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RDS & Surfactant Flashcards

1
Q

When was Surfactant deficiency determined to be the cause of RDS and when the first report of UAC for blood sampling?

A

1959

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2
Q

In what decade was:
the first NICU in the world
phototherapy
& First PKU developed?

A

1960’s

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3
Q

Who was the “mother of neonatology” who worked at Vanderbilt?

A

Mildred Stahlman-Initial research in Pediatric Cardiology–then moved in to premature lung dz, got grant for HMD research

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4
Q

Who was the famous president’s baby born early (34.5 wks) and died from HMD?

A

JFK’s (Patrick Bouvier Kennedy)

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5
Q

Baby Kennedy’s death sparked interest in research on?

Gave rise to what subspecialty? When?

A

Prematurity, specifically RDS

“Neonatology”–recognized in 1975

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6
Q

When did NNP’s emerge as a role?

A

1970’s

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7
Q

In 1970’s, what equipment became available?

A

Ventilators, ECMO (no sats, just ABG’s avail)

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8
Q

When did certification for NNP’s develop?

A

1983

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9
Q

What else happened in 1980’s besides NNP certification?

A

Jet vents
Pulse ox
Increased use perinatal steroids
Wide spread surfactant use

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10
Q

When did FDA approve surfactant Therapy for RDS?

A

1990’s

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11
Q

Bedsides Surfactant, what other treatments became available?

A

Partial liquid ventilation
HFOV
iNO-FDA approved for PPHN

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12
Q

Along with the development of RDS, oxygen, ventilation, we created what?

A

BPD

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13
Q

What is the most common diagnosis in NICU?

A

RDS

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14
Q

RDS is characterized by?

A

Increased WOB, Grunting, Flaring

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15
Q

What GA is affected by RDS?

A

All GA’s–but the causes differ

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16
Q

If you are suspecting RDS, what are some differentials?

A 
TTN
Pneumonia/Sepsis
Meconium Aspiration
Pulmonary 
         Hypoplasia/dysplasia
Symptomatic polycythemia
Pulmonary Hemorrhage
Perinatal Asphyxia
Pneumothorax
Congential cardiac 
                         malformation
Chromosomal/Metabolic  D/O
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17
Q

What is another name for RDS?

A

HMD (hyaline membrane dz)

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18
Q

Which group of infants has the highest rate RDS?

A

< 1500 gm

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19
Q

More than ____ of ELBW’s have some type of respiratory distress

A

1/2

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20
Q

RDS is characterized by development of?

A

Hyaline membranes (within the lung tissue)

-leakage of protein debris into airways–>can impair what surfactant is present

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21
Q

How soon after a baby is born can Hyaline Membranes develop?

A

w/in 30 minutes

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22
Q

RDS onset is with in _____ of birth

Gets worse/better over first 1-3 days

Improves/worsens gradually with duration usually 3-5 days

A

hours

worse

improves gradually

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23
Q

True/False: TTN will show improvement w/in first 12 hours of birth.

A

True

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24
Q

Name risk factors for RDS

A 
Prematurity
Perinatal asphyxia
Maternal DM
C/S deliver
Absence of antenatal steroid 
                    administration
Male
Caucasian
Multiple gestation
Surfactant dysfunction or 
          inactivation (MAS, 
           pulm. hemorrhage)
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25
Q

How is RDS prevented? (2 things)

A

Antenatal Steroids

Prevent Asphyxia

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26
Q

When are Antenatal Steroids recommended?

A

24-34 wks (w/anticipated

delivery situation

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27
Q

When are Antenatal steroids most effective?

A

> 24 hours before delivery

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28
Q

What do Antenatal steroids reduce?

A

Neonatal death, development of RDS, IVH, & NEC

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29
Q

When does the benefit of Antenatal steroids begin to wane?

What could be done?

A

> 1 wk before delivery

Repeat dosing–possibly

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30
Q

To prevent RDS, why would you want to prevent Asphyxia?

A

Asphyxia –>hypoxemia & acidosis–>reduce surfactant synthesis

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31
Q

What could you do to prevent asphyxia if in an outlying facility?

A

Transfer mom to experienced center if safe

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32
Q

What 8 things are noted in the clinical presentation of RDS?

