Newborn Respiratory Distress Syndrome Flashcards

1
Q

Major factors in the pathophysiology of RDS

A
  • Surfactant Deficiency
  • Decreased alveolar surface area
  • Increased small airways
  • Presence of ductus arteriosus
  • Decreased FRC and lung compliance
  • Increased pulmonary vascular resistance
  • V/Q mismatch
  • Pulmonary edema that is rich in protein and dying epithelial cells
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2
Q

Respiratory Distress Syndrome

A
  • Disorder of prematurity
  • Prevalence: 20,000-30,000 newborns affected each year or about 1% of pregnancies(USA)
  • Inversely related to gestational age and birth weight
    • <28 weeks: 60-80% occurrence
    • 32-36 weeks: 15-30% occurrence
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3
Q

Surfactant in RDS

A

Surfactant production depends on both the relative maturity of the lung and the adequacy of fetal perfusion.

In preterm infants, adequate amounts of surfactant are present in the lung; however, the surfactant is trapped inside type II cells. In infants with RDS, type II cells do not release adequate amounts of surfactant.

  • The surfactant that is released is incompletely formed, so it does not make tubular myelin and does not decrease alveolar surface tension.
  • Because the surfactant molecule in the alveolus is structurally abnormal, the type II cells and alveolar macrophages have more rapid uptake for recycling. Thus, there is a qualitative deficiency of alveolar surfactant.
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4
Q

Maternal Factors that Impair fetal blood flow

A

Abruptio placentae and maternal diabetes, which may lead to RDS.

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5
Q

The decrease in surfactant results in

A
  • A qualitative decrease in surfactant increases alveolar surface tension forces, which causes alveoli to become unstable and collapse and leads to atelectasis and increased work of breathing. The increased surface tension draws fluid from the pulmonary capillaries into the alveoli.
  • In combination, these factors impair oxygen (O2) exchange and cause severe hypoxemia. The severe hypoxemia and acidosis increase pulmonary vascular resistance (PVR). As pulmonary arterial pressure increases, extrapulmonary right-to-left shunting in- creases, and hypoxemia worsens. Hypoxemia and acidosis also impair further surfactant production.
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6
Q

Steroid Administration for ARDS

A
  • Steroids given before birth (antenatally) have been shown to mature surfactant function in the fetus, decrease the severity of RDS, and improve outcomes
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7
Q

RDS Clinical Manifestations

A

1st signs of distress will appear right after birth

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8
Q

RDS Clinical Manifestation

A
  • Tachypnea is normally the first sign and will be followed with worsening retractions, paradoxical breathing, nasal flaring, and grunting (to maintain FRC)
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9
Q

How do Retractions Appear

A
  • Retractions have a See-Saw appearance: Abdomen protrudes as the chest is pulled in
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10
Q

Chest radiograph for ARDS

A
  • A definitive diagnosis of RDS usually is made with chest radiography
    • Diffuse, hazy, reticulogranular densities with the presence of air bronchograms with low lung volumes are typical of RDS.
    • The reticulogranular pattern is caused by aeration of respiratory bronchioles and collapse of the alveoli.
    • Air bronchograms appear as aerated, dark, major bronchi surrounded by the collapsed or consolidated lung tissue.
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11
Q

CXR “Stages” for RDS

A

Stage I RDS with fine, diffuse reticulogranular pattern over the lung fields

Stage II RDS reveals a denser lung, with the presence of air bronchograms within the heart border.

Stage III RDS shows increased density and the presence of air bronchograms beyond the heart border.

Stage IV RDS, termed “whiteout,” infant with severe disease complicated by pulmonary edema. The view of the heart border and edge of the diaphragm is obliterate

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12
Q

prevntion of RDS

A
  • Delayed premature delivery with the use of tocolytics (weak evidence that they work
    • Tocolytics will delay birth
  • Promote the surfactant production with the use of steroids (bethamethasone)
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13
Q

Betamethasone

A
  • Betamethasone: A corticosteroid used to stimulate lung maturation in fetal lungs
    • Clinically proven to reduce perinatal mortality in RDS
    • Treatment should consist of two 12mg doses of betamethason given IM 24 hours apart, or four 6mg doses given IM 12 hours apart.
    • Due to insufficient data, repeated courses of corticosteroids should not be used routinely
    • Pregnant women between 24 and 34 weeks’ gestation who are at risk of preterm delivery within 7 days
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14
Q

