Nur 1210 Pedia Module #1 Newborn

FAR EASTERN UNIVERSITY
INSTITUTE OF NURSING
SECOND SEMESTER – AY 2020 – 2021
NUR 1210 – NCM 109 CARE OF THE MOTHER AND CHILD AT RISK OR WITH PROBLEM
MODULE 1: NURSING CARE OF AT RISK /HIGH RISK /SICK CLIENT - NEWBORN

INTRODUCTION
This module discusses care during pregnancy, screening women for risk factors that
could lead to illness in a newborn such as younger or older than average maternal age,
concurrent disease conditions such as diabetes or human immunodeficiency virus (HIV)
infection, pregnancy complications such as placenta previa, or an unhealthy maternal lifestyle
such as drug abuse is essential to identify infants who may need greater-than-usual care at
birth (Pinheiro, 2007). Unfortunately, not all instances of high risk can be predicted. Even a
newborn from a “perfect” pregnancy may require specialized care or develop a problem over
the first few days of life necessitating special interventions. Any infant who is born dysmature
(before term or postterm, or who is underweight or overweight for gestational age) is also at
risk for complications at birth or in the first few days of life. Parents need thorough education
about their baby’s health because these problems may require rehospitalization or additional
follow-up at home. Being able to predict an infant is at high risk allows for advanced
preparation so that specialized, skilled health care personnel can be present at the child’s birth
to perform necessary interventions, such as resuscitating a newborn who has difficulty
establishing respirations. Immediate, skilled handling of any problems that occur may help to
save the newborn’s life and also prevent future problems, such as neurologic disorders (Saigal
& Doyle, 2008).
LEARNING OUTCOME
After the successful completion of the module you should be able to:
LO1 Integrate concepts, theories and principles of sciences and humanities in the formulation and
application of appropriate nursing care to mothers and children at-risk / high risk,
LO2 Apply maternal and child nursing concepts and principles to at risk/high risk/ and sick clients during
childbearing and child rearing years holistically and comprehensively.
LO3 Assess mothers and children at – risk / high risk /with acute or chronic conditions with the use of
specific methods and tools to address existing health needs.
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NUR 1210 –PEDIA CONCEPT( Anna Liza R. Alfonso DNM,MAN,RN,RM)
Prepared by MCN FEU Faculty Lecturers January, 2021
LO4 Formulate nursing diagnoses to address needs / problems of mothers and children at - risk/high
risk/with acute or chronic conditions.
LO5 Implement safe and quality nursing interventions addressing health needs/ problems of mothers
and children at - risk / high risk/s with acute or chronic conditions.
LO9 Provide nursing care utilizing evidence-based practices to mothers and children at – risk / high risk /
with acute or chronic conditions.
LO11 Apply ethical reasoning and decision making process to address situations of ethical distress and
moral dilemma in caring for mothers and children who are at - risk/high risk/with acute or chronic
conditions.
TOPIC OUTLINE
Nursing care of the high-risk newborn to maturity
1. Problems related to maturity
a. Prematurity
b. Post maturity
2. Problems related to gestational weight
a. Small for gestational age (SGA)
b. Large for gestational age (LGA)
3. Acute conditions of the neonates such as:
a. Respiratory distress syndrome
b. Meconium aspiration syndrome
c. Sepsis
d. Hyperbilirunemia
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CONTENT
The High-Risk Newborn

• Newborn regardless of the gestational age or birth weight, who has a greater- than-
average chance of morbidity or mortality because of conditions or circumstances
superimposed on the normal course of events associated with birth and adjustments to
extrauterine life.
APGAR Scoring:
The 1-minute score determines how well the baby tolerated the birthing
process.
The 5-minute score tells the doctor how well the baby is doing outside the
mother's womb.
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Interpretation:
0 – 3 = severely depressed
4 – 6 = moderately depressed
7 – 10 = good/ healthy
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SILVERMAN – ANDERSEN INDEX - NEONATAL RESPIRATORY DISTRESS GRADING

Grading : 0 = No Respiratory Distress
4 - 6 = Moderate Distress
7 - 10 = Severe Distress
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Ballard Maturational Assessment:

The sum of all 12 criteria represents the neuromuscular and physical maturation of the fetus.
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I. PROBLEMS RELATED TO MATURITY:

A. Full-term infant
• delivered at 37 to 40 weeks of development in the uterus
B. Preterm infant
• delivered before 37 weeks of development in the uterus
• weigh less than 5½ pounds (2.5 kg)
Determining the maturity of newborn

a. Physical findings ( Ballard’s Maturity Testing)
b. Neurologic findings that reveal gestational age
c. Mother’s report of LMP

d. Sonographic estimation of gestation age
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Etiology
a. Low socio economic level
b. Poor nutritional status (Low BMI)
c. Lack of prenatal care
d. Multiple pregnancy (twins, triplets, etc.)

e. Previous early birth
f. Race (higher incidence in non-whites)
g. Use of tobacco, cocaine, and excessive alcohol during pregnancy
h. Age of mother (younger than 18y/o and older than 35 y/o)
i. Order of birth (1st and beyond 4th pregnancy)

j. Maternal height and weight
k. Closely spaced pregnancies (6 month or less)
l. Abnormalities of mother’s reproductive system (Intrauterine septum)
m. Infections (UTI; Intrauterine inflammation/infection)
n. OB complications (Premature rupture of membranes / separation of the placenta/ decidual

bleeding)
o. Early induction of labor
p. Elective caesarean birth
q. type of work and physical activity of mother (stressful conditions, hard labor, and long hours)
r. history of spontaneous (i.e., miscarriage) or surgical abortion
s. Pregnancies that are unwanted or unintended

t. unmarried mothers
u. Women with abnormal amounts of amniotic fluid
v. Mental status of women
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Characteristics of a Preterm Infant

