CARE OF MOTHER AND CHILD SEM 02 | 02

LECTURE / AT RISK OR WITH ACUTE/CHRONIC PROBLEMS AUF-CON

NCM 0109 MODULE 08 – NURSING CARE OF AT-RISK/HIGH-RISK SICK CLIENT: NEWBORN

OUTLINE
I Problems Related to Maturity
A Prematurity
B Postmaturity
II Problems Related to Gestational Weight
A Small for Gestational Age
B Large for Gestational Age
III Alterations in Oxygenation
A Respiratory Distress Syndrome
B Sudden Infant Death Syndrome
5. A small for gestational age newborn has a
birthweight of:
a. Below 10th percentile on an intrauterine growth
curve for that age
b. Above 10th percentile on an intrauterine growth
curve for that age
c. Below 20th percentile on an intrauterine growth
curve for that age
d. Above 20th percentile on an intrauterine growth
curve for that age

INTRODUCTION 6. Which of the following therapeutic management is

PRETEST
1. Which of the following is the most appropriate
nursing action in a newborn with risk for deficient fluid
volume related to insensible water loss at birth and
small stomach?
a. Provide gavage feeding
b. Monitor baby’s weight, urine output, specific
gravity, serum electrolytes
c. Keep the newborn warm
d. Perform frequent handwashing
2. All of the following are characteristic appearances of
a premature newborn, EXCEPT:
a. Head is disproportionately large
b. Lanugo is extensive at the back, forearms,
forehead, and sides of the face
c. Fingernails have grown well beyond the end of
the fingertips
d. Unusually ruddy because of little subcutaneous
fat
3. An infant large for gestational age is also called a:
a. Macrosomia
b. Microsomia
c. Monosomia
d. Midsomia
4. Which of the following is the MOST common cause of
small for gestational age (SGA) newborn?
a. Cigarette smoking
b. Use of narcotics
c. Women with severe diabetes mellitus
d. Placental anomaly
used to convert excess bilirubin into a soluble,
excretable form?
a. Early and frequent breastfeeding
b. Administration of Phenobarbital
c. Phototherapy
d. Administration of intravenous immunoglobulin
7. The peak age of incidence of Sudden Infant
Syndrome is:
a. 2–4 months of age
b. 4–6 months of age
c. 6–8 months of age
d. 8–10 months of age
8. Infants are highly susceptible of Sepsis
a. True
b. False
9. All of the following are therapeutic management of
Meconium Aspiration Syndrome, EXCEPT:
a. Antibiotic therapy
b. Administer oxygen under pressure until the
infant has been intubated and suctioned
c. Perform chest physiotherapy with clapping and
vibration
d. Maintain a temperature-neutral environment
10. Which of the following is the case of Respiratory
Distress Syndrome in a newborn?
a. High level of surfactant
b. High level of surface tension
c. Low level of surface tension
d. Low level of surfactant

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MODULE PROPER ○ Adulthood problems include learning

disabilities, growth deficiencies, and asthma
OVERVIEW OF NURSING CARE AT RISK/HIGH RISK ○ NR: They need intensive care from the moment
SICK CLIENT: NEWBORN
of birth to give them their best chance of
survival without neurologic aftereffects
● ASSESSMENT
○ Must be done to all infants to identify obvious
I. ASSESSMENT
congenital anomalies and gestational age
○ Assessment for High-Risk Infants
● Involves the use of technology and PREGNANCY HISTORY OF THE MOTHER OF A
PRETERM BABY:
equipment such as cardiac, apnea, oxygen
● Although a detailed pregnancy may sometimes
saturation, and blood pressure monitoring
reveal the reason for a preterm birth, the
● Note that these do not replace the role of
pregnancy history is often normal up to the
frequent, close, common sense
beginning of labor
observations by a nurse
● When interviewing parents of a preterm newborn,
○ They know the infant well because they
be careful not to convey disapproval of reported
took care of the baby consistently; they
pregnancy behaviors such as cigarette smoking
sense changes before a monitor or
that may have contributed to the early birth
other equipment begins to put a
● An accurate but comforting answer to a direct
quantitative measurement on the
inquiry about why preterm birth occurs is, “No one
change
really knows what causes prematurity”
● NEWBORN AND NEONATE: similar concepts that
refer to children aged 4 weeks (28–30 days or 1
RISK FACTORS
month)

I. PROBLEMS RELATED TO MATURITY ● OBSTETRIC FACTORS

○ Multiple pregnancy d/t risk of developing HPN
A. PREMATURITY ● If not controlled properly, vasoconstriction of
the uterine arteries occurs which decreases
● DEFINING A PRETERM INFANT blood flow to fetus → decreased nutritional
○ A live-born infant born before the end of week intake from the development of HPN
37 of gestation (full term is 38–42 weeks AOG)
○ Previous early birth
○ Classifications ● The body has not fully recovered to carry
● Early: 24–34 weeks AOG another full-term pregnancy
● Late: 34–37 weeks AOG ○ Order of birth
○ Epidemiology: 12.18% of all births (80-90% ● Early birth is highest in first pregnancies and
mortality) in those beyond the fourth pregnancy
○ Basis ○ Closely-spaced pregnancies
● Weeks of gestation (<37 weeks) ● Body has not yet fully recovered from
● Weight (<2500 g) previous pregnancy
○ Low Birth Weight: 1,500–2,500 g ○ Obstetric complications
○ Very Low Birth Weight: 1,000–1,500 g ● PROM, AP, PIH, placental problems, etc.
○ Extremely very low birth weight: ○ Early induction of labor (less than Week 39)
500–1,000 g
● Elective cesarean birth (there is a chosen
● PHYSIOLOGICAL COMPLICATIONS date for the surgery)
○ Increased risk for hypoglycemia and
○ According to dates rather than fetal
intracranial hemorrhage maturity; if the baby is supposed to be
○ Respiratory Distress Syndrome delivered at an earlier date/ mother is in
● Lung surfactant (which lowers surface danger
tension) does not form until about the 34th GYNECOLOGIC FACTORS
●
week of pregnancy
○ Age of the mother
● A newborn who has difficulty
● Highest incidence is in birthing parents
accomplishing effective breathing may younger than age 20 years
experience residual neurologic morbidities
● The body of a young child is not yet ready for
as a result of cerebral hypoxia pregnancy

