Meconium Aspiration Syndrome & Transient Tachypnea of the Newborn

In Partial Fulfillment of the Requirements

in Clinical Education I

Submitted to:
Prof. Lloyd Deocades, RTRP
Clinical Instructor

Submitted by:
Amirulhadj, Shariza S.
Evediente, Aira Faye A.
Maluag, Rafael L.
Morastil, Dario Jr. A.
Perales, Karina Isabel C.
Ragasa, Alyssa P.

Group 3

Date Submitted:
July 29, 2021
 TABLE OF CONTENTS
Cover Page………………………………………………………………………………….. i
Table of Contents ..............................................................................................…….. ii

I. DEFINITION
II. CLINICAL FINDINGS AND SYMPTOMS
III. RISK FACTORS
IV. PATHOPHYSIOLOGY
V. DIAGNOSIS
VI. MANAGEMENT & TREATMENT

BIBLIOGRAPHY:

Des Jardins, T., Burton, G. (2016). Clinical Manifestations and Assessment of

Respiratory Disease (7th ed.). Elsevier Inc.

Farrash R. (2015). Neonatal and Pediatric Respiratory Care (4th

ed.). Elsevier Inc.

Hanse, A., Levin, J. (2019). Neonatal and pediatric disorders (5th

ed.) Elsevier Inc.

Mola, S., Oldenburg, G., Polin, S., et. al., (2014). Neonatal and pediatric respiratory care: a
patient case method. F.A Davis Company.

Perretta, J. (2014). Neonatal and Pediatric Respiratory Care Pageburst E-book on Kno (pp. 151,
157). F. A. Davis Company.

Perreta, P. S. (2014). Disease of full-term infants. Cain, J. Neonatal and Pediatric Respiratory
Care (pp. 151-157). Quincy McDonald

Walsh, B. K. (2015). Neonatal and Pediatric Respiratory Care Pageburst E-book on Kno
(Fourth, pp. 424, 429). W B Saunders Company

Zanelli, S., Kaufman, D. (2019). Neonatal and pediatric disorders (5th ed.) Elsevier Inc.
 Meconium Aspiration Syndrome

I. DEFINITION

The inhalation of meconium by a fetus or newborn is known as meconium aspiration syndrome

(MAS). It can obstruct the airways, preventing the lungs from expanding or causing other
respiratory problems like pneumonia or emphysema (Des Jardins & Burton, 2016).

Meconium aspiration syndrome (MAS) affects 5% to 10% of newborns born with

meconium-stained fluid. Mechanical airway obstruction, chemical pneumonitis, and secondary
infection are all part of the MAS pathophysiology. Mechanisms of surfactant inactivation in MAS
include Disruption of the surfactant monolayer by fatty acids present in the meconium, producing
holes in type II cells by phospholipids, causing asymmetry surfactant monolayer, Bile acid-
induced calcium influx in type II cells, an influx of neutrophils producing proteases that degrade
surfactant 1 to 2 hours after aspiration, decreased levels of SP-A and SP-B (Zanelli & Kaufman,
2019).

II. CLINICAL MANIFESTATIONS

Chief Complaint: Respiratory distress, including cyanosis, gasping respirations, grunting,

retractions, nasal flaring, and tachypnea.

Patient History

a. Past Health History

No past health history

b. Maternal Health History

A mother at the age of 33 had a prolonged labor of her child. The mother was
thought to be at her post-term pregnancy (43 wG).

c. Present Health History

Upon the completion of delivery, abnormal respiratory rate of the patient was observed
and increased respiratory effort was noticed, seen as audible grunting, nasal flaring, and
retractions. The patient was distinguished with cyanosis.

Initial laboratory was immediately performed. Arterial Blood Gas results revealed that
the patient had hypoxemia and hypercapnia. Chest radiograph shows patchy infiltrates or
irregular streaky, linear densities and consolidation throughout the lung fields.
Physical Assessment
General Survey

The infant quickly exhibits signs of respiratory distress, including cyanosis, gasping
respirations, grunting, retractions, nasal flaring, and tachypnea. The newborn has a 5-
minute Apgar score of 4 (Activity: 0- absent, Pulse: 2-over 100 bpm, Grimace: 0-flaccid,
Appearance: 0- pale, blue, Respiration: 2- vigorous cry). Glasgow coma scale of 8 (Eye response:
2- to pain, Verbal response: 2-grunts or moan to pain, Motor response: 4- withdraws to pain). The
initial vital signs of the newborn show the respiratory rate of 75cpm, Systolic Blood pressure of
65 mmHg, Pulse rate of 160bpm, SpO2 85%, Temperature of 36.4℃.

