
is produced, if this fluid isn’t cleared from the pressures on
chest from birth, then TTN. C-Section don’t get this squeeze.)
– Mild intrauterine asphyxia
• Maternal over sedation, bleeding, IDM
– Difficult birth
• Breech birth, prolapsed cord
• C/Section birthInfant may have tachypnea with shallow rapid
respirations or grunting respirations. Retractions and increased
effort with breathing nasal flaring.
• REVIEW:
• Normal Respiratory Rate 30-60 per minute
19
TTN Nursing Assessment
• Little or no difficulty breathing at birth
• Shortly after…
– Grunting
– Flaring
– Mild cyanosis
– Tachypnea- usually by 6 hours of age
•RR as high as 100-140/min.
20
TTN Nursing Care
– Supplemental O2
– IV Fluids
21
15:05
WTF
16:35
4) Meconium Stained
Amniotic Fluid
As the baby stays in the fluid, this fluid will stain the baby
• MAS
•
- 13% of births have meconium stained fluid
•
- of those 4-11% develop MAS
Represents a fetal asphyxial insult
• before/during labor
Risk factors
• Term SGA’s
• Postterm
• Long labors
22
Meconium Aspiration Syndrome
(MAS)
Meconium fluid has aspirated into the baby’s lungs
• Air trapping, if not released can
rupture/pneumothorax
• Alveoli overdistention
• Possible pneumothorax
• Chemical pneumonitis
23
19:40
Nursing Care of the Newborn with
Meconium Aspiration Syndrome
• Prevention of aspiration (Prevent!!)
–
–
–
–
–
–
Detect meconium stained amniotic fluid
Suction ASAP
Mechanical ventilation
Surfactant
Antibiotics
Supportive care
24
20:35
5) Newborn at Risk
Cold Stress
• Cold stress- excessive heat loss resulting in the use of
compensatory mechanisms (increased respirations,
nonshivering thermogenesis)
• Infant heat production is by nonshivering
thermogenesis
• Burning of brown fat
• Requires energy – utilizes O2 and glucose
– Leading to Hypoxemia ( < 40mg/dL )
• Which Produces acids
• Decreases surfactant production
25
Cold Stress Chain of Events
26
Ladewig et al, P. 697
• Figure 26–8 Cold stress chain of events. The
hypothermic, or cold-stressed, newborn attempts to
compensate by conserving heat and increasing heat
production. These physiologic compensatory
mechanisms initiate a series of metabolic events that
result in hypoxemia and altered surfactant production,
metabolic acidosis, hypoglycemia, and
hyperbilirubinemia.
• Cold stress is excessive heat loss resulting in the use of
compensatory mechanisms to maintain core body
temperature
• Heat loss occurs in the newborn through evaporation,
convection, conduction, and radiation.
27
21:55
Methods of Heat Loss
• Evaporation– loss of heat incurred when water is converted
to a vapor. Drying the newborn and etc.
• Convection-the loss of hear from the warm body surface to the
cooler air currents (ie. air conditioned rooms, air currents, O2 by
mask, & removal from incubator into cooler air)
• Conduction-the loss of heat to a coolder surface by direct skin
contact (cold hands, cool scales, cold stethoscope etc)
• Radiation– heat transfers from heated body surface to cooler
surfaces and objects NOT in direct contact with the body (wall of a
room or incubator, objects near the infant
28
Newborn at Risk
Cold Stress
• Signs/Symptoms
– ↑ movement
– ↑ respirations
– ↓ skin temperature
– ↓ peripheral perfusion (cyanotic looking)
– Hypoglycemia- producing heat uses up
stores
– Metabolic acidosis
29
Newborn at Risk
Cold Stress
• Nursing care
– Don’t let it happen!!
– Assess skin temperature q 15-30 minutes
– Warm slowly – rapid temperature elevation may produce
apnea
– Remove plastic wrap, caps, or heat shields while re-warming
– Warm intravenous fluids prior to infusion
– Block heat loss by evaporation, radiation, convection, and
conduction
– Asses for hypoglycemia
30
• Don’t let it happen!!