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○ Abnormalities of the mother’s reproductive ○ Deep tendon reflexes such as

system the Achilles tendon reflex are
● Intrauterine septum (the pregnancy process also diminished
cannot proceed to full term) Unusually ruddy and translucent
○ Infections (bright pink, smooth and shiny)
● Especially those involving the urinary tract SKIN
because the infant has little
○ UTI is one of the danger signs of subcutaneous fat beneath it
pregnancy: can precipitate preterm Easily noticeable; high degree of
contractions = prematurity acrocyanosis (bluish color of
● Damages amniotic sac VEINS
extremities; very immature circulatory
● PHYSICAL AND SOCIAL FACTORS system)
○ Low socioeconomic level (10–20%) ● Late Preterm: extensive on the
● Financial constraints result in difficulty back, forearms, forehead, and
purchasing healthy foods LANUGO
sides of the face
● Limited healthcare access and knowledge ● Very Premature: scant
about nutrition = poor nutritional status and ● Preterm (25-26 weeks): Typically
lack of prenatal care covered with vernix caseosa
○ Race (before shedding, some vernix
● People of color experience a higher caseosa is inside the uterus; the
incidence of prematurity than White people longer the baby stays inside the
VERNIX
do, potentially related to social determinants CASEOSA uterus, the more vernix caseosa
of health dissolved)
○ Cigarette smoking ● Very Preterm (<25 weeks): Vernix
● Vasoconstriction → delayed blood flow → is absent (vernix caseosa has not
slows down growth of fetus, damage developed)
developing brain and lungs
● Few or no creases on the soles of
APPEARANCE OF A PREMATURE NEWBORN feet (smooth appearance)
● Scarf sign: elbow is easily brought
Appears small and underdeveloped; across the chest with no
SIZE
appear scrawny (skinny) resistance
● Disproportionately large (3 cm or EXTREMITIES ○ Flexion is the attitude of term
more greater than chest size) infants = resistance with
● Development of baby is extension
cephalocaudal, since premature, ● Heel to ear maneuver: place heel
the baby’s head is enlarged but of foot of the infant to ears with no
the body is tiny resistance
● Anterior and posterior fontanelles ● Eyes appear small, papillary
are small reaction is present (although
○ Small fontanelles lead to slow difficult to elicit)
EYES
brain development and ● Varying degrees of myopia
learning disabilities as they (near-sightedness d/t lack of eye
HEAD/BRAIN globe depth)
grow older
● Preemie head: soft cranium is ● Cartilage is immature (soft and
subject to unintentional pliable) and allows the pinna to
deformation fall forward
○ NR: frequent positioning or gel ● The level of the ears should be
mattress as it follows the carefully inspected to rule out
shape of the head EARS chromosomal abnormalities
● Immature neurologic system ○ Deep set ears: down
● Reflex such as sucking and syndrome/Trisomy 21
swallowing will be absent if an ○ Check level of outer canthus of
infant’s age is below 33 weeks eye to ears
● Appear large in relation to head

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● During an examination, a preterm
infant is much less active than a
mature infant and rarely cries
○ If the infant does cry, the cry is
ACTIVITY
weak and high-pitched
● Vagal response is low =
greater tension in the
vocal cords
● MALE: few scrotal rugae; some of
them have undescended testes
(cryptorchidism)
○ 34th week: testes are already
fully descended
○ If still not descended at 34
weeks and beyond, prepare for
surgery (orchidopexy) and
GENITALS should be done as soon as
possible as the undescended
testes can cause testicular
cancer when the newborn
grows
● FEMALE: prominent labia minora
and clitoris rather than majora
(labia majora is not yet
developed)
● Overall attitude of extension
ATTITUDE (normal attitude of full-term are
fully flexed)
II. POTENTIAL COMPLICATIONS
A. ANEMIA OF PREMATURITY
A.1. ASSESSMENT
● DEVELOPMENT OF NORMOCHROMIC, NORMOCYTIC
ANEMIA
○ Normal cells, just few in number
○ CAUSE: the effective production of red cells by
the bone marrow with an elevated reticulocyte
count may not begin until 32 weeks of
pregnancy
● CHARACTERISTICS: pale and may be lethargic; poor
feeding, decreased oxygen saturation, tachycardia,
tachypnea, diminished activity, and anorectic
CONTRIBUTING FACTORS TO ANEMIA OF PREMATURITY
● Combined with destruction of
RBC to low levels of Vitamin E,
Immaturity of which normally protects RBC
the against oxidation = lesser RBC
hematopoietic produced
system ○ It should take 114–117 days
before RBC becomes
replaced or destroyed
● Low levels of vitamin E makes
the baby prone to anemia of
prematurity
Excessive
blood drawing ● Potentiates the existing problem
for electrolyte (kaunti na nga lang,
or blood gas mababawasan pa)
analysis
A.2. NURSING MANAGEMENT
● Keep a record of the amount of blood drawn for
analysis
● RBC production can be stimulated by the
administration of DNA recombinant erythropoietin
(a synthetic erythropoietin given through SQ)
○ Given as last resort as this may cause
retinopathy of prematurity [ROP; stops normal
development of blood vessels in the retina]
causing blindness in prematurity
● Supplementations
○ Blood transfusion
○ Vitamin E and Iron (supply needed RBCs)
● iron supplements RBC
● Vitamin E protects RBC against unnecessary
destruction
● Delaying cord clamping at birth
○ Allows a little more blood from the placenta to
enter the newborn may also help reduce the
development of anemia
B. KERNICTERUS
(Acute Bilirubin Encephalopathy)
B.1. ASSESSMENT
● DESTRUCTION OF BRAIN CELLS BY INDIRECT
BILIRUBIN
○ INDIRECT VS DIRECT: direct (conjugated) is
excreted and eliminated while indirect
(unconjugated) is not due to its fat-soluble
nature
● Due to immaturity of the liver, indirect
bilirubin cannot be converted
● Premature neonates also have less serum
albumin available to bind indirect bilirubin
and inactivate its effect
○ CAUSE: high concentrations of indirect bilirubin
in the blood from excessive breakdown of RBC
NORMAL PROCESSING OF BILIRUBIN
Worn out RBC = breakdown of heme and
1 globin
Globin (protein component) is recycled
2 while heme becomes converted to bilirubin
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When the liver takes in bilirubin, it becomes
processed in the intestines (excreted as
feces) and in the kidneys (excreted as
urine)
3
In kernicterus, the bilirubin does not get
converted into its direct form. Because of
this, it stays in the body and affects the
brain.
B.2. PATHOPHYSIOLOGY
● Poor respiratory exchange (hindi nalalabas ‘yung
carbon dioxide) → acidosis → brain cells are more
susceptible to the effect of indirect bilirubin
○ Acidosis comes from poor respiratory exchange
of immature newborn (lack of surfactant)
● Poor carbon dioxide and oxygen exchange
→ carbon dioxide (acid) will be retained
● Preterm infant has less serum albumin
○ Serum albumin binds to indirect bilirubin to
inactivate its effect
● Since the preterm has less of this, there is
lesser inactivation of indirect bilirubin
○ WOF for edema d/t decreased albumin, a
protein that regulates colloidal osmotic pressure
● Albumin (already low in number) would bind
with the indirect bilirubin and will try to
inactivate its action → fluid from
extracellular spaces will move to interstitial
spaces
B.3. NURSING MANAGEMENT
● These may be done to prevent excessively high
indirect bilirubin levels
● PHOTOTHERAPY
○ A treatment using an artificial light to help
convert indirect bilirubin into direct d/t liver
enzyme maturity
○ Make sure to cover the eyes and genitals
● EXCHANGE TRANSFUSION
○ Find a donor that
matches preterm
○ Replace blood with
excessive bilirubin,
waste blood is
removed through the
umbilical cord
○ Cord bilirubin levels must be assessed
✅ Cord bilirubin level: >5 mg/dl or increase of
1 mg/dL/hr
✅ Current bilirubin level: > 1 mg/dL per hr
✅ Indirect bilirubin level: >20 mg/dL
○ If one of these are present, exchange
transfusion is indicated
C. PERSISTENT PATENT DUCTUS ARTERIOSUS
C.1. ASSESSMENT
● DUCTUS ARTERIOSUS: found between the
pulmonary artery and the aorta
○ Normal: 15 hours after delivery, as the baby
takes his/her first breath in life, the massive
contraction of the muscles of the ductus
arteriosus leads to its closure
○ Preterm: due to lack of surfactant, their lungs are
noncompliant → more difficult for them to move
blood from the pulmonary artery into the lungs
(pulmonary HPN) → may interfere with closure of
the ductus arteriosus
C.2. NURSING MANAGEMENT
● CAREFUL FLUID REGULATION
○ Always administer intravenous therapy
cautiously to premature neonates because
increased fluid also increases blood pressure
which could further compound this problem
● INDOMETHACIN OR IBUPROFEN
○ Inhibits prostaglandin synthesis which is known
to keep ductus arteriosus open (nonsteroidal
anti-inflammatory and prostaglandin inhibitor)
○ May be used to cause closure of a patent ductus
arteriosus, making ventilation more efficient
○ Indomethacin is given cautiously to preterm
infants because it has been associated with
adverse effects such as decreased renal
function, decreased platelet count, and gastric
irritation
● Carefully monitor urine output and observe
for bleeding, especially at injection sites, if
this is prescribed
D. PERIVENTRICULAR/INTRAVENTRICULAR
HEMORRHAGE
D.1. ASSESSMENT
● PERIVENTRICULAR HEMORRHAGE: bleeding into the
tissue surrounding the ventricles of the brain
● INTRAVENTRICULAR HEMORRHAGE: bleeding into
the ventricles
● Preterm infants have both fragile capillaries and
immature cerebral vascular development
○ When there is a rapid change in cerebral blood
pressure, such as could occur with hypoxia,
intravenous infusion, ventilation, or
pneumothorax (lung collapse), capillary rupture
could occur; brain anoxia then occurs distal to
the rupture
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CLASSIFICATIONS (GRADE) III. NURSING DIAGNOSES