APGAR SCORING SYSTEM

Activity 0 (absent)

Pulse 2 (over 100 bpm)

Grimace 0 (flaccid)

Appearance 0 (pale, blue)

Respiration 2 (Vigorous cry)

4 - Moderately Depressed

GLASGOW COMA SCALE

Eye Response 2 (To Pain)

Verbal Response 2 (Grunts or moan to pain)

Motor Response 4 (Withdraws to pain)

GCS SCORE: 8
Severe

Vital Signs:
RR- 60 cpm, Systolic BP- 65 mmHg, PR- 160bpm, SpO2 85%, Temperature of 36.4℃.
Cephalocaudal Assessment

Head
• Microcephalic, no lesions and deformities present, Hair color is black and fine

Eyes
• Eyes of newborn were amblyopia
• Color of both eyes were dark brown

Ears
• Position of the ears is lower than the head

Nose
• Nasal flaring are observe

Mouth
• Blue discoloration can be seen around the lips and mouth

Neck
• Clavicles are intact, tonic neck reflex is present, neck-righting reflex is present,
short and thick

Thorax and Lungs

• Gasping respirations, grunting, retractions,

Abdomen
• Dome-shaped abdomen, Abdominal respirations
• Soft to palpation, Well-formed umbilical cord, cord dries at base

Upper extremities
• Hypothermia is present on the hands
• Cyanosis is seen

Lower extremities
• Hypothermia is present on the feet
• Cyanosis is seen
Reflex

Root Reflex MET The corner of a baby's mouth touches the skin or nipple

Suck Reflex UNMET The baby is newborn

Moro Reflex UNMET The newborn has no active movements

Tonic neck UNMET The side of the infant's spine is stroked or tapped while the infant lies
Reflex on the stomach.

Grasp Reflex MET Stroking the palm of a baby's hand causes the baby to close his or
her fingers in a grasp.

Babinski MET The sole of the foot has been firmly stroked. The big toe then moves
Reflex upward or toward the top surface of the foot.

Step Reflex UNMET The baby is newborn

Differential Diagnosis

• Respiratory Distress Syndrome

• Transient Tachypnea of Newborn
• Congenital heart disease
III. RISK FACTORS

Factors associated with increased risk of meconiumstained fluid and subsequent

development of MAS include the following:

• Maternal hypertension
• Maternal diabetes
• Preeclampsia or eclampsia
• Maternal heavy smoking or chronic respiratory or cardiovascular disease
• Post-term pregnancy (greater than 42 wG)
• Intrauterine growth retardation
• Abnormal biophysical profile
• Oligohydramnios
• Abnormal fetal heart rate and nonreassuring fetal heart rate tracing
• Presence of fetal distress
• Low 5-minute Apgar
• Ethnicity: Black Americans and Africans have increased risk when compared with
other groups. Those of Pacific Islander and indigenous Australian ethnicity are also
at increased risk.
• Home births

IV. PATHOPHYSIOLOGY
Fetal passage of meconium is accepted as a sign of intrauterine stress or hypoxia.
The infant becomes hypoxic in utero (possibly because of cord or fetal head compression or
prolonged labor), which exhausts oxygen reserves, causing a vagal response, relaxed anal
sphincter tone, and passage of meconium into the amniotic fluid (Farrash, 2015).

The fetus exhibits normal rapid, shallow respiratory chest movements during normal
intrauterine fetal development. While the glottis remains closed, this normal action moves
pulmonary fetal fluid into and out of the oropharynx. However, during periods of fetal hypoxia,
the fetus may exhibit very deep, gasping inspiratory movements, which may force the contents
of the naso-oropharynx to pass through the glottis and into the airways. The aspiration of
minimal amounts of clear amniotic fluid is not usually associated with serious anatomic or
functional problems of the lungs. During fetal hypoxemia, however, the aspirate may contain
meconium and amniotic fluid (Des Jardins & Burton, 2016).

