ILLNESS IN THE

NEWBORN
Presented by: John LLoyd Paghid

&
Daniela Ngoho
 Topics
Topic 1: Respiratory Distress
Syndrome

Topic 2: Transient tachypnea of

newborn
 Topics
Topic 3: Meconium Aspiration
Syndrome

Topic 4: Apnea
Respiratory Distress
Syndrome
formerly termed hyaline membrane disease, most often occurs in
preterm infants, infants of diabetic mothers, infants born by
cesarean birth, or those who for any reason have decreased blood
perfusion of the lungs, such as occurs with meconium aspiration

The pathologic feature of RDS is a hyaline-like (fibrous) membrane

formed from an exudate of an infant’s blood that begins to line the
terminal bronchioles, alveolar ducts, and alveoli. This membrane
prevents exchange of oxygen and carbon dioxide at the alveolar–
capillary membrane.

 CAUSES
The cause of RDS is a low level or absence of surfactant, the
phospholipid that normally lines the alveoli and reduces
surface tension to keep the alveoli from collapsing on
expiration. Because surfactant does not form until the 34th
week of gestation, as many as 30% of low-birth-weight
infants and as many as 50% of very-low-birth-weight
infants are susceptible to this complication

 SIGNS AND SYMPTOMS

1. LOW BODY TEMPERATURE

2. NASAL FLARING

3. STERNAL AND SUBCOSTAL RETRACTIONS

4. TACHYPNEA (more than 60 respirations per minute)

5. CYANOTIC MUCOUS MEMBRANES

A partially closed glottis this way is helpful as it increases

the pressure in the alveoli on expiration, helps to keep the
alveoli from collapsing, and makes oxygen exchange
more complete. As the disease progresses, infants become
cyanotic and their PO2 and oxygen saturation levels fall
in room air.

 On auscultation, there may be fifine rales and diminished breath

sounds because of poor air entry. As distress increases, an infant
may exhibit:

• Seesaw respirations (on inspiration, the anterior chest wall retracts

and the abdomen protrudes; on expiration, the sternum rises)

• Heart failure, evidenced by decreased urine output and edema of the

extremities

• Pale gray skin

• Periods of apnea

• Bradycardia

• Pneumothorax

 DIAGNOSTIC PROCEDURES

1. The diagnosis of RDS is made on the clinical signs of grunting, central

cyanosis in room air, tachypnea, nasal flaring, retractions, and
shock
2. CHEST CARDIOGRAPH

3. BLOOD GAS STUDIES

A -hemolytic, group B streptococcal infection may

mimic RDS, as this infection is so severe in newborns that
the insult to the lungs is enough to stop surfactant produc
tion. Cultures of blood, cerebrospinal fluid, and skin may
be obtained to rule out this condition. An antibiotic (peni
cillin or ampicillin) and an aminoglycoside (gentamicin
or kanamycin) may be started while culture reports are
pending

 THERAPEUTIC MANAGEMENT

1. Surfactant Replacement- . As a preventive measure, synthetic

surfactant is sprayed into the lungs by a syringe or catheter through an
endotracheal tube at birth while an infant is first positioned with the
head held upright and then tilted downward
Mucus plugging from the solution, do occur. An infant who is
receiving surfactant and then is placed on a ventilator needs close
observation because lung expansion can improve rapidly.
Anticipate the need to adjust ventilator settings to prevent
excessive lung pressure.

2. Oxygen Administration- Administration of oxygen is necessary to

maintain correct PO2 and pH levels. Continuous positive airway
pressure (CPAP) or assisted ventilation with positive end-expiratory
pressure (PEEP) will exert pressure on the alveoli at the end of
expiration and keep the alveoli from collapsing
3. Ventilation- Normally, on a ventilator, inspiration is
shorter than expiration, or there is an inspiratory/expiratory
ratio (I/E ratio) of 1:2. Infant ventilators are therefore available with
a reversed I/E ratio (2:1). These are pressure-cycled to control the force
with which air is delivered. High-frequency, oscillatory, and jet
ventilation are other methods of introducing oxygen to infants with
noncompliant lungs. These systems maintain airway pressure and
then intermittently “jet” or oscillate at a rapid rate (400–600 times
a minute) an additional amount of air to inflate alveoli.

Complications: Pneumothorax, impaired cardiac output. Being

certain that infants are not overhydrated is important to help
prevent increased blood pressure and increased pulmonary artery
pressure.

Indomethacin or ibuprofen may be used to cause closure of a patent

ductus arteriosus, making ventilation more efficient. Indomethacin
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, es
pecially at puncture sites, if this is prescribed.
4. Additional Therapy- using muscle relaxants Pancuronium (Pavulon)
can be administered intravenously to the point of abolishing
spontaneous respiratory action. Infants who have no spontaneous
respiratory function because of drug administration need critical
observation and frequent ABG analysis because they totally depend on
caregivers at this point

The effect of pancuronium decreases as the life of the drug expires; its
effect can be interrupted by the administration of atropine or
injectable neostigmine methylsulfate (Prostigmin Methylsulfate
Injectable)

Some infants are maintained on extracorporeal membrane

oxygenation n (ECMO) to ensure adequate oxygenation

Other therapies include liquid ventilation or administration of

perfluorocarbons and inhalation of nitric oxide
 Extracorporeal Membrane Oxygenation. ECMO was first developed as a
means of oxygenating blood during cardiac surgery. Its current use has
expanded to the management of chronic severe hypoxemia in newborns
with illnesses such as meconium aspiration, RDS, pneumonia, and
diaphragmatic hernia. With 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.

