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RSPT 2353 – Neonatal Pediatric Cardiopulmonary Care
Neonatal Lung Disease & Problems with
Prematurity
Lecture Notes
Reference & Reading:
Whitaker, Chapter 10
I. TRANSIENT TACHYPNEA OF THE NEWBORN (TTN): aka – type II RDS
a. Etiology – unclear; usually related to retention of fetal lung fluid: more common in term
& near-term neonates with hx of C-section
b. Diagnosis – PT shows signs of respiratory distress, CXR appears like RDS , but gradually
clear within 24 – 48 hours. Dx made after everything else is rule out.
c. Treatment – Usually requires O2, CPAP for more severe symptoms
II. RESPIRATORY DISTRESS SYNDROME (RDS): aka Hyaline Membrane Disease (HMD)
a. Etiology – underlying etiology is related to surfactant deficiency. Although immature
surfactant is produced at approximately 22 weeks gestation, it is easily disrupted by
hypoxemia, hypothermia, and acidosis. Mature surfactant is not affected by these
stressors and lung are considered mature.
b. Pathophysiology – although surfactant deficiency is the main problem with RDS,
overall prematurity also contributes to the disease:
Poor gas exchange: immature terminal airways & sacs, vasculature
Chest walls: not stable,  negative pressure creates poor inspiratory effort
Inspiratory difficulty: immature muscle development
Apnea: immature CNS system
c. With all these factors combined the vicious cycle of RDS presents
Decreased surfactant, lead to widespread atelectasis
Atelectasis contributes to  FRC & worsening V/Q mismatch
Hypoxia & hypercapnia lead to respiratory acidosis. Metabolic acidosis is a
result of  O2 at the cellular level
Condition worsens and damages alveoli & capillaries = more surfactant
deficiency
Combined acidosis also leads to pulmonary vasospasm, causing worsening
hypoxemia
If left untreated, the conditions worsens until patient can’t compensate for the
disease
d. Clinical signs & Diagnosis – involves manifestations of respiratory distress
Tachypnea
Grunting – effort to  FRC by partially closing glottis
Retractions
Nasal flaring
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Cyanosis
CXR – ground glass appearance, air bronchograms with presence of atelectasis
Hypothermia may present
Flaccid muscle tone & general hypoactivity
Symptoms worsen at around 48 – 72 hours followed by stabilization & very slow
recovery
e. Treatment – Ideally, prevent it before it starts
Antenatal steroids – mimics stress & promotes fetal lung & surfactant
development; must be administered at least 48 hours prior to delivery
Nasal CPAP – used to recruit alveoli & increase FRC.
Intubation – if patient shows  signs of respiratory distress
Artificial surfactant replacement – Usually common practice when alternative
supportive methods are ineffective
Steroids – sometimes used to improve pulmonary compliance & Vt
Thermoregulation – must be maintained, patients will not respond to
treatment as well
f. Complications – Many are secondary to use of ventilation
Intracranial hemorrhage – because of use of positive pressure ventilation
Barotraumatic injury – affects of inadequate ventilation can lead to barotrauma
& pneumothoraces
Disseminated Intravascular Coagulation (DIC) – disease caused by disruption of
coagulation factors
Infections – can result in pneumonias
III. BRONCHOPULMONARY DYSPLASIA (BPD) aka Chronic Lung Disease (CLD)
a. Etiology: BPD occurs following the tx of RDS – high FiO2 and high pressures over a
length of time.
b. Pathophysiology
O2 toxicity: high concentrations of O2thickens the alveolar membrane leading
to edema, tissues hemorrhage & necrosis. As the lung attempts to heal itself,
new cell s are damaged as well.
Positive Pressure Ventilation: Incidence of BPD increases with higher peak
pressure
Presence of PDA: causes left-to-right shunting that develops into CHF lead to
pulmonary congestion & worsens compliance. Requires increase pressures &
O2
Fluid Overload: common in small preemies, may be related to an exacerbation
of pulmonary edema
c. Diagnosis – based on chronic need for O2 and ventilator support
Stage I (first 3 days): typical of RDS, ground glass appearance
Stage II (day 3 – 10): opaque lungs with granular infiltrates, cardiac markings .