Aspiration may also occur after delivery when the expansion of the chest allows the
fluid or meconium, or both, to be dispersed even deeper into the infant’s lungs. After delivery,
the normal pulmonary mechanisms are hindered in the setting of MAS. Aspirated meconium
causes a ball-valve effect because of partial obstruction of the airways. Inflammation of the
airways and secretion production (a normal response to a foreign substance within the lungs)
occurs, and chemical pneumonitis often develops. Meconium also inactivates surfactants,
which may lead to atelectasis and decreased pulmonary compliance. It has been proposed
that intrauterine hypoxia not only stimulates meconium passage but also causes pulmonary
vascular bed restructuring. The hypoxia may result in pulmonary vasoconstriction, which
causes many infants with MAS to then develop PPHN (Hansen & Levin, 2019).
 V. DIAGNOSTICS

a. Meconium Aspiration Syndrome

Diagnosis is suspected when a neonate shows respiratory distress in the setting of

Meconium-tinged amniotic fluid and is confirmed by chest x-ray showing hyperinflation with
variable areas of atelectasis and flattening of the diaphragm. The aspiration of meconium (the
neonate’s intestinal discharge) into the lungs. Typically occur with the first breath or while the
neonate is in utero (Perretta, J. S., 2014).
VI. MANAGEMENT & TREATMENT

a) MECONIUM ASPIRATION SYNDROME (MAS)

The focus of the management in MAS is respiratory support, and it may vary from
supplemental oxygen via nasal cannula to HFOV, inspired nitric oxide(iNO)v, and ECMO,
depending on the severity of disease. Singh reported the use of the following modalities in the
first day after birth to treat more than 7,000 infants over a 10-year period: RA (11%); oxygen
by hood (33%); nasal cannula (10%); continuous positive airway pressure (7%); CMV (28%);
high-frequency ventilation (8%); surfactant (16%); iNO (6.1%), and extracorporeal
oxygenation (1.4%). From 2000 to 2006, iNO and surfactant use increased. High-frequency
ventilation use remained constant at 6% to 9%, and vasopressors and extracorporeal
oxygenation use decreased (Perretta, 2014).

Care for newborns with MSAF begins in the delivery room and is adjusted based on the
level of hypoxemia, physical respiratory distress, and respiratory acidosis. PPHN is treated as
needed, using the strategies discussed in the previous section (Perretta, 2014).

• Delivery Room Interventions

Until 2005, all infants born through MSAF were routinely intubated and suctioned
with a meconium aspirator repeatedly until no meconium was observed in the ETT.
Several randomized studies,most recently published in 2004 by Lancet,concluded that, if
meconium-stained fluid is observed during a delivery, the infant’s oral and nasal pharynx
may be suctioned by the obstetrician once the head is delivered to prevent the additional
aspiration of meconium; however, intubation andtracheal suctioning should only be
attempted if the infant is unresponsive immediately after birth. Attempting an intubation on
a vigorous newborn may cause vocal cord trauma or initiate a vagal response caused by
the insertion of the laryngoscope (Perretta, 2014).

Although the evidence is not strong regarding suctioning versus non-suctioning,

the American Academy of Pediatrics (AAP) still recommends endotracheal suctioning of
non-vigorous babies with MSAF. A non-vigorous baby is defined as having:

o a depressed respiratory effort,

o poor muscle tone,
o and/or heart rate less than 100 bpm.

In this instance, it is acceptable to perform an intubation to suction the trachea

immediately after birth. Suction is limited to 5 seconds, and if no meconium is aspirated,
no further intubations for suctioning are recommended. If meconium is aspirated and no
bradycardia is present, a judgment is made whether to re-intubate and suction a second
time. If the heart rate is low, proceed to resuscitative efforts with drying, stimulating,
repositioning, and administering oxygen or positive-pressure ventilation (Perretta, 2014).
• A vigorous baby is one with:

o a normal respiratory effort,

o normal muscle tone,
o and heart rate greater than 100 bpm.

