6. TransientTachypnea of Newborn
TTN (known as wet lung) is a relatively mild,
self limiting disorder of near-term or term
Delay in clearance of fetal lung fluid results in
transient pulmonary edema. The increased
fluid volume causes a reduction in lung
compliance and increased airway resistance.
7. TransientTachypnea of Newborn
Risk factors:
Maternal asthma
C- section
Macrosomia, maternal diabetes
Prolonged labor, Excessive maternal sedation
Fluid overload to the mother,Delayed clamping of the
umbilical cord .
8. TransientTachypnea of Newborn
Usually near-term or term
Tachypnea immediately after birth or within 6 hrs
after delivery, mild to moderate respiratory distress.
These manifestations usually persist for 12-24 hrs,
but can last up to 72 hrs
Auscultation usually reveals good air entry with or
without crackles
Spontaneous improvement of the neonate is an
important marker of TTN.
9. TransientTachypnea of Newborn
Chest x-ray :
Prominent perihilar streaking (due to engorgement of
periarterial lymphatics)
Fluid in the minor fissure
Prominent pulmonary vascular markings
Hyperinflation of the lungs, with depression of
diaphragm
► Chest x-ray usually shows evidence of clearing by 12-
18 hrs with complete resolution by 48-72 hrs
11. General Management of Respiratory Distress
Supplemental oxygen or MV, if needed.
Continuously monitor with pulse oximeter.
Obtain a chest radiograph.
Correct metabolic abnormalities
(acidosis,hypoglycemia).
Obtain a blood culture & begin an antibiotic
coverage (ampicillin + gentamicin)
12. General Management
Provide an adequate nutrion. Infants with
sustained RR >60 breaths/min should not be fed
orally & should be maintained on gavage feedings
for RR 60-80 breaths/min, and NPO with IV fluids
or TPN for more severe tachypnea
14. Respiratory Distress Syndrome
Also called as hyaline membrane disease
Most common cause of respiratory distress in
premature infants, correlating with structural &
functional lung immaturity.
primarily affects preterm infants; its incidence is
inversely related to gestational age and
birthweight.
15-30% of those between 32-36 weeks‘ gestation,
in about 5% beyond 37 weeks' gestation
15. Physiologic abnormalities
Surfactant deficiency- increase in alveolar
surface tension.
Lung compliance decreased to 10-20% of
normal
Atelectasis…areas not ventilated
Decrease alveolar ventilation
Reduce lung volume
Areas not perfused
20. Clinical Manifestations
Appear within minutes of birth may not be recognized for several
hours in larger preterm
Tachypnea (>60 breaths/min), nasal flaring, subcostal and intercostal
retractions, cyanosis & expiratory grunting
Breath sounds may be normal or diminished and fine rales may be
heard
Progressive worsening of cyanosis & dyspnea. BP may fall; fatigue,
cyanosis and pallor increase & grunting decreases.
Apnea and irregular respirations are ominous signs
In most cases, symptoms and signs reach a peak within 3 days, after
which improvement occurs gradually.
21. Findings can be graded according to the severity:
Grade 1 (mild cases): the lungs show fine
homogenous ground glass shadowing
Grade 2: widespread air bronchogram become
visible
Grade 3: confluent alveolar shadowing
Grade 4: complete white lung fields with obscuring
of the cardiac shadow
Chest x-ray:
26. Management
Prevention:
Lung maturity testing: lecithin/sphingomyelin (L/S) ratio
Tocolytics to inhibit premature labor.
Antenatal corticosteroid therapy:
► They induce surfactant production and accelerate fetal lung
maturation.
► Are indicated in pregnant women 24-34 weeks' gestation at
high risk of preterm delivery within the next 7 days.
► Optimal benefit begins 24 hrs after initiation of therapy and
lasts seven days.
27. Prevention
Antenatal corticosteroid therapy consists of either :
□ Betamethasone 12 mg/dose IM for 2 doses, 24 hrs apart, or
□ Dexamethasone 6 mg/dose IM for 4 doses, 12 hrs apart
Early surfactant therapy: prophylactic use of
surfactant in preterm newborn <27 weeks'
gestation.
Early CPAP administration in the delivery room.
28. Treatment
Administer oxygen
Initiate CPAP as early as possible in infants with mild
RDS
Start MV if respiratory acidosis (PaCO2 >60 mmHg,
PaO2 <50 mmHg or SaO2 <90%) with an FiO2 >0.5, or
severe frequent apnea.