•
- the amount of heat loss of an infant
•
depends a great deal on the nurses actions
•
What are some ways we can decrease heat loss?
•
- NTE
•
- prewarm surfaces
•
- avoid drafts
•
- …..
• Warm slowly
•
- rapid temperature elevation may cause
•
HYPOTENSION
•
APNEA
31
25:20
6) Hypoglycemia
• Why treat?
– To prevent CNS damage or death
32
Hypoglycemic Neonate
• At Risk
–
–
–
–
–
–
–
Sick and stressed neonates
Infants of diabetic mothers
SGA infants
Smaller twin will have less stores
Male infant
Preterm AGA
Mother with preeclampsia
33
Signs of hypoglycemia
•
•
•
•
•
•
•
Lethargy or jitteriness/tremor
Poor feeding
Vomiting
Pallor, cyanosis
Apnea, Irregular Respirations, Respiratory Distress
Tremors, jerkiness, seizure activity
High pitched cry (meaning neurological origin)
34
Glucose level
•
•
Hypoglycemic newborn’s plasma glucose
concentration is 40 mg/dl or lower.
Signs of hypoglycemia may occur before
40 mg/dl and require intervention
35
27:55
Capillary blood specimen site
• To check blood glucose,
capillary blood is
usually drawn from
newborn’s heel. Avoid
the shaded areas to
prevent injury to
arteries or nerves in the
foot.
36
Care of the Hypoglycemic Neonate
• Early formula feeding or breastfeeding
• If too ill, gavage feeding or IV infusion of
D5W
• Continue to monitor adequacy of
treatment
• Conserve energy stores
• Maintain a neutral thermal environment
37
30:40
7a) Hyperbilirubinemia
• Bilirubin (Normal bilirubin level is ~10-14)
– potential toxin collects in fatty tissue and brain kernicterus
– Jaundice – skin yellow due to deposit of bilirubin
in tissues
• Up to 60% of term newborns will have clinical
jaundice; ↑ for premature infants
• Unconjugated bilirubin is a breakdown product derived from
hemoglobin released from destroyed RBC’s=indirect bilirubin
• To be eliminated from the body, conjugation of bilirubin occurs.
Conjugation is the conversion of yellow lipid soluble pigment into
water-soluble pigment=direct bilirubin
38
31:55
Newborn at Risk
Hyperbilirubinemia
• Risk factors
–
–
–
–
–
–
–
Fetal-maternal ABO/Rh incompatibilities
Prematurity
Cephalohematomas- from birth trauma
Bruising
Birth trauma
Polycythemia
Delayed meconium passage, which are normally
excreted thru stool
39
Newborn at Risk
Hyperbilirubinemia
• Classification
– Physiologic jaundice
– Breastfeeding / Breast milk jaundice
– Pathologic jaundice
40
• Physiologic jaundice in the term
newborn
•
- typically peaks at 3-4 days
then declines over the first week of life
• usually the total bili will be < 12 mg/dLbili can go as high as 17 with multiple
risk factors
41
• Breastfeeding jaundice (early onset)
- compared to formula fed infants--breast fed infants
are 3-6X more likely to develop
moderate to severe
jaundice (moderate = bili> 12, severe=
bili >15 mg/dL)
- due to mild dehydration (decreased
volume of breast milk)
- dehydration may cause a delay in
meconium passage
42
• Breastmilk jaundice (late onset)
•
- occurs later—bili usually peaks at day 614 can develop in up to 1/3 of healthy breast
fed infants bili can vary from 12-20, at this
age it would not be considered pathologic- bili
level usually continually falls after 2 wks of
age, however, it may remain elevated for 1-3
months. if the cause of the jaundice is in
question, the mom may be asked to stop
breastfeeding, but continue to express
breastmilk, with formula substitution, if the
bili drops rapidly over 48 hours, this confirms
breastmilk jaundice and breastfeeding may be
resumed.
43
32:52
Hyperbilirubinemia - Physiologic
• RBCs shorter life span
• Immature liver
• Lack of intestinal bacteria to conjugate
bilirubin
• Poor hydration hinders urine & bowel
elimination
44
Newborn at Risk
Hyperbilirubinemia
• Nursing Care
–
–
–
–
–
I&O
Hydration
Observe for jaundice
Phototherapy
Transfusions
– Nursing care plan, page 779-780
45
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
I&O
- monitor for first stool WHY?