Strategies for Surfactant Therapy

A
  • Prophylactic or preventative
    • Surfactant is administered at the time of birth of shortly thereafter to neonates who are high risk for developing RDS
      • <32 weeks gestational age
      • Low birth weight(<1300g)
      • L:S ratio < 2:1
  • Rescue or therapeutic
    • Surfactant is administered after the initiation of mechanical ventilation in neonates with confirmed RDS
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15
Q

RDS CPAP THerapy

A
  • Continuous positive airway pressure (CPAP) and positive end expiratory pressure (PEEP) are the traditional support modes used to manage RDS.
  • Unless the infant’s condition is severe, a trial of nasal CPAP is indicated (4 to 6 cm H2O).
    • For CPAP your 5 is normal but the 8 is high
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16
Q

Indication for Mechanical Ventilation with RDS

A
  • Mechanical ventilation with PEEP should be initiated if oxygenation does not improve with CPAP or if the patient is apneic or acidotic.
    • pH< 7.2 and PaCO >60 indication is the indication for mechanical ventilation
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17
Q

Aim of Mechanical Ventilation

A

The aim of mechanical ventilation for RDS is to prevent lung collapse and maintain alveolar inflation. In severe RDS, collapse of alveoli with every breath necessitates very high reinflation pressure. To prevent the need for this high reinflation pressure, use of end-tidal pressure is necessary.

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18
Q

relationship between arterial partial pressure of carbon dioxide (PaCO2) and functional residual capacity (FRC)

A
  • Because of the relationship between arterial partial pressure of carbon dioxide (PaCO2) and functional residual capacity (FRC), PaCO2 is lowest when PEEP is used to optimize FRC. The time constant of the lungs in RDS is short, so the lung empties very quickly with each ventilator cycle.
  • If alveolar ventilation is inadequate, either peak inspiratory pressure or rate should be increased. For minimizing the possibility of volutrauma, the peak inspiratory pressure should be kept less than 30 cm H2O for larger premature infants, and even lower peak inspiratory pressure is indicated for more immature infants.
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19
Q

What is RDS caused by?

A

Immaturity of the lungs.

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20
Q

What is the reason for immaturity of the lungs?

A

Lack of surfactant.

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21
Q

What causes low alveolar compliance?

A

A decrease in surfactant.

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22
Q

What is the biggest problem with RDS?

A

Surfactant deficiency.

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23
Q

What is known as lung tissue underdevelopment?

A

Lung hypoplasia.

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24
Q

What is the primary cause of respiratory distress?

A

Lung hypoplasia.

25
Q

What are surfactant molecules exerted and made of?

A

Alveolar type 2 cells.

26
Q

At what gestational week will surfactant appear?

A

17-26.

27
Q

Which cells in the alveoli produce surfactant?

A

Type II Pneumocytes.

28
Q

What is the cause of Neonatal Respiratory Distress Syndrome?

A

Pathology is due to a lack of surfactant due to the immaturity of the neonate’s lungs. This leads to an increase in surface tension, decreased compliance, and increased work of breathing and alveolar collapse.

29
Q

What will a Neonatal Respiratory Distress Syndrome chest x-ray show?

A

Will see these diffuse interstitial infiltrates.

30
Q

Who is at risk for neonatal respiratory distress syndrome?

A

Pre-term infants (born before <35 weeks).

31
Q

During what stage of lung development do pneumocytes develop?

A

The saccular stage (week 26 to birth).

32
Q

How do we test a pregnant mother to see if her baby’s lungs have reached maturity?

A

Look at the Lecithin:Sphingomyelin ratio in the amniotic fluid. Both lecithin and sphingomyelin are lipids in surfactant- mostly lecithin that gives surfactant its qualities.

33
Q

What lecithin molecule is most important in surfactant?

A

Dipalmitoyl phosphatidylcholine.

34
Q

In NRDS, what is the Lecithin:Sphingomyelin ratio?

A

Less than 1.5. A ratio of greater than 2.0 indicates a low risk for NRDS.

35
Q

What happens to the oxygen tension in NRDS?

A

Oxygen tension is decreased.

36
Q

Persistently low oxygen tension within the blood can result in an increased risk for what cardiac complication?

A

Patent Ductus Arteriosus.

37
Q

What is the risk of decreased oxygen tension?

A

Necrotizing enterocolitis.