a. very small and appear scrawny
b. have a proportionately large head in relation to the body; with
scant hair
c. Skin - bright pink, smooth, and shiny, with small blood vessels
clearly visible underneath the thin epidermis
d. Fine lanugo - abundant over the body but is sparse, fine, and fuzzy on the head
e. Ear cartilage - soft and pliable
f. Skin - bright pink, smooth, and shiny, with small blood vessels clearly visible underneath
the thin epidermis
g. Soles and palms - minimum creases
h. Bones of the skull and the ribs - feel soft
i. Eyes may be fused.
j. Sleeping for most of the time
k. Inactive and listless
l. Underdeveloped breast tissue
m. Male infants - few scrotal rugae, testes are undescended;
n. Females - labia minora and clitoris are prominent
o. Extremities - maintain an attitude of extension and remain in any position in which they
are placed
p. Unable to maintain body temperature, have limited ability to excrete solutes in the
urine, and have increased susceptibility to infection.
q. A pliable thorax, immature lung tissue, and an immature regulatory center
r. More susceptible to biochemical alterations
s. Higher extracellular water content
t. Preterm infants exchange fully half their extracellular fluid volume every 24hours
u. Soft cranium - subject to characteristic unintentional deformation, or "preemie head,"
caused by positioning from one side to the other on a mattress
v. Head - looks disproportionately longer from front to back, is flattened on both sides,
and lacks the usual convexity seen at the temporal and parietal areas. This positional
molding is often a concern to parents and may influence their perception of the infant’s
attractiveness and their responsiveness to the infant.
w. Frequent repositioning of the infant and positioning on a gel mattress can reduce or
minimize cranial molding.
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Problems due to Prematurity
A. ANEMIA OF PREMATURITY
Erythropoiesis decreases after birth as a result of increased
tissue oxygenation due to the onset of breathing and
closure of the ductus arteriosus, and a reduced production
of erythropoietin
Therapeutic Management:
a. DNA recombinant erythropoietin
b. Vitamin E supplement (assist in
formation of RBCs)
c. Blood transfusion (RBC
transfusion)
d. Iron supplement
B. APNEA OF PREMATURITY
refers to short episodes of stopped breathing in babies who were born before they were
due.
Causes:
a. Their brain is not fully developed
b. The muscles that keep the airway open are weak
c. Anemia
d. Feeding problems
e. Heart or lung problems
f. Infection
g. Low oxygen levels
h. Overstimulation
i. Temperature problems
a. Gently stimulate during periods when breathing stops
b. Give caffeine preparation to help stimulate their breathing
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c. Suction children with apnea

d. Change the position
e. Use a bag and mask to help them breathe
f. Slower feeding time
g. Give oxygen
C. RETINOPATHY OF PREMATURITY (ROP)

• Causes blood vessels to grow abnormally and randomly in the eye. These abnormal
vessels tend to leak or bleed, which leads to scarring of the retina. When the scars
shrink, they pull on the retina, causing it to detach from the back of the eye which
can cause blindness
• Caused by disorganized growth of retinal
blood vessels
• Immature retinal blood vessels constrict

when exposed to high oxygen
concentrations. In addition, endothelial cells
in the layer of nerve fibers in the periphery of the retina proliferate, leading to
retinal detachment and blindness. Infants who are most immature and most ill (and
consequently receive the most oxygen) are at highest risk.
• A preterm infant who is receiving oxygen must have blood PO2 levels monitored by
pulse oximeter, transcutaneous oxygen saturation, or blood gas monitoring.
Keeping blood PO2 levels within normal limits lowers the risk. When blood PO2
levels rise to higher than 100 mm Hg, the risk of the disease increases greatly. In the
past, once ROP occurred, there was no reversing it.
THERAPEUTIC MANAGEMENT
• Antibiotics are administered. Gentamicin, ampicillin, and penicillin are all effective
against GBS infections.
• Parents may have difficulty understanding how their infant could suddenly become this
ill and may need a great deal of support in caring for their infant. This is even more
important if the newborn survives the infection but is left neurologically challenged.
• In the future, immunization of all women of childbearing age against streptococcal B

organisms could decrease the incidence of newborns infected at birth.
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• Cryosurgery or laser therapy may be effective in preserving sight.
• Newborns and those who have received oxygen therapy before discharge from a
hospital nursery and again at age 4 to 6 weeks of age to detect any occurrence of the
syndrome.
D. PERIVENTRICULAR / INTRAVENTRICULAR HEMORRHAGE

• Neurodevelopmental problems have been linked to lack of maternal thyroid
hormones at a time when their own thyroid is unable to meet postnatal needs
a. Cranial ultrasound performed after the first few days of life to detect if a hemorrhage has
occurred
F. NECROTIZING ENTEROCOLITIS
• Because specific IgG production is delayed in
newborns, and 33% of VLBW neonates have
substantial hypogammaglobulinemia, the IgA
content of breastmilk may be an important facet of
GI mucosal protection. Breastmilk promotes the
growth of bifidobacterial, which produce acetic and
lactic acid that in turn inhibits the growth of many
pathogenic, gram-negative organisms. VLBW infants
have a delay in the establishment of GI bifidobacterial. This delay appears related to
decreased intake of human milk.
Management for Necrotizing enterocolitis:
• Encourage all mothers to initially provide

breastmilk for their preterm neonates
NURSING DIAGNOSIS
1. Impaired gas exchange r/t immature pulmonary functioning
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2. Ineffective thermoregulation r/t immaturity

3. Deficient diversional activity (lack of stimulation) r/t preterm infant’s rest needs
4. Risk for deficient fluid volume r/t insensible water loss at birth and small stomach
capacity
5. Risk for infection r/t immature immune defenses in preterm infant
6. Risk for imbalanced nutrition, less than body requirements r/t additional nutrients
needed for maintenance of rapid growth, possible sucking difficulty, and small stomach
7. Risk for impaired parenting r/t interference with parent-infant attachment secondary to
hospitalization
8. Risk for disorganized infant behavior r/t prematurity and environmental overstimulation
9. Parental health-seeking behaviors r/t preterm infant’s needs for health maintenance
PREVENTION OF PREMATURITY
Expectant mother should:
1. Eat nutritious diet
2. Avoid alcohol, tobacco, and drugs unless they are needed to treat a medical condition
3. Receive early and regular prenatal care for early recognition and treatment of complications
of pregnancy
NURSING DIAGNOSIS
1. Impaired gas exchange r/t immature pulmonary functioning
2. Ineffective thermoregulation r/t immaturity
3. Deficient diversional activity (lack of stimulation) r/t preterm infant’s rest needs
4. Risk for deficient fluid volume r/t insensible water loss at birth and small stomach capacity
5. Risk for infection r/t immature immune defenses in preterm infant
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6. Risk for imbalanced nutrition, less than body requirements r/t additional nutrients needed
for maintenance of rapid growth, possible sucking difficulty, and small stomach
7. Risk for impaired parenting r/t interference with parent-infant attachment due to
hospitalization
8. Risk for disorganized infant behavior r/t prematurity and
environmental overstimulation
9. Parental health-seeking behaviors r/t preterm infant’s needs for health maintenance
MANAGEMENT
1. Glucocorticosteroids
Severely premature infants may have underdeveloped lungs, because they are not yet
producing their own surfactant. This can lead directly to RDS, also called hyaline membrane
disease, in the neonate.
• Prior to 34 weeks at least one course of glucocorticoids (Betamethasone or

