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HIGH RISK NEWBORNS Increased respiratory rate to better use the

surface available
PRETERM INFANT
Predisposing factors:
o A live infant born before the end of
37th week of pregnancy o Cesarean birth (thoracic cavity not
o Weighs less than 2,500 grams at birth compressed thus less lung fluid is
o The earlier the infant is born, the expelled)
greater the chance of complications. o Mother received extensive fluid
administration during labor
Etiology o Prematurity
o Maternal risk factors: smoking, poor Complications:
nutrition, placental problems,
incompetent cervix. o Tiring effort
o Other risk factors: Low socioeconomic o Mild retractions
status, environmental exposure to o Mild hypoxia
harmful substance. o Difficult feeding

Respiratory Distress Syndrome (RDS) Interventions:

Etiology: 1. Close observation:

o Lack of surfactant o See to it that increased effort is not

o Insufficient surfactant allows alveoli to
collapse with each expiration
o Respiratory failure is most common
cause of death in preterm infants within 2. Oxygen administration
the first 72 hours of life
Assessment:
o Tachypnea
o Tachycardia
o Cyanosis Apnea
o Grunting
o Nasal flaring
o Chest wall retractions
Interventions:
1. Put the patient on NPO to decrease risk
for aspiration
2. Administer Oxygen therapy
3. Assist physician in inserting
endotracheal tube
4. Instill artificial surfactant via the ET tube
5. Maintain respirations 30-60/min
6. 6. Assess every 1-2 hrs and prn Causes:
Transient tachypnea in newborn
o Rapid respiratory rate up to 80
breaths/minute when crying
o Within 1 hour, slows to 30-60 bpm
Causes:
Slow absorption of lung fluid --- Slight decrease
in mature surfactant production --- decreased
alveolar surface area for oxygen exchange ---
tiring
o Watch out for more serious disorder
(respiratory obstruction)
o Peaks in intensity at 36 hours of life &
then begins to fade
o By 72 hours, spontaneously fades (lung
fluid is absorbed)
o Pause in respiration longer than 20sec.
o Apnea of 15 seconds or less is normal at
any age
o Can be a sign of sepsis, seizures, upper
airway abnormalities, gastro-
esophageal reflux, hypoglycemia, or
impaired regulation of sleep or feeding.
o Usually presents as an apparent life-
threatening event.
o Associated with cyanosis, marked
pallor, hypotonia or bradycardia
o Fatigue
o Immaturity of respiratory mechanisms
o Secondary stresses:
o Infection
o Hyperbilirubinemia
o Hypoglycemia
o Hypothermia
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Interventions: o Assess for abdominal distention and

emesis (neonate is not tolerating the
1. Stimulate the baby to breathe again
feedings)
o Shake the baby gently
Infection (Sepsis Neonatorum)
o Flick the sole of the foot
o Theophylline (bronchodilator) ETIOLOGY:

2. Resuscitation o Immature immune system

o Lack of immunoglobulin from the
Prevention:
mother
o Maintain a neutral thermal
ASSESSMENT:
environment
o Avoid excessive fatigue (gentle o Redness
handling) o Hypoactivity
o Always suction gently o Poor sucking
o Burp after feeding
INTERVENTIONS:
Hypothermia
o Provide antibiotic therapy
ETIOLOGY: o Adhere to ASEPTIC PROTOCOL
o Administer O2 therapy
o Lack of subcutaneous fat to insulate
o Monitor v/s, activity level.
body
o Small muscle mass Hemorrhage
o Absent sweat or shiver mechanisms
ETIOLOGY:
ASSESSMENT:
o Rupture of thin fragile capillaries within
Mottling the ventricles of the brain
o Immature production of clotting factors
o Tachypnea
o Increased activity ASSESSMENT:
o Increased crying
1. Lethargy - degree of inactivity &
INTERVENTIONS: unresponsiveness nearing
unconsciousness
1. Place infant under radiant warmer or in
2. Bulging fontanels
double-wall isolette.
3. Bradycardia
2. Assess infant’s temp q 2-3 hours and
prn INTERVENTIONS:
3. Warm equipment and linen before in
1. Monitor for signs of hemorrhage.
contact with infant.
2. Administer Vitamin K
Aspiration
Hyperbilirubinemia
Etiology:
o Excessive amounts of bile pigment
o Weak suck/swallow reflexes until 33 to bilirubin in the blood.
34 weeks gestation
ETIOLOGY:
o Poor gag/cough reflexes increase risk of
aspiration o Related to immature liver
o Difficulty in eliminating bilirubin
INTERVENTIONS:
released by normal breakdown of red
o Monitor suck/swallow reflex to assess blood cells
the risk of aspiration; if poor, gavage
ASSESSMENT:
feed as indicated
o Use “preemie” nipple if bottle feeding o Jaundice
o Burp frequently o Dark/Tea colored