A
  1. Tachypnea (tries to increase CO2 & O2 exchange)
  2. Grunting (attempt at PEEP)
  3. Increased WOB
  4. Cyanosis, Pallor, Lethargy
  5. Poor Feeding
  6. Apnea
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33
Q

What radiographic features are common to RDS? (5 things)

A
  • Reticulogranular pattern (ground-glass)
  • Air bronchograms
  • Homogenously dense (wide-spread alveolar collapse)
  • “white out” severe
  • Low lung volumes
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34
Q

In absence of surfactant there is widespread?

A

Alveolar collapse with over-distension of open Alveoli

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35
Q

Reopening collapsed Alveoli requires what?

How is this clinically manifested in baby?

A

Increased pressure

Retractions during inspiration

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36
Q

Widespread alveolar collapse causes intrapulmonary shunting of?

How is this clinically manifested in baby?

A

blood past areas of atelectasis

Pulmonary HTN

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37
Q

Name the 4 steps in developing RDS.

A
  1. Surfactant Deficiency
  2. Alveoli Collapse
  3. Atelectasis & V/Q mismatch
  4. Hypoxemia and Respiratory Acidosis
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38
Q

Who’s law explains why some alveoli collapse while others are over-expanded?

A

La Place law

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39
Q

What does surfactant do?

A

Decreases surface tension

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40
Q

The amount of pressure required to KEEP alveoli open during expiration is ________compared to complete loss of gas.

A

Minimal

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41
Q

During inflation, surface tension increases faster/slower?

If Alveoli are inter-connected, air will flow into smaller/larger Alveoli?

A

Faster

Smaller (keeping them the same size)

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42
Q

What does a lack of Surfactant cause? (5 things)

A
  1. Increased pressure requirements
  2. Decreased compliance
  3. Decreased FRC
  4. Decreased V/Q mismatch
  5. R–>L shunting
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43
Q

If supportive therapy of RDS is successful, the repair phase begins on what day?

A

2nd day after birth

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44
Q

During repair, what happens to the debris?

What happens to the damage tissue?

What happens to edema?

A

It is phagocytosed

It is regenerated

It is mobilized into the lymphatic system–>diuretic phase of RDS (high UOP)

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45
Q

How is RDS Diagnosed? (6 things)

A 
1. Arterial or cap blood gas:
PaCO2 near normal (d/t tachypnea) usually elevated
PaO2 low d/t hypoxia
2. Blood glucose:  <40
3. CBC Hct :  >65
4. Blood culture &amp; CRP
5. AP and lateral CXR
6. Echo (if indicated)
46
Q

Almost all NB’s have elevated CRP’s, how long do most nurseries wait to collect one?

A

12-24 hours

47
Q

Name some complications of RDS (3)

A
  1. Airleak (PIE, Pneumo)
  2. Pulmonary Hemorrhage (hemorrhagic pulm. edema)
    -L.V. failure & excessive
    L–>R flow through PDA = over-circulation to lungs
  3. BPD or CLD
    -Abnormal lung repair following RDS
48
Q

What is the tx of RDS? (5 things)

A
  1. Nutritional support
    - 60-80 mL/kg/day
    - parenteral nutrition
  2. Abx
  3. Oxygen
  4. CPAP or vent
  5. Exogenous surfactant
    - Surfactant deficiency
    - Surfactant Deactivation (pulm. hemorrhage and MAS)
49
Q

What 3 types of resp support can you provide to babies with RDS?

A
  1. Intubation
  2. CPAP
  3. HFNC
50
Q

When would you think about intubation for RDS (2 times)?

A

To support respiratory effort

Give surfactant

51
Q

What does CPAP provide?

A
  1. Prevents end-expiratory alveoli collapse
  2. Reduces WOB
  3. Improves ventilation to perfusion V/Q
  4. improve & maintain FRC
  5. Recruitment
52
Q

What are some draw backs to using humidified HFNC?

