RESPIRATORY DISORDERS OF THE NEWBORN  When the baby exhales, because of no established functional

residual capacity, the alveoli collapse back. Hence on the

SURFACTANT SYSTEM succeeding respiration, the baby will always require a high
inspiratory pressure.
 produced by pneumocyte II  because of surfactant deficiency, this leads to atelectasis of the
 reduces alveolar surface tension hence preventing collapse of alveoli 
the alveoli o V/Q mismatch or inequality
 gets recycled after release into the alveoli in 72 hours o hypoventilation
 both of the above leads to:
COMPOSITION o hypoxia
 phosphatidylcholine (50-60%) o hypercarbia
o saturated phosphatidylcholine (35%)  the baby will lead into combined respiratory and metabolic
o unsaturated phosphatidylcholine (30%) acidosis  pulmonary (and systemic) vasoconstriction 
 neutral lipids (10%) impaired endothelial and epithelial integrity  proteinaceous
 surfactant proteins (10%) exudate into the alveoli (seen on xray as ground glass
o surfactant protein A appearance)  which again leads to further decrease of
 hydrophobic collectin surfactant or available lung area for adequate respiration, and
 has immune defense function hence become a vicious cycle until the baby’s demise
o surfactant protein B o if pulmonary constriction persists for considerable
 spreading factor of the surfactant period of time, this will eventually lead to persistent
 genetic absence: lethal form or RDS (even among pulmonary hypertension of the newborn
term babies)  because of hypoxia and hypercarbia, the tendency to treat them
o surfactant protein C is to provide mechanical ventilation:
 hydrophilic o the baby requires high inspired oxygen and
 aids in spreading surfactant inspiratory to improve the baby’s oxygenation
 genetic absence: chronic lung disease  but due to structural immaturity, and
o surfactant protein D deficiency as well of anti-oxidant
 small hydrophobic collectin (superoxide dismutase)  free radicals
 also helps in immune defense reaction  lung injury
 other phospholipids:  these two also will tend to recruit
o phosphatidylinositol – elevated among more preterm inflammatory cells into the alveolar space,
infants and releases cytokines. Inflammatory cells
o phosphatidylethanolamine and cytokines can work together to further
o phosphatidylglycerol – found in high amounts when the cause injury to the alveolar epithelium and
baby is near term capillary endothelium hence more exudate
can escape further into the alveoli
FORMS  cytokines likewise help in lung injury
 tubular myelin sheath o lung injury then eventually leads to chronic lung
o surface active form of surfactant disease of the newborn (BPD)
o arrange themselves either in monolipid layer or
multilayer RADIOLOGY
 lamellar bodies  reticulogranular pattern
o nascent storage form prior to its release into the  air bronchogram
alveolar surface  white lung pattern/ground glass appearance
 vesicular bodies
o recycled form of surfactant PREVENTION
 antenatal steroids
o given between 24-34 weeks
RESPIRATORY DISTRESS SYNDROME o besides lung maturation, antenatal steroids also help
prevent the following:
CAUSES  NEC
RISK FACTORS MECHANISM  PDA
Prematurity, low birth weight Surfactant deficiency  ICH
Genetic defect Absence of surfactant protein  BPD
(spreading factors) o betamethasone 12 mg OD x 2 doses
Perinatal asphyxia, neonatal Surfactant inactivation o dexamethasone 6 mg q12h x 4 doses
pneumonia o ideally last dose should be given at least 24 hours
Uncontrolled maternal diabetes Immature form of surfactant prior to termination of pregnancy.
 in case of inevitable delivery, any dose
CLINICAL MANIFESTATIONS given prior to delivery will still be of benefit
o in cases when mother gets repeated preterm labor,
 onset may be immediately within or few hours after birth
only one course of antenatal steroid will do.
 main characteristic: increasing oxygen requirement
o repeated administration of antenatal steroids
 tachypnea
whenever the mother has preterm labor may also
 alar flaring attenuate the alveolarization of the fetal lung and
 grunting hence prolonged oxygen dependence on the baby
 retractions
 cyanosis TREATMENT
 apnea  exogenous surfactant therapy:
 pallor (anemia, peripheral vasoconstriction) o bovine (survanta) 4mL/kg
o porcine (curosurf) 100 mg/kg
PATHOPHYSIOLOGY  ventilatory support:
 because of atelectasis, the alveoli will require very high o mechanical ventilator
inspiratory pressure to open and distend them (shown as deep o nasal CPAP
retractions clinically)  INSURE therapy:
o INtubate
 o administer SURfactant o fetus gasps  with rapid inhalation of amniotic fluid,
o Extubated to NCPAP including all particulates dissolved in it
 maintain oxygen saturation between 88-95% strictly. o meconium thus can occur antenatally
o higher oxygen saturation predisposes the preterm to
oxygen radical injuries: RISK FACTORS
 bronchopulmonary dysplasia  fetal tachycardia
 retinopathy of prematurity  MSAF
o when the baby is maintained on low oxygen  non-reassuring fetal heart rate pattern (fetal distress)
saturation, they tend to develop more septated alveoli  oligohydramnios
compared to when they are exposed to high oxygen  post-maturity
saturation.
 general supportive measures: PATHOPHYSIOLOGY
o acid-base balance  when meconium is aspirated, there are three effects to the
o nutrition lungs:
o temperature o mechanical obstruction of the airways
o infection o chemical inflammation
o surfactant inactivation
TRANSIENT TACHYPNEA OF THE NEWBORN  Mechanical Obstruction:
(RESPIRATORY DISTRESS SYNDROME II) o complete
 when the entire airway is occluded by meconium
 transient respiratory distress secondary to alveolar fluid  leads to resorptive atelectasis of the distal alveoli
retention o partial
 risk factors:  more dangerous
o CS delivery without prior labor  when baby inhales, air enters the airway to the
 labor causes elevation of epinephrine  distal aveoli
transmitted to the fetus  greater oncotic  when the baby exhales, the meconium, like in a
pressure  greater alveolar fluid resorption into ball-valve effect, obstructs the airways, causing now
the fetal circulation air trapping in the alveoli
o failure to initiate first breaths effectively  when this gets repeated and the alveoli is distended
 inability to breath effectively immediately at birth beyond its capacity, it can lead to rupture of the
can delay replacement of alveolar fluid with air alveoli  air leak syndrome
 can sustain the relatively hypertensive o air trapping causes:
pulmonary pressure  air leak syndrome
o prolonged administration of hypotonic fluid  V/Q mismatch
 both of the above can lead to hypoxemia and
CLINICAL MANIFESTATIONS acidosis
 mild cyanosis  Chemical inflammation:
 grunting o can lead to atelectasis  intrapulmonary shunting 
 flaring hypoxemia, acidosis
 retractions  Surfactant inactivation
 tachypnea o leads to intrapulmonary shunting  hypoxemia and
 most resolves within 12-24 hours, 72 hours in severe cases acidosis
 when hypoxemia and acidosis do not get corrected, this leads to
ROUTES OF ALVEOLAR FLUID ABSORPTION thickening of the walls of the pulmonary capillaries surround the
 hematogenous (60%) alveoli  requires prolonged transport of oxygen from alveoli to
 lymphatics (12 %) the capillaries  cyanosis (persistent pulmonary hypertension)
 vaginal squeeze
 aspiration CLINICAL FEATURES
  signs of postmaturity
 neurologic and respiratory depression
RADIOLOGY: o severe respiratory distress incongruent with the
 perihilar streaks benign radiologic findings
 patchy infiltrates  hyperinflation (increased AP diameter)
 hyperaeration  rales
 clears within 48 hours
RADIOLOGY
TREATMENT  patchy infiltrates with interspersed areas of aeration
 oxygen support  hyperaeration, flattened diaphragm
 NCPAP in severe cases  cardiomegaly