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Stage III (day 10-20): multiple small cyst formations with visible cardiac
silhouette
Stage IV (following day 28): increase lung density, & formation of larger,
irregular cysts
d. Treatment
Prevention: reduce factors that lead to its development & perpetuation. Use
pressures, rates & FiO2 to maintain PaO2 50-70 mmHg, PaCO2 45-55 mmHg
Mechanical Ventilation: Appropriate ETT size to prevent subglottic stenosis,
tracheostomy may be recommended. Extubate ASAP and tolerated. Use
NCPAP as a transition. HFV shown some success as tx. Adequate
humidification to avoid mucus plugging from thickened secretions.
RT Procedures: CPT to mobilize secretions. Maintain good bronchopulmonary
hygiene. Bronchodilators help with bronchospasm
Fluid Therapy: aim at maintaining adequate hydration & urination. Diuretics
may be required.
Right Heart Failure: close PDA. May require used of digoxin and diuretics.
Nutrition: adequate nutrition required to meet increased metabolic needs. 120
– 150 cal/kg/day to achieve growth & needs of tissue repair. Watch for O2
consumption & CO2 retention
e. Prognosis –with changes in mechanical ventilation long-term effects are hard to
examine. Some suggest that there  risk for Asthma or COPD later in life.
IV. RETINOPATHY OF PREMATURITY (ROP) - literally means formation of scar behind the lens;
a. Etiology - there is a link between O2 use and ROP; but other factors such as
retinovascular immaturity, circulatory & respiratory instability.
b. The developing eye: Capillaries in the eye begin to grow at 16 weeks. They grow from
optic nerve towards the ora serrata – retina’s anterior end; they do not reach the entire
ora serrata until 40 weeks. Premature neonate’s capillaries do not have the time to
reach the ora serrata. In this population the capillaries can either develop normally or
cease to grow and cause ROP
c. Pathophysiology
Presence of  PaO2 retinal vessels constrict which leads to necrosis of vessels
(vaso-obliteration).
 In an attempt to reestablished blood supply to retinas, remaining vessels begin
to proliferate may cause hemorrhage in liquid portion of eye.
Results in formation of scarring behind retina with traction, detachment and
blindness.
Once stopped, no further damage occurs
d. Diagnosis – Use ophthalmologic exam of internal eye anatomy.
Five stages ( see Table 10-2)
Appears between 35-45 weeks gestational age and can progress from stage I to
stage 5 over several weeks
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e. Treatment & Prevention
Prevention involves cautious use of O2 delivery to patient
Do not let PaO2 to reach >80 mmHg
Cryotherapy – probe is cooled to -20 degrees with nitrous oxide, placed behind
eye and freezing the avascular portion of retina to prevent further damage.
Laser therapy – alternative to cryotherapy; lasers are used to photocoagulate
avascular portion of retina. Less invasive & less traumatic to eye.
V. INTRACRANIAL/INTRAVENTRICULAR HEMORRHAGE (ICH/IVH)
a. Etiology – Bleeding in the cranium can result in several places
Subdural/subarachnoid bleeds occur secondary to trauma or asphyxia in space
of cranial bone. Usually birth trauma
Cerebral tissue – seen in preterm neonates. Associated with periventircularintraventricular hemorrhages (IVH); usually occur in neonates between 24 -32
weeks gestation, birth weight of <1500 g are also at high risk
b. Pathophysiology
Bleeds occur in choroids plexus in the term neonate; the germinal matrix in the
preterm neonate
Caused by the inability of the cerebral vascular system to regulate blood flow –
mostly due to immaturity
Small bleeds may be confined to the immediate area, but if larger blood may
enter the ventricles enlarging in size and pushing on the parenchyma of brain.