A
  1. Pressure variable
  2. Unpredictable
  3. Unregulated
  4. Not FDA approved
53
Q

Name some treatment complications of RDS

A
  1. Equipment issues
    -keeping in place
    -pressure necrosis of nasal
    septum
    -clefts in palates
  2. Hyperoxic injuries
    -ROP
  3. Added lung injury
    -Infection from prolonged
    intubation
    -BPD
54
Q

Surfactant Provides: (6 things)

A
  1. Thin layer at air liquid interface
  2. lowers surface tension
  3. Prevents Alveolar collapse w/expiration
  4. Reduces pressure needed for next alveolar inflation
  5. Maintains FRC
  6. Improves compliance & thus WOB
55
Q

What is surfactant made up of?

A

90% lipids

10% protein

56
Q

What is the main phospholipid of surfactant?

A

DPPC (dipalmitoylphosphatidylcholine) or lecithin

57
Q

Surfactant has a ________ head and a _______ tail

A

hydrophilic head

hydrophobic tail

58
Q

What cells make surfactant?

A

Type II pneumocytes

59
Q

What is phosphatidylglycerol (PG) used for?

A

A marker for lung maturity

60
Q

What are the names of the 4 surfactant proteins that make up surfactant?

A
  1. SP-A
  2. SP-B
  3. SP-C
  4. SP-D
61
Q

What does SP-A do?

Which other protein has this characteristic?

A

Plays role in immune defense

Also SP-D too

62
Q

What is characteristic of SP-B & SP-C? (4 things)

A
  1. Hydrophobic
  2. Essential for transiiton to a monolayer at the air-liquid surface
  3. Facilitate absorption and spreading of DPPC–>lower surface tension
  4. Commercially available
63
Q

Name the three component types of surfactants

A
  1. Nonprotein Synthetic Surfactants
  2. Protein-Containing Animal Surfactants
  3. Peptide-Containing Synthetic Surfactants
64
Q

What do nonprotein synthetic surfactants contain?

What do they lack?

A

Contained DPPC

Lack SP-B

65
Q

Name 2 nonprotein synthetic surfactants.

A
  1. Adsurf

2. Exosurf

66
Q

Name the 3 protein-containing animal surfactants and what they are made from

A
  1. Curosurf (poractant)-Porcine (pig)
  2. Infrasurf (Calactant)-Bovine/calf
  3. Survanta (Beractant)-Bovine-cow
67
Q

Name the type of Peptide-containing Synthetic Surfactant

A

Surfaxin (Lucinactant)

68
Q

Do natural or artificial surfactants act faster?

This type also has lower incidence of what?

A

Natural

Pneumothorax and Mortality

69
Q

Clinical trials comparing natural surfactants are ______________.

True/False: there are no differences in long-term outcomes between types of natural surfactants

A

Inconclusive

True

70
Q

There is a new generation of synthetic surfactants (peptide-containing) produced due to what concerns?

A

Concerns from current synthetics and immunlogic/infectious complications from animal-derived

71
Q

The new generation synthetic surfactant (peptide-containing) mimics what?

A

Actions of Natural surfactant proteins SP-B and SP-C

72
Q

What is the name of the peptide containing synthetic surfactant?

A

Lucinactant

73
Q

Lucinactant is superior to what?

Is their superiority proven from animal-derived?

A

The old synthetic surfactants

No

74
Q

In what patients is prophylactic surfactant given?

A

The highest-risk patients

75
Q

When is prophylactic surfactant given?

To whom?

A

Within 15 minutes of birth

< 26 wks or
26-30 wks without antenatal steroids or need intubation

76
Q

When is Early Rescue Surfactant given?

To whom?

A

1-2 hours of age

< 30 wks at risk w/first signs of RDS

77
Q

What is the latest time surfactant is given?

Why?

A

within 12 hours of age

To treat established RDS
Ventilated & at least 30-40% FiO2

78
Q

True/False: Prophylactic or early surfactant is more beneficial than late in highest-risk populations

79
Q

True/False: Surfactant dosing provides improved CPAP administration

A

True

~advocate for early tx & CPAP

80
Q

When multiple doses are used, what do Meta-analysis suggest?

A

Reduction in pneumothorax and mortality

81
Q

What is the greatest number of doses of Surfactant that can be given?

82
Q

When should Surfactant be discontinued?