ECMO is typically used for 4 to 7 days

complications, chief of which is intracranial hemorrhage, possibly

from the anticoagulation therapy necessary to prevent
thromboembolism.

ensure that the child’s blood volume remains adequate, bleeding

does not occur, and adequate oxygen is being supplied
 Liquid ventilation. Liquid ventilation involves the use of
perfluorocarbons, substances used in industry to assess for
leakage in pipes. When perfluorocarbons are introduced into lungs that
inflate poorly because they are deficient in surfactant, or in lungs
damaged by trauma or disease, the weight of the fluid, which is heavy
compared with air, helps to distend the lungs. As the liquid moves into
a lung, oxygen is carried along with it; as the liquid spreads over all
lung surfaces, an exchange of oxygen occurs (Lindemann et al., 2007).
The administration of liquid ventilation can also be used to deliver
surfactant to a newborn’s lungs.

Nitric Oxide. An additional measure that can help to oxygenate a

newborn’s lungs is the administration of nitric oxide. This causes
pulmonary vasodilation, which can be helpful to increase blood flow to
the alveoli when persistent pulmonary hypertension is present
Supportive Care. An infant with RDS must be kept warm because cooling
increases acidosis in all newborns, and for the newborn with RDS it may
increase to lethal levels. Keeping an infant warm also reduces the
metabolic oxygen demand. Provide hydration and nutrition with
intravenous fluids, glucose, or gavage feeding because the respiratory
effort makes an infant too exhausted to suck
 PREVENTION

RDS rarely occurs in mature infants. Dating a pregnancy by sonogram

and by documenting that the level of lecithin in surfactant obtained
from amniotic fluid exceeds that of sphingomyelin by 2:1 are important
ways to be certain an infant born by cesarean birth or has labor
induced is mature enough that RDS is not likely to occur.

Using a tocolytic agent such as terbutaline can help to prevent preterm

birth for a few days. Because steroids appear to quicken the formation
of lecithin, it may be possible to prevent RDS in infants by
administering two injections of a glucocorticosteroid, such as
betamethasone, to the mother at 12 and 24 hours during this time. This
is most effective when given between weeks 24 and 34 of pregnancy.
Unfortunately, there is often no warning that preterm birth is
imminent until hours before birth. Because the steroid does not take
effect before 24 to 48 hours, some labors and births will progress too
rapidly for this preventive measure to be effective.
Transient Tachypnea
of the Newborn
At birth, a newborn may have a rapid rate of respirations, up
to 80 breaths per minute when crying, caused by retained
lung fluid. Within 1 hour, however, this rapid rate slows to
between 30 and 60 breaths per minute. In about 10 in 1000 live
births, the respiratory rate remains at a high level, between 80
and 120 breaths per minute.

Mild retractions but not marked cyanosis, mild hypoxia, and

hypercapnia may be present. Feeding is difficult because the
child cannot suck and breathe this rapidly at the same time.
A chest radiograph will reveal some fluid in the central lung, but
aeration is, overall, adequate. An ultrasound may show like findings.

Transient tachypnea occurs more often in infants who are born by

cesarean birth, in infants whose mothers received extensive fluid
administration during labor, and in preterm infants.