Hemorrhaging may extend to brain tissue – results in further damage
Factors that may trigger IVH include
1. Shock
2. Acidosis
3. Hypernatremia
4. Transfusion f blood
5. Seizures
6. Rapid expansion of blood volume
7. Increased ICP – trendelenburg
8. Mechanical ventilation
9. Alcohol during pregnancy
c. Signs depend on severity of bleed
Signs of germinal matrix include:
1. Apnea
2. Hypotension
3. Drop in hematocrit
4. Flaccidity
5. Bulging fontanelles
6. Tonic posturing
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d. Grading an IVH
Graded from grade 0 to grade IV
Grade I: limited to germinal matrix
Grade II: include germinal matrix with blood extending into ventricles; no
ventricular dilation
Grade III: comparable to grade II, but ventricles are dilated
Grade IV: most severe; dilate ventricles & extend in to brain parenchyma
e. Complications – depend on severity of the bleed
Posthemorrhagic Hydrocephalus (PHH): Most serious complication;
1. Caused by obstruction of CSF outflow & impairment of CSF resorption
in the brain.
2. Tx initially is a lumbar punctures are used to maintain normal cerebral
perfusion pressure as ICP increases
3. Placement of a reservoir is used until a peritoneal shunt is placed
4. If problems arise with the shunt a venticulostomy is placed with
external drainage.
Cerebral Palsy
Vision loss
Hearing loss
Epilepsy
Mental retardation
f. Treatment – avoid factors that lead to this occurrence
Avoid wide fluctuations in oxygenation, blood pressure, and pH
Once it occurs care is more supportive
VI. ASPHYXIA – combination of hypoxia, hypercarbia, & acidosis in fetus or neonate.
a. In utero: Result of placental insufficiency with an inability for gas exchange to occur
b. After delivery: result of pulmonary or cardiac problems
c. Any maternal, placental or umbilical cord problem that interferes with exchange of gas
can lead to asphyxia (see table 10-4)
d. Maternal hypoxia can impair blood flow to placenta and cause less O2 to reach the
fetus. Blood shunts away from lungs, skeletal muscle, liver, kidneys & gut and directed
to brain, heart & adrenal glands
e. Symptoms
Begins with  HR & BP; baby attempts to correct with gasping reflex
If continues, primary apnea; baby commences with deep, ineffective gasps then
secondary apnea.
If still continues, then permanent damage or death
f. In utero – asphyxia is detected by fetal heart monitor & presence of meconium in
amniotic fluid. Fetal heart monitor will show
loss of baseline variability
late decelerations
prolong periods of bradycardia
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g. Complications
Hypoxic-ischemic encephalopathy which also can result in IVH.
Periventircular leukomalacia – infarction in periventricular region
Tubular necrosis of kidneys & GI - bowel ischemia, NEC
Liver damage with sever asphyxia
Lung damage – from  pulmonary vascular resistance, hemorrhage & possible
damage to surfactant production
h. Treatment – requires immediate reversal of hypoxemia and acidosis
If occurs in utero immediate delivery of fetus possibly by C-section is indicated.
Proper resuscitation and close monitoring is required depending on severity
VII. MECONIUM ASPIRATION SYNDROME – predominately a disease of term/postterm neonate that
experiences some form of asphyxia either before or after onset of labor
a. Etiology
Actual aspiration of meconium occurs in about ½ of neonates born with
meconium staining
Occurs with first breath, before or during delivery
Risk for postterm due to diminishing amniotic fluid levels dilute meconium;
diminishes placental function, and  asphyxia
Meconium is the contents of the fetal bowel – includes amniotic fluid, bile salts
& acids, squamous cells, vernix, intestinal enzymes
b. Pathophysiology
During an asphyxia episode the fetsus’ bowel relaxes and the meconium enters
the amniotic fluid
In response to asphyxia the fetus begins to gasp – meconium in the fluid may
enter the oropharynx & tracheobronchial tree
1. Physical presence of meconium can lead to blockage of the airway
2. Results in a ball-valve effect; leading to air-trapping and a
pneumothorax can result
Second response is an inflammatory response in the tracheobronchial tree –
chemical pneumonitis; mucosal edema,  lung compliance, impairment of gas
exchange
1. Vasospasm in the pulmonary vasculature because of MAS can lead to
Persistent Pulmonary Hypertension (PPHN) aka Persistent Fetal
circulation (PFC)- blood flow follows fetal routs bypassing lungs and
leading to  shunt & worsening ABGs
Pulmonary infection is another problem with MAS
c. Diagnosis & treatment
Baby is considered meconium stained until meconium aspiration into trachea is
verifies
Upon delivery of the head the OB must sxn out the mouth and oropharynx and
clear meconium
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Proper NRP procedures should be performed during resuscitation
If ventilation is required, low pressures are recommended, but use whatever
pressure is necessary to ventilate the patient.