INTERVENTIONS:
1. Provide for phototherapy (bili light
exposure) – 18” from the baby (Protect
eyes & the genitals)
2. Regular turning to the side every 2
hours
3. Promote feeding and hydration and
give water in between feedings
Abo incompatibility
o Maternal blood is O and the fetal blood
is either A, B, AB
Pathophysiology:
o The mother’s body forms an antibody
against such particular blood group
antigen and hemolysis (destruction of
RBC) begins.
o The process of antibody formation is
maternal sensitization.
o The antibodies are of large class & do
not cross the placenta
o Hemolysis of blood begins at birth
during the mixing of maternal & fetal
blood as the placenta is loosened.
Complications:
o Fetal anemia
o Jaundice
o Kernicterus (excessively high bilirubin
levels)
ASSESSMENT:
o Blood incompatibility between mother
& fetus
o Jaundice & increasing bilirubin levels
during first 24 hrs
o Decreased hematocrit & hemoglobin
o Lethargy & irritability
o Poor feeding pattern; vomiting
o Enlargement of the liver & spleen
o Signs of kernicterus:
- Absence of Moro reflex
- Apnea
- High pitched cry
- Opisthotonos -
- Tremors
- Seizures
Management:
1. Phototherapy - to reduce mild to moderate
kernicterus
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o Care for neonate receiving
phototherapy:
o Protect eyes from light
o Monitor for signs of dehydration
2. Exchange transfusions
o done on severely affected infants to
decrease the antibody level & increase
infant RBC & hemoglobin levels.
Retinopathy of Prematurity
o Disorder of the retina resulting to
impairment or loss of vision.
ETIOLOGY:
Prolonged exposure to high O2 conc. ---
Hemorrhage within the retina --- Retinal
detachment --- Loss of vision
Intervention:
1. Cautious administration of oxygen
o Administer the minimum amount of
oxygen to maintain PaO2 (partial
pressure of oxygen in arterial blood) of
50-70 mmHg
POSTMATURE INFANTS
o Born after completion of 42 weeks of
pregnancy
Etiology:
o Problems are caused by progressively
less efficient actions of placenta.
ASSESSMENT
o Absence of vernix and minimal lanugo
o Minimal subcutaneous fats
o OLD MAN’s face – leather like skin; long
fingernails
o Skin and cord yellow/green
Hypoglycemia
ETIOLOGY:
o Inadequate glucose stores
o Placental insufficiency
ASSESSMENT:
o High-pitched cry
o Jittery movements (jerky/rapid jumpy
movements)
o Convulsions