Dexamethasone)
2. Tocolysis
• delays delivery beyond 24–48 hours to allow for transfer and give administered
corticosteroids the possibility to reduce neonatal organ immaturity.
• Calcium-channel blockers and an oxytocin antagonist can delay delivery by 2–7 days
• β2-agonist drugs delay by 48 hours but carry more side effects.

Neonatal care
1. Keep the newborn warm

a. Plastic wraps or warm mattresses
b. Radiant warmers or in incubators (also
called isolettes)
c. kangaroo care (skin to skin warming)
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o placing a premature baby in an upright position on a mother’s bare chest

allowing tummy to tummy contact and placing the premature baby in
between the mother’s breasts.
o Baby’s head is turned so that the ear is above the parent’s heart
2. Fluids and nutrition through intravenous catheters
3. Oxygen supplementation
4. Mechanical ventilator support
5. Medications
6. Encourage breastfeeding
7. Basic infection control measures
8. Bili lights to treat newborn jaundice (hyperbilirubinemia)
9. Prophylactic treatments like indomethacin
PROGNOSIS OF PRETERM
1. Risk of death and long-term problems (delayed development, cerebral palsy, and vision
impairment) begins to increase in infants born before 26 weeks of pregnancy and particularly in
those born before 24 weeks.
2. Many newborns extremely premature have normal intelligence, but some have learning
disorders
3. Children born between 22 and 25 weeks:
• 46 % had moderate to severe disabilities (cerebral palsy, vision or hearing loss and
learning disabilities)
• 34 % had mild disabilities
• 20 % had no disabilities
• 12 % had disabling cerebral palsy
POST TERM (POST MATURE INFANTS)
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• Infants born of a gestation that extends beyond 40 weeks

Calculated from:
• Mother’s LMP
• Ultrasonography
CHARACTERISTICS OF POST TERM INFANTS
1. Absence of lanugo
2. Skin is often loose, cracked, parchment like, and desquamating
3. The little vernix caseosa that remains in the skinfolds may be stained a
deep yellow o r green, an indication of meconium staining
4. Abundant scalp hair
5. Wasted physical appearance (intrauterine nutritional deprivation)
6. Depletion of subcutaneous fat

7. Elongated appearance.
8. Long fingernails and toenails
9. Umbilical cord and nails may be stained green if meconium was
present in the amniotic fluid
TREATMENT FOR POST TERM
a. Resuscitation if in distress
b. If lethargic because of
meconium aspiration, intubate to
suction as much meconium
c. Mechanical ventilator may be needed to support breathing

d. If hypoglycemic, glucose solutions by IV or frequent breast milk or formula feedings
• Induction of labor is usually recommended when infants are significantly overdue.
II. PROBLEMS RELATED TO GESTATIONAL WEIGHT
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Appropriate for gestational age

full term infant heavier than 2,500 grams (about 5.5 lbs.) and lighter than 4,000 grams (about
8.75 lbs.)
A. SMALL FOR GESTATIONAL AGE (SGA)

 Birth weight falls below the 10th percentile
on intrauterine growth curves.

 SGA infants are small for their age because they
have experienced Intrauterine growth restriction or
retardation (IUGR) failed to grow at the expected rate in utero.
ETIOLOGY OF SGA
1. Placental anomaly:
2. Women with systemic diseases that decrease blood flow to the placenta:
3. Infants with uterine infections:
a. Rubella (German measles)

b. Toxoplasmosis
4. Mothers who smoke heavily or use narcotics
5. Babies with chromosomal abnormalities
6. Maternal nutrition during pregnancy
7. Pregnant adolescents
8. Parents are small
CHARACTERISTICS / APPEARANCE OF SGA

1. Below average in weight, length, and head circumference (deprivation early in pregnancy)
2. Reduction in weight (deprivation Iate in pregnancy)

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3. Overall wasted appearance

4. May have a small liver, which may cause difficulty regulating glucose, protein and bilirubin
levels.
5. Poor skin turgor
6. Large head because the rest of the body is so small.
7. Skull sutures may be widely separated from lack of normal bone growth.
8. Hair is dull and lusterless

9. Abdomen may be sunken
10. Cord often appears dry may be stained yellow
11. Because the NB’s age is more than the weight implies, the child may have better-developed
neurologic responses, sole creases and ear cartilage than expected for a baby of that weight
12. Skull may be firmer
13. Infant may seem unusually alert and active for that weight.
14. Hematocrit level is more than 65% to 70%.
SGA are at increased risk of the following problem:

1. Meconium aspiration
2. Excess red blood cells (polycythemia)
3. Low blood sugar levels (hypoglycemia)
4. Difficulty regulating body temperature

5. An impaired immune system
NURSING DIAGNOSIS FOR SGA

1. Ineffective breathing pattern r/t underdeveloped body systems at birth
2. Risk for ineffective thermoregulation r/t lack of subcutaneous fat

