A.

Nursing Care of the High- Risk

Newborn to Maturity
Learning Objectives

Week 1
1.Define related terms.
2.Identify At- Risk Newborn.
3.Explain Newborn Classification based on
Gestational Age.
4.Identify Problems related to Prematurity.
5.Explain the causes of prematurity.
6. Discuss the characteristics of prematurity.
7. Identify the complications of prematurity.
8. Enumerate the interventions of prematurity.
9. Discuss the diagnostic interventions.
10. Explain the problems related to
Gestational weight
Week 2

1. Discuss the acute conditions of the neonates such

as:
a. Respiratory Distress Syndrome
b. Transient Tachypnea of NB
c. Meconium Aspiration Syndrome
d. Apnea
e. Sudden Infant Death Syndrome
f. Hyperbilirubinemia
g. Hemolytic Disease of the NB
Week 3- Holiday
&4
 Week 4
 Discuss Care of Pediatric Client with
Respiratory Disorder:
1. Upper Respiratory Tract Disorders
a. Choanal Atresia
b. Acute Nasopharygitis
c. Pharyngitis e. Epistaxis
d. Tonsillitis f. Laryngitis
g. Croup h. Epiglotitis
Week 5, Week 6- Prelim Exam

2. Lower Respiratory Tract Disorders

a.Bronchitis
b.Bronchiolitis
c.Cystic fibrosis
d.Asthma
3. Complication of Acute Respiratory Infection
a. Otitis Media
Week 7, 8, 9

C. Care of Pediatric Client with Cardiovascular

Disorder: Discuss
1.Congenital Heart Defects
A.Increased Pulmonary Blood Flow
a.Ventricular Septal Defect
b.Atrial Septal Defect
c.Atrioventricular Septal Defect
d.Patent Ductus Arteriosus
B. Obstruction to Blood Flow
a.Pulmonary Stenosis
b.Aortic Stenosis
c.Coarctation of the Aorta
C. Defects with Mixed Blood Flow
a. Transposition of the Great Vessels
b. Total Anomalous Pulmonary Venous Return
c. Truncus Arteriosus
d. Hypoplastic Left Heart Syndrome
D. Defects with Decreased pulmonary Blood
Flow
a.Tricuspid Atresia
b.Tetralogy of Fallot
2. Acquired Heart Disease
A. Rheumatic fever
B. Kawasaki Disease
C. Bacterial Endocarditis
Week 10 & 11
D. Care of Pediatric Client with GIT Disorder
1. Cleft Lip & Plate
2. Tracheoesophageal Atresia
3. Tracheoesophageal fistula
4. Imperforate Anus
5. Pyloric Stenosis
6. Intussusception
7. Necrotizing Enterocolitis
8. Celiac Disease
9. Hirschsprung Disease
10. Failure to Thrive
Week 12 Midterm Exam
13, 14
E. Care of Pediatric Client with Neurologic
Disorder
1.Hydrocephalus
2.Spina bifida
3.Meningitis
4.Talipes Deformities
5.Developmental Dysplasia of the Hip
6. Trisomy 21
7. Autism/ ADHD
8. Febrile Seizure
9. Cerebral Palsy
Week 15, 16
F. Care pf Pediatric Client with HEMATOLOGIC
disorder
1. Thalassemia
2. Hemophilia
G. Care of pediatric Client with Renal & Urinary
Disorder
1.Hypospadia
2.Epispadia
3.Glomerulonephritis
4.Nephrotic Syndrome
5.Nephroblastoma(Wilm’s Tumor)
Week 17

H. Care of Pediatric Client with Dermatologic

Disorder
1.Pediculosis
2.Scabies
3.Impetigo
Week 18 Final Exam
1.Identification of At-Risk Newborn
High- risk neonate is a newborn, regardless of
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 the
adjustments to extrauterine existence.
The – risk period encompasses human growth
& development from the time of viability, the
gestational age at which survival outside the
uterus is believed to be possible, or as early
as 23 weeks of gestation up to 28 weeks
following threats to life & health that occur.
Classification of high risk infants

2. NB Classification Based on Gestational Age

1. Appropriate- for gestational –age (AGA)
infant- an infant whose weight falls between
the 10th& 90th percentile on intrauterine
growth curves or birth weight expected for
the gestational age. Ex. 34th week who
weighs 5 lbs.
2. Small-for-date (SFD) or small-for-
gestational- age (SGA) infant- if the birth
weight is below the 10th percentile on
intrauterine growth curve for that age or
birth weight less than expected for the
specific gestational age. The infant maybe
born preterm(before38th week gestation),
term(between weeks 38 & 42), or post term
(past 42 weeks). Ex. 38 weeks gestation who
weighs 5 lbs.
SGA infants are small for their age because
they have experienced Intrauterine growth
retardation (IUGR)- or restriction or failed to
grow at the expected rate in utero.
 Causes:
1. Mothers nutrition during pregnancy plays a
major role in fetal growth outcome & lack of
adequate nutrition maybe a major
contributor to IUGR & most common cause
of IUGR is placental anomaly:
 either the placenta did not obtain sufficient
nutrients from the uterine arteries or it was
insufficient at transporting nutrients to the
fetus.
2. Placental damage such as partial placental
separation with bleeding limits placental
function.
3. Women with systemic diseases that
decrease blood flow to the placenta as severe
diabetes mellitus or pregnancy –induced
hypertension.
4. Mothers who smoke heavily or use narcotics.
5. Placental supply of nutrients is adequate but
the infant can’t use them- intrauterine
infections of rubella or toxoplasmosis.
Assessment:
Prenatal Assessment- maybe detected in the
utero by taking the fundal height during
pregnancy.
Sonogram can demonstrate the decreased
size, biophysical profile including a non-stress
test, placental grading ultrasound examination
can provide placental function.
Appearance:
1. Below average in weight, length, & head
circumference.
2. Skin is dry, little fat -Wasted appearance
3. Small liver, which may cause difficulty
regulating glucose, protein, & bilirubin levels.
4. Poor skin turgor & generally appears to have
large head because the rest of the body is so
small.
5. Skull sutures may be widely separated from
lack of normal bone growth.
6. Hair is dull & lusterless
7. Abdomen may be sunken.
8. The cord often appears dry & maybe stained
yellow.
9. Better neurologic responses, sole creases, &
ear cartilage expected for a baby of that weight
.
10. Skull may be firmer & the infant may seem
unusually alert & active for that weight.
Laboratory Findings.
High hematocrit level- due to lack of fluid in
the utero.
Polycythemia - increase in RBC due to a state of
anoxia during intrauterine life.
Acrocyanosis results due to blood viscosity & is
difficult to circulate thick blood.
Common Problem
1. Hypoglycemia- decreased glycogen stores
-decreased blood glucose or level below
40mg/dL- IVF to sustain blood sugar until able
to suck vigorously enough to take oral feedings.
2. Birth Asphyxia- due to under developed
chest muscles & risk for developing meconium
aspiration syndrome due to anoxia during
labor. Fetal hypoxia causes reflex relaxation of
the anal sphincter & increased intestinal
movement.
 With gasping the fetus draws meconium
discharged into the amniotic fluid into the
Tracheobronchial tree. As a foreign substance it
blocks airflow into the alveoli leading to
hypoxemia, acidosis & hypercapnia.
Nursing Diagnosis

Ineffective breathing pattern related to

underdeveloped body systems at birth.
Outcome Identification
NB will initiate & maintain respirations at birth.
Evaluation
NB maintains normal respirations at a rate of 30
-60 breaths/ min. after resuscitation at birth.
3. Less able to control body temperature than
normal newborn because they lack
subcutaneous fat. Controlled environment is
essential to keep the infant’s body temperature
in neutral zone.
Nursing Diagnosis

 Nursing Diagnosis
 Risk for ineffective thermoregulation related
to lack of subcutaneous fat.
 Outcome Identification: NB will maintain body
temperature within normal limits.
 Outcome Evaluation:
 Infant’s temp is maintained at 36.5C of 97.8F.
Nursing Diagnosis