PREVENTION
MECONIUM ASPIRATION SYNDROME  amnio-infusion
o to relieve in-utero cord compression  no hypoxia 
 meconium aspiration of amniotic fluid/fetus usually indicates no meconium passage
fetal distress  direct tracheal suctioning
o passage of meconium in utero accompanies 8-20% of all o upon baby’s birth, he is intubated and meconium is
deliveries aspirated before the baby’s first cry/breath
o SGA and postmature, those with fetal distress o may repeat doing it as long as HR is >60 bpm
o seldom meconium is passed out before 34 weeks of  if HR is <60 bpm, even with still meconium
gestational age present, stop suctioning then continue with
 meconium aspiration syndrome occus in 4% of deliveries with resuscitation
MSAF
 during normal respiration: fluid moves rhythmically from alveoli TREATMENT
into the amniotic fluid cavity  meconium is STERILE
 during fetal distress:  antibiotics for suspected chorioamnionitis
 ventilatory assistance: o increased cerebral blood flow (superior vena cava
o CPAP syndrome)  intracranial hemorrhage, especially
o mechanical ventilator among preterms
o high frequency oscillator ventilator  pneumopericardium:
 extracorporeal membrane oxygenation (ECMO) o rare
 surfactant administration o can cause cardiac tamponade
o suspected in patients with
PROGNOSIS  air leak syndrome
 oxygenation index  sudden cardiovascular collapse
= (FiO2 x Paw) x 100  narrow pulse pressure
paO2
if > 25 cmH2O/mmHg – indicative of severe respiratory distress DIAGNOSIS:
if > 43 cmH2O/mmHg – poor prognosis, impending death  transillumination test
o darkened room
o >1cm ring around the light source
NEONATAL PNEUMONIA  x-ray
 needling aspiration
TRANSMISSION
 transplacental TREATMENT
 vertical  asymptomatic: no treatment
 horizontal (nosocomial)  nitrogen wash off:
o 100% oxygen delivered via oxygen hood
CLINICAL MANIFESTATIONS  needle aspiration/thoracentesis
 clinical signs are nonspecific:  thoracotomy tube insertion
o thermal instability  PIE: HFOV
o apnea
o neurologic depression
o abdominal distention
o retractions

RADIOLOGY
 unilateral/bilateral streaky densities
 confluent mottled opacified areas
 diffusely granular appearance with air bronchogram

TREATMENT
 broad spectrum coverage:
 EO: penicillin/ampicillin + aminoglycosides
 LO: anti-staph coverage + aminoglycoside
 Staphylococcus epidermidis: vancomycin
 most effective drug/drug combination: continued x 10 – 14 days

PULMONARY AIR LEAK SYNDROMES

 includes:
o pneumothorax
o pneumomediastinum
o pneumopericardium
o pulmonary interstitial emphysema
o pneumoperitoneum
o subcutaneous emphysema
 occur mostly on patients with pulmonary pathology where
positive pressure was introduced
 pneumothorax may occur spontaneously during cry (PIP > 40
cmH2O)
 distended alveoli ruptures  air tracks towards hilum, pleura:
o prematures: interstitium more abundant, less
dissectible  PIE
 risk factors:
o pulmonary pathology
o ventilatory support (bag-mask ventilation)

CLINICAL PRESENATTION
 sudden worsening of respiratory distress
 tachypnea, alar flaring, retractions, grunting
 hypoxemia, cyanosis, increasing oxygen requirement 
hypercarbia
 distant breath sounds, overdistended chest, bulging of abdomen
ipsilaterally
 thread pulses
 displaced cardiac apex, trachea
 increased thoracic pressure:
o causes impaired venous return  decreased cardiac
output  shock