3. Risk for impaired parenting r/t child’s high-risk status and possible cognitive impairment from
lack of nutrients in utero
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MANAGEMENT OF SGA
1. Exchange transfusion to dilute the blood
2. Intravenous glucose to sustain blood sugar until they are able to suck vigorously enough to
take sufficient oral feedings
• SGA infants have decreased glycogen stores: one of the most common problems is
hypoglycemia (decreased blood glucose, or a level below 40 mg/dL).
B. LARGE FOR GESTATIONAL AGE (LGA)
• An infant whose birth weight falls above the 90th percentile

on intrauterine growth charts;
• also termed Macrosomia

ETIOLOGY OF LGA
1. Overproduction of growth hormone in utero
2. Extreme macrosomia may occur in diabetic mothers whose conditions are poorly controlled
hence have high glucose levels.
3. Multiparous women
4. Large parents
5. Genetic factors
a. Beckwith-Wiedemann syndrome (an overgrowth
syndrome, affected infants are larger than normal
(macrosomia) and continue to grow and gain weight at
an unusual rate during childhood. Growth begins to slow by about age 8, and adults
with this condition are not unusually tall, macroglossia (large tongue)
b. Sotos' syndrome (Cerebral Gigantism, extraordinary physical

growth in children in the first 2 to 3 years of their life, accompanied
with subtle mental retardation, autistic behavior, motor skills delays,
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cognitive disorder, muscle tone and dysarthria. Large at birth, taller, have more weight, and
also tend to have larger hands and feet)
CHARACTERISTICS / APPEARANCE OF LGA

1. May show immature reflexes
2. Low scores on gestational age examinations in
relation to his size.

3. May have extensive bruising
4. Birth injury:
a. Broken clavicle
b. Erb-Duchenne paralysis
5. Prominent caput succedaneum, cephalhematoma, or

molding.
PROBLEMS IN LGA
a. Cardiovascular Dysfunction
•
Cyanosis may be a sign of transposition of the great vessels, a serious heart
anomaly.
b. Excess amount of red blood cells (polycythemia)
• caused by the infant's system attempting to fully oxygenate all body tissues.
c. Hyperbilirubinemia
• LGA newborns may have a ruddy complexion because too many red blood
cells are produced. As the excess red blood cells are broken down, bilirubin is
formed, which, along with poor feeding, results in jaundice.
d. Hypoglycemia
• If the mother has diabetes that is poorly controlled, the infant will have an
increased blood glucose level in utero, which causes the infant to produce
elevated levels of insulin. After birth, these increased insulin levels will
continue for up to 24 hours of life, possibly causing rebound hypoglycaemia
because the infant uses up nutritional stores readily to sustain his weight.
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NURSING DIAGNOSIS FOR LGA

1. Ineffective breathing pattern r/t possible birth trauma in large-for-gestational-age
newborn
2. Risk for imbalanced nutrition, less than body requirements r/t additional nutrients
needed to maintain weight and prevent hypoglycemia
3. Risk for impaired parenting r/t high-risk status of large-for-gestational-age infant
THERAPEUTIC MANAGEMENT LGA

1. Glucose given intravenously or frequent feedings by mouth or by tube into the stomach for
hypoglycemia
2. Supplemental oxygen (Nasal or Mechanical ventilator) for RDS
3. Phototherapy for jaundice
III. ACUTE CONDITIONS OF THE NEAONATE
A. Respiratory Distress Syndrome

B. Meconium Aspiration Syndrome
C. Hyperbilirubinemia
D. Neonatal Sepsis
A. RESPIRATORY DISTRESS SYNDROME
• A condition of surfactant deficiency and physiologic immaturity of the thorax
• Also known as “Hyaline Membrane

Disease”
• Between 24 and 28 weeks of

gestation, a fetus begins producing
"surfactant" in his or her lungs.
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Surfactant is a slippery substance produced by cells in the airways and contains

phospholipids and proteins. Sufficient amounts of surfactant are important because
they help the lungs fill with air and keep the air sacs from deflating thereby keeping the
alveoli open during the oxygen/carbon dioxide transfer in the lungs. If there isn't
enough, the alveoli will collapse. The cells that produce the surfactant are hyaline
membranes. Usually by 35 weeks, a fetus has developed enough surfactant for his or
her lungs to function normally.
ETIOLOGY OF RDS
 Delivery before 37 weeks gestation
 Precipitous delivery
 Sepsis
 Cardiac defects
 Airway obstruction
 Hypoglycemia
 Metabolic acidosis
 Multiple pregnancy
 Maternal diabetes
 Caucasian or male babies
 Perinatal asphyxia
 Preeclampsia or eclampsia
 Maternal hypertension
 Prolonged rupture of membranes

 Maternal corticosteroid use
 Previous birth of a baby with HMD
 Caesarean delivery or induction of labor before full-term
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 Problems with delivery that reduce blood flow to the baby

 Cold stress
 Perinatal infection
Pathophysiology
There is fetal respiratory activity before birth. The lungs make feeble respiratory
movements, and fluid is excreted through the alveoli. Because the final unfolding of the
alveolar septa, which increases the surface area of the lungs occur During the last trimester of
pregnancy, preterm infants are born with numerous underdeveloped and many uninflatable
alveoli. There is limited pulmonary blood flow, which results from the collapsed state of the
fetal lungs-from poor vascular development in general and an immature capillary network in
particular. Because of increased pulmonary vascular resistance, the major portion of fetal blood
is shunted from the lungs by way of the ductus arteriosus and foramen ovale.
At birth, infants must initiate breathing and keep the previously fluid-filled lungs inflated with
air. At the same time, the pulmonary capillary blood flow must be increased approximately
tenfold to provide for adequate lung perfusion and to alter the intracardiac pressure that closes
the fetal cardiac structures.
The alveolar epithelium secretes the surfactant which reduces the surface tension of the
fluids that line the alveoli and respiratory passages, resulting in uniform expansion and
maintenance of lung expansion at low intra alveolar pressure. Deficient surfactant production
causes unequal expansion of alveoli on inspiration and the collapse of alveoli on end expiration.
Without surfactant, infants are unable to keep their lungs inflated and therefore exert a great
deal of effort to reexpand the alveoli with each breath. With increasing exhaustion, infants are
able to open fewer and fewer alveoli. This inability to maintain lung expansion produces
widespread atelectasis.
Inadequate pulmonary perfusion and ventilation produce hypoxemia and hypercapnia.
Pulmonary arterioles, with their thick muscular layer, are markedly reactive to diminished
oxygen concentration. Thus a decrease in oxygen tension causes vasoconstriction in the
pulmonary arterioles that is further enhanced by a decrease in blood pH. This vasoconstriction
contributes to a marked increase in PVR. In normal ventilation with increased oxygen
concentration, the ductus arteriosus constricts and the pulmonary vessels dilate to decrease
PVR.
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Prolonged hypoxemia activates anaerobic glycolysis, which produces increased amounts