Administer surfactant therapy: early rescue therapy
within 2 hrs after birth is better than late rescue
treatment when the full picture of RDS is evident.
29. Types of Surfactant
Natural Surfactants: contain appoproteins SP-B & SP-C
Curosurf (extract of pig lung mince)
Survanta (extract of cow lung mince)
Infasurf (extract of calf lung)
Synthetic Surfactants:do not contain proteins
Exocerf
ALEC
Lucinactant (Surfaxin)
30. 30
SurfactantTherapy for RDSSurfactantTherapy for RDS
Improvement in compliance, functional
residual capacity, and oxygenation
Reduces incidence of air leaks
Decreases mortality
31. Mode of administration of Surfactant
Dosing may be
divided into 2
alliquots and
adminitered via
a 5-Fr catheter
passed in the
ET
35. Clinical Manifestations
Meconium staining amniotic fluid (meconium stained
nails, skin & umbilical cord )
Some infants may have mild initial respiratory
distress, which becomes more severe hours after
delivery.
Pneumothorax and/or pneumomediastinum
PPHN in severe cases
Hypoxia to other organs (e.g., seizures, oliguria)
37. Chest x-ray: Areas of hyperexpansion mixed with patchy
densities and atelectasis
38. Management
In the DR or OR:
Visualization of the vocal cords & tracheal suctioning before
ambu-bagging should be done only if the baby is not vigorous
In the NICU:
Empty stomach contents to avoid further aspiration.
Suction frequently & perform chest physiotherapy.
39. Management
Consider CPAP, if FiO2 requirements >0.4; however CPAP
mayaggravate air trapping and must be used cautiously.
Mechanical ventilation: in severe cases (paCO2 >60 mmHg
orpersistent hypoxemia (paO2 <50 mmHg).
Correct systemic hypotension (hypovolemia, myocardial
dysfunction).
Manage PPHN, if present
Manage seizures or renal problems, if present.
Surfactant therapy in infants whose clinical status continue
todeteriorate.
42. Clinical Manifestations
Early manifestations may be nonspecific (e.g., poor
feeding, lethargy, irritability, cyanosis, temperature
instability
Respiratory distress signs may be superimposed upon RDS
or BPD.
In a ventilated infant, the most prominent change may be
the need for an increased ventilatory support.
Signs of pneumonia (dullness to percussion, change in
breathsounds, rales or rhonchi) are difficult to appreciate.
44. 44
Chlamydia pneumonia with features of an interstitial
pneumonitis and characteristic widespread interstitial changes.
45. Management
Initiate ampicillin and gentamicin IV;
modify according to culture results
and continue therapy for 14 days.
If there is a fungal infection, an
antifungal agent is used.
47. Air Leak Syndromes
Risk Factors:
MV,MAS, surfactant therapy without
decreasing pressure support in ventilated
infants
vigorous resuscitation,
prematurity
pneumonia
48. Clinical Manifestations
Spontaneous pneumothorax may be asymptomatic or
only mildly symptomatic (i.e., tachypnea and ↑O2
needs).
In unilateral cases, chest asymmetry is noted,
mediastinum shift to the opposite side.
If the infant is on ventilatory support will have sudden
onset of clinical deterioration (i.e., cyanosis,
hypoxemia, hypercarbia & respiratory acidosis
associated with decreased breath sounds and shifted
heart sounds).
49. Tension pneumothorax
(a life-
threatening
condition) →
↓cardiac
output and
obstructive
shock; urgent
drainage prior
to a radiograph
is mandatory.
52. Left-sided pneumothorax under tension.There is pulmonary interstitial
emphysema in the right lung and a small basal right pneumothorax.
53. Others
Pneumomediastinum
It can occur with aggressive ETT insertion, Ryle's feeding tube
insertion, lung disease, MV, or chest surgery (e.g., TEF).
Pneumopericardium
Pneumoperitoneum
Subcutaneous emphysema
Systemic air embolism
57. Severe bilateral PIE affecting the right more than the left lung; there is gross
cardiac compression. A chest drain is in situin the right hemithorax.
58. Management
Conservative therapy: close observation of the
degree of respiratory distress as well as oxygen
saturation, without any other intervention aiming
at spontaneous resolution and absorption of air.
Needle aspiration should be done for suspected
cases of pneumothorax with deteriorating general
condition until intercostal tube is inserted.
Decompression of air leak according to the type
(intercostal tube insertion in case of pneumothorax).