Risk for impaired parenting related to child’s

high-risk status & possible cognitive
impairment from lack of nutrients in utero.
Outcome Identification
Parents will demonstrate beginning bonding
behavior with infant while in the hospital.
Outcome Evaluation
Parents express interest in infant & ask
questions about what the child’s care needs
will be at home.
Intervention
1. Adequate stimulation
2. Provide toys suitable for their chronological
Nursing Interventions
1. Care of SGA infant is similar in many
instances to care of preterm infant.
2. Tailor high-level nursing care to meet
specific needs of infant with regard to
functioning of all body systems, psychologic
growth & development, parental support &
teaching, & prevention of complications.
3. Large- for- gestational- age ( LGA termed
macrosomia) infant – an infant whose birth
weight falls above the 90th percentile or birth
weight more than expected on an
intrauterine growth chart for the specific
gestational age. Ex. Baby born on the 30th
week of gestation weighing 5 lbs. on
intrauterine growth charts.
Causes:
1. Overproduction of growth hormone in utero in
diabetic mothers with poorly controlled glucose
levels.
2. Multiparous women because with each
succeeding pregnancy, babies tend to grow
larger.
3. Other conditions: Transposition of the great
vessels- group of congenital heart defects
4. Beckwith Syndrome- overgrowth disorder
usually present at birth, characterized by
increased risk of childhood cancer & certain
congenital features.
5. Congenital anomalies- omphalocele-
Abnormal contents small & large intestines,
stomach & liver, protrude through a hole in the
abdominal wall.
Assessment:
Fetus is suspected LGA when the uterus is
unusually large for date of pregnancy.
CS may be necessary because of CPD (the
biparietal diameter is closer to 10 cm than
usual 9 cm)or shoulder dystocia( wide
shoulders are unable to pass through the outlet
of the pelvis.
Assessment Criteria for an LGA Infant
1. Skin color for ecchymosis, jaundice, &
erythema.
2. Motion of extremities on spontaneous
movement & in response to a Moro’s reflex to
detect fracture.
3. Symmetry of the anterior chest or unilateral
lack of movement to detect diaphragmatic
paralysis from edema of the phrenic nerve.
4. Eyes for evidence of unresponsive or dilated
pupils, vomiting, bulging fontanelles, & high-
pitched cry suggestive of increased intracranial
pressure.
5. Activities such as jitteriness, lethargy, &
uncoordinated eye movement that suggest
seizure activity.
Large for gestational age
Assessment/ Diagnostic test
1. A sonogram to confirm the suspicion
2. Non stress test to assess the placenta’s ability
to sustain the large fetus during labor
3. Lung maturity may be assessed by
amniocentesis.
4. Recognized during labor when infant can pass
through the pelvic brim.
Appearance:
1.At birth show immature reflexes & low scores
on gestational age examinations in relation to
his size.
2.May have extensive bruising or a birth injury
such as broken clavicle or Erb Duchenne
paralysis from trauma to the cervical nerves if
born vaginally.
Caput succedaneum
3. Head is large due to pressure at birth prone
to caput succedaneum, cephal- hematoma, or
molding.
Cephalhematoma
Molding of the head
Cardiovascular Dysfunction
Heart rate should be observed.
Cyanosis may be a sign of transposition of the
great vessels, a serious heart anomaly.
Polycythemia is caused by the infant’s systems
attempting to fully oxygenate all the body
tissues.
Hyperbilirubinemia- increased bilirubin level
which may result from absorption of blood
from bruising & polycythemia.
Hypoglycemia- in the early hours of life
because the infant uses up nutritional
Stores readily to sustain his weight. If the
mother has diabetes that is poorly controlled,
the infant will have an increased blood glucose
level in the utero, which causes the infant to
produce elevated levels of insulin. At birth,
these increased insulin will continue for up to
24 hours of life, causing rebound
hypoglycemia.
Nursing Diagnosis
Ineffective breathing pattern related to
possible birth trauma in large for-gestational
age NB.
Outcome identification
NB will initiate & maintain respirations at birth.
Evaluation- NB initiates breathing at birth;
 maintains normal NB respiratory rate of 30-
60 breaths / minute.
 Difficulty establishing respiration because of
birth trauma.
 Increased intracranial pressure from birth of
the larger-than usual head may lead to
pressure on the respiratory center causing a
decrease in respiratory function.
 Nursing Diagnosis
 Risk for imbalanced nutrition, less than body
requirements related to additional nutrients
needed to maintain weight & prevent
hypoglycemia
 Outcome Identification
 Infant will ingest adequate fluid for growth
during neonatal period.
 Outcome Evaluation
 Infant’s weight follows percentile growth
curve; skin turgor is good; specific gravity of
urine is 1.003 to 1.030; serum glucose is
above 40mg/dL.
 As a rule LGA infants needs to be breastfed
immediately to prevent hypoglycemia.
Supplemental formula feedings after breast
feeding to supply enough fluid & glucose for
the larger than normal for the first few days.
 Nursing Diagnosis- Risk for impaired parenting
related to high risk status of large for
gestational age infant.
 Outcome Identification
 Parents demonstrate adequate bonding
behavior during neonatal period.
 Outcome Evaluation- Parents hold infant;
speak of the child in positive terms, state
accurately why infant needs to be observed
closely during postnatal period.
3. Problems related to Maturity

a. Premature (preterm) infant- an infant born

before the end of 37 weeks of gestation,
regardless of birth weight or born before
the 38th week.
Weight of less than 2500g (5 lb. 8 oz.) at
birth.
Low Birth Weight infant(LBW)- an infant
whose birth weight is1500 to 2500g,
regardless of gestational age.
Extremely- Low Birth Weight infant (ELBW)-
an infant whose birth weight is 500 to 1000g(
2 lbs. & 3 oz.) born at 27 weeks gestation or
even younger.
Minimum age of viability is 23 weeks gestation.
Very LBW infant(VLBW)- an infant whose birth
weight is 1000 to 1500g born before 30
weeks of pregnancy (3 lbs. & 5 oz.)
Moderately Low Birth Weight infant(MLBW) –
an infant whose birth weight is 1501 to
2500g
Causes include:
a. Maternal factors: age, smoking, poor
nutrition, placental problems,
preeclampsia/ eclampsia.
b. Fetal factors: multiple pregnancy, infection,
intrauterine growth retardation (IUGR)
 c. Other: low socioeconomic status, early
termination of pregnancies, environmental
exposure to harmful substance, iatrogenic
causes, such as elective cesarean birth &
inducement of labor according to dates
rather than fetal maturity.
Factors Associated with Preterm Birth
1. Low socio economic level
2. Poor nutritional status
3. Lack of prenatal care
4. Multiple pregnancy
5. Prior previous early birth
6. Race ( non whites higher incidence)
7. Cigarette smoking
8. Age of the mother( highest incidence
younger than age 20)
9. Order of birth( early termination is highest in
first pregnancies than those beyond the 4th)
10. Closely spaced pregnancies
11. Abnormalities of the mother’s reproductive
system, such as intrauterine septum
12. Infections ( especially UTI)
13. Obstetric complications such as PROM or
premature separation of placenta
14. Early induction of labor
15. Elective cesarean birth
Characteristics:
Appearance- small & underdeveloped. The
head is disproportionately large(3cm or more
greater than chest size). The skin is generally
or usually ruddy because the infant has little
subcutaneous fat beneath it; veins are easily
noticeable; & a high degree of acrocyanosis
may be present.
Preterm neonate, 24-36 weeks, typically is
covered with vernix caseosa. In very preterm
newborns (less than 25 weeks’ gestation),
vernix is absent because it is not formed this
early in pregnancy. Lanugo is usually
extensive,
covering the back, forearms, forehead, & sides
of the face, because this amount is present
until late in pregnancy. Both anterior &
posterior fontanelles are small. Few or no
creases on the soles of the feet.
The eyes are small, with varying degrees of
myopia (nearsightedness) because of lack of
eye globe depth.
The cartilage of the ear is immature & allows
the pinna to fall forward. The ears appear
large in relation to head. The level of the ears
should be carefully inspected to rule
out chromosomal abnormalities.
Neurologic function is difficult to evaluate.
Sucking & swallowing is weak & immature,
deep tendon reflexes such as Achilles tendon
are markedly diminished. Cry is weak & high-
pitched.
Generally activity is more feeble & weak; often
assume frog-like position;
Scarf sign- elbow passes the midline of the
body.
Square window- wrist at a 90 degree angle
Preterm with vernix caseosa
Preterm- SGA
Intensive incubator
Radiant Warmer
With acrocyanosis- AGA
Radiant warmer with Mechanical
ventilator
Mechanical ventilator
Components of Neuromuscular
Assessment