Such a baby would not be intubated; insteadthe mouth and nose may be suctioned
with a bulb syringe or a large-bore suction catheter for remaining meconium before
proceeding to neonatal resuscitative efforts with drying, stimulating, repositioning, and
administering oxygen or positive-pressure ventilation (Perretta, 2014).

To perform an intubation with intent to suction meconium from the trachea, an

appropriate-sized ETT is used, with a meconium aspirator connected to it, which will allow
attachment of wall suction and use of the ETT as a large-bore suction device within the
trachea. The infant should be placed in the sniffing position by the nurse, RT, or physician
with a small neck roll under the infant’s shoulders. This will create a straight view of the
vocal cords. The laryngoscope is inserted with the left hand by gently opening the infant’s
mouth with thumb or finger and then gently sliding the blade into the mouth. The blade
should be inserted only far enough to lift the epiglottis up out of the way to bring the chords
into view. Care should be taken to not rock back onto the gums, which could cause
damage and bleeding. Once the cords are visualized, the ETT is inserted down the right
side of the mouth, being careful not to obstruct the view, only far enough to watch the
glottis markings pass through the vocal cords. If a stylet was used to facilitate intubation,
this is removed before the meconium aspirator is attached to the end of the ETT. The 15-
mm adapter end of the meconium aspirator is attached to the ETT, and the nipple adapter
is attached to suction tubing connected to a suction regulator. Occlude the thumb port on
the meconium aspirator and withdraw the ETT. Assess the contents of the aspiration. If
there was a large amount of meconium and the infant’s heart rate has not dropped
significantly, try aspirating again. If the infant’s heart rate decreases or not much
meconium was aspirated, proceed to resuscitative efforts with drying, stimulating,
repositioning, and administering oxygen or positive-pressure ventilation (Perretta, 2014).

There was also a time when performing an amnioinfusion to reduce the incidence
of MAS was a common practice. Amnioinfusion is a procedure in which normal saline or
lactated Ringer’s solution is placed into the uterus after rupture of the amniotic sac. The
thought is that a dilution of meconium with warm sterile saline will minimize the severity
ofMAS. The evidence does not support amniofusion to prevent MAS, which may be
because an infant may pass meconium in utero long before it is noted clinically, thus
having no effect on the health out- comes for the baby (Perretta, 2014).

• Neonatal Management

There is currently no strategy to prevent MAS; therefore, treatment is mainly

supportive. Therapy goals are to maintain normoxemia and ventilation, to assure adequate
systemic blood pressure, and to correct acidosis and hypoglycemia when needed
(Perretta, 2014).
 • Oxygen Therapy

For mild cases of MAS, supplemental oxygen may be the only therapy required for
stabilization. Oxygen should be titrated as needed to maintain higher SpO2, preferably
monitoring preductal SpO2 for 94% to 98%. If a right arterial line is available (preductal),
oxygen should be titrated to maintain a PaO2 of 60 to 100 mm Hg. In mild cases, delivery
devices may include a nasal cannula or oxygen hood. NCPAP can also be used to provide
alveolar stabilization, airway stenting, and supplemental oxygen delivery. Pressures of 5 to 8
cm H2O can be used, and patients should be monitored for agitation and discomfort while on
NCPAP, which can exacerbate PPHN and necessitate intubation. If necessary, intubation and
mechanical ventilation will be provided for hypoxemic and hypercarbic respiratory failure
(Perretta, 2014).

• Mechanical Ventilation

Roughly 30% of newborns developing MAS will require some degree of ventilator
suppor. Indications for intubation and ventilation include the following:

o FIO2 greater than 0.80

o Respiratory acidosis with pH less than 7.25 forseveral hours
o Pulmonary hypertension
o Poor systemic blood pressure and perfusion

Initial management should focus on normalizing pH to 7.3 to 7.4 and maintaining PaCO2
of 40 to 60 mm Hg. There are few clinical trials regarding ventilator management for MAS, so few
definitive recommendations are available. General guidelines for ventilator support are similar to
those made for other neonates and include the following:

o Use a synchronized mode of ventilation whenever possible (Perretta, 2014).