Bleeding in the periventricular germinal matrix 1. IMPAIRED GAS EXCHANGE R/T IMMATURE PULMONARY
1 regions or germinal matrix, occurring in one FUNCTIONING
ventricle
Bleeding within the lateral ventricle without CAUSES
2 dilatation of the ventricle
3 Bleeding causing enlargement of the ventricles ● Inadequate lung surfactant: leads to alveolar
Bleeding in the ventricles and collapse with each expiration
4 intraparenchymal hemorrhage ○ This collapse forces the neonate to use
maximum strength to inflate lung alveoli each
D.2. COMPLICATIONS
time
○ Because this is so tiring, it becomes very difficult
● HYDROCEPHALUS (long term effect)
for neonates to maintain effective ventilations
○ May occur from clots and other debris (blocks
under these stressful conditions
the aqueduct of Sylvius) that can obstruct the
● CS Birth: there would be more fluid retained in
passages between the ventricles, causing it to
lungs; abdominal incision + uterine incision = not
dilate; thus, hydrocephalus occurs
pass through canal = excess fluid will not be
● Diagnosed through cranial ultrasound (done
removed
after the first few days of life)
○ In NSD, as the chest area of baby passess
● Maintain head in midline position
through the vaginal canal → compressed chest
● BRAIN ANOXIA
→ removal of excess fluid from lungs
○ Hypoxia or IV infusion (given in large amount) →
● Breech presentation: fetus expel meconium to
rapid change in cerebral BP → rupture of
amniotic fluid → aspiration → pneumonia
capillaries bleeding → intracranial bleeding
● Soft rib cartilage: causes the ribs to collapse on
E. OTHER POTENTIAL COMPLICATIONS expiration
● Underdeveloped accessory muscles: premature
● RESPIRATORY DISTRESS SYNDROME neonate has no backup muscles to use when they
○ Lack of lung surfactant, causing lung collapse become fatigued
○ Diagnosed through amniocentesis (ratio of
lecithin and sphingomyelin [2:1]), a procedure NURSING MANAGEMENT
that determines fetal lung maturity; and
● Resuscitation within 2 minutes: prevents acidosis
ultrasound (determines AOG)
and initiates effective respiration
● APNEA
○ Birthing room teams need to be prepared with
○ Lapse of spontaneous breathing for 20 or more
preterm-size laryngoscopes, endotracheal
seconds or shorter pause accompanied by
tubes, suction catheters, and synthetic
bradycardia or oxygen desaturation
surfactant to be administered by the
● RETINOPATHY OF PREMATURITY
endotracheal tube so resuscitation can be
○ Retinal changes due to vascular constriction,
accomplished immediately
followed by hypoxia
● Warmth: to not spend extra energy to increase BMR
○ Compensatory proliferation follows resulting to
● Continued oxygen: do not stop oxygenating the
turbidity in the aqueous and vitreous humor →
baby after resuscitation
retina becomes edematous leading to
○ Giving the birthing parent oxygen by mask
hemorrhage, scarring, and retinal detachment
during the birth can help provide the premature
leading to blindness (excessive oxygen
neonate with optimal oxygen saturation at birth
concentration can bring rupture to the eyes)
(85% to 90%)
● NECROTIZING ENTEROCOLITIS
○ Use preterm size equipment: O2 mask, cannula
○ Vascular compromise in the GI tract causing
to supply O2 → to maximize supply that we are
distended abdomen and bloody stool leading to
going to give to newborn
inability to digest
● Minimal maternal analgesia and anesthesia:
offers the premature newborn the best chance of
initiating effective respirations
○ These two tends to suppress the respiratory
system of the fetus as well