1. Posture
2. Square window
3. Arm recoil
4. Popliteal angle
5. Scarf sign
6. Heel to ear
Assess posture
for degree of
flexion.
Term- legs & arms
are moderately
Flexed at rest.
Preterm- lesser
degrees of flexion
Assess square window by
grasping the NB’s forearm
& gently flexing the wrist
toward the inner arm. Do
not allow rotation of the
wrist.
Term the hand should
touch the wrist resulting to
0 degree angle.
Preterm- greater angles of
flexion. The younger, the
less flexibility of the wrist.
Measure arm recoil by first
flexing & holding both
forearm for 5 sec. then
extending the hands &
arms fully at the NB’s side.
Release the hands & allow
the arms to recoil( return
to flexion)
Term full recoil to a
position of flexion.
Preterm less flexion
Term NB’S are less flexible,
with about 90 degree
angle,
Measure the popliteal
angle by moving the foot
gently toward the head
until you meet resistance.
Then measure the distance
behind the knee in the
popliteal area.
Preterm – the leg
straightens to 180 degree
angle.
Scarf sign by grasping
the NB”s hand &
attempting to cross
the arm over the body
at the neck.
Arms of the Term NB
meet resistance
before crossing
midline.
Premature NB cross
the elbow past
midline.
Assess heel to ear by raising
the NB’s heel towards his
head in an attempt to bring
the foot to ear. Don’t bring
the NB’s buttocks off the
examination surface. Stop
when you meet resistance &
measure the degree of
extension of the leg.
Preterm you’ll come close to
touching the heel to the ear.
Term- you’ll meet resistance
almost immediately..
Physical Maturity:
Components:
1.Skin
2.Lanugo
3.Plantar surface
4.Breast
5.Eye/ear
6.Genitals
Skin ranges from
translucent & friable in
preterm.
Post term- leathery,
cracked to wrinkled.
Lanugo- very fine body
hair.
Extremely premature NB’s
have none.
Term NB’s have very little.
Post term- nearly absent.
Term NB’s have
creases over the
entire plantar surface..
Preterm- from absent
to faint red markings.
Inspect the breast to
assess the size of the
breast bud in milliliters
& the development of
the areola.
Preterm NB’s lacked
developed breast tissue.
Term- have a raised to a
full areola with breast
buds that are 3 to 10
milliliters in diameter.
The eye/ear assessment
is an analysis of the ear
cartilage & shape of the
pinna.
Preterm –pinna is less
curved.
Term- well-curved pinna
with firm cartilage. Ear
recoil goes back quickly.
Preterm eyes fused
eyelids.
Term- testes usually
descend near term & rugae
are visible on the scrotum.
Palpate testes to
determine if they have
descended. & note the
rugae.
Premature- flat & smooth
Female NB at term- labia
majora are larger then the
clitoris & the labia minora.
Preterm have prominent
clitoris & small labia
minora.
CNS center for respiration is underdeveloped, which
results in irregular breathing w/ short periods of
apnea. O2 administered should never be more
than 40% because it can lead to blindness due to
retrolenthal fibroplasia, an overgrowth of retinal
blood vessels causing blindness.
Potential Complications
1. Anemia of prematurity- develop
normochromic, normocytic anemia. Blood
cells may be fragmented or irregularly
shaped. The reticulocyte count is low because
bone marrow does not increase its
production until approximately 32 weeks.
Infant appear pale, lethargic & anorectic &
fail to thrive.
The fault appears to be immaturity of the
hematopoietic system combined with destruction of
RBC due to low levels of vitamin E, which normally
protects RBC against oxidation. They have less iron
stores (because transfer of iron stores from the
mother to the baby also occurs during the last
weeks of pregnancy) & smaller RBC mass (since
cord was cut immediately after delivery).
Intervention:
Blood transfusion, vitamin E & iron provided by
preterm formula, administration of DNA
recombinant erythropoietin.
2. Hyperbilirubinemia –because of immaturity of the
liver, Kernicterus (staining of brain cells with
bilirubin, causing irreversible brain damage or even
death) or destruction of brain cells by invasion of
indirect bilirubin. This invasion results from
excessive breakdown of RBC. More prone because
with acidosis that occurs from poor respiratory
exchange, brain cells are
Susceptible to the effect of indirect bilirubin
than normally. They have less serum albumin
available to bind indirect bilirubin &
therefore inactivate its effect. Because of
this, kernicterus may occur at lower level( as
low as 12mg/ 100ml of indirect
bilirubin) in these infants. If jaundice occurs,
phototherapy or exchange transfusion can be
started to prevent excessively high indirect bilirubin
levels.
3. Persistent Patent Ductus Arteriosus
Because preterm infants lack surfactant, their lungs
are noncompliant. It is more difficult for them to
move blood from the pulmonary artery
into the lungs. This condition leads to pulmonary
artery hypertension, which may interfere with
closure of the ductus arteriosus. Administer IV
Therapy cautiously to avoid increasing blood
pressure. Indomethacin may be administered to
initiate closure of the patent ductus arteriosus.
4. Periventricular/ Intraventricular hemorrhage
Preterm infants are particularly prone to peri-
ventricular hemorrhage(bleeding into the
tissue surrounding the ventricles) or
intraventricular hemorrhage( bleeding into
the ventricles). Preterm infants have fragile
capillaries & immature cerebral vascular
development their susceptibility.
When there is rapid change in cerebral blood
pressure, such as with hypoxia, IV infusion,
ventilation, & pneumothorax, the capillaries rupture
. The infant experiences brain anoxia beyond the
rupture. Hydrocephalus may occur from bleeding
into the aqueduct of Sylvius with resulting
obstruction of the aqueduct.
Diagnostic intervention
Cranial ultrasound done after the first few days
of life to detect if hemorrhage has occurred.
An infant’s prognosis is guarded until it can
show that development in the infant is
normal after an intracranial bleeding.
Other Potential Complications:
1. RDS
2. Apnea
3. Retinopathy of prematurity
4. Necrotizing enterecolitis
Nursing diagnosis
Impaired gas exchange related to immature
pulmonary functioning.
Outcome Identification:
Newborn will initiate & maintain respirations
after surfactant therapy.
Evaluation: Newborn initiates breathing at
birth
 Apnea of Prematurity

 Is a common phenomenon in the preterm infant.

Infants less than 33 weeks gestation & healthy
infants less than 30 weeks of gestation. Resolves
as the infant approaches 37 weeks gestation.
 Apnea is a lapse of spontaneous breathing
for 20 seconds or more, or shorter pauses
accompanied by hypotonia, bradycardia or
color change.
Classification

According to origin:
1. Central apnea, an absence of diaphragmatic &
other respiratory muscle function that causes a
lack of respiratory effort & occurs when CNS does
not transmit signals to the respiratory muscle.
2. Obstructive apnea, when air flow ceases
because of upper airway obstruction, yet chest
or abdominal wall movement is present.
3. Mixed apnea, a combination of central &
obstructive apnea, & the most common form of
apnea seen in preterm infants.
Pathophysiology

Apnea of Prematurity reflects the immature &

poorly refined neurologic & chemical
respiratory control mechanisms in premature
infants. These infants are not responsive to
hypercarbia & hypoxemia, & their neurons
have fewer dendritic associations than those of
more mature infants. Respiratory reflexes are
significantly less mature.
Overall weakness of the thorax, diaphragm & upper
airway may also contribute to apneic episodes.
Apnea is characteristically observed during the
period of REM sleep. Worsened by variety of
factors:
Infection, intracranial hemorrhage, or PDA.
Therapeutic Management:
1.Administer Methylxanthines
(aminophylline, theophylline, or caffeine). Act
as CNS stimulants to breathing. Observe for
symptoms of toxicity. Serum theophylline levels
are determined by the
infant’s weight, gestational age, & chronological
age & maintained within a therapeutic range.
Caffeine has fewer side effects, once daily, more
predictable plasma concentrations, slower
elimination, & wider therapeutic range(rough, 5-
20 mcg/ml)
Weight & urinary output should be closely
monitored because both has mild diuretics.
Nasal CPAP IMV ventilation – acts to maintain
airway patency, effective for obstructive &
mixed apnea.
 Nursing Care

1. Monitoring respiration & heart rate.

2. Cardiorespiratory monitors alert staff-preset
delay time-15-20 seconds.
3. If begun early, gentle tactile stimulation
(rubbing back & chest gently, turning infant to
supine position)
4. If tactile stimulation fails to reinstitute
respiration, flow-by oxygen & suctioning of
nose & throat, if breathing does not begin, the
chin is raised gently to open the airway, &
resuscitate by mask & bag to lift the rib cage.
Never shake.
5. If breathing is restored, assess infant for
temperature, abdominal distention.
6. Use pulse oximetry.
7. Record apneic episodes.
8. If persistent & recurrent apnea, put baby on
mechanical ventilation / CPAP.
Nursing diagnosis
Impaired gas exchange related to immature
pulmonary functioning.
Outcome Identification:
Newborn will initiate & maintain respirations
after surfactant therapy.
Evaluation:
Newborn initiates breathing at birth
after resuscitation; maintains normal newborn
respirations of 30 to 60 breaths / minute free of
assisted ventilation; exhibits oxygen saturation
levels of at least 90% as evidenced by arterial blood
gases.
Preterm infants have great difficulty initiating
respiration at birth because the pulmonary
capillary bed is immature. Lung surfactant
does not form in adequate amounts until
about the 34th to 35th week of pregnancy.
Thus, it may be inadequate, leading to alveolar
collapse with each expiration.
Breech born infants are apt to expel meconium
into the amniotic fluid. If fetus aspirates
either vaginal secretions or meconium, the
respiratory problem is further compromised.
Medical Intervention:

