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tas neonatal medicine ✅ > Respiratory Distress Syndrome ✅ > Flashcards

Respiratory Distress Syndrome ✅ Flashcards

1
Q

What is the most common lung problem accompanying prematurity?

A

Respiratory distress syndrome

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2
Q

What can RDS lead to?

A

Severe respiratory failure and death

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3
Q

What causes RDS?

A

Surfactant deficiency

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4
Q

How does surfactant deficiency lead to RDS?

A

It leads to higher surface tension at the alveolar surface, difficulty in achieving adequate functional residual capacity, and interferes with the normal exchange of respiratory gases

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5
Q

What is the incidence and severity of RDS related to?

A

Inversely proportional to gestational age

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6
Q

Why is the incidence and severity of RDS inversely proportional to gestational age?

A

Because of the smaller number of functional alveoli with decreasing gestational age

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7
Q

Other than surfactant deficiency, what problems are there with premature infants lungs?

A

The airways are incompletely formed and lack sufficient cartilage to remain patent

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8
Q

What does the incomplete formation of airways and lack of cartilage in premature infants contribute to?

A

Collapse of lungs and increased airway resistance

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9
Q

What is the result of the higher surface tension in RDS?

A

Greater distending pressure is required to inflate the alveoli

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10
Q

What law describes the concept of higher surface tension requiring greater distending pressure to inflate the alveoli?

A

Laplace’s law

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11
Q

What is Laplace’s law?

A

P = 2T/r

P = pressure 
T = surface tension 
r = radius
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12
Q

How does the compliance of the lungs compare to that of the chest wall in a preterm infant?

A

The compliance of the chest wall is greater than that of the lungs

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13
Q

What is the result of the compliance of the chest wall being greater than that of the lungs in a newborn infant?

A

The lungs tend to collapse when the infant attempts to increase negative intrathoracic pressure

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14
Q

What functional abnormalities contribute to respiratory failure in preterm newborns?

A
  • Decreased compliance
  • Increased resistance
  • Ventilation-perfusion imbalance
  • Impaired gas exchange
  • Increased work of breathing
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15
Q

What cells are involved with pulmonary surfactant?

A

Type 2 epithelial cells

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16
Q

What is the role of type 2 epithelial cells with regard to pulmonary surfactant?

A

They synthesise and secrete it into alevelar spaces

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17
Q

What is pulmonary surfactant made up of?

A
  • Phospholipids (85%)

- Proteins (10%)

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18
Q

What do most of the phospholipids in pulmonary surfactant consist of?

A

Polyphatidylcholine (PC)

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19
Q

What molecule of PC is particularly important in pulmonary surfactant?

A

DPPC (dipalmitoyl phosphatidylcholine)

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20
Q

Why is DPPC important in pulmonary surfactant?

A

The structure of DPPC is suited to form a stable monolayer generating the lower surface tension required to prevent alveolar collapse at end-expiration

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21
Q

Do phospholipids alone exhibit all the biophysical properties of pulmonary surfactant?

A

No

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22
Q

What, alongside phospholipids, gives pulmonary surfactant its biophysical probelms?

A

The low-molecular weight surfactant specific SP-B and SP-C proteins

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23
Q

What is the role of SP-B and SP-C?

A
  • Contribute to structural organisation and functional durability
  • Promote rapid absorption of phospholipids at the air-liquid interface
  • Account for sustained low surface tension activity after dynamic compression
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24
Q

What is the inheritance of SP-B deficiency?

A

Autosomal recessive

25
Q

How severe is SP-B deficiency?

A

It is lethal and results in fulminant respiraotry failure

26
Q

What effect does SP-C have on phospholipids?

A

It dramatically enhances the spread of phospholipids

27
Q

How does SP-C gene mutation present?

A

Later in life as chronic interstitial lung disease

28
Q

What other surfactant specific proteins are there

A

SP-A and SP-D

29
Q

What is the role of SP-A and SP-D?

A

Play important role in defence barrier against pathogenic organisms and in recycling of surfactant

Only marginally involved in surface tension lowering ability of pulmonary surfactant

30
Q

How does the total surfactant lipid pool in preterm babies compare to term infants?

A

10mg/kg in preterm babies, 100mg/kg in full term infants

31
Q

How does the content of surfactant differ in preterm babies compared to term infants?