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 MODULE 08 – NURSING CARE OF AT-RISK/HIGH-RISK SICK CLIENT: NEWBORN
● Carry out procedures gently: prevents trauma and
bleeding
○ Tissues are extremely sensitive to trauma can be
damaged/bruised → bleeding → ●
hyperbilirubinemia → kernicterus
2. RISK FOR DEFICIENT FLUID VOLUME R/T INSENSIBLE
WATER LOSS AT BIRTH AND SMALL STOMACH CAPACITY
CAUSES
Large body surface relative to total body weight
●
● They cannot concentrate urine well because of
immature kidney function
○ Because of this, a high proportion of body fluid is
excreted = deficient fluid volume
NURSING MANAGEMENT
● IVF administration: done via a continuous infusion
pump to ensure a constant infusion rate and to
prevent accidental overload
○ 160–200 mL/KBW weight daily; G26/27 or
umbilical venous catheter
○ Also used to provide glucose and prevent
hypoglycemia
● Monitor baby’s weight, UO (weigh diapers),
specific gravity, serum electrolytes
○ ↑ Fluid: non-nutritional weight gain, pulmonary
edema, and heart failure
○ ↓ Fluid: DHN, starvation, acidosis, and weight loss
● There should be an accurate fluid
replacement to prevent these complications
○ Normal UO: 40–100 mL/kg/24 hours
● Measured by weighing diapers rather than
using urine collection bags because these
can lead to skin irritation and breakdown
from frequent changing and leaking
● NOTE: The amount of urine output for the first
few days of life in premature neonates is
high in comparison with that of term
neonates because of poor urine
concentration
○ Normal SG: 1.012
● Determines the kidney’s ability to
concentrate urine
○ Normal blood glucose: 40–60 mg/dL
● Test urine for glucose and ketones as they
can indicate hyperglycemia caused by the
glucose infusion, which then can lead to
diuresis and extreme fluid loss
○ If too little glucose is being supplied and
body cells are using protein for
metabolism, ketone bodies will appear
in the urine
○ Might also indicate type 1 juvenile DM
which might occur even in the first few
months of life
Elimination process: most premature neonates
void and pass meconium within 24 hours after birth,
although this is delayed in very premature
neonates
○ Check for presence of blood in stool
3. RISK FOR IMBALANCED NUTRITION, LESS THAN BODY
REQUIREMENTS R/T ADDITIONAL NUTRIENTS NEEDED
FOR MAINTENANCE OF RAPID GROWTH, POSSIBLE
SUCKING DIFFICULTY, AND SMALL STOMACH
CAUSES
● Attempt to continue to maintain the rapid rate of
intrauterine growth appropriate for the gestational
age (↑ metabolic rate)
○ Requires a relatively larger amount of nutrients
than the term neonate does, 115–140 calories/kg
of body weight/day
● FEEDING SCHEDULE OF A PRETERM NEONATE
○ They have a smaller stomach capacity than
term neonates, as a rule, they must be fed more
frequently with smaller amounts (1–2 mL/2–3
hours)
● Small stomach = quickly-filled = risk for
distention = pressure on the diaphragm
○ Immature cardiac sphincter (between the
stomach and esophagus) allows regurgitation
to occur readily (hindi nagko-contract; stays
relaxed)
● The lack of a cough reflex may lead the
neonate to aspirate regurgitated formula
○ Delayed feeding and a resultant decrease in
intestinal motility may also add to
hyperbilirubinemia
● No milk = no meconium (manner of
excreting bilirubin)
○ As meconium is rich in bilirubin, if the
meconium passage will be delayed, the
amount of meconium will be reabsorbed
in the neonatal circulation →
hyperbilirubinemia
○ Immature reflexes causes difficulty in
swallowing and sucking
● Increased activity that occurs from
ineffective sucking may further increase the
metabolic rate and oxygen requirements
● Inconsistent ability (until 32 weeks AOG) to
coordinate sucking and swallowing
○ 💡 NR: Offering a pacifier during gavage
feeding can help strengthen the sucking
reflex, better prepare the neonate for
bottle feeding or breastfeeding
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● Non-intact (until 32 weeks AOG) gag reflex
NURSING MANAGEMENT
● Safely delaying feedings: must be done with early
administration of intravenous fluid to prevent
hypoglycemia and supply fluid
○ Proceed with feedings when respiratory status
stabilizes
○ Very premature neonates may be fed by total
parenteral nutrition until they are stable enough
for enteral feedings
● 115-140 calories/KBW/day
○ Provide protein requirements of 3-3.5g/KBW
● NOTE: If these nutrients are not supplied, the
neonate can develop hypocalcemia
(decreased serum calcium) or azotemia
(build up of nitrogenous waste products due
to low protein level in the blood)
● Gavage feedings (breast/bottle): tube is inserted
into the oral cavity up to the stomach to prevent
deterioration of intestinal villi
○ Premature neonates may have a chest X-ray
taken before the first feeding
● The presence of air in the stomach shows
that the route to the stomach is clear
○ SCHEDULE:
📅 Delayed to establish effective
respirations before feeding the newborn
📅 Given intermittently every few hours or
continuously via tubes passed into the
stomach or intestine through the mouth
or nose
○ Measure the aspirate (gaano pa karami yung
natirang amount sa nabigay kanina) to
determine if the feeding is being used by the
newborn
○ Manual expression or use of breast pump for
breast milk may be used for gavage feeding
● Breast milk: immunologic properties and nutritional
properties
○ Digestion and absorption of nutrients in the
stomach and intestine may be immature,
making the digestion of milk difficult
○ Immunologic properties of breast milk may play
a major role in preventing neonatal NEC as well
as increase immune defenses
○ Sodium content of breast milk of mother to
preterm baby is higher vs milk of mother to term
baby
● Sodium is necessary for fluid retention
○ To avoid tiring, bottles with preterm nipples that
are softer with a slightly larger hole than regular
nipples are used for bottle feedings
○ A neonate who has a large amount of milk left
in the stomach (volume depends on the
amount of milk the infant is receiving) is not
digesting the milk
● Inability to digest can be a sign that NEC
(necrotizing enterocolitis), a destructive
intestinal disorder that often occurs in
preterm babies, may be developing
4. INEFFECTIVE THERMOREGULATION R/T IMMATURITY
CAUSES
● Have difficulty maintaining their body
temperature because they have a relatively large
surface area per kilogram of body weight
● They do not flex their body well but remain in an
extended position, rapid cooling from evaporation
is more likely to occur
● POIKILOTHERMIC: has little subcutaneous fat for
heat insulation and poor muscular development
and therefore cannot move as actively as an older
infant to produce body heat and regulate their own
body temperature = dependent on environmental
temperature for warmth
❌ Brown fat: special tissue present in
newborns that helps maintain body
❌
temperature
Shivering: useful mechanism to increase
❌
body temperature
Sweating: immature sweat glands, central
nervous system and hypothalamic control
NURSING MANAGEMENT
● Keep the baby warm under radiant heat warmers,
in incubators, or by skin-to-skin contact
○ A 1,500g newborn exposed to this low
temperature loses 1°C of body heat every 3
minutes if left unprotected in a birthing room,
typically kept at 62–68°F (16.6–20°C) [must be
increased to 76°F or 24°C]
○ Be certain a radiant heat warmer is prewarmed
before the newborn is born
● Use of additional heat shield or plastic wrap
○ Prevents heat loss by radiation and conduction
○ A portable warming mattress can be placed
under the neonate to help conserve heat during
transport
5. RISK FOR INFECTION R/T IMMATURE IMMUNE
DEFENSES IN PRETERM INFANT
CAUSES
● Less resistance to infection: skin of the premature
neonate (first line of defense) is easily traumatized
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 MODULE 08 – NURSING CARE OF AT-RISK/HIGH-RISK SICK CLIENT: NEWBORN
● Lowered resistance to infection: difficulty
producing phagocytes to localize infection as well
as a deficiency of immunoglobulin M (IgM)
antibodies because of insufficient production
NURSING MANAGEMENT
● To prevent infection, linen and equipment must not
be shared with other infants to prevent
cross-contamination
● Staff members must be free of infection,
handwashing and gowning must be strictly
enforced
6. RISK FOR IMPAIRED PARENTING RELATED TO
INTERFERENCE WITH PARENT–NEWBORN ATTACHMENT
RESULTING FROM HOSPITALIZATION OF NEWBORN AT
BIRTH
CAUSES
● PERIOD OF REACTIVITY
○ If done to stimulate respiratory function:
● Greater threat of respiratory failure because
respiratory efforts may not be stimulated
○ Delayed periods of reactivity
● Observed in the first and second periods
● Expect a delay in what is normally observed
in the first four hours of life
○ In some newborns, no period of
increased activity or tachycardia may
appear until 12 to 18 hours of age
● Results in loss of an opportunity for
interaction between parents and the
newborn in the early postpartum period
NURSING MANAGEMENT
● Premature neonates appear to need as much
attention and affection as term neonates
● Rocking, singing, talking, and gentle holding are
measures to help premature neonates develop a
sense of trust in people and also increases sensory
stimulation
B. POSTMATURITY
● POST TERM INFANT: born after the 42nd week of a
pregnancy regardless of birth weight