Hydration
- early frequent feeds
- more severe IVF
Jaundice
- note when it occurs
- monitor progression
- transcutaneous bili check before discharge
Phototherapy
- use of visible light to convert bilirubin into
water soluble isomers that can be eliminated
without being conjugated in the liver
Transfusions
- for severe anemia
- exchange transfusions
to replace the baby’s damaged blood
↑ RBC count and ↓ bili level
46
35:30
Hyperbilirubinemia
Pathologic Jaundice
• Hemolytic disease of the newborn (HDN) due to a
– Rh incompatibility
– ABO incompatibility
• Jaundice at birth or in the first 24 hours of life
– Physiologic jaundice occurs after 24hrs
• Hydrops fetalis- massive edema in the fetus or newborn, usually
in association with RBC destruction. (blood incompatibility)
Rhogam to prevent.
• Kernicterus- toxic accumulation of bilirubin in tissues caused by
hyperbilirubinemia.
47
• Rh incompatibility
•
- Rh negative Mom/Rh positive Dad
•
have an Rh positive baby
•
- baby’s blood cells cross over to the Rh negative Mom
•
- Mom develops antibodies (Rh sensitization)
•
- subsequent pregnancies are at risk for HDN
•
- How do we avoid this? RhoGAM
• Signs/Symptoms
•
During pregnancy
•
- placenta helps rid some bili, but not all =
•
mild anemia/hyperbilirubinemia/jaundice
•
- liver/spleen and bone marrow can’t keep
•
up with RBC destruction=
•
severe anemia & liver/spleen enlargement
•
- baby’s organs can’t handle the severe anemia
•
leading to heart failure with fluid buildup in tissues
•
and organs= hydrops fetalis
•
•
•
•
After birth
- baby’s liver can’t conjugate the large amount of bili
severe hyperbilirubinemia and jaundice
- leading to the most severe form of hyperbilirubinemia kernicterus
48
7b) Hemolytic Disease of
the Newborn
• Rh incompatibility
– Rh neg mother with Rh positive newborn
– Jaundice, anemia, hemolysis of RBC’s, increased
immature RBCs
– Most severe form of hemolytic disease of
newborn – Hydrops Fetalis
– Multi-organ system failure due to severe anemia
– Rhogam for the block
49
• Hemolytic disease of the newborn secondary to
Rh incompatibility
– Isoimmune
– Rh neg mother with Rh positive newborn
passes maternal antibodies to fetal circulation
that destroy the fetal RBC
• Jaundice, anemia, increased immature RBCs
(erythroblasts) r/t hemolysis of RBC’s,
• Most severe form is hydrops fetalis – occurs
when maternal antibodies attach to the Rh site
on the fetal RBC, making them susceptible to
destruction by phagocytes; multi-organ system
failure; frequently fatal
50
38:20
Hemolytic Disease of the Newborn
Same thing, but not as severe
• ABO incompatibility
• Mother blood type O & infant A or B can result in
jaundice but rarely hemolytic disease
– Jaundice, hyperbilirubinemia,
hepatosplenomegaly r/t hemolysis of RBC’s
– Rh is not a factor
51
Care of Newborn at Risk for
Hyperbilirubinemia
• Identifying the Cause of Hemolytic Disease
– Blood type
– Coombs’ test
• Indirect- amount of Rh + antibodies in mother’s
blood
• Direct- presence of antibody coated Rh+ RBC’s in
newborn
– Serum bilirubin
– CBC
– Reticulocyte count
52
39:35
Care of Newborn at Risk for
Hyperbilirubinemia
• Alleviate anemia
• Exchange transfusion
– Withdraw & replace all newborn’s blood with
donor blood
• Increase serum albumin levels
• Reduce serum bilirubin
– Phototherapy
– Drug therapy- Phenobarbital (Bilirubin binds to
Phenobarbital, so when it goes… the bilirubin
does too)
53
8) Newborn at Risk
for Anemia
• Normal Hgb
– Term 15-20 g/dL, less 14 = anemia