1. Giving mother oxygen by mask during birth will

help provide the preterm infant with optimal
oxygen saturation at birth (85-90%).
2. Keeping maternal analgesia & anesthesia to a
minimum offers the infant the best chance of
initiating effective respiration.
3. Cesarean birth, although it has the advantage of
reducing pressure on the immature head
may lead to additional respiratory complications
because of retained lung fluid.
Preterm is unable to initiate effective respirations as
quickly as the mature infant, he is prone to
irreversible acidosis. To prevent, the infant must be
resuscitated within 2 minutes after birth.
Birthing room should be prepared with preterm-
size laryngoscope, ET, suction catheters, &
synthetic surfactant to be administered by
endotracheal tube.
The infant must be kept warm during resuscitation
procedures so he is not expending extra energy
to increase the metabolic rate to maintain body
temperature. Handle infants gently.
Giving 100% oxygen during resuscitation or to
maintain respirations presents the danger of
pulmonary edema & retinopathy of
prematurity( blindness of prematurity) when
saturation of the blood with oxygen (PO2 of more
than 100 mm hg which usually occurs when oxygen
is administered at a concentration over 70%).
With true apnea, the pause of respirations is more
than 20 seconds & bradycardia does occur.
Nursing diagnosis:
Risk for deficient fluid volume related to
insensible water loss at birth & small
stomach capacity.
Outcome Identification: Newborn will
demonstrate intake of adequate fluid &
electrolytes to meet body needs.
Outcome Evaluation:
Plasma glucose is between 40 & 60 mg per 100ml;
specific gravity of urine is maintained at 1.003 to
1.030; urine output is maintained at a minimum of
1ml/kg/h; electrolyte levels are within normal
levels.
The preterm newborn has a high insensible
water loss due to large body surface
compared with total body weight. The infant
also is unable to concentrate urine well
because of immature kidney function & thus
excretes a high proportion of fluid from the
body.
All these factors make it important that the
preterm baby receive up to 160-200ml of
fluid / kg of body weight daily( higher than
the term infant).
IV fluid administration begins within hours after birth
to fulfill this fluid requirement & provide glucose to
prevent hypoglycemia. Given via continuous
infusion pump to ensure a constant infusion rate &
prevent accidental overload.
IV sites checked conscientiously because if
infiltration should occur, the lack of
subcutaneous tissue places the preterm
newborn at risk for damaged tissue. They
lack adequately sized peripheral veins,
therefore IV/ umbilical venous catheter is
used.
Nursing Outcomes Classification & Nursing
Interventions Classifications
Monitor baby’s weight, urine output & specific gravity,
& serum electrolytes to ensure adequate fluid
intake.
Over hydration may lead to non-nutritional
Weight gain, pulmonary edema & heart failure.
Range of urine output for the first few days of life in
preterm babies is high with that of the term
baby:40 to 100ml / 24 hours, compared with 10 to
20 ml/ kg/ 24 hours.
Specific gravity is low-1.012,normal babies up to
1.030.
Test urine for ketones & glucose. Hyperglycemia
caused by glucose infusion may lead to glucose
spillage into the urine & an accompanying diuresis. If
too little glucose is supplied & body cells are using
protein for metabolism, ketone bodies will appear
in the urine.
Blood glucose determinations every 4-6 hours help
determine hypoglycemia or hyperglycemia.
Blood glucose should range between 40 &
60mg/dl.
Check for blood in the stools to evaluate for
possible bleeding from intestinal tract.
Nursing Diagnosis:
Risk for imbalanced nutrition, less than body
requirements related to additional nutrients
needed for maintenance of rapid growth,
possible sucking difficulty, & small stomach.
Outcome Identification:
Infant will receive adequate fluid & nutrients for
growth during hospitalization.
Outcome Evaluation:
Infant’s weight follows percentile growth curve; skin
turgor is good; specific gravity of urine is maintained
between 1.003 & 1.030; infant has no more than
15% weight loss in first 3 days of life & continuous
to gain weight after.
Nutritional problems arise because the body is
attempting to continue to maintain the rapid
rate of intrauterine growth. Therefore the
preterm newborn requires a larger amount
of nutrients in the diet than the mature
infant does. If these nutrients are not
supplied, the infant will develop
hypocalcemia
(decreased serum calcium) or azotemia (low protein
level in blood).
Delayed feeding & a resultant decrease in intestinal
motility may add to hyperbilirubinemia when fetal
RBC begin to be destroyed.
Nutrition problems are compounded by the preterm
infant’s immature reflexes, which make swallowing
& sucking difficult. The stomach’s capacity is small,
possibly impeding nutrition.
A distended stomach puts pressure on the
diaphragm, which could lead to respiratory
distress. Increased activity necessitated by
ineffective sucking may increase the
metabolic rate & oxygen requirements.
Immature cardiac sphincter( between the
stomach & the esophagus allows
regurgitation to occur
readily.
The lack of cough reflex may lead the infant to
aspirate regurgitated formula.
Feeding Schedule
W/ the early administration of IVF to prevent
hypoglycemia & supply fluid, feedings may be
delayed until the infant has stabilized his respiratory
effort from birth.
Fed by Total Parenteral Nutrition until they are
stable.
Breastfeeding, gavage, or bottle feedings are
begun as soon as the infant is able to tolerate
them to prevent deterioration of the
intestinal villi.
Needs 115-140 calories / kg of body weight / day,
compared with 100-110 needed by term infant.
Protein requirement are 3 to 3.5 g/kg of body weight,
compared with 2.0 to 2.5 for term newborn.
Because preterm infant has a smaller stomach
capacity, she should be fed more frequently with
smaller amounts as 1 or 2 ml. every 2 to 3
hours.
Gavage Feeding
The gag reflex is not intact until an infant is 32
weeks gestation. The ability to coordinate
sucking & swallowing is inconsistent until
approximately 34 weeks’ gestation.
Thus infants born 32 to 34 weeks gestation & those
who are ill or experiencing respiratory distress are
usually started on gavage feedings because
preemies have ineffective sucking which is not
coordinated with swallowing & therefore, may
aspirate.
When inserting NGT measure from the earlobe
to the tip of the nose to the distal end of
the sternum. Check for correct placement
of the tube by:
a. Aspirate gastric contents, Acidic- NGT in
place
b. Inject 5 cc of air then auscultate. If no sound
is heard as air is injected, it means NGT is not
in the stomach.
c. Measure the amount of residual , Subtract
the same amount from the next feeding
because this means that the baby is not able to
digest all the milk that has been given to him.
Put back the residual since it contains acids & the baby
can develop metabolic alkalosis/
d. Keep NGT always closed to avoid abdominal
distention.
e. Fill syringe with formula before opening NGT, let it
flow by gravity.
f. Flush NGT w/ sterile water after giving formula in
order to prevent clogging the NGT
Minimal handling is necessary in order to conserve
energy.
May be given intermittently every few hours or
continuously via tubes passed through the mouth or
nose. They may be fed by continuous drip feedings
at about 1 ml/h. Helpful for infants on ventilators or
those who experience oxygen deprivation with
handling. As long as the infant is being gavage-fed,
stomach secretions are usually aspirated, measured,
& replaced before
the feeding. An infant who has a stomach
content of more than 2ml just before a
feeding is receiving more formula than he
can digest in the time allowed. Feedings
should not be increased but possibly even
cut back to ensure better digestion &
decrease the possibility of regurgitation &
aspiration.
Formula
The caloric concentration of formulas used for
preterm infants is usually 24 cal/oz, compared with
20 cal/oz for term infants. Supplementing minerals
such as iron, calcium, & phosphorus & electrolytes
such as sodium, potassium & chloride may be
necessary.
Vitamin K 0.5 is administered instead of 1 ml to
term baby because of the infant’s small size.
Vitamin A is important in improving healing &
possibly reducing the incidence of lung
disease.
Vitamin E important in preventing hemolytic
anemia in preterm.
Breast milk is the best milk for preterm because of
the immunologic properties play a major role in
preventing neonatal necrotizing enterocolitis, a
destructive intestinal disorder that often occurs in
preterm babies. The mother can manually express
breast milk for gavage feeding.
Nursing Diagnosis
Ineffective thermoregulation related to
immaturity.
Outcome Identification: Infant will maintain
body temperature within normal limits until
term age.
Outcome Evaluation: Infant’s temperature is
97.6 degrees F ( 36.5degrees C)
Preterm has little subcutaneous fat for insulation &
poor muscular development does not allow the
child to move as actively as the older infant. Has
limited amount of brown fat, the special tissue
present in the newborns to maintain body
temperature. The infant is unable to shiver, a useful
mechanism to increase body
temperature; on the other hand, the child is
unable to sweat & thereby reduce body
temperature because of an immature central
nervous system & hypothalamic control.
Thus the infant depends on the
environmental temperature provided.
In the delivery room, temperature is kept at 62 to 68
degrees F (16.6 to 20degrees C), the infant must be
kept in a radiant heat warmer. A 1500g infant
exposed to this low, a temperature loses 1 degree C
of body heat every 3 minutes if left unprotected.
Nursing Diagnosis: Risk for infection related to
immature immune defenses in preterm
infant.