○ Common among Australian, Greek, Italian
○ May be due to inaccurate estimation of EDD
POSTMATURITY AND PLACENTAL FUNCTION
📌
●
○ REMEMBER: A placenta appears to function
effectively for only 40 weeks and the infant is
continuously exposed to AF
● After that time, it begins to lose its ability to
carry nutrients effectively to the fetus, and
the fetus begins to lose weight leading to
post term syndrome/death
POST-TERM SYNDROME
CHARACTERISTICS
● Dry, cracked, almost leather-like skin d/t lack of
fluid
● Absence of vernix (dissolves as the pregnancy
progresses)
● Desquamation (nagbabalat) and wasted physical
appearance
○ Since they had an intrauterine nutritional
deprivation d/t the aging placenta, they may
also appear older
● Lightweight d/t recent weight loss
○ Occurred because of the poor placental function
● Amniotic fluid
○ Lesser than normal and meconium-stained
● Long fingernails (beyond the end of the fingertips)
● Alertness similar to 2-week-old baby
DIAGNOSIS
● Sonogram to measure the biparietal diameter of
the fetus (>9.5 cm)
● Nonstress test or complete biophysical profile to
establish if placenta is still functioning adequately
○ If non-stress test reveals that there is a
compromised placental functioning → baby is
delivered through CS
HANDLING A POST-TERM BABY
CHARACTERISTICS EXPECTED AT BIRTH
● Difficulty establishing respirations: esp. if
meconium aspiration occurred
○ Prone to fetal distress (aging placenta,
macrosomia, MAS)
● Meconium aspiration occurred (uterine
hypoxia): aspiration pneumonia
● MGT: amnio-transfusion (normal saline/LRS)
○ Inject catheter directly to uterus to add
fluid in decreasing amt of AF inside
uterus to dilute AF = lesser chance to
swallow meconium
● Hypoglycemia: may develop as the fetus had to
use stores of glycogen for nourishment in the last
weeks of intrauterine life
○ Placenta does not supply enough nutrients
○ NR: glucose tests to check glucose level
● ↓ subcutaneous fat levels: may be low after having
been used in utero → can make temperature
regulation difficult
NCM 0109|9
 MODULE 08 – NURSING CARE OF AT-RISK/HIGH-RISK SICK CLIENT: NEWBORN
● Polycythemia: may develop from decreased
oxygenation in the final weeks
○ Increased number of RBC and elevated Hct
(higher amounts of formed elements than the
plasma [liquid portion], making the blood more
viscous and sticky → difficulty in circulation)
○ TOO MUCH RBC: since the placenta does not
deliver enough oxygen and nutrients, the fetus
produces RBC as a compensatory mechanism
for low O2 levels
● Elevated hematocrit: because of the polycythemia
and dehydration, which lowers the circulating
plasma level
● ADDITIONAL OBSERVATIONS
○ Congenital anomalies of unknown cause
○ Seizure activity (increased electrical activity of
the irritated brain from hypoxia)
NURSING RESPONSIBILITIES
● Allow the woman to spend enough time with her
newborn
● Follow up care until school age to track
developmental abilities because of the lack of
nutrients and to check for neurologic symptoms d/t
hypoxia
NURSING DIAGNOSES
● Hypothermia r/t decreased liver glycogen and
brown fat stores
● Imbalanced nutrition less than body requirements
r/t increased use of glucose secondary to
intrauterine stress and decreased placental
perfusion
● Impaired gas exchange r/t airway obstruction from
meconium aspiration (MA)
● Ineffective peripheral tissue perfusion r/t increase
blood viscosity caused by polycythemia
II. PROBLEMS RELATED TO GESTATIONAL WEIGHT
A. SMALL FOR GESTATIONAL AGE
(SGA/MICROSOMIA)
● An infant is SGA if the birth weight is below the 10th
percentile on an intrauterine growth curve for that
age
○ WHY?: they have experienced intrauterine
growth restriction (IUGR) or failed to grow at the
expected rate in utero, advanced gestation and
limited fetal growth
● May be born preterm (before week 38 of gestation),
term (between weeks 38 and 42), or postterm (past
42 weeks)
● SGA infants are small for their age
I. ASSESSMENT
CAUSES
● Lack of adequate nutrition, especially among
adolescents
○ Adolescents are prone to having a high
incidence of SGA infants
● If they eat only enough to meet their own
nutritional and growth needs, the needs of
the growing fetus may be compromised
● Chromosomal abnormality or intrauterine
infection
○ The placental supply of nutrients is adequate
but an infant cannot use them because of a
chromosomal abnormality or an intrauterine
infection such as rubella or toxoplasmosis
● Placental anomaly: most common cause
○ Either the placenta did not obtain sufficient
nutrients from the uterine arteries or it was
inefficient at transporting nutrients to the fetus
● Placental underdevelopment/damage
○ Area of placenta that separated infarcted and
fibrose reduces the placental surface available
for nutrient exchange
● Women with systemic diseases (ex. severe DM, PIH)
○ Decreased blood flow to the placenta due to
narrowed blood vessel lumen → decreased
supplements going to the fetus
Cigarette smoking and use of narcotics
●
(vasoconstriction)
○ Diminished blood supply to fetus
ASSESSMENT
A. PREGNANT MOTHER
● Fundal height during pregnancy becomes
progressively less than expected
● EARLY NUTRITIONAL DEFICIENCY
○ Few new cells formed
○ Organs are small with ↓ organ weight
○ ↓ weight, length, head circumference
● LATE NUTRITIONAL DEFICIENCY
○ Decreased cell size
○ Normal organs = diminished size
○ ↓ weight
B. SGA INFANT
● Overall wasted appearance
● ↓ weight, length, head circumference
● Small liver
○ Causes difficulty regulating glucose, protein, and
bilirubin levels after birth
● Poor skin turgor
NCM 0109|10
 MODULE 08 – NURSING CARE OF AT-RISK/HIGH-RISK SICK CLIENT: NEWBORN
● Appear to have a large head, rest of the body is
smaller
● Skull sutures may be widely separated from lack of
normal bone growth
● Hair is dull and lusterless
Abdomen may be sunken (organs are smaller than
●
usual)
● Cord appears dry and may be stained yellow
More prominent sole creases, and ear cartilage
●
than expected for a baby of that weight
● Unusually alert and active d/t well-developed
neurologic responses
○ Appears to be more mature as infant’s age is
more advanced than the weight
Prolonged, marked acrocyanosis
●
○ Extra work on infant’s heart
○ Unable to circulate thick blood
Hyperbilirubinemia
●
○ Due to polycythemia
II. DIAGNOSIS
● SONOGRAM: to check size of the baby
● BIOPHYSICAL PROFILE: including a non-stress test,
placental grading, and amniotic fluid amount
○ Documents additional information on placental
function and fetal growth
○ If poor placental function is apparent from such
determinations, it can be predicted that the
infant will do poorly during labor during the
periods of relative hypoxia, which occur during
contractions
● Cesarean birth is preferred d/t poor
placental function (hypoxia during
contraction)
● LABORATORY TESTS
○ Increased hematocrit level
● Less than normal amounts of plasma in
proportion to red blood cells are present
because of a lack of fluid in the utero
● If the hematocrit level is more than 66–70%,
an exchange transfusion to dilute the blood
may be necessary (para matanggal ang
viscous/thick blood)
○ Increased RBC (polycythemia)
● Occurs because anoxia during intrauterine
life stimulated excess development of them
● Causes increased blood viscosity, which
puts extra work on the infant’s heart
because it is more difficult to effectively
circulate thick blood = prolonged
acrocyanosis
Increased blood viscosity (more formed
1 elements than plasma in blood)
Extra work on infant’s heart (to circulate the
2 thick blood)
Inefficient circulation leads to blocked
3 vessels and thrombus formation
● Hyperbilirubinemia
○ Related to polycythemia
○ Part of the heme (one of the components of
hemoglobin) becomes bilirubin after RBC
destruction
○ Under normal circumstances, this is to be picked
up by the liver. However, the infant’s immature
and small liver is unable to perform its task
○ The difficult regulation (conversion into direct
from to allow excretion) causes increased levels
of bilirubin in the blood
● Hypoglycemia/decreased blood glucose (<40
mg/dL)
○ Decreased glycogen stores
○ Not enough glucose stored in the body because
placenta is not providing enough nutrients to the
growing fetus in the intrauterine life
○ NR: May need intravenous glucose to sustain
blood sugar until they are able to suck
vigorously enough to take sufficient oral
feedings
III. NURSING MANAGEMENT
1. INEFFECTIVE BREATHING PATTERN R/T
UNDERDEVELOPED BODY SYSTEMS AT BIRTH
● CAUSES
○ Birth asphyxia: underdeveloped chest muscles
and MAS
○ Risk for MAS: fetal anoxia triggers the relaxation
of the anal sphincter and the increase of
intestinal motility → passage of meconium in the
intrautero (meconium aspiration) → blocks
airflow into alveoli → hypoxemia
● MANAGEMENT
○ Resuscitation at birth: aspiration meconium is a
foreign substance that blocks airflow into the
alveoli
○ Closely observe both respiratory rate and
character in the first few hours of life
● As underdeveloped chest muscles not only
make taking the first breath difficult, but it
can also make SGA infants unable to sustain
an adequate newborn respiratory rate
2. RISK FOR INEFFECTIVE THERMOREGULATION R/T LACK
OF SUBCUTANEOUS FAT
● Infant’s temperature is maintained at 36-36.5°C
(97.8°F; axillary)
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 MODULE 08 – NURSING CARE OF AT-RISK/HIGH-RISK SICK CLIENT: NEWBORN