INTERVENTIONS:
o Provide glucose infusion (10 – 25 % IV
glucose)
o Monitor patient closely
o Provide milk feedings
o Decrease stimuli to prevent seizures
Meconium Aspiration Syndrome (MAS)
ETIOLOGY:
o Occurs when infants take meconium
into their lungs during or before
delivery.
ASSESSMENT:
o Greenish or yellowish appearance of
the amniotic fluid
o Infant's skin, umbilical cord, or nail beds
may be stained
INTERVENTIONS:
o Adequate suctioning
o Oxygen administration
Small-for-gestational-age infant
o A baby who is smaller than the usual
amount for the number of weeks of
pregnancy.
o Usually has birth weight below the 10th
percentile for babies of the same
gestational age (they are smaller than
90 percent of all other babies of the
same GA)
o May appear physically and
neurologically mature but is smaller
than other babies of the same GA.
o May be preterm, term or post term
ETIOLOGY
Maternal causes:
o Hypertension
o Cardiac, pulmonary or renal disease
o Diabetes Mellitus
o Poor nutrition
o Use of alcohol, tobacco or drugs
o Age
o Multiple gestation
o Placental insufficiency
o Placental fetal abnormalities
o Pregnancy that occurred at high
altitudes
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Fetal factors:
o Normal genetically small infant
o Chromosomal abnormality
o Malformations
o Congenital infections (rubella &
cytomegalovirus)
Clinical manifestations
o Soft tissue wasting and dysmaturity
o Loose, dry and scaling skin
o Perinatal asphyxia
o Polycythemia (increase hgb conc.),
respiratory distress, and CNS
aberrations and persistent acrocyanosis
o Congenital anomalies
Lab. & diagnostic study findings
o Glucose testing will reveal decreased
glycogen stores (increases the potential
for hypothermia & hypoglycemia)
o Hematocrit level may be increased
Nursing management
1. Provide adequate fluid and electrolytes and
nutrition.
o High calorie formula for feeding
2. Decrease metabolic demands when possible
o Small frequent feedings
o Gavage feedings (if no steady weight
gain)
o Neutral thermal environment
o Decrease iatrogenic stimuli
3. Prevent hypoglycemia
o Monitor glucose
o Provide early feedings
o Frequent feedings (q 2 to 3 hrs)
o IV glucose if glucose level does not
normalize with oral feedings
4. Maintain a neutral thermal environment
5. Monitor serum hematocrit
6. Provide education and emotional support
Large-for-gestational age infant
o Is one who weighs more than 4,000
grams
o Is above the 90th percentile of the
normal variation for gestational age.
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Predisposing factors: o Assess for adduction of affected arm

with internal rotation & elbow
o Genetic predisposition
extension
o Excessive maternal weight gain during
o Moro reflex is absent on the affected
pregnancy
side
o Poorly controlled maternal diabetes
o Grasp reflex is intact
o Pathophysiology:
o Overproduction of growth hormone in Klumpke paralysis
utero
- Affects lower trunk from nerve roots C7 and
o Multiparous pregnancies
T1
Manifestations:
o Assess for absent grasp on the affected
Birth injuries: side
o The hand appears as claw-shaped
o Fractured clavicle
o Facial nerve injury Erb – Duchenne palsy & Klumpke paralysis
o Erb – Duchenne palsy or brachial plexus
Management:
paralysis
o Klumpke paralysis o X-ray of shoulder & upper arm
o Phrenic nerve palsy o Delay passive movement of affected
o Possible skull fracture joints until nerve edema resolves (7-10
days)
Management:
o Possible splinting to prevent wrist &
Fractured clavicle digit contractures on the affected side

o X-ray Phrenic nerve palsy (phrenic nerve - supplies the

o Assess for crepitus, hematoma, or muscles of the diaphragm)
deformity over the clavicle; decreased
Management:
movement of arm on the affected side;
absent Moro reflex o Assess for respiratory distress with
o Limit motion diminished breath sounds
o Pain reliever o X-ray usually shows elevation of the
diaphragm on the affected side
Facial nerve injury
o Avoid pneumonia during the recovery
o Assess for asymmetry of mouth while phase (1-3 months)
crying
Skull fracture
o Wrinkles are deeper on the unaffected
side Manifestations:
o The paralyzed side is smooth, with a
swollen appearance. o Soft tissue swelling over fracture site
o If the eye is affected, protect it with o Visible indentation in scalp
patches and artificial tears o Cephalhematoma
o Positive skull x-rays
Erb – Duchenne palsy o CNS signs & symptoms with intracranial
hemorrhage:
 A paralysis of the arm caused by injury
 Lethargy
to the upper group of the arm's main
 Seizures
nerves, specifically, spinal roots C5-C7.
 Apnea
 Hypotonia