of lactic acid. An increase in lactic acid causes metabolic acidosis, inability of the atelectatic
lungs to blow off excess carbon dioxide produces respiratory acidosis. Acidosis causes further
vasoconstriction. With deficient pulmonary circulation and alveolar perfusion, partial pressure
of oxygen in arterial blood continues to fall, pH falls, and the materials needed for surfactant
production are not circulated to the alveoli.
SIGNS AND SYMPTOMS
1. Subtle signs:
a. ↓ Body temperature
b. Nasal flaring
c. Suprasternal, sternal and subcostal retractions (early signs)
d. Tachypnea
e. Cyanotic mucous membranes
2. Several hours later:

a. Expiratory grunting
b. Cyanotic - central (late sign)
c. PO2 and O2 saturation fall in room air
d. Auscultation:
1. Fine rales
2. Diminished breath sounds
3. Distress increases:
a. Seesaw respiration / Shallow breathing
b. Heart failure
c. ↓ UO and edema on extremities

d. Pale gray skin
e. Lethargy, irregular breathing, and apnea
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f. Bradycardia
g. Pneumothorax
COMPLICATIONS OF RDS
1. Hypoxia
2. Respiratory Acidosis
3. Metabolic acidosis
Diagnostic and Laboratory Procedures

1. ABG
 ABG: acceptable level is Pao2 of 50-70 mmHg, Paco2 of 45-60 mmHg, pH of 7.25 of
above, O2 sat at 89-95%
2. Blood Glucose
3. Blood serum calcium
4. Pulse oximetry
5. Chest X-ray
6. Tests of fetal lung maturity

7. Blood, cerebrospinal fluid, and skin culture and sensitivity
MANAGEMENT OF RDS
 Head elevated
 Proper suctioning
 Oxygen administration with increased humidity

 Client will be placed on
 CONTINUOUS POSITIVE AIRWAY PRESSURE
 POSITIVE END EXPIRATORY PRESSURE
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o Purpose is to maintain the alveoli open and prevent alveoli collapse

PROGNOSIS OF RDS
 The condition often gets worse for 2 to 4 days after birth. It often improves slowly after
that. Some infants with severe RDS will die.
 If this occurs, it often happens between days 2 and 7.
PREVENTIVE MANAGEMENT OF RDS

1. Good and regular prenatal care
2. Level of lecithin in surfactant
3. Corticosteroids
4. Proper timing of a Caesarean delivery
5. Preventing premature delivery

6. Tocolytic agent (Terbutaline)
7. Surfactant replacement postnatal
THERAPEUTIC MANAGEMENT OF RDS
1. Provide a calm setting

2. Gentle handling
3. Maintain an ideal body temperature
4. Give warm, moist oxygen
5. Use of CPAP
6. Fluids and nutrition via NGT or TPN

7. Monitoring ABG
8. Give medications right away
9. Blood transfusion
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10. Monitoring ABG
11. Administer medications: Antibiotics, bronchodilators, sedatives, inotropes
13. Therapy with recombinant erythropoetin
14. Give intrathecal surfactant therapy within 24-36 hrs
15. Give warm, moist oxygen (Avoid side effects from too much oxygen)
16. Use of a continuous positive airway pressure (CPAP) to prevent need for a breathing
machine
17. Provide a calm setting
18. Gentle handling
19. Staying at an ideal body temperature (Cooling increases Acidosis; Reduces metabolic oxygen
demand)
20. Management of fluids and nutrition
21. Treat infections right away
22. Provide muscle relaxant
NURSING MANAGEMENT
1. Keep infant thermoregulated
2. Clear infants airway

3. Administer warm humid oxygen
4. Monitor IV fluids per infusion pump and regulate as ordered
5. Provide nutrition via NGT or TPN when indicated
Monitor and Assess:
1. Respiratory rate and rhythm, pulse blood pressure and activity

2. Skin color, Signs of cyanosis, duskiness and pallor
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3. Sucking, swallowing, gag and cough reflex
• Surfactant replacement and rescue
COMPLICATIONS OF RDS
1. Retinopathy of Prematurity and blindness
2. High pressures delivered to the lungs
3. Intraventricular hemorrhage of the NB
4. Pulmonary hemorrhage
5. Severe hypoxemia can result in multiple organ failure and death

6. Air or gas may build up in:
a. Tension pneumothorax
b. Pneumomediastinum
c. Pneumopericardium
7. Blood clots due to an umbilical arterial catheter

28 | P a g e
8. Bronchopulmonary dysplasia
9. Delayed mental development and intellectual
disability
B. MECONIUM ASPIRATION SYNDROME (MAS)
 Before or during labor and delivery.
 Infants born at term and post term.
Meconium
o the first intestinal discharge from
newborns
o a sterile viscous, dark-green substance
composed of lanugo, swallowed
amniotic fluid, and intestinal
secretions (eg, bile); 85-95% is water,
the major liquid constituent
o Meconium-stained amniotic fluid may
be aspirated before or during labor
and delivery. Because meconium is rarely found in the amniotic fluid prior to 34
weeks' gestation, meconium aspiration chiefly affects infants born at term and
post term.
FACTORS THAT PROMOTES THHE PASSAGE MECONIUM TO THE UTERO
1. Placental insufficiency
 Placental insufficiency. When a mother has placental insufficiency, there is a
lack of adequate blood flow to the baby, which can cause fetal distress, leading
to the untimely passage of meconium.
2. Maternal hypertension
3. Preeclampsia
 Preeclampsia. When the placenta does not carry adequate oxygen and nutrition
for the fetus due to maternal underperfusion such as preeclampsia, the placental
villi show increased syncytial knots, villous agglutination, intervillous fibrin, and
distal villous hypoplasia, while maternal vessels in the deciduadisclose atherosis
or mural hypertrophy of the arterioles.
29 | P a g e
4. Oligohydramnios
5. Maternal drug abuse
6. Intrauterine distress
7. Maternal infection/ chorioamnionitis
 Maternal infection/chorioamnionitis. When the placental membranes are
ruptured and amniotic fluid infection occurs, the placenta shows acute
chorioamnionitis (as the maternal inflammatory response) and funisitis (as the
fetal inflammatory response).
8. Fetal hypoxia
 Fetal hypoxia. Fetal hypoxia leads to passage of meconium from neural
stimulation of a maturing gastrointestinal system.
Pathophysiology
In utero meconium passage results from neural stimulation of a maturing GI tract and
usually results from fetal hypoxic stress. As the fetus approaches term, the GI tract matures,
and vagal stimulation from head or cord compression may cause peristalsis and relaxation of
the rectal sphincter leading to meconium passage. Meconium directly alters the amniotic fluid,
reducing antibacterial activity and subsequently increasing the risk of perinatal bacterial
infection. Additionally, meconium is irritating to fetal skin, thus increasing the incidence of
erythema toxicum. However, the most severe complication of meconium passage in utero is
aspiration of stained amniotic fluid before, during, and after birth.
SIGNS AND SYMPTOMS OF MAS
1. Cyanosis
2. Grunting
3. Alar flaring
4. Intercostal retractions
5. Tachypnea
6. Barrel chest
7. Auscultated rales and rhonchi
30 | P a g e
8. Yellow-green staining of fingernails, umbilical cord, skin