○ A carefully controlled environment is essential to ● Transposition of the great arteries (TGA)

keep an infant’s body temperature in a neutral ○ The right ventricle’s blood is received by the
zone aorta, while the left ventricle’s blood is received
● SGA infants are less able to control body by the pulmonary artery (magkabaliktad)
temperature than other newborns because they ● Beckwith–Wiedemann syndrome (general body
lack subcutaneous fat overgrowth)
● MANAGEMENT: PREVENTING HEAT LOSS ○ Overgrowth + neonatal hypoglycemia +
○ Evaporation: keep skin dry immediately after hyperinsulinemia (mas maraming sugar ang
delivery papasok = overgrowth)
○ Radiation and Convection: place incubators
and cribs away from windows:
○ Conduction: do not place surrounding cold
objects (such as metal objects)
● Different temperature of baby’s body from
the surrounding objects that is in contact
with the baby’s body ● Congenital anomalies (e.g., omphalocele [genetic
○ Check cold stress (decreased temperature, defect in the abdominal wall with organs protruding
lethargy, pallor) outside])
3. RISK FOR IMPAIRED PARENTING R/T CHILD’S ● Genetics
HIGH-RISK STATUS AND POSSIBLE COGNITIVE OR ● Male infants
NEUROLOGIC IMPAIRMENT FROM LACK OF NUTRIENTS IN ● Erythroblastosis fetalis
UTERO
APPEARANCE
● Impaired cognitive development d/t lack of oxygen
A. PREGNANT MOTHER
and nourishment in utero despite seemingly
normal physical development (weight gain)
● Uterus is unusually large size for the date of
● MANAGEMENT
pregnancy
○ Promote early parental bonding with the child
● Deceptive abdominal size: because a fetus lies in a
by discussing ways parents can promote an
flexed fetal position, they do not occupy
infant’s development once they are at home
significantly more space at 10 lb than at 7 lb
● Done until the child reaches school age
○ Cannot fit into pelvic rim (cephalopelvic
(follow-up care after discharge) to
disproportion)
determine presence of neurologic defects
● CS birth may be necessary d/t risk of
○ Encourage parents to provide toys suitable for
shoulder dystocia
their child’s chronological age, not physical size
○ Because an infant tires easily in the first few B. LGA INFANT
weeks of life, urge them to space play periods
with rest periods or hypoglycemia or apnea can ● Immature reflexes and low scores on gestational
occur age examinations
● Extensive bruising
B. LARGE FOR GESTATIONAL AGE ● Birth injury (broken clavicle and Erb-Duchenne
(LGA/MACROSOMIA) paralysis from trauma to cervical nerves if born
vaginally)
● Birth weight is above the 90th percentile on an
● Prominent molding, cephalhematoma, and caput
intrauterine growth chart for that gestational age
succedaneum
○ Head is too large due to increased pressure
I. ASSESSMENT
during birth
CAUSES
IMPORTANT ASSESSMENT CRITERIA FOR LGA INFANT
● Overproduction of nutrients and growth hormone in
utero Asymmetry of the anterior
Skin color for
chest or unilateral lack of
● Diabetic/obese mothers ecchymosis (bruising
movement (diaphragmatic
● Multiparity (with each succeeding pregnancy, with vaginal birth),
paralysis from edema of
jaundice, and erythema
babies tend to grow larger) the phrenic nerve)