38
Q

What are the complications of too much oxygen during the perinatal period?

A

Retinopathy which is more involved with O2 tension- once the O2 is removed, the relative hypoxia in the eye causes blood vessel overgrowth- which can result in blindness. Intraventricular Hemorrhage and Bronchopulmonary Dysplasia are also complications of too much oxygen.

39
Q

Why does RDS happen?

A

It occurs because of a deficiency of alveolar surfactant, and is mainly seen in premies. It leads to alveolar collapse and reinflation with each breath – exhausts the baby and causes respiratory failure.

40
Q

What signs can result from hypoxia in RDS?

A

Reduced cardiac output, Hypotension, Acidosis, Renal failure, and Death.

41
Q

What are the signs of RDS?

A

Respiratory distress shortly after birth (in first 4h), and Tachypnoea (>60/min), grunting, nasal flaring, intercostal recession, cyanosis.

42
Q

What would you see on a CXR in RDS?

A

Air bronchograms and Diffuse granular patterns (ground glass appearance).

43
Q

What are the differentials for RDS?

A

Transient tachypnoea of newborn (due to excess lung fluid, normally resolves after 24h), Meconium aspiration, Congenital pneumonia (group B strep), Tracheoesophageal fistula, suspect if respiratory problems after feeds, and Congenital lung abnormalities.

44
Q

How to prevent RDS?

A

Betamethasone or dexamethasone to all women at risk of premature delivery from 23-35 weeks.

45
Q

How to treat RDS?

A

Delay cord clamping by 3 mins to promote placento-fetal transfusion. Give oxygen via o2/air blender at lowest possible concentration. If spontaneous breathing, stabilize with CPAP. If at high risk of RDS – give surfactant.

46
Q

When do you suspect pulmonary hypoplasia?

A

All infants with persistent neonatal tachypnoea and feeding difficulties, especially if prenatal oligohydramnios. In a diaphragmatic hernia, it is due to a ‘SOL’. It can also be due to cystic adenomatoid malformations.

47
Q

What are the 4 most common causes of respiratory distress?

A

Respiratory distress syndrome (RDS)– like her case, Transient Tachypnea of the Newborn, Pneumonia/Aspiration syndromes, and Pneumothorax.

48
Q

How do we assess fetal lung maturity?

A

Amniocentesis (check the fluid in utero, only done in high risk), Lecithin, and phospholipid.

49
Q

What is a more specific indicator of lung maturity in babies?

A

Saturated phosphatidylcholine or phosphatidylglycerol.

50
Q

When are mature alveoli present?

A

36 weeks.

51
Q

What helps the neonates to get a good first breath?

A

Vaginal delivery that causes intermittent compression of the thorax and helps with the removal of lung fluid. Surfactant helps to decrease surface tension which lowers pressure needed to open the alveoli.

52
Q

What are the 6 parts of the definition of respiratory distress?

A

Tachypnea (over 60 breaths/minute), grunting (stints alveoli open), nasal flaring, retractions, Cyanosis, and decreased breath sounds.

53
Q

What are the tests that must be done for respiratory distress?

A

Chest x-ray, serum glucose, blood gas, CBC with differential, CRP, blood culture, obtain maternal history (diabetes, premature, ultrasound abnormalities), details of labor and delivery (where was placenta).

54
Q

What should you rule out with respiratory distress?

A

Cardiac disease; via murmurs, gallops, poor capillary refill, weak/delayed pulses, single heart sound, central cyanosis, hyperactive precordium.

55
Q

What are the causes of respiratory distress syndrome?

A

Surfactant deficiency which causes an increase in surface tension and alveolar collapse, they cannot establish and maintain an FRC (functional residual capacity) and then the lungs become atelectatic. Classic chest x-ray appearance for respiratory distress syndrome ground glass appearance, diminished lung volume, air bronchograms.

56
Q

What is the ABG of a child with respiratory distress syndrome?

A

Hypoxemia, hypercapnia, and metabolic acidosis.

57
Q

How can we prevent respiratory distress syndrome?

A

Antenatal corticosteroids 24-34 weeks in preterm labor; speeds up fetal lung maturation should also avoid c-section if unnecessary. Give prophylactic doses of surfactant to premature infants.

58
Q

What is the biggest complication of respiratory distress syndrome?

A

Chronic lung disease (bronchopulmonary dysplasia).