o Monitor for ETT leak and avoid auto-triggering (Perretta, 2014).

o Use synchronized intermittent mandatory ventilation (SIMV) rather than assist/control

(A/C)to avoid air trapping and hyperinflation caused by inadvertent high respiratory rates
(Perretta, 2014).

o Use PEEP set at 4 to 7 cm H2O, increasing it when atelectasis is present and decreasing
it if significant overdistension is observed as flattened diaphragms on chest radiograph, or
if the patient exhibits signs of hemodynamic instability indicative of decreased venous
return (Perretta, 2014).

o Set inspiratory time (TI) around 0.5 seconds and use close monitoring to assure that TI
and expiratory time (TE) settings are enough for full exhalation, as evidenced by expiratory
flows returning to zero and end-expiratory pressures reaching set PEEP before the next
breath begins. TI may be increased to facilitate alveolar recruitment, but only if it does not
cause air trapping. Normal RRs for a healthy neonate are 30 to 60 breaths/min, but
patients with MAS should be maintained on a relatively low RR of less than 50 breaths/min
(Perretta, 2014).
o Target tidal volume at 4 to 6 mL/kg. This may require high peak inspiratory pressures
(PIP). If PIP must be maintained at greater than 30 cm H2O, then high-frequency
ventilation should be considered (Perretta, 2014).

Correctly selected ventilator settings should allow the patient’s work of breathing
(WOB) to diminish, as evidenced by a resolution of hypoxemia and retractions and a decrease
in spontaneous RR. As discussed previously, sedation may be needed to prevent agitation
and hypoxemic crisis in patients with MAS and PPHN (Perretta, 2014).

If the infant cannot be stabilized on a conventional ventilator as evidenced by blood

gases that are not improving and/or hemodynamic instability, then HFOV is an alternative
ventilation strategy to provide alveolar ventilation in patients with poor lung compliance. HFOV
employs an open-lung strategy to minimize volutrauma and atelectrauma and may prevent
air-leak syndrome in MAS patients. A combination of HFV and iNO administration has been
linked to a greater improvement in oxygenation in severe MAS with PPHN (Perretta, 2014).

Initiation of HFOV may require a high Paw to recruit atelectatic alveoli, and most
infants with MAS should be able to be stabilized with a Paw of 16 to 20 cm H2O. Paw should
be weaned as tolerated to prevent interference with systemic blood pressure. Because of the
risk of air trapping with MAS, hertz levels used are lower than those typical for other
populations of neonates. An initial hertz of 10 is reasonable, and 8 or 6 may be necessary if
PaCO2 cannot be managed using ΔP. As previously recommended, TI should be set to 33%
and ΔP set to provide adequate chest wiggle factor.Hypoxia, acidosis, and hypoxia from
increased pulmonary vascular resistance are common in this patient population, and arterial
blood gases are frequently monitored (Perretta, 2014)

• Surfactant-Replacement Therapy

Surfactant-replacement therapy is an appealing therapy for MAS because meconium

can cause surfactant dysfunction and inactivation. Meconium may also outcompete for space
in the alveoli, making it necessary to replace lost surfactant. Surfactant has not been shown
to decrease the mortality rate in this population, but it has been demonstrated to reduce the
severity of the disease and decrease hospital length of stay. It is presumed that surfactant
administration may be more beneficial after the meconium is no longer in the airway (Perretta,
2014).

• Pulmonary Vasodilators

Infants with MAS and PPHN can benefit from pulmonary vasodilators in the same way
as newborns with idiopathic PPHN, and the most frequently used pulmonary vasodilator is
inhaled nitric oxide (iNO). Around one-quarter of all ventilated MAS newborns are treated with
inhaled nitric oxide(iNO), with about half showing a positive response. The focus of iNO
therapy with MAS should be to optimize lung inflation prior to initiation to maximize the
likelihood of a positive response. Gupta and colleagues used gentle CMV with permissive
hypercapnia and iNO and reported an overall mortality rate of 9.8% in infants with MAS and
PPHN (Perretta, 2014).
 • Extracorporeal Membrane Oxygenation

MAS is one of the most common diagnoses among neonates treated with ECMO.
MAS patients make up about 35% of patients requiring ECMO, and the initiation criteria
are the same as for other causes of hypoxic respiratory failure. ECMO survival is high for
MAS, nearing 95%, even with ECMO being used less frequently since the advent of iNO
(Perretta, 2014).