– Preterm 14-18 g/dL, less 13 = anemia
• Hemoglobin levels < 14g/dl in term infant or
13 g/dl in preterm
54
Common Causes of Anemia
• Blood Losses
– Placental bleeding
– Intrapartal blood loss
– Umbilical cord bleeding
– Birth trauma
– Cerebral bleeding
• Hemolysis
• Impaired red blood cell production
55
42:10
Physiologic anemia
• Decreased hgb first 6-12 weeks
• Production of RBC’s stopped in response to
elevated O2
• Hgb levels decrease, bone marrow
production resumes
56
Care of the Newborn with Anemia
• Early Detection and correction of pathological
anemia
– Pale infant, poor weight gain, tachycardia,
tachypnea, apneic episodes
• Ensure newborn well-being. Follow checklist:
airway, breathing, circulation, neutral thermal
environment, early detection and intervention of
hypoglycemia, promote comfort & bonding
• Monitor: total blood out
57
Anemia
• Signs & Symptoms
– ↓ Hgb
– Pallor
– ↓ BP
– Tachycardia
– Tachypnea
– Apneic episodes
58
Nursing Care - Anemia
• Mild anemia
– Iron supplement
• More severe
– Hydration
– Blood Transfusion
59
9) Newborn at Risk
Polycythemia
•
•
•
•
↑ blood volume
↑Hct > 65%-70%
Hgb > 22 g/dl
More common in:
–
–
–
–
–
–
IDM
SGA
Postmature
Term infants with delayed cord clamping
Maternal-fetal transfusion
Twin-to-twin transfusion
60
Newborn at Risk
Polycythemia
Often asymptomatic
– S/S
•CHF - Tachycardic, Respiratory distress
(30-60 is normal)
•↑ bili
•↓ peripheral pulses
61
Nursing Care
• Exchange transfusion with FFP or albumin
• Monitor VS during transfusion
• +/- phototherapy
• Treatment goal
– Reduce hematocrit to a range of 55%-60%, this
is a success
62
48:38
Newborn at Risk
Infection
• Sepsis Neonatorum
– Newborns up to 1 month of age are particularly
susceptible
– Prematurity increases risk
• Caused by organisms that do not cause
infection in older children
63
Predisposing Factors
• Maternal antepartal infections
– TORCH - Toxoplasmosis, Rubella, Cytomegalic
Inclusion Disease, Herpes (all deadly to newborns)
• Intrapartal
– Amnionitis, passage through the birth canal,
Group B hemolytic Strep, Herpes, Gonococci,
Listeria
• Nosocomial
– Pseudomonas, Staphylococcus aureas and epi
64
50:43
Diagnosis
• Usual Lab work
– CBC, Blood Cultures (best) and Sensitivity with
Gram Stain, Urine for antibody screen, C-Reactive
Protein level, other cultures as recommended or
ordered
• Chest x-ray
• If viral infection is suspected TORCH
(toxoplasmosis, other, rubella,
cytomegalovirus, herpes virus) titers are
drawn. Skull and bone x-rays to check for any
damage.
65
51:42
•
•
•
•
Nursing care
Infants with sepsis can rapidly deteriorate!
Supportive care
Administer medications as ordered
Recognition of the signs of sepsis- hypotonia, color
changes – pallor, dusky, cyanosis, grey, temperature
instability, feeding intolerance, hyperbilirubinemia,
tachycardia, apnea, behavioral changes, RDS-type
symptoms
– Respiratory Distress symptoms:
• Incr respirations, nasal flaring, retractions, grunting, peripheral edema
• A sub normal temperature, is a cardinal sign of sepsis.
66
53:42
10) Antibiotic Therapy
Review proper dose/kg
Therapeutic peak/trough values
Method of administration (thru IV, Central line
is better)
Incompatibilities
Side effects
67
54:23
Duration of Antibiotic Therapy
• Therapy initiated before test results are final
• Treatment of infection with 2 broad spectrum
antibiotics per intravenous route
• When the pathogen and its sensitivities are
determined appropriate specific antibiotic
therapy is implemented for 7-14 days.
68