Outcome Identification: Infant will remain free

of infection during hospital stay.
Outcome Evaluation: Temperature instability
decreasing, being maintained at 97.6 degrees
F ( 36. 5degrees C)axillary; absence of further
s/s of infection such as poor growth or a
reduced temperature
Severity of problems related to level of maturity:
the earlier the infant is born, the greater the
chance of complications.
Major complicating conditions:
a. Respiratory distress syndrome
b. Thermoregulatory problems
c. Conservation of energy
d. Infection
e. Hemorrhage
Assessment findings
1. Respiratory system
a. insufficient surfactant
b. Apneic episodes
c. Retractions, nasal flaring, grunting, seesaw
pattern of breathing, cyanosis
d. Increased respiratory rate
2. Thermoregulation: body temperature fluctuates
easily (premature newborn has less subcutaneous
fat & muscle mass)
3. Nutritional status
a. Poor sucking & swallowing reflexes
b. Poor gag & cough reflexes
4. Skin: lack of subcutaneous fat; reddened;
translucent
5. Drainage from umbilicus/ eyes
6. Cardiovascular
a. Petechiae caused by fragile capillaries & prolonged
prothrombin time
b. Increased bleeding at injection sites
7. Neuromuscular
a. Poor muscle tone
b. Weak reflexes
c. Weak, feeble cry
C. Nursing Interventions
1. Maintain respirations at less than 60/
minute, check every 1-2 hours
2. Administer oxygen as ordered; check
concentration every 2 hours to avoid
retrolental fibroplasia while providing
adequate oxygenation.
3. Auscultate breath sounds to assess lung expansion.
4. Encourage breathing with gentle rubbing of back &
feet.
5. Suction as needed.
6. Reposition every 1-2 hours for maximum lung
expansion & prevention of exhaustion.
7. Monitor for signs of infection; these infants
have little antibody production & decreased
resistance.
8. Monitor blood gases & electrolytes.
9. Maintain appropriate humidity level.
11. Feed according to abilities.
12. Monitor sucking reflex; if poor, gavage feeding
indicated. Most preterm infants require at least
some gavage feeding as it diminishes the effort
required for sucking while improving the caloric
intake.
13. Use “premie” nipple if bottle- feeding.
14. Monitor intake & output, weight gain or
loss; these infants are easily dehydrated,
with poor electrolyte balance.
15. Monitor for hypoglycemia & hyper-
bilirubinemia.
16. Handle carefully, organize care to minimize
disturbances.
17. Provide skin care with special attention to
cleanliness & careful positioning to prevent
breakdown.
18. Monitor heart rate & pattern at least every 1-2
hours; listen apically for 1 full minute.
19. Monitor potential bleeding sites( umbilicus,
injection sites, skin); these infants have lowered
clotting factors.
20. Monitor growth & development of infant;
check weight, length, head circumference.
21. Provide tactile stimulation when caring for
or feeding infant.
22. Provide complete explanations for parents.
23. Encourage parental involvement in infant’s
care.
24. Provide support for parents; refer to self-help
group or other parents if necessary.
25. Promote parental confidence with infant care
before discharge.
Infants born after the 37th week are considered term.
Infants who are weighing 1500 to 2500g are
considered low-birth weight infants; those
weighing 1000 to 1500g are considered
very- low birth-weight infants. Those born
weighing 500 to 1000g are considered
extremely- very-low birth weight infants.
All such infants need neonatal intensive care from the
moment of birth to give them their best chance of
survival without neurologic after effects.
A lack of lung surfactant makes them extremely
vulnerable to respiratory distress syndrome.
 The maturity of the newborn is determined
by physical findings such as sole creases,
skull firmness, ear cartilage, & neurologic
findings that reveal gestational age, as well
as the mother’s report of the date of her last
menstrual period & sonographic estimations of
gestational age.
Amniocentesis or ultrasound– is a test for fetal
maturity to avoid inducing labor prematurely.
Post Maturity

b. Post-Maturity or Post Term Infants- born after the

completion of 42 weeks of pregnancy or
gestation.
Problems of the post- term infant are associated with
the progressively less efficient actions or capacity
of placenta to sustain intrauterine life. The fetus
who remains in utero w/ a failing placenta may
die or develop post term syndrome.
Assessment Findings

1. Skin
a. Vernix & lanugo completely disappeared or absent
b. Dry, cracked, parchment like appearance of skin or
leather- like skin from lack of fluid & absence of
vernix
c. Color: yellow to green skin, nails & cord from
meconium staining
2. Depleted or little subcutaneous fat with
newborn old looking
3. Hard nails or long nails extending beyond
fingertips
4. Old man wrinkled appearance or “old man face”,-
due to intrauterine weight loss, dehydration, &
chronic hypoxia.
5. Signs of birth injury or poor tolerance of birth
process
6. Wide- eye alertness of a 1 month old baby, firm
skull
Diagnostic Procedure
1. Ultrasound to measure the biparietal
diameter of the fetus.
2. Non-stress test or complete biophysical
profile to establish whether the placenta is
still functioning.
3. Cesarean birth
Management
1. Monitor vital signs
2. IV as ordered
Problems:
1. Difficulty establishing respirations especially if
meconium stained or perinatal asphyxia.
2. Hypoxia due to asphyxia & cause increased in
production of RBC
3. Meconium aspiration
4. Hypoglycemia owing to insufficient stores of
glycogen which were used for nourishment in
the last weeks of intrauterine life.
5. Subcutaneous fat levels may be low having
been used up in the utero.
6. Tolerate stress of labor poorly
7. Temperature regulation difficult- cold stress,
protect from chilling
Management – Provide warm blanket, exposed to
drop light or keep in isolette
8. Polycythemia from decreased oxygenation in the
final weeks.
Management- Partial exchange transfusion
9. Elevated hematocrit because of
polycythemia & dehydration which lowers
the circulating plasma level.
Long term Problem
1. Poor weight gain
2. Low IQ scores
C. Nursing Interventions
1. Nursing care of the post mature infant has many
characteristics in common with the care given to
the premature infant.
2. Design high- level nursing care to identify the
infant’s specific physical & psychologic needs or
parental teaching of newborn care
3. Monitor functioning of all body systems, growth &
development, parental support & teaching, &
prevention of complications.
Parents hold infant, speak of the child in positive
terms; state accurately why the infant needs to be
closely observed in postnatal period.

Intervention
Have the same developmental care that all other
infants need.
Singing or talking to the baby, stroking the
child’s back & rocking the baby.
Encourage parents to treat their baby as a
fragile NB who needs warm nurturing, not as
a tough big infant who has grown past that
stage.
Remind parents that the infant’s birth weight is
not correlation of the child’s projected adult
size.
3. Problems related to gestational weight.
a. Low Birth Weight
b. Very Low birth Weight
c. Extremely very low birth weight
5. Acute Conditions of the Neonates:
a. Respiratory Distress Syndrome (RDS) or
Hyaline Membrane Disease.
Occurs in preterm infant, infants of diabetic mother,
infants born by CS or those with decreased blood
perfusion of the lungs. The pathologic feature of
RDS is a hyaline-like (fibrous) membrane
comprising products formed from exudate of the
infant’s
Blood that lines the terminal bronchioles,
alveolar ducts, & alveoli. This membrane
prevents exchange of oxygen & carbon dioxide
at the alveolar –capillary membrane. The cause
is a low level or absence of surfactant , the
phospholipid that normally lines the alveoli &
reduces surface tension on expiration to keep
the alveoli from collapsing on expiration.
Pathophysiology
High Pressure is required to fill the lungs with
air for the first time & overcome the pressure
of lung fluid. It takes a pressure between 40 &
70 cm H2O to inspire a first breath but only 15
to 20 cm H2O to maintain quite, continued
breathing. If alveoli collapse with each
expiration, as happens when surfactant is
deficient & continues to take forceful
inspiration to inflate them.
A very immature infants release a bolus of
surfactant at birth into their lungs from the
stress of birth. However, w/ deficient
surfactant areas of hypoinflation occur &
pulmonary resistance is increased.
Blood then shunts through the foramen ovale
& the ductus arteriosus as it did during fetal
life. The lungs are poorly perfused, affecting
gas exchange. As a result, the production of
surfactant decreases even further. The poor
O2 exchange leads to tissue hypoxia which
causes the release of lactic acid.
This combined with the increasing carbon
dioxide level resulting from the formation of
the hyaline membrane on the alveolar
surface, leads to severe acidosis. Acidosis
causes vasoconstriction, & decreased
pulmonary perfusion from vasoconstriction
further limits surfactant production.
With decreased surfactant production, the
ability to stop alveoli from collapsing with
each expiration becomes impaired. This
vicious cycle continues until the oxygen
carbon dioxide exchange in the alveoli is no
longer adequate to sustain life without
ventilator support.
Decreased pulmonary surfactant – increased
surface tension- alveolar walls will not
separate- lack of expansion of affected
alveoli – decreased alveolar ventilation –
inadequate exchange of O2 & carbon dioxide
– hypoxia increased capillary permeability
which causes effusion from the
pulmonary capillaries into the alveoli &
terminal – bronchioles- hyaline –like
membrane found in the alveoli & bronchioles
composed of mainly of fibrin – atelectasis.
4. Additional factors:
a.Hypoxia,
b.Patent ductus arteriosus
c. Hyperbilirubinemia
d. Retrolenthal fibroplasia
e. Brochopulmonary dysplasia (BPD)-damaged
to the alveolar epithelium of the lungs rel.to
high O2 concentration &+ pressure ventilation
f. Necrotizing enterocolitis
Diagrammatic Presentation of RDS
Assessment/ Signs & Symptoms
1. Low body temperature
2. Nasal flaring
3. Sternal & subcostal retractions
4. Tachypnea or Increased RR- more than 60/ m
5. Expiratory grunting- major symptom
6. Cyanotic mucous membranes
7. Rales
8. Respiratory acidosis
a. Low Ph level ( normal- 7.35- 7.45)
b. Low PO2 level (normal -40-60 mm Hg)
c. High PCO2 level ( normal- 35-45)
As distress increases:
1.Seesaw respirations-diaphragm descends
causing the abd. to lift & the chest to sink
2.Heart failure evidenced by decreased urine
output & edema of the extremities
3.Pale gray skin
4.Periods of apnea
5.Bradycardia
6.Pneumothorax
Diagnostic Evaluation
1. Blood glucose- test hypoglycemia
2. Serum Calcium- test hypocalcemia
3. Blood gas- respiratory acidosis, PaO2- for
hypoxia
4. Chest X-Ray (haziness)
Beta –hemolytic B Streptococcus mimic RDS.
Therapeutic Management
1. Administer Surfactant- through ET tube
2. Oxygen therapy, high humidity, warmth, -to
provide adequate oxygen to tissues, to prevent
lactic accumulation resulting from hypoxia &
prevent the negative effects of oxygen therapy.
CPAP- Continues Positive Airway Pressure –
Continues application of 3 to 8 cm
H2O(positive) pressure to the airway, uses
the infant’s spontaneous respiration to
improve O2 by helping prevent alveolar
collapse.
Greatly improves oxygen exchange.
IMV is used with Positive End-Expiratory
Pressure(PEEP) allows to breath at their own rate
but provides + pressure w/ end-expiratory pressure
to prevent alveolar collapse & overcome airway
resistance.
The PIP is the maximum amount of + pressure
applied to infant on inspiration. The total
amount of pressure transmitted to the airway
throughout an entire respiratory cycle is called
mean airway pressure(MAP), improve
oxygenation by maintaining functional residual
capacity & overcoming the resistive forces of
the atelectic lung.
SIMV-Synchronized Intermittent Mandatory
Ventilation- breaths delivered by the ventilator are
synchronized to the onset of spontaneous infants
breaths.
Complication of Positive Pressure Ventilation:
Pneumothorax, pulmonary interstitial emphysema,
pneumomediastinum
3. Monitor vital signs, arterial blood gases, skin color muscle
tone
4. Proper positioning; NPO; IV, NGT care
5. Suction PRN
6. Prevent complications
7. Sodium bicarbonate – for acidosis
8. Changing infant’s position frequently
9. Indomethacin –to cause closure of the patent ductus
arteriosus
 Additional Therapy