• Cardiovascular Support

Cardiovascular support will include intravenous fluids and inotropic agents, such
as:

o dopamine,
o dobutamine,
o and epinephrine.

This support should be provided when the patient exhibits a decreased cardiac
output, as evidenced by hypotension, decreased pulses, and slow capillary refill. Fluid
management will begin as clear fluids for initial resuscitation and stabilization. Total
parenteral nutrition will begin after 12 to 24 hours, which will be based on electrolyte
values.In addition to respiratory and cardiovascular compromise (hypoxia and hypoxemia,
hypotension), infants with MAS are also at risk for hypoglycemia, hypothermia, sepsis,
and limited parental involvement (Perretta, 2014).

Transient Tachypnea of Newborn

I. DEFINITION

Transient tachypnea of the newborn (TTN) is a condition of term or near-term infants,

characterized by mild respiratory distress during the first few hours of life. It is caused by failure
to clear fetal lung fluid prior to delivery. It is a self-limiting disorder, typically resolving itself within
48 to 72 hours of life. At delivery, TTN maybe be difficult to differentiate from other causes of
respiratory distress, such as sepsis, aspiration, and pneumonia. The exact incidence of TTN is
not known, but a 2012 publication estimated that it occurs in 0.5% to 2.8% of live births and in as
many as 30% of elective cesarean section (Peretta, 2014).

Transient tachypnea of the newborn (TTN) is a breathing disorder seen shortly after delivery in
early term or late preterm babies. Transient means it is short-lived (most often less than 48 hours).
Tachypnea means rapid breathing (faster than most newborns, who normally breathe 40 to 60
times per minute)
Transient tachypnea of the newborn (TTN) is a benign, self-limited condition that can present in
infants of any gestational age, shortly after birth. It is caused due to delay in clearance of fetal
lung fluid after birth which leads to ineffective gas exchange, respiratory distress, and tachypnea
(Perretta, 2014)

II. CLINICAL FINDINGS

Chief Complaint: Tachypnea, cyanosis, grunting, retractions, and nasal flaring within the first
hours after birth.

Patient History

A. Past Health History

No past health history

B. Maternal Health History

A mother at the age of 29 years old diagnosed with maternal asthma and had a breech
delivery, so the mother underwent cesarean section.

C. Present Health History

Upon the completion of delivery, abnormal respiratory rate of the patient was observed,
seen as audible grunting, retractions, and nasal flaring within the first few hours after birth.
The patient was distinguished with cyanosis as well.

Also, Infant’s History includes maternal analgesia or anethesia during labor and
delivery or episodes of interuterine hypoxia.

Initial laboratory was immediately performed. ABG analysis reveals mild to moderate
hypoxemia, hypercapnia, and respiratory acidosis. CXR may show pulmonary vascular
congestion, prominent perihilar streaking, fluid in the interlobular fissures, hyperexpansion,
and a flat diaphragm. Mild cardiomegaly and pleural effusions are also present.
Physical Assessment
General Survey

Upon assessment, the newborn exhibits tachypnea, cyanosis, seen as audible grunting,
w/ chest retractions, and manifests nasal flaring.The newborn has a 5-minute Apgar score of 8
(Activity: 2- active movement, Pulse: 2-over 100 bpm, Grimace: 2- active motion, Appearance: 0-
pale, blue, Respiration: 2- vigorous cry) and Glasgow coma scale of 8 (Eye response: 2- to pain,
Verbal response: 2-grunts or moan to pain, Motor response: 4- withdraws to pain).