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 MODULE 08 – NURSING CARE OF AT-RISK/HIGH-RISK SICK CLIENT: NEWBORN

● PELVIMETRY/ULTRASOUND
Motion of extremities on
Eyes for evidence of ● SONOGRAM: to determine the size of the fetus and
spontaneous
unresponsive or dilated
movement and in to compare the size of the fetus with the woman’s
pupils; vomiting, bulging
response to a pelvic capacity
fontanelles, high-pitched
Moro/startle reflex NST: to check for placental function
cry (increased intracranial ●
(clavicle fracture/Erb
pressure) ● AMNIOCENTESIS: to check for fetal lung maturity
palsy)
Activities such as jitteriness, lethargy, uncoordinated
eye movements (suggests seizure activity d/t
III. NURSING MANAGEMENT
increased ICP or hypoglycemia; absent seizure may
also be possible wherein the neonate would suddenly ● INEFFECTIVE BREATHING PATTERN RELATED TO
stop moving or there is unusual movement) POSSIBLE BIRTH TRAUMA IN LGA NEWBORN
○ Some LGA neonates have difficulty establishing
COMMON COMPLICATIONS respirations at birth because of birth trauma
● Increased intracranial pressure from birth of
● Birth trauma from CPD, breech position, and the larger-than-usual head lead to pressure
shoulder dystocia on the respiratory center causing a
● COMPLICATION IF WE TRIED TO DELIVER VIA NSD: decrease in respiratory function
○ Asphyxia, clavicular fracture, facial paralysis, ○ BORN VIA CS: ineffective gas exchange d/t
depressed skull fracture d/t repeated pressure transient fluid in the lungs
and friction of the fetal head to the vaginal canal ○ BORN VIA NSD: ineffective lung function d/t
diaphragmatic paralysis or broken clavicle
CARDIOVASCULAR DYSFUNCTION
● RISK FOR IMBALANCED NUTRITION, LESS THAN BODY
● POLYCYTHEMIA REQUIREMENTS R/T ADDITIONAL NUTRIENTS NEEDED
○ Fetus attempts to fully oxygenate more than the TO MAINTAIN WEIGHT AND PREVENT
average amount of body tissue; will try to HYPOGLYCEMIA
increase RBCs ○ As a rule, an LGA infant needs to be fed
● SIGNS OF HYPERBILIRUBINEMIA (EX. JAUNDICE) immediately after birth (preferably by
○ Absorption of blood from bruising and breastfeeding) to prevent hypoglycemia
breakdown of the extra red blood cells created ○ Sucking may not be effective enough to obtain
by polycythemia the larger than usual amount of milk needed
○ As hematoma or bruises heal, there would be a ○ May need supplemental formula feedings after
release of bilirubin which would lead to a breastfeeding to supply enough fluid and
yellowish discoloration and hyperbilirubinemia glucose for the larger than normal size for the
● PRESENCE OF CYANOSIS first 24 hours
○ May be a sign of poor heart function, but it could ● RISK FOR IMPAIRED PARENTING R/T HIGH-RISK OF
also be from transposition of the great vessels, a LGA INFANT
serious heart anomaly associated with ○ Parents may also underestimate this infant’s
macrosomia needs because of the child’s large size
● Make sure to correct these misconceptions
HYPOGLYCEMIA to allow the parents to properly care for their
child
● After birth, these increased insulin levels will
○ If they are worried the infant must be sick in
continue for up to 24 hours of life, possibly causing some way they are not being told about, it can
rebound hypoglycemia interfere with bonding happening as
● Large newborns require large amounts of instinctively as it might
nutritional stores to sustain their weight
III. ALTERATIONS IN OXYGENATION
II. DIAGNOSIS
A. RESPIRATORY DISTRESS SYNDROME
(Surfactant Deficiency Disorder)
● REMINDER: MAY BE MISSED IN AN OBESE WOMAN
○ Fetal contours are difficult to palpate ● Formerly termed as HYALINE MEMBRANE DISEASE
○ Obesity does not necessarily indicate a larger ● Most often occurs in conditions that decrease the
than usual pelvis amount of blood perfused to the lungs:
○ Preterm infants

NCM 0109|13
 MODULE 08 – NURSING CARE OF AT-RISK/HIGH-RISK SICK CLIENT: NEWBORN

○ Infants of diabetic mothers

Blood then shunts through the foramen ovale and
○ Infants born by cesarean birth 2 the ductus arteriosus as it did during fetal life
○ Meconium aspiration
● PATHOLOGIC FEATURE: HYALINE-LIKE/FIBROUS The lungs become poorly perfused (POOR
OXYGEN EXCHANGE)
MEMBRANE
● This leads to tissue hypoxia, which causes
○ Formed from an 3 the release of lactic acid
exudate of an infant’s
● Decreased oxygen level in the tissues =
blood that begins to anaerobic metabolism
line the terminal As a result, the production of surfactant
bronchioles, alveolar 4 decreases even further
ducts, and alveoli
Acidosis occurs when decrease in lung surfactant
○ Injured alveoli d/t lack is accompanied by increase in carbon dioxide
of lung surfactant = levels
collection of
5
damaged cells/debris ACIDOSIS = VASOCONSTRICTION = DECREASED
PULMONARY PERFUSION = ALVEOLAR COLLAPSE
= goes into the alveolar lining (instead of
surfactant) and becomes the hyaline
membrane I. ASSESSMENT
● This membrane prevents the exchange of
● Most infants who develop RDS have difficulty
oxygen and carbon dioxide at the
initiating respirations at birth
alveolar–capillary membrane, interfering
● INITIAL RELEASE OF SURFACTANT AFTER
with effective oxygenation
RESUSCITATION
● ROLE OF SURFACTANT
○ They appear to have periods of hours or a day
○ Phospholipid that lines alveoli on top of the
when they are free of symptoms
water layer, lowering the surface tension and
allowing alveolar expansion (prevents collapse)
SUBTLE SIGNS AFTER RESUSCITATION
○ What happens when surfactants are in low
levels or are absent? ● Sternal and subcostal
● Low body retractions (use of all
● These factors result to unequal inflation of
alveoli on inspiration and the collapse of temperature accessory muscles to
alveoli on end of expiration ● Nasal flaring prevent lung
● Cyanotic mucous collapse)
● Infants are unable to keep their alveoli
inflated and therefore exert a great deal of membranes ● Tachypnea (more
effort to re-expand the alveoli with each than 60 bpm)
breath S/SX WITHIN SEVERAL HOURS
Initial effect of surfactant has already winded off
● This inability to maintain lung expansion
● Expiratory grunting
produces widespread atelectasis
(brought about by
● Fine rales and
closing of the glottis
diminished breath
during expiration to
sounds upon
increase pressure
auscultation (signs of
and prevent the lungs
poor air entry)
from collapsing
● Central cyanosis
[expiration is longer
even in room air
than inspiration];
temperature
produces sound
similar to snoring)
S/SX AS DISTRESS INCREASES
● Seesaw respirations
PATHOPHYSIOLOGY OF RESPIRATORY DISTRESS ● Heart failure (AEB
SYNDROME (on inspiration, the
decreased urine
anterior chest wall
With deficient surfactant, areas of hypoinflation output [blood is not
retracts and the
1 begin to occur and pulmonary resistance perfused to major
increases abdomen protrudes;
organs] and edema
on expiration, the

NCM 0109|14
 MODULE 08 – NURSING CARE OF AT-RISK/HIGH-RISK SICK CLIENT: NEWBORN

sternum rises): sign of extremities [stasis ○ Complications: pulmonary hemorrhage,