1. Pancuronium(Pavulon) IV- muscle relaxant.

2. Extracorporeal Membrane
oxygenation(ECMO)Management for chronic
hypoxemia.
3. Nitric Oxide- causes pulmonary vasodilatation
to help increase blood flow to the alveoli when
persistent pulmonary hypertension is present.
4. Liquid Ventilation- Perfluorocarbons-
effective in delivering O2 & surfactant.
5. Supportive Care- kept warm reduces
metabolic oxygen demand.
Prevention:
1.Check the level of Lecithin/ Sphingo-
myelin ratio in amniotic fluid by 2:1
2. Use tocolytic agents- terbutaline-prevents
preterm birth by 2 injections of Glucocor
ticosteroid- Ex. Betamethasone at 12 & 24
hours before birth at 24to 34 weeks pregnancy.
Signs of respiratory distress usually begins
within 2 hours after birth:
- Grunting on expiration,
- Flaring of nostrils
- Tachypnea
- Chest retractions
- Generalized cyanosis
- Pallor
- Decreased breath sounds on auscultation of the
lungs as lesser areas are functional
- Cough due to excessive lung secretions
- Chin lug
- Hypotension & shock
The important surfactant that must be present at
birth:
a. Lecithin/ Sphingomyelin – 2:1
b. Phosphatidylcholine
c. Phosphatidylglycerol
Nursing intervention
1. Maintain infant’s body temperature at
97.6degrees F( 36.2degreesC).
2. Provide sufficient caloric intake for size, age, &
prevention of catabolism (usually IV glucose with
gradual increase in feedings) Nasogastric tube
may be used.
3. Organize care for minimal handling of infant.
4. Administer oxygen therapy as ordered.
a. Monitor oxygen concentration every 2-4 hours;
maintain less than 40% concentration if possible.
b. Oxygen may be administered by hood, nasal
prongs, intubation, or mask.
c. Oxygen may be atmospheric or increased
pressure.
d. Continuous positive air pressure(CPAP) or
positive end-expiratory pressure
(PEEP) may be used to prevent collapse & to
keep alveoli expanded.
. Therapeutic range is 10-12 cm of water pressure.
- First 72 hours – increase pressure to keep airway
open
- After 72 hours – decrease pressure for airways are
already open
e. Oxygen should be warmed & humidified
f. Monitor infant’s blood gases
g. If intubated, suction (for less than 5 seconds)
prn using sterile catheter.
h. Glucocorticoid( Celestone) – Artificial
surfactant given at birth before the first
breath or after diagnosis of RDS which is
effective for up to 72 hours.
 Surfactant can be administered by aerosol spray or ET
tube. This surfactant will help to hasten lung
maturity.
i. BT to replace extracted blood used for tests.
j. Give milk by gavage if NB has mild tachypnea
k. Auscultate breath sounds.
l. Provide chest physiotherapy, postural
drainage, & percussion if ordered.
m. Encourage parental involvement in care
(visiting, stroking infant, talking).
n. Administer surfactant via endotracheal tube
& other medications as ordered.
o. Place newborn on the back or in a side lying
position with the neck slightly extended.
p. Hold breastfeeding to conserve energy. Newborn
may be on NPO & given IVF.
Normal Arterial Blood gases
Temperature : 36.5- 37.5
pH : 7.35 -7.45
pCO2 : 35 – 45
pO2 : 80- 100
HCO3 : 22- 26
O2 saturation : 94-100%
Base excess :+-2
Transient Tachypnea of the Newborn

 At birth, a newborn may have a rapid rate of

respiration, up to 80 breathes / minute when
crying.
 Within 1 hour, this rapid rate slows between
30-60 breaths / minute.
 The respiratory rate remains at a high level,
between 80-120 breathes/ minute.
Signs & Symptoms:
1.The infant does not appear to be in a great
deal of distress, aside from the tiring effort of
breathing so rapidly.
2.Has mild retractions but not marked
cyanosis.
3.Mild hypoxia & hypercapnia
4. Feeding is difficult because the child cannot
suck & breath deeply at the same time.
5. Chest X-ray reveals some fluid in the central
lung but aeration is adequate.
Cause:
Result from slow absorption of lung fluid.
Reflect a slight decrease in production of
phosphatidyl glycerol or mature surfactant.
These factors limit the amount of alveolar
surface area available to the infant for gas
exchange. Thus the infant must increase the
respiratory rate & depth to better use the
surface available.
Occurs more often in infants who are:
1.Born by cesarean section- because the
thoracic cavity is not compressed by the force of
vaginal birth, less lung fluid is expelled than
normally.
2.Infants whose mothers received extensive fluid
administration during labor
3.In preterm infants
Nursing Care:
1.Close observation of the NB is the priority.
2.Watch carefully that increased effort in not
tiring.
3.Watch for beginning signs of a more serious
disorder because rapid RR is the first sign of
respiratory obstruction.
4. Oxygen administration
Transient Tachypnea of the NB peaks at
approximately 36 hours of life & slowly begins
to fade at 72 hours as lung fluid is absorbed &
respiratory activity becomes effective .
Meconium Aspiration Syndrome

Meconium is present in the fetal bowel as early

as 10 weeks gestation. An infant with hypoxia
in utero experiences a vagal reflex relaxation of
the rectal sphincter, which releases meconium
into the amniotic fluid from pressure on the
buttocks. Appears green to greenish black.
 Asphyxia or other stress can cause passage of
meconium before the fetus is born.
 Meconium aspiration syndrome occurs when
the meconium stained amniotic fluid is
aspirated by the fetus before or after
delivery. Aspiration of meconium in utero
can cause chemical pneumonitis
Meconium can cause severe respiratory
distress in 3 ways:
1. It can bring about inflammation of
bronchioles because it is a foreign
substance
2. It can block small bronchioles by
mechanical plugging.
3. It can cause a decrease in surfactant production
through lung cell trauma.
Hypoxemia, carbon dioxide retention, &
intrapulmonary & extrapulmonary shunting occur.
A secondary infection of injured tissue may lead to
pneumonia.
Causes:
1. Relaxation of anal sphincter
2. Accelerated intestinal peristalsis & passage
of meconium
3. Reflex gasping & aspiration of meconium
mixed in amniotic fluid
Complications
1. Air leak
2. Pulmonary hemorrhage
3. Pulmonary interstitial emphysema
4. Pulmonary hypertension
5. Pneumonia
6. Infection
7. Thrombocytopenia-deficiency of platelet
8. Asphyxia
Assessment
1.Difficulty establishing respirations at birth-
meconium stained amniotic fluid.
Not born breech- hypoxia
2. Apgar score low
3. Tachypnea, retractions & cyanosis
4. Poor gas exchange- decreased PO2 &
increased PCO2
5. Continue to have retractions due to
inflammation of bronchi tends to trap air in the
alveoli causing enlargement of the antero-
posterior diameter of the chest(barrel chest)
Diagnostic Tests
1. Chest X-ray will show bilateral coarse
infiltrates in the lungs, w/ spaces of
hyperaeration, (honeycomb effect),
diaphragm will be pushed downward.
2. Complete blood count
3. C-reactive protein
4. Blood cultures
Therapeautic Management
1. Intrapartally, amniotransfusion may be used to
dilute the amount of meconium in amniotic fluid
to reduce the risk of aspiration.
2. Suctioning after head is delivered with a bulb
syringe, or a catheter after endotracheal tube
is inserted while at the perineum.
3.After tracheal suction, oxygen administration
& assisted ventilation.
4. Administer prescribed:
- Antibiotic therapy- prevent pneumonia
- Bicarbonate for acidosis
5. Monitoring of blood gases
6. Watch out for seizures, GIT bleeding & renal
failure
7. Observe closely for pneumothorax- due to
trapping of air in the alveoli.
8. Observe for signs of heart failure(increased
RR & signs of respiratory distress)
9. Maintain a temperature-neutral
environment to prevent increasing the
metabolic oxygen demands.
10. Chest physiotherapy with clapping &
vibration- remove remnants of meconium.
Apnea