APGAR SCORING SYSTEM

Activity 2 (active movement)

Pulse 2 (over 100 bpm)

Grimace 2 (active motion)

Appearance 0 (pale, blue)

Respiration 2 (Vigorous cry)

8 - Excellent Condition

GLASGOW COMA SCALE

Eye Response 2 (To Pain)

Verbal Response 2 (Grunts or moan to pain)

Motor Response 4 (Withdraws to pain)

GCS SCORE: 8
Severe coma

Vital Signs:

• RR - 100cpm, HR - 168/min, SpO2 - 85%, BP - 75/45

Cephalocaudal Assessment

Head
• Microcephalic, no lesions and deformities present, Hair color is black and fine

Eyes
• Eyes of newborn were amblyopia
• Color of both eyes were dark brown

Ears
• Position of the ears is lower than the head

Nose
• Nasal flaring is observe

Mouth
• Blue discoloration can be seen around the lips and mouth

Neck
• Clavicles are intact, tonic neck reflex is present, neck-righting reflex is present,
short and thick

Thorax and Lungs

• Grunting, Intercostal retractions

Abdomen
• Dome-shaped abdomen, Abdominal respirations
• Soft to palpation, Well-formed umbilical cord, cord dries at base

Upper extremities
• Hypothermia is present on the hands
• Cyanosis is seen

Lower extremities
• Hypothermia is present on the feet
• Cyanosis is seen

Reflex

Root Reflex MET The corner of a baby's mouth touches the skin or nipple.

Suck Reflex UNMET The baby is newborn

 Moro Reflex MET The newborn suddenly splaying their arms and moving their
legs before bringing their arms in front of their body

Tonic neck UNMET The side of the infant's spine is stroked or tapped while the infant lies
Reflex on the stomach.

Grasp Reflex MET Stroking the palm of a baby's hand causes the baby to close his or
her fingers in a grasp.

Babinski MET The sole of the foot has been firmly stroked. The big toe then moves
Reflex upward or toward the top surface of the foot.

Step Reflex UNMET The baby is newborn

Differential Diagnosis

• Respiratory Distress Syndrome

• Meconium Aspiration Syndrome

III. RISK FACTOR

Below are the risk factors that have been suggested to increase the likelihood of TTN:

• Delivery via cesarean section

• Macrosomia
• Maternal asthma
• Maternal diabetes
• Male gender
• Negative PG presence test of amniotic
 • Maternal fluid overload
• Delayed clamping of umbilical cord
• Breech delivery
• Polycythemia
• Prematurity
• Very low birth weight (less than 1,500 g)
• Maternal drug dependence
• Maternal sedation
• Perinatal depression
• Precipitous delivery
• Prolonged labor

IV. PATHOPHYSIO

Fetal lung fluid is necessary for normal fetal lung development. It is secreted by type II
alveolar cells to stabilize the structure of the lung in utero. In late gestation and shortly before
birth, fetal lungs convert from fluid secretion to fluid reabsorption. Fetal adrenaline released during
labor inhibits the chloride channel within type II cells, which causes the secretion of lung fluid. It
simultaneously stimulates sodium channels, which absorb lung fluid. This signals the epithelial
cells of the lung to stop secreting and start reabsorbing lung fluids. Through this mechanism, the
lungs of a healthy term neonate at birth contain only a minimal amount of lung fluid. The majority
of the fluid left is mechanically expelled during delivery, with additional clearance being facilitated
by the ciliary escalator through the upper airway, mediastinum, and pleural space (Mola et al.,
2014).

TTN causes a delay in lymphatic and pulmonary capillary absorption of pulmonary fluid.
This condition is thought to be caused in part by the infant's hypoxia and insufficient inspiratory
effort, which causes a delay in pulmonary fluid clearance. The infant develops pulmonary capillary
congestion, interstitial edema, decreased lung compliance, decreased tidal volume, and
increased dead space as this condition worsens. The clearance of bronchial secretions is
compromised in infants with TTN because their swallowing and coughing efforts are commonly
depressed. Although TTN is primarily a restrictive lung disorder, excessive airway secretions may
lead to air trapping and alveolar hyperinflation. Excessive fluid accumulation throughout the
alveolar-capillary interstitial tissue can compress the bronchial airways in severe cases. The
abnormal anatomic alterations of the lungs associated with TTN, on the other hand, usually begin
to resolve 48 to 72 hours after birth. The major pathologic or structural changes associated with
TTN decreased removal of fluid by pulmonary lymphatics, pulmonary capillary congestion,
interstitial edema, excessive bronchial secretions and incomplete absorption of pulmonary fetal
fluid, air trapping and alveolar hyperinflation, and compressed bronchial airways (from excessive
alveolar-capillary interstitial fluid) (Des Jardins & Burton, 2016).
 V. DIAGNOSIS