A

Lower percent of saturated phosphatidylcholine species, phosphatidylglycerol, and surfactant associated proteins

32
Q

Where can exogenous surfactant preparations be derived from?

A

Either animal sources (bovine and porcine) or can be prepared synthetically

33
Q

What do animal-derived surfactants consist of?

A
  • More than 80% phospholipids

- Specific proteins SP-B and SP-C, but not SP-D

34
Q

What are synthetic surfactants composed of?

A

Mainly DPPC

35
Q

What are the advantages of administration of exogenous surfactant in a surfactant-deficient preterm newborn?

A
  • Decreases minimum pressure required to open lungs
  • Increases functional residual capacity and maximal lung volume
  • Diminishes work of breathing
  • Stabilises respiratory tract
  • Improves mucociliary transport
  • Prevents oedema
  • Contributes to lung defence against pathogens
36
Q

What is the result of increasing functional residual capacity and maximal lung volume with the administration of exogenous surfactant?

A

It prevents lung collapse at low pressures and end-inspiration

37
Q

How is RDS diagnosed?

A

Using combination of clinical features, including;

  • Gestational age
  • Presence of respiratory distress with impaired gas exchange
  • Characteristic radiographic abnormalities
38
Q

What is involved in the management of RDS

A
  • Prevention
  • Exogenous surfactant replacement therapy
  • Artificial respiratory support
  • Adjunctive measures
  • Avoidance of complications
39
Q

How is RDS prevented?

A

Use of antenatal glucocorticoid to induce endogenous surfactant formation

40
Q

In what forms can artificial respiratory support be given in RDS?

A
  • Continuous distending pressure, such as CPAP

- Intermittent positive airway pressure ventilation through mechanical ventilator

41
Q

What adjunctive measures may be used in RDS?

A
  • Maintenance of adequate blood pressure
  • Maintenance of adequate oxygen carrying capacity
  • Maintenance of physiological pH
42
Q

What complications should be avoided in RDS?

A
  • Air leaks

- Bronchopulmonary dysplasia

43
Q

Is exogenous surfactant replacement given prophylactically or as rescue therapy?

A

Can be either

44
Q

What stages can the clinical response to surfactant therapy be divided into?

A
  1. Acute treatment response
  2. Sustained response to initial dose
  3. Continued response to initial dose
45
Q

When does the acute treatment response to surfactant therapy occur?

A

Within 10 minutes

46
Q

What does the acute treatment response to surfactant therapy result from?

A

The biophysical properties of surfactant to distal lung areas

47
Q

What is usually the first clinical response to surfactant instillation?

A

An improvement in oxygenation

48
Q

When does the second stage of response to surfactant therapy (sustained response to initial dose) occur?

A

Hours post administration

49
Q

What does the sustained response to surfactant therapy result from?

A
  • Improving lung mechanics

- Recycling of of surfactant components from air spaces into type 2 cells

50
Q

How are surfactant components recycled in the sustained response to surfactant therapy?

A

Lipids are, in part, diverted into lamellar bodies for re-secretion

51
Q

How does the recycling rates of surfactant therapy in pre-term infants compare to that of term?

A

They are higher in preterm lungs, as high as 80-90%

52
Q

Does the recycling of surfactant components guarantee that only one dose of surfactant will be effective?

A

No

53
Q

When will an infant receiving surfactant therapy require re-treatment?

A

If they are still receiving mechanical ventilation with FiO2 of more than 30-40% several hours after the first dose

54
Q

What % of infants receiving surfactant therapy require re-treatment?

A

20-30%

55
Q

What is the third stage of response to surfactant therapy?

A

Continued response to the initial surfactant dose

56
Q

What is the continued response to the initial surfactant dose attributed to?

A

The long half life of surfactant components

57
Q

What allows an infant with RDS to accumulate a large amount of surfactant over many daysu?

A

The net balance of slow synthesis, secretion, metabolism, and clearance of surfactant and its components

58
Q

What are the advantages of surfactant therapy in preterm infants with RDS?

A

Reduces neonatal mortality and complications such as pneumothoraces

59
Q

What is the limitation of surfactant therapy for preterm infants with RDS?

A

None of the trials or meta-analysis have shown any benefit in terms of reducing incidence of BPD

tas neonatal medicine ✅ (35 decks)

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