2a Respiratory Diseases (RDS) Yen Flashcards

1
Q

What is the usual duration for a full term baby, and their normal weight?

A

38-40 weeks GA. 3.6kg (8 lbs)

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2
Q

At what age is a baby considered premature?

A

< 38 weeks

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3
Q

What is a “Low Birth Weight”?

A

< 1.5kg (3.3 lbs)

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4
Q

What is “Very Low Birth Weight”?

A

< 1kg (2.2 lbs)

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5
Q

What is an overview of Respiratory Distress Syndrome (RDS)?

A

Also called hyaline membrane disease. Respiratory distress common in newborns. RDS major cause of respiratory distress

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6
Q

Which neonates are at higher risk of RDS?

A

White male infants. Infants born to mothers with diabetes. Infants born by means of cesarean delivery. Second born twins. Infants with a family history of RDS

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7
Q

How does the incidence of RDS decrease?

A

Use of antenatal steroids. Pregnancy-induced or chronic HTN. Prolonged rupture of membranes. Maternal narcotic addiction

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8
Q

Why does RDS often occur in premature infants?

A

RDS is the result of pulmonary surfactant deficiency. Lungs of premature infants lack pulmonary surfactant (inadequate production until 34 weeks GA). Full term infants can develop surfactant inactivation with sepsis, pneumonia, meconium, aspiration, asphyxia

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9
Q

What are the clinical signs that result from abnormal pulmonary function in RDS?

A

Tachypnea. Nasal flaring. Grunting. Retractions. Cyanosis

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10
Q

When do the clinical signs of RDS usually present?

A

Typically presents at birth. Will worsen over 48 hrs if untreated. If no improvements, death usually occurs in 2-7 days

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11
Q

What is the Prevention for RDS?

A

Best intervention is to prevent premature birth. Cervical cerclage. Tocolytic agents. Treatment of maternal infections (ex. UTI). Smoke and alcohol cessation. Avoid unnecessary C-sections. Prenatal care

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12
Q

What is Antenatal Corticosteroid Therapy (ACS) like for RDS?

A

Enhances maturational changes in the preterm lung. Results in improved lung function. Increases surfactant synthesis and release

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13
Q

When is ACS recommended?

A

All women less than 34 weeks gestation. Optimal benefit begins 24 hrs after initial dose, effect lasts 7 days. ACS for less than 24 hrs still associated with reductions in RDS and infant mortality

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14
Q

What are the ACS regimens to use?

A

Betamethasone 12mg IM Q24hrs x2 doses. Dexamethasone 6mg IM Q12hr x4 doses. Both of these are 48 hr regimens

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15
Q

What is the theory behind surfactant use?

A

Widely used and is effective in reducing mortality and morbidity rate in RDS. Prevents development of RDS. Once RDS has been established, reduces severity of RDS

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16
Q

What is Prophylactic Surfactant Therapy?

A

Administered at the time of delivery to those at risk of RDS (< 30 weeks GA)

17
Q

What is Early Surfactant Therapy?

A

Administered within 2 hrs of life. Prophylactic or Early therapy are superior to rescue therapy alone

18
Q

What is Rescue Surfactant Therapy?

A

Given once diagnosis of RDS is established

19
Q

What is a Surfactant?

A

A complex lipoprotein complex (phospholipoprotein) with 6 phospholipids and 4 apoproteins. Naturally found in Type II alveolar cells

20
Q

What are the 4 surfactant apoproteins identified?

A

Surfactant Protein A (SP-A), B, C, D

21
Q

What do Surfactant Proteins A (SP-A) and SP-D do?

A

Innate host defense. SP-A involved in negative feedback mechanism to control production of surfactant

22
Q

What do Surfactant Proteins B (SP-B) and SP-C do?

A

Required for proper biophysical lung function. Work in concert to facilitate rapid absorption and spreading of a thin monolayer

23
Q

What is the MOA of Surfactants?

A

Lung surfactant lines the alveolar surfaces and terminal airways. Reduces the surface tension of pulmonary fluids and stabilizes alveoli. Contributes to the elastic properties of pulmonary tissue (pulmonary compliance). Facilitates recruitment of collapsed airways

24
Q

What can surfactant deficiency lead to?

A

Atelectasis and impaired gas exchange. Hypoxemia. CO2 retention. Secondary lung injury

25
Q

What is Natural vs. Synthetic Surfactant?

A

Natural surfactants superior to synthetic surfactant without SBP (non-protein containing). Synthetic products that contain peptide analogs of SBP are superior to non-protein containing synthetic product. New synthetic product with peptide analogs of SBP are COMPARABLE to natural surfactant

26
Q

What is the synthetic surfactant currently used?

A

Lucinactant (Surfaxin)

27
Q

Which surfactant uses the lowest dose?

A

Poractant alfa (Curosurf)

28
Q

Which surfactant is porcine derived?

A

Poractant alfa (Curosurf)

29
Q

What are the side effects with surfactant therapy (many attributed to installation: intubation)?

A

Transient bradycardia, hypotension, endotracheal tube blockage, oxygen desaturation, pulmonary hemoorhage. Pulmonary hemorrhage may prevent further instillation

30
Q

What are postnatal steroids for RDS used for?

A

Improves pulmonary function and decreases incidence of CLD

31
Q

What are the short term complications with Postnatal steroids in RDS?

A

Intestinal perforations, HTN, hyperglycemia, increased risk of infections

32
Q

What are the long term complications with Postnatal steroids in RDS?

A

Abnormal neurodevelopmental outcomes, increased incidence of cerebral palsy

33
Q

What is the recommendation for postnatal steroids?

A

AAP does NOT recommend the use of postnatal steroids unless the infant is doing poorly on maximal support. Dexamethasone mostly used in low doses, short duration

34
Q

What is the management for RDS?

A

Used to correct atelectasis. Increases concentration of supplemental oxygen to avoid hypoxemia. Facilitates repeat administration of surfactant. Correct CO2 retention. Associated with volutrauma and barotrauma (along with oxygen toxicity leads to development of chronic lung disease). Avoid fluid overload (excess can lead to pulmonary edema)

35
Q

Which surfactant is produced by calf lung lavage?

A

Calfactant (Infasurf)