Infants born by cesarean birth are probably more prone to develop

this form of respiratory distress because the thoracic cavity is not
compressed as it is in vaginal birth, so less lung fluid is expelled than
normally
Close observation of such a newborn is a priority. Watch carefully to
be certain the increased effort is not tiring. Also watch for beginning
signs of a more serious disorder, because a rapid respiratory rate is
often the first sign of respiratory obstruction. Oxygen
administration may be necessary. Transient tachypnea of the
newborn peaks in intensity at approximately 36 hours of life and
then begins to fade. Typically, by 72 hours of life, it spontaneously
fades as the lung fluid is absorbed and respiratory activity becomes
effective.
Meconium Aspiration
Syndrome
Meconium is present in the fetal bowel as early as
10 weeks gestation. If hypoxia occurs, a vagal
reflex is stimulated, resulting in the relaxation of
the rectal sphincter. This releases meconium into
the amniotic fluid. Babies born breech may expel
meconium into the amniotic fluid from pressure on
the buttocks. In both instances, the appearance of
the fluid at birth is green to greenish-black from
the staining. Meconium staining occurs in
approximately 10% to 12% of all pregnancies; in 2%
to 9% of these pregnancies, infants will aspirate
the meconium.
Meconium Aspiration
Syndrome
An infant may aspirate meconium either in utero
or with the first breath at birth. Meconium can
cause severe respiratory distress in three ways: it
causes inflammation of bronchioles because it is a
foreign substance; it can block small bronchioles
by mechanical plugging; and it can cause a
decrease in surfactant production through lung
trauma. Hypoxemia, carbon dioxide retention, and
intrapulmonary and extrapulmonary shunting
occur. A secondary infection of injured tissue may
lead to pneumonia.
 ASSESSMENT
With meconium-stained amniotic fluid, an infant
should be suctioned with a bulb syringe or catheter
while at the perineum, before the birth of the
shoulders, to avoid meconium aspiration. Although
there is some dispute regarding whether all infants
with meconium staining need intubation, those with
severe staining are intubated and meconium is
suctioned from their trachea and bronchi.
Do not administer oxygen under pressure (bag and
mask) until an infant has been intubated and
suctioned, so that the pressure of the oxygen does
not drive small plugs of meconium farther down
into the lungs, worsening the irritation and
obstruction.
 ASSESSMENT
After the initiation of respirations, an infant's
respiratory rate may remain elevated (tachypnea)
and coarse bronchial sounds may be heard on
auscultation. An infant may continue to have
retractions because the inflammation of the bronchi
tends to trap air in the alveoli, limiting the entrance
of oxygen. This air trapping may also cause
enlargement of the anteroposterior diameter of the
chest (barrel chest). Blood gases will reveal a poor
gas exchange, evidenced by a decreased PO2 and an
increased PCO2. A chest radiograph will show
bilateral corse infiltrates in the lungs, with spaces of
hyperaeration (a peculiar honeycomb effect). The
diaphragm will be pushed downward by the
overexpanded lungs.
Therapeutic Management
Amnioinfusion can be used to dilute the amount of

1. meconium in amniotic fluid and reduce the risk of

aspiration although this is usually reserved for
instances where the fetus shows sistress.

2.
After birth and tracheal suction, infants may need
to be treated with oxygen administration and
assisted ventilation.

Antibiotic therapy may be used to forsetall the

3. development of pneumonia as a secondary

problem. Surfactant may be administered to
increase lung compliance.
Therapeutic Management
Infants must be observed closely for signs of

1. trapping air in the alveoli, because the alveli can

expand only so far and then will rupture, sending
air into the plueral space (pneumothorax).

Observe an infant closely for signs of heart failure

2. such as increased heart rate respiratory distress.

Maintain a temperature-neutral environment to
prevent incresing metabolic oxygen demands.

Chest physiotherapy with clapping and vibration

3. may be helpful to encourage removal of remnants

of meconium from the lungs.
Therapeutic Management
Some infants will be maintained ECMO to ensure

1. adequate oxygenation.

2.
 APNEA
Apnea is a pause in respirations longer than 20 seconds
with accompanying bradycardia. Beginning cyanosis
also may be present. Many preterm infants have
periods of apnea as a result of fatigue or the immaturity
of their respiratory mechanisms. Babies with secondary
stresses, such as infection, hyperbilirubinemia,
hypoglycemia, or hypothermia, tend to have a high
incidence of apnea.
 ASSESSMENT
Result 1

Gently shaking an infant or flicking

the sole of the foot often stimulates
the baby to breathe again, almost as
if the child needed to be reminded to
maintain this function. If an infant
does not respond to these simple
measures, resuscitation is necessary.
 ASSESSMENT
Result 2
Closely observe all newborns, but especially
preterm ones, to detect these apneic
episodes. Apnea monitors that record
respiratory movements are invaluable tools
to detect failing respiration and sound a
warning an infant needs attention. Infants
with frequent or difficult-to-correct
episodes may be placed on ventilators to
provide respiratory coordination until they
are more mature.
 Therapeutic Management
Result 3
Result 4
To help prevent episodes of apnea,
maintain a neutral thermal environment After feeding, observe an infant
and use gentle handling to avoid carefully because a full stomach can
excessive fatigue. Always suction gently put pressure on the diaphragm and
to minimize nasopharyngeal irritation, potentially compromise respirations.
which can cause bradycardia because of Careful burping also helps to reduce
vagal stimulation. Using indwelling this effect.
nasogastric tubes rather than
intermittent ones can also reduce the
amount of vagal stimulation.
 Therapeutic Management
Result 5
Never take rectal temperatures in Result 6
infants prone to apnea; the resulting Theophylline or caffeine sodium
vagal stimulation can reduce the benzoate may be administered to
heart rate (bradycardia), which can stimulate respirations. The mechanism
lead to apnea. by which these drugs reduce the
incidence of apneic episodes is
unclear, but they appear to increase
an infant’s sensitivity to carbon
dioxide, ensuring better respiratory
function.
 Therapeutic Management
Result 7
Infants who have had an apneic
episode severe enough to require
resuscitation are at a high risk for
sudden infant death syndrome (SIDS).
Such infants may be discharged home
with a monitoring device to be used
for 2 to 6 months.
Question
Time
 Our Team

Alfredo Torres Yanis Petros

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