9. Green urine observed less than 24 hours after birth
DIAGNOSTIC STUDIS FOR

MECONIUM ASPIRATION
1. Meconium stained amniotic fluid
2. Neonatal respiratory distress

3. Characteristic radiographic
abnormalities
 Chest radiography is essential in order to confirm the diagnosis of meconium
aspiration syndrome (MAS) and determine the extent of the intrathoracic
pathology; identify areas of atelectasis and air leak syndromes; ensure
appropriate positioning of the endotracheal tube and umbilical catheters.
MANAGEMENT OF MECONIUM ASPIRATION SYNDROME

1. Close monitoring of fetal status
2. When meconium is detected, amnioinfusion with warm, sterile saline is theoretically
beneficial to dilute the meconium in the amniotic fluid, thereby minimizing the severity
of the aspiration.
3. When aspiration occurs, intubation and immediate suctioning of the airway to remove
much of the aspirated meconium.
4. Suction for no longer than 5 seconds. If the baby is vigorous (defined as normal
respiratory effort, normal muscle tone, and heart rate >100 beats/min) Clear secretions
and meconium from the mouth and nose with a bulb syringe or a large-bore suction
catheter.
5. Dry, stimulate, reposition, and administer oxygen as necessary.
6. Maintain an optimal thermal environment to minimize oxygen consumption.
7. Minimal handling because these infants are easily agitated. Agitation can increase
pulmonary hypertension and right-to-left shunting, leading to additional hypoxia and
acidosis.
a. Sedation to decrease agitation.
31 | P a g e
b. Umbilical artery catheter be inserted to monitor blood pH and blood gases

without agitating infant.
8. Oxygen therapy via hood or positive pressure to maintain adequate arterial
oxygenation.
9. Mechanical ventilation to minimize mean airway pressure and tidal volume if pulmonary
interstitial emphysema or a pneumothorax is present
10. Oxygen saturations should be maintained at 90-95%
11. Surfactant therapy to replace displaced or inactivated surfactant and as a detergent to
remove meconium.
12. Volume expansion, transfusion therapy, and systemic vasopressors (Dopamine) to
maintain systemic blood pressure greater than pulmonary blood pressure, thereby
decreasing the right-to-left shunt through the patent ductus arteriosus.
13. Ensure adequate oxygen carrying capacity by maintaining the hemoglobin concentration
of at least 13 g/dL.
C. SEPSIS NEONATORUM (SEPTICEMIA)

 Refers to a generalized bacterial infection in the
bloodstream that occurs in an infant younger than
90 days old
 Infant’s poor response to pathogenic agents, ➔
usually no local inflammatory reaction at the portal of entry to signal an infection, ➔
symptoms tend to be vague and nonspecific ➔ Delayed diagnosis and treatment
SOURCES OF INFECTION
1. Transplacental transfer from maternal bloodstream or during labor from ingestion or

aspiration of infected amniotic fluid.
2. Prolonged rupture of the membrane always presents a risk for maternal-fetal transfer of
pathogenic organisms.
3. Microorganisms transmitted through transplacental transfer:

a. Cytomegalovirus (CMV)
32 | P a g e
b. Toxoplasma gondii
c. Treponema pallidum
Factors increasing the risk of infection:
1. Transplacental transfer
2. Prematurity
3. Congenital anomalies
4. Acquired injuries that disrupt the skin or mucous membranes
5. Invasive procedures (placement of IV lines and ET tubes)
6. Administration of TPN
7. Nosocomial exposure
33 | P a g e
Pathophysiology of Sepsis
• Premature withdrawal of the placental barrier leaves the infant vulnerable to most
common viral, bacterial, fungal, and parasitic infections. Immunoglobulin G (IgG), are
normally acquired from the maternal system and stored in fetal tissues during the
final weeks of gestation to provide NBs with passive immunity to a variety of
infectious agents. Early birth (interrupts) ➔ *transplacental transmission➔
preterm infants have a low level of circulating IgG. IgA- against viral infections, and
IgM – against gram-negative organisms, are not transferred to the fetus. ➔ highly
vulnerable to invasion by these organisms Defense mechanisms of neonates are
further hampered by:
a. low level of complement
b. diminished opsonization ability
c. monocyte dysfunction
d. reduced number and inefficient function of circulating leukocytes are unable to
concentrate their limited numbers at the site
e. A hypofunctioning adrenal gland contributes only a meager anti-inflammatory
response ➔These deficiencies permit rapid invasion, spread, and multiplication
of organisms.
TYPES OF SEPSIS
A. Early-onset sepsis
o (less than 3 days after birth)
o acquired in the perinatal period
o Infection can occur from direct contact
with organisms from the maternal GI
and genitourinary tracts.
B. Late-onset sepsis
o (1 to 3 weeks after birth or Day 8 and 9 of NB)
o primarily nosocomial
o Offending organisms are usually:

a. Staphylococci d. E. Coli
34 | P a g e
b. Klebsiella organisms e. Pseudomonas or Candida species

c. Enterococci f. Coagulase-negative staphylococci
CLINICAL MANIFESTATION OF SEPSIS

