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RSPT 2353 – Neonatal Pediatric Cardiopulmonary Care
Neonatal Lung Disease & Problems with
Prematurity
Lecture Notes
Reference & Reading:
Czverinske Chapter 28 & 30
I. 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 lungs are considered mature.
b. Pathophysiology – although surfactant deficiency is the main problem with RDS,
overall prematurity also contributes to the disease:
Poor gas exchange
Chest walls
Inspiratory difficulty
Apnea
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
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
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e. Treatment – Ideally, prevent it before it starts
Antenatal steroids
Nasal CPAP
Intubation – if patient shows  signs of respiratory distress
Artificial surfactant replacement
Steroids
Thermoregulation
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
II. 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. Clinical Presentation & 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
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 memebrane
leading to edema, tissues hemorrhage & necrosis. As the lung attempts to heal
itself, new cell s are damaged as well.
Positive Pressure Ventilation
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 or presence of pulmonary hypertension
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 4 – 10): opaque lungs with granular infliatrates, cardiac markings .
Stage III (day 10-20): multiple small cyst formations with visible cardiac
silhouette
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Satge IV (beyond 30 days): increase lung density, & formation of larger,
irregular cysts
d. Treatment
Prevention: reduce factors that lead to its development & perpetuation.
Mechanical Ventilation: Appropriate ETT size to prevent subglottic stenosis,
tracheostomy may be recommended.
Pharmacologic agents: corticosteroids, caffine
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 reestablish 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
Appears between 35-45 weeks gestational age and can progress from stage I to
stage 5 over several weeks
e. Treatment & Prevention
Prevention
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.
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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 .
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. Transfusiono 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
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
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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
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. 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
Pesisitant Pulmonary Hypertension (PPHN) aka Persistant Fetal
circulation (PFC)- blood flow follows fetal routs bypassing lungs and
leading to  shunt & worsening ABGs
Pulmonary infection is another problem with MAS
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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
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
VII. 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. Pathophysiology
Air dissects and collects in interstitium
Small airways and vessels are compressed
Massive V/Q mistmatches occur, vicious cycle
c. 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
VIII. PESISTANT 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, persistant pulmonary vasoconstriction, causing increase
pressures & decreased pulmonary flow.
R sided heart pressures rises higher than arterial pressure
Continuation of factors that allow fetal circulation to occur
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
Preductal and postductal PaO2 level
Hyperoxia-hyperventilation test:
Echocardiogram:
c. Treatment
Hyperventilation – caution must be taken to avoid barotraumas, HFV is
recommended
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Drug-induced vasodilation
1. Tolazoline
2. Isoproterenol
3. iNO – now considered drug of choice
ECMO Nitric Oxide