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RES-30 Neonatal Respiratory Distress Syndrome crc

Terms in this set (37)

Embryonic (4-5 weeks)
Pseudoglandular (8-12 weeks)
Canalicular (17-22 weeks)
What are the major stages of lung development?
Pseudoglandular (8-12 weeks)
What stage?
Embryonic (4-5 weeks)
What stage?
Canalicular (17-22 weeks), in which the canals of the airways develop
What stage?
23 weeks (past the canalicular stage)
Earliest stage of survival for a fetus?
General appearance of mature alveoli in the respiratory parenchyma.
Reviewed
What is this?
Respiratory bronchiole
A
Alveolar sac
B
Alveolar ducts
C
Alveoli
D
Dipalmitoyl phosphatidylcholine. Soap-like molecule lowers surface tension.
Primary constituent phospholipid of surfactant?
GO BACK TO OTHER LECTURE
A healthy L/S (lecithin/sphingomyelin) ratio that signifies a mature amount of surfactant?
Lung compliance. How easy is it to open the lung? If you washed out surfactant, the compliance decreases, as does the total volume the lung is able to handle.
Too much surface tension in the alveoli that want to close the lungs.
Slope of the upswinging curve signifies what?
Blue curve
What curve would best signify the lungs of a surfactant-deficient patient?
Rib cage is not ossified yet. Chest wall is not stiff and will collapse upon movement of the diaphragm. Cannot create same pressure difference in this case.
Besides deficient surfactant and underdeveloped accessory muscles of respiration, what other problems would a premature (or even term) infant have that might impede respiration?
Neonatal respiratory distress syndrome (nRDS), which is primarily a failure of type II cell maturation.
What is the leading cause of perinatal morbidity and mortality in the world?
Note the extreme sternal concavity associated with the child's strenuous inspiratory efforts. This sternal concavity creates insufficiencies that add to the work of breathing. Tidal volumes are smaller, so breathing will be very fast.

This infant will also probably have nasal flaring.
What is most remarkable about the physical appearance of this baby?
No. May increase P(a)O2, but any increase is merely transient. This was the last ditch medical treatment option available in the 60s.
Is hyperbaric oxygen effective in curing neonatal RDS?
Tachypnea
Grunting (to stent alveoli open)
Sternal retraction
Nasal flaring
Perioral cyanosis

Effort to breath actually increases oxygen demand.
What clinical findings are indicative of neonatal respiratory distress syndrome?
Low PaO2, and if very severe, increased PaCO2
What lab findings are indicative of neonatal respiratory distress syndrome?
Decreased lung volume (heart appears larger), "ground glass" opacities (hazy diffuse appearance), air bronchograms (normally you cannot see the bronchi out peripherally). Airways are collapsed down, and thus they take on a fluid-like density that is readily apparent on CXR.

AP chest x-ray of a premature infant, in which lengthy air bronchograms(arrows) are visible as nearly vertical dark streaks against bilateral fields of lung parenchyma that show characteristic "ground glass" appear-anceof immaturity.
What is going on with this CXR of a neonate?
Very severe variation of neonatal RDS in which the entire lung takes on very dense fluid density. A virtual "white out" of the parenchyma is evident on standard AP CXR.
What is going on with this CXR of a neonate?
Hyaline membranes
Atelectatic distal airways
Underinflation
Pathologic findings of neonatal respiratory distress syndrome?
Poorly aerated thus creating undersized lungs on gross appearance of neonatal respiratory distress syndrome. "Hepatization" of the lungs.
What is this?
Cut appearance of gross lung speciment in nRDS showing "red hepatization" of the lungs in neonates with this condition.
What is this?
Diffuse alveolar damage (DAD) and numerous pink-stained hyaline membranes are seen lining the immature airways of this lung from an infant dying of neonatal RDS. This is "hyaline membrane disease," which is practically synonymous with nRDS. Hyaline membranes made up of dead cell debris

Looks hypercellular, but only because lungs are collapsed down.
What is up with this lung tissue?
Prematurity
Male gender
Caucasian race
Caesarean section
Maternal diabetes
Second-born twin
Family history of nRDS/prematurity
What is associated with increased risk of neonatal respiratory distress syndrome?
Fetal "stress"
Maternal hypertension
Placental insufficiency
Prolonged vaginal delivery
Mild maternal trauma

Stress hormones triggers earlier lung development, thus opening the possibility of corticosteroid therapies to trigger earlier lung development in people at risk of delivering a premature baby.
What is associated with decreased risk of neonatal respiratory distress syndrome?
Yes if intrapulmonary and combined with PEEP
No if extrapulmonary in nature.
Will a right-to-left pulmonary physiological shunt respond to increased F(I)O2?
Intrapulmonary means probably a collapsed or blocked airway (can respond to supplemental oxygen with PEEP to open up closed alveoli). Ventilation goes up in one area of the lung, goes down in the other. Circulation flowing through underventilated area contributes to intrapulmonary shunting.

Extrapulmonary means outside the lungs (like a PDA etc.)
Difference between intrapulmonary or extrapulmonary right to left shunt?
Reviewed
Review neonatal circulation via Kaplan videos
Nitric oxide breathing, which lowers the vascular resistance of pulmonary blood vessel beds. Increases the blood flow to these areas.
Also CPAP (continuous positive airway pressure), and intubation for MV + PEEP.
Besides supplemental oxygen, what are other gas-based therapy options for the treatment of neonatal RDS?
Give supplemental surfactant.
How to correct fundamental defect in neonatal respiratory distress syndrome?
Big babies can sometimes have problems with shunting, just as small babies can. Diabetic mother = LGA. Would also see hypoglycemia in these infants (because pancrease producing a large amount of insulin in response to being bathed by maternal insulin).

Despite CPAP at 0.40 FIO2, pHa = 7.20, PaCO2 = 67mmHg. Intubated w/ P(PEAK) = 28 cmH2O to get appropr. V(T). This is a lot of pressure, should be around 15 cmH2O.
Treat with poractant alfa intratracheal suspension, which is synthetic surfactant.
This would decreased P(PEAK) required for tidal volume, in this case to 20 cmH2O.

Except for mild glycemia, course uncomplicated and extubaqted 48 hours later.
♂"Alec" born by Csection (as siblings) at 37 wk and 3.51 kg; tachypneic, given "blow-by" O2.
Still grunting, nasal flaring, sternal retractions; x-ray: streaky hilar infiltrates, diffuse granular infiltrates.
Poractant alfa, 3 mL intratracheal suspension, in half doses
What synthetic surfactant is used to treat nRDS?
D.
The P(PEAK) required to sustain any given V(T) will decline when surfactant dosing has been successful, due to the rapid reduction in alveolar surface tension; additional doses beyond the first or second day are usually unnecessary (answer E). Although C(a)O2 declines in anemia, P(a)O2 usually does not. The infant has primarily respiratory acidosis (answer b) likely due to the diffusion block, and adding only an endotracheal tube will increase V(D) rather than decrease it.
D. Surgical closure of a PDA that has remained open despite exposure to a relatively high P(A)O2.

The "venous admixture" of PDA-shunted blood from the RV joins the aortic outflow tract distal to emergence of systemic arteries to the head and upper torso. Thus, the disparate oximetry readings are both correct (answer a) and indeed guide the clinician to the diagnosis without required additional echo studies (answer e). True anatomical shunts like PDA are not appreciably improved by supplemental oxygen alone (answer b). There is no evidence from the blood gas values or oximetry data that the infant is hypoventilating (answer c).
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