Apnea is a pause in respirations longer than 20

seconds with accompanying bradycardia.
Beginning cyanosis may be present.
Preterm infants have periods of apnea due to
fatigue or the immaturity of their respiratory
mechanism.
Babies with secondary stresses such as
infection, hyperbilirubinemia, hypoglycemia, or
hypothermia have high incidence of apnea.
Management:
1. Gently shaking the baby or flicking the sole
of the foot stimulates the baby to breath.
2. If infant does not respond, resuscitation is
necessary.
3. Apnea monitors that record respiratory
movement.
4. Ventilator- for infants with frequent or difficult
to correct episodes.
5. Maintain a neutral thermal environment &
gentle handling to avoid excessive fatigue.
6. Suction gently to minimize nasopharyngeal
irritation, which can cause bradycardia due to
vagal stimulation.
7. Use indwelling NGT rather than intermittent
reduce the amount of vagal stimulation.
8. After feeding, observe the infant carefully
because the full stomach can put
Pressure on the diaphragm. Burp to reduce the
effect.
9. Never take rectal temperatures
10. Theophylline or caffeine sodium benzoate
administered to stimulate respirations-
increase an infant’s sensitivity to carbon
dioxide, ensuring better respiratory function.
Sudden Infant Death Syndrome

Sudden Infant Death Syndrome (SIDS) is the

sudden, unexplained death in infancy or
unexpected death of an apparently healthy
infant under 1 year of age in which a
thorough autopsy fails to demonstrate an
adequate cause of death.
It tends to occur at a higher rate in the infants
of:
1.Adolescent mothers
2.Infants of closely spaced pregnancies
3.Underweight infants
4.Preterm infants
5.Bronchopulmonary dysplasia
6. Twins
7. Siblings of another child with SIDs
8. Native American & Alaskan infants
9. Economically disadvantage black infants
10. Infants of narcotic-dependent mothers
Other possible contributing factors:
1.Viral respiratory or botulism infection
2.Pulmonary edema
3.Brain stem abnormalities
4.Neurotransmitter deficiencies
5.Heart rate abnormalities
6.Distorted familial breathing patterns
7. Decreased arousal
8. Possible lack of surfactant in alveoli
9. Sleeping prone( resp. muscles restricted)
Age : Peak incidence is between 2-4 months of
age
Time of Year: esp. during winter months.
Time of Death: During Sleep
Cause- unknown
Sleep Risk Habits:
a.prone sleeping position
b.Overheating( thermal stress)
c.Use of soft bedding
d.Possibly sleeping with an adult
e.Respiratory disorders,
f.History of life threatening event,
Maternal risk factors:
a. Maternal smoking
b. Young mothers age
c. High risk pregnancy
d. Substance abuse
Specific cause of SIDS cannot be explained,
placing the infant in a supine position or
side has been shown to decrease the
incidence of the syndrome.
Assessment
Death typically occurs during sleep.
Appearance when found:
1. Apneic, blue, lifeless
2. Frothy blood-tinged fluid in the nose &
mouth
3. May be found in any position
4. May be clutching bedding
5. Diaper is wet & full of stool
Diagnostic
No test can predict risk
Cardiopneumogram or pneumocardiogram

Nursing Intervention / Prevention

1. Apparent life- threatening event
a. Home cardiorespiratory event monitor-
discontinue monitor 2-3 months without
episodes.
b. Administer respiratory stimulant
medications-theophylline or caffeine as
prescribed

Emergency
1.Review scenario
2. Healthy infants should be placed in supine
position for sleep
3. Infants with gastroesophageal reflux
or other airway anomalies that predispose to
airway obstruction my be placed in a prone
position.
 2. Soft moldable mattress & bedding, such as
pillows should not be used
 3. Stuffed animals should be removed from
the crib while sleeping.
4. Allow the parents & family to say good-bye
to their infant
5. Clean the infant before allowing the family
to see him.
6. Make an appropriate referral for follow-up
with the family.
Public health nursing
Encourage the expression of feelings
Explore coping mechanisms & evaluate
effectiveness
Assess parental intellectual knowledge
Provide written information about SIDS
Hyperbilirubinemia