that the baby is not d/t poor circulation]) mucous plugging
receiving enough ● Pale gray skin ○ Monitoring of blood gas analysis and
oxygen and there is ● Periods of apnea oxygenation
ineffective gas ● Bradycardia ○ Newborn is suctioned before surfactant
exchange ● Pneumothorax (air or administration and suctioning is delayed after to
gas in the pleural allow maximum effects
space) ● OXYGEN ADMINISTRATION
○ Rationale:
✅ To maintain correct PO2 and pH levels
✅ To provide adequate oxygen to the tissues
✅ To prevent lactic acid accumulation from
II. DIAGNOSIS hypoxia
○ Use warm oxygen and humidifiers
● CHEST X-RAY ○ Provide via cannula with CPAP
○ Atelectasis: diffuse pattern of radiopaque areas ○ Provide good oral hygiene using sterile water
that look like ground glass (haziness) ● Oxygen can thicken oral secretions and
cause drying of the mucous membrane
○ High levels of oxygen should also be prevented
as it can cause damage to the blood vessels of
the newborn’s eye (could lead to retinopathy of
prematurity [blindness])
● VENTILATION
○ Infant ventilators that are pressure-cycled to
control the force with which air is delivered
● Forces air in lungs at high pressure so that
○ Lung collapse they would not totally collapse
● Ipsilateral shift of ● NR: close observation on ventilator to adjust
the trachea, if needed
carina, and ○ Complications: pneumothorax, impaired
mediastinum cardiac output (decreased blood flow through
● Bronchial cut-off the pulmonary artery from increased lung
sign (left pressure), increased intracranial and arterial
mainstem pressure (changes in BP)
bronchus) ● NR: Limit fluid intake or give IV cautiously to
● Rib crowding help lower BP
(compensation of ○ LIQUID VENTILATION
the other lung [hyperinflation]) ● Perfluorocarbons
● Loss of volume ● Bubbled oxygen = damaged lungs = fluid is
○ Dilated, air filled bronchioles: dark streaks within heavier = distention of lungs (filled with
the ground glass more oxygen)
● BLOOD GAS STUDIES ● NITRIC OXIDE (vascular dilator)
○ Taken from an umbilical vessel catheter ○ To reverse pulmonary hypertension, pulmonary
○ Will reveal respiratory acidosis vasoconstriction, subsequent acidosis, and
severe hypoxia
III. THERAPEUTIC MANAGEMENT ● Decreases pulmonary resistance and
increases blood flow to alveoli = more
● SURFACTANT REPLACEMENT (Poractant alfa,
oxygen supplied to the lungs
Calfactant, Beractant)
○ Causes smooth muscle relaxation and reduces
○ Synthetic surfactant is sprayed into the lungs by
pulmonary vasoconstriction
a syringe or catheter by an endotracheal tube
○ Administered via ventilator circuit blended with
at birth while an infant is first positioned with the
oxygen
head held upright and then tilted downward
● Administer only 6–20 ppm (below toxic
levels)

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 MODULE 08 – NURSING CARE OF AT-RISK/HIGH-RISK SICK CLIENT: NEWBORN
○ Attaches readily to hemoglobin → deactivated;
does not affect systemic vasculature
● ADDITIONAL THERAPY
○ Pancuronium (Pavulon; IV): muscle relaxant to
improve lung compliance and to decrease
muscle resistance
● Allows easy accomplishment of mechanical
ventilation
○ Atropine (neostigmine methylsulfate):
increases pulmonary blood flow
○ Extracorporeal membrane oxygenation (ECMO)
● Blood is removed from the baby by gravity
using a venous catheter advanced into the
right atrium of the heart
● The blood circulates from the catheter to the
ECMO machine, where it is oxygenated and
rewarmed
○ It is then returned to an infant’s aortic
arch by a catheter advanced through
the carotid artery
● Ensures adequate oxygenation supplied to
the body tissues
● Typically used for 4–7 days only
● SUPPORTIVE CARE
○ An infant with RDS must be kept warm because
cooling increases acidosis in all newborns
● Also decreases oxygen demand and
workload of the heart
○ FEEDINGS
❌ Nipple feedings are contraindicated as this
creates a marked increase in respiratory
rate
✅ Nutrition is provided by parenteral therapy
during acute stage
✅ Minimal enteral feeding is provided to
enhance maturation of the GI system
○ Suction only when necessary: evidence of
decreased oxygenation, excess moisture in the
ET tube, or increased infant irritability
● Use water-soluble ointment to reduce
irritation to the external nares from O2
equipment
PREVENTION
● AMNIOCENTESIS: to assess fetal lungs for adequate
surfactant formation
● TOCOLYTIC AGENTS (terbutaline; magnesium
sulfate): to prevent preterm birth
● STEROIDS AND SURFACTANTS: administered before
delivery (maternal steroid) and postnatally
(surfactant)
○ 2 injections of glucocorticosteroid to quicken
formation of lecithin or lung surfactant
● Betamethasone at 12 and 24 hours before
birth
B. SUDDEN INFANT DEATH SYNDROME (SIDS)
● Peak age of incidence is 2–4 months of age
I. ASSESSMENT
RISK FACTORS
● Generally unknown
● Babies of adolescent mothers
● Babies of closely-spaced pregnancies
● Underweight infants (lack nutrition in utero =
underdeveloped body systems)
● Preterm infants (lack of surfactant)
● Infants with bronchopulmonary dysplasia
● Twins (compete with each other)
● Siblings of another child with SIDS
● Native American, Native Alaskan, and
economically-disadvantaged black infants
● Infants of narcotic-dependent mothers (what is
taken by the mother is taken by the fetus;
suppression of the CNS)
SIGNS AND SYMPTOMS
● WELL-NOURISHED INFANT BUT WITH SLIGHT HEAD
COLD
○ After being put to bed at night or for a nap, the
infant is found dead a few hours later
● Infants who die this way do not appear to
make any sound as they die, which
indicates that they die with laryngospasm
●
(nag-close ‘yung airway)
BLOOD-FLECKED SPUTUM/VOMITUS
○ Commonly found in the mouths and on the
bedclothes of affected infants
○ This occurs as a result of death, and not as its
cause
● PETECHIAE IN THE LUNGS AND MILD
INFLAMMATION/CONGESTION
○ Revealed by autopsy
NCM 0109|16
 MODULE 08 – NURSING CARE OF AT-RISK/HIGH-RISK SICK CLIENT: NEWBORN

○ Not severe enough to cause sudden death = ANSWER KEY: PRE-TEST

these infants do not suffocate from bedclothes 1. B 8. A
5. A
or choke from overfeeding, underfeeding, or 2. C 9. B
6. C
crying 3. A 10. D
7. A
4. D
CAUSE OF DEATH
Banaag, Cato, Diala, Ingal, Mallari, Malonzo, Navarro,
● Attributed to prolonged and unexplained apnea Paras | CAHAYA 2025
● CONTRIBUTING FACTORS
○ Viral respiratory or botulism infection (release of REFERENCES
toxins that cause CNS paralysis) Synchronous Lecture: 13–14 April 2023
Module: NCM 0109 Module 08
○ Exposure to secondary smoke
Book: Maternal and Child Health Nursing
○ Pulmonary edema
○ Brainstem abnormalities (location of respiratory
center)
○ Neurotransmitter deficiencies
○ Heart rate abnormalities
○ Distorted familial breathing patterns
○ Decreased arousal responses (mahirap gisingin
‘yung baby)
○ Sleeping in a room without air currents
(rebreathes expired air = metabolic acidosis)
○ Possible lack of surfactant in alveoli
○ Sleeping prone (respiratory muscles are
restricted; limited lung expansion)

II. NURSING INTERVENTIONS

● PATIENT EDUCATION
○ Risk of prone sleeping in infants
● Place infants on supine when sleeping
○ Appropriate bedding surfaces
○ Association of SIDS with maternal smoking
○ Dangers of co-sleeping with adults or other
children
● COUNSELING
○ Parents should be counseled by a nurse or
someone else trained in counseling at the time
of the infant’s death
○ It helps if they can talk to this same person
periodically for however long it takes to resolve
their grief
● They have a difficult time accepting the
death of any child, especially when it
happens so suddenly and to an infant
● GIVE AUTOPSY REPORTS AS SOON AS POSSIBLE
○ Reading the report that their child died an
unexplained death can help to reassure them
that the death was not their fault
○ Assurance plan for other children
● SLEEP STUDY OF SIBLING OF SIDS INFANT
○ Done as a precaution within the first 2 weeks of
life
○ Infant is placed on a sleep apnea monitoring

NCM 0109|17