1. Hypothermia
2. Diarrhea
3. Low blood sugar
4. Swollen belly area
5. Vomiting
6. Jaundice
7. Poor sucking
8. Sudden episodes of apnea
9. Unexplained desaturation
 A few neonatal infections (e.g., pyoderma, conjunctivitis, omphalitis, and mastitis) are
easily recognized.
DIAGNOSTIC EVALUATION OF SEPSIS
1. Radiographic examination
2. Cultures of blood, urine, and CSF
3. CBC
4. C-Reactive Protein serial measurements
PREVENTION OF SEPSIS
1. Screen pregnant women for GBS
2. Screening other maternal infections
3. Handwashing techniques
35 | P a g e
4. Isolation precautions
5. Standards for spacing of infant beds (3 feet spacing)
THERAPEUTIC MANAGEMENT OF SEPSIS

1. Prompt initiation of antibiotic therapy
2. Supportive therapy
4. Electronic monitoring of vital signs
5. Regulation of thermal environment
D. HYPERBILIRUBINEMIA
 Jaundice of the newborn
 Neonatal hyperbilirubinemia
 Bili lights – jaundice
CAUSES OF JAUNDICE
1. ABO Incompatibility
2. Rh Incompatibility
3. Sepsis
4. Extensive bruising
5. Cephalhematoma
36 | P a g e
RISK FACTORS OF HYPERBILIRUBINEMIA

1. Postnatal age
2. Total Serum Bilirubin value
3. Prematurity
4. Health of the neonate
5. SGA
Pathophysiology
Bilirubin is one of the breakdown products of the haemoglobin that results from red blood cell
destruction (RBC) When RBCs are destroyed, the breakdown products are released into the
circulation, where the haemoglobin splits into two fractions: heme and globin. The globin
(protein) portion is used by the body, and the heme portion is converted to unconjugated
bilirubin, an insoluble substance bound to albumin.
In the liver, the bilirubin is detached from the albumin molecule and, in the presence of the
enzyme glucuronyl transferase, is conjugated with glucoronic acid to produce a highly soluble
substance, conjugated bilirubin, which is then excreted into the bile. In the intestine, bacterial
action reduces the conjugated bilirubin to urobilinogen, the pigment that gives stool its
characteristic color. Most of the reduced bilirubin is excreted through the feces; a small amount
is eliminated in the urine.
Normally, the body is able to maintain a balance between the destruction of RBCs and the use
or excretion of by-products. However, when developmental limitations or a pathologic process
interferes with this balance, bilirubin accumulates in the tissues to produce jaundice.
On average, newborns produce twice as much bilirubin as do adults because of higher
concentrations of circulating erythrocytes and a shorter life span of RBCs (only 70 to 90 days, in
contrast to 190 days in older children and adults). In addition, the ability of the liver to
conjugate bilirubin is reduced because of limited production of glucuronyl transferase.
Newborns also have a lower plasma-binding capacity for bilirubin because of reduced albumin
concentrations as compared with older children. Normal changes in hepatic circulation after
birth may contribute to excess demands on liver function.
Normally, conjugated bilirubin is reduced to urobilinogen by the intestinal flora and excreted in
feces. However, the sterile and less motile newborn bowel is initially less effective in excreting
urobilinogen. In the newborn intestine the enzyme β glucuronidase is able to convert
37 | P a g e
conjugated bilirubin into the unconjugated form, which is subsequently reabsorbed by the
intestinal mucosa and transported to the liver. This process known as enterohepatic circulation,
or shunting, is accentuated in the newborn and is thought to be a primary mechanism in
physiologic jaundice. Feeding (1) stimulates peristalsis and produce more rapid passage of
meconium thus diminishing the amount of reabsorption of unconjugated bilirubin, and (2)
introduces bacteria to aid in the reduction of bilirubin to urobilinogen.
Colostrum, a natural cathartic, facilitates meconium evacuation. When there is bruising, as the
bruising heals and the red blood cells are hemolyzed, additional indirect bilirubin is released.
With increasing bilirubin levels, jaundice advance in a head-to-foot direction. Jaundice is visible
on the sclera at a level of 2 to 3 mg/dL (34 to 51μmol/L) and on the face at about 4 to 5 mg/dL
(68 to 86 μmol/L), at the umbilicus at about 15 mg/dL (258 μmol/L) and at the feet at about 20
mg/dL (340 μmol/L).
SYMPTOMS OF HYPERBILIRUBINEMIA
1. Jaundice causes a yellow color of the skin.
1. The color begins on the head to feet fashion
2. Lethargy
3. Poor sucking
DIAGNOSTIC EVALUATION
1. Signs of jaundice
2. Blood exams
3. Serum Bilirubin
a. Preterm infants > 10 mg/dL (> 170 μmol/L)
b. Term infants > 18 mg/dL in term infants
4. Blood, urine and CSF culture
Jaundice in Breastfeeding Infant

 Breast-feeding is associated with an increased incidence of jaundice.
38 | P a g e
Two types:
A. Breast-feeding—associated jaundice (early-onset jaundice)
 begins at 2 to 4 days of age and occurs in approximately 12% to 13% of breast-fed
newborns.
THERAPEUTIC MANAGEMENT OF HYPERBILUBINEMIA
1. Early feeding
2. Pharmacologic: Phenobarbital
3. Fiberoptic panel / blanket
4. Intravenous immunoglobulin
5. Phototherapy
6. Exchange transfusion
PHOTHOTHERAPY
1. The infants eyes are shielded by
an opaque mask to prevent exposure to the
light – protective Plexiglas shield.
a. infant's eyelids are closed
b. checked at least every 4 to 6
hours
c. Eye shields are removed during
feedings
2. Temperature is closely monitored
3. Flexed position with rolled blankets along

the sides of the body
4. Minimal clothing and turn patient

to sides
5. An overhead phototherapy unit may be combined with a bili blanket that can be placed
under the infant.
39 | P a g e
6. Accurate charting includes:

a. Time
b. shielding of the eyes
c. type of fluorescent lamp
d. number of lamps
e. distance between surface of lamps and infant

f. use of phototherapy + incubator or bassinet
g. Occurrence of side effects.
Maximize phototherapy
1. Distance between the lamps and the infant, no less than 18 inches.
2. Increasing the skin surface area exposed to phototherapy will also maximize
treatment.
3. An overhead phototherapy unit is combined with a bili blanket that can be place
under the infant.
4. Lining the sides of the bassinet with white blankets or aluminum foil can increase
effectiveness of therapy
MINOR SIDE EFFECTS OF PHOTOTHARAPY