Hyperbilirubinemia(an elevated level of

bilirubin in the blood)results from destruction
of red blood cells by either a normal
physiologic process or the abnormal
destruction of red blood cells.
Refers to an excessive level of accumulated
bilirubin in the blood & is characterized by
jaundice, or icterus, a yellowish discoloration
of the skin, sclera, & nails.
Hyperbilirubinemia may result from increased
unconjugated or conjugated bilirubin. Most
common is unconjugated bilirubin.
Pathophysiology
Bilirubin is one of the breakdown products of
the hemoglobin that results from red blood
cell (RBC) destruction. When RBC’s are
destroyed the breakdown products are
released into the circulation, where the
hemoglobin splits into two fractions heme &
globin. The globin (protein) portion is used
by the body, & 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 &, in the presence of the
enzyme glucuronyl transferase, is conjugated
with glucuronic acid to produce a highly
soluble substance, conjugated bilirubin
glucuronide, 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 excreted in the urine.
Normally the body is able to maintain a
balance between the destruction of RBC’s
& the use of excretion of by-products.
However, when developmental limitations
or a pathologic process interferes with this
balance, bilirubin accumulates in the
tissues to produce jaundice.
Possible causes of hyperbilirubinemia:
1. Physiologic (developmental) factors
(prematurity)
2. An association with breast feeding or
breastmilk due to substances in the
maternal milk such as B-glucurorinadase &
non- sterified fatty acids which may
inhibit normal bilirubin metabolism or
pregnanediol(a breakdown product of
progesterone) in breastmilk depresses the
action of glucoronyl transferase, the enzyme
that converts indirect bilirubin to the direct
form, which is readily excreted in bile.
3. Excess production of bilirubin( hemolytic
disease, biochemical defects, bruises)
4. Disturbed capacity of the liver to secrete
conjugated bilirubin ( enzyme deficiency,
bile duct obstruction- plugging of biliary
secretions- when obstructed bile is unable to
enter the intestinal tract, accumulates in
the liver. Bile pigments(direct bilirubin)
enter the bloodstream & jaundice occurs.)
5. Combined overproduction & undersecretion
(sepsis)
6. Some disease states( hypothyroidism,
galactosemia- genetic metabolic disorder
that affects an individual’s ability to
metabolize the sugar galactose properly,
infant of diabetic mother)
7. Genetic predisposition to increased
production (Native Americans, Asians)
2 Types of Jaundice:
1. Physiologic jaundice or icterus – term infants,
starts on the 2nd day or 3rd day of life in about
50% of all newborns as a result of the
breakdown of fetal RBC. Bilirubin levels
gradually increase to approximately 6mg/dl
on the 3rd day of life or 72 hours, then
decrease to a plateau of 2 to 3 mg/dl by the
5th day
Preterm infants – serum bilirubin levels may
peak as high as 10 to 12 mg/dl at 4 to 5
days & decrease slowly over a period of 2
to 4 weeks.
2.Pathologic jaundice - usually appears early,
up to 24 hours after birth; represents a
process ongoing before birth. Pattern of
progression is from head to feet. Blanch
the skin over bony area or look at
conjunctiva & buccal membranes in dark
skinned infants.
Diagnostic evaluation
The degree of jaundice is determined by serum
bilirubin measurements.
Normal values of unconjugated bilirubin are
0.2 to 1.4 mg/dl.
In the newborn, levels must exceed 5mg/dl
before jaundice is observable.
Evaluation of jaundice is based on:
1. Serum bilirubin levels
2. Timing of the appearance of clinical
jaundice
3. Gestational age at birth
4. Family history including maternal Rh factors
5. Age in days since birth
6. Feeding method
7. Infant’s physiologic status
8. The progression of serial serum bilirubin
levels
Criteria of pathologic jaundice
1. Appearance of jaundice within 24 hours
2. Persistent jaundice after 1 (term neonate)
or 2 preterm weeks
If the level of indirect serum bilirubin rises
above 10 to 12 mg./ 100ml. Treatment will
be considered although age, maturity &
breastfeeding affect this.
At about 20mg/ 100ml. Enough indirect
bilirubin has left the bloodstream that it
could interfere the chemical synthesis
of brain cells, resulting in permanent cell
damage & scarring of the basal ganglia &
brain stem called kernicterus.
Nursing Intervention for physiologic jaundice in
NB is rarely necessary except for:
1. early feeding to speed passage of feces
through the intestine & prevent reabsorption
of bilirubin from the bowel
2. Phototherapy ( exposure to infant to light)
to initiate maturation of liver enzymes may be
used, used to help convert unconjugated
bilirubin to conjugated & move from the skin
to the blood plasma & then excreted.
Completely undress the infant except for the
diaper with eye patches to protect the eyes
from the high intensity fluorescent lights.
Remove eye patches during assessment &
feeding.
4. Maintain temperature regulation due to
large surface area being exposed to
environmental temperatures.
5. Maintain adequate hydration due to
increased excretion of conjugated bilirubin
through the bowel & urinary system.
6. Monitor serial fractionated bilirubin levels to
evaluate the infant’s condition.
7. Instruct the parents on the disease & the
expected care of the infant.
Diagnostic tests
a. Physical examination to check for
cephalocaudal progression of dermal icterus
b. Serum bilirubin determination
Type of Jaundice
Physiological Pathological Breast-Fed
On- appears after appears before early onset:
set 24 h of age & 24 h of age appears by
disappears by - day 4 of life
the end of day Late onset:
5-7 of life appears bet-
ween days 6
& 14 of life
& may per-
sist 2-3 mo.
Incidence 50% full- Appx. 0.3% Apprx. 2%
term infant of bottle fed of breastfed
80% prema- & 2% of BF infants deve-
ture infant infants lop jaundice
Bilirubin usually does increases by early
onset:
Level not exceed more than 5 bilirubin
12mg/100 dl mg/dl in 24 h peaks less
in fullterm than 17 mg /
infant & 15 mg 100 / dl
/ 100 dl in Late Onset:
prem. 12-20mg/100
dl
Etiology liver imma- the most Exact etiology
turity lead common unknown but
ing to the causes are suspected to be
inability to Rh & ABO substances in
to convert blood incom- in maternal
fat-soluble patibilities, milk, such as B
unconjuga liver disease glucuronidase
ted bilirubin or infection & nonsterified
to water- fatty acids, w/c
soluble con- may inhibit nor
jugated bi- mal bilirubin
lirubin metabolism
Hemolytic Disease of the
Newborn( Erythroblastosis fetalis)
Hemolytic- characterized by destruction(lysis) of
red blood cells
Caused by:
1.ABO incompatibility
2.Rh factor
3.Maternal antibodies
4.Complications include anemia,
kernicterus(neurological damage)
Assessment
a.Jaundice due to hyperbilirubinemia
b.Pallor due to hemolytic anemia
Diagnostic Test
a. Cord blood studies
b. Complete blood count
c. Reticulocyte count
d. Bilirubin
Mechanism of Rh Incompatibility:
a. Sensitization of Rh-negative woman by
transfusion of Rh-positive blood.
b. Sensitization of Rh-negative woman by
presence of Rh positive RBC’s from her fetus
conceived with Rh-positive man
c. 65% of infants conceived by this combination
of parents will be Rh +.
d. Mother is sensitized by passage of fetal Rh-
positive RBC’s through placenta, either during
pregnancy( break/leak in membrane) or at the
time of separation of the placenta after delivery.
e. This stimulates the mother’s immune response
system to produce anti-Rh-positive antibodies
that attack fetal RBC’s & cause hemolysis.
f. If this sensitization occurs during pregnancy,
the fetus is affected in utero; if sensitization
occurs at the time of delivery, subsequent
pregnancies may be affected.
ABO incompatibility:
a.Same underlying mechanism
b.Mother is blood type O; infant is A,B, or AB
c.Reaction in ABO incompatibility is less severe.
Nursing Interventions:
a.Provide phototherapy
b.Monitor laboratories
c.Assist with exchange transfusion
Rh Incompatibility
No direct connection exists between the fetal &
maternal circulation, & no fetal blood cells enter
the maternal circulation.
If the mother’s blood type is Rh (D) negative &
the fetal blood type is Rh positive(contains the D
antigen), the introduction of fetal blood causes
sensitization to occur, & the mother begins to
form antibodies against the D antigen.
 Most form in the mother’s blood stream in the
first 72 hours after birth because there is an
active exchange of fetal –maternal blood as
placental villi loosen & the placenta is delivered.
 After this, sensitization, in a second pregnancy,
there will be a high level of antibody D
circulating in the mother’s bloodstream, which
acts to destroy the
 fetal red blood cells early in pregnancy if the
fetus is Rh positive. By the end of the second
pregnancy, a fetus can be severely
compromised by the action of these
antibodies crossing the placenta & destroy
RBC.
1. First pregnancy: mother may become
sensitized, baby rarely affected
2. Indirect Coomb’s test(tests for anti-Rh-
positive antibodies in mother’s circulation)
performed during pregnancy at first visit &
again about 28 weeks’ gestation. If indirect
Coombs’ test is negative at 28 weeks, a
small dose of (MicRhogam) is given
 prophylactically to prevent sensitization in
the third trimester. Rhogam may also be
given after second trimester amniocentesis.
3. If positive, levels are titrated to determine
extent of maternal sensitization & potential
effect on fetus.
4. Direct Coombs’ test done on cord blood at
delivery to determine presence of anti-Rh –
positive antibodies on fetal RBCs.
5. If both indirect & direct Coombs tests are
negative(no formation of anti-Rh-positive
antibodies) & infant is Rh positive, then Rh-
negative mother can be given RhoGam(RhoD)
human immune globulin) to prevent develop-
 ment of anti-Rh- positive antibodies as the
result of sensitization from present(just
terminated) pregnancy.
 6. In each pregnancy, an Rh-negative mother
who carries an Rh-positive fetus can receive
RhoGam to protect future pregnancies if the
mother has had negative indirect Coombs’
tests & the infant has have positive
direct Coombs tests.
7. If mother has been sensitized(produced anti-
Rh positive antibodies), RhoGam is not
indicated.
8. RhoGam must be injected into unsensitized
mother’s system within first 24 hours if
possible , by 72 hours the latest.
ABO Incompatibility
1. The maternal blood type is O & the fetal blood
type is A
2. Occur when the fetus has type B or AB blood
3. A reaction in an infant with type B blood is
often serious.
4. Hemolysis can become a problem with a first
pregnancy in which there is ABO
incompatibility.
ABO Incompatibility

1. Reaction less severe than with Rh incompatibility.

2. First born may be affected because Type O
mother may have anti-B antibodies even before
pregnancy.
3. Fetal RBCs with A,B, or AB antigens evoke less
severe reaction on part of mother, thus fewer
anti- A, anti-B, or anti-AB –antibodies are
produced.
4. Clinical manifestations of ABO
Incompatibility are milder & shorter duration
than those of Rh incompatibility.
5. Care must be taken to observe for hemolysis &
jaundice.
Assessment
Rh incompatibility of the NB can be predicted by
rising anti-Rh titer or a rising level of anti-
bodies( indirect Coombs test) in the mother
during pregnancy. Confirmed by detecting
antibodies on the fetal erythrocytes in cord
blood (positive direct Coombs’ test) by
umbilical cord sampling. The mother have Rh-
negative blood (dd), & the baby will be Rh
positive)DD or Dd).
 Indirect bilirubin is fat-soluble & can’t be
excreted from the body. The liver enzyme
glucuronyl transferase converts indirect
bilirubin to direct bilirubin.
 Direct bilirubin is water-soluble & combines
with bile for excretion from the body with
feces. In preterm, the liver is unable to
convert bilirubin thus jaundice is extreme.
 Normally cord blood has an indirect bilirubin
level of 0 to 3 mg/100ml.
 An increasing indirect bilirubin level is
dangerous if the level rises above 20mg/dl in
term infant or 12mg/dl in a preterm infant-
brain damage from kernicterus (invasion of
bilirubin in brain cells) occur.
 Therapeutic Management
1. Early feeding
2. Phototherapy
3. Exchange blood transfusion- Monitor HR,RR, & BP
a. 5mg/ 100 ml at birth
b. 10mg/ 100ml at age 8 hours
c. 12 mg/100ml at age 16 hours
d. 15 mg/100ml at 24 hours
Assessment
1. Jaundice
2. Anemia
3. Erythropoiesis- production of RBC
4. Enlarged placenta
5. Edema & ascites
Nursing Intervention
1. Determine blood type & Rh early in
pregnancy.
2. Determine results of indirect Coombs’ test
early in pregnancy & again at 28-32 weeks.
3. Determine results of direct Coombs test on
cord blood (type & Rh, hemoglobin &
hematocrit).
4. Administer RhoGam IM to mother as
ordered.
5. Monitor carefully infants of Rh-negative &
type O mothers for jaundice.
6. Set up phototherapy as ordered & monitor
infant during therapy..
7. Support parents with explanations &
information.