A

After 48 hours or w/minimal ventilator/O2 requirement

83
Q

Name an advantage of Curosurf (versus Survanta and others)

A

It has a higher concentration, so less volume to lung, infant may handle it better

84
Q

Is the dosing frequency the same among types of survanta?

A

No, some are 8 hrs, some are 12 hrs, etc.

85
Q

What are some complications of surfactant? (7)

A
  1. Quickly improved lung compliance and FRC
  2. Air leak syndrome
  3. Lung injury
  4. Pulmonary Hemorrhage
  5. Plugging of ETT
  6. Administration to one lung
  7. Lack of response
86
Q

In pulmonary hypoplasia are both lungs or just one lung affected?

A

either both or one :-)

87
Q

what 2 common conditions mentioned in lecture might lead to pulmonary hypoplasia?

A
  1. CDH

2. Renal Anomalies

88
Q

True/false: it is often difficult to diagnose the severity of pulmonary hypoplasia?

89
Q

Is pulmonary hypoplasia fatal in preemies?

A

Yes, usually

90
Q

What 5 types of anomalies can cause pulmonary hypoplasia?

A
  1. Space occupying lesions (CDH, CCAM, Effusion)
  2. Oligohydramnios (Renal anomalies, PPROM)
  3. Skeletal anomalies (OI)
  4. Neuromuscular (anencephaly)
  5. Cardiac (HLHS, HRHS, pulmonary stenosis, ebstein’s)
91
Q

What is the risk of pulm. hypoplasia if PPROM occurs:
15 wks, ____%
19 wks, ____%
After 26 wks, ____%

A

80%
50%
near 0%

92
Q

What is the treatments of PPROM? (2)

A
  1. Amnioinfusion

2. Tracheal Occlusion

93
Q

What are the risks of Amnioinfusion? (2)

A
  1. Chorioamnionitis

2. Abruption

94
Q

What is the benefit of amnioinfusion?

A

Increasing latency period & stimulating fetal lung growth

95
Q

What should happen if Tracheal Occlusion is performed?

A

Delivery within 1 week

96
Q

What happens with tracheal occlusion?

A

Increased lung blood flow and increased fetal lung volume (it’s controversial)

97
Q

True/False: Impairment of lung development directly corresponds to time in gestation when these structures are developing

98
Q

What are 7 signs of Pulmonary Hypoplasia?

A
  1. Immediate signs of RDS & cyanosis
  2. Small or bell-shaped thorax
  3. Flattening of faces or deformation ie. contractures
  4. Resp Failure (w/in minutes)
  5. Hypercarbia
  6. Pulmonary Hypertension
  7. Pneumothorax
99
Q

What is the treatment for pulmonary hypoplasia? (7)

A
  1. Supportive, similar to RDS
  2. Assisted ventilation (HFO-is gentler, less expansion)
  3. Exogenous Surfactant replacement
  4. Decompression of pneumo
  5. iNO
  6. ECMO (if reversible-if not, it is a contraindication to ECMO)
100
Q

What is the incidence of Pneumonia in infants w/resp distress (mostly term)?

101
Q

Pneumonia is the ____ most likely cause of resp distress?

102
Q

What are the previously common pathogens to cause pneumonia?

A

GBS, E-Coli, H. influenza

103
Q

What are the most recent pathogens to cause pneumonia?

A

E-Coli, GBS, CONS

104
Q

Clinical signs of Pneumonia are indistinguishable from what?

A

RDS

-there’s surfactant deficiency

105
Q

Bacterial pneumonia is usually accompanied by what?

106
Q

True/False: the clinical signs of pneumonia include those of RDS, sepsis, shock

107
Q

What are 2 signs of shock/sepsis?

A

Poor perfusion

hypotension

108
Q

With pneumonia, what would you see on CBC?
CRP?
Blood culture?

A 
Leukopenia
Increased
Could have low yield 
                      (w/maternal abx)
Tracheal culture
109
Q

What would an x-ray taken later in Pneumonia course look like?

A

Infiltrates

110
Q

What is the tx of pneumonia?

A 
Abx
  -Amp/Gent (broad range and synergistic effect)
  -Narrow if org. ID'd
Exogenous Surfactant
Respiratory Support

Neo Pathophys 2 (20 decks)

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