Antibiotics with patients with infiltrates on CXR
VIII. PNEUMOTHORAX – most common of air leak disorders
a. Spontaneous – result of rupture of weak alveolar area
b. Tension – gets larger and larger eventually affecting venous return
c. Diagnosis – onset can be gradual or rapid
Patient may be bradycardic, cyanotic, or have periods of apnea & hypotension
Asymmetric chest expansion is easily seen in neonates
Transillumination - fiberoptic light is placed on patient’s chest to determine if
there is a pneumothorax present. Very quick
d. Treatment – depends on severity
Close observation
Needle aspiration
Chest tube - -15 cmH2O for small leaks, -25 cmH2O for large leaks
IX. Pulmonary Interstitial Emphysema (PIE) – air dissects into interstitial tissue of lungs
a. Result of chronic use of high PEEP, PIP and prolonged inspiratory times
b. Two classifications –
Intrapulmonary interstitial pneumatosis – air remains in lung tissue
Intrapleural pneumatosis – extra – alveolar air is confined by the visceral pleura,
forms blebs
c. Pathophysiology
Air dissects and collects in interstitium
Small airways and vessels are compressed
Massive V/Q mismatches occur, vicious cycle
d. Treatment – prevention
Use as little pressures as possible to maintain oxygenation & ventilation
HFV – studies show successful management
There is a high incidence of BPD in these patients
X. PERSISTENT PULMONARY HYPERTENSION OF THE NEONATE (PPHN) – aka Persistent Fetal Circulation
a. Etiology –
Seen in term & postterm infants w/ hx of asphyxia, MAS, sepsis, CDH,
pulmonary hypoplasia, congenital heart, or premature closure of ductus
arteriosus
Neonates have severe, persistent pulmonary vasoconstriction, causing increase
pressures & decreased pulmonary flow.
R sided heart pressures rise higher than arterial pressure
Continuation of factors that allow fetal circulation to occur
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b. Diagnosis
When there is worsening hypoxemia three things must be ruled out:
1. Parenchymal lung disease
2. Cyanotic congenital heart lesion
3. PPHN
Hyperoxia test – place on 100% FiO2 for 5 – 10 minutes draw ABG; if PaO2is
below 100 mmHg, R-to-L shunting is present
Preductal and postductal PaO2 level: if preductal is 15-20 mmHg higher,R-to-L
shunting is present
Hyperoxia-hyperventilation test: PaCO2 is lowered to 20 – 25 mmHg or pH
raised to 7.50 or greater; if PaO2 is less than 50 mmHg before hyperventilation
and rises to >100 mmHg following hyperventilation it is almost certain it is
PPHN
Echocardiogram: shows  pulmonary artery pressures, R-to-L shunting at
ductal or atrial level, regurgitation through tricuspid valve and dilation of R
ventricle
c. Treatment
Hyperventilation – caution must be taken to avoid barotraumas, HFV is
recommended
Drug-induced vasodilation
1. Tolazoline
2. Isoproterenol
3. iNO – now considered drug of choice
ECMO – many with severe PPHN require ECMO; supports cardiopulmonary
system and corrects acidosis, allowing time for HTN to resolve