1. Loose, greenish stools - Frequent stooling can cause perianal irritation; therefore
meticulous skin care, keeping the skin clean and dry, is essential.
2. Bronze baby syndrome - Infants develop a dark, gray-brown discoloration of skin, urine,
and serum due to the accumulation of porphyrins and other metabolites
3. Frying effect - Increased tanning due to use of oily lubricants or lotions on the skin
4. Purpura or bullae - In infants with cholestatic jaundice or congenital erythropoietic
porphyria
Exchange Transfusion
Serum Bilirubin levels greater than 20-25 mg/dL
40 | P a g e
Using an estimate of 80-90 mL/kg total blood volume X 2 is usually removed and replaced
sequentially in aliquots (10-15 mL in term babies; 5-10 mL in smaller preterm babies) over
several hours.
Using O negative blood rather than the baby's blood type is important because not all
circulating antibodies may be removed.
Packed RBCs resuspended in fresh frozen plasma must be used for this procedure.
COMPLICATIONS OF HYPERBILIRUBINEMIA
1. Kernicterus - indirect bilirubin levels as high as 20 mg/100ml
a. decreased activity f. fever
b. lethargy g. seizures
c. irritability h. opisthotonus
d. rigid extension of all four extremities
e. loss of interest in feeding
NURSING DIAGNOSIS
 1. Risk for Injury r/t abnormal blood profile
(increased breakdown of products of red blood cells), developmental age (immature blood-
brain barrier and immature liver function)
 2. Readiness for Enhanced Parenting r/t birth of a new family member
LEARNING RESOURCES:
Jaundice - https://www.youtube.com/watch?v=6akhmBqAe2g
41 | P a g e
Neonatal distress Syndrome -https://www.youtube.com/watch?v=xWe7Xwh7O1Y
Meconium Aspiration Syndrome - https://youtu.be/w10Z8mYZv-U
Sepsis- https://youtu.be/MdDD9n7Cz-o
LEARNING ACTIVITIES:
Answer the following question – 50 points

1. Using the table below, list the common problems related to maturity . Include the
description, characteristics, symptoms, and treatment. 25pts
MATURITY DESCRIPTION CHARACTERISTICS SIGNS AND TREATMENT

PROBLEM SYMPTOMS
2. Make a list of the maternal risk factors that may cause your chosen problems related to
maturity . For each of these risk factors, state what could be done to decrease the occurrence
of these risks. 10pts
3. What interventions should the nurse plan and/or implement to meet this newborn ’s and his
or her family’s needs? List down 5 and include rationale for each nursing intervention – 10 pts
4. What client outcomes should the nurse evaluate regarding the effectiveness of the nursing
interventions? 5 points
Goodluck
42 | P a g e
REFERENCES
Pillitteri, A. (2014). Maternal and child health nursing (8th ed.) Philadelphia: Lippincott,
Williams and Wilkins.
Bowden, V. R., & Greenberg, C.S. (2016). Pediatric nursing procedures (4thed.).
Philadelphia, PA: Wolters Kluwer.
Cunningham, F. (2014). Williams Obstetrics (24th ed)
43 | P a g e

Nur 1210 Pedia Module #1 Newborn

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FAR EASTERN UNIVERSITY

MODULE 1: NURSING CARE OF AT RISK /HIGH RISK /SICK CLIENT - NEWBORN

Nursing care of the high-risk newborn to maturity

1. Problems related to maturity

2. Problems related to gestational weight

a. Small for gestational age (SGA)

b. Large for gestational age (LGA)

3. Acute conditions of the neonates such as:

a. Respiratory distress syndrome

b. Meconium aspiration syndrome

The High-Risk Newborn

SILVERMAN – ANDERSEN INDEX - NEONATAL RESPIRATORY DISTRESS GRADING

Ballard Maturational Assessment:

I. PROBLEMS RELATED TO MATURITY:

Determining the maturity of newborn

c. Mother’s report of LMP

d. Multiple pregnancy (twins, triplets, etc.)

i. Order of birth (1st and beyond 4th pregnancy)

n. OB complications (Premature rupture of membranes / separation of the placenta/ decidual

s. Pregnancies that are unwanted or unintended

Characteristics of a Preterm Infant

Problems due to Prematurity

c. Suction children with apnea

C. RETINOPATHY OF PREMATURITY (ROP)

• Immature retinal blood vessels constrict

• In the future, immunization of all women of childbearing age against streptococcal B

• Cryosurgery or laser therapy may be effective in preserving sight.

D. PERIVENTRICULAR / INTRAVENTRICULAR HEMORRHAGE

Management for Necrotizing enterocolitis:

• Encourage all mothers to initially provide

2. Ineffective thermoregulation r/t immaturity

• Prior to 34 weeks at least one course of glucocorticoids (Betamethasone or

• β2-agonist drugs delay by 48 hours but carry more side effects.

1. Keep the newborn warm

o placing a premature baby in an upright position on a mother’s bare chest

3. Children born between 22 and 25 weeks:

• 34 % had mild disabilities

• 12 % had disabling cerebral palsy

POST TERM (POST MATURE INFANTS)

• Infants born of a gestation that extends beyond 40 weeks

6. Depletion of subcutaneous fat

c. Mechanical ventilator may be needed to support breathing

• Induction of labor is usually recommended when infants are significantly overdue.

II. PROBLEMS RELATED TO GESTATIONAL WEIGHT

Appropriate for gestational age

A. SMALL FOR GESTATIONAL AGE (SGA)

on intrauterine growth curves.

a. Rubella (German measles)

CHARACTERISTICS / APPEARANCE OF SGA

2. Reduction in weight (deprivation Iate in pregnancy)

3. Overall wasted appearance

8. Hair is dull and lusterless

14. Hematocrit level is more than 65% to 70%.

SGA are at increased risk of the following problem:

4. Difficulty regulating body temperature

NURSING DIAGNOSIS FOR SGA

2. Risk for ineffective thermoregulation r/t lack of subcutaneous fat

B. LARGE FOR GESTATIONAL AGE (LGA)

• An infant whose birth weight falls above the 90th percentile

• also termed Macrosomia

b. Sotos' syndrome (Cerebral Gigantism, extraordinary physical

CHARACTERISTICS / APPEARANCE OF LGA

relation to his size.