A. Transient Tachypnea of the Newborn (TTN)

Doctors usually diagnose transient tachypnea of the newborn in the first few hours
after a baby is born.It is confirmed by radiograph. The Chest X-ray is safe and painless
test uses a small amount of radiation to take a picture of the chest. Doctors can see if the
lungs have fluid in them. However, it may be difficult to tell whether the problem is TTN or
another kind of respiratory problem, such as respiratory distress syndrome (also known
as hyaline membrane disease). Often, TTN is diagnosed when symptoms suddenly
resolve by the third day of life. (Mola et.al., 2014)

VI. MANAGEMENT & TREATMENT

A. Transient Tachypnea of the Newborn (TTN)

The normal course of treatment in neonatal pneumonia is multifaceted and

includes appropriate antibiotic or antiviral therapy, oxygenation, adequate ventilation, and
pharmacotherapy. To prevent rapid deterioration, early intervention, aggressive
management, and continuous monitoring are required, especially in the infant with early-
onset GBS disease (Perretta, 2014).

Also, the treatment of TTN is supportive, including supplemental oxygen,

withholding of enteral feeds, and administration of intravenous fluids and antibiotics.
Infants with TTN are also at risk for hypoglycemia, hypothermia, and sepsis, and support
for these are given on an as-needed basis (Walsh, 2015).

Oxygen therapy is a mainstay of care fornewborns with TTN. Typical oxygen

delivery includes an oxygen hood or nasal cannula connected to an air-oxygen blender,
titrated to maintain SpO2 90% to 96%. Moderate respiratory distress may require NCPAP
of 4 to 6 cm H2O to resolve grunting or retracting. Gradual improvement will be seen over
48 to 72 hours, and an FIO2 of less than 0.40 is usually sufficient. Armangil et al. attempted
a trial of salbutamol, an inhaled beta-2 agonist, for the treatment of TTN and found that it
improved blood gas values, decreased RR, and allowed for weaning of FIO2 when
compared with placebo (Perretta, 2014).

Supportive care for thermoregulation, fluid, and nutrition is indicated. Nutritional

status should be supported as needed because nursing or bottle feeding may initially be
unsuccessful owing to tachypnea. Parental nutrition may be included, but continuous
enteral feeds are often tolerated after initial stabilization. Hypothermia can be monitored
and infants should be in a neutral thermal environment such as an incubator or radiant
warmer. Evaluation is necessary to rule out sepsis as a cause of respiratory dis- tress.
Additional cardiovascular support is rarely indicated (Perretta, 2014).

Maternal corticosteroids have been suggested to accelerate resorption of fetal lung

fluid. A single, 2-day course of antenatal steroids 48 hours before elective cesarean at 37
 to 38 weeks appears to improve respiratory morbidity from TTN. Its mechanism of action
may be twofold: Antenatal steroids accelerate lung maturation and surfactant maturation,
and they may also enhance sodium channel activity (Perretta, 2014).

• Respiratory Support

Assurance of airway patency may be more challenging in neonates with

pneumonia because of the often profuse, potentially obstructive secretions and
mucopurulent exudates of variable viscosity. Judicious suctioning is warranted. Deep
suctioning should be avoided because it can cause airway trauma and swelling, which in
turn may cause large airway obstruction.The infant with cyanosis, hypoxemia, and
hypercapnia may require mechanical ventilation to maintain oxygenation. The most
critically ill infants may need high ventilatory settings with high PIP, ventilatory rate, and
oxygen levels. ABG values and transcutaneous monitors, or pulse oximetry, or both, are
used to monitor the patient’s respiratory status (Walsh, 2015).

• Extracorporeal Membrane Oxygenation

Near-term and term infants who are unresponsive to conventional ventilation and
other supportive measures may benefit from extracorporeal membrane oxygenation
(ECMO). Improved rates of survival have been reported